Sam Dagogo-Jack Eds. Diabetes Mellitus in Developing Countries and Underserved Communities

Diabetes Mellitus in
Developing Countries
and Underserved
Communities
Sam Dagogo-Jack
Editor
123
Diabetes Mellitus in Developing
Countries and Underserved
Communities
Sam Dagogo-Jack
Editor
Diabetes Mellitus in
Developing Countries
and Underserved
Communities
Editor
Sam Dagogo-Jack
University of Tennessee Health
Science Center
Memphis, Tennessee
USA
ISBN 978-3-319-41557-4 ISBN 978-3-319-41559-8 (eBook)

DOI 10.1007/978-3-319-41559-8
Library of Congress Control Number: 2016959999
Springer International Publishing Switzerland 2017

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way,
and transmission or information storage and retrieval, electronic adaptation, computer software,
or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in
this book are believed to be true and accurate at the date of publication. Neither the publisher nor
the authors or the editors give a warranty, express or implied, with respect to the material
contained herein or for any errors or omissions that may have been made.
Printed on acid-free paper
This Springer imprint is published by Springer Nature

The registered company is Springer International Publishing AG Switzerland
The registered company address is Gewerbestrasse 11, 6330 Cham, Switzerland
This volume is dedicated to all persons who struggle with the
syndrome of diabetes mellitus, the global community of
clinicians who manage diabetes, and the researchers dedicated
to finding better methods for the treatment, prevention, and,
ultimately, cure of diabetes mellitus.
Preface
No other disorder exerts a more pervasive and catholic global burden on

humanity and society than does diabetes. The current diabetes epidemic is
felt on all continents, by all ethnic groups, among the rich and poor, and
across gender and age groups. In the first Global Diabetes Report released in
2016, the World Health Organization noted that diabetes is no longer a dis-
ease of predominantly rich nations and that the prevalence of diabetes is
steadily increasing everywhere, most markedly in the worlds middle-income
countries. There were an estimated 108 million adults with diabetes globally
in 1980. By 2014, that number had risen to 422 million adults, and the global
estimate is projected to increase to 592 million adults with diabetes by 2035.
Sadly, low- and middle-income countries are projected to experience the
steepest increase as they transition to lower-middle and upper-middle income
status. The complications of diabetes, such as blindness, kidney failure,
amputations, heart disease, stroke, and mortality, are a personal tragedy as
well as a threat to national and global security, through their negative effects
on the vitality and economic productivity of afflicted citizens.
Low- and middle-income countries have limited resources for dealing
with the costs of controlling diabetes and its complications. Even in the
developed economies, the quality of diabetes control is suboptimal for
approximately 50 % of the affected population. Moreover, socioeconomically
vulnerable demographic subgroups have always existed in North America,
Europe, Australia, and New Zealand; individuals from those groups often
experience disparities in diabetes prevalence, quality of care, and outcomes.
Autochthonous or aboriginal people and migrant groups predominate among
the vulnerable and often underserved populations with regard to diabetes.
The chronic low-grade human migration trends (usually from lower-income
to upper-income regions) have escalated exponentially as a result of recent
geopolitical upheavals. The flood of new immigrants to Europe and elsewhere
has added to the challenges of providing optimal diabetes care in a setting of
rapid cultural, linguistic, and socioeconomic metamorphosis.
Diabetes Mellitus in Developing Countries and Underserved Communities,
a global textbook of diabetes, presents a detailed consideration of the epide-
miology, genomic landscape, clinical presentation, complications, manage-
ment, and prevention of diabetes in all regions of the world. The regions
covered include sub-Saharan Africa, the Middle East and North Africa,
Eastern Europe, China and the Western Pacific, India and Southeast Asia,
Latin America and the Caribbean, as well as Australia, New Zealand, North
vii
viii Preface
America, and Western Europe. In the latter more affluent regions, appropriate
focus is placed on vulnerable indigenous and immigrant populations.
Additional attention is given to a description of regional coordination of dia-
betes care, diabetes prevention services, preferences and imperatives regard-
ing pharmacotherapy, and the status of diabetes research. The chapters
conclude with the identification of future directions, unmet needs, unan-
swered questions, or even unquestioned answers, with regard to diabetes in
specific regions.
The availability, in a single volume, of comprehensive information on the
peculiarities of diabetes pathophysiology, genetics, and best practices in
major regions of the world, crafted by leading authorities in the field, is a
valuable resource for clinicians, researchers, scholars, public health leaders,
students, and everyone interested in diabetes. The authors are to be com-
mended for their hard work in creating this informed and informative treatise
on global diabetes.
The conceptual insight of Kristopher Spring (editor, Clinical Medicine)
and logistical support from Ms. Saanthi Shankhararaman (project coordina-
tor), both at Springer, greatly facilitated the creation of this book. Much grati-
tude is owed to them for their professionalism and engagement that resulted
in the successful execution of the book project.
Memphis, TN, USA Sam Dagogo-Jack

Contents
1 The Global Burden of Diabetes: An Overview . . . . . . . . . . . . . . . . 1

William H. Herman
2 Primary Prevention of Type 2 Diabetes: An Imperative
for Developing Countries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
Sam Dagogo-Jack
3 Diabetes in Sub-Saharan Africa . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Felix Assah and Jean Claude Mbanya
4 Type 2 Diabetes in the Middle East and
North Africa (MENA) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
Yasmin Khan and Osama Hamdy
5 Diabetes in China and the Western Pacific Region . . . . . . . . . . . 63
Juliana C.N. Chan, Elaine Y.K. Chow, and
Andrea A.O. Luk
6 Diabetes in India and Southeast Asia . . . . . . . . . . . . . . . . . . . . . . 85
Shashank R. Joshi and S.R. Aravind
7 Diabetes in Latin America . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
Omar Y. Bello-Chavolla and Carlos A. Aguilar-Salinas
8 Diabetes in the Caribbean . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Michael S. Boyne
9 Diabetes in Indigenous Australians and Other
Underserved Communities in Australia . . . . . . . . . . . . . . . . . . . 151
Stephen Colagiuri
10 Diabetes Among Mori and Other Ethnic Groups
in New Zealand . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
Evan Atlantis, Grace Joshy, Margaret Williams,
and David Simmons
11 Diabetes in Eastern Europe . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
Mykolay Khalangot, Vitaliy Gurianov,
Alexander Vaiserman, Ieva Strele, Vasile Fedash,
and Victor Kravchenko
ix
x Contents
12 Diabetes in Ethnic Minorities and Immigrant

Populations in Western Europe . . . . . . . . . . . . . . . . . . . . . . . . . . 225
Oliver Razum and Helmut Steinberg
13 Diabetes Among Indigenous Canadians . . . . . . . . . . . . . . . . . . . 235
Sudaba Mansuri and Anthony J. Hanley
14 Diabetes in Native Populations and Underserved
Communities in the USA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251
Joshua J. Joseph and Sherita Hill Golden
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285
Contributors
S.R. Aravind, MBBS, DNB, FRCP, FDRC, DHA, FRSSDI Columbia

Asia Hospital, Yeshwanthpur, Bangalore, India
Felix Assah, MD, PhD Faculty of Medicine and Biomedical Sciences,
University of Yaound I, Yaound, Cameroon
Evan Atlantis, PhD Western Sydney University, Campbelltown, NSW,
Australia
Omar Y. Bello-Chavolla Department of Endocrinology and Metabolism,
Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn,
Mexico City, Mexico
Facultad de Medicina, Universidad Nacional Autnoma de Mxico, Mexico
City, Mexico
Michael S. Boyne, MD, FRCPC Tropical Metabolism Research Unit,
Tropical Medicine Research Institute, The University of the West Indies,
Mona, Kingston, Jamaica
Juliana C.N. Chan, MD, FRCP The Chinese University of Hong Kong,
Prince of Wales Hospital, Shatin, Hong Kong, China
Elaine Y.K. Chow, MBChB, PhD Department of Medicine and Therapeutics,
Hong Kong Institute of Diabetes, Hong Kong, SAR, China
Obesity and Li Ka Shing Institute of Health Sciences, The Chinese University
of Hong Kong, Prince of Wales Hospital, Hong Kong, SAR, China
Stephen Colagiuri, MD W.H.O. Collaborating Centre on Physical Activity,
Nutrition and Obesity, The University of Sydney, Sydney, NSW, Australia
Sam Dagogo-Jack, MD, MBBS, MSc, FRCP, FACP, FACE Division of
Endocrinology, Diabetes & Metabolism, University of Tennessee Health
Science Center, Memphis, TN, USA
Vasile Fedash, MD, PhD Institute of Physiology and Sanocreatology of
ASM, Chisinau, Moldova
Sherita Hill Golden, MD, MHS Department of Medicine, Johns Hopkins
University School of Medicine, Baltimore, MD, USA
xi
xii Contributors
Vitaliy Gurianov, PhD Bogomolets National Medical University, Kyiv,

Ukraine
Osama Hamdy, MD, PhD, FACE Joslin Diabetes Center, Harvard Medical
School, Boston, MA, USA
Anthony J. Hanley, PhD Departments of Nutritional Sciences and Public
Health Sciences, Faculty of Medicine, University of Toronto, Toronto, ON,
Canada
William H. Herman, MD, MPH University of Michigan, Ann Arbor, MI,
USA
Joshua J. Joseph, MD Division of Endocrinology, Diabetes and Metabolism,
Johns Hopkins University School of Medicine, Baltimore, MD, USA
Shashank R. Joshi, MD, DM, FICP, FACP, FACE, FRCP Joshi Clinic,
Lilavati & Bhatia Hospital, Mumbai, India
Grace Joshy, PhD Australian National University, Canberra, ACT, Australia
Mykolay Khalangot, MD, Sc D Shupyk National Academy of Postgraduate
Medical Education, Kyiv, Ukraine
Yasmin Khan, MD, MPH Adult Diabetes Section, Joslin Diabetes Center,
Boston, MA, USA
Victor Kravchenko, Sc D Komisarenko Institute of Endocrinology and
Metabolism, National Academy of Medical Sciences, Kyiv, Ukraine
Andrea A.O. Luk, MBBS, MRCP Department of Medicine and Therapeutics,
Hong Kong Institute of Diabetes, Hong Kong, SAR, China
Obesity and Li Ka Shing Institute of Health Sciences, The Chinese University
of Hong Kong, Prince of Wales Hospital, Hong Kong, SAR, China
Sudaba Mansuri Department of Nutritional Sciences, Faculty of Medicine,
University of Toronto, Toronto, ON, Canada
Jean Claude Mbanya, MD, PhD, FRCP Faculty of Medicine and Biomedical
Sciences, University of Yaounde I, Yaounde, Cameroon
Oliver Razum Fakultt frGesundheitswissenschaften, Universitt Bielefeld,
School of Public Health, Bielefeld, Germany
Carlos A. Aguilar Salinas Departamento de Endocrinologia y Metabolismo,
Instituto Nacional de CienciasMdicas y Nutricion, Mexico City, Mexico
Christopher D. Saudek, MD Division of Endocrinology, Diabetes and
Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD,
USA
David Simmons, MBBS, MA, FRACP, FRCP, MD Western Sydney University,
Campbelltown, NSW, Australia
Contributors xiii
Helmut Steinberg, MD Department of Medicine, Division of Endocrinology,

Diabetes and Metabolism, University of Tennessee Health Science Center,
Memphis, TN, USA
Ieva Strele, MD, PhD Riga Stradins University, Riga, Latvia
Alexander Vaiserman, Sc D Chebotariov Institute of Gerontology, National
Academy of Medical Sciences, Kyiv, Ukraine
Margaret Williams, PhD Auckland University of Technology, Auckland,
New Zealand
About the Editor
Sam Dagogo-Jack, MD, is Professor of

Medicine and Chief of the Division of
Endocrinology, Diabetes and Metabolism at
the University of Tennessee Health Science
Center, Memphis, Tennessee, where he holds
the A. C. Mullins Endowed Chair in
Translational Research. He is also Director of
the Endocrinology Fellowship Training
Program and Director of the General Clinical
Research Center at UTHSC. A global citizen,
Dr. Dagogo-Jack has studied, practiced,
researched, and/or taught medicine and dia-
betology in Africa, Asia, Australia, Europe, North and South America,
Caribbean countries, and the Middle East. His current research focuses on the
interaction of genetic and environmental factors in the prediction and preven-
tion of prediabetes and diabetes. Dr. Dagogo-Jack is a recipient of the Banting
Medal for Leadership from the American Diabetes Association and the
Distinction in Endocrinology Award from the American College of
Endocrinology. He served as the 2015 President, Medicine & Science, of the
American Diabetes Association.
xv
The Global Burden of Diabetes:
An Overview 1
William H. Herman
Introduction [5]. Whatever the causes, the estimates are con-

servative, and the future burden of diabetes is
The global burden of diabetes is enormous and likely to be even greater than projected.
growing. Between 1997 and 2010, four research In 2015, the International Diabetes Federation
groups estimated the numbers of people with dia- (IDF) estimated that globally, 415 million adults
betes globally and projected the future burden of 2079 years of age or 8.8 % of the adult popula-
diabetes (Fig. 1.1) [14]. In each instance, the pre- tion have diabetes [5]. There are 321 million
vious estimate was shown to have underestimated people of working age (2064 years) with diabe-
the number of people with diabetes, and the pro- tes and 94 million people aged 6579 with diabe-
jections painted an ever more alarming picture of tes. There are slightly more men than women
the future burden of diabetes. The latest study with diabetes (215 million men vs. 200 million
estimated that between 2010 and 2030, the num- women). Currently, there are more people with
ber of adults with diabetes worldwide would diabetes in urban areas (270 million) than in rural
increase by 54 %, from 285 million to 439 million areas (145 million). Age-adjusted diabetes preva-
[4]. Much of the growth in the numbers of people lence rates among adults 2079 years of age vary
with diabetes would occur in middle-aged work- by region and by country. In 2015, the age-
ing adults [4]. The number of adults with diabetes adjusted diabetes prevalence was 11.5 % in North
would increase by 20 % in developed countries America and the Caribbean, 10.7 % in the Middle
and by 69 % in developing countries [4]. A part of East and North Africa, 9.6 % in South and Central
the increase in the number of people with diabetes America, 8.8 % in the Western Pacific and
worldwide is due to increased incidence of type 2 Southeast Asia, 7.3 % in Europe, and 3.8 % in
diabetes related to urbanization, obesogenic diets, Africa [5]. Perhaps most alarmingly, approxi-
and decreased physical activity [5]. A larger part mately 75 % of people with diabetes live in low-
of the increase is due simply to population growth, and middle-income countries [5].
aging of the population, and decreased mortality Diabetes prevalence rates vary greatly among
indigenous communities. These communities are
characterized by unique languages, knowledge
systems, and beliefs [5]. Many have a special
W.H. Herman, MD, MPH
Departments of Internal Medicine and Epidemiology, relationship with their traditional land which
University of Michigan, often has a fundamental importance for their cul-
1000 Wall Street, Room 6108/SPC 5714, Ann Arbor, ture [5]. In many cases, the prevalence of diabe-
MI 48105-1912, USA tes is greater in indigenous populations than in
e-mail: [email protected]
Springer International Publishing Switzerland 2017 1

S. Dagogo-Jack (ed.), Diabetes Mellitus in Developing Countries and Underserved Communities,
DOI 10.1007/978-3-319-41559-8_1
2 W.H. Herman
500
450
400
350 Amos, McCarty & Zimmet, 1997
300
Millions
King, Aubert & Herman, 1998

250
200 Wild, Roglic, Green, Sicree & King,
2004
150
Shaw, Sicree & Zimmet, 2010
100
50
0
1990 2000 2010 2020 2030 2040
Year
Fig. 1.1 Global estimates and projections of the number of people with diabetes
the surrounding population such as in indige- in diabetes prevalence will occur in regions where
nous Australian [6], New Zealand Mori [7], economies are moving from low-income to mid-
Greenland Inuit [8], Canadian Inuit [9], and dle-income levels. By 2040, the IDF has estimated
Native American populations [10]. Some indig- that the age-adjusted prevalence of diabetes will
enous populations that still live very traditional be 12.0 % in North America, 9.7 % in South and
lifestyles have a relatively low prevalence of dia- Central America, 9.0 % in the Western Pacific,
betes [5]. 9.1 % in Southeast Asia, 7.6 % in Europe, and
Not every person with diabetes has been diag- 4.2 % in Africa [5].
nosed. Globally, it is estimated that one-in-two The global epidemic of type 2 diabetes has
adults with diabetes is undiagnosed [5]. In major implications for healthcare expenditures.
regions where healthcare resources are lacking Most countries dedicate between 5 % and 20 % of
such as in sub-Saharan Africa, the proportion of their total healthcare resources to treat diabetes
people with diabetes who are undiagnosed is as and its complications [5]. In 2015, the IDF esti-
high as 67 % [5]. Even in high-income regions mated that total diabetes healthcare expenditures
such as North America, slightly more than one- for persons 2079 years of age were $673 billion
third of people with diabetes have not been diag- or 12 % of total healthcare expenditures world-
nosed [5]. Globally, 81 % of people with diabetes wide [5]. The IDF has projected that this number
who are undiagnosed live in low- and middle- will increase to $802 billion by 2040 assuming
income countries [5]. constant per capita healthcare expenditures [5].
The IDF has estimated that by 2040, 642 mil- The increase in healthcare expenditures for diabe-
lion adults 2079 years of age or 10.4 % of the tes by 2040 is projected to be proportionately
world population will have diabetes [5]. In 2040, less than the increase in the number of people
proportionately more people with diabetes will be with diabetes because countries with the largest
6579 years of age. The gender difference increases in the numbers of people with diabetes
between men and women is expected to decrease are those with the lowest per capita spending for
modestly by 2040, but the global difference in the diabetes. In 2015, an average of $1,622 was spent
number of people with diabetes in urban and rural per person with diabetes [5]. The range in expen-
areas is expected to widen with 478 million peo- ditures for diabetes varied by almost 85-fold:
ple with diabetes living in urban areas and 164 from $7,859 per person per year in North America
million living in rural areas. The largest increases and the Caribbean, $2,610 in Europe, $1,169 in
1 The Global Burden of Diabetes: An Overview 3
South and Central America, $693 in the Western increased demand for and access to expensive but
Pacific, $483 in the Middle East and North Africa, lifesaving care. As low- and middle-income coun-
$243 in Africa, and $93 in Southeast Asia [5]. tries develop economically, the demand for and
Not surprisingly, these dramatic differences in per capita expenditures for the treatment of diabe-
mean annual healthcare expenditures per person tes and its complications will increase substan-
with diabetes are associated with major differ- tially. The future costs of healthcare for diabetes
ences in the types of expenditures for diabetes. In are likely to be many times higher than projected
developed countries where mean annual health- by the IDF and, if costs remain unchecked, have
care expenditures are high, a large absolute the potential to bankrupt healthcare systems and
amount but a small proportion of total healthcare indeed national economies.
expenditures are for antihyperglycemic therapy What can be done? All countries, but especially
[11]. The greatest proportion of healthcare expen- low- and middle-income countries with limited
ditures for diabetes go for the treatment of com- resources, must carefully balance the benefits and
plications and comorbidities. In contrast, in costs of allocating scarce healthcare resources for
developing countries where mean annual health- population-level and targeted interventions for
care expenditures are low, the greatest proportion diabetes prevention, for antihyperglycemic and
of expenditures go for antihyperglycemic therapy cardiovascular therapies to delay or prevent the
[11]. Although some resources go to the treat- development of complications among people with
ment of acute metabolic and infectious complica- diabetes, and for the treatment of advanced dia-
tions, little is spent on the treatment of chronic betic complications. Addressing only the health-
complications and comorbidities such as renal care needs of individuals with diagnosed diabetes
and cardiovascular disease. will leave the epidemic of type 2 diabetes and its
Economic development is associated with downstream complications, comorbidities, and
increased per capita healthcare expenditures. In a costs unchecked. Clearly, tailored strategies that
recent study, Seuring and colleagues examined allocate resources to prevent diabetes, to treat dia-
the factors associated with the heterogeneity in betes, and to treat its complications and comor-
diabetes healthcare expenditures among coun- bidities will be required.
tries [12]. Their work demonstrated that the direct Population-level policy interventions address-
costs of diabetes are positively associated with a ing food supply, the built environment, tax pol-
countrys per capita gross domestic product icy, and financial incentives and disincentives all
(GDP). Healthcare expenditures increase with offer great promise in addressing the obesogenic
national economic wealth. Per capita GDP and diabetogenic environment at a relatively low
explained about one-third of the variation in dia- cost. Examples abound in the area of tobacco
betes healthcare expenditures among countries control [14]. Unfortunately, there are many dif-
such that every additional dollar in per capita ferences between smoking, diet, and physical
GDP translated into an average increase in direct activity and the evidence base for population-
diabetes expenditures of about $0.04 [12]. level interventions for diabetes prevention is
This phenomenon is further illustrated by a limited.
study that assessed rates of end-stage renal dis- The evidence base for targeted interventions
ease (ESRD) treatment by national wealth [13]. In to delay or prevent the development of type 2 dia-
low- and middle-income countries with per capita betes is extensive, robust, and consistent. At least
GDP less than ~$10,000, rates of ESRD treatment four trials from China [15], Finland [16], the
were very low but tended to increase with per United States [17], and India [18] have demon-
capita GDP. In contrast, in high-income countries strated that lifestyle interventions that achieve a
with per capita GDP above ~$10,000, rates of 57 % reduction in initial body weight and
ESRD treatment were consistently higher, reflect- increase brisk walking to approximately 150 min
ing greater access to ESRD treatment. Economic per week can reduce the incidence of type 2 dia-
development thus appeared to be associated with betes by 2958 % in high-risk individuals with
4 W.H. Herman
impaired glucose tolerance. Other trials have change from glucose to HbA1c possible in all popula-
tions? J Clin Endocrinol Metab. 2010;95:E3336.
demonstrated the efficacy of metformin [17, 18],
9. Diabetes in Canada: facts and figures from a public
alpha-glucosidase inhibitors [19, 20], and thia- health perspective. Ottawa Ont: Public Health Agency
zolidinediones [2123] for diabetes prevention. of Canada; 2011.
Unfortunately, such interventions required sub- 10. Lee ET, Howard BV, Savage PJ, Cowan LD, Fabsitz
RR, Oopik AJ, Yeh J, Go O, Robbins DC, Welty
stantial resources to identify at-risk individuals,
TK. Diabetes and impaired glucose tolerance in three
to implement interventions, and to maintain long- American Indian populations aged 4574 years. The
term adherence. In addition, the evidence that Strong Heart Study. Diabetes Care. 1995;18:599610.
targeted interventions can be translated into long- 11. Zhang P, Zhang X, Brown J, Vistisen D, Sicree R,
Shaw J, Nichols G. Global healthcare expenditure on
term clinical practice in large, less highly selected
diabetes for 2010 and 2030. Diabetes Res Clin Pract.
populations is lacking. 2010;87:293301.
The challenge is clear. As reported by the IDF, 12. Seuring T, Archangelidi O, Suhrcke M. The economic
Type 2 diabetes is a global epidemic with devas- costs of type 2 diabetes: a global systematic review.
Pharmacoeconomics. 2015;33:81131.
tating humanitarian, social, and economic conse-
13. Grassmann A, Gioberge S, Moeller S, Brown G. End-
quences [5]. We must understand the global stage renal disease: global demographics in 2005 and
burden of diabetes to increase awareness, to plan observed trends. Artif Organs. 2006;30:8957.
for future needs, and to inform interventions. An 14. Reducing risks and preventing disease: population-
wide interventions. In: World Health Organization
understanding of the present and future burden of
(editor). Global status report on noncommunicable
diabetes in developing countries and underserved diseases 2010. Chapter 4. Geneva; 2011. http://www.
communities is essential to this task. who.int/nmh/publications/ncd_report2010/en/ .
Accessed 5 Jan 2016.
15. Pan XR, Li GW, Hu YH, et al. Effects of diet and
exercise in preventing NIDDM in people with
References impaired glucose tolerance. The Da Qing IGT and
Diabetes Study. Diabetes Care. 1997;20:53744.
1. Amos AF, McCarty DJ, Zimmet P. The rising global 16. Tuomilehto J, Lindstrm J, Eriksson JG, Finnish
burden of diabetes and its complications: estimates Diabetes Prevention Study Group, et al. Prevention of
and projections to the year 2010. Diabet Med. 1997;14 type 2 diabetes mellitus by changes in lifestyle among
Suppl 5:S185. subjects with impaired glucose tolerance. N Engl
2. King H, Aubert RE, Herman WH. Global burden of J Med. 2001;344:134350.
diabetes, 19952025: prevalence, numerical estimates 17. Knowler WC, Barrett-Connor E, Fowler SE, Diabetes
and projections. Diabetes Care. 1998;21:141431. Prevention Program Research Group, et al. Reduction in
3. Wild S, Roglic G, Green A, Sicree R, King H. Global the incidence of type 2 diabetes with lifestyle interven-
prevalence of diabetes: estimates for the year 2000 tion or metformin. N Engl J Med. 2002;346:393403.
and projections for 2030. Diabetes Care. 18. Ramachandran A, Snehalatha C, Mary S, Mukesh B,
2004;27:104753. Bhaskar AD, Vijay V, Indian Diabetes Prevention
4. Shaw JE, Sicree RA, Zimmet PZ. Global estimates of Programme (IDPP). The Indian Diabetes Prevention
the prevalence of diabetes for 2010 and 2030. Diabetes Programme shows that lifestyle modification and met-
Res Clin Pract. 2010;87:414. formin prevent type 2 diabetes in Asian Indian sub-
5. International Diabetes Federation. IDF diabetes atlas. jects with impaired glucose tolerance (IDPP-1).
7th ed. Brussels: International Diabetes Federation; Diabetologia. 2006;49:28997.
2015. http://www.diabetesatlas.org. Accessed 5 Jan 19. Chiasson JL, Josse RG, Gomis R, Hanefeld M,
2015. Karasik A, Laakso M, STOP-NIDDM Trail Research
6. Minges KE, Zimmet P, Magliano DJ, Dunstan DW, Group. Acarbose for prevention of type 2 diabetes
Brown A, Shaw JE. Diabetes prevalence and determi- mellitus: the STOP-NIDDM randomised trial. Lancet.
nants in Indigenous Australian populations: a system- 2002;359:20727.
atic review. Diabetes Res Clin Pract. 2011;93:13949. 20. Kawamori R, Tajima N, Iwamoto Y, Kashiwagi A,
7. Coppell KJ, Mann JI, Williams SM, Jo E, Drury PL, Shimamoto K, Kaku K, Voglibose Ph-3 Study Group.
Miller J, et al. Prevalence of diagnosed and undiag- Voglibose for prevention of type 2 diabetes mellitus: a
nosed diabetes and prediabetes in New Zealand: find- randomised, double-blind trial in Japanese individuals
ings from the 2008/09 Adult Nutrition Survey. N Z with impaired glucose tolerance. Lancet. 2009;373:
Med J. 2013;126:2342. 160714.
8. Jrgensen ME, Bjerregaard P, Borch-Johnsen K, 21. Buchanan TA, Xiang AH, Peters RK, et al.
Witte D. New diagnostic criteria for diabetes: is the Preservation of pancreatic beta-cell function and pre-
1 The Global Burden of Diabetes: An Overview 5
vention of type 2 diabetes by pharmacological treat- fasting glucose: a randomised controlled trial. Lancet.
ment of insulin resistance in high-risk hispanic 2006;368:1096105. Erratum in: Lancet 2006;
women. Diabetes. 2002;51:2796803. 368:1770.
22. DREAM (Diabetes REduction Assessment with 23. DeFronzo RA, Tripathy D, Schwenke DC, ACT
ramipril and rosiglitazone Medication) Trial NOW Study, et al. Pioglitazone for diabetes preven-
Investigators, Gerstein HC, Yusuf S, Bosch J, et al. tion in impaired glucose tolerance. N Engl J Med.
Effect of rosiglitazone on the frequency of diabetes in 2011;364:110415. Erratum in: N Engl J Med
patients with impaired glucose tolerance or impaired 2011;365:189. N Engl J Med 2011;365:869.
Primary Prevention of Type 2
Diabetes: An Imperative 2
for Developing Countries
Sam Dagogo-Jack
Introduction again with the fastest increases occurring in

developing countries. Although sub-Saharan
In 2015, the International Diabetes Federation Africa (SSA) currently has the lowest estimate
(IDF) estimated that 415 million adults had dia- for diabetes prevalence, the steepest proportion-
betes worldwide (1). Type 2 diabetes mellitus ate increase in diabetes (240 %) is projected to
(T2DM) accounts for 9095 % of all diabetes occur in that region [1] (Fig. 2.1). In contrast,
cases. The 2015 IDF estimates for people with recent data indicate that the incidence of diabetes
diabetes in regions of the world (descending is leveling off in the United States of America,
order) were 153.2 million in the Western Pacific, presumably as a result of increased awareness
59.8 million in Europe, 44.3 million in North and national diabetes prevention initiatives [2].
America and the Caribbean, 35.3 million in the Furthermore, major declines in the rates of diabe-
Middle East/North Africa, and 14.2 million in tes complications have also occurred in the
sub-Saharan Africa [1]. The country-specific United States [3]. Unfortunately, these encourag-
estimates showed that the top 10 nations with the ing developments in the United States are not
highest numbers of people with diabetes are shared by most regions of the world, where the
China (109.6 million), India (99.2 million), the escalating prevalence of diabetes and ravages
United States of America (29.3 million), Brazil from the disease persist inexorably [1, 46].
(14.3 million), the Russian Federation (12.1 mil-
lion), Mexico (11.5 million), Indonesia (10 mil-
lion), Egypt (7.8 million), Japan (7.2 million), Risk Factors for Type 2 Diabetes
and Bangladesh (7.1 million) [1]. Thus, countries
in the developing economies contribute dispro- Both genetic and environmental factors underlie
portionately to the escalating global diabetes bur- the development of T2DM [6, 7]. To date, more
den (13). By 2040, the number of adults with than 60 gene variants associated with T2DM
diabetes is projected to increase to 642 million, have been identified; however, the effect size of
these individual gene variants is rather modest
[812]. The environmental risk factors strongly
associated with T2DM risk include obesity, phys-
S. Dagogo-Jack, MD, MBBS, MSc, FRCP,
FACP, FACE ical inactivity, history of gestational diabetes,
Division of Endocrinology, Diabetes & Metabolism, hypertension, and dyslipidemia, among others
University of Tennessee Health Science Center, (Table 2.1) [6, 7, 13]. These risk factors interact
920 Madison Avenue, Memphis, TN 38163, USA with genetic predisposition (indicated by a family

DOI 10.1007/978-3-319-41559-8_2
8 S. Dagogo-Jack
Fig. 2.1 Projected

55%
increases in diabetes
WORLD
prevalence in different
regions of the world, 642
20152040 (Source:
International Diabetes million
Federation [1]) people
living with
diabetes
WORLD
415 Africa 141%
million Middle East & North Africa 104%
South East Asia 82%
South and Central America 65%
Western Pacific 40%
Europe 19%
North America & Caribbean 37%
2015 2040
history of diabetes and/or high-risk ethnic heri- Table 2.1 Risk factors for type 2 diabetes
tage) to promote the development of diabetes. Physical inactivity
Such a phenomenon was clearly demonstrated in Overweight/obesity
the studies that showed a threefold increase in the First-degree relative with diabetes
rate of T2DM in recent Japanese immigrants to High-risk ethnicity
the United States compared with native Japanese Gestational diabetes or delivery of a baby weighing
[14]. Since a dramatic increase in disease preva- 9 lb or greater
lence over a relatively short time frame in humans HDL cholesterol <35 mg/dl TG >250 mg/dl
is unlikely to be due to sudden new genetic muta- Hypertension (>140/90 mmHg or on therapy)
tions, environmental factors (notably changes in A1C 5.7, IGT, or IFG on previous testing
diet, physical activity, and perhaps microbial Conditions associated with insulin resistance:
acanthosis nigricans, polycystic ovary disease, etc.
flora) probably trigger the surging diabetes rates
History of cardiovascular disease
among genetically predisposed populations. The
exact mechanisms whereby these environmental
triggers induce diabetes in genetically predis- resistance, impaired insulin secretion, impaired
posed persons remain to be fully elucidated. glucagon suppression, increased lipolysis, exag-
gerated hepatic glucose production, incretin defi-
ciency/resistance, maladaptive renal glucose
Pathophysiology reabsorption, and central nervous system defects
(including impaired dopaminergic tone and dys-
Current understanding indicates that multiple regulation of satiety) [1517] (Fig. 2.2). Insulin
pathophysiological defects underlie T2DM. resistance can be inherited or acquired. Obesity,
Generally, at least eight unique pathophysiological aging, physical inactivity, overeating, increased
defects are currently recognized in T2DM: insulin lipolysis, and accumulation of excessive amounts
2 Primary Prevention of Type 2 Diabetes: An Imperative for Developing Countries 9
Fig. 2.2 The major

pathophysiological Insulin
defects that lead to the resistance
Im
in d
p
m se
development and se aire
e
pa ea
progression of type 2 cre d i
do ecr
tio nsu
diabetes. Many of the n lin
D
same defects (notably
Increased glucose
insulin resistance,
impaired insulin
reabsorption
secretion, lipolysis,
Increased
lipolysis
and subnormal incretin
response) at some
Hyperglycemia
degree of expression
have also been
described in people
with prediabetes
cr go d
se ca ase
et n
Incr
n
e
gl cre
def tin
io
ic
In
res iency
u
ista /
nce Increased hepatic
glucose production
of nonesterified (free) fatty acids are known causes the formation of intracellular DAG. Thus, multiple
of insulin resistance. Normally, cytoplasmic long- metabolic pathways link intracellular glucose
chain fatty acids are transported into mitochondria abundance (usually derived from carbohydrate
as long-chain fatty acyl coenzyme A (LCFA-CoA) consumption) to impaired fat oxidation, fatty acid
for beta-oxidation, a process that is gated by carni- synthesis, accumulation of long-chain fatty acids,
tine palmitoyl transferase (CPT)-1 and CPT-2 (the risk of lipotoxicity, and insulin resistance (Fig. 2.3).
shuttle enzymes located in the outer and inner Among the potent interventions that have been
mitochondrial membrane). This shuttle process demonstrated to ameliorate the pathological cellu-
ensures that fatty acids do not accumulate exces- lar and molecular processes leading to insulin
sively in the cytoplasm. Inhibition of that process resistance are caloric restriction (reduction of car-
leads to intracellular accumulation of long-chain bohydrate and fat intake), physical activity, and
fatty acids, which can induce lipotoxicity, cellular weight loss [1927].
dysfunction, and cell death [16, 17]. Further, intra-
cellular accumulation of long-chain fatty acids
along with diacylglycerol (DAG) can activate cer- Prediabetes
tain isoforms of protein kinase C (PKC), leading
to aberrant phosphorylation of the insulin receptor The term prediabetes refers to impaired glu-
and consequent insulin resistance. cose tolerance (IGT) and impaired fasting glu-
Acetyl-CoA, a product of glycolysis in the cose (IFG), two intermediate metabolic states
Krebs cycle, can be converted to malonyl CoA by between normal glucose tolerance and diabetes.
the enzyme acetyl-CoA carboxylase (ACC). IGT is defined by a plasma glucose level of
Malonyl-CoA is the activated two-carbon donor 140 mg/dl to 199 mg/dl (7.811.1 mmol/l), 2 h
required for fatty acid synthesis. Malonyl-CoA following ingestion of a 75-g oral solution. IFG is
also is a potent inhibitor of CPT-1, thereby block- defined by a fasting plasma glucose level of 100
ing the delivery and oxidation of fatty acids in the 125 mg/dl (5.66.9 mmol/l) [13] (Fig. 2.4). There
mitochondria. The result is accumulation of long- is considerable overlap in the risk factors and
chain fatty acids in the cytosol and eventual lipo- pathophysiological defects that underlie T2DM
toxicity [17, 18]. Glucose abundance also increases and prediabetes. Although the exact sequence of
10 S. Dagogo-Jack
Insulin
Insulin receptor
Tyr
G (-)
PKC
IRS-1
PI3K
GLUT4 DAG
Akt/PKB
GLUT4
LCFA-CoA
G
(-)
Malonyl CoA CPT
Krebs
ACC
cycle
Acetyl CoA
Fig. 2.3 Schematic diagram of insulin signaling path- tylpalmitoyltransferase (CPT), the mitochondrial enzyme
ways and interactions with glucose (G) and fatty acid that transports long-chain fatty acids (LCFA) into the inner
metabolism. Increased intracellular glucose flux generates mitochondrial space for oxidation. The resultant accumu-
acetyl coenzyme A molecules which can be converted to lation of LCFA in the cytosol is linked to insulin resistance
malonyl coenzyme, a process catalyzed by acyl coenzyme via mechanisms involving protein kinase C (PKC) and
A carboxylase (ACC). Malonyl coenzyme A inhibits carni- altered phosphorylation of the insulin receptor
evolution of individual pathophysiological following features: (1) baseline fasting plasma

defects has not been determined precisely, many glucose (FPG) and the 2-h OGTT glucose values
of the defects coevolve during the pathogenesis are positively associated with diabetes risk; (2)
of T2DM and are demonstrable even at the stage the rate of progression from IGT to T2DM was
of prediabetes (Fig. 2.1) [2838]. Estimates by exponential among subjects in the top quartile of
the Centers for Disease Control and Prevention baseline FPG but increased linearly with increas-
(CDC) in the United States indicated that there ing 2-h OGTT glucose levels; (3) incident diabe-
were ~29 million adults with diabetes and 86 mil- tes occurred at higher rates in Hispanic,
lion with prediabetes in 2014 [39]. Worldwide, Mexican-Americans, Pima, and Nauruan popula-
there are more than 400 million people with pre- tions than among Caucasians; (4) the degree of
diabetes [1]. Individuals with prediabetes prog- obesity, as measured by the BMI, predicted
ress to T2DM at an annual rate of ~10 % [31, 32]. T2DM risk in three studies with the lowest inci-
dence rates of diabetes but not in the studies that
recorded the highest incidence of T2DM; and (5)
Predictors of Progression a family history of diabetes did not predict the
from Prediabetes to Type 2 risk of progression from IGT to diabetes in these
Diabetes studies, suggesting that genetic effects probably
are fully established by the stage of IGT [40].
An analysis of six prospective studies [40] on Thus, the magnitude of fasting and post-challenge
progression from IGT to diabetes revealed the dysglycemia (a reflection of insulin action and
Fig. 2.4 Criteria for

the definition of normal Criteria for the Diagnosis of Diabetes and Prediabetes
glucose regulation and
diagnosis of prediabetes
and diabetes. FPG Normal Prediabetes Diabetes
fasting plasma glucose,
2hPG two-hour
post-load plasma
glucose, OGTT oral
Fasting FPG < 100 mg/dl 100 125 mg/dl FPG 126 mg/dl
glucose tolerance test, Glucose (<5.6 mmol/l) (5.6 6.9 mmol/l) (7.0 mmol/l)
using standard 75 g
200 mg/dl (11.1

OGTT 2hPG <140mg/dl 140 199 mg/dl mmol/l) or random
(<7.8 mmol/l) (7.8 - 11.0 mmol/l) BG 200 + typical
symptoms
HbA1c < 5.7% 5.7 6.4% HbA1c > 6.5%

HbA1c
insulin secretion), ethnicity, and weight gain are beta-cell dysfunction. The role of beta-cell dys-
major predictors of progression to T2DM. function in predicting progression to T2DM indi-
Longitudinal studies in subjects from a high- cates that interventions that prevent or replenish
risk population (Pima Indians) [41] with baseline the progressive decline in insulin secretion can be
normal glucose tolerance (NGT) indicated that expected to prevent the development of diabetes.
weight gain, insulin resistance, and progressive
loss of insulin secretory response to glucose pre-
dicted the development of T2DM [34]. Weight Predictors of Initial Transition
gain also predicted progression from NGT to IGT to Prediabetes
(5.2 kg vs. 2.6 kg in nonprogressors) and progres-
sion from IGT to T2DM during a 6-year follow-up In contrast to the numerous studies on the transi-
period [34]. The greater weight gain in the pro- tion from prediabetes to T2DM [34, 4042],
gressors was accompanied by ~ 30 % worsening of information on the incidence of prediabetes
insulin resistance and >50 % decline in acute insu- among initially normoglycemic persons is scant.
lin secretory response to intravenous glucose [34]. In a study of 254 Pima Indians with normoglyce-
Weight gain also predicted incident T2DM in mia, 79 subjects (31 %) progressed to prediabetes
African-Americans in the Atherosclerosis Risk in (IGT) during a mean follow-up period of 4 years
Communities study [42]. It follows therefore that [43]. Based on those results, the incidence of pre-
interventions that induce weight loss (e.g., diet, diabetes among Pima Indians can be estimated at
exercise, medications) could prevent progression ~8 %/year [43]. Of the 468 subjects with NGT at
from prediabetes to T2DM. In the prospective enrollment in the Baltimore Longitudinal Study
study of Pima Indians [34], progressive impair- on Aging (BLSA), over half were followed for at
ment of first-phase insulin secretion proved to be a least 10 years [44]. By 10 years, 62 % of the ini-
critical determinant of progression from NGT to tially NGT participants had progressed to predia-
IGT and from IGT to T2DM. Progression from betes, yielding an incidence rate of prediabetes
IGT to diabetes was associated with ~75 % decline 6.2 % in the BLSA cohort (96 % of whom were
in acute insulin secretory response to intravenous European-American) [44]. Dagogo-Jack et al.
glucose [34]. A high concordance rate for impaired followed 343 healthy African-American and
insulin secretion has also been reported among European-American offspring of parents with
elderly identical twins discordant for T2DM (42), T2DM in the Pathobiology of Prediabetes in a
which suggests a genetic basis for pancreatic Biracial Cohort (POP-ABC) study and observed
12 S. Dagogo-Jack
that 100 had developed incident prediabetes (IGT levels [4547]. Obesity is a likely unifying factor
and/or IFG) during a mean follow-up period of that links the various pathophysiological mecha-
~3 years, without evidence of ethnic disparities nisms leading to dysglycemia. Comparison of
[45]. Thus, among black and white subjects with several measures of adiposity indicates higher
parental history of T2DM, the incidence of pre- values in people who progress from normoglyce-
diabetes was ~10 %/year. These data indicate that mia to prediabetes compared with those who
the risk of incident prediabetes among offspring maintain normal glucose metabolism (Table 2.2).
of parents with T2DM in the general United
States population is similar to or higher than the
risk observed among Pima Indians, a group with Rationale for Primary Prevention
the worlds highest rate of T2DM [41]. The POP- of Type 2 Diabetes
ABC data underscore the importance of heredity,
familial, and genetic T2DM. Taken together, There are compelling reasons why the primary
these studies found that normoglycemic individ- prevention of T2DM ought to be an urgent policy
uals develop prediabetes at an annual rate of priority in developing countries. Undoubtedly,
610 %, the higher rate being more likely among the prohibitive costs of managing diabetes and its
those with a strong family history of T2DM. Based complications could easily overwhelm the bud-
on findings in the Pima Indian [34] and the POP- gets of many low- and middle-income countries.
ABC [45] studies, the predictors of incident pre- In many such countries, competing pressures
diabetes include older age, male gender, from infectious diseases and periodic epidemics
overweight/obesity, lower insulin sensitivity, and can easily relegate considerations for diabetes
impaired acute insulin secretory response to glu- care to the bottom of the totem pole of noncom-
cose [45]. Other predictors of incident prediabe- municable diseases. However, the unique demo-
tes included food habits, physical inactivity, graphic (increased diabetes susceptibility at
higher C-reactive protein, and lower adiponectin younger age and female preponderance) and the
Table 2.2 Selected baseline demographic and clinical characteristics of participants who developed prediabetes (pro-
gressors) compared to those who remained free of incident prediabetes during 5 years of follow-up in the POP-ABC
study
Characteristic Progressors Nonprogressors P-value
Number 111 232
White/black 53/58 97/135 0.3
Female/male 65/46 180/52 0.0003
Age (year) 47 8.9 43.9 10.7 0.0017
Age 1840/4065 23/88 85/147 0.0030
Weight (kg) 90 20 83 22 0.0036
BMI (kg/m2) 31.4 6.9 29.6 7.4 0.0013
Waist (cm) 99 14 92 16 <0.0001
Female 98 12 91 16 0.0006
Male 101 15 96 15 0.14
Total fat mass (kg) 32.0 12.6 29.9 14.0 0.0025
Female 37.2 12.0 32.1 14.4 0.02
Male 24.2 9.1 22.4 9.1 0.0004
Trunk fat mass (kg) 16.6 6.8 14.3 7.3 <0.0001
Female 18.9 6.7 15.1 7.6 0.0064
Male 13.1 5.4 11.5 5.5 0.07
Plusminus values are means SD
BMI body mass index, POP-ABC pathobiology of prediabetes in a biracial cohort (see [47])
Fig. 2.5 Human

capital investment in
building a
multidisciplinary Endocrinologist/
team-based diabetes Diabetologist
care service. A Ophthalmologist Podiatrist
well-informed and
highly motivated
patient is critical to the
success of diabetes
care Diabetes Patient
Nurse, Educated Dietitian/
Diabetes Motivated Nutritionist
Educator Self-actualizing
Other
Behaviorist
specialists
Primary Care
Physician
geographical (urban vs. rural) distribution of the monitoring supplies, laboratory support, and the
diabetes provide clear targets for preventive professional care team (comprising of physician
intervention. Moreover, there is interplay between specialists, nurses, dietitians, diabetes educators,
diabetes and chronic infectious diseases (e.g., podiatrists, and other experts) is often elusive in
tuberculosis) as well as between successful con- many countries that face challenges in health-
trol of HIV infection and iatrogenic diabetes. care infrastructure (Fig. 2.5). Where some or all
But, the strongest argument for prioritizing dia- of these essential resources for effective diabetes
betes prevention is the premium availability of control are available, their distribution often is
effective tools that have been developed in land- lopsided, and most rural areas are underserved. In
mark studies conducted in different parts of the the absence of comprehensive national health
world that established the feasibility of prevent- coverage, affordability of medications and self-
ing T2DM [4851]. management supplies, even when available, can-
Diabetes mellitus imposes a huge drain on not be guaranteed for most low-income patients.
national health budgets. The annual diabetes- For example, in sub-Saharan Africa, insulin secu-
related health-care costs exceed $240 billion in rity and affordability have been major concerns
the United States [52]. Although precise figures [55, 56]. Lacking cost defrayment by government
are hard to come by, on average, developing or reimbursement by third-party insurers, the
countries spent at least 5 % of their total health limitations imposed by the significant out-of-
expenditures on diabetes in 2010 [53]. The 5 % pocket costs of diabetes care translate to chronic
budgetary allocation is suboptimal and could be suboptimal care, which increases the burden of
much higher if diabetes-related medical costs diabetes-related complications [57].
were to be adjusted to account for the >50 % rate Type 2 diabetes, a global epidemic, now ranks
of undiagnosed diabetes in developing countries among the leading noncommunicable public
[53, 54]. Optimal control of glycemia and related health challenges of the present era [1, 4, 5]. The
comorbidities is difficult and expensive to achieve public health burden imposed by diabetes is
in patients with established diabetes. Availability underscored by the fact that diabetes now is the
of antidiabetes medications, diabetes testing and leading cause of blindness, end-stage renal failure,
14 S. Dagogo-Jack
100
US (n=1,444) AUS (n=146) BEL (n=173) FRA (n=144) GER (n=256)
90
GRE (n=176) NOR (n=142) RUS (n=95) SPA (n=182) SWE (n=164)
80
SWI (n=205) TUR (n=210) UK (n=153)
70
60
At Goal,%
52.2
48.4
50 43.8 41.9
39.7 41.5 40.6 41.8
40 33.7
26.2 26 27.7
30 23.4
20
10
0
Country
Fig. 2.6 Percentage of patients with diabetes achieving optimal control in the United States (HbA1c target <7 %) or
several European countries (HbA1c target <6.5 %) (Source: see [67, 68])
and nontraumatic limb amputations and a major multiple-related risk factors. Consequently, the
contributor to heart disease, stroke, and peripheral long-term complications of diabetes flourish
vascular disease [5760]. These complications unchecked. Ironically, many developing countries
can be prevented or delayed by achieving and lack the infrastructure, technology, and human
maintaining excellent control of glycemia and resources for adequate management of diabetes
comorbid conditions, such as hypertension and complications. Services like dialysis, renal trans-
dyslipidemia [6164]. However, the achievement plantation, laser surgery for retinopathy, interven-
of sustained glycemic control to the level neces- tional cardiology, and rehabilitation services for
sary for prevention of complications often proves amputees are not routinely available. It is, thus,
elusive, even in countries in the developed econo- self-evident that primary prevention of T2DM is
mies [65, 66] (Fig. 2.6). Optimal glycemic control an imperative for developing countries [68, 69].
requires a highly motivated patient, working with
a diabetes care team comprising physicians and
several cadres of clinicians (Fig. 2.5). The care Unique Vulnerabilities
processed involves the use of multiple medica- in Developing Countries
tions; frequent clinic visits; adherence to chal-
lenging lifestyle prescriptions; performance of Data from surveys in developing countries indi-
demanding self-management tasks; paying for cate that diabetes predominantly affects younger
cumulative costs of home blood glucose test age-groups: the majority of people with diabetes
strips; sustained engagement by a team of physi- fall within the age range of 4059 years, as com-
cians, nurses, dietitians, diabetes educators, oph- pared to 60 years or older in developed countries
thalmologists, podiatrists, behaviorists, and other [69]. It has also been predicted that future increases
specialized professionals; and the implementa- in diabetes numbers would affect all age-groups in
tion of sundry other recommendations [13, 67] developing countries, whereas in developed coun-
(Fig. 2.5). Lacking the requisite resources and tries an increase is expected predominantly among
support for excellence in diabetes care, many persons older than 60 years, with a slight decrease
patients in developing countries face the specter in the younger age-groups [69]. This younger age
of chronic suboptimal control of glycemia and predilection means that individuals in developing
countries in their prime productivity years are the efficacious in decreasing the rate of progression
ones burdened with diabetes and its complica- from prediabetes to T2DM during study periods
tions, with dire consequences on national econo- that ranged from ~3 to 6 years [4851].
mies. Besides the enormous direct medical costs,
the additional lost productivity from absenteeism
and presenteeism inflicts compounding negative Da Qing Study
effects on current and future economic perfor-
mance in the developing world. Furthermore, the Investigators in the Da Qing study (49) screened
preponderance of diabetes in young women of 110,660 men and women from 33 health-care
childbearing age perpetuates a vicious cycle clinics in the city of Da Qing, China, and enrolled
through the effects of intrauterine fetal program- 577 adults (mean age 45 years; mean BMI 26 kg/
ming for increased susceptibility to cardiometa- m2) with IGT. The participants were randomized
bolic disorders in postnatal life [70, 71]. A more by clinic to a control group or to one of three
recent vulnerability is the unexpected association active treatment groups diet only, exercise only,
of successful antiretroviral therapy in HIV or diet plus exercise and were followed every
patients with treatment-emergent metabolic per- 2 weeks during the first 3 months and quarterly
turbations, including diabetes, dyslipidemia, and thereafter for 6 years.
lipodystrophy [72, 73]. The primary end point, development of T2DM
at 6 years, occurred in 67.7 % of subjects in the
control group, 43.8 % in the diet-only group,
Approach to Prevention of Type 2 41.1 % in the exercise-only group, and 46.0 % in
Diabetes the diet-plus-exercise group. Interestingly, rela-
tive decrease in diabetes incidence in the active
Lifestyle Modication treatment groups was similar in lean or over-
weight (BMI >25 kg/m2) subjects. After adjust-
Three landmark studies have demonstrated the ments for baseline differences in BMI and fasting
efficacy of lifestyle intervention in preventing the glucose, the diet, exercise, and diet-plus-exercise
development of T2DM in high-risk individuals interventions produced 31 %, 46 %, and 42 %
[4851]. All studies targeted persons with predia- reductions in diabetes risk, compared with control
betes (principally IGT and high-normal fasting [48]. However, there was apparently no additive
plasma glucose). The lifestyle counseling focused efficacy of combined diet plus exercise versus
on dietary intervention and increased physical either component of the lifestyle intervention.
activity and a weight loss target of approximately
5 to <10 % of initial body weight. The dietary
intervention was aimed at encouraging partici- Finnish Diabetes Prevention Study
pants to adopt healthy eating patterns and to
decrease caloric consumption (by ~500700 kcal/ In the Finnish Diabetes Prevention Study (FDPS)
day) through selective reduction in saturated fat [49], 522 middle-aged subjects (mean age,
calories and limitation of excessive carbohydrate 55 years; mean BMI 31 kg/m2) with IGT were
intake. The physical activity component moti- randomly assigned to either an intervention or
vated high-risk individuals to accrue 150 control group. Each participant in the interven-
240 min of moderate-intensity activity per week tion group received individualized sessions with
(~3060 min daily on 5 days or more each week). a health counselor (approximately every
The target intensity (~55 % VO2 max) of physical 2 months) and was encouraged to aim for ~5 %
activity is equivalent to walking at a brisk pace weight loss through reduction of total and satu-
[4851]. Compared with the control groups (who rated fat intake and increased intake of fiber. The
merely received passive health information), lifestyle participants also were instructed to
these lifestyle modifications proved remarkably increase their physical activity by ~210 min per
16 S. Dagogo-Jack
week. The primary end point was development of After cessation of the active phase of the stud-
T2DM (confirmed by OGTT). The cumulative ies, follow-up assessment showed continued ben-
incidence of diabetes after 4 years was 11 % in efit of lifestyle intervention in decreasing diabetes
the intervention group and 23 % in the control incidence during post-study follow-up periods
group, a significant 58 % reduction in diabetes spanning 1020 years [7577], clearly demon-
incidence. The mean weight loss in the lifestyle strating a legacy effect.
group was ~3.5 kg compared with ~0.8 kg in the
control group. Improvement in insulin and pres-
ervation of insulin secretion also occurred differ- Indian Diabetes Prevention Program
entially in the lifestyle group compared with
control [49]. The Indian Diabetes Prevention Program (IDPP)
randomized South Asians with IGT to four arms:
control (with standard advice, N = 136), lifestyle
Diabetes Prevention Program modification (N = 133), low-dose metformin
(N = 133), and lifestyle modification plus low-
The Diabetes Prevention Program (DPP) enrolled dose metformin (N = 136) [51]. Participants in
3,234 participants with IGT and high-normal lifestyle modification groups received counseling
fasting glucose and assigned them randomly to sessions aimed at promoting healthy eating hab-
intensive lifestyle intervention (ILI), metformin, its (decreased intake of refined carbohydrates and
or placebo treatment [50]. The enrollees included fats and increased intake of dietary fiber) and
representation from all ethnic and racial groups boosting physical activity (at least 30 min daily).
in the US population; persons of non-European After a median follow-up of 30 months, the rela-
ancestry constituted 45 % of the entire cohort. tive reductions in diabetes incidence were 28.5 %
The ILI targets were a minimum of 7 % weight with lifestyle modification, 26.4 % with metfor-
loss/weight maintenance and a minimum of min, and 28.2 % with lifestyle modification and
150 min of physical activity per week. Subjects metformin [71]. Remarkably, these benefits of
in the ILI group received a 16-lesson curriculum lifestyle modification occurred despite the lack of
covering diet, exercise, and behavior modifica- significant weight change in the two groups that
tion delivered by case managers on a one-to-one focused on lifestyle change.
basis during the first 24 weeks after enrollment.
Subsequently, monthly individual sessions and
group sessions with the case managers were pro- Translating Diabetes Prevention
vided, to reinforce the behavioral changes. to Communities in Developing
After an average follow-up period of Countries
2.8 years, the participants randomized to ILI
showed a 58 % reduction in the incidence of dia- Collectively, the extant data show that lifestyle
betes, as compared with placebo [50]. This ben- modification is remarkably and consistently
eficial effect of lifestyle intervention was seen effective in preventing the development of T2DM
in all demographic subgroups defined by age, in high-risk populations in China, India, Europe,
gender, race, or ethnicity. Furthermore, rever- and the United States. To date, no large RCTs of
sion to normal glucose tolerance (NGT) diabetes prevention have been published from
occurred in ~40 % of subjects in the lifestyle Africa, Latin America, Australia, New Zealand,
intervention arm, as compared with ~18 % in the the Middle East, or the Caribbean regions,
control arm [50]. Participants who experienced although a number of pilot projects have been
reversion to NGT (even if transiently) were implemented or are ongoing. Some of these pilot
50 % less likely to develop diabetes during long- projects have reported promising results among
term follow-up, as compared with those who indigenous (Maori) New Zealanders [78]. There
had persistent IGT status [74]. is overwhelming evidence that lifestyle
modification is a more compelling approach to general public, through demonstrative education

diabetes prevention than medications. However, by convinced professionals; and (4) adoption of
the landmark lifestyle intervention programs that evidenced-based changes in practices and behav-
achieved remarkable success in preventing diabe- iors, triggered by the new knowledge. The pre-
tes were designed as randomized controlled trials ceding construct of translational cascade is
(RCTs) and conducted predominantly at aca- somewhat akin to the sequential steps in
demic medical centers. The protocols of many of Prochaskas transtheoretical model of behavior
the RCTs entailed frequent clinic visits, utilized modification: pre-contemplative, contemplative,
specialized multidisciplinary teams (including preparation, action, and change [83, 84].
physicians, nurses, dietitians, psychologists,
exercise physiologists, and others), and con-
sumed substantial resources and support from Dissemination of Diabetes
institutions and funding agencies. Notably, all Prevention Knowledge
protocol-mandated services and interventions
were provided at no cost to participants in the The preponderance of evidence from randomized
diabetes prevention RCTs, many of whom also clinical trials on the efficacy of lifestyle interven-
received incentives and stipends. Thus, the odds tion in preventing T2DM has established the
were stacked heavily toward success in these rationale for diabetes prevention as self-evident
RCTs, and it is crucial to determine whether the among health professionals. However, the screen-
sterling results obtained in the landmark RCTs ing for prediabetes and institution of prompt life-
could be reproduced in the community, without style counseling have not become routine
all of the inbuilt advantages, specialized profes- practice, even in economically advanced coun-
sionals, and resources. Some community initia- tries. Bridging the hiatus between philosophical
tives are currently underway to determine the acceptance of the idea of diabetes prevention
feasibility of community programs for diabetes among health professionals and the adoption of
prevention [79, 80]. The United States Centers pragmatic steps to detect and act upon high-risk
for Disease Control and Prevention (CDC) has persons requires a methodical approach.
been training and certifying community diabetes The information and knowledge base of health-
prevention personnel under the aegis of the care professional must be steered toward a more
National Diabetes Prevention Program [81]. pragmatic approach to primary prevention of dia-
Programs using trained lay persons to deliver betes through a number of established approaches.
adaptations of the DPP lifestyle intervention to First, curriculum development in primary and
groups (rather than one-on-one sessions) in the high schools should begin to introduce seminal
community have been shown to produce promis- data from the behavioral components of the land-
ing results [79, 80, 82]. mark diabetes prevention studies within a wider
context of instruction in wellness and health pro-
motion. Second, students in schools of medicine,
Keys to Translation nursing, pharmacy, and allied medical fields
should receive exposure to formal instruction in
In general, the keys to the translation of any new the design and key findings of the major diabetes
concept or discovery related to health consist of prevention studies, again, within the wider con-
(1) adequate comprehension, evaluation, and text of wellness and health promotion. Third,
acceptance of the new information within a spe- mastery of the principles and methods of primary
cialized professional community; (2) processing prevention of T2DM ought to be a priority item in
and conversion of the new information into the the core curriculum of residency training pro-
professional knowledge base and dissemination grams for physicians. The latter can be imple-
to a wider circle of professionals and students; mented through lectures and workshops by
(3) diffusion of the conceptual information to the intramural experts and invited speakers. Finally,
18 S. Dagogo-Jack
practicing physicians in all disciplines (including local, national, and international diabetes associ-
internists, family physicians, endocrinologists, ations, can be invaluable during the process of
cardiologists, nephrologists, general and special- program building and facilitation.
ist surgeons), podiatrists, nurse practitioners, and
other primary care providers must have their
knowledge base updated to include the tenets of Strategies for Diabetes Prevention
primary prevention of diabetes. in the Community
Operationally, the increased awareness about
diabetes prevention at the primary care level Five key elements can be distilled from the life-
should lead to increased zeal for screening and style intervention protocols utilized by the DPP
detection of individuals with prediabetes (often and other major diabetes prevention trials. Most
relatives of patients with established T2DM). or all of these strategies can readily be adapted
Once individuals have been diagnosed with pre- for widespread application in the community.
diabetes (Fig. 2.4), appropriate referral for life-
style counseling can follow, as recommended by 1. Selection of persons at risk
the American Diabetes Association [13]. All diabetes prevention trials targeted, screened,
Convinced health-care workers and their fami- and enrolled a defined group of at-risk persons,
lies become conduits for the dissemination and using well-known risk factors for T2DM
diffusion of diabetes prevention ideas in targeted (Table 2.2). The merit of that approach is
segments of the public (hospital communities, underscored by the finding that the participants
established patients and their relatives, schools, randomized to placebo did in fact develop dia-
neighborhoods, social media and outlets, reli- betes at an alarming rate (~12 % per year in
gious forums, etc.). Most human societies have DPP, ~18 % per year in IDPP) [50]. Thus, the
encountered diabetes and are probably precondi- published criteria used for selecting at-risk per-
tioned for receptive attention to diabetes cam- sons for diabetes prevention appear to be of
paigns, having been primed by awareness of the high fidelity and can be adopted for translation
more obvious complications, such as blindness, of diabetes prevention in the general populace.
amputation, and end-stage kidney disease. Such a Specifically, a positive family history of T2DM
preconditioning of societal awareness of diabetes in first-degree relatives, overweight or obesity
and its complications bodes well for the dissemi- (using ethnic-specific BMI cutoffs), and a fast-
nation of ideas regarding the rationale and feasi- ing plasma glucose in the range of 96125 mg/
bility of diabetes prevention. Yet, the fact that dl predict a high yield of eligible individuals for
T2DM can be prevented by modest caloric restric- community diabetes prevention efforts. The
tion and physical activity is yet to enter folklore. appropriate BMI cutoff for identifying over-
That gap in the popular consciousness (despite the weight subjects appears to be >22 kg/m2 for
raging global epidemic of diabetes) presents an Asians compared with >25 kg/m2 for most
enormous opportunity for leadership by health- other ethnicities [85, 86]. The inclusive age
care professionals and civic leaders. To convince range for the published diabetes prevention
and motivate large segments of society for pre- studies was >25 years for DPP and Da Qing
ventive action against diabetes requires coordi- studies, 4065 years for FDPS, and 3055 years
nated efforts at the local, regional, state, national, for IDPP [4851]. None of the published dia-
and international leadership levels. Creative pro- betes prevention studies enrolled individuals
grams anchored by ministries and departments of younger than age 25 years, which is a major
health, information, education, and other agencies limitation, given the increasing prevalence of
would also be important catalysts for public edu- T2DM in children and adolescents [87, 88].
cation, awareness, and action. The expertise and Obesity and physical inactivity are major risk
contributions from philanthropic organizations factors for T2DM in children, as in adults.
and other nongovernmental bodies, especially Other risk factors include female gender,
ethnicity, family history of T2DM, peripubertal for the prevention of T2DM [4851, 95].
age, and intrauterine exposure to diabetes [89 Walking was the preferred activity for the vast
91]. Because the long-term complications of majority of participants in these studies.
diabetes become established over a >10-year Given the generally low rates of voluntary
period, the epidemic of T2DM in children and physical activity in urbanized communities
adolescents predicts dire consequences for [75, 76], innovative motivational strategies
patients at the prime of their youth [92]. [96, 97] will be required to build physical
Primary prevention of childhood T2DM, there- activity into daily routine, especially in high-
fore, is of utmost public health importance. For risk populations. In clinical trials, the physical
the aforementioned reasons, it is desirable for activity intervention component often required
community diabetes prevention initiatives to exercise physiologists or other skilled staff to
lower the inclusive age for screening at-risk implement. For large-scale community trans-
persons well into the childhood and adolescent lation, these specialists may not be essential,
years. A school-based pilot study sponsored by as lay persons can be trained to deliver physi-
the US National Institutes of Health showed cal activity intervention. However, the infra-
that obesity and diabetes risk factors can be structure required for effective large-scale
decreased by lifestyle intervention in sixth implementation of physical activity interven-
grade pupils [93]. tion well-lit and safe walkways, public
2. Delivery of physical activity intervention parks, biking trail, health and fitness clubs,
The physical activity component of lifestyle etc. may not be readily available in many
intervention in the reported diabetes preven- developing countries, especially at over-
tion studies was of moderate intensity (~55 % crowded urban centers. One innovative
VO2 max) and duration (~30 min daily in the approach to the problem of space for physical
DPP). Out of an abundance of caution, partici- activity is to establish partnerships with
pants in the DPP lifestyle intervention arm schools and houses of religious worship, so
underwent submaximal cardiac stress testing that their large real estate can be utilized for
prior to commencement of the physical activ- diabetes prevention activity after school hours
ity program [94]; however, that was not a rou- and during non-worship days.
tine requirement for physical activity in the The tropical environment (especially, high
majority of diabetes prevention trials [48, 49, temperature, humidity, and torrential rain)
51]. It must be stressed that physical activity constitutes an additional barrier to regular out-
was well-tolerated in the DPP, and no untow- door exercise. Cultural barriers to exercise
ard cardiovascular events or musculoskeletal may also exist in some communities, where
injuries were reported. A routine requirement obesity may be venerated as a sign of well-
for prescreening with cardiac stress would be a being and evidence of freedom from wasting
serious logistical and economic hindrance to diseases (such as malnutrition, HIV/AIDS,
the widespread translation of diabetes preven- and tuberculosis). A less obvious obstacle is a
tion and may not be necessary for the majority cultural mindset among blue collar workers
of free-living individuals who are candidates that associates exercise with the privileged
for diabetes prevention in the community. The elite. These (mis)-perceptions must be con-
DPP exercise goal of 150 min per week was fronted using education and public awareness
similar to that prescribed in the Malmo [95] campaigns. Such grassroots educational cam-
and Da Qing [48] studies but lower than the paigns should emphasize the risks of obesity
210 min per week prescribed in the Finnish and the health benefits of modest increases in
study [49]. The DPP and all other landmark physical activity, thereby shifting the focus
studies have demonstrated the efficacy, tolera- from exercise as indulgent leisure of the bour-
bility, and safety of moderate-intensity physi- geoisie to exercise as an engine of health pro-
cal activity (150210 min per week) as used motion among the proletariat. Civic and local
20 S. Dagogo-Jack
government leadership should collaborate to face-to-face counseling sessions in group for-

create community resources for participatory mat, supplemented by virtual contacts (via
health promotion and wellness. The lowest SMS text messaging, e-mail, or web-based
reported dose of exercise which was effective platforms) could be a less expensive approach
in preventing diabetes was ~150 min/week (or to harnessing the power of contact in diabetes
~30 min/day) [50]; however, significant meta- prevention efforts. Along these lines, web-
bolic benefits can be derived from shorter based lifestyle programs have been reported
bouts of activity (1015 min spread across two to have modest but variable effects on weight
or three periods during the day) [98]. This spe- loss in studies reported from Australia, the
cific point is worth emphasizing when coun- United States, Europe, and Asia [99103];
seling time-pressed subjects. Additionally, however, extrapolation to populations with
whenever appropriate, participatory physical lower literacy and uncertain digital access is
activity and health promotion should be built questionable.
into scheduled cultural festivals and other 4. Delivery of dietary intervention
activities. The latter could include student The participants in the landmark diabetes pre-
teacher and parentchild low- to moderate- vention studies [4851] were asked to reduce
intensity sporting events, parades, pageants, their daily intake of fat calories and total calo-
mini-carnivals, and other civic celebrations. ries. Consumption of meals high in dietary
3. Frequent contacts fiber was also promoted. To help participants
The frequency of contacts between partici- maintain a healthy eating pattern, additional
pants in diabetes prevention programs and life- training regarding reading and understanding
style interventionists was weekly, monthly, food labels was provided. The nutritional
bimonthly, or quarterly, depending on the spe- counseling was delivered in person during the
cific study protocols and phase of study. In the regular visits. As already discussed, there
DPP, the greatest weight loss occurred during appeared to be a relationship between fre-
the initial 24 weeks of intensive individual quency of counseling visits and the magnitude
weekly sessions with lifestyle coaches [50]. of weight loss in the DPP. However, other pro-
When the visit frequency was relaxed to grams that used less frequent visits achieved
monthly sessions, some weight regain was comparable efficacy in diabetes prevention.
noted. Other studies, notably FDPS and Da Thus, following initial run-in and initiation of
Qing, used lower overall contact frequency the dietary intervention, maintenance visits at
(every 2 months to quarterly) and achieved approximately 3-month intervals may be suf-
comparable results to those achieved by the ficient to yield desirable results in a commu-
DPP [48, 49]. Clearly, regular contact at some nity setting.
frequency between interventionists and partic- Pragmatically, implementing dietary inter-
ipants is desirable for successful diabetes prevention for diabetes prevention in local com-
vention. Such contacts could create favorable munities in sub-Saharan Africa and other
dynamics and bonding between lifestyle developing regions would be fraught with
coach and participant. Moreover, the repeated challenges. First, of course, is the shortage of
objective recording of weight, waist circum- trained and culturally adapted dietitians and
ference, and other metabolic measures could medical nutritionists. Second, mandatory food
have important motivational effects. However, labeling, the result of legislation passed some
the optimal frequency of physical contacts decades ago in the West, is not yet a routine
necessary for successful diabetes prevention in practice in many developing countries. In fact,
the community is unclear and could well differ nutritional information may be lacking for
by cultural and regional peculiarities. Thus, many staple foods. Thirdly, even where food
such data would need to be determined through labeling exists, low literacy rates mitigate
pilot studies in different communities. Fewer against their comprehension. Furthermore, the
popularity of informal retail markets (espe- to incorporate some element of self-monitor-

cially for grains, flour, corn, cereal, rice, beans, ing component into a community-based dia-
cassava powder {garri}, and other tuber- betes prevention campaign. The focus of such
derived staples) that do not offer standardized monitoring could be the type and amount
packaging calls for creative approaches to the (serving size) of food intake, daily physical
implementation of caloric control. Thus, effec- activity minutes, and other lifestyle end
tive dietary intervention strategies for diabetes points, as appropriate. In low literacy situa-
prevention in developing countries must antic- tions, the use of domestic surrogates (spouses,
ipate and creatively overcome or circumvent relatives, school age children, neighbors, fam-
these apparent translational obstacles. In that ily friends, etc.) to capture these end points
regard, the value of local pilot and feasibility could be considered. Where feasible, self-
studies cannot be overemphasized. In low lit- monitored data can be transmitted via SMS
eracy regions, a visual (pictorial) approach to text to the Community Diabetes Prevention
dietary modification could be an effective Centers, for tracking and real-time interven-
alternative to text-based formats. The Dietary tional feedback purposes.
Guidelines for Americans, issued by the
United States Department of Agriculture
(USDA), advocates a simple plate method: Community Diabetes Prevention
half of the plate contains fruits and vegetables; Centers
the other half is divided roughly equally into
grains and protein [104]. The plate method The sheer magnitude of the current and projected
[104, 105] is an attractive model that can be escalation of the diabetes epidemic in developing
evaluated as the basis for teaching portion con- countries mandates the broadest possible response
trol and optimal dietary habits in developing at the community level. One practical, efficient
countries. The visual approach uses a graphic approach is the establishment of Community
display of a typical plate, divided into seg- Diabetes Prevention Centers (CDPC) at several
ments that contain desirable food classes in locations on the African continent, the Caribbean
optimal proportions [105]. region, India and South Asia, the Pacific Rim,
5. Self-monitoring South and Central America, Australia and New
Extensive self-monitoring of nutrient intake Zealand, as well as in communities inhabited by
and minutes spent each day in physical activ- high-risk populations in Europe and North
ity (and type of activity) was an integral part America (Fig. 2.7). Such a groundswell of
of the lifestyle intervention in the DPP [50, CDPCs can serve as essential focal points for the
94]. In other studies, the frequent self-moni- dissemination of diabetes prevention practices.
toring of weight and anthropometrics has Operationally, the CDPCs can be administered
been reported to be associated with long- and staffed by the noncommunicable disease
term maintenance of weight loss [106]. The branch of Ministries and Departments of Health or
exact mechanism whereby self-monitoring through partnership with nongovernmental organi-
of eating and exercise behavior predicts good zations. The primary purpose of CDPCs would be
metabolic outcome is unclear. It is plausible to test and implement culturally and regionally
that such a level of involvement in ones appropriate models for the delivery of physical
health could have a beneficial heuristic effect activity and dietary interventions. Referral to
by guiding food choices and lifestyle deci- CDPCs can be based on a risk factor approach that
sions. For most persons in psychic equilib- focuses on genetic (e.g., family history of diabe-
rium, the potential adverse psychological tes) and other risk markers (Table 2.1). Individuals
impact of frequent self-monitoring of nutri- with diagnosed T2DM can be the conduits for
ent intake and physical activity is probably referral of family members to CDPCs for predia-
negligible. For these reasons, it seems prudent betes screening and intervention.
22 S. Dagogo-Jack
Fig. 2.7 Diabetes

prevention strategies for Low-cost, lifestyle intervention models Partnerships: local, regional, national and
delivered by lay persons in the community international Stakeholders
developing countries,
culminating in the
Community support programs: School-based Engagement of the private sector, workplace,
creation of Community physical activity and nutrition education food industry
Diabetes Prevention
Centers (see [68, 69]) Urban designs that facilitate physical activity Laws: Food pricing, labelling, advertising
Training in T2DM prevention (nursing and Mass media: Promote DM knowledge and
medical school curricula) Motivated behavior
Community Diabetes Prevention Centers
Medications for Diabetes placebo [50]. The STOP-NIDDM (Study to

Prevention Prevent Non-Insulin-Dependent Diabetes
Mellitus) employed acarbose as the intervention
Even in the most successful of the randomized drug and demonstrated a 25 % decrease in the rate
controlled trials, the risk reduction for incident of progression to diabetes, compared to placebo
diabetes following lifestyle intervention was [108]. In the XENDOS (XENical in the Prevention
~60 % [4851]. That raises the argument as to of Diabetes in Obese Subjects) study, the pancre-
whether medications could be offered to high- atic lipase inhibitor orlistat (when prescribed in
risk persons who are unable or unwilling to combination with lifestyle modification) resulted
implement lifestyle changes or in whom the latter in a 37 % risk reduction in incident diabetes
have failed to halt glycemic progression. In fact, among subjects with impaired glucose tolerance,
several of the landmark diabetes prevention trials compared with lifestyle intervention alone [109].
also included pharmacological arms, and addi- Thiazolidinedione drugs were tested in the
tional studies have specifically tested medica- DREAM (Diabetes Reduction Assessment with
tions for diabetes prevention. Given the linear Ramipril and Rosiglitazone Medication) [110],
relationship between diabetes risk reduction and ACT NOW (ACTos NOW for the Prevention of
the amount of weight loss (~10 % for every 1 kg Diabetes) [111], and CANOE (CAnadian
weight loss) [50, 107], a medication that enhances Normoglycemia Outcomes Evaluation) [112]
or maintains weight loss would be a rational studies, which showed diabetes risk reduction
adjunct to lifestyle. What follows is a summary rates of >5075 %, compared with placebo. In
of medications that have been studied for the pre- the NAVIGATOR trial, the use of valsartan for
vention of T2DM (Table 2.4). 5 years, along with lifestyle modification, led to
The list of medications that have been tested a relative reduction of 14 % in the incidence of
includes sulfonylureas, metformin, acarbose, orli- diabetes among subjects with IGT, but the effect
stat, rosiglitazone, and pioglitazone (Table 2.3). of nateglinide was not better than placebo [113].
The DPP demonstrated that intervention with The CANOE trial showed that low-dose combi-
metformin decreased the development of diabetes nation therapy with metformin (500 mg twice
in adults with impaired glucose tolerance by 31 % daily) and rosiglitazone (2 mg daily) decreased
[50]. Curiously, the diabetes prevention efficacy incident type 2 diabetes by 66 % compared with
of metformin was observed only in younger, placebo in IGT subjects. Of note, the low doses
obese (BMI >35 kg/m2) individuals; among older were well tolerated, with minimal effect on clini-
or leaner participants, the effect of metformin in cally relevant adverse events of the individual
diabetes risk reduction was no better than that of drugs [112].
Table 2.3 Diabetes prevention studies using lifestyle modification and medications
Year Study acronym Follow-up Intervention Outcome
1997 Da Qing 6 years Diet + exercise Decrease, 51 %
2001 DPS, Finland 3 years Diet + exercise Decrease, 58 %
2002 DPP 2.8 years Diet+ Ex vs. Met Decrease, 58 %
2002 STOP-NIDDM 3.3 years Acarbose + diet Decrease, 25 %
2004 XENdos 4 years Orlistat + diet Decrease, 37 %
2006 DREAM 3 years Rosiglitazone Decrease, 60 %
2008 ACT NOW 24 years Pioglitazone Decrease, 72 %
2006 IDPP-1 3 years L/S Met Decrease, 2628 %
Met not additive to
L/S
2009 IDPP-2 3 years L/S Pio Pio not additive to
L/S
2010 Navigator 5 years Nateglinide No effect
Valsartan Decrease, 14 %
2010 CANOE 4 years Rosi+Met Decrease 69 %
Ex exercise, L/S lifestyle, Met metformin, Pio pioglitazone, Rosi troglitazone
Limitations of Medications Table 2.4 Desirable characteristics of an ideal drug for

diabetes prevention
The drugs that have been tested for diabetes pre- Efficacy: should equal or exceed the efficacy of
vention are associated with a range of adverse lifestyle intervention
effects, the need for continuous therapy to main- Mechanism(s): should repair the pathophysiologic
defects that underlie prediabetes
tain their effects, and consequent adherence bar-
Glucoregulation: should normalize glucose
riers. In the studies that tested the effect of metabolism
interruption of metformin, rosiglitazone and pio- Durability: effects should outlast the period of
glitazone therapy for diabetes prevention, no sus- medication exposure
tained effect off medication was observed, which Adiposity: should induce weight loss or be
indicates that those medications did not funda- weight-neutral
mentally improve the underlying pathophysiol- Safety: should have minimal toxicity and require no
safety monitoring
ogy of prediabetes [114116]. Moreover, in the
Tolerability: should be well tolerated, without GI or
Indian Diabetes Prevention Program (IDPP)-1 other adverse effects
and IDPP-2, neither low-dose metformin nor pio- Cost: should cost less than the least expensive drug for
glitazone, when tested in combination with life- diabetes treatment
style modification, achieved additive reduction of Adapted from [28, 69]
diabetes risk, compared to the effects of lifestyle
modification alone [51, 117]. Clearly, the cumu-
lative costs of long-term (probably life-long) and durable medications for diabetes prevention.
therapy with medications (even where generic Indeed, the poor human record of long-term
versions are available and no adverse effects adherence to behavioral recommendations and
occur) can be prohibitive, particularly for devel- the known physiological adaptations that limit
oping countries. weight loss and trigger counter-veiling mecha-
For reasons that have already been argued, the nisms that promote weight regain [118] create a
use of drugs for diabetes prevention cannot be need for such adjunctive pharmacological agents.
recommended as a first-line approach in the gen- The ideal drug for diabetes prevention (Table 2.4)
eral population. The latter conclusion is not to should be nontoxic, well-tolerated, and at least as
eschew societal expectation of safe, effective, efficacious as lifestyle modification [28, 69].
24 S. Dagogo-Jack
Additionally, such a drug should repair or first 6 months (i.e., approximately 1 % per month).
improve the pathophysiological defects that Thus, candidates for diabetes prevention who are
underlie prediabetes, so that a durable effect that unable to meet the lifestyle response target of los-
outlasts the period of medication can be expected. ing ~1 %/month of body weight during the initial
The latter attribute would permit withdrawal of 36 months of behavioral intervention may be
the medication after a defined period of interven- considered for adjunctive metformin therapy.
tion, without the risk of prediabetes relapse. The guidelines on the management of predia-
Finally, the cost of such a drug must not be pro- betes, issued by the Indian Health Services (IHS)
hibitive, bearing in mind the large number of and the Australian Diabetes Society/Australian
people with prediabetes (86 million in the United Diabetes Educators Association, emphasize life-
States and more than 400 million worldwide). style intervention prior to consideration of medi-
cations. The Australian guidelines recommend
trying lifestyle intervention for a minimum of
Current Guidelines for Use 6 months before considering drugs for diabetes
of Medication for Diabetes prevention [120]. The IHS guidelines recom-
Prevention mend addition of either metformin or piogli-
tazone if initial lifestyle intervention fails to
The ADA consensus statement [119] recom- improve dysglycemia in people with prediabetes
mends lifestyle modification with a weight loss [121]. The IHS guidelines state that the decision
goal of 510 % along with moderate physical to use medication for diabetes prevention must be
activity of about 30 min daily for patients with made on an individual basis and with the patients
IFG or IGT. Although no drug has been approved full understanding [121].
by the Food and Drug Administration for diabe- Prediabetes is diagnosed based on the presence
tes prevention, the ADA has suggested that treat- of either IFG alone, IGT alone (determined during
ment with metformin be considered as an adjunct oral glucose tolerance test), or both IFG and
to diet and exercise for the prevention of type 2 IGT. Individuals who have both IFG and IGT (so-
diabetes in selected high-risk persons [13, 119]. called double prediabetes) show more severe insu-
Based on the subgroup analysis of the efficacy of lin resistance and impairment of beta-cell function
metformin in the DPP, metformin was most compared to persons with a single prediabetes
effective in preventing diabetes in high-risk, very marker [119, 122, 123]. Nearly all persons with
obese (BMI >35 kg/m2) prediabetic subjects double prediabetes (~96 %) would qualify for met-
younger than 60 years of age [50]. Additional formin therapy, based on the ADA consensus cri-
selection criteria when considering metformin teria, whereas only ~30 % of persons with isolated
use in prediabetic subjects include a family his- IFG would be eligible for metformin treatment
tory of diabetes in first-degree relatives, prior using the same criteria [119, 124]. This means that
gestational diabetes mellitus, hypertriglyceride- the use of oral glucose tolerance testing can refine
mia, subnormal HDL cholesterol levels, hyper- and sharply tailor the selection of individuals at
tension, and HbA1c 5.76.4 % [13, 119]. greatest risk (i.e., those with IFG + IGT) for met-
Even in persons who harbor all or most of these formin adjunctive treatment [119, 124]. This
risk factors, active lifestyle modification is the pre- maximalist risk and minimalist drug interven-
ferred initial intervention; metformin can then be tion approach has much to commend it, as it would
considered for individuals who fail to make sig- spare individuals and governments the huge
nificant progress. Currently, there are no clear expense of covering the costs of medications and
guidelines for determining the optimal timing of related expenses for a much wider range of indi-
metformin therapy, but failure of lifestyle inter- viduals from lower risk pools. Indeed, the ADA
vention can be determined fairly empirically. The consensus statement stipulates that the presence of
DPP participants assigned to lifestyle intervention both IFG and IGT must be documented if metfor-
lost ~7 % of their baseline body weight during the min is to be used for diabetes prevention [119].
Costs of Preventing T2DM agencies) would need to be explored and mobi-

lized for successful implementation of diabetes
Analysis of costs associated with the DPP indi- prevention initiatives in most low- and middle-
cates that the overall expense to society of pre- income countries.
venting diabetes was cost-effective [125128].
For over 3 years, the direct medical costs of the
DPP interventions were US $79 per participant Conclusion
in the placebo group, US $2,542 in the metfor- Nearly 90 million adults in the United States
min group, and US $2,780 in the lifestyle group and more than 400 million people around the
[125, 126]. Further longer-term analysis indi- world have prediabetes. Perhaps, one of the
cated that lifestyle modification remained cost- most significant public health advances of the
effective, and metformin was potentially cost present era is the demonstration that progres-
saving when used for preventing diabetes [128]. sion from prediabetes to type 2 diabetes can
Cost analysis in the IDPP showed that the be interrupted by effective interventions. In
T2DM prevention strategies in India, especially addition to the compelling arguments for pri-
lifestyle intervention, were cost-effective [129]. oritizing diabetes prevention, there is an even
The total cost of identifying one person with more urgent need for action in low-income
IGT was US $117. The direct medical costs countries, where a narrow window of opportu-
were US $61 per person in the control group and nity currently exists. In those countries, diabe-
US $225 in the lifestyle intervention group tes is currently not featured among the top ten
[129]. The cost of preventing one case of T2DM causes of death; however, as countries emerge
through lifestyle modification in India was US from poverty, the role of diabetes as a leading
$1,052 [129]. The DPP, IDPP, and other trials cause of death becomes firmly established
were by the nature of their design quite (Fig. 2.8). This nefarious association between
resource-intensive. economic progress and death from diabetes is
Clearly, the adaptation of diabetes prevention not inevitable; economic transition from pov-
programs to developing countries would require erty to wealth can and must be uncoupled
extensive cost-containment and cost-shifting from increased morbidity and mortality from
strategies. Reduction in contact frequency, diabetes [131]. Among the different interven-
optimization of the size of the intervention per- tions of proven efficacy in preventing diabe-
sonnel, and the use of group (rather than one-on- tes, lifestyle modification is the most appealing
one) counseling format should decrease costs because of its high efficacy, nontoxicity, and
significantly. Furthermore, the use of trained generalizable effects in persons from various
lay (nonmedical) workers to implement life- ethnic backgrounds [4851]. Most of the med-
style modification protocols in group sessions ications that have been tested for diabetes pre-
at the Community Diabetes Prevention Centers vention fall short of the efficacy achieved by
and prorated cost sharing could be additional lifestyle intervention. Although the efficacy of
approaches to the implementation of afford- thiazolidinedione drugs on diabetes preven-
able diabetes prevention programs in develop- tion when administered to persons with pre-
ing countries [79, 130]. Even with a markedly diabetes can match or somewhat exceed that
scaled down cost schedule, the low gross domes- of lifestyle intervention, the drug effect is not
tic product (~$500 per capita) in many develop- sustained and quickly dissipates following
ing countries suggests that these nations cannot cessation of therapy [114, 115]. In contrast
afford to underwrite the costs of even a limited such a rapid washout effect is not seen with
national diabetes prevention program. Given the lifestyle intervention, where sustained bene-
immense future benefits to society from preven- fits of diabetes prevention have been reported
tion of T2DM, novel funding sources (private, up to 20 years following cessation of formal
industry, international, philanthropic, and other intervention [7577].
26 S. Dagogo-Jack
Lower respira- Ischaemic

91 95
tory infections heart disease
HIV/AIDS 65 Stroke 78
Diarrhoeal Lower respira-
53 53
diseases tory infections
Stroke 52 COPD 52
e e s
Ischaemic
co
m Diarrhoeal dl ie
heart disease
39
i n s diseases
37
id ntr
m u
w- rie Preterm r - o
Malaria 35
Lo unt birth complic...
28
we e c
Preterm
33 co HIV/AIDS 23
Lo com
birth complic...
Diabetes
in
Tuberculosis 31 22
mellitus
Birth
29 Tuberculosis 21
asphyxia and...
Protein Cirrhosis of
27 19
energy maln... the liver
0 20 40 60 80 100 0 20 40 60 80 100
Deaths per 100,000 population Deaths per 100,000 population
Ischaemic
158 Stroke 126
heart disease
Ischaemic
Stroke 95 107
heart disease
Trachea
49 COPD 50
bronchus, lu...
Alzheimer Trachea
42 31
Disease and ... e bronchus, lu...
e ies
m dl
COPD 31 co Diabetes
23
id ntr
- in s mellitus
m u
Lower respira-
gh rie Lower respira- r- o
tory infections
31
Hi unt tory infections
23
pe e c
Colon
27 co Road injury 21
Up com
rectum cance...
Diabetes Hypertensive
in
20 20
mellitus heart disease
Hypertensive Liver
20 18
heart disease cancer
Breast Stomach
16 17
cancer cancer
0 32 64 96 128 160 0 26 52 78 104 130
Deaths per 100,000 population Deaths per 100,000 population
Fig. 2.8 Top ten causes of death in countries of the world of death. COPD chronic obstructive pulmonary disease
grouped by income status. Diabetes does not appear (Source: World Health Organization. Available from
among the top causes of death in low-income countries, http://www.who.int/mediacentre/factsheets/fs310/en/
but as countries experience upward economic transition, index1.html. Accessed 20 May 2015)
diabetes becomes firmly established among the top causes
The effective translation of diabetes pre- Diabetes Prevention Centers, to serve as a

vention across global communities requires hub for harmonizing the planning, delivery,
engagement and coordination at multiple and evaluation of lifestyle intervention activi-
levels within the health-care establishment, ties, would be an efficient approach to global
civic society, and government agencies. diabetes prevention. Appropriate legislation
Environmental and policy changes are needed that promotes food labeling, rewards healthful
to stimulate broad societal participation in well- behavior, and redistributes revenue from sin
ness and diabetes prevention activities. Pilot tax on tobacco and alcohol to fund community
and feasibility projects are needed to custom- diabetes prevention initiatives would be well
ize generally proven methodologies to local directed. Clearly, great opportunities exist for
specificities and realities in developing coun- innovative partnerships among governmental,
tries and underserved communities. Ecological civic, philanthropic, and other nongovernmen-
improvements that result in improved access tal organizations toward a common purpose
to safe walking trails, well-lit and well-kept of stemming the global diabetes epidemic by
public parks, subsidized or affordable neigh- focusing on primary prevention.
borhood fitness centers, and other appurte-
nances for health promotion would all augur Acknowledgments SD-J is supported, in part, by grants
well for the practice of community diabetes (R01 DK067269, DK62203, DK48411) from the National
prevention. The establishment of Community Institutes of Health.
Disclosures The author has no conflicts of inter- 15. Dagogo-Jack S, Santiago JV. Pathophysiology of
est with regard to the content of this chapter. type 2 diabetes and modes of action of therapeutic
interventions. Arch Intern Med. 1997;157:
180217.
16. Defronzo RA. Banting lecture. From the triumvirate to
References the ominous octet: a new paradigm for the treatment of
type 2 diabetes mellitus. Diabetes. 2009;58:77395.
1. International Diabetes Federation. IDF diabetes atlas 17. DeFronzo RA. Insulin resistance, lipotoxicity, type 2
2015. 7th ed. Brussels: International Diabetes diabetes and atherosclerosis: the missing links. The
Federation; 2015. Claude Bernard Lecture 2009. Diabetologia. 2010;
2. Geiss LS, Wang J, Cheng YJ, Thompson TJ, Barker L, 53:127087.
Li Y, et al. Prevalence and incidence trends for diag- 18. Rasmussen BB, Holmbck UC, Volpi E, Morio-
nosed diabetes among adults aged 20 to 79 years, Liondore B, Paddon-Jones D, Wolfe RR. Malonyl
United States, 19802012. JAMA. 2014;312:121826. coenzyme A and the regulation of functional carni-
3. Gregg EW, Li Y, Wang J, Burrows NR, Ali MK, tine palmitoyltransferase-1 activity and fat oxidation
Rolka D, et al. Changes in diabetes-related compli- in human skeletal muscle. J Clin Invest. 2002;
cations in the United States, 19902010. N Engl 110:168793.
J Med. 2014;370:151423. 19. Kitabchi AE, Temprosa M, Knowler WC, Kahn SE,
4. World Health Organization. Global status report on Fowler SE, Haffner SM, et al. Role of insulin secre-
noncommunicable diseases 2014. Geneva: WHO tion and sensitivity in the evolution of type 2 diabe-
Press; 2014. tes in the diabetes prevention program: effects of
5. Shaw JE, Sicree RA, Zimmet PZ. Global estimates lifestyle intervention and metformin. Diabetes.
of the prevalence of diabetes for 2010 and 2030. 2005;54:240414.
Diabetes Res Clin Pract. 2010;87:414. 20. Larson-Meyer DE, Heilbronn LK, Redman LM,
6. Hu F. Globalization of diabetes: the role of diet, life- Newcomer BR, Frisard MI, Anton S, et al. Effect of
style, and genes. Diabetes Care. 2011;34:124957. calorie restriction with or without exercise on insulin
7. Egede LE, Dagogo-Jack S. Epidemiology of type 2 sensitivity, -cell function, fat cell size, and ectopic
diabetes: focus on ethnic minorities. Med Clin N lipid in overweight subjects. Diabetes Care. 2006;
Am. 2005;89:94975. 29:133744.
8. Tanizawa Y, Riggs AC, Dagogo-Jack S, Vaxillaire 21. Kelley DE. Effects of weight loss on glucose homeo-
M, Froguel P, Liu L, et al. Isolation of the human stasis in NIDDM. Diabetes Rev. 1995;3:36677.
LIM/homeodomain gene islet-1 and identification of 22. Schneider SH, Morgado A. Effects of fitness and
a simple sequence repeat polymorphism. Diabetes. physical training on carbohydrate metabolism and
2004;43:93541. associated cardiovascular risk factors in patients
9. Ehm MG, Karnoub MC, Sakul H, Gottschalk K, with diabetes. Diabetes Rev. 1995;3:378407.
Holt DC, Weber JL, American Diabetes Association 23. Rogers MA, Yamamoto C, King DS, Harberg JM,
GENNID Study Group. Genetics of NIDDM, et al. Ensani AA, Holloszy JO. Improvement in glucose
Genome wide search for type 2 diabetes susceptibil- tolerance after one week of exercise in patients with
ity genes in four American populations. Am J Hum mild NIDDM. Diabetes Care. 1988;11:6138.
Genet. 2000;66:187181. 24. Eriksson KF, Lindgarde F. Prevention of type 2 dia-
10. McCarthy M, Zeggini E. Genome-wide association betes mellitus by diet and physical exercise.
studies in type 2 diabetes. Curr Diab Rep. 2009;9: Diabetologia. 1991;34:8918.
16471. 25. Mikines KJ, Sonne B, Farrell PA, Tronier B, Galbo
11. Hivert MF, Jablonski KA, Perreault L, Saxena R, H. Effect of physical exercise on sensitivity and
McAteer JB, Franks PW, et al. Updated genetic responsiveness to insulin in humans. Am J Physiol.
score based on 34 confirmed type 2 diabetes Loci is 1988;254:E24859.
associated with diabetes incidence and regression to 26. Goodyear LJ, Kahn BB. Exercise, glucose transport,
normoglycemia in the diabetes prevention program. and insulin sensitivity. Annu Rev Med. 1998;
Diabetes. 2011;60:13408. 49:23561.
12. Dagogo-Jack S. Predicting diabetes: our relentless 27. Steven S, Hollingsworth KG, Al-Mrabeh A, Avery
quest for genomic nuggets. Diabetes Care. 2012; L, Aribisala B, Caslake M, et al. Very-low-calorie
35:1935. diet and 6 months of weight stability in type 2 diabe-
13. American Diabetes Association. Standards of medi- tes: pathophysiologic changes in responders and
cal care in diabetes2016. Diabetes Care. 2016; nonresponders. Diabetes Care. 2016. pii: dc151942.
39:S1112. [Epub ahead of print].
14. Fujimoto WY, Leonetti DL, Kinyoun JL, Newell- 28. Dagogo-Jack S, Edeoga C. Understanding and iden-
Morris L, Shuman WP, Stolov WC, et al. Prevalence tifying pre-diabetes can we halt the diabetes epi-
of diabetes mellitus and impaired glucose tolerance demic? Eur Endocrinol. 2008;4:168.
among second-generation Japanese-American men. 29. Pour OR, Dagogo-Jack S. Prediabetes as a therapeu-
Diabetes. 1987;36:7219. tic target. Clin Chem. 2011;57:21520.
28 S. Dagogo-Jack
30. Maschirow L, Khalaf K, Al-Aubaidy HA, Jelinek 46. Boucher AB, Adesanya EAO, Owei I, Gilles AK,
HF. Inflammation, coagulation, endothelial dysfunc- Ebenibo S, Wan J, Edeoga C, Dagogo-Jack
tion and oxidative stress in prediabetes biomark- S. Dietary habits and leisure-time physical activity
ers as a possible tool for early disease detection for in relation to adiposity, dyslipidemia, and incident
rural screening. Clin Biochem. 2015;48:5815. dysglycemia in the Pathobiology of Prediabetes in
31. Nyenwe EA, Dagogo-Jack S. Metabolic syndrome, A Biracial Cohort Study. Metabolism. 2015;64:
prediabetes and the science of primary prevention. 10607.
Minerva Endocrinol. 2011;36:12945. 47. Jiang Y, Owei I, Wan J, Ebenibo S, Dagogo-Jack
32. Tabk A, Herder C, Rathmann W, Brunner E, S. Adiponectin levels predict prediabetes risk: the
Kivimki M. Prediabetes: a high-risk state for diabe- pathobiology of prediabetes in a biracial cohort
tes development. Lancet. 2012;379:227990. (POP-ABC) study. BMJ Open Diabetes Res Care.
33. Weir G, Bonner-Weir S. Five stages of evolving pro- 2016;4:e000194. doi:10.1136/bmjdrc-2016.
gression to diabetes. Diabetes. 2004;53:S1621. 48. Pan XR, Li GW, Hu YH, Wang JX, Yang WY, An
34. Weyer C, Bogardus C, Mott DM, Pratley R. The ZX, et al. Effects of diet and exercise in preventing
natural history of insulin secretory dysfunction and NIDDM in people with impaired glucose tolerance:
insulin resistance in the pathogenesis of type 2 dia- the Da Qing IGT and Diabetes Study. Diabetes Care.
betes mellitus. J Clin Invest. 1999;104:78794. 1997;20:53744.
35. Toft-Nielsen MB, Damholt MB, Madsbad S, Hilsted 49. Tuomilehto J, Lindstrom J, Eriksson J, Valle T,
LM, Hughes TE, Michelsen BK, et al. Determinants Hamalainen H. Prevention of type 2 diabetes melli-
of the impaired secretion of glucagon-like peptide- tus by changes in lifestyle among subjects with
1 in type 2 diabetic patients. J Clin Endocrinol impaired glucose tolerance. N Engl J Med. 2001;344:
Metab. 2001;86:371723. 134350.
36. Papaetis G. Incretin-based therapies in prediabetes: 50. DPP Research Group. Reduction in the incidence of
current evidence and future perspectives. World type 2 diabetes with lifestyle intervention or metfor-
J Diabetes. 2014;5:81734. min. N Engl J Med. 2002;346:393403.
37. Lopategi A, Lpez-Vicario C, Alcaraz-Quiles J, 51. Ramachandran A, Snehalatha C, Mary S, Mukesh B,
Garca-Alonso V, Titos E, Clria J, et al. Role of bio- Bhaskar AD, Vijay V, Indian Diabetes Prevention
active lipid mediators in obese adipose tissue inflam- Programme (IDPP). The Indian Diabetes Prevention
mation and endocrine dysfunction. Mol Cell Programme shows that lifestyle modification and
Endocrinol. 2016;419:4459. metformin prevent type 2 diabetes in Asian Indian
38. Cerasi E, Luft R. The prediabetic state, its nature and subjects with impaired glucose tolerance (IDPP-1).
consequences a look toward the future. Diabetes. Diabetologia. 2006;49:28997.
1972;21 Suppl 2:68594. 52. American Diabetes Association. Economic costs of
39. Centers for Disease Control and Prevention. National diabetes in the U.S. in 2012. Diabetes Care. 2013;36:
diabetes statistics report: estimates of diabetes and 103346.
its burden in the United States, 2014. Atlanta: US 53. Zhang P, Zhang X, Brown J, Vistisen D, Sicree R,
Department of Health and Human Services; 2014. Shaw J, Nichols G. Global healthcare expenditure on
40. Edelstein SL, Knowler WC, Bain RP, et al. Predictors diabetes for 2010 and 2030. Diabetes Res Clin Pract.
of progression from impaired glucose tolerance to 2010;87:293301.
NIDDM: an analysis of six prospective studies. 54. Barcel A, Aedo C, Rajpathak S, Robles S. The cost
Diabetes. 1997;46:70110. of diabetes in Latin America and the Caribbean. Bull
41. Knowler WC, Bennett PH, Hamman RF, Miller World Health Organ. 2003;81:1927.
M. Diabetes incidence and prevalence in Pima 55. Deeb LC, Tan MH, Alberti KGMM. Insulin availabil-
Indians: a 19-fold greater incidence than in Rochester, ity among International Diabetes Federation member
Minnesota. Am J Epidemiol. 1978;108:497505. associations. Diabetes Care. 1994;17:2203.
42. Brancati FL, Kao WH, Folsom AR, Watson RL, 56. Dagogo-Jack S. DCCT results and diabetes care in
Szklo M. Incident type 2 diabetes mellitus in African developing countries. Diabetes Care. 1995;18:4167.
American and white adults: the Atherosclerosis Risk 57. Beran D, Yudkin JS. Diabetes care in sub-Saharan
in Communities Study. JAMA. 2000;283:22539. Africa. Lancet. 2006;368:168995.
43. Weyer C, Tataranni PA, Bogardus C, Pratley 58. Dagogo-Jack S. Pattern of foot ulcer in diabetic
R. Diabetes Care. 2000;24:8994. Nigerians. Pract Diabetes Dig. 1991;2:758.
44. Meigs JB, Muller DC, Nathan DM, Blake DR, 59. Dagogo-Jack S. Diabetic in-patient mortality in
Andres R. Diabetes. 2003;52:147584. Nigeria. Pract Diabetes Dig. 1991;2:1179.
45. Dagogo-Jack S, Edeoga C, Ebenibo S, Nyenwe E, 60. Dagogo-Jack S. Primary prevention of cardiovascu-
Wan J. Lack of racial disparity in incident prediabe- lar disease in diabetic patients. Cardiol Q. 2006;12:
tes and glycemic progression among black and white 205.
offspring of parents with type 2 diabetes: the patho- 61. Nathan DM, Bayless M, Cleary P, Genuth S,
biology of prediabetes in a biracial cohort (POP- Gubitosi-Klug R, Lachin JM, DCCT/EDIC Research
ABC) study. J Clin Endocrinol Metab. 2014;99: Group, et al. Diabetes control and complications
E107887. trial/epidemiology of diabetes interventions and
complications study at 30 years: advances and con- follow-up of the Finnish Diabetes Prevention Study.
tributions. Diabetes. 2013;62:397686. Lancet. 2006;368:16739.
62. UK Prospective Diabetes Study (UKPDS) Group. 77. Li G, Zhang P, Wang J, An Y, Gong Q, Gregg EW,
Intensive blood-glucose control with sulphonylureas et al. Cardiovascular mortality, all-cause mortality,
or insulin compared with conventional treatment and and diabetes incidence after lifestyle intervention for
risk of complications in patients with type 2 diabetes people with impaired glucose tolerance in the Da
(UKPDS 33). Lancet. 1998;352:83753. Qing Diabetes Prevention Study: a 23-year follow-up
63. Hayward RA, Reaven PD, Wiitala WL, Bahn GD, study. Lancet Diabetes Endocrinol. 2014;2:47480.
Reda DJ, Duckworth, VADT Investigators, et al. 78. Simmons D, Rush E, Crook N. Development and
Follow-up of glycemic control and cardiovascular piloting of a community health worker-based inter-
outcomes in type 2 diabetes. N Engl J Med. 2015; vention for the prevention of diabetes among New
372:2197206. Zealand Maori in Te Wai o Rona: diabetes preven-
64. Gaede P, Lund-Andersen H, Parving HH, Pedersen tion strategy. Public Health Nutr. 2008;11:131825.
O. Effect of a multifactorial intervention on mortality 79. Ackermann RT, Marrero DG. Adapting the Diabetes
in type 2 diabetes. N Engl J Med. 2008;358:58091. Prevention Program lifestyle intervention for deliv-
65. Banegas JR, Lpez-Garca E, Dallongeville J, ery in the community: the YMCA model. Diabetes
Guallar E, Halcox JP, Borghi C, et al. Achievement Educ. 2007;33(69):745, 778.
of treatment goals for primary prevention of cardio- 80. Albright AL, Gregg EW. Preventing type 2 diabetes
vascular disease in clinical practice across Europe: in communities across the U.S.: the National
the EURIKA study. Eur Heart J. 2011;32:214353. Diabetes Prevention Program. Am J Prev Med.
66. Ali MK, Bullard KM, Saaddine JB, Cowie CC, 2013;44(4 Suppl 4):S34651.
Imperatore G, Gregg EW. Achievement of goals in 81. Albright A. The National Diabetes Prevention
U.S. diabetes care, 19992010. New Engl J Med. Program: from research to reality. Diabetes Care
2013;368:161324. Educ Newsl. 2012;33(4):47.
67. Dagogo-Jack S. Preventing diabetes-related morbid- 82. Hays LM, Finch EA, Saha C, Marrero DG,
ity and mortality in the primary care setting. J Natl Ackermann RT. Effect of self-efficacy on weight
Med Assoc. 2002;94:54960. loss: a psychosocial analysis of a community-based
68. Dagogo-Jack S. Primary prevention of type 2 diabe- adaptation of the diabetes prevention program life-
tes in developing countries. J Natl Med Assoc. style intervention. Diabetes Spectr. 2014;27:2705.
2006;98:4159. 83. Velicer WF, Brick LA, Fava JL, Prochaska
69. Echouffo-Tcheugui JB, Dagogo-Jack S. Preventing JO. Testing 40 predictions from the transtheoretical
diabetes mellitus in developing countries. Nat Rev model again. With confidence. Multivar Behav Res.
Endocrinol. 2012;8:55762. 2013;48:22040.
70. Dabelea D, Knowler WC, Pettitt DJ. Effect of dia- 84. Norcross JC, Krebs PM, Prochaska JO. Stages of
betes in pregnancy on offspring: follow-up research change. J Clin Psychol. 2011;67:14354.
in the Pima Indians. J Matern Fetal Med. 2000; 85. Pan WH, Flegal KM, Chang HY, Yeh WT, Yeh CJ,
9:838. Lee WC. Body mass index and obesity-related meta-
71. Francis-Emmanuel PM, Thompson DS, Barnett AT, bolic disorders in Taiwanese and US whites and
Osmond C, Byrne CD, Hanson MA, et al. Glucose blacks: implications for definitions of overweight
metabolism in adult survivors of severe acute malnu- and obesity for Asians. Am J Clin Nutr. 2004;79:
trition. J Clin Endocrinol Metab. 2014;99:223340. 319.
72. Dagogo-Jack S. HIV therapy and diabetes risk 86. Yang W, Lu J, Weng J, Jia W, Ji L, Xiao J. Prevalence
(Editorial). Diabetes Care. 2008;31:12678. of diabetes among men and women in China. N Engl
73. Yarasheski K, Tebas P, Sigmund CM, Dagogo-Jack S, J Med. 2010;362:1090101.
Bohrer A, Turk J, Cryer PE, Powderly WG. Insulin 87. Pohl JH, Greer JA, Hasan KS. Type 2 diabetes mel-
resistance in HIV-protease inhibitor-associated diabe- litus in children. Endocr Pract. 1998;4:4136.
tes. J Acquir Immune Defic Syndr. 1999;21:20916. 88. Kaufman FR. Type 2 diabetes mellitus in children
74. Perreault L, Pan Q, Mather KJ, Watson KE, Hamman and youth: a new epidemic. J Pediatr Endocrinol
RF, Kahn SE, Diabetes Prevention Program Research Metab. 2002;15 Suppl 2:73744.
Group. Effect of regression from prediabetes to normal 89. Alberti G, Zimmet P, Shaw J, Bloomgarden Z,
glucose regulation on long-term reduction in diabetes Kaufman F, Silink M, Consensus Workshop Group.
risk: results from the Diabetes Prevention Program Type 2 diabetes in the young: the evolving epidemic:
Outcomes Study. Lancet. 2012;379:224351. the international diabetes federation consensus
75. Diabetes Prevention Program Research Group. workshop. Diabetes Care. 2004;27:1798811.
10-year follow-up of diabetes incidence and weight 90. Wiegand S, Maikowski U, Blankenstein O,
loss in the Diabetes Prevention Program Outcomes Biebermann H, Tarnow P, Gruters A. Type 2 diabetes
Study. Lancet. 2009;374:167786. and impaired glucose tolerance in European children
76. Lindstrm J, Ilanne-Parikka P, Peltonen M, Aunola and adolescents with obesity - a problem that is no
S, Eriksson JG, Hemi K. Sustained reduction in the longer restricted to minority groups. Eur
incidence of type 2 diabetes by lifestyle intervention: J Endocrinol. 2004;151:19920.
30 S. Dagogo-Jack
91. Caprio S. Development of type 2 diabetes mellitus in a visual method of teaching meal planning. DAIS
the obese adolescent: a growing challenge. Endocr Project Group. Diabetes Atherosclerosis Intervention
Pract. 2012;18:7915. Study. J Am Diet Assoc. 1998;98:11558.
92. TODAY Study Group. Rapid rise in hypertension and 106. Wing RR, Phelan S. Long-term weight loss mainte-
nephropathy in youth with type 2 diabetes: the TODAY nance. Am J Clin Nutr. 2005;82(Suppl):222S5.
clinical trial. Diabetes Care. 2013;36:173541. 107. Hamman RF, Wing RR, Edelstein SL, Lachin JM,
93. HEALTHY Study Group. A school-based interven- Bray GA, Delahanty L, Hoskin M, Kriska AM,
tion for diabetes risk reduction. N Engl J Med. Mayer-Davis EJ, Pi-Sunyer X, Regensteiner J,
2010;363:4435. Venditti B, Wylie-Rosett J, Diabetes Prevention
94. The Diabetes Prevention Program Research Group. Program Research Group. Effect of weight loss with
The Diabetes Prevention Program (DPP): descrip- lifestyle intervention on risk of diabetes. Diabetes
tion of lifestyle intervention. Diabetes Care. 2002;25: Care. 2006;29:21027.
216571. 108. Chiasson JL, Josse RG, Gomis R, Hanefeld M,
95. Eriksson KF, Lindgarde F. Prevention of type 2 Karasik A, Laakso M, STOP-NIDDM Trial Research
(noninsulin-dependent) diabetes mellitus by diet and Group. Acarbose for prevention of type 2 diabetes
physical exercise: the 6-year Malmo feasibility mellitus: the STOP-NIDDM randomised trial.
study. Diabetologia. 1991;4:8918. Lancet. 2002;359:20727.
96. Pate RR, Pratt M, Blair SN, Haskell WL, Macera 109. Orgerson JS, Hauptman J, Boldrin MN, Sjstrm
CA, Bouchard C, et al. Physical activity and public L. XENical in the prevention of Diabetes in Obese
health: recommendation from the Centers for Disease Subjects (XENDOS) study: a randomized study of
Control and Prevention and the American College of orlistat as an adjunct to lifestyle changes for the pre-
Sports Medicine. JAMA. 1995;273:4027. vention of type 2 diabetes in obese patients. Diabetes
97. Kimm SY, Glynn NW, Kriska AM, Barton BA, Care. 2004;27:15561.
Kronsberg SS, Daniels SR, et al. Decline in physical 110. DREAM (Diabetes REduction Assessment with
activity in black and white girls during adolescence. ramipril and rosiglitazone Medication) Trial
N Engl J Med. 2002;347:70915. Investigators. Effect of rosiglitazone on the fre-
98. Hood MS, Little JP, Tarnopolsky MA, Myslik F, quency of diabetes in patients with impaired glucose
Gibala MJ. Low-volume interval training improves tolerance or impaired fasting glucose: a randomised
muscle oxidative capacity in sedentary adults. Med controlled trial. Lancet. 2006;368:1096105.
Sci Sports Exerc. 2011;43:184956. 111. DeFronzo RA, Tripathy D, Schwenke DC, Banerji
99. Tate DF, Wing RR, Winett RA. Using Internet tech- M, Bray GA, Buchanan TA, ACT NOW Study, et al.
nology to deliver a behavioral weight loss program. Pioglitazone for diabetes prevention in impaired glu-
JAMA. 2001;285:11727. cose tolerance. N Engl J Med. 2011;364:110415
100. Neve M, Morgan PJ, Jones PR, Collins (Erratum in: N Engl J Med. 2011;365:189).
CE. Effectiveness of web-based interventions in 112. Zinman B, Harris SB, Neuman J, Gerstein HC,
achieving weight loss and weight loss maintenance Retnakaran RR, Raboud J, et al. Low-dose combina-
in overweight and obese adults: a systematic review tion therapy with rosiglitazone and metformin to
with meta-analysis. Obes Rev. 2010;11:30621. prevent type 2 diabetes mellitus (CANOE trial): a
101. Kodama S, Saito K, Tanaka S, Horikawa C, Fujiwara double-blind randomised controlled study. Lancet.
K, Hirasawa R, et al. Effect of Web-based lifestyle 2010;376:10311.
modification on weight control: a meta-analysis. Int 113. NAVIGATOR Study Group. Effect of valsartan on
J Obes (Lond). 2012;36:67585. the incidence of diabetes and cardiovascular events.
102. Kohl LF, Crutzen R, de Vries NK. Online prevention N Engl J Med. 2010;362:147790 (Erratum in: N
aimed at lifestyle behaviors: a systematic review of Engl J Med. 2010;362:1748).
reviews. J Med Internet Res. 2013;15:e146. 114. DPP Research Group. Effects of withdrawal from
doi:10.2196/jmir.2665. metformin on the development of diabetes in the dia-
103. Watson S, Woodside JV, Ware LJ, Hunter SJ, betes prevention program. Diabetes Care. 2003;26:
McGrath A, Cardwell CR, et al. Effect of a web- 97780.
based behavior change program on weight loss and 115. DREAM Trial Investigators. Incidence of diabetes
cardiovascular risk factors in overweight and obese following ramipril or rosiglitazone withdrawal.
adults at high risk of developing cardiovascular dis- Diabetes Care. 2011;34:12659.
ease: randomized controlled trial. J Med Internet 116. Tripathy D, Schwenke DC, Banerji M, Bray GA,
Res. 2015;17(7):e177. doi:10.2196/jmir.3828. Buchanan TA, Clement SC, et al. Diabetes incidence
104. US Department of Agriculture Center for Nutrition and glucose tolerance after termination of piogli-
Policy and Promotion. Dietary guidelines for tazone therapy: results from ACT NOW. J Clin
Americans. http://www.cnpp.usda.gov/dietaryguide- Endocrinol Metab. 2016:jc20154202. [Epub ahead
lines.htm. Accessed 5 Apr 2016. of print].
105. Camelon KM, Hdell K, Jmsn PT, Ketonen KJ, 117. Ramachandran A, Snehalatha C, Mary S, Selvam S,
Kohtamki HM, Mkimatilla S, et al. The Plate Model: Kumar CK, Seeli AC, Shetty AS. Pioglitazone does
not enhance the effectiveness of lifestyle modifica- have pre-diabetes and should be considered for met-
tion in preventing conversion of impaired glucose formin therapy. Diabetes Care. 2010;33:4954.
tolerance to diabetes in Asian Indians: results of the 125. Diabetes Prevention Program (DPP) Research
Indian Diabetes Prevention Programme-2 (IDPP-2). Group. Cost associated with the primary prevention
Diabetologia. 2009;52:101926. of type 2 diabetes mellitus in the Diabetes Prevention
118. Greenway FL. Physiological adaptations to weight Program. Diabetes Care. 2003;26:3647.
loss and factors favouring weight regain. Int J Obes 126. Diabetes Prevention Program Research Group.
(Lond). 2015. doi:10.1038/ijo.2015.59. Within-trial cost-effectiveness of lifestyle interven-
119. Nathan DM, Davidson MB, DeFronzo RA, Heine tion or metformin for the primary prevention of type
RJ, Henry RR, Pratley R, Zinman B. Impaired fast- 2 diabetes. Diabetes Care. 2003;26:251823.
ing glucose and impaired glucose tolerance. Diabetes 127. Herman WH, Hoerger TJ, Brandle M, Hicks K,
Care. 2007;30:7539. Sorensen S, Zhang P, Diabetes Prevention Program
120. Twigg SM, Kamp MC, Davis TM, Neylon EK, Flack Research Group, et al. The cost-effectiveness of life-
JR. Australian Diabetes Society and Australian style modification or metformin in preventing type 2
Diabetes Educators Association. Prediabetes: a posi- diabetes in adults with impaired glucose tolerance.
tion statement from the Australian Diabetes Society Ann Intern Med. 2005;142:32332.
and Australian Diabetes Educators Association. 128. Diabetes Prevention Program Research Group. The
Med J Aust. 2007;186:4615. 10-year cost-effectiveness of lifestyle intervention or
121. Indian Health Services. 2008 IHS guidelines for care of metformin for diabetes prevention: an intent-to-treat
adults with prediabetes and/or the metabolic syndrome analysis of the DPP/DPPOS. Diabetes Care. 2012;
in clinical settings. http://aianp.ucdenver.edu/sdpi/com- 35:72330.
mon/initiative/DP_Appendices/DPIAN6%20IHS%20 129. Ramachandran A, Snehalatha C, Yamuna A, Mary S,
Guidelines%20PreDiabetes%20Metsyn%20Sept%20 Ping Z. Cost-effectiveness of the interventions in the
2008.pdf. Accessed 3 Apr 2016. primary prevention of diabetes among Asian Indians:
122. Dagogo-Jack S, Askari H, Tykodi G. Glucoregulatory within-trial results of the Indian Diabetes Prevention
physiology in subjects with low-normal, high- Programme (IDPP). Diabetes Care. 2007;30:254852.
normal, or impaired fasting glucose. J Clin 130. Ackermann RT, Marrero DG, Hicks KA, Hoerger
Endocrinol Metab. 2009;94:20316. TJ, Sorensen S, Zhang P, et al. An evaluation of cost
123. Kanat M, Mari A, Norton L, Winnier D, DeFronzo sharing to finance a diet and physical activity inter-
RA, Jenkinson C, Abdul-Ghani MA. Distinct -cell vention to prevent diabetes. Diabetes Care. 2006;29:
defects in impaired fasting glucose and impaired 123741.
glucose tolerance. Diabetes. 2012;61:44753. 131. Dagogo-Jack S. 2015 Presidential address: 75 years
124. Rhee MK, Herrick K, Ziemer DC, Vaccarino V, of battling diabetes-our global challenge. Diabetes
Weintraub WS, Narayan KM, et al. Many Americans Care. 2016;39:39.
Diabetes in Sub-Saharan Africa
3
Felix Assah and Jean Claude Mbanya
Overview Diabetes prevalence in adults is in general

much higher on islands in sub-Saharan Africa,
Type 2 diabetes1 is a global problem with major compared to the mainland. The highest prevalence
public health and socioeconomic challenges. is found in the Seychelles (17.4 % age-adjusted
From recent estimates of the International comparative prevalence, 17.4 % raw prevalence),
Diabetes Federation (IDF) [1], the number of followed by the island of Reunion (15.8 % age-
adults with diabetes in the world currently stands adjusted, 18.2 % raw) and Comoros (9.9 % age-
at 415 million with a projected rise to 642 million adjusted, 7.5 % raw). Some of Africas most
by 2040. An estimated 14.2 (9.529.4) million populous countries have the highest numbers of
people aged 2079 have diabetes in the sub- people with diabetes, including South Africa (2.3
Saharan Africa (SSA) region, representing a [1.24.6] million), Democratic Republic of
regional prevalence of 2.16.7 %. SSA has the Congo (1.8 [1.52.2] million), Nigeria (1.6 [1.2
highest proportion of undiagnosed cases of dia- 3.8] million) and Ethiopia (1.3 [0.83.5] mil-
betes; over two-thirds (66.7 %) of people with lion). Nearly half of all adults with diabetes in the
diabetes are unaware of their status. The majority region live in these four countries [1].
of people with diabetes (58.8 %) live in cities, Despite the paucity of data from Africa, over
even though the population in the region (61.3 %) the past few decades, diabetes, which was previ-
is predominantly rural. With increasing urbanisa- ously considered to be rare or unknown in rural
tion and population ageing, diabetes will pose an Africa, has emerged as an important non-
even greater threat. It is expected that by 2040 communicable disease (NCD) in the region
there will be 34.2 million adults in the region liv- [24]. Global estimates and projections [1, 57]
ing with diabetes, more than double the number confirm the diabetes epidemic, through the
in 2015 [1]. increasing numbers of people with diabetes and
impaired glucose tolerance (IGT). These reports
not only show that diabetes in adults is a global
1
This chapter will focus on type 2 diabetes and will be problem but also that populations of developing
referred to as diabetes throughout.
countries, minority groups and disadvantaged
communities in industrialised countries face the
F. Assah, MD, PhD (*) J.C. Mbanya, MD, PhD, FRCP greatest risk. The large increase that is expected
Faculty of Medicine and Biomedical Sciences,
to occur in developing regions of the world has
University of Yaound I, Yaound, Cameroon
e-mail: [email protected]; principally been attributed to population ageing
[email protected] and urbanisation [1, 5, 7].

DOI 10.1007/978-3-319-41559-8_3
34 F. Assah and J.C. Mbanya
Epidemiology of Diabetes in Africa The burden of diabetes in sub-Saharan Africa is

already substantial and continues to increase at a
Historical Perspective very rapid rate. A recent review paper reported that
diabetes in sub-Saharan African countries has
In 1901, Doctor Cook, a medical missionary reached epic proportions. The overall pooled prev-
working in Uganda, reported that diabetes was alence was estimated at 5.7 % for diabetes, 4.5 %
rather uncommon, but very fatal in sub-Saharan for impaired fasting glycaemia and 7.9 % for
Africa [8]. For over half a century after that, dia- impaired glucose tolerance [13]. Diabetes preva-
betes continued to be regarded as a disease of lence in sub-Saharan African countries varies by
affluent societies. Almost no data was available two factors: the first is the level of urbanisation,
as very few studies were carried out on diabetes from 1 % in rural Uganda to 12 % in urban Kenya,
in sub-Saharan Africa until the latter half of the and the second is by ethnicity, from 8 % in
twentieth century. The limited number of early Zimbabwe to 18 % in sub-Saharan African coun-
studies completed between the 1960s and early tries with advanced economies or with significant
1980s reported prevalence rates of mostly <1 %, numbers of Indian subpopulations such as South
except for South Africa with 0.63.6 % and Africa, Kenya and Seychelles [10, 14]. Data from
Ivory Coast with 5.7 % [2]. Doctor Cooks ini- several point prevalence studies in Cameroon show
tial report is no longer accurate today as it is a more than tenfold increase in diabetes prevalence
known that most of the people living with diabe- over a period of one decade [15]; Fig. 3.1.
tes are in developing countries. The burden of Current predictions estimate that the number
diabetes in sub-Saharan Africa is already sub- of people living with diabetes on the continent
stantial and continues to increase at a very rapid will almost double over the coming 20 years [1,
rate. Current predictions estimate that the num- 51, 110]. This, together with the growing inci-
ber of people living with the chronic condition dence of type 2 diabetes in younger age groups
on the continent will almost double over the (including in some obese children even before
next 20 years [1]. puberty), constitutes a serious cause for concern.
In developed countries, most people with diabetes
are above the age of retirement (>60 years), whilst
Current Trends in developing countries, those most frequently
affected are in the middle, productive years of
Sub-Saharan Africa is currently facing a multi- their lives, aged between 35 and 64 [16]. All types
ple disease burden characterised by simultane- of diabetes are on the increase, particularly type 2
ous health challenges from chronic diabetes, and the number of people with diabetes
non-communicable diseases (NCDS), HIV/ will increase by 55 % by 2035 [1] (Fig. 3.2) (IDF
AIDS, other infectious diseases and malnutrition 2015). This underlines the fact that the economic
[9]. The emerging and increasing burden of obe- burden of diabetes in developing countries will be
sity, diabetes and other NCDs is not accompa- amplified by its effect on the working age group.
nied by any marked improvements in control of
infections or undernutrition. Studies have
reported high rates of coexistence of obesity and Risk Factors for Diabetes in Africa [9]
undernutrition in the same communities and
even same households [10, 11]. The current epi- Age, Gender and Family History
demiologic transition in sub-Saharan Africa is
unique and not the same as most Western coun- Similar to data from other parts of the world, stud-
tries. The transition in Africa follows a delayed ies from sub-Saharan Africa (SSA) show that dia-
model [12] which is characterised by high fertil- betes prevalence increases with age (Fig. 3.3)
ity and high but reducing mortality, resulting in a [1821]. Therefore, as living standards improve
double demographic disease pattern. in SSA with a resulting increase in life expectancy,
3 Diabetes in Sub-Saharan Africa 35
9
Men urban
8
Women urban
7
Men rural
Prevalence (%)
6
Women rural
5
4
3
2
1
0
1994 1998 2003
Fig. 3.1 Prevalence of type 2 diabetes in Cameroon, 19942003 (prevalence standardised to new world population
distribution)
IDF 2013 2035 Increase

region Millions Millions %
Africa 19.8 41.4 109 %
Middle East and North Africa 34.6 67.9 96 %
South-East Asia 72.1 123 71 %
South and Central America 24.1 38.5 60 %
Western Pacific 138.2 201.8 46 %
North America and Caribbean 36.7 50.4 37 %
Europe 56.3 68.9 22 %
World 381.8 591.9 55 %
Fig. 3.2 The number of people living with diabetes in Africa, EUR Europe, NAC North America and Caribbean,
2013 and projections for 2035 (in millions of cases), with SACA South and Central America, SEA South-East Asia,
projected percent changes (Source of data: IDF Diabetes WP Western Pacific)
Atlas [17]. AFR Africa, MENA Middle East and North
Prevalence (%) estimates of

diabetes by age
(2079 years) and sex
Male
Female
7
<2 2
24
46 1
68
810
>10 0
20-29 30-39 40-49 50-59 60-69 70-79
* Comparative prevalence
Fig. 3.3 An estimated number of adults with diabetes in sub-Saharan Africa by age group and sex (Source of data: IDF [1])
the prevalence of diabetes is expected to increase Asian Indians [2729] and when compared with a
accordingly. In addition, the age at onset of diabe- population of mixed ancestry (Khoi-East Indian-
tes may shift more towards younger adults due to Europid) [30] (Table 3.1). The prevalence rates in
the effects of urbanisation and westernisation Caucasians in SSA have been quite similar to those
increasing obesity, sedentary lifestyle and other in Europe (610 %), also relatively high [31].
diabetes risk factors in younger age groups. SSA is experiencing the fastest rate of urban-
There is no discernable gender difference in isation worldwide, with an average annual rate of
either the prevalence or distribution of diabetes in change of the urban population of more than 3 %
SSA [22]. This is consistent with observations [34]. Currently, more than one-third of the popu-
from other parts of the world as well as with lation in SSA live in urban areas. It is estimated
global estimates [23]. It must also be noted that a that this could increase to 45 % by 2025, with a
positive family history of diabetes is an indepen- demographic inflection point to be attained by
dent diabetes risk factor [18, 19, 24]. 2035 more urban than rural residents [35]. This
increase in the urban population is influenced by
both the inherent growth of the urban population
Ethnicity, Urbanisation, Migration due to persistent high fertility and longer life
and Diabetes expectancy, and also a massive rural-urban
migration [34]. This rapid urbanisation in SSA
Studies from Tanzania and South Africa have shown has been identified as a major determinant of the
that diabetes prevalence is lower in the indigenous rising burden of diabetes and other cardiovascu-
African community [20, 25, 26] than in migrant lar diseases [12, 23, 36, 37].
Table 3.1 Ethnic differences in the prevalence of diabetes mellitus (D) and impaired glucose tolerance (IGT) and the
effect of migration in Africa
Country Author year Ethnic group Prevalence (%)a
Locality (Reference) D IGT
Tanzania McLarty (1989) [26] Native African 1.1 8.4
Ramaiya (1991) [27] Asian Indian 9.1 16.2
Swai (1990) [28] Asian Indian 7.1 21.5
South Africa
KwaZulu Natal Omar (1993) [25] Native African 5.3 7.7
Omar (1994) [29] Asian Indian 13.0 6.9
Cape Province Levitt (1993) [20] Native African 8.0 7.0
Levitt (1999) [30] Mixed ancestry 10.8 10.2
(Khoi-East
Indian-Europid)
Sudan Elbagir (1996) [19] Native African 3.4b 2.9b
Elbagir (1998) [18] Mixed Egyptian 10.4 9.8
ancestry
Nigeria Cooper (1997) [32] Native African 2.0
Caribbean African origin 7.2
United States African origin 10.8
United Kingdom African origin 10.6
Cameroon Rural Mbanya (1999) [33] Native African 0.8 6.4/3.1c
Cameroon Urban Native African 2.0 1.6/4.6c
Caribbean African origin 8.5 16.3/19.6c
United Kingdom African origin 14.6 11.1/14.4c
a
Age-adjusted prevalence except where indicated
b
For crude prevalence
c
Male/female
Many studies have clearly demonstrated a first 6 months of urban residence, there was no
positive rural-urban gradient in the prevalence of significant change in their HbA1c level compared
diabetes and its risk factors, particularly obesity. to an age, sex and village-matched nonmigrant
Urban residence is associated with a two- to five- cohort. However, there was an increase in mean
fold increased risk of prevalent diabetes or body mass index (BMI) in the recent migrants
impaired fasting glycaemia (Fig. 3.4) [18, 21, 33, compared to the nonmigrants. More data is
36, 3842]. Most of these studies considered needed to provide answers about societal changes
only the current residence and so may be con- and their influence on human behaviour and car-
founded by the effects of recent rural-urban diovascular risk factors such as diabetes.
migration or vice versa. A study from Cameroon A limitation to the discussion on urban and
[43] that examined both current urban residence rural differences is the lack of a universally
as well as total lifetime exposure to an urban accepted definition for an urban area. Studies
environment found that both lifetime exposure to of rural-urban differences in diabetes have
an urban environment and current residence were used local or national norms to define urban-
independently associated with diabetes. Lifetime ised regions, which may not be similar across
exposure to an urban environment was strongly studies. The existence of geographically sepa-
associated with fasting blood glucose (r = 023; rate residential areas by social class within
P < 0001), with the prevalence of diabetes or IFG urban areas may further confound observed
being higher for individuals with a longer expo- differences between studies. Apart from het-
sure to the urban environment. erogeneity in the definition and attributes of
Most of these studies from SSA are cross- urban area across studies, the degree of
sectional studies, requiring that inferences about urbanisation may influence the magnitude of
causality or direction be made with caution. differences in estimates of diabetes or its risk
Longitudinal studies to provide more robust data factors. A study in Benin [44] that recruited
on direction and magnitude of change are almost participants from rural, semiurban and urban
inexistent. In a prospective study of recent rural- areas observed a positive rural and semiurban
to-urban migrants in Tanzania [42], during the to urban gradient in metabolic syndrome and
10
Fig. 3.4 Prevalence of 0

diabetes mellitus (D) in
4)
7)
4)
3)
9)
0)
6)
(2
(2
(3
(3
(2
(3
(3
rural [ ] and urban [ ]

n
ia
ia
a
n
n
a
oo
ric
da
da
ne
an
an
communities in community
Af
er
Su
Su
ui
nz
nz
G
am
studies in Africa, using

Ta
Ta
ut
C
So
randomly selected samples

obesity, but not for blood glucose or prevalence generally neglected in terms of healthcare and
of diabetes. The prevalence of high fasting research, hence the scanty nature of data about
blood glucose was significantly lower in urban them. A study from South Africa reported a dia-
dwellers compared to their semiurban or rural betes prevalence of about 5 % among the QwaQwa
counterparts. people [46]. There is currently an increasing
The impact of environmental influence global awareness of the vulnerability of indige-
(migration) in populations of similar genetic ori- nous peoples as a result of their socioeconomic
gin has been confirmed in two studies which disadvantage, limited access to care and margin-
showed that diabetes prevalence was lower in alisation from the majority of the population [17].
native West African populations in Nigeria and From the above data, it appears to be difficult
Cameroon than in West Africanorigin commu- to categorise ethnicity, urbanisation and migra-
nities living abroad, in the Caribbean, United tion as distinct and separate risk factors for diabe-
Kingdom and United States [32, 33] (Table 3.1). tes. Instead, the correlation should be noted and
In a study comparing rural and urban Ghanaians further study undertaken in this area.
in Ghana with Ghanaians in the Netherlands [45]
adjusting for age and educational level, the Diabetes and Obesity
Ghanaians living in the Netherlands were more Published studies indicate a simultaneous rise in
likely to be obese than those in rural Ghana. overweight/obesity and diabetes prevalence in
Currently, there are growing concerns about most SSA countries [47] (Fig. 3.5). Most people
the diabetes burden in indigenous populations with diabetes are obese at the time of diagnosis
because these populations may be experiencing a [48]. Studies conducted in African countries
very rapid lifestyle transition. Active subsistence (Ghana [49, 50], Togo [51], Rwanda [52], South
lifestyle is rapidly giving way to sedentary Africa [53] and Nigeria [69]) have reported sig-
Western lifestyles. Indigenous populations are nificant associations between type 2 diabetes and
80
70
60
50
40
Overweight/obesity
30
Diabetes
20
10
0
a n a i n bia ea ya wi ali ia e n s a o ia e
gol ni an nd oo n n la M tan iqu nio elle fric Tog an bw
An Be tsw uru er am Gui Ke Ma r i b eu ch A n z ba
Bo
B am G q au am R ey uth Ta Zim
C E M oz S So
M
Fig. 3.5 Comparison of overweight/obesity and diabetes prevalence in sub-Saharan Africa (SSA)
obesity. Many studies of people living with dia- escalate the development of these disorders. This
betes in Africa have consistently reported excess combination of childhood stunting and adulthood
body weight in >50 % of studied samples. obesity has led to the proposition that such indi-
However, there is lack of agreement regarding viduals in their early years acquire the conten-
which of the anthropometric variables used to tious thrifty phenotype such that when they
measure obesity can best predict the develop- rapidly adapt to sedentary lifestyles and high-
ment of diabetes. One case-control study con- calorie diets later in their lives, they will be highly
ducted in a Ghanaian sample [50] suggests that prone to obesity-related disorders [59, 63]. The
measures of central, rather than general, obesity thrifty phenotype hypothesis seems to apply bet-
appear to be significantly related to type 2 diabe- ter for the sub-Saharan African populations
tes in Africans. There is little or no data from rather than the thrifty gene hypothesis (theorises
longitudinal studies with hard endpoints that can that genes derived from times of deprivation may
shed more light on the predictive value of these result in adaptations that have adverse effects in
different measures of obesity in Africans. This times of plenty) [59, 64]. This is because the
means that there are no African-specific cut-off prevalence rates of T2DM and obesity have been
points for estimating obesity risk, hence the con- on the increase since the advent of dramatic
tinued use of Caucasian cut-off points for nutritional/lifestyle changes.
Africans. Further research is needed to establish
cut-off points based on African data [55].
Physical Activity, Diet and Diabetes
Adiposity Available data strongly links the current epide-

miological transition in SSA with rapid urbanisa-
In most studies in sub-Saharan Africa (SSA), tion and westernisation of lifestyle. This changing
adiposity has generally been found to be associ- lifestyle is characterised by decreased levels of
ated with diabetes. These studies have shown physical activity and increased consumption of
that diabetes prevalence is higher with increased energy dense or high-fat diets. Although the sug-
BMI (BMI-specific rates) [24, 26, 32, 56], gestion of lower physical activity in urban areas
waist-hip ratio (WHR-specific rates) [20, 24, compared to rural areas is intuitively plausible,
57] and waist circumference (WC-specific rates) most of the studies on physical activity levels
[24]. This means that overall obesity (BMI) as have used self-reported information, mainly
well as central obesity (WC and WHR) are asso- using physical activity questionnaires which have
ciated with an increased risk for diabetes. not been validated in the population [30, 43, 65
Some researchers have been proposing theories 69]. Few studies have used locally validated
suggesting that some alternate distributions of physical activity questionnaires to demonstrate
body fat (such as in the hips, thighs or legs) could an urbanisation gradient [42, 70] and the
confer lower risk for diabetes. The protective role increased risk of diabetes associated with reduced
of hip circumference as observed in rural South physical activity levels [30].
Africans, confirming recent findings in Australians, Studies documenting temporal trends of phys-
requires further evaluation in Africa [24]. ical activity levels in SSA using comparable
Emerging evidence is demonstrating that pres- methods are lacking. The adoption and use of the
ent day lifestyle habits are not the only contribut- WHO STEPS Global Physical Activity
ing factor to adiposity. The developmental origins Questionnaire for surveillance of habitual physi-
of adult disease suggest that intrauterine growth cal activity by many SSA countries [71] will
retardation and the resulting low birth weight hopefully provide some answers in the near
predispose individuals to metabolic disorders in future about trends in population levels of physi-
their adulthood [5860]; the high prevalence of cal activity over time despite the limitations of
stunting and malnutrition [61, 62] in SSA might self-reported physical activity [68, 69].
Most of the studies which have used objective that the adult population will be decimated by
methods to measure physical activity or energy HIV/AIDS and that few will live long enough to
expenditure are small etiologic studies in specific develop such diseases. However, a South African
populations or questionnaire validation studies study [80], which modelled the impact of HIV/
[6567, 70, 7274] and may not be representative AIDS for the years 1995 and 2010, clearly
of the general population. However, a study in showed that the total number of people with dia-
Cameroon [65] using the doubly labelled water betes and the number of people with diagnosed
method to measure physical activity in free-living diabetes (patient load) will increase regardless of
adults found physical activity energy expenditure the expected impact of HIV/AIDS on population
to be inversely associated with 2-h glucose levels growth rates and any change (no change, increase)
independent of age, sex, adiposity or aerobic fit- in diabetes prevalence. Since this analysis did not
ness. Larger studies in Cameroon and Kenya take into consideration the potential impact of
have used a combined heart rate and motion sen- antiretroviral therapy (ART) on improving sur-
sor to objectively measure physical activity in vival rates or possible increase in diabetes inci-
free-living individuals [39, 75, 76]. These studies dence, it is likely to be a conservative estimate.
demonstrate a significantly higher physical activ- However, the ART of choice in sub-Saharan
ity level in rural compared to urban dwellers, and Africa, with its limited healthcare resources, has
a beneficial association between physical activity been linked with an increase in the numbers of
and abnormal glucose tolerance. people developing prediabetes, and its increased
A high-fat, high-calorie diet is associated use in the treatment of HIV/AIDS is also pro-
with the development of obesity and diabetes. jected to cause adverse metabolic abnormalities
The difficulties of assessing diet and nutritional among patients in SSA [81]. Because of the sheer
data in free-living individuals in epidemiologic numbers of people with HIV/AIDS, this effect
studies pose an even bigger challenge in could directly influence the emerging diabetes
many resource-limited settings. Consequently, crisis in sub-Saharan Africa. Long-term studies
population level dietary data relevant to diabe- to examine the effect of ART on the rising burden
tes and other chronic NCDs in SSA are scanty of diabetes in SSA are needed.
[7779]. A study in South African Blacks
showed a temporal trend of increasing con-
sumption of fat and decreasing carbohydrates Clinical Manifestations
in both urban and rural areas [77]. However,
urbanisation may also lead to a better supply of The presence of atypical forms of diabetes in
fruits and vegetables which improve the micro- sub-Saharan Africa makes it sometimes difficult
nutrient and fibre content of the diet in urban to classify persons living with diabetes based on
compared to rural areas [79]. The notion of established clinical criteria. The disease process
increased consumption of fat as a marker of may involve peripheral resistance to insulin,
urbanisation and westernisation of the African increased hepatic production of glucose and lack
diet is not supported by the findings of a study of insulin production from the pancreas. There
by Mennen et al. which reported the highest are also other causes of diabetes such as genetic
consumption of fat in rural Cameroonians, abnormalities, surgery, drug usage and infectious
compared to urban Cameroonians, Black diseases [82].
Jamaicans and Blacks in Manchester, UK [78]. Diabetes mellitus is defined as a metabolic
disorder caused by different factors characterized
by a chronic high level of blood sugar with distur-
Impact of HIV/AIDS bances to carbohydrate, fat, and protein metabo-
lism resulting from defects in insulin secretion,
In SSA, chronic NCDs such as diabetes receive insulin action, or both [83]. Scientists have
limited attention due in part to misconceptions divided diabetes into three different types: Type 1
diabetes mellitus (formerly insulin-dependent hope for widespread use in both clinical and
diabetes mellitus IDDM) or type 1 diabetes is research settings even in remote parts of the
also known as juvenile onset diabetes. Type 2 continent.
diabetes mellitus (non-insulin-dependent diabe- Beran et al. surveyed the availability of diag-
tes mellitus (formerly non-insulin-dependent dia- nostic testing tools in a sample of healthcare set-
betes, NIDDM) or type 2 diabetes adult-onset tings in three countries and found that in
diabetes) is found in individuals who are insulin- Mozambique, urine glucose strips were available
resistant and who usually have relative insulin in only 18 % of health facilities surveyed, ketone
deficiency. Gestational diabetes mellitus (GDM), testing strips in 8 % and blood glucose metres in
the third type, is defined as any degree of glucose 21 %, whilst availability in Mali was 54, 43 and
intolerance with onset or first recognition during 13 % and in Zambia 61, 54 and 49 %, respectively
pregnancy. Recently, diabetologists have added a [87, 88]. Low levels of adequate glucose control
fourth category, tropical diabetes, suggested first in those diagnosed with diabetes were reported in
in 1907, but made popular by Hugh Jones (J-type several prevalence studies [89, 90]. Only 27 % of
diabetes) during the mid-1950s by his study of people diagnosed with type 2 diabetes receiving
13 Jamaican patients [84, 85]. However, tropical treatment in a study conducted in Cameroon had
diabetes is less than 1 % of the diabetes cases in adequately controlled glucose levels [89]. Of the
Africa and is thought to be related to malnutri- 99 people with type 1 diabetes in a Tanzanian
tion [31]. survey, only one person achieved suggested glu-
The diagnosis of diabetes usually involves cose targets [90]. None of the 99 people with type
symptoms of diabetes plus either casual plasma 1 diabetes had the ability to monitor their glucose
glucose concentration 200 mg/dl (11.1 mmol/l), levels at home, and hospitals were unable to rou-
a fasting plasma glucose 126 mg/dl (7.0 mmol/l) tinely do this [68]. A regular supply of insulin
or a 2-h post-load glucose 200 mg/dl was unaffordable for many people with diabetes,
(11.1 mmol/l) during an oral glucose tolerance with 1 months insulin supply costing 19.6 days
test (OGTT) conducted as per WHO recommen- wages in Malawi [91] and 25 % of the minimum
dations using a glucose load containing the wage in Tanzania [92]. One Sudanese study
equivalent of 75 g anhydrous glucose dissolved found that 65 % of a familys annual household
in water [48]. In 2010, a WHO expert committee expenditure on health was spent on caring for a
further adopted cut-off points for using glycated diabetic child [93].
haemoglobin (HbA1c) in the diagnosis of diabe- Beran and Yudkin found that state interven-
tes. It concluded that HbA1c can be used as a tions affected insulin price, reporting that an
diagnostic test for diabetes providing that strin- annual supply of insulin cost 5 % of GDP in
gent quality assurance tests are in place and Mozambique, where it was subsidised by the
assays are standardised to criteria aligned to the government, whereas it cost 25 % of GDP in Mali
international reference values, and there are no without subsidies [88]. One study investigated
conditions present which preclude its accurate insulin availability and reported that one in five
measurement. An HbA1c of 6.5 % was therefore hospitals and none out of six health centres sur-
recommended as the cut-off point for diagnosing veyed had a regular insulin supply [87].
diabetes, though a value less than 6.5 % does not
exclude diabetes diagnosed using glucose tests
[86]. The practicality of using HbA1c for diabe- Economic Cost of Diabetes
tes diagnosis in Africa still faces challenges, par-
ticularly the high cost of the test relative to blood Healthcare in most of SSA is almost entirely pri-
glucose measurements and also the high preva- vately purchased, even though the majority of the
lence of haemoglobinopathies such as sickle cell poorest people on earth live in SSA. A recent study
anaemia. As the OGTT is much more demanding by Kirigia et al. [94] clearly demonstrates that the
in terms of time and logistics, HbA1c offers real cost of diabetes care is going to be overwhelming
for the poorest countries of the region. This study insulin. In a study on type 1 diabetes patients in
shows that whilst the direct cost of diabetes per Sudan, Elrayah et al. [93] reported a partial direct
person with diabetes is only a fraction (<25 %) of cost of care for each child with type 1 diabetes of
the GNI per capita for the 12 richest countries, the USD 283, in a country with a GDP per capita of
direct cost for the 34 poorest countries of the USD 300 and a per capita government expendi-
region is 125 % of their GNI per capita (Fig. 3.6). ture on health of USD 300.
For these poorest countries, the total cost (direct These data indicate undeniably that the cost of
and indirect costs) of diabetes per person with dia- diabetes care constitutes a huge burden for
betes is more than double the GNI per capita. SSA. In the absence of a publicly funded health-
The few studies which have examined the cost care system, these costs are borne almost entirely
of diabetes care (usually in small samples) in the by individuals individuals who are among the
region confirm the above estimates. Akoussou- poorest people in the world. In this context, poor
Zinsou and Amedegnato reported in 2001 that the disease prognosis, with high morbidity and mor-
direct cost of diabetes care at a teaching hospital tality seem to be the unavoidable outcome.
in Togo was USD 342 and USD 110 per person
for complicated and uncomplicated diabetes
patients, respectively. The estimated GNI per Healthcare Access for Diabetes
capita for Togo at the time was approximately and its Complications
USD 385. Chale et al. [95] reported an average
annual direct cost of diabetes care in Tanzania in Many SSA countries have made significant
19891990 of USD 287 for a patient requiring efforts in initiating and improving care for diabe-
insulin and USD 103 for a patient not requiring tes and other chronic diseases. However, two-
12
Average GNI per capita

Amount (thousands of International dollars)
10
Average direct cost per person with diabetes
Average indirect cost per person with diabetes

8
Average total cost per person with diabetes

6
0
Group 1 Group 2 Group 3
Countries
Fig. 3.6 Direct, indirect and total cost of diabetes per ing to the average GNI per capita of the countries (Adapted
person with diabetes compared to the average GNI per from Kirigia et al. [94])
capita in countries of WHO Africa region grouped accord-
thirds of people with diabetes in low- and Control of blood glucose and blood pressure is
middle-income countries have poor diabetes con- very poor.
trol because of inadequate access to care oral Referral systems are inadequate.
antidiabetic agents and insulin are not available Patient education is almost nonexistent.
at all times in many parts of the developing world Organisation of services is generally poor.
[96]. A few countries have now established suc- Better record keeping will assist improve-
cessful National Diabetes Programmes and ments in care.
guidelines for the management of diabetes [97
99]. For most countries, there is still much Therefore, even when diabetes care pro-
improvement required. Limited financial grammes are introduced, a lot will still need to be
resources are a major handicap even with the done to enable them meet their objective of
availability of scientific information and political reducing morbidity and mortality linked to diabe-
will both of which are still largely lacking in tes and its complications. A few of the drawbacks
many SSA countries. above relate to inadequate healthcare staff levels
It is possible to set up effective diabetes as well as patient-related factors. Patient educa-
care at the peripheral level using basic tion and empowerment in the form of a peer sup-
resources in terms of personnel and equipment. port system could offer some hope of better
Nurse-led care including education has been diabetes control by improving compliance and
shown to be successful in resource-limited set- optimising self-care practices.
tings over an 18-month period [100]. It would
however be a real challenge to translate such
experiments over a larger scale and a much Advocacy and Policy for Diabetes
longer period. Work carried out by the Control and Prevention
International Insulin Foundation [101] identi-
fied key areas to be addressed in the fight The adoption of a World Diabetes Day
against diabetes in SSA, encompassing policy Resolution by the United Nations General
improvement, better organisation and delivery Assembly [103] is acknowledgement of the
of care and patient education. Whiting et al. fact that diabetes is a real and imminent threat
[102] reviewed challenges to the delivery of to social and economic development globally.
diabetes care in a few countries which had The UN resolution calls for member states to
reported data on diabetes healthcare delivery, develop national policies for the prevention,
and could still identify the following barriers treatment and care of diabetes in line with the
to adequate diabetes care: sustainable development of their healthcare
systems, taking into account the internation-
Patient attendance is poor (there are many rea- ally agreed development goals, including the
sons for this and more work is required to Millennium Development Goals. In SSA spe-
explore them). cifically, the IDF Africa Region, the World
Consultation times are very short, leaving lit- Health Organization (WHO)-AFRO and the
tle or no time for patient education. African Union have jointly issued a Diabetes
Staff levels are inadequate and more use could Declaration and Strategy for Africa [104]. The
be made of trained nurses and other health declaration is a call to action for governments
workers. of African countries and all partners and
Staff training is limited, and continuing edu- stakeholders in diabetes to prevent diabetes
cation or in-service training, especially of and related non-communicable diseases and
lower cadres, is needed. to improve quality of life and reduce morbid-
Complications are not monitored or evaluated ity and premature mortality from diabetes
in a systematic manner. (Panel).
Future Perspectives of Diabetes

The IDF-Africa, the WHO-AFRO and Prevention and Control
the Africa Union call on governments of
African countries, non-government organ- Diabetes is perhaps the index case of the general
isations, international donor agencies, problem of non-communicable disease health-
industry, health care providers and all part- care delivery in developing countries. There have
ners in diabetes to ensure: been scattered reports [100, 105109] of success-
ful attempts to improve diabetes care delivery
Adequate, appropriate and affordable and outcome, but sadly these have largely been
medications and supplies for people liv- initiated either by local hospitals or by external
ing with diabetes funding and support. The lessons appear to be
Earlier detection and optimal quality of that real improvements in diabetes care and
care for diabetes outcome in Africa are achievable. However,
Effective efforts to create healthier envi- although external support, local health facilities,
ronments and prevent diabetes support groups and diabetes associations all have
The identification and dissemination of a role to play, national government health depart-
information, education and communica- ments need to take the responsibility of instigat-
tion to empower people with diabetes to ing widespread permanent change and
access appropriate diabetes services and improvement. The costs need not be great, as
improve self-care patient education (one of the least expensive of
Equitable access to care and prevention diabetes treatments) has been shown to be a
services for people with or at risk of major and effective part of all the currently
diabetes described care delivery packages [100, 105109].
Awareness of diabetes in the community The integration of traditional healers should also
and among health care providers be considered as part of these reforms, since, to
A truly integrated approach which uti- the everyday African, they are very much a part
lises the whole health workforce to of illness management.
address infectious and non-
communicable diseases simultaneously
Government commitment to reducing References
the personal and public health burden of
diabetes 1. International Diabetes Federation. IDF diabetes atlas.
Partnership and collaboration within Brussels, Belgium: International Diabetes Federation;
7th ed. 2015.
and between government sectors, pri-
2. McLarty DG, Pollitt C, Swai AB. Diabetes in Africa.
vate sectors, non-government organisa- Diabet Med. 1990;7(8):67084.
tions and communities to create 3. Motala AA, Omar MA, Pirie FJ. Diabetes in Africa.
community and workplace environ- Epidemiology of type 1 and type 2 diabetes in Africa.
J Cardiovasc Risk. 2003;10(2):7783.
ments that promote better health.
4. Levitt NS. Diabetes in Africa: epidemiology, man-
agement and healthcare challenges. Heart. 2008;
94(11):137682.
5. International Diabetes Federation. IDF diabetes atlas.
Brussels, Belgium: International Diabetes Federation;
The advocacy for diabetes prevention and
3rd ed. 2008.
control in SSA is largely based on general prin- 6. King H, Aubert RE, Herman WH. Global burden
ciples that are generally accepted. There is very of diabetes, 19952025: prevalence, numerical esti-
little evidence available from local data to sub- mates, and projections. Diabetes Care. 1998;21(9):
141431.
stantiate the implementation of prevention or
7. Wild S, Roglic G, Green A, Sicree R, King
control interventions. H. Global prevalence of diabetes: estimates for the
year 2000 and projections for 2030. Diabetes Care. 23. International Diabetes Federation. IDF diabetes atlas.
2004;27:104753. Brussels, Belgium: International Diabetes Federation;
8. Cook A. Notes on the diseases met with in Uganda, 4th ed. 2009.
Central Africa. J Trop Med. 1901;4:1758. 24. Motala AA, Esterhuizen T, Gouws E, Pirie FJ, Omar
9. Mbanya JC, Motala AA, Sobngwi E, Assah FK, MA. Diabetes and other disorders of glycemia in a
Enoru ST. Diabetes in sub-Saharan Africa. Lancet. rural South African community: prevalence and
2010;375(9733):225466. associated risk factors. Diabetes Care. 2008;31(9):
10. Hall V, Thomsen RW, Henriksen O, Lohse N. Diabetes 17838.
in Sub-Saharan Africa 19992011: epidemiology and 25. Omar MA, Seedat MA, Motala AA, Dyer RB, Becker
public health implications. A systematic review. BMC P. The prevalence of diabetes mellitus and impaired
Public Health. 2011;11:564. glucose tolerance in a group of urban South African
11. Kimani-Murage EW, Muthuri SK, Oti SO, Mutua blacks. S Afr Med J. 1993;83(9):6413.
MK, Van de V, Kyobutungi C. Evidence of a dou- 26. McLarty DG, Swai AB, Kitange HM, Masuki G,
ble burden of malnutrition in urban poor settings in Mtinangi BL, Kilima PM, et al. Prevalence of diabe-
Nairobi, Kenya. PLoS One. 2015;10(6):e0129943. tes and impaired glucose tolerance in rural Tanzania.
12. Omran AR. The epidemiologic transition: a theory Lancet. 1989;1(8643):8715.
of the epidemiology of population change. 1971. 27. Ramaiya KL, Swai AB, McLarty DG, Alberti
Milbank Q. 2005;83:73157. KG. Impaired glucose tolerance and diabetes mellitus
13. Hilawe EH, Yatsuya H, Kawaguchi L, Aoyama in Hindu Indian immigrants in Dar es Salaam. Diabet
A. Differences by sex in the prevalence of diabetes Med. 1991;8(8):73844.
mellitus, impaired fasting glycaemia and impaired 28. Swai AB, McLarty DG, Sherrif F, Chuwa LM, Maro
glucose tolerance in sub-Saharan Africa: a systematic E, Lukmanji Z, et al. Diabetes and impaired glu-
review and meta-analysis. Bull World Health Organ. cose tolerance in an Asian community in Tanzania.
2013;91(9):671682D. Diabetes Res Clin Pract. 1990;8(3):22734.
14. Bovet P, Gabriel A, Shamlaye C, Paccaud F. Diabetes in 29. Omar MA, Seedat MA, Dyer RB, Motala AA, Knight
Africa: the situation in the Seychelles. Heart. 2009;95(6): LT, Becker PJ. South African Indians show a high
5067. prevalence of NIDDM and bimodality in plasma
15. Mbanya JC, Kengne AP, Assah F. Diabetes care in glucose distribution patterns. Diabetes Care. 1994;
Africa. Lancet. 2006;368(9548):16289. 17(1):703.
16. Tabish SA. Is diabetes becoming the biggest epidemic 30. Levitt NS, Steyn K, Lambert EV, Reagon G,
of the twenty-first century? Int J Health Sci (Qassim). Lombard CJ, Fourie JM, et al. Modifiable risk
2007;1(2):VVIII. factors for type 2 diabetes mellitus in a peri-urban
17. International Diabetes Federation. IDF diabetes atlas. community in South Africa. Diabet Med. 1999;16:
Brussels, Belgium: International Diabetes Federation; 94650.
6th ed. 2013. 31. Sobngwi E, Mauvais-Jarvis F, Vexiau P, Mbanya JC,
18. Elbagir MN, Eltom MA, Elmahadi EM, Kadam IM, Gautier JF. Diabetes in Africans part 1: epidemi-
Berne C. A high prevalence of diabetes mellitus ology and clinical specificities. Diabetes Metab.
and impaired glucose tolerance in the Danagla com- 2001;27:62834.
munity in northern Sudan. Diabet Med. 1998;15(2): 32. Cooper RS, Rotimi CN, Kaufman JS, Owoaje EE,
1649. Fraser H, Forrester T, et al. Prevalence of NIDDM
19. Elbagir MN, Eltom MA, Elmahadi EM, Kadam IM, among populations of the African diaspora. Diabetes
Berne C. A population-based study of the prevalence Care. 1997;20:3438.
of diabetes and impaired glucose tolerance in adults 33. Mbanya JCN, Cruickshank JK, Forrester T, Balkau B,
in Northern Sudan. Diabetes Care. 1996;19(10): Ngogang JY, Riste L, et al. Standardised comparison
11268. of glucose intolerance in West African-origin popu-
20. Levitt NS, Katzenellenbogen JM, Bradshaw D, lations of rural and urban Cameroon, Jamaica, and
Hoffman MN, Bonnici F. The prevalence and identi- Caribbean migrants to Britain. Diabetes Care. 1999;22:
fication of risk factors for NIDDM in urban Africans 43440.
in Cape Town, South Africa. Diabetes Care. 1993; 34. United Nations Population Fund. State of world popu-
16(4):6017. lation 2007: unleashing the potential of urban growth.
21. Balde NM, Diallo I, Balde MD, Barry IS, Kaba L, 35. Population Division of the Department of Economic
Diallo MM, et al. Diabetes and impaired fasting glu- and Social Affairs of the United Nations Secretariat.
cose in rural and urban populations in Futa Jallon World urbanization prospects: the 2007 revision. 2008
(Guinea): prevalence and associated risk factors. 36. Mayosi BM, Flisher AJ, Lalloo UG, Sitas F, Tollman
Diabetes Metab. 2007;33(2):11420. SM, Bradshaw D. The burden of non-communicable
22. Motala AA, Omar MAK, Pirie FJ. Epidemiology diseases in South Africa. Lancet. 2009;374:93447.
of diabetes in Africa. In: Ekoe J-M, Rewers M, 37. Popkin BM, Gordon-Larsen P. The nutrition transi-
Williams R, Zimmet P, eds. The epidemiology of tion: worldwide obesity dynamics and their determi-
diabetes mellitus (2nd edn). Chichester: Wiley, 2008; nants. Int J Obes Relat Metab Disord. 2004;28 Suppl
13346. 3:S29.
38. Aspray TJ, Mugusi F, Rashid S, Whiting D, Edwards 53. Erasmus RT, Blanco BE, Okesina AB, Gqweta Z,
R, Alberti KG, et al. Rural and urban differences in Matsha T. Assessment of glycaemic control in stable
diabetes prevalence in Tanzania: the role of obesity, type 2 black South African diabetics attending a peri-
physical inactivity and urban living. Trans R Soc Trop urban clinic. Postgrad Med J. 1999;75(888):6036.
Med Hyg. 2000;94:63744. 54. Oguntibeju OO, Odunaiya N, Oladipo B, Truter
39. Christensen DL, Friis H, Mwaniki DL, Kilonzo B, EJ. Health behaviour and quality of life of patients
Tetens I, Boit MK, et al. Prevalence of glucose intol- with type 2 diabetes attending selected hospitals in
erance and associated risk factors in rural and urban South Western Nigeria. West Indian Med J. 2012;
populations of different ethnic groups in Kenya. 61(6):61926.
Diabetes Res Clin Pract. 2009;84:30310. 55. Mbanya JC, Assah FK, Saji J, Atanga EN. Obesity
40. Mbanya JC, Ngogang J, Salah JN, Minkoulou E, and type 2 diabetes in Sub-Saharan Africa. Curr Diab
Balkau B. Prevalence of NIDDM and impaired glu- Rep. 2014;14(7):501.
cose tolerance in a rural and an urban population in 56. Fisch A, Pichard E, Prazuck T, Leblanc H, Sidibe Y,
Cameroon. Diabetologia. 1997;40:8249. Brucker G. Prevalence and risk factors of diabetes mel-
41. Mollentze WF, Moore AJ, Steyn AF, Joubert G, Steyn litus in the rural region of Mali (West Africa): a practi-
K, Oosthuizen GM, et al. Coronary heart disease risk cal approach. Diabetologia. 1987;30(11):85962.
factors in a rural and urban orange free state black 57. Fisch A, Pichard E, Prazuck T, Leblanc H, Cisse
population. S Afr Med J. 1995;85:906. H. Suitability of reflectometry in epidemiology of dia-
42. Unwin N, McLarty D, Machibya H, Aspray T, Tamin betes mellitus in Africans. Lancet. 1990;335(8690):
B, Carlin L, et al. Changes in blood pressure and lipids 6612.
associated with rural to urban migration in Tanzania. 58. Prentice AM, Moore SE. Early programming of adult
J Hum Hypertens. 2006;20:7046. diseases in resource poor countries. Arch Dis Child.
43. Sobngwi E, Mbanya JC, Unwin NC, Porcher R, 2005;90(4):42932.
Kengne AP, Fezeu L, et al. Exposure over the life 59. Joffe B, Zimmet P. The thrifty genotype in type 2 dia-
course to an urban environment and its relation with betes: an unfinished symphony moving to its finale?
obesity, diabetes, and hypertension in rural and urban Endocrine. 1998;9(2):13941.
Cameroon. Int J Epidemiol. 2004;33:76976. 60. Pettitt DJ, Aleck KA, Baird HR, Carraher MJ,
44. Ntandou G, Delisle H, Agueh V, Fayomi B. Bennett PH, Knowler WC. Congenital susceptibil-
Abdominal obesity explains the positive rural-urban ity to NIDDM. Role of intrauterine environment.
gradient in the prevalence of the metabolic syndrome Diabetes. 1988;37(5):6228.
in Benin, West Africa. Nutr Res. 2009;29:1809. 61. Martorell R, Kettel Khan L, Hughes ML, Grummer-
45. Agyemang C, Owusu-Dabo E, de Jonge A, Martins Strawn LM. Overweight and obesity in preschool
D, Ogedegbe G, Stronks K. Overweight and obesity children from developing countries. Int J Obes Relat
among Ghanaian residents in The Netherlands: how Metab Disord. 2000;24:95967. (8): 959967.
do they weigh against their urban and rural counter- 62. de Onis M, Blossner M. Prevalence and trends of
parts in Ghana? Public Health Nutr. 2009;12:90916. overweight among preschool children in developing
46. Mollentze WF, Osthuizen GM, et al. The prevalence countries. Am J Clin Nutr. 2000;72(4):10329.
of diabetes mellitus in two South African black popu- 63. Hossain P, Kawar B, El NM. Obesity and diabetes in
lations. Diabetologia. 1992;5:511. 1992. the developing world a growing challenge. N Engl
47. World Health Organization. Global status report on J Med. 2007;356:2135.
noncommunicable diseases 2010. Geneva: World 64. Levitt NS, Lambert EV. The foetal origins of the
Health Organization; 2011. 2011. metabolic syndrome a South African perspective.
48. American Diabetes Association. Position statement: Cardiovasc J S Afr. 2002;13(4):17980.
diagnosis and classification of diabetes mellitus. 65. Assah FK, Ekelund U, Brage S, Mbanya JC,
Diabetes Care. 2004;27(1):s510. Wareham NJ. Free-living physical activity energy
49. Danquah I, Bedu-Addo G, Terpe KJ, Micah F, expenditure is strongly related to glucose intoler-
Amoako YA, Awuku YA, et al. Diabetes mellitus type ance in Cameroonian adults independently of obesity.
2 in urban Ghana: characteristics and associated fac- Diabetes Care. 2009;32(2):3679.
tors. BMC Public Health. 2012;12:210. 66. Cole AH, Ogbe JO. Energy intake, expenditure and
50. Frank LK, Heraclides A, Danquah I, Bedu-Addo G, pattern of daily activity of Nigerian male students. Br
Mockenhaupt FP, Schulze MB. Measures of gen- J Nutr. 1987;58:35767.
eral and central obesity and risk of type 2 diabetes 67. Luke A, Dugas LR, Ebersole K, Durazo-Arvizu
in a Ghanaian population. Trop Med Int Health. RA, Cao G, Schoeller DA, et al. Energy expenditure
2013;18(2):14151. does not predict weight change in either Nigerian or
51. Barruet R, Gbadoe AD. Type 2 diabetes mellitus in African-American women. Am J Clin Nutr. 2009;89:
children in black Africa: description of first five cases 16976.
in Togo. Med Trop (Mars). 2006;66(5):4813. 68. Neilson HK, Robson PJ, Friedenreich CM, Csizmadi
52. Buresi D. Clinical study of diabetes mellitus in hospi- I. Estimating activity energy expenditure: how valid
tal practice in Northern Rwanda (apropos of 86 case are physical activity questionnaires? Am J Clin Nutr.
reports). Med Trop (Mars). 1988;48(3):22935. 2008;87:27991.
69. Wareham NJ, Rennie KL. The assessment of physical 83. World Health Organisation. Definition, diagnosis and
activity in individuals and populations: why try to be classification of diabetes mellitus and its complica-
more precise about how physical activity is assessed? tions. WHO/NCD/NCS/99.2. Geneva: World Health
Int J Obes Relat Metab Disord. 1998;22 Suppl 2: Organization; 1999.
S308. 84. McMillan DE. Tropical malnutrition diabetes.
70. Singh J, Prentice AM, Diaz E, Coward WA, Ashford Diabetologia. 1986;29(2):1278.
J, Sawyer M, et al. Energy expenditure of Gambian 85. Ducorps M, Ndong W, Jupkwo B, Belmejdoub G,
women during peak agricultural activity measured by Poirier JM, Mayaudon H, et al. Epidemiological
the doubly-labelled water method. Br J Nutr. 1989;62: aspects of diabetes in Cameroon: what is the role of
31529. tropical diabetes? Diabetes Metab. 1997;23(1):617.
71. World Health Organization. STEPwise approach 86. World Health Organization. Use of glycated hemo-
to chronic disease risk factor surveillance. Geneva: globin (HbA1c) in the diagnosis of diabetes mellitus.
World Health Organization; 2009. Geneva: World Health Organization; 2010.
72. Heini AF, Minghelli G, Diaz E, Prentice AM, Schutz 87. Beran D, Yudkin JS, de Court. Access to care for
Y. Free-living energy expenditure assessed by two dif- patients with insulin-requiring diabetes in developing
ferent methods in rural Gambian men. Eur J Clin Nutr. countries: case studies of Mozambique and Zambia.
1996;50:2849. Diabetes Care. 2005;28(9):213640.
73. Huss-Ashmore R, Goodman JL, Sibiya TE, Stein 88. Beran D, Yudkin JS. Looking beyond the issue of
TP. Energy expenditure of young Swazi women as access to insulin: what is needed for proper diabe-
measured by the doubly-labelled water method. Eur tes care in resource poor settings. Diabetes Res Clin
J Clin Nutr. 1989;43:73748. Pract. 2010;88(3):21721.
74. Kolbe-Alexander TL, Lambert EV, Harkins JB, 89. HoPiT Research Group. Cameroon burden of diabetes
Ekelund U. Comparison of two methods of measur- project (Cambod): baseline survey report. Yaound:
ing physical activity in South African older adults. HoPiT Research Group; 2004.
J Aging Phys Act. 2006;14:98114. 90. Majaliwa ES, Munubhi E, Ramaiya K, Mpembeni R,
75. Dirk Lund Christensen. Glucose intolerance in rela- Sanyiwa A, Mohn A, et al. Survey on acute and chronic
tion to body composition, physical activity and other complications in children and adolescents with type
predictors among the Luo, Kamba and Maasai of 1 diabetes at Muhimbili National Hospital in Dar es
Kenya. PhD Thesis, University of Copenhagen. 2008. Salaam, Tanzania. Diabetes Care. 2007;30(9):218792.
76. Assah FK. Physical activity, cardiorespiratory fit- 91. Mendis S, Fukino K, Cameron A, Laing R, Filipe Jr
ness and metabolic health in Cameroon. PhD Thesis, A, Khatib O, et al. The availability and affordability
University of Cambridge. 2009. of selected essential medicines for chronic diseases
77. Bourne LT, Lambert EV, Steyn K. Where does the in six low- and middle-income countries. Bull World
black population of South Africa stand on the nutri- Health Organ. 2007;85(4):27988.
tion transition? Public Health Nutr. 2002;5:15762. 92. Neuhann HF, Warter-Neuhann C, Lyaruu I, Msuya
78. Mennen LI, Jackson M, Sharma S, Mbanya JCN, L. Diabetes care in Kilimanjaro region: clinical pre-
Cade J, Walker S, et al. Habitual diet in four popula- sentation and problems of patients of the diabetes
tions of African origin: a descriptive paper on nutri- clinic at the regional referral hospital - an inven-
ent intakes in rural and urban Cameroon, Jamaica and tory before structured intervention. Diabet Med.
Caribbean migrants in Britain. Public Health Nutr. 2002;19(6):50913.
2001;4:76572. 93. Elrayah H, Eltom M, Bedri A, Belal A, Rosling H,
79. Vorster HH, Venter CS, Wissing MP, Margetts Ostenson CG. Economic burden on families of child-
BM. The nutrition and health transition in the North hood type 1 diabetes in urban Sudan. Diabetes Res
West Province of South Africa: a review of the Clin Pract. 2005;70(2):15965.
THUSA (Transition and Health during Urbanisation 94. Kirigia JM, Sambo HB, Sambo LG, Barry
of South Africans) study. Public Health Nutr. 2005;8: SP. Economic burden of diabetes mellitus in the
48090. WHO African region. BMC Int Health Hum Rights.
80. Levitt NS, Bradshaw D. The impact of HIV/AIDS on 2009;9:6.
type 2 diabetes prevalence and diabetes healthcare 95. Chale SS, Swai AB, Mujinja PG, McLarty DG. Must
needs in South Africa: projections for 2010. Diabet diabetes be a fatal disease in Africa? Study of costs
Med. 2006;23(1):1034. of treatment. BMJ Clin Res Ed. 1992;304(6836):
81. Young F, Critchley JA, Johnstone LK, Unwin NC. A 12158.
review of co-morbidity between infectious and 96. Deeb LC, Tan MH, Alberti KG. Insulin availability
chronic disease in Sub-Saharan Africa: TB and dia- among International Diabetes Federation member
betes mellitus, HIV and metabolic syndrome, and the associations. Report of the Task Force on Insulin
impact of globalization. Glob Health. 2009;5:9. Distribution. Diabetes Care. 1994;17(3):2203.
82. Idemyor V. Diabetes in sub-Saharan Africa: health- 97. Njamnshi A, Hiag AB, Mbanya J-C. From research
care perspectives, challenges, and the economic to policy: the development of a national diabetes pro-
burden of disease. J Natl Med Assoc. 2010;102(7): gramme in Cameroon. Diabetes Voice. 2006;51(3):
6503. 1821.
98. Ramaiya K. Tanzania and diabetes a model for 106. Acheampong JW, Boateng KA, Eghan BA, Story
developing countries? BMJ. 2005;330(7492):679. P, Parry EHO, Tomlinson S. The impact of diabe-
99. Daniels A, Biesma R, Otten J, Levitt NS, Steyn K, tes nurses in the Komfo Anokye Teaching Hospital,
Martell R, et al. Ambivalence of primary healthcare Ghana. Diabetes Int. 2000;10:8193.
professionals towards the South African guidelines 107. Mamo Y, Seid E, Adams S, Gardiner A, Parry E. A
for hypertension and diabetes. S Afr Med J. 2000; primary healthcare approach to the management of
90(12):120611. chronic disease in Ethiopia: an example for other
100. Gill GV, Price C, Shandu D, Dedicoat M, Wilkinson countries. Clin Med (Lond). 2007;7(3):22831.
D. An effective system of nurse-led diabetes care 108. Coleman R, Gill G, Wilkinson D. Noncommunicable
in rural Africa. Diabet Med. 2008;25(5):60611. disease management in resource-poor settings: a
101. Beran D, Yudkin JS. Diabetes care in sub-Saharan primary care model from rural South Africa. Bull
Africa. Lancet. 2006;368(9548):168995. World Health Organ. 1998;76(6):63340.
102. Whiting DR, Hayes L, Unwin NC. Diabetes in 109. Windus DW, Ladenson JH, Merrins CK, Seyoum
Africa. Challenges to health care for diabetes in M, Windus D, Morin S, et al. Impact of a multidis-
Africa. J Cardiovasc Risk. 2003;10(2):10310. ciplinary intervention for diabetes in Eritrea. Clin
103. United Nations. World diabetes day. A/RES/61/225. Chem. 2007;53(11):19549.
12-20-2006. 110. Otaigbe BE, Imafidon EE. Type 2 diabetes mellitus
104. IDF Africa. Diabetes declaration and strategy for in a Nigerian child: a case report. Afr Health Sci.
Africa. International Diabetes Federation; 2006. 2011;11(3):4546.
105. Huddle KR, Gill GV. Reducing acute hyperglycae-
mic mortality in African diabetic patients. Diabet
Med. 1989;6(1):646.
Type 2 Diabetes in the Middle East
and North Africa (MENA) 4
Yasmin Khan and Osama Hamdy
Introduction lion) [1]. The rapid rise is due to a multitude of

factors, including economic and demographic
The Middle East and North Africa (MENA) changes over the last few decades that have led
region encompasses approximately 22 countries to a decrease in physical activity and rise in obe-
and comprises 6 % of the worlds population. It is sity. The MENA region has among the highest
a geographic area with rich history and linguistic, obesity rates in the world (Fig. 4.3).
ethnic, and cultural diversity. According to WHO Diabetes is associated with early mortality
statistics from 2010, Egyptians account for more and increased risk for microvascular and macro-
than one-third of the population in this region, vascular complications. Approximately 40 % of
followed by North Africans and Arabs from the patients with diabetes have chronic kidney dis-
Gulf (Fig. 4.1). The MENA region has one of the ease, and almost 6070 % of patients with dia-
highest prevalence rates of diabetes in the world betes have mild to severe forms of nervous
(11 %) (Fig. 4.2). system damage. In addition, patients with diabe-
Diabetes is a global pandemic affecting more tes are two to four times more likely to have
than 415 million adults worldwide. This number fatal or nonfatal coronary events or stroke.
is expected to surge to 642 million by 2040 [1]. Almost 7080 % of patients with diabetes die
According to the International Diabetes from one of these two conditions. The American
Federation (IDF), over 35 million people in Heart Association considers diabetes to be one
MENA have diabetes. Saudi Arabia leads the of the six major controllable risk factors for car-
MENA region with the highest prevalence of diovascular disease. Researchers also consider
diabetes (23.9 %), and Egypt is the country with diabetes as a risk equivalent to having a prior
the largest number of diabetes patients (7.5 mil- heart attack.
In addition to being a major public health
problem, diabetes is also associated with signifi-
Y. Khan, MD, MPH (*) cant healthcare costs. Worldwide, the global cost
Adult Diabetes Section, Joslin Diabetes Center, of diabetes continues to soar and is now estimated
Boston, MA, USA
to be 825 billion dollars per year [2]. The IDF
estimates that in 2015, countries in the Middle
O. Hamdy, MD, PhD, FACE
Joslin Diabetes Center, Harvard Medical School,
East spent over 17 billion dollars on diabetes care.
Boston, MA, USA This figure accounts for only 2.5 % of global
e-mail: [email protected] spending on the disease [1]. Healthcare expenditure

DOI 10.1007/978-3-319-41559-8_4
50 Y. Khan and O. Hamdy
Fig. 4.1 Ethnicity of the 26.7 (1%) (3%)

MENA region (Source: (8%)
2010 WHO statistics) lestinians jordanians
Iraqis
Egyptians/
38.9
Sudaneses 108.4 (33%)
(12%)
Gulf Arabs 58.9

(18%)
North Africans 83.6
Fig. 4.2 Comparative

prevalence of diabetes in
MENA (Source: IDF
Diabetes Atlas)
<5 10-12
5-8 12-15
8-10 >15
*comparative prevalence
varies greatly across the region due to economic diabetes to avoid major spending on healthcare in
inequalities. In Egypt, a cost analysis from 2010 the coming years.
estimated the economic impact of diabetes to be
$1.29 billion. This number excluded the cost
associated with prediabetes and also the cost Epidemiology of Diabetes in MENA
related to loss of productivity. This figure, adjusted
for inflation, can be expected to double by the The MENA region can be described as a global
year 2030. According to the IDF, in Egypt the cur- hotspot for diabetes. According to the IDF, approx-
rent spending on diabetes is among the lowest in imately 37 million adults aged 2079 are living
the MENA at $116 per patient per year (16 % of with diabetes across the region. By 2040, this num-
total healthcare expenditure). Countries with the ber is expected to rise to 72 million. Of particular
highest spending per person with diabetes are concern is that over 40 % of individuals with diabe-
Qatar, Kuwait, UAE, and Bahrain, with a range of tes are undiagnosed and are at increased risk for
$1,0002,000 per year. This is still lower than developing complications from diabetes. Moreover,
spending for developed countries, which usually in 2015 there were 342,000 deaths related to diabe-
ranges from $2,000 to 7,000 per patient per year tes. A further 30.2 million people in the region, or
[1]. The rising epidemic will continue to strain the 7.8 % of the adult population, are estimated to have
economies of the MENA region, and health impaired glucose tolerance and are therefore at
authorities should urgently address the problem of high risk of developing diabetes in the future [1].
4 Type 2 Diabetes in the Middle East and North Africa (MENA) 51
GLOBAL OBESITY - MEN

Frequency of BMI (%) Overweight (>25 to <30 kg/m2) Obese (> 30 kg/m2)
80
70
60
50
40
30
20
10
lia
ll
pe st
As ast
ric h
As uth
st e
a
ric h
ro th
ra
Af out
Ea ddl
ad
ro t
Af ort
ro e
Eu Eas
er in
ra
Eu ou
pe
pe
ia
a
a
ve
Eu th W
So
ia
an
Am Lat
ic
N
st
i
S
M
S
O
Au
C
or
N
SOURCE: American Heart Association
GLOBAL OBESITY - WOMEN

Frequency of BMI (%) Overweight (>25 to <30 kg/m2) Obese (> 30 kg/m2)
80
70
60
50
40
30
20
10
0
lia
ll
pe st
As ast
ric h
As uth
st e
a
ric h
ro th
ra
Af out
Ea ddl
ad
ro t
Af ort
ro e
Eu Eas
er in
ra
Eu ou
pe
pe
ia
a
a
ve
Eu th W
So
ia
an
Am Lat
ic
N
st
i
S
M
S
O
Au
C
or
N
SOURCE: American Heart Association
Fig. 4.3 Global prevalence of obesity (Source: AHA)

Prevalence of Diabetes individuals in Egypt have diabetes and another 2.2

million have prediabetes. Furthermore, reports
Diabetes prevalence varies greatly across the indicate that 43 % of patients with diabetes and
region. The highest prevalence is seen in the Gulf most patients with prediabetes in Egypt are likely
countries, with Saudi Arabia, Kuwait, and undiagnosed. It is estimated that 42 % of patients
Bahrain leading the way (Fig. 4.4). The high rates with diabetes in Egypt have retinopathy, 5 % are
of diabetes are due in large part to the economic legally blind, and 22 % have peripheral neuropa-
growth of the last few decades and the subse- thy. Diabetes is also the leading cause of end-stage
quent change in diet and lifestyle of these popula- renal disease and leg amputation in Egypt [57]. It
tions. Saudi Arabia has a diabetes prevalence of is especially alarming that the prevalence of diabe-
23.9 % among adults. The prevalence is higher tes in Egypt has increased rapidly within a rela-
among Saudis residing in urban areas (25.5 %) tively short period of time from approximately 4.4
when compared to rural areas (19.5 %) [3]. There million in 2007 to 7.5 million in 2013. This number
is little gender difference with respect to diabetes is projected to rise to 13.1 million by 2035 (Fig. 4.5).
prevalence in the region. As expected, type 2 dia-
betes (T2D) cases predominate and constitute
approximately 9095 % of all patients with dia- Prevalence of Diabetes Complications
betes. However, it is worth mentioning that Saudi
Arabia has one of the worlds highest annual inci- Among patients with diabetes, the prevalence of
dence rates of type 1 diabetes in children, with microvascular and macrovascular complications is
31.4 new cases per 100,000 individuals per year relatively high in Arab populations. A recent cross-
[4]. This is the highest incidence of type 1 diabe- sectional study from Saudi Arabia showed that the
tes of any country outside of Europe. prevalence of peripheral neuropathy among patients
The countries with the largest number of people with diabetes was 19.9 % [8]. Among Saudi patients
affected by diabetes are Egypt (7.5 million), with T2D for at least 10 years, the prevalence of reti-
Pakistan (7 million), and Iran (4.5 million) (Fig. 4.4). nopathy was 31 % [9]. In Jordan, data from a national
These figures reflect the large populations of diabetes center showed that 45 % of patients had reti-
these countries. In Egypt, the prevalence of dia- nopathy, 33 % had nephropathy, and 5 % had a his-
betes is around 15.6 % among adults between 20 tory of amputation [10]. Diabetes is also frequently
and 79 years of age. The International Diabetes associated with psychological distress. A study from
Federation (IDF) estimates that 7.5 million UAE demonstrated that up to 33.8 % of patients with
diabetes had depression or anxiety or both [11].
Top 5 countries for number of pepole with diabetes Diabetic patients with depression are less likely to
(20-79 years), 2014 adhere to medical treatment and engage in self-care.
Countries/territories Millions Overall, the high prevalence of diabetic complica-
Egypt 7.593
tions in this region highlights the need for early
Pakistan 6.944
Iran (Islamic Republic of) 4.582
detection and prompt treatment of this disease.
Saudi Arabia 3.806
Sudan 3.007
Risk Factors for Type 2 Diabetes
Top 5 countries for diabetes comparative
prevalence (%) (20-79 years), 2014 in the MENA Region
Countries/territories %
Saudi Arabia 23.9 Obesity
Kuwait 23.1*
Bahrain 21.9* Obesity and physical inactivity are the two major
Qatar 19.8 risk factors for diabetes in the MENA region. The
United Arab Emirates 19
countries with the highest prevalence of obesity
Fig. 4.4 Diabetes in the MENA region, 2014 (Source: are Saudi Arabia, United Arab Emirates, and
IDF Atlas, sixth edition) Egypt (Fig. 4.6). Over the last few decades, there
Fig. 4.5 The rising a Prevalence of T2D in Egypt

prevalence of type 2 20%
diabetes in Egypt. (a) 18%
Projected trends of the
16%
prevalence rate of T2D in
Egypt. (b) The projected 14%
trend of the total number 12%
of patients with T2D in 10%
Egypt 8%
6%
4%
2%
0%
2007 2011 2030
Number of T2D patients in Egypt
b
(in millions)
14
12
10
0
2007 2013 2035
has been a dramatic increase in obesity, particu- among children has been reported in Bahrain
larly among Arab women. Results from a national (38.5 %), while the lowest was reported in Iran
survey conducted in Saudi Arabia showed the (3 %) [17]. Cross-sectional data from Saudi
prevalence of obesity was 44 % among women Arabia showed that a very high proportion of
and 26 % among men [12]. Similar results were Saudi adolescents (84 % of males and 91.2 % of
seen in the 2008 Egypt Demographic and Health females) spent more than 2 h on TV or video
Survey, which assessed the nutritional status of screen daily and almost half of the males and
adults aged 1559 years old, and found that three-quarters of the females did not meet daily
approximately 50 % of men and 6580 % of physical activity guidelines [18]. In Egypt, data
women were overweight or obese [13]. The from the most recent Demographic and Health
Egyptian National Hypertension Survey pro- Survey show that 35 % of males and 36 % of
gram, which was conducted in six Egyptian gov- females aged 519 are overweight [13]. These
ernorates and included 2,313 adults older than trends are largely the result of an unhealthy eat-
25 years of age, showed that 50 % of surveyed ing pattern and decreased physical activity that
individuals had central obesity. This was shown has emerged over the last few decades.
to be strongly associated with increased risk of
diabetes and cardiovascular disease [1416].
An alarming trend is the increased rates of Genetics of Diabetes
obesity among children and adolescents. Obesity
during childhood is a risk factor for obesity and Central adiposity is common among Arab popula-
related chronic diseases during adulthood, such tions and genetic factors are likely to play a role in
as cardiovascular disease, diabetes mellitus, and the development of obesity and diabetes. The genet-
hypertension. The highest prevalence of obesity ics underlying T2D is multifactorial and complex in
40
35.6
33.7
35
30.3 28.8
30 28.9
25
19.5
20
17.2
16
15 13.5
10
a
t
AE
a
co
t
an
n
ai
yp
si
bi
ai
no
w
ac
rd
ni
U
ra
hr
Eg
ba
Ku
Tu
Jo
or
iA
Ba
Le
M
ud
Sa
Fig. 4.6 Prevalence (%) of obesity in Arab countries (Source: 2010 WHO statistics)
nature. Although genetic studies from the region are computers and television have all contributed to a
limited, there is evidence that variations in the sedentary lifestyle. Low levels of physical activity
ADIPOQ gene, which encodes adiponectin, are are prevalent throughout the region. In a cross-sec-
associated with increased BMI and waist circumfer- tional study of adults in Saudi Arabia aged 3070,
ence [19]. Adiponectin is released by adipocytes the prevalence of inactivity was very high at 96.1 %
and is found in lower levels among obese subjects. [24]. In Cairo, absence of weekly physical activity
Recent studies from Jordan and Tunisia have also was reported among 81 % of the 4,918 households
shown that variants in the ADIPOQ gene strongly surveyed in 1995 [13]. The majority of individuals
correlate with risk of T2D [20, 21]. In the Lebanese did not engage in any physical activity or walk
population, mutations in both CDKAL1 and regularly. Physical activity levels were especially
IGF2BP2 genes have been shown to be associated low among women [24]. The major reasons for
with T2D [22, 23]. Interestingly, variants of the decreased physical activity, particularly among
TCF7L2 gene, which have been associated with Egyptian women, include the general lack of exer-
T2D across multiple ethnic groups, have only a cise facilities, overcrowded urban cities, and poor
weak association with diabetes in Arab populations. physical education in schools [13]. Furthermore,
Another consideration is that the genetic risk is urban planning in many cities does not encourage
increased among populations that have traditions of or support an active lifestyle. The lack of regular
consanguineous marriages. Certainly more research physical activity represents a major public health
is needed to further our understanding of the genetic concern that needs to be addressed by each indi-
basis of diabetes in this region. vidual country in a culturally appropriate way.
Physical Inactivity Chronic Hepatitis C Infection
Physical inactivity is the other major risk factor for The burden of hepatitis C virus (HCV) is growing
the development of T2D in MENA. Rapid eco- in the MENA region. If untreated, HCV can
nomic development, increased availability of cars, lead to liver cirrhosis, hepatocellular cancer, and
access to migrant labor, and widespread use of death. Egypt has the highest prevalence of chronic
hepatitis C infection in the world. This is attributed can affect multiple pathways involved in glucose
to the mass intravenous treatment campaign of bil- regulation. Organophosphorus and organochlorine
harziasis between 1960 and 1980 with the use of pesticides in particular lead to a deleterious effect
poorly sterilized needles. The Egypt Demographic on glucose metabolism and insulin secretion. It is
and Health Survey showed that 15 % of Egyptians hypothesized that the involved mechanisms include
are serologically positive for HCV antibodies and oxidative stress, pancreatitis, and inhibition of cho-
10 % have active infection [13]. Meanwhile in the linesterase [30, 31].
Gulf region, infection rates are relatively low. In Pesticides are widely used in the MENA
Qatar, 1.1 % of the population carries the virus. region, as 43 % of the population lives in rural
The prevalence of T2D among patients with areas and depends on farming for livelihood.
HCV is 1333 %. A meta-analysis of the associa- Pesticide usage is high in Lebanon, Kuwait, and
tion of HCV and T2D showed that patients with Egypt. Egypt ranks fifth among African nations
HCV are more likely to develop T2D. The odds with respect to pesticide consumption. The most
ratio was particularly high among male patients commonly used pesticides in Egypt are dichloro-
(OR, 1.26; 95 % CI, 1.031.54) and those older diphenyltrichloroethane (DDT), which is an
than 40 years of age (OR, 7.39; 95 % CI, 5.82 organochlorine compound, and chlorpyrifos and
9.38). Not only does HCV increase the risk of malathion, which are organophosphorus com-
diabetes, it is also associated with poor glycemic pounds [3235]. Growing evidence suggests a
control and increased prevalence of diabetes strong association between exposure to these
complications. A study of 438 patients with T2D pesticides and increased risk for insulin resis-
(113 Egyptians and 325 Kuwaitis) showed that tance and T2D. Raafat et al. found a positive
poor glycemic control was mostly seen in patients association between chronic exposure to mala-
positive for HCV. In another cross-sectional thion and insulin resistance [36]. Another study
study of 489 patients with T2D who attended an showed a U-shaped dose-response association
outpatient clinic and dialysis unit in Egypt, the between features of metabolic syndrome, such as
prevalence of HCV infection was 12.9 % among high body mass index, dyslipidemia (increased
patients attending the outpatient clinic and 18.7 % serum triglycerides, increased LDL cholesterol,
among patients on dialysis [2528]. decreased HDL cholesterol), and insulin resis-
Early treatment of HCV can help delay or pre- tance with exposure to various pesticides [37].
vent T2D. It has been shown that effective elimi- Currently, pesticide regulations are inadequate
nation of HCV in patients with prediabetes and a greater commitment to food safety is
improved glycemic tolerance and significantly needed to protect the health of consumers.
reduced A1C levels. Prospectively, 34.8 % of
patients who were treated became normoglyce-
mic and only 5.5 % developed diabetes. The sus- Cultural Factors Affecting Type 2
tained response to antiviral therapy was the only Diabetes in the MENA Region
independent predictor of improved glycemic
control [29]. With the development of newer and Dietary Pattern
effective medications for HCV, the risk for T2D
may significantly reduce in Egypt. Over the last three decades, the MENA region has
experienced a major shift in its traditional eating
patterns, referred to as the nutrition transition,
Pesticide Exposure due to urbanization and rapid economic develop-
ment. The traditional diet was rich in vegetables,
There is growing evidence that pesticide use is asso- legumes, fruits, whole wheat bread, and fish, with
ciated with T2D. Exposure to pesticides may occur low to moderate in amount of animal protein.
either directly among farmers and applicators or Presently, a dietary pattern with high consump-
indirectly due to chronic exposure to low levels of tion of saturated fat, refined carbohydrates,
pesticides through contaminated food. Pesticides processed meat, and sugar-sweetened beverages
has emerged throughout the region. This pattern countries, reduced exposure to sunlight with tra-
has been associated with an increased risk of ditional clothing among women contributes to
T2D. Meanwhile, diets characterized by high vitamin D deficiency, which has been linked to
intakes of vegetables, fruits, and whole grains have increased rates of obesity and T2D [40].
been shown to be protective against T2D [38]. Women are facing more obstacles to physical
Recent meta-analyses of observational and activity compared to men. In Bahrain, for exam-
prospective cohort studies have shown a strong ple, the main barriers to exercise perceived by
association between high consumption of white women were home commitments (49 %), care of
rice and an increased risk of T2D [39]. High con- children (36 %), and negative attitudes by family
sumption of trans fat has also been shown to be a members toward women practicing exercise/
risk factor for cardiovascular disease. Egypt and sports (24 %) [41, 42]. Of the women studied, the
Pakistan are the worlds highest consumers of majority believed that there is gender discrimina-
this unhealthy type of fat. Partially hydrogenated tion when it comes to sports, since sports and
oil, which contains trans fat, is also used fre- other recreational facilities are provided mostly
quently for daily cooking and for preparing fried for men [42]. Furthermore, in the Middle East,
foods throughout the region. women athletes continue to struggle for womens
Sociocultural factors also play an important role participation in sports at the national and interna-
in the pattern of food consumption. With longer tional level. In 2012, Sarah Attar and Wojdan
working hours and more women entering the work- Shaherkani made history when they became the
force, there has been a gradual shift toward larger first women to compete for Saudi Arabia in the
and later dinner. Dining out is also on significant London Olympics.
rise, especially among youth. Western fast-food
restaurants have also proliferated throughout the
MENA region. Together with a strong culture of Smoking
hospitality and frequent family gatherings around
food, these trends have nudged society toward con- Smoking represents a major public health crisis
sumption of bigger portions and no doubt are con- in the MENA region. Smoking is directly linked
tributing to the increased prevalence of obesity and to increased incidence of microvascular and mac-
T2D in the MENA region. rovascular diseases in patients with diabetes. In
Jordan, 43.4 % of men smoke, which represents
the highest prevalence in the region. Among
Sedentary Lifestyle women, Lebanon leads the way with a smoking
prevalence of 21.2 %. Egypt represents one of the
Low levels of physical activity are further exac- largest tobacco markets in the world, with over
erbating the problem of obesity and diabetes. 20 billion cigarettes smoked annually and a
The increased number of cars, vast expansion smoking prevalence of 39.7 % among adult men.
of cities, and hot climate contribute to decreased Smoking is still rare among Egyptian women.
physical daily activity. In addition, there are Despite high taxes on cigarettes and increasing
various cultural and social norms that may dis- public health education, smoking remains a com-
courage exercise. In Egypt, there is a tendency mon unhealthy habit in the MENA region [43].
to avoid exercise in public areas, while few are
able to afford membership in private athletic
facilities. Overall, exercise facilities are limited Health Illiteracy
and community sports facilities are scarce. Even
in schools, reduced time for physical activity Health literacy may be defined as the degree to
and limited availability of spaces for sports rein- which an individual has the capacity to obtain and
forces a sedentary lifestyle for Egyptian youth. It understand basic health information to make
is also worth mentioning that in Egypt and Gulf appropriate health decisions. Health illiteracy is
common in the MENA region. Obesity is fre- effective prevention. Unfortunately, many
quently regarded as a cosmetic problem and rarely patients consider their disease and its complica-
viewed as a disease. Most patients with T2D tions as inevitable and feel powerless to alter the
believe that diabetes should only be treated by course of the disease. A recent study from Egypt
oral medications and often resist insulin injections showed that improvement with medication adher-
when indicated. Routine daily glucose monitoring ence can be achieved through improving patient
is essentially nonexistent or limited due to cost or education about the disease, simplifying the drug
fear of frequent finger sticks. Furthermore, it has regimen, and reducing medication cost [46].
been demonstrated that patients rarely change
their diet or exercise habits following a diagnosis
of diabetes. A recent survey of 575 patients from Healthcare Quality
a diabetes outpatient clinic in the UAE showed
that the majority (72 %) of patients had negative The high prevalence of diabetes and other chronic
attitudes toward having the disease, and 31 % of diseases has placed a great burden on the regions
patients had poor knowledge of diabetes [44]. health systems. Many patients with diabetes are
In a study from Egypt, the majority of 560 either treated in the limited number of public hos-
patients with T2D surveyed believed that T2D is pitals, in the private healthcare sector through out-
an infectious disease originally caused by stress. of-pocket fee for service, or in the scarce diabetes
Moreover, only 38.4 % of patients had a positive centers in major cities. Furthermore, patients with
attitude toward self-management. Interestingly, diabetes face many barriers to care including cost,
these study patients believed that the efficacy of access to physicians and diabetes educators, and
herbal medicine in treating T2D was sufficiently access to medicines such as insulin.
high and neglected the positive role of regular Human resources for diabetes care are often
exercise in diabetes management. Most of inadequate. Overall, there is a shortage of physi-
patients also believed that patients suffering from cians, nurses, and health educators in the region.
polyuria should reduce their volume of drinking For example, a study in Saudi Arabia found that
water [45]. All of these factors result in poor gly- less than 10 % of health centers were staffed
cemic control, late diagnosis, and increased prev- with diabetes educators, and only 40 % of
alence of diabetes complications. patients with retinopathy were referred to eye
clinics [47]. Another study examined the deliv-
ery of health education to T2D patients in four
Poor Adherence healthcare centers (two rural and two urban) in
Alexandria, Egypt. Although diabetes knowl-
In the MENA region, as elsewhere, nonadher- edge was satisfactory among the 88 physicians
ence with diabetes management is common and surveyed in this study, 95.5 % of physicians
is one of the main factors for poor glycemic con- from rural areas and 89.8 % of those from urban
trol. Daily testing of blood glucose is very rare health centers neglected the fundamental role of
and frequent omission of insulin injections is patient education and regular exercise in man-
common, even in patients with type 1 diabetes. aging T2D [45]. All of these factors contribute
Even among educated patients, poor adherence to suboptimal quality of care for patients with
with healthy eating and physical activity is com- diabetes.
mon. Furthermore, fear of hypoglycemia among
patients treated with insulin leads to suboptimal
control and frequent reduction in insulin dosing Prevention of T2D
either intentionally or upon recommendation of
treating physicians. Frequently, diagnosis of dia- Type 2 diabetes is a largely preventable disease.
betes complications, especially retinopathy and Research has shown that lifestyle modification
nephropathy, is too late and does not allow for can significantly reduce the incidence of type 2
diabetes by up to 58 % [48]. Early diagnosis and further insight into the prevention and treatment
prevention of diabetes is a key priority for coun- of this disease.
tries of the MENA region. The Arab Taskforce To curb the diabetes epidemic, public health
for Obesity was created in 2010 to limit the rise strategies that focus on primary prevention
of obesity among Arab countries. This repre- through promotion of a healthy diet and lifestyle
sented a collaboration of 14 Arab countries. The should be prioritized. Primary care is now seen as
goals of the taskforce are to promote healthy eat- having a key role in prevention and early detec-
ing, increase physical activity, raise awareness tion of diabetes. Traditionally, diabetes has been
about obesity and its complications, and develop managed by specialist centers, but the majority of
national guidelines for controlling the rise in obe- people with diabetes can be effectively managed
sity, especially in children. by multidisciplinary teams of physicians, diabe-
Effective screening is one of the most impor- tes educators, nurses, and pharmacists. Countries
tant factors in diabetes prevention and control. should develop and organize their health systems
The Weqaya program in Abu Dhabi is an exam- to provide integrated and continuous care for
ple of a successful screening program. The pro- patients from prediabetes to severe diabetes with
gram was launched in 2008, and to date over complications.
94 % of the national population has been screened
for cardiovascular risk factors, including diabe-
tes, using A1c criteria [49]. Approximately 45 % Strategies to Improve Diabetes Care
of the screened population was found to have dia- in the MENA Region
betes or prediabetes. In Oman, a diabetes risk
score was developed that used age, waist circum- As outlined in this chapter, the diabetes epidemic
ference, body mass index, family history of dia- is driven by a complex multitude of factors. As
betes, and hypertension status to correctly awareness of diabetes in the region rises, a tar-
identify individuals at high risk of type 2 diabetes geted multi-sector response is necessary to
in a community setting. Interestingly, testing address this global crisis. Fundamental changes in
with Dutch, Thai, and Finnish diabetes risk scores public policies and health systems are required.
showed poor performance in this population [50]. The following points should be urgently
This suggests that customized screening tools considered:
may be of benefit in Arab populations. Ideally,
screening for diabetes should be part of a larger 1. Screen for diabetes.
national prevention program. Abu Dhabi, Qatar, Health authorities should implement efficient
UAE, and Kuwait are examples of countries that screening programs for high-risk individuals,
are leading the way with national strategies for especially adults who are overweight and
diabetes prevention. obese with a positive family history of diabe-
tes. Focusing on primary care and preventive
services will avoid costly complications of
Future Directions diabetes down the road.
2. Create a National Diabetes Prevention
Although the prevalence of diabetes is increasing Program.
throughout the MENA region, data on obesity Develop a comprehensive and accessible life-
and diabetes in many countries are lacking. style program with simple methods to facili-
Healthcare research is not seen as a priority in tate implementation on large scale. Increase
many countries of the region. Gaps exist in our public awareness of diabetes and emphasize
knowledge of epidemiological variation of diabe- that early diagnosis can reduce the risk of dia-
tes, as Arab populations are widely distributed betes and its complications. Addressing
across both Asia and Africa. Research on social childhood obesity and obesity among women
and cultural barriers to diabetes care can add should be a priority of such programs.
3. Improve diabetes education. 7. Develop clinical guidelines.

Diabetes education remains the cornerstone of Guidelines should be published for diabetes
diabetes management. General diabetes and management that are culturally suitable for
nutrition education should be conducted at patients. Such guidelines should consider the
schools, community centers, and healthcare unique risk factors highlighted in this chapter.
facilities. Public and private media can also play Guidelines can help standardize clinical prac-
vital role in disseminating accurate informa- tice to improve patient care. There is a great
tion about diabetes to the public. The goal is to opportunity for local diabetes associations
encourage citizens to be engaged in a healthy and scientific bodies to champion the devel-
lifestyle and also to reduce consumption of pro- opment of these guidelines and audit their
cessed food, refined carbohydrates, and trans fat. implementation.
4. Strengthen clinical care for diabetes.
Improve human resources for healthcare. The
concept of a diabetes management team should Summary and Conclusions
be introduced that includes a certified diabetes
educator (CDE) and registered dietitian (RD). Diabetes is a growing public health problem in the
Health authorities should develop or encour- MENA region. Its high prevalence continues to
age training programs that aim to prepare rise due to the increased prevalence of central obe-
enough CDEs and RDs to treat the growing sity, sedentary lifestyle, change in diet patterns,
number of patients with diabetes. Education increased prevalence of hepatitis C, and possibly
programs should emphasize self-management the increased use of uncontrolled pesticides.
and dispel fears about finger sticks and insulin Smoking among men, health illiteracy, and poor
injections. Physicians and patients alike should adherence increase the frequency of diabetes com-
be encouraged to be involved in this process. plications. Health authorities, through a limited
In addition, mobile technology in the form of healthcare budget, are striving to improve diabetes
apps, reminders, and education material can care, but many strategies and guidelines for stan-
also be used to enhance a comprehensive dia- dard of care are still needed to augment this effort.
betes management plan.
5. Treat hepatitis C infection.
The risk of hepatitis C infection should be References
reduced to minimize the health and economic
burden of diabetes. Early management with a 1. International Diabetes Federation. IDF diabetes. 7th
focus toward elimination of HCV in infected ed. Brussels: International Diabetes Federation; 2015.
http://www.diabetesatlas.org.
patients can also reduce T2D risk. Newer and 2. NCD Risk Factor Collaboration. Worldwide trends in
effective medications should be available at diabetes since 1980: a pooled analysis of 751
reduced price or provided through the national population-based studies with 4.4 million partici-
insurance service. pants. Lancet. 2016;387(10027):151330.
3. Al-Nozha MM, Al-Maatouq MA, Al-Mazrou YY,
6. Regulate pesticide use. Al-Harthi SS. Diabetes mellitus in saudi arabia. Saudi
Implementation of an effective pesticide regula- Med J. 2004;25:160310.
tory program, with regular surveying of pesti- 4. Habeb AM, Al-Magamsi MS, Halabi S, Eid IM,
cide residues in drinking water and food, should Shalaby S, Bakoush O. High incidence of childhood
type 1 diabetes in Al-Madinah, North West Saudi
be mandated. Health education is also war- Arabia (20042009). Pediatr Diabetes. 2011;12(8):
ranted to reduce uncontrolled exposure to pesti- 67681.
cides by minimizing the misuse and improper 5. Al-rubeaan K. International journal of diabetes mel-
handling of pesticides and providing protective litus type 2 diabetes mellitus red zone. Int J Diabetes
Mellitus. 2010;2:12.
personal equipment. Special attention should be 6. Jain S, Saraf S. Type 2 diabetes mellitusits global
made to avoid the involvement of women and prevalence and therapeutic strategies. Diabetes Metab
children in pesticide application. Syndr: Clin Res Rev. 2010;4:4856.
7. Whiting DR, Guariguata L, Weil C, et al. IDF diabetes haplotypes in the adiponectin gene contribute to the
atlas: global estimates of the prevalence of diabetes for genetic risk for type 2 diabetes in Tunisian Arabs.
2011 and 2030. Diabetes Res Clin Pract. 2011;94: Diabetes Res Clin Pract. 2012;97(2):2907.
31121. 22. Nemr R, Almawi AW, Echtay A, Sater MS, Daher HS,
8. Wang DD, Bakhotmah BA, Hu FB, Alzahrani Almawi WY. Replication study of common variants
HA. Prevalence and correlates of diabetic peripheral in CDKAL1 and CDKN2A/2B genes associated with
neuropathy in a saudi arabic population: a cross- type 2 diabetes in Lebanese Arab population. Diabetes
sectional study. PLoS One. 2014;9(9):e106935. Res Clin Pract. 2012;95(2):e3740.
9. El-Asrar AMA, Al-Rubeaan KA, Al-Amro SA, 23. Nemr R, Echtay A, Dashti EA, Almawi AW,
Kangave D, Moharram OA. Risk factors for diabetic Al-Busaidi AS, Keleshian SH, Irani-Hakime N,
retinopathy among Saudi diabetics. Int Ophthalmol. Almawi WY. Strong association of common variants
1998;22(3):15561. in the IGF2BP2 gene with type 2 diabetes in Lebanese
10. Jbour AS, Jarrah NS, Radaideh AM, Shegem NS, Arabs. Diabetes Res Clin Pract. 2012;96(2):2259.
Bader IM, Batieha AM, Ajlouni KM. Prevalence and 24. Al-Nozha MM, Al-Hazzaa HM, Arafah MR,
predictors of diabetic foot syndrome in type 2 diabe- Al-Khadra A, Al-Mazrou YY, Al-Maatouq MA, Khan
tes mellitus in Jordan. Saudi Med J. 2003;24(7): NB, Al-Marzouki K, Al-Harthi SS, Abdullah M,
7614. Al-Shahid MS. Prevalence of physical activity and
11. El-Rufaie OE, Bener A, Ali TA, Abuzeid inactivity among Saudis aged 3070 years. A
M. Psychiatric morbidity among type II diabetic population-based cross-sectional study. Saudi Med
patients: a controlled primary care survey. Prim Care J. 2007;28(4):55968.
Psychiatry. 1997;3:18994. 25. Miller FD, Abu-Raddad LJ. Evidence of intense
12. AlQuaiz AM, Siddiqui AR, Qureshi RH, Fouda MA, ongoing endemic transmission of hepatitis C virus
AlMuneef MA, Habib FA, Turkistani IM. Women in Egypt. Proc Natl Acad Sci U S A. 2010;107:
health in Saudi Arabia: a review of non-communicable 1475762.
diseases and their risk factors. Pak J Med Sci. 26. Chehadeh W, Abdella N, Ben-Nakhi A, et al. Risk
2014;30(2):422. factors for the development of diabetes mellitus in
13. EL-Zanaty F, Way A. Egypt demographic and health chronic hepatitis C virus genotype 4 infection.
survey 2008. Cairo: Ministry of Health, El-Zanaty and J Gastroenterol Hepatol. 2009;24:428.
Associates, and Macro International; 2009. p. 431. 27. Chehadeh W, Kurien SS, Abdella N, et al. Hepatitis C
14. Population Council. http://www.popcouncil.org/uploads/ virus infection in a population with high incidence of
pdfs/2010PGY_SYPEFinalReport_FrontMatter. type 2 diabetes: impact on diabetes complications.
pdf. J Infect Public Health. 2011;4:2006.
15. Ibrahim MM, Elamragy AA, Girgis H, et al. Cut off 28. Greca LF, Pinto LC, Rados DR, et al. Clinical features
values of waist circumference & associated cardiovas- of patients with type 2 diabetes mellitus and hepatitis
cular risk in Egyptians. BMC Cardiovasc Disord. C infection. Braz J Med Biol Res Rev Bras Pesqui
2011;11:53. Md Biol Soc Bras Biofs [et al]. 2012;45:28490.
16. Herman WH, Ali MA, Aubert RE, et al. Diabetes mel- 29. Huang JF, Yu ML, Huang CF, et al. The outcomes of
litus in Egypt: risk factors and prevalence. Diabet glucose abnormalities in pre-diabetic chronic hepati-
Med. 1995;12(12):112631. tis C patients receiving peginterferon plus ribavirin
17. Mirmiran P, Sherafat-Kazemzadeh R, Jalali-Farahani therapy. Liver Int. 2012;32:9629.
S, Azizi F. Childhood obesity in the Middle East: a 30. FAO/RNEA. Report of the workshop on implementa-
review/Revue sur lobsit de lenfant au Moyen- tion of the International Code of Conduct on the dis-
Orient. East Mediterr Health J. 2010;16(9):1009. tribution and use of pesticides in the Near East, 1621
18. Al-Hazzaa HM, Abahussain NA, Al-Sobayel HI, Sept 1995, Cairo; 1995.
Qahwaji DM, Musaiger AO. Physical activity, seden- 31. WRI. Pesticides and the immune system: the public
tary behaviors and dietary habits among Saudi adoles- health risks. Washington, DC: World Resources
cents relative to age, gender and region. Int J Behav Institute; 1996.
Nutr Phys Act. 2011;8(1):140. 32. Ambio O. Pesticide use, habits and health awareness
19. Zadjali F, Al-Yahyaee S, Hassan MO, Albarwani S, among Egyptian farmers. Ann Occup Hyg. 1996;
Bayoumi RA. Association of adiponectin promoter 40(5):499509.
variants with traits and clusters of metabolic syndrome 33. Wessels D, Barr DB, Mendola P. Use of biomarkers to
in Arabs: family-based study. Gene. 2013;527(2): indicate exposure of children to organophosphate pes-
6639. ticides: implications for a longitudinal study of chil-
20. Alkhateeb A, Al-Azzam S, Zyadine R, Abuarqoub drens environmental health. Environ Health Perspect.
D. Genetic association of adiponectin with type 2 dia- 2003;111(16):193946.
betes in Jordanian Arab population. Gene. 2013; 34. Mansour SA. Pesticide exposureEgyptian scene.
512(1):613. Toxicology. 2004;198(13):91115.
21. Mtiraoui N, Ezzidi I, Turki A, Chaieb A, Mahjoub T, 35. El-Sebae AH, Zeid MA, Saleh MA. Status and envi-
Almawi WY. Single-nucleotide polymorphisms and ronmental impact of toxaphene in the third worlda
case study of African agriculture. Chemosphere. M, Rashid N, El Hasnaoui A, BREATHE Study

1993;27(10):206372. Group. Smoking habits in the Middle East and North
36. Raafat N, Abass MA, Salem HM. Malathion expo- Africa: results of the BREATHE study. Respir Med.
sure and insulin resistance among a group of farmers 2012;106:S1624.
in Al-Sharkia governorate. Clin Biochem. 2012; 44. Al-Maskari F, El-Sadig M, Al-Kaabi JM, Afandi B,
45:15915. Nagelkerke N, Yeatts KB. Knowledge, attitude and
37. Lee DH, Steffes MW, Sjdin A, et al. Low dose practices of diabetic patients in the United Arab
organochlorine pesticides and polychlorinated biphe- Emirates. PLoS One. 2013;8(1):e52857.
nyls predict obesity, dyslipidemia, and insulin resis- 45. Koura MR, Khairy AE, Abdel-Aal NM, et al. The role
tance among people free of diabetes. PLoS One. of primary health care in patient education for diabe-
2011;6(1), e15977. tes control. J Egypt Public Health Assoc. 2001;
38. Brunner EJ, Mosdl A, Witte DR, Martikainen P, 76(0013-2446 (Print)):24164.
Stafford M, Shipley MJ, Marmot MG. Dietary patterns 46. Shams ME, Barakat EA. Measuring the rate of thera-
and 15-y risks of major coronary events, diabetes, and peutic adherence among outpatients with T2DM in
mortality. Am J Clin Nutr. 2008;87(5):141421. Egypt. Saudi Pharm J. 2010;18(4):22532.
39. Hu EA, Pan A, Malik V, Sun Q. White rice consump- 47. Al-Ahmadi H, Roland M. Quality of primary health
tion and risk of type 2 diabetes: meta-analysis and care in Saudi Arabia: a comprehensive review.
systematic review. BMJ. 2012;344:e1454. International J Qual Health Care. 2005;17(4):331.
40. Fields J, Trivedi NJ, Horton E, et al. Vitamin D in the 48. Diabetes Prevention Program Research Group.
Persian Gulf: integrative physiology and socioeco- Reduction in the incidence of type 2 diabetes with
nomic factors. Curr Osteoporos Rep. 2011;9:24350. lifestyle intervention or metformin. N Engl J Med.
41. Musaiger AO. Overweight and obesity in the Arab coun- 2002;346(6):393.
tries: the need for action. Arab Cent Nutr. 2007;1:18. 49. Hajat C, Harrison O, Al Siksek Z. Diagnostic testing
42. Musaiger AO, Al-Ansari MS. Barriers to practicing for diabetes using HbA1c in the Abu Dhabi popula-
physical activity in the Arab countries, in nutrition tion Weqaya: the Abu Dhabi cardiovascular screening
and physical activity in the arab countries of the near program. Diabetes Care. 2011;34(11):24002.
east. Musaiger AO and Meladi SS, (eds). FAO/Cairo 50. Al-Lawati JA, Tuomilehto J. Diabetes risk score in
Regional Office, Cairo, Egypt. 2000. Oman: a tool to identify prevalent type 2 diabetes
43. Khattab A, Javaid A, Iraqi G, Alzaabi A, Kheder AB, among Arabs of the Middle East. Diabetes Res Clin
Koniski ML, Shahrour N, Taright S, Idrees M, Polatli Pract. 2007;77(3):43844.
Diabetes in China and the Western
Pacic Region 5
Juliana C.N. Chan, Elaine Y.K. Chow,
and Andrea O.Y. Luk
Introduction lion people, have diabetes which is expected to

increase to 201.8 million in the next 20 years.
According to the International Diabetes While China has the biggest diabetic population
Federation (IDF) Atlas, 382 million people have with 98 million people affected, the WP Region
diabetes in 2013, and by 2035, this will rise to also has areas with the highest prevalence, such
582 million, with China, India and the United as some Pacific Islands with a diabetes preva-
States of America (USA) as the top three coun- lence of 30 %. A major concern is the high preva-
tries contributing to half of the global population lence of undiagnosed diabetes and prediabetes
of diabetes. The Western Pacific (WP) Region is which can lead to late presentation with expen-
the worlds most populous region with 39 coun- sive and difficult-to-treat complications.
tries and territories and home to 35 % of the Figure 5.1 summarises the IDF estimates regard-
world population. It has the largest country, ing the prevalence, disease burden and distribu-
China, with one billion people and the smallest tion of type 1 and type 2 diabetes in different age
Pacific Island nations with less than 1000 people. and gender groups as well as countries within the
It is also a region of transition with enormous WP Region in 2013 (Table 5.1) [1].
diversity in terms of ethnicity, demographics, Adding to this health-care challenge are the
cultures, politics, religions, technological and rapid societal transition and changing demograph-
socioeconomic development as well as health- ics occurring within an unprepared health-care
care systems, all of which are implicated in the system designed for provision for acute and epi-
causality and consequences of diabetes [1]. sodic rather than chronic care. In many emerging
According to the latest estimates by the IDF, economies, the lack of societal, environmental
8.6 % of adults in the WP Region, i.e. 138.2 mil- and financial protection has led to the widening
social disparity which has exposed the genetically
vulnerable and socially disadvantaged to develop
this silent killer often due to lack of information,
awareness and intervention [2, 3]. In this chapter,
J.C.N. Chan, MD, FRCP (*) E.Y.K. Chow, MB, we will review the epidemiology, aetiology, mor-
ChB, PhD A.O.Y. Luk, MBBS, MRCP bidity, diagnosis, treatment and care delivery for
Department of Medicine and Therapeutics, Hong
Kong Institute of Diabetes and Obesity and Li Ka diabetes focusing in China and WP Region. We
Shing Institute of Health Sciences, The Chinese will also discuss the current unmet needs and pos-
University of Hong Kong, Prince of Wales Hospital, sible solutions for the prevention and control of
Shatin, Hong Kong, SAR, China diabetes in this populous region.

DOI 10.1007/978-3-319-41559-8_5
64 J.C.N. Chan et al.
Diabetes 2010 60,000

14
11.6
GDP
Diabetes prevalence (%)
12 2007 50,000
GDP (million RMB)

9.7
10
40,000
2000 40151
8 5.5 30,000
6
1994
26581 20,000
4 2.5
1980
2 0.9 10,000
9921
4820
0 0
455
1978 1983 1988 1993 1998 2003 2008 2013
Year
Fig. 5.1 The growth of gross domestic product (GDP) and prevalence of diabetes increased in a parallel manner in
China during the last three decades [3]
Rapid Transition and the Obesity decades, while the GDP has increased by 100-
Epidemic fold, the prevalence of diabetes has also increased
by tenfold. In the 2010 National Survey of
The impact of rapid urbanisation on the diabetes 98,658 adults and using both 75 g oral glucose
epidemic is exemplified by the parallel increase tolerance test (OGTT) and glycated haemoglo-
in gross domestic product (GDP) and diabetes bin (A1c) as diagnostic criteria, one in nine
prevalence in China (Fig. 5.1). In less than three Chinese had diabetes, one in three had obesity
(general or central) closely associated with
hypertension and dyslipidemia and one in two
Table 5.1 Key facts and figures about diabetes in the had prediabetes. Amongst those with diabetes,
Western Pacific Region [1] only 30 % were diagnosed and amongst the diag-
At a glance 2013 2035 nosed, only 30 % were treated and amongst the
Total population (millions) 2278 2476 treated, only 40 % were controlled, defined as
Adult population (2079 years, 1613 1818 A1c less than 7 % [4].
millions) According to the Diabetes Epidemiology
Diabetes (2079 years)
Collaborative Analysis of Diagnostic Criteria in
Regional prevalence (%) 8.6 11.1
Asia (DECODA) data, 3050 % of subjects in the
Comparative prevalence (%)* 8.1 8.4
WP Region had metabolic syndrome, character-
Number of people with diabetes 138.2 201.8
(millions)
ised by central obesity and clustering of cardio-
IGT (2079 years) metabolic risk factors, and a strong predictor for
Regional prevalence (%) 6.8 9.0 future development of diabetes [5]. In 2008,
Comparative prevalence (%)* 6.6 7.8 6070 % of people in Tonga, Nauru and Cook
Number of people with IGT (millions) 110.1 164.5 Islands were considered obese [6]. In 2004, the
Type 1 diabetes (014 years) sex-standardised diabetes prevalence was reported
Number of children with type 1 32.5 to be 13.0 % in men and 14.4 % in women in
diabetes (thousands) Nauru. The age-specific prevalence rose from
Number of newly diagnosed cases 5.3 4.5 % in the 1524 age group to 42.7 % in the
per year (thousands) 5564 age group [7]. Tables 5.2 and 5.3 sum-
Health expenditure due to diabetes (2079 years, USD) marise the prevalence and number of people with
Total health expenditure, R = 2#, 88.4 98.4 diabetes in the WP countries based on the IDF fig-
(billions)
ures published in 2013 [8].
*Age-adjusted
# Rapid quantitative and qualitative changes in
R=2 (the diabetes cost ratio assumes that healthcare costs
for people with diabetes are on average two fold higher nutritional intake, notably a shift from a
than people without diabetes). traditional high-fibre, low-fat diet to an energy-
5 Diabetes in China and the Western Pacific Region 65
Table 5.2 Top ten countries in the Western Pacific Region Table 5.3 Top ten countries in the Western Pacific
in terms of number of subjects affected by diabetes [8] Region in terms of prevalence of diabetes [8]
Number of subjects (in 1000s), Prevalence (%),
Country/territory 2013 Country/territory 2013
1. China 98,407.379 1. Tokelau 37.49
2. Indonesia 8554.165 2. Federated States of Micronesia 35.03
3. Japan 7203.776 3. Marshall Islands 34.89
4. Republic of Korea 3323.903 4. Kiribati 28.77
5. Vietnam 3299.113 5. Cook Islands 25.66
6. Philippines 3256.215 6. Vanuatu 23.97
7. Thailand 3150.670 7. Nauru 23.29
8. Myanmar 1988.846 8. French Polynesia 22.41
9. Malaysia 1913.236 9. New Caledonia 19.49
10. Taiwan 1721.062 10. Guam 19.48
dense diet with increased meat and fat consump- Besides, Asians had the lowest body mass index
tion as well as reduced physical activity due to (BMI) and AIRg and developed diabetes only
mechanisation and increased use of mobile vehi- with a small increase in BMI compared to the
cles, are important drivers for this global epi- Caucasians and Africans [13].
demic [9]. In the islands of Vanuatu, researchers Compared to their Europid counterparts, peo-
reported close associations of economic develop- ple of Asian ethnicity are more prone to develop
ment with increased consumption of animal pro- diabetes for the same level of BMI or waist cir-
teins and simple carbohydrates, as well as cumference due to their propensity to store
increased tobacco and alcohol consumption in excessive body or visceral fat [14]. Even amongst
men in areas with high tourism [10]. In China, lean subjects and given the same amount of vis-
during the last two decades, changes in food tech- ceral fat, Asians were more insulin resistant than
nology with production of high-calorie foods Europids due to increased concentration of free
together with reduced physical activity have con- fatty acids and inflammatory markers [15].
tributed to the rising burden of obesity in both Using insulin clamp studies, researchers from
adults and children [11]. Thailand reported insulin deficiency as the pre-
dominant feature in lean subjects and insulin
resistance and in the overweight and obese sub-
Unique Aspects jects [16].
of Pathophysiology: Beta-Cell In autopsy studies, Korean researchers have
Function Versus Visceral Obesity reported close correlations between BMI and
relative percentage of beta cells in both diabetic
Age, family history and obesity are the main risk (r = 0.55) and nondiabetic specimens (r = 0.35).
factors for diabetes [4] although inadequate beta- However, diabetic subjects had a lower percent-
cell response to overcome insulin resistance due age of beta cells than nondiabetic subjects for
to factors such as ageing, obesity and inflam- the same BMI [17]. In healthy subjects, both
mation remains the primary culprit [12]. In an Chinese and South Asian subjects with normal
analysis of 74 study cohorts comprising 3813 glucose tolerance exhibit higher glucose excur-
individuals (19 African, 31 Caucasian and 24 sion during an OGTT with reduced rate of glu-
East Asian cohorts), the authors examined the cose disposal than their Caucasian counterparts
hyperbolic relationship between insulin sensitiv- [18]. This inherently low beta-cell function
ity index (IS) and acute insulin response to glu- together with propensity to develop obesity
cose (AIRg) in healthy cohorts. Amongst these which will impose metabolic stress has provided
three subpopulations, Asians had a steep and a highly plausible explanation for the high risk
non-linear relationship with small changes in one of diabetes in Asian populations undergoing
variable having large effect sizes on the other. rapid transition (Fig. 5.2).
D Plasma Glucose (mmol/L)

SE Asian (n= 10) Insulin Sensitivity (euglycemic clamp)
2.00
4.5 Caucasian (n= 20)
M value (mmol/min/m2)
4.0
1.50
3.5
3.0
1.00
2.5
2.0 0.50
1.5
1.0 0.00
0.5 Caucasian Chinese SE Asian
0.0 n = 15 n=9 n=7
0 15 30 45 60 75 90 105 120
Time (minutes)
25 Insulin Resistance (HOMA)
Chinese (n= 10)
4.5
Caucasian (n= 20) 20
4.0
3.5
3.0 15
2.5 HOMA
2.0 10
1.5
1.0 5
0.5
0.0 0
0 15 30 45 60 75 90 105 120 SE Asian Indian Arabic Chinese Caucasian
Time (minutes) n = 10 n = 10 n = 10 n = 10 n = 10
Fig. 5.2 Lean Chinese and Southeast Asians (open studies compared to their Europid counterparts (black
circle) with normal glucose tolerance exhibited higher circle), supporting their biological vulnerability to
glucose excursion during a 75 g oral glucose tolerance test develop diabetes under conditions of metabolic stress [18]
and reduced insulin sensitivity during euglycaemic clamp
Genomic Landscape of Diabetes generations [19] may contribute to this Asian epi-
in the Region demic with increasingly young age of onset. On
the other hand, monogenic diabetes and latent
Most of the genetic variants discovered in the autoimmune diabetes in adults [25] are not uncom-
genome-wide association studies (GWAS) in mon in young Asian populations which further
Caucasians have been replicated in Asian popula- increase the genotypic and phenotypic heterogene-
tions, albeit often with subtle differences in loca- ity of diabetes in Asian populations [26] (Fig. 5.3).
tions and frequency of genetic variants given the In a recent epigenome-wide association study
same locus [19] and larger effect size on beta-cell of South Asians and Caucasians, the methylation
function in Asians for the same variant [20]. levels of several genetic loci associated with lipid
Besides, GWAS performed in Japanese, Chinese metabolism and beta-cell biology were found to be
and Caucasian populations have revealed signifi- associated with increased risk of diabetes in a
cant interethnic differences in genomic architec- dose-dependent manner [27]. These findings are in
ture as well as novel genetic variants in Asian line with the preponderance of noncoding variants
populations which are implicated in protein syn- linked to diabetes in GWAS, suggesting that dys-
thesis and developmental and beta-cell biology regulation of expression may be more important
[19, 21, 22]. Some of these novel variants were than protein changes as a genetic cause for the
first discovered in patients with familial young- common form of diabetes [28]. In this light, mater-
onset diabetes, suggesting that more variants may nal obesity and gestational diabetes may influence
be discovered in these populations [23, 24]. These the in utero environment to cause dysregulation of
findings also support the notion that insufficient expression of interlinking biological networks
beta-cell response to rapid weight gain with through DNA methylation and chromatin modifi-
progressive personal affluence through multiple cation and contribute towards the high prevalence
Fig. 5.3 A schematic

diagram showing the
phenotypic and
genotypic heterogeneity Non-obese T2D with
of diabetes in Asian genetic variants
populations with and other risk factors
complex interactions Atypical T2D T1D with or
between genetic, Non-diabetic with uncommon without typical
autoimmune and subjects with or variants presentation
external risk factors without common
genetic variants Monogenic
familial
T2D
Obese T2D common

genetic variants and other risk
factors
Not to scale
T1D-type 1diabetes
T2D-type 2 diabetes
of childhood metabolic syndrome [29] and young- Amongst these risk factors, low-grade inflam-
onset diabetes in Asian population [30, 31]. In this mation [48] associated with endemic infections
context, the thrifty genotype or phenotype theory such as chronic hepatitis B viral infections
which states that a trait conducive to survival dur- affecting over 10 % of the Asian population [49,
ing energy-scare condition may become maladap- 50] as well as beta-cell dysfunction associated
tive in an energy-abundant environment may be with the use of tobacco, with smoking rates as
particularly relevant to emerging economies like high as 50 % amongst Asian men from China,
China and the WP Region [32]. In support of this Japan, Korea and Indonesia [51], may be partic-
notion, early-life exposure to the 19501960 fam- ularly relevant to the Asian environment. These
ine in China was found to be associated with external factors may interact with cultural fac-
increased risk of diabetes and metabolic syndrome tors such as high consumption of rice with high
[33] especially in subjects with low birth weight glycaemic index [52] to cause metabolic stress
and adult obesity [34, 35]. especially in those with compromised beta-cell
function. Adding to this multicausality and com-
plexity, environmental pollutants such as persis-
Nature Versus Nurture tent organic pollutants (POPs) [53] and bisphenol
A (BPA) [54] are endocrine or mitochondrial
The combination of low BMI and obesity has put disruptors which tend to hit emerging economies
Asians at high risk of diabetes although many of and/or subjects with low socioeconomic status
these risk factors are modifiable [36]. First and hardest. By inducing insulin resistance and/or
foremost, health illiteracy and social disparity beta-cell dysfunction, these chemicals may
[37] remain the most important socioeconomic increase the risk of obesity and hyperglycaemia
determinant for diabetes and obesity [38, 39]. In especially in subjects with genetic predisposi-
these subjects, lack of awareness, poor education, tion [54].
psychosocial stress [40, 41] and long working
hours [42] may amplify the adverse effects of
behavioural risk factors such as poor sleep Morbidity and Mortality
hygiene [43] and the use of tobacco [44], alcohol
[45] and sugar-sweetened beverages [46] which According to the estimates by IDF in 2013, 36 %
can unmask diabetes especially in those with of global deaths in adults are due to diabetes
genetic predisposition [47]. affecting 5.1 million people. The most populous
WP Region had the highest number of diabetes- foot care (11 %) [60] are the main reasons for
related deaths affecting more men (1,080,000) amputation.
than women (789,000). Of note, 44 % of deaths On the other hand, several local, national and
due to diabetes occurred in people under the age regional registries have provided insights regard-
of 60 [1]. On average, diabetes reduces life ing the interethnic differences in diabetic compli-
expectancy by 612 years, especially in people cations and the impact of ageing and care
diagnosed young, and increases the risk of vascu- provision on the secular changes of these clinical
lar, cancer, nonvascular, non-cancer deaths by outcomes. Apart from renal failure, stroke is a
1.33-fold. The nonvascular, non-cancer-related major disease burden in Asian diabetic popula-
deaths are mainly due to renal failure, mental ill- tions [61]. Depending on the demographic pat-
nesses, hepatobiliary disease and sepsis with fast- tern and stage of societal transition, cancer is now
ing plasma glucose having linear relationships emerging as a leading cause of death especially
with all clinical outcomes, even after adjustment in ageing societies and areas with high rate of
for confounders such as age, sex, BMI and life- endemic infections (e.g. hepatitis B for liver can-
style factors [55]. cer) and high survival rates from cardiovascular-
In the WP Region, in contrast to Europids in renal complications [62]. In the Australian
whom cardiovascular disease is a leading cause National Diabetes Registry of nearly one million
of mortality and morbidity, diabetic kidney dis- subjects, researchers have reported 1.3-fold
ease is a major complication in Asia [26], affect- increased standardised incidence risk of all-site
ing 5060 % of type 2 diabetic patients in cancer in both type 1 and type 2 diabetes except
different clinic settings [56]. In prospective stud- for prostate and melanoma [63]. In a national
ies, the annual incidence of diabetic kidney dis- insurance database from Taiwan, diabetes-related
ease in Chinese population was 24 %, driven death rates have declined over time (men, women:
primarily by disease duration, smoking, meta- 3.92 %, 3.29 % in 2000; 3.64 %, 3.11 % in 2005;
bolic syndrome, blood pressure and glycaemic and 3.12 %, 2.71 % in 2009). In 2009, the esti-
control [57]. Other factors such as the use of mated loss of life due to diabetes was 6.1 years in
over-the-counter medications including herbal women and 5.3 years in men amongst people
medicine [58] and chronic hepatitis B infection diagnosed at the age of 40. The four major causes
[50] might also contribute to this high rate of dia- of death were diabetes, malignancies, heart dis-
betic kidney disease in the WP Region. While ease and cerebrovascular disease [64].
many patients in the WP Region die from end- In the Hong Kong Diabetes Registry estab-
stage renal disease due to lack of access to renal lished as a quality improvement programme since
replacement therapy, this devastating condition 1995, researchers were able to track the secular
can be prevented by intensive control of all risk changes in clinical outcomes in Chinese adults
factors using a protocol-driven and collaborative with diabetes, captured by a territory-wide clinical
approach [59]. management system. In the early 1990s when uni-
Countries in the WP Region differ consider- versal health-care coverage was still being devel-
ably in the ecosystem of health-care provision oped, stroke and end-stage renal failure were the
and health literacy. In low-income areas such as leading causes of death. With ageing, societal
some Pacific Islands where health illiteracy is affluence and access to interventions, coronary
common and access to care is poor, leg amputa- heart disease, cancer and heart failure became the
tion continues to be a major cause of morbidity leading causes of death. In 2005 and after a follow-
and mortality. In a recent survey of amputations up period of 5.5 years, amongst the 7534 type 2
involving 85 people with diabetes from diabetic patients enrolled in the registry since
Solomon Islands, Nauru and Vanuatu, delayed 1995, 763 died with the main causes of death being
treatment (42 %), the use of traditional treat- neoplasms (24.5 %) and cardiovascular (23.5 %),
ments (18 %) and insufficient knowledge about respiratory (15.3) and renal disease (15.3 %) [65].
200 2007 2039 years 2014 2039 years 2007 4059 years
No. with diabetes
(million)
150 2014 4059 years 2007 6079 years 2014 6079 years
100
50
0
Africa Europe MENA North SACA Southeast Western World
Amercia Asia Pacific
160
2039 years 4059 years 6079 years
Percentage change
110
(20072014)
60
10
Africa Europe MENA North SACA Southeast Western World

-40 Amercia Asia Pacific
Fig. 5.4 Rates of increase and number of people with from IDF Atlas 2015 [1]) (MENA Middle East and North
diabetes in different age groups showing the growing epi- Africa, SACA South America and Central America)
demic of young-onset diabetes especially in Asia (Adapted
Emerging Epidemic of Young-Onset implications on the individual, family and society

Diabetes and Its Comorbidities [66]. Between 2007 and 2014, the number of
people with diabetes worldwide has increased by
In the WP Region, 32,500 children under the age 74 % in the 2039 years age group, from 38 mil-
of 15 were estimated to have type 1 diabetes, lion to 67 million. This compares to a 63 %
with the largest number living in the Philippines increase in the 4059 years age group and a 43 %
(7900), followed by China (7700), while increase in the 6079 years age group with an
Australia has the highest estimated incidence rate especially sharp increase in the WP Region and
of 22.3 cases per 100,000 children. In 2013, 5300 Southeast Asia where China and India are located
children were diagnosed to have type 1 diabetes (Fig. 5.4).
in the WP Region [1]. Although type 1 diabetes is In the same registry, the researchers reported
often considered a rare disease in non-Caucasian the rarity of classical type 1 diabetes which
populations, the rising prevalence of young-onset accounted for 3 % in the entire cohort and less
type 2 diabetes is a major health-care challenge. than 10 % amongst those diagnosed before the
Arbitrarily defined as age of diagnosis less than age of 40. Overall, one in five adults with type 2
40 years, these youths and young adults are diabetes had young-onset disease, with 50 %
high-risk populations for premature noncommu- higher risk of cardiovascular-renal disease than
nicable disease (NCD) including but not limited their late-onset counterparts at any given age,
to cardiovascular-renal disease and cancer. This mainly driven by long disease duration [67].
growing epidemic of young-onset diabetes is in Amongst these young-onset type 2 diabetic
part driven by the high prevalence of maternal patients, 40 % were lean and 60 % were obese or
obesity, gestational diabetes and childhood met- overweight. Compared to their counterparts with
abolic syndrome which sets up a vicious cycle type 1 diabetes, these young-onset type 2 dia-
of diabetes begetting diabetes with enormous betic patients had considerably higher rates of
cardiovascular-renal complications, often due to for the prevention and control of type 2 diabetes
poor control of risk factors, frequent default and last updated in 2010 has not yet endorsed the use
treatment non-adherence. By contrast, due to of HbA1c as an alternative to glucose-based tests
their propensity to develop an acute ketotic pre- for diagnosing diabetes [71]. Similarly, the
sentation, type 1 diabetic patients were less likely UNITE FOR Diabetes Philippines in its 2014
to default, and with access to education and insu- practice guideline also recommended against
lin, these patients tended to have low incidence of using A1c. They also proposed the use of OGTT
complications despite long disease duration [68]. for diabetes screening only in individuals with
In a regional database established through the known impaired fasting glucose or metabolic
web-based Joint Asia Diabetes Evaluation syndrome [72]. In the latest report published in
(JADE) programme which enables care providers 2010, the Japan Diabetes Society adopted the use
to establish registries using a common protocol in of A1c to complement glucose-based tests in dia-
a real-world setting, high prevalence of young- betes screening but stipulated that an individual
onset diabetes (~20 %) and treatment gaps was meeting the A1c threshold of 6.5 % must concur-
confirmed in 41,029 adult patients from over ten rently fulfil one other criteria of either fasting
countries in Asia. These real-world data highlight plasma glucose 7.0 mmol/L or 2-h post-OGTT
the heterogeneity in terms of attainment of treat- plasma glucose 11.1 mmol/L to establish the
ment targets often due to differences in health- diagnosis [73]. This differs from international
care coverage and financial support for essential guidelines which assign similar weights to
laboratory investigations and medications as key glucose-based studies and A1c in the diagnostic
components for diabetes care. Yet irrespective of schema and allows the diagnosis to be made on
these diversities, in all countries, there was a con- the basis of A1c measurement alone. The Korean
sistent trend that patients with young-onset dia- Diabetes Association fully applied the ADA cri-
betes were less likely to attain treatment targets teria for diagnosing diabetes since 2011 [74].
for blood glucose and blood lipids and were less Glycated haemoglobin has a number of advan-
likely to be prescribed organ-protective drugs tages over plasma glucose in that it summarises
such as statins and renin-angiotensin system long-term glucose exposure, has less intra-
(RAS) inhibitor despite having clear indications individual variability and does not require testing
such as cardiovascular-renal complications [30]. during a fasted state [75]. The recommendation
to include A1c in diagnostic criteria of diabetes
by the international expert committee was based
Diagnosis of Diabetes on epidemiological studies which demonstrated a
and Prediabetes in Asia tight association between A1c and diabetic reti-
nopathy in mixed populations [7577]. Progress
The criteria for diagnosing diabetes and predia- in analytic procedures and global movement to
betes in Asia for the most part take references certify A1c assay to the National Glycohemoglobin
from international guidelines including those of Standardization Program facilitated its wider use
the World Health Organization (WHO) and as a diagnostic tool as well as in disease monitor-
American Diabetes Association (ADA) [69, 70]. ing [75, 78]. In developing countries such as
The measurement of fasting plasma glucose for China and the Philippines, however, the measure-
diabetes screening is widely accepted and prac- ment of A1c has not yet achieved standardisation
tised. On the other hand, there are differences in across the nation, and this remains the key limita-
regional recommendations for oral glucose tol- tion to its application [72].
erance test (OGTT) and glycated haemoglobin Notwithstanding logistics of costs and instru-
(A1c) in the routine diagnostic process. mentation, inclusion of A1c in diagnostic crite-
Approaches to screening are also closely related ria will uncover more patients with diabetes than
to health-care access and resources available. For using glucose-based criteria alone. In large pop-
instance, the Chinese Diabetes Society guideline ulation surveys in China and Japan, over half of
the participants with newly diagnosed diabetes ducted in Asia which showed that fasting plasma
and prediabetes were detected with A1c. This glucose alone could only identify half of the peo-
may be due to the high prevalence of high post- ple with diabetes and that individuals with pre-
glucose challenge blood glucose levels which dominantly post-load hyperglycaemia are
may be detected by an integrated value like A1c phenotypically different from those with fasting
but missed by using fasting plasma glucose only hyperglycaemia [86]. As discussed, Asian dia-
[4, 79]. betic patients have lower BMI and less beta-cell
Increasingly, it is recognised that ethnicity reserve than their Caucasian counterparts and
may modify the relationship between measured thus are more likely to fail glucose stress test. On
A1c and blood glucose levels. Several studies this premise, a lower threshold to perform OGTT
have shown that for similar distribution of blood in Asians should be considered. In Chinese, a
glucose, A1c levels were consistently higher in paired value of A1c 6.1 % and fasting plasma
Asians compared to Caucasians and that amongst glucose 6.1 mmol/L had 1317 times increased
Asians, higher in Indians and Malays relative to likelihood to occur in diabetic subjects compared
Chinese [80, 81]. A few factors may contribute to to nondiabetic subjects [87, 88]. In resource-
such racial disparities such as differences in hae- limited setting, OGTT will have the greatest yield
moglobin glycation rate and in population preva- in detecting diabetes when paired A1c and fasting
lence of haemoglobinopathies which interfere plasma glucose are above these cut-off values.
with A1c measurement.
Against this background, concerns are raised
regarding the optimal A1c threshold for detecting Translating Primary Prevention
diabetes in Asian groups and whether ethnic- of Type 2 Diabetes
specific standards are required. Studies carried
out in Asians have suggested that lower cut-offs The chronic, silent and nonurgent nature of dia-
of A1c correlated more closely with diabetes as betes often leads to late diagnosis and delayed
defined using the gold standard of OGTT [82 treatment. Once diagnosed, people with diabetes
84]. In a recent population-based study compris- have pluralistic needs including information,
ing three ethnic groups of Malay, Chinese and social and psychological support, education,
Indian which examined the cross-sectional rela- medical and surgical treatment, to name but a
tionship between A1c and moderate retinopathy, few. Given these multiple demands, large popula-
it was found that although A1c differed slightly tion size, lack of capacity and resource restraints,
in its sensitivity and specificity in predicting reti- prevention and control of diabetes is often chal-
nopathy amongst different ethnic groups, eye lenged with care fragmentation, clinical inertia
complication was generally rare when A1c fell and treatment non-adherence with insufficient
below 6.5 % [85]. Results from this Asian study community support [3, 89, 90]. In both ran-
concurred with those of a large multinational domised disease management programmes and
database which confirmed that an A1c threshold observational cohorts, attaining multiple treat-
of 6.5 % has similar discriminatory power for the ment targets and the use of organ-protective
presence or absence of diabetic retinopathy in drugs such as statins and RAS inhibitors have
Caucasians and Asians [77, 85]. been shown to reduce cardiovascular-renal com-
Oral glucose tolerance test is the gold standard plications and related deaths in the WP Region
test for the diagnosis of diabetes and is necessary [91, 92]. Yet large-scale surveys have demon-
in making a diagnosis of impaired glucose toler- strated only 30 % of patients with diabetes ever
ance (IGT). The requirement of a second blood had assessments for risk factors and complica-
sample and being more time consuming has tions. Amongst those who had assessments,
greatly limited its practice in many Asian coun- only 3040 % attained one of the three ABC
tries. However, the importance of the 2-h plasma targets (A1c <7 %, BP <130/80 mmHg, LDL-C
glucose has been highlighted in studies con- <2.6 mmol/L) and 510 % attained all three
targets [93] with particularly low rates amongst strategic alliance between the WHO Regional
people with young-onset diabetes [30, 94]. Office for the WP, the Secretariat of the Pacific
Diabetes is a lifelong disease which requires Community and the IDF-Western Pacific Region
acquisition of knowledge, change of attitudes and as a regional voice to advocate for prevention and
formation of new habits in order to reduce dis- control of diabetes. In the WPDD Plan of Action
ease burden. It is also a biological problem that (20052010), experts from the region sum-
requires medications, technologies and monitor- marised the multidimensional nature of diabetes
ing which have resource implications. In a survey (Fig. 5.5) and the need to use a multipronged
from Guam involving 125 patients, 40 % were strategy including policies and legislations
not aware of the type of diabetes they had, 20 % (Fig. 5.6) to create a health-enabling environment
had not received education on self-management and reform the health-care system to make pre-
and 3060 % had not received advice on tobacco vention and control of diabetes accessible, afford-
cessation, immunisation services, nutritional able and sustainable [101].
counselling and/or regular eye and foot examina-
tions. Over 50 % of patients expressed their desire
to have preventive and education services with Some Examples of Diabetes
enhanced access to specialists and specialised Prevention and Control Strategies
care as well as financial support to cover the costs from China and WP
of chronic care and medications [95].
There is now consensus that a chronic care National Plan for Diabetes and NCD
model involving community mobilisation and Prevention
engagement supported by an integrated health- In the China National Plan for NCD Prevention
care system with country/area appropriate financ- and Treatment (20122015), the government pro-
ing and health-care organisation is needed to posed to use public measures including environ-
promote interactions between an informed per- mental protection, food safety, clean drinking
son with diabetes and a proactive health-care water, tobacco control and occupational safety to
team to achieve positive clinical outcomes [96]. create a health-enabling environment through
In this information and technology era, there is a broad social participation and multisector collab-
growing advocacy to use improvement science, orations. Other proposed practices and policies
often entailing the use of real-world data, to included universal vaccination, maternal and
inform and change clinical practice [97]. In the child health programmes and primary care. Since
case of diabetes, changing the workflow and then, the Chinese government has introduced dif-
using protocols to collect data systematically for ferent health insurance packages at the rural and
establishing registry can generate personalised urban areas and built more than 30,000
report to promote shared decision-making. On a community-based clinics to provide basic preven-
broader perspective, data transparency and com- tive care programme including regular risk factor
parison of performance indexes may also moti- surveillance and provision of essential medica-
vate practice and policy changes through ongoing tions for control of blood pressure and blood glu-
evaluation and sharing of best care models cose [102]. Despite these ongoing efforts, given
[98100]. the vastness of the country and size of the popula-
tion, there remain challenges in communications
amongst relevant stakeholders, patient flow
Western Pacic Diabetes Declaration between hospitals and primary care clinics, capac-
(WPDD) Plan for Action (20062010) ity building and public education [103].
In 2000, at the 51st session of the WHO Regional Tobacco Control

Committee for the WP, the Committee endorsed Several meta-analyses have indicated a dose-
the establishment of the WPDD as a regional dependent risk association of smoking with dia-
Diabetes and cardio-

renal complications
Chronic disease,
Obesity and morbidity and
metabolic syndrome mortality
Personal lifestyle
Physical activity e.g. Unhealthy diet e.g. Smoking,alcohol

TV watching, video soft drink junk food, binge drinking
game playing, low fruit/vegetable
computer use and high meat
Environment and consumption
policy
Socio-economical Employment, income, Demographics and Political environment Other factors e.g. low
status,education, access, to care and culture e.g. aging and eg.health policy and grade infections,
psychosocial stress medical insurance migrant populations legislations maternal and
perinatal health, low
birth weight
Genetics
Fig. 5.5 A schematic diagram summarising the interac- in the Western Pacific Diabetes Declaration Plan for
tions amongst predisposing, precipitating and perpetuat- Action (20052010) [154]
ing factors in the epidemic of diabetes and its comorbidities
Policy makers Health care team
Collection of information (STEPS) at Development of clinical guidelines

periodic intervals
Information dissemination Patient education and self-care

Health awareness Periodic assessments and default
recall
Mass media Treatment to targets
Personnel training
School
Resource redistribution
Community
New funding model
Nongovernmental organizations
Medical insurance
Other sectors
Health Promotion Programmes Disease management

(diet, exercise, tobacco and alohol) Integrated and continual care
School Screening for Community Hospital

Policy diabetes in high care care
risk subjects
Ongoing data Ongoing data

collection collection
Reduce obesity and diabetes Reduce diabetes complications
Fig. 5.6 A multipronged strategy using policies, commu- Western Pacific Diabetes Declaration Plan for Action
nity mobilisation, intersectoral partnerships and clinical (20052010) [154]
leaderships to detect, prevent and control diabetes in the
betes [104] as well as that with cardiovascular WHO has now called for early prevention of dia-
disease and total mortality in people with diabetes betes using a life-course strategy that starts with
[105]. Although it remains to be confirmed maternal health [116]. However, screening for
whether smoking cessation will reduce the risk of gestational diabetes is only practised in a few
diabetes, it is likely that tobacco control would countries in Asia [117]. Several countries such as
reduce the amplifying effects of tobacco on mor- Japan [118] and Taiwan [119] have embarked
bidities associated with diabetes, notably, cancer upon national urine glucose screening pro-
and cardiovascular-renal disease. To this end, gramme, while a few countries such as Singapore
there have been successful stories in tobacco con- have introduced national school programme to
trol through strong political will and tough mea- control childhood obesity [120].
sures in the WP Region, such as New Zealand and
Hong Kong [106].
Rational Selection of Antidiabetes
Early Detection and Prevention Medications
There is high-level evidence confirming that many
cases of diabetes can be prevented or delayed by In previous sections, we have highlighted differ-
structured lifestyle modification [107]. That said, ences in pathophysiology in Asian populations.
most experts and professional bodies proposed tar- Beta-cell dysfunction may be the primary defect
geted or opportunistic screening using known risk in lean individuals, while Asians exhibit greater
factors (e.g. age, sex, family history, obesity (BMI insulin resistance and visceral adiposity at a lower
and waist circumference), blood pressure and ges- BMI compared with Caucasian counterparts.
tational diabetes) and/or simple risk scores [108] Therefore, treatment may be tailored to reflect
rather than population screening [109]. Given the these ethnic differences. Metformin is widely
high prevalence of young-onset diabetes in the WP used as a first-line oral antidiabetic agent. Despite
Region and the importance of disease duration as a a lower BMI, metformin appears efficacious in
determinant for all diabetes-related complications Asian populations [121]. Asian diabetic subjects
[110], targeted screening in young subjects with treated with metformin show a similar reduction
family history and/or obesity is likely to be cost- in insulin resistance and improved glycaemic con-
effective due to the high prevalence of diabetes trol as compared with non-Asians [122].
amongst the relatives of affected subjects [111] Therefore, metformin, unless contraindicated, is
and the high lifetime risk for complications, once recommended as the first-line therapy according
affected [109]. to global guidelines by the IDF [123].
In the early 1990s, China conducted the first Alpha glucosidase inhibitors (AGI) may have a
randomised 6-year lifestyle modification pro- particular role in early therapy amongst Asians
gramme in a workforce who had IGT. These sub- due to high carbohydrate content of Asian diets.
jects continued to be observed for more than The typical Chinese diet has a carbohydrate con-
20 years after completion of the trial which content of up to 67 % as compared with 40 % amongst
firmed that early intervention reduced the inci- Europeans [124]. In one study, treatment with
dence of diabetes, retinopathy and cardiovascular acarbose 50100 mg three times a day effectively
disease [112, 113]. Similar prevention pro- reduced A1c by 0.7 % and improved both fasting
grammes have also been successfully translated and 1 h plasma glucose as compared with placebo
and adapted to meet the special needs in primary in Asians with type 2 diabetes [125]. In the met-
care settings in Australia [114] and indigenous formin and acarbose in Chinese as the initial
populations in Pacific Islands [115]. hypoglycaemic treatment (MARCH) study,
The negative impact of gestational diabetes on nearly 800 newly diagnosed Chinese patients with
childhood obesity may underlie the growing epi- type 2 diabetes were randomised to 24 weeks of
demic of young-onset diabetes and NCD. The either acarbose or metformin monotherapy [126].
The reduction in A1c was comparable in the acar- to-head trials comparing glinides versus other
bose- and metformin-treated groups (1.17 % first-line oral antidiabetic drugs; therefore, their
versus 1.19 %), demonstrating noninferiority in role in early therapy remains unclear.
overall glucose lowering. In contrast to Caucasians, the incretin response
Further, there is a strong evidence that AGI is preserved in Asians with type 2 diabetes [131].
may prevent progression from IGT to type 2 dia- DPP4 inhibitors may have a larger effect in glucose
betes. In the STOP-NIDDM trial that was con- reduction in Asians as compared with non-Asians.
ducted in Canada and Europe, the use of acarbose In a systematic review of randomised controlled
reduced progression to type 2 diabetes by 25 % trials of DPP4 inhibitors, those involving higher
[127]. These findings have been replicated in the proportion of Asian subjects demonstrated greater
VICTORY study which compared voglibose A1c lowering [132]. Similarly, GLP-1 analogues
versus placebo amongst 1780 Japanese individu- lowered A1c to a greater extent in Asian-dominant
als with IGT. The use of voglibose was associ- as compared with non-Asian-dominant studies
ated with an impressive 40 % lower risk of [133]. Although there are no ethnic-specific data of
progression to type 2 diabetes [128]. The control long-term safety of incretin-based therapies, sev-
of postprandial glucose excursions may theoreti- eral large-scale cardiovascular end point studies of
cally confer cardioprotection via reduction of saxagliptin and sitagliptin have enrolled over 10 %
oxidative stress. However, the jury is still out as of Asians and demonstrated neutral effects on car-
to whether AGI confers any cardiovascular ben- diovascular outcomes [134, 135].
efit. In an analysis of a large Taiwanese cohort Severe beta-cell dysfunction is common at
comparing type 2 diabetes patients treated with diagnosis, and there is evidence that early inten-
AGI versus metformin monotherapy, the risk of sive insulin therapy may preserve beta-cell func-
cardiovascular events was significantly higher tion or even induce remission in Asians. An initial
amongst those on AGI, adjusted for baseline dif- study showed that continuous subcutaneous insu-
ferences by propensity score [129]. Ongoing tri- lin infusion for 2 weeks in newly diagnosed type
als, such as the Acarbose Cardiovascular 2 diabetes Chinese patients led to restoration of
Evaluation (ACE) study which evaluates the early-phase insulin secretion and beta-cell func-
effect of acarbose on recurrent cardiovascular tion. As such, 42 % of patients maintained optimal
events and incident diabetes amongst those with glycaemic control after 2 years on diet alone
history of cardiovascular disease and IGT, may [136]. A subsequent study led by Weng and col-
provide much needed answers [130]. leagues randomised 410 newly diagnosed type 2
Insulin secretagogues including sulfonylureas diabetes patients to multiple daily injections
and glinides are widely used and are generally (MDI), continuous subcutaneous insulin infusion
efficacious in glucose lowering amongst Asians. (CSII) or oral agents, and treatment was stopped
The glinides target early-phase insulin release, as after normoglycaemia was reached for 2 weeks
compared with sulfonylureas which tend to have a [137]. The study demonstrated superior remission
longer half-life. Thus, glinides may be particu- rates at 1 year in insulin-treated patients regard-
larly effective in Asian Chinese where a defect in less of route (CSII 51 %, MDI 45 %) as compared
early-phase insulin is common [124]. In a trial in with those treated with oral agents (27 %). Similar
Chinese patients which compared repaglinide levels of A1c reduction were achieved in all three
plus metformin versus repaglinide alone, both groups, suggesting the restoration of beta-cell
arms achieved a similar reduction in A1c (4.45 % function is not merely linked to amelioration of
with repaglinide plus metformin versus 4.15 % hyperglycaemia. These studies argue for a possi-
with repaglinide only) from baseline A1c of 10 %. ble use of intensive insulin therapy to reverse
However, combination treatment with metformin acute glucotoxicity for preserving beta-cell func-
achieved lower fasting plasma glucose as com- tion in Asian patients especially in those with
pared with repaglinide alone. There are no head- early diabetes and without complications.
Given the phenotypic heterogeneity, subtle dif- patients who need additional informational, medi-
ferences in disease mechanisms and lifestyle fac- cal and social support (Fig. 5.7) [140].
tors, the goal of a personalised regimen is to By combining service provision and epide-
match the right drug to the right patient at the miological research, these cohorts, databases
right time for the right outcome. In particular the and biobanks have provided clinicians unique
risk-benefit of each therapeutic agent should be opportunities to track clinical progress, develop
considered for in the individual in order to achieve risk equations and identify treatment gaps such
the best outcomes [138]. as the associations between hypoglycaemia, can-
cer and diabetic kidney disease [141] as well as
interactions amongst genotypes, phenotypes,
Coordination and Delivery treatment and clinical outcomes [142, 143]. In
of Diabetes Care Services 2009, the Hong Kong government fully adopted
this integrated care model and introduced the
In a meta-analysis, quality improvement initia- risk assessment management programme and
tives targeting at patients, systems and care pro- patient empowerment programme to the primary
viders have been shown to reduce blood pressure, care clinics which were shown to improve con-
blood glucose and blood lipids although amongst trol of all risk factors and reduce cardiovascular
these strategies, patient education, task delega- disease and all-cause death [144146].
tion, self-care and case management were found
to have the largest effect sizes [99]. Hong Kong is
one of the most cosmopolitan cities in China with Using the JADE Registry to Promote
a population of seven million. It has a public Quality Assurance and Cooperative
health-care system delivered through the Hospital Learning
Authority which funds and governs all public hos-
pitals and clinics, modelled after the UK National In 2007, this concept of using structured processes
Health Scheme. to personalise care [147], augmented by informa-
In response to the growing epidemic of diabetes tion technology and collaborative care [148], was
since the early 1990s and given limited resources, digitalised through the establishment of the web-
clinical researchers and care providers used knowl- based Joint Asia Diabetes Evaluation (JADE) pro-
edge transfer and changed care settings to cope gramme using private-public partnerships [139].
with the patient volume. By setting up a hospital- By joining the JADE programme, practitioners can
based diabetes centre, located away from the busy establish their own clinic registry using built-in
clinics, coordinated by specialised nurses and templates and protocols for quality assurance while
health-care assistants and supported by endocri- contributing anonymous data to form the JADE
nologists, the diabetes team offers regular risk Registry to identify treatment gaps and share best
assessment and education services to diabetic practices [139]. Using this regional registry, first of
patients referred by all specialties. A key feature of its kind, the researchers were able to confirm the
this model is the use of protocols, task delegation high prevalence of young-onset diabetes (20 %) in
and data management to establish the Hong Kong Asia and the treatment gaps [30] as well as the ben-
Diabetes Registry for risk stratification and quality efits of providing informational and social support
assurance [139]. These data were used to generate on reducing clinical inertia, treatment non-adher-
personalised report for improving communica- ence and hospitalisations [140, 149].
tions amongst specialists, doctors and patients as
well as triaging patients into primary or hospital-
based care. The Diabetes Center also serves as a Future Directions
central point for coordinating various activities
including peer support, group medical follow-up In 2009, the United Nations General Assembly
and behavioural programmes for difficult-to-treat identified diabetes, cardiovascular disease, cancer
Comminity Diabetes Public health

Empowerment assessment Measures & policy
& education
centre
Registry
Treat early,
Case safely and to Information
finding multiple technology
targets
Family
Specialists
doctors
Ongoing
Support
Resourcing Health literacy
Fig. 5.7 A conceptual framework of using diabetes cen- linked by information technology and protocols to estab-
tres run by paramedical staff, supported by internists, to lish registry for quality assurance. Through community
provide assessment, education, outreach and peer support empowerment, capacity building and health-care policies,
programmes to complement medical care provided by these centres can contribute towards early detection, pre-
specialists and family doctors. All parties concerned are vention and control of diabetes and its comorbidities
and respiratory disease as the four NCDs as top pri- centres for education to develop, produce and dis-
orities for prevention and control [150]. Recently, seminate diabetes education in order to enhance
universal health coverage is ranked a top WHO professional education for which two of the nine
agenda for ensuring people with NCD to have centres were located in the WP Region (Australia
access to medications, technologies and basic and Hong Kong) [152].
medical care [151]. Given the diversity of the WP
Region, different countries will have their unique Conclusion
transition patterns in terms of political, socio-eco- Although the definition of health by the
nomical, technological, cultural and health-care WHO as a state of complete physical, mental
development which will interact to influence the and social well-being and not merely the
diabetes landscapes in these countries. As such, absence of disease or infirmity [153] may not
each country/area will have to develop its own be easily attained, collective efforts through
prevention and control strategies tailored to its government mandates, clinical leaderships,
special needs and circumstances to meet the man- intersectoral partnerships, community
dates set by the WHO and UN Assembly. empowerment, ongoing research and advo-
Policies aside, from a more operational per- cacy and prevention and control of diabetes
spective, health-care providers who are equipped are aspiration that is feasible, achievable and
with knowledge about the nature of diabetes and indeed essential. To this end, with increasing
stand between evidence and patients in need of globalisation, more countries/areas will
evidence-based care, knowledge transfer and undergo urbanisation and as such, the expo-
application become their armamentarium in the sures to, and experiences gained with diabetes
pursuit of health protection and disease preven- in the WP Region, will provide invaluable les-
tion. In this regard, the IDF, as a global voice for sons in our common pursuit of prevention and
people with diabetes, has established reference control of diabetes and its comorbidities.
References 17. Yoon KH, Ko SH, Cho JH, et al. Selective beta-cell
loss and alpha-cell expansion in patients with type 2
diabetes mellitus in Korea. J Clin Endocrinol Metab.
1. IDF Atlas 2015: International Diabetes Federation
2003;88:23008.
2015.
18. Dickinson S, Colagiuri S, Faramus E, Petocz P,
2. Chan JC, Cho NH, Tajima N, Shaw J. Diabetes in the
Brand-Miller JC. Postprandial hyperglycemia and
Western Pacific Region-past, present and future.
insulin sensitivity differ among lean young adults of
Diabetes Res Clin Pract. 2014;103:24455.
different ethnicities. J Nutr. 2002;132:25749.
3. Chan JC, Zhang Y, Ning G. Diabetes in China: a
19. Ma RC, Chan JCN. Type 2 diabetes in East Asians:
societal solution for a personal challenge. Lancet
similarities and differences with populations in
Diabetes Endocrinol. 2014;2:96979.
Europe and the United States. Ann N Y Acad Sci.
4. Xu Y, Wang L, He J, et al. Prevalence and control of
2013;1281:6491.
diabetes in Chinese adults. JAMA J Am Med Assoc.
20. Hong KW, Chung M, Cho SB. Meta-analysis of
2013;310:94859.
genome-wide association study of homeostasis model
5. DeCODA Study Group. Prevalence of the metabolic
assessment beta cell function and insulin resistance in
syndrome in populations of Asian origin.
an East Asian population and the European results.
Comparison of the IDF definition with the NCEP
Mol Genet Genom MGG. 2014;289:124755.
definition. Diabetes Res Clin Pract. 2007;76:5767.
21. Cho YS, Chen CH, Hu C, et al. Meta-analysis of
6. Stevens GA, Singh GM, Lu Y, et al. National,
genome-wide association studies identifies eight
regional, and global trends in adult overweight and
new loci for type 2 diabetes in East Asians. Nat
obesity prevalences. Popul Health Metrics. 2012;
Genet. 2011;44:6772.
10:22.
22. Yamauchi T, Hara K, Maeda S, et al. A genome-
7. Khambalia A, Phongsavan P, Smith BJ, et al. wide association study in the Japanese population
Prevalence and risk factors of diabetes and impaired identifies susceptibility loci for type 2 diabetes at
fasting glucose in Nauru. BMC Public Health. 2011; UBE2E2 and C2CD4A-C2CD4B. Nat Genet. 2010;
11:719. 42:8648.
8. International Diabetes Federation, ed. International 23. Ma RC, Lee HM, Lam VK, et al. Familial young-
Diabetes Atlas 2013. onset diabetes, pre-diabetes and cardiovascular dis-
9. Hu FB. Globalization of diabetes: the role of diet, ease are associated with genetic variants of
lifestyle, and genes. Diabetes Care. 2011;34: DACH1 in Chinese. PLoS ONE. 2014;9, e84770.
124957. 24. Ma RC, Hu C, Tam CH, et al. Genome-wide associa-
10. Dancause KN, Dehuff C, Soloway LE, et al. tion study in a Chinese population identifies a sus-
Behavioral changes associated with economic devel- ceptibility locus for type 2 diabetes at 7q32 near
opment in the South Pacific: health transition in PAX4. Diabetologia. 2013;56:1291305.
Vanuatu. Am J Hum Biol Off J Hum Biol Counc. 25. Kong APS, Chan JCN. Other disorders with type 1
2011;23:36676. phenotype. In: Holt R, Goldstein B, Flyvbjerg A,
11. Ma RC, Lin X, Jia W. Causes of type 2 diabetes in Cockram CS, editors. Textbook of diabetes. 4th ed.
China. Lancet Diabetes Endocrinol. 2014;2:98091. Chichester: Wiley-Blackwell, Wiley; 2010. p. 1529.
12. Kahn SE. The relative contributions of insulin resis- 26. Kong AP, Xu G, Brown N, So WY, Ma RC, Chan
tance and beta-cell dysfunction to the pathophysiol- JC. Diabetes and its comorbidities-where East meets
ogy of Type 2 diabetes. Diabetologia. 2004;46 West. Nat Rev Endocrinol. 2013;9:53747.
:319. 27. Chambers JC, Loh M, Lehne B, et al. Epigenome-
13. Kodama K, Tojjar D, Yamada S, Toda K, Patel CJ, wide association of DNA methylation markers in
Butte AJ. Ethnic differences in the relationship peripheral blood from Indian Asians and Europeans
between insulin sensitivity and insulin response: a with incident type 2 diabetes: a nested case-control
systematic review and meta-analysis. Diabetes Care. study. Lancet Diabetes Endocrinol. 2015;3:52634.
2013;36:178996. 28. Lou S, Lee HM, Qin H, et al. Whole-genome bisul-
14. Deurenberg-Yap M, Schmidt G, van Staveren WA, fite sequencing of multiple individuals reveals com-
Deurenberg P. The paradox of low body mass index plementary roles of promoter and gene body
and high body fat percentage among Chinese, Malays methylation in transcriptional regulation. Genome
and Indians in Singapore. Int J Obes. 2000;24:10117. Biol. 2014;15:408.
15. King GL, McNeely MJ, Thorpe LE, et al. 29. Ma RC, Tutino GE, Lillycrop KA, Hanson MA, Tam
Understanding and addressing unique needs of dia- WH. Maternal diabetes, gestational diabetes and the
betes in Asian Americans, native Hawaiians, and role of epigenetics in their long term effects on off-
Pacific Islanders. Diabetes Care. 2012;35:11818. spring. Prog Biophys Mol Biol. 2015;118:5568.
16. Suraamornkul S, Kwancharoen R, Ovartlarnporn M, 30. Yeung RO, Zhang Y, Luk A, et al. Metabolic profiles
Rawdaree P, Bajaj M. Insulin clamp-derived mea- and treatment gaps in young-onset type 2 diabetes in
surements of insulin sensitivity and insulin secretion Asia (the JADE programme): a cross-sectional study
in lean and obese Asian type 2 diabetic patients. of a prospective cohort. Lancet Diabetes Endocrinol.
Metab Syndr Relat Disord. 2010;8:1138. 2014;2:93543.
31. Chan JC, Yeung R, Luk A. The Asian diabetes phe- style factors in Chinese: the Better Health for Better
notypes: challenges and opportunities. Diabetes Res Hong Kong health promotion campaign. Eur J Clin
Clin Pract. 2014;105:1359. Nutr. 2010;64:138692.
32. Diamond JM. Diabetes running wild. Nature. 47. Qi Q, Chu AY, Kang JH, et al. Sugar-sweetened bev-
1992;357:3623. erages and genetic risk of obesity. N Engl J Med.
33. Li Y, Jaddoe VW, Qi L, et al. Exposure to the Chinese 2012;367:138796.
famine in early life and the risk of metabolic syn- 48. Pickup JC. Inflammation and activated innate immu-
drome in adulthood. Diabetes Care. 2011;34:10148. nity in the pathogenesis of type 2 diabetes. Diabetes
34. McCance DR, Pettitt DJ, Hanson RL, Jacobsson Care. 2004;27:81323.
LTH, Knowler WC, Bennett PH. Birth weight and 49. Lao TT, Chan BC, Leung WC, Ho LF, Tse
non-insulin dependent diabetes: thrifty genotype, KY. Maternal hepatitis B infection and gestational
thrifty phenotype, or surviving small baby geno- diabetes mellitus. J Hepatol. 2007;47:4650.
type? Br Med J. 1994;308:9425. 50. Cheng AY, Kong AP, Wong VW, et al. Chronic hepa-
35. Neel JV. Diabetes mellitus: a thrifty genotype ren- titis B viral infection independently predicts renal
dered detrimental by progress? Am J Hum Genet. outcome in type 2 diabetic patients. Diabetologia.
1962;14:35362. 2006;49:177784.
36. Boyko EJ, Fujimoto WY, Leonetti DL, Newell- 51. Ueshima H, Sekikawa A, Miura K, et al.
Morris L. Visceral adiposity and risk of type 2 diabe- Cardiovascular disease and risk factors in Asia: a
tes: a prospective study among Japanese Americans. selected review. Circulation. 2008;118:27029.
Diabetes Care. 2000;23:46571. 52. Yu R, Woo J, Chan R, et al. Relationship between
37. Wong MC, Leung MC, Tsang CS, Lo SV, Griffiths dietary intake and the development of type 2 diabe-
SM. The rising tide of diabetes mellitus in a Chinese tes in a Chinese population: the Hong Kong Dietary
population: a population-based household survey on Survey. Public Health Nutr. 2011;14:113341.
121,895 persons. Int J Public Health. 2013;58:26976. 53. Lim S, Cho YM, Park KS, Lee HK. Persistent
38. Demakakos P, Nazroo J, Breeze E, Marmot organic pollutants, mitochondrial dysfunction, and
M. Socioeconomic status and health: the role of sub- metabolic syndrome. Ann N Y Acad Sci. 2010;1201:
jective social status. Soc Sci Med. 2008;67:33040. 16676.
39. Ko GTC, Chan JCN, Cockram CS. A low socioeco- 54. Bi Y, Wang W, Xu M, et al. Diabetes genetic risk
nomic class is associated with diabetes and meta- score modifies effect of bisphenol A exposure on
bolic syndrome in Hong Kong Chinese. Eur deterioration in glucose metabolism. J Clin
J Epidemiol. 2001;17:28995. Endocrinol Metab. 2016;101:14350.
40. Williams ED, Magliano DJ, Tapp RJ, Oldenburg BF, 55. Seshasai SR, Kaptoge S, Thompson A, et al.
Shaw JE. Psychosocial stress predicts abnormal glu- Diabetes mellitus, fasting glucose, and risk of cause-
cose metabolism: the Australian diabetes, obesity specific death. N Engl J Med. 2011;364:82941.
and lifestyle (AusDiab) study. Ann Behav Med Publ 56. Wu AY, Kong NC, de Leon FA, et al. An alarmingly
Soc Behav Med. 2013;46:6272. high prevalence of diabetic nephropathy in Asian type
41. Harding JL, Backholer K, Williams ED, et al. 2 diabetic patients: the MicroAlbuminuria Prevalence
Psychosocial stress is positively associated with (MAP) Study. Diabetologia. 2005;48:1726.
body mass index gain over 5 years: evidence from 57. Luk AO, So WY, Ma RC, et al. Metabolic syndrome
the longitudinal AusDiab study. Obesity. 2014;22(1): predicts new onset of chronic kidney disease in
27786. 5,829 patients with Type 2 diabetes: a 5-year pro-
42. Ko GT, Chan JC, Chan AW, et al. Association spective analysis of the Hong Kong Diabetes
between sleeping hours, working hours and obesity Registry. Diabetes Care. 2008;31:235761.
in Hong Kong Chinese: the better health for better 58. Wen CP, Cheng TY, Tsai MK, et al. All-cause mor-
Hong Kong health promotion campaign. Int J Obes. tality attributable to chronic kidney disease: a pro-
2007;31:25460. spective cohort study based on 462 293 adults in
43. Cappuccio FP, DElia L, Strazzullo P, Miller Taiwan. Lancet. 2008;371:217382.
MA. Quantity and quality of sleep and incidence of 59. Chan JC, So WY, Yeung CY, et al. Effects of struc-
type 2 diabetes: a systematic review and meta- tured versus usual care on renal endpoint in type 2
analysis. Diabetes Care. 2010;33:41420. diabetes: the SURE study: a randomized multi-
44. Cho NH, Chan JC, Jang HC, Lim S, Kim HL, Choi center translational study. Diabetes Care. 2009;32:
SH. Cigarette smoking is an independent risk factor 97782.
for type 2 diabetes: a four-year community-based pro- 60. Win Tin ST, Gadabu E, Iro G, Tasserei J, Colagiuri
spective study. Clin Endocrinol. 2009;71:67985. R. Diabetes related amputations in Pacific Islands
45. Xu M, Zhou Y, Xu B, et al. Associations of smoking countries: a root cause analysis of precipitating
and alcohol consumption with impaired beta-cell events. Diabetes Res Clin Pract. 2013;100:2304.
function in Chinese men. J Diabetes. 2016;8(3): 61. Morrish NJ, Wang S, Stevens LK, Fuller JH, Keen
43441. H. Mortality and causes of death in the WHO
46. Ko GT, So WY, Chow CC, et al. Risk associations of Multinational Survey of Vascular Diseases in Diabetes.
obesity with sugar-sweetened beverages and life- Diabetologia. 2001;44:S1421.
62. Yang X, Lee HM, Chan JC. Drug-subphenotype globin standardization program: a five-year progress
interactions for cancer in type 2 diabetes mellitus. report. Clin Chem. 2001;47:198592.
Nat Rev Endocrinol. 2015;11:3729. 79. Heianza Y, Hara S, Arase Y, et al. Impact of introduc-
63. Harding JL, Shaw JE, Peeters A, Cartensen B, ing HbA1c into the diagnostic criteria on prevalence
Magliano DJ. Cancer risk among people with type 1 and cardiovascular risk profiles of individuals with
and type 2 diabetes: disentangling true associations, newly diagnosed diabetes in Japan: the Toranomon
detection bias, and reverse causation. Diabetes Care. Hospital Health Management Center Study 2
2015;38:26470. Diabetes care 2015;38:7345. (TOPICS 2). Diabetes Res Clin Pract. 2012;95:
64. Li HY, Jiang YD, Chang CH, Chung CH, Lin BJ, 28390.
Chuang LM. Mortality trends in patients with dia- 80. Venkataraman K, Kao SL, Thai AC, et al. Ethnicity
betes in Taiwan: a nationwide survey in 20002009. modifies the relation between fasting plasma glucose
J Formos Med Assoc Taiwan yi zhi. 2012;111: and HbA1c in Indians, Malays and Chinese. Diabet
64550. Med. 2012;29:9117.
65. So WY, Yang X, Ma RC, et al. Risk factors in 81. Herman WH, Cohen RM. Racial and ethnic differ-
V-shaped risk associations with all-cause mortal- ences in the relationship between HbA1c and blood
ity in type 2 diabetes-The Hong Kong Diabetes glucose: implications for the diagnosis of diabetes.
Registry. Diabetes Metab Res Rev. 2008;24:23846. J Clin Endocrinol Metab. 2012;97:106772.
66. Chan JC, Malik V, Jia W, et al. Diabetes in Asia: epi- 82. Lee H, Oh JY, Sung YA, et al. Optimal hemoglo-
demiology, risk factors, and pathophysiology. JAMA bin A1C cutoff value for diagnosing type 2 diabetes
J Am Med Assoc. 2009;301:212940. mellitus in Korean adults. Diabetes Res Clin Pract.
67. Chan JC, Lau ES, Luk AO, et al. Premature mortal- 2013;99:2316.
ity and co-morbidities in young-onset diabetes a 83. Ko GT, Chan JC, Tsang LW, Cockram CS. Combined
7 year prospective analysis. Am J Med. 2014;127: use of fasting plasma glucose and HbA1c predicts
61624. the progression to diabetes in Chinese subjects.
68. Luk AO, Lau ES, So WY, et al. Prospective study on Diabetes Care. 2000;23:17703.
the incidences of cardiovascular-renal complications 84. Wu S, Yi F, Zhou C, et al. HbA1c and the diagno-
in Chinese patients with young-onset type 1 and type sis of diabetes and prediabetes in a middle-aged
2 diabetes. Diabetes Care. 2014;37:14957. and elderly Han population from northwest China
69. Diagnosis and classification of diabetes mellitus. (HbA1c). J Diabetes. 2013;5:28290.
Diabetes Care. 2010;33(Suppl 1):S629. 85. Sabanayagam C, Khoo EY, Lye WK, et al. Diagnosis
70. Federation WHOaID. Definition and diagnosis of of diabetes mellitus using HbA1c in Asians: rela-
diabetes mellitus and intermediate hyperglycemia: tionship between HbA1c and retinopathy in a mul-
report of a WHO/IDF consultation. World Health tiethnic Asian population. J Clin Endocrinol Metab.
Organization Geneva; 2006. 2015;100:68996.
71. China Diabetes Society. China Guideline for Type 2 86. Qiao Q, Nakagami T, Tuomilehto J, et al. Comparison
diabetes. 2010 edition (in Chinese) Beijing: Peking of the fasting and the 2-h glucose criteria for diabetes
University Medical Press; 2011, p. 5. in different Asian cohorts. Diabetologia. 2000;43:
72. Philippines United for Diabetes Philippine practice 14705.
guidelines on diagnosis and management of diabetes 87. Ko GT, Chan JC, Yeung VT, et al. Combined use of
mellitus. Compendium of Philippine Medicine, 16th a fasting plasma glucose concentration and HbA1c
edition 2014. or fructosamine predicts the likelihood of having
73. Seino Y, Nanjo K, Tajima N, et al. Report of the diabetes in high-risk subjects. Diabetes Care. 1998;
committee on the classification and diagnostic crite- 21:12215.
ria of diabetes mellitus. J Diabetes Investig. 2010;1: 88. Ko G, Chan J, Cockram C. Use of a paired value of
21228. fasting plasma glucose and glycated hemoglobin in
74. Ko SH, Kim SR, Kim DJ, et al. 2011 clinical prac- predicting the likelihood of diabetes in a community.
tice guidelines for type 2 diabetes in Korea. Diabetes Diabetes Care. 1999;22:1909.
Metab J. 2011;35:4316. 89. Narayan KMV, Gregg EW, Engelgau MM, et al.
75. International Expert Committee report on the role of Translation research for chronic diseases. The case
the A1C assay in the diagnosis of diabetes. Diabetes for diabetes. Diabetes Care. 2000;23:17948.
Care. 2009;32:132734. 90. Fisher EB, Chan JCN, Nan H, Sartorius N,
76. Buell C, Kermah D, Davidson MB. Utility of A1C Oldenburg B. Co-occurrence of diabetes and depres-
for diabetes screening in the 1999 2004 NHANES sion: conceptual considerations for an emerging
population. Diabetes Care. 2007;30:22335. global health challenge. J Affect Disord. 2012;
77. Colagiuri S. Glycated haemoglobin (HbA1c) for the 142(Suppl):S5666.
diagnosis of diabetes mellitus practical implica- 91. Kong AP, Yang X, Ko GT, et al. Effects of treat-
tions. Diabetes Res Clin Pract. 2011;93:3123. ment targets on subsequent cardiovascular events in
78. Little RR, Rohlfing CL, Wiedmeyer HM, Myers GL, Chinese patients with type 2 diabetes. Diabetes Care.
Sacks DB, Goldstein DE. The national glycohemo- 2007;30:9539.
92. Leung WYS, So WY, Tong PCY, Chan NN, Chan 107. Inzucchi SE, Sherwin RS. The prevention of type
JCN. Effects of structured care by a pharmacist- 2 diabetes mellitus. Endocrinol Metab Clin N Am.
diabetes specialist team in patients with type 2 diabetic 2005;34:199219, viii.
nephropathy. Am J Med. 2005;118:1414.e421e427. 108. Brown N, Critchley J, Bogowicz P, Mayige M,
93. Chan JCN, Gagliardino JJ, Baik SH, et al. Multi- Unwin N. Risk scores based on self-reported or
faceted determinants for achieving glycaemic con- available clinical data to detect undiagnosed Type
trol: the International Diabetes Management Practice 2 diabetes: a systematic review. Diabetes Res Clin
Study (IDMPS). Diabetes Care. 2009;32:22733. Pract. 2012;98:36985.
94. Chuang LM, Soegondo S, Soewondo P, et al. 109. CDC Diabetes Cost-effectiveness Study Group. The
Comparisons of the outcomes on control, type of cost-effectiveness of screening for Type 2 diabetes.
management and complications status in early onset J Am Med Assoc. 1998;280:175763.
and late onset type 2 diabetes in Asia. Diabetes Res 110. Chan JC, So WY, Ma RCW, Tong P, Wong R,
Clin Pract. 2006;71:14655. Yang XL. The complexity of both vascular and
95. David AM, Rubio JM, Luces PS, Zabala RV, Roberto non-vascular complications of diabetes: the Hong
JP. Getting the patients perspective: a survey of diabe- Kong Diabetes Registry. Curr Cardiovasc Risk Rep.
tes services on Guam. Hawaii Med J. 2010;69:459. 2011;5:2309.
96. Wagner EH, Groves T. Care for chronic diseases. Br 111. Li JK, Ng MC, So WY, et al. Phenotypic and genetic
Med J. 2002;325:9134. clustering of diabetes and metabolic syndrome in
97. Marshall M, Pronovost P, Dixon-Woods Chinese families with type 2 diabetes mellitus.
M. Promotion of improvement as a science. Lancet. Diabetes Metab Res Rev. 2006;22:4652.
2013;381:41921. 112. Gong Q, Gregg EW, Wang J, et al. Long-term effects
98. Stock S, Pitcavage JM, Simic D, et al. Chronic care of a randomised trial of a 6-year lifestyle intervention
model strategies in the United States and Germany in impaired glucose tolerance on diabetes-related
deliver patient-centered, high-quality diabetes care. microvascular complications: the China Da Qing
Health Aff. 2014;33:15408. Diabetes Prevention Outcome Study. Diabetologia.
99. Tricco AC, Ivers NM, Grimshaw JM, et al. 2011;54:3007.
Effectiveness of quality improvement strategies on 113. Li G, Zhang P, Wang J, et al. Cardiovascular mortal-
the management of diabetes: a systematic review ity, all-cause mortality, and diabetes incidence after
and meta-analysis. Lancet. 2012;379:225261. lifestyle intervention for people with impaired glu-
100. Welin L, Wilhelmsen L, Bjornberg A, Oden A. Aspirin cose tolerance in the Da Qing Diabetes Prevention
increases mortality in diabetic patients without car- Study: a 23-year follow-up study. Lancet Diabetes
diovascular disease: a Swedish record linkage study. Endocrinol. 2014;2:47480.
Pharmacoepidemiol Drug Saf. 2009;18:11439. 114. Laatikainen T, Dunbar JA, Chapman A, et al.
101. Western Pacific Declaration on Diabetes (WPDD) Prevention of type 2 diabetes by lifestyle interven-
Steering Committee, On behalf of International tion in an Australian primary health care setting:
Diabetes Federation Western Pacific Region, World greater green triangle (GGT) diabetes prevention
Health Organization Western Pacific Region, project. BMC Public Health. 2007;7:249.
Secretariat of Pacific Community. Plan of Action 115. Sukala WR, Page R, Cheema BS. Targeting the type
(20062010) for the Western Pacific Declaration on 2 diabetes epidemic in Polynesia: historical perspec-
Diabetes: from Evidence to Action: WHO-WPRO tive and rationale for exercise intervention trials.
Publication Office. 2007. Ethn Dis. 2012;22:1238.
102. Wang HH, Wang JJ, Wong SY, Wong MC, Mercer 116. World Health Organization. Updated revised draft
SW, Griffiths SM. The development of urban com- global action plan for the prevention and control of
munity health centres for strengthening primary care noncommunicable diseases 20132020. 2013.
in China: a systematic literature review. Br Med 117. Tutino GE, Tam WH, Yang X, Chan JC, Lao
Bull. 2015;116:13954. TT, Ma RC. Diabetes and pregnancy: perspec-
103. Chen Z. Launch of the health-care reform plan in tives from Asia. Diabet Med J Br Diabet Assoc.
China. Lancet. 2009;373:13224. 2014;31:30218.
104. Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz 118. Urakami T, Suzuki J, Mugishima H, et al. Screening
J. Active smoking and the risk of type 2 diabetes: and treatment of childhood type 1 and type 2 diabe-
a systematic review and meta-analysis. JAMA J Am tes mellitus in Japan. Pediatr Endocrinol Rev PER.
Med Assoc. 2007;298:265464. 2012;10 Suppl 1:5161.
105. Pan A, Wang Y, Talaei M, Hu FB. Relation of 119. Wei J, Sung F, Lin C, Lin R, Chiang C, Chuang
smoking with total mortality and cardiovascular L. National surveillance for type 2 diabetes melli-
events among patients with diabetes mellitus: a tus in Taiwanese children. JAMA J Am Med Assoc.
meta-analysis and systematic review. Circulation. 2003;290:134550.
2015;132:1795804. 120. Toh C, Cutter J, Chew S. School based intervention
106. Mackay J, Ritthiphakdee B, Reddy KS. Tobacco has reduced obesity in Singapore. Br Med J. 2002;
control in Asia. Lancet. 2013;381:15817. 324:427.
121. Chan JC, Deerochanawong C, Shera AS, et al. Role 135. Green JB, Bethel MA, Armstrong PW, et al. Effect
of metformin in the initiation of pharmacotherapy of sitagliptin on cardiovascular outcomes in type 2
for type 2 diabetes: an Asian-Pacific perspective. diabetes. N Engl J Med. 2015;373:23242.
Diabetes Res Clin Pract. 2007;75:25566. 136. Li Y, Xu W, Liao Z, et al. Induction of long-term
122. Nagi DK, Yudkin JS. Effects of metformin on insu- glycemic control in newly diagnosed type 2 diabetic
lin resistance, risk factors for cardiovascular disease, patients is associated with improvement of beta-cell
and plasminogen activator inhibitor in NIDDM sub- function. Diabetes Care. 2004;27:2597602.
jects. A study of two ethnic groups. Diabetes Care. 137. Weng J, Li Y, Xu W, et al. Effect of intensive insulin
1993;16:6219. therapy on beta-cell function and glycaemic control
123. Global guideline for type 2 diabetes. Diabetes Res in patients with newly diagnosed type 2 diabetes: a
Clin Pract. 2014;104:152. multicentre randomised parallel-group trial. Lancet.
124. Yang W, Weng J. Early therapy for type 2 diabe- 2008;371:175360.
tes in China. Lancet Diabetes Endocrinol. 2014;2: 138. Pozzilli P, Leslie RD, Chan J, et al. The A1C and
9921002. ABCD of glycaemia management in type 2 diabe-
125. Chan JC, Chan KW, Ho LL, et al. An Asian multi- tes: a physicians personalized approach. Diabetes
center clinical trial to assess the efficacy and toler- Metab Res Rev. 2010;26:23944.
ability of acarbose compared with placebo in type 2 139. Chan JC, Ozaki R, Luk A, et al. Delivery of inte-
diabetic patients previously treated with diet. Asian grated diabetes care using logistics and information
Acarbose Study Group. Diabetes Care. 1998;21: technology the Joint Asia Diabetes Evaluation
105861. (JADE) program. Diabetes Res Clin Pract. 2014;106
126. Yang W, Liu J, Shan Z, et al. Acarbose compared Suppl 2:S295304.
with metformin as initial therapy in patients with 140. Chan JC, Sui Y, Oldenburg B, et al. Effects of
newly diagnosed type 2 diabetes: an open-label, telephone-based peer support in patients with type
non-inferiority randomised trial. Lancet Diabetes 2 diabetes mellitus receiving integrated care: a ran-
Endocrinol. 2014;2:4655. domized clinical trial. JAMA Intern Med. 2014;174:
127. Chiasson JL, Josse RG, Gomis R, Hanefeld M, 97281.
Karasik A, Laakso M. Acarbose for prevention of 141. Kong AP, Yang X, Luk A, et al. Severe hypoglyce-
type 2 diabetes mellitus: the STOP-NIDDM ran- mia identifies vulnerable patients with type 2 diabe-
domised trial. Lancet. 2002;359:20727. tes at risk for premature death and all-site cancer:
128. Kawamori R, Tajima N, Iwamoto Y, Kashiwagi A, the Hong Kong diabetes registry. Diabetes Care.
Shimamoto K, Kaku K. Voglibose for prevention of 2014;37:102431.
type 2 diabetes mellitus: a randomised, double-blind 142. Ma RC, So WY, Tam CH, et al. Genetic variants for
trial in Japanese individuals with impaired glucose type 2 diabetes and new-onset cancer in Chinese
tolerance. Lancet. 2009;373:160714. with type 2 diabetes. Diabetes Res Clin Pract. 2014;
129. Chang CH, Chang YC, Lin JW, Chen ST, Chuang 103:32837.
LM, Lai MS. Cardiovascular risk associated with 143. Kong AP, Yang X, So WY, et al. Additive effects
acarbose versus metformin as the first-line treat- of blood glucose lowering drugs, statins and renin-
ment in patients with type 2 diabetes: a nation- angiotensin system blockers on all-site cancer
wide cohort study. J Clin Endocrinol Metab. risk in patients with type 2 diabetes. BMC Med.
2015;100:11219. 2014;12:76.
130. Holman RR, Bethel MA, Chan JC, et al. Rationale for 144. Jiao F, Fung CS, Wan YF, et al. Long-term effects
and design of the Acarbose Cardiovascular Evaluation of the multidisciplinary risk assessment and man-
(ACE) trial. Am Heart J. 2014;168:239.e2. agement program for patients with diabetes melli-
131. Cho YM. Incretin physiology and pathophysiol- tus (RAMP-DM): a population-based cohort study.
ogy from an Asian perspective. J Diabetes Investig. Cardiovasc Diabetol. 2015;14:105.
2015;6:495507. 145. Fung CS, Wan EY, Jiao F, Lam CL. Five-year change
132. Kim YG, Hahn S, Oh TJ, Kwak SH, Park KS, Cho of clinical and complications profile of diabetic
YM. Differences in the glucose-lowering efficacy patients under primary care: a population-based lon-
of dipeptidyl peptidase-4 inhibitors between Asians gitudinal study on 127,977 diabetic patients. Diabetol
and non-Asians: a systematic review and meta- Metab Syndr. 2015;7:79.
analysis. Diabetologia. 2013;56:696708. 146. Wong CK, Wong WC, Wan YF, et al. Patient
133. Kim YG, Hahn S, Oh TJ, Park KS, Cho Empowerment Programme in primary care reduced
YM. Differences in the HbA1c-lowering efficacy of all-cause mortality and cardiovascular diseases in
glucagon-like peptide-1 analogues between Asians patients with type 2 diabetes mellitus: a population-
and non-Asians: a systematic review and meta- based propensity-matched cohort study. Diabetes
analysis. Diabetes Obes Metab. 2014;16:9009. Obes Metabol. 2015;17:12835.
134. Scirica BM, Bhatt DL, Braunwald E, et al. 147. Raz I, Riddle MC, Rosenstock J, et al. Personalized
Saxagliptin and cardiovascular outcomes in patients management of hyperglycemia in type 2 diabetes:
with type 2 diabetes mellitus. N Engl J Med. reflections from a Diabetes Care Editors Expert
2013;369:131726. Forum. Diabetes Care. 2013;36:177988.
148. Institute of Medicine Crossing the quality chasm: a 2015. Accessed 9th Feb 2016, at http://www.idf.org/
new health system for the 21st century. 2001. http:// centres-education.
www.nap.edu/books/0309072808/html/. 153. WHO. WHO definition of health. Preamble to the
149. Yin J, Wong R, Au S, et al. Effects of providing Constitution of the World Health Organization as
peer support on diabetes management in people adopted by the International Health Conference,
with type 2 diabetes. Ann Fam Med. 2015;13 Suppl New York, 1922 June 1946, and entered into force
1:S429. on 7 April 1948. 1948.
150. United Nation General Assembly. Political dec- 154. Western Pacific Declaration on Diabetes Steering
laration of the High-level Meeting of the General Committee. Plan of action (20062010) for the
Assembly on the Prevention and Control of Non- Western Pacific declaration on diabetes: from evi-
communicable Diseases A/66/L.12011. dence to action. Manila: World Health Organization
151. Holmes D. Margaret Chan: committed to universal Western Pacific Regional Office; 2008. Available at
health coverage. Lancet. 2012;380:879. www.wpdd.org.
152. International Diabetes Federation Reference Centre
of Education http://www.idf.org/centres-education.
Diabetes in India and Southeast
Asia 6
Shashank R. Joshi and S.R. Aravind
Epidemiological Trends Moreover, Asians have a strong ethnic and

and Emerging Disease Burden genetic predisposition for diabetes and have
lower thresholds for the environmental risk fac-
Diabetes is a multisystem disorder associated tors. There are 387 million people with diabetes
with complications, and the prevalence of which in the world with 78.3 million people in the SEA
is increasing globally. Diabetes imposes region which is expected to rise to 131 million
immense public health burden with unaccept- by the year 2040.
ably high burdens on individuals, their families, The last three decades have witnessed an epi-
and national economies. As the urbanrural demic rise in the number of people with diabetes,
divide narrows consistently, it adversely affects especially type 2 diabetes, and particularly in
the lifestyle of populations. The rapid emerging developing countries, where more than 80 % of
economies of Southeast Asia (SEA) are a victim the people with diabetes live. The recent land-
to the epidemiological transition which results in mark study for the pooled analysis across 751
the shifting of the disease burden from the com- studies with 4.4 million adults from 200 coun-
municable to the non-communicable diseases. tries published in Lancet reflects that between
1980 and 2014 the number of adults with diabe-
tes in the world increased fourfold from 108 mil-
S.R. Joshi, MD,DM,FICP,FACP,FACE,FRCP (*)
lion to 422 million. The increase has particularly
Joshi Clinic, Lilavati & Bhatia Hospital, been sharp in low- and middle-income countries.
Mumbai, India In 2014, 50 % of adults with diabetes lived in five
Endocrine Society of India, New Delhi, India
Association of Physicians of India (API) (2014-15),
Columbia Asia Hospital,
Mumbai, India
Yeshwanthpur, Bangalore, India
Indian Academy of Diabetes, Mumbai, India
Post Graduate Studies in Diabetology (RGUHS &
RSSDI (Research Society for the Study of Diabetes RSSDI), Bangalore, India
in India 2011), Mumbai, India
PESIMSR, Kuppam, India
AIAARO (All India Association of Advancement for
RSSDI (Research Society for Study of Diabetes in
Research in Obesity), Mumbai, India
India), Bangalore, India
DiabetesIndia, Hyderabad, India
S.R. Aravind, MBBS,DNB,FRCP,FDRC,DHA,FRSSDI
Diacon Hospital, Bangalore, India KRSSDI, Bangalore, India

DOI 10.1007/978-3-319-41559-8_6
86 S.R. Joshi and S.R. Aravind
countries: China, India, the USA, Brazil and the region during 2015. India is home to the
Indonesia. The prevalence of diabetes in adults second largest number of children with type 1
more than doubled for men in India and China diabetes in the world (70,200), after the USA,
(3.79.1 % in India, 3.59.9 % in China) but and accounts for the majority of the children
increased by 80 % amongst women in India (4.6 with type 1 diabetes in the region. More than
8.3 %) but only 50 % in women in China half (53.2 %) of these deaths occurred in people
(57.6 %). The total number of adults with diabe- under 60 years of age.
tes in India increased from 11.9 million in 1980 With an estimated 69.2 million people suffer-
to 64.5 million in 2014. In China, the increase ing from the condition, the largest in any country
was from 20.4 million in 1980 to 102.9 million in in the world, diabetes has become a major health-
2014. While India contributed 15.3 % of the care problem in India (refer to Figs. 6.2 and 6.3).
global share of adults with diabetes in 2014, it Recent epidemiological studies from India point
was 24.4 % for China. Across the region, approx- to the great burden due to diabetes and its micro-
imately 72 million people have diabetes close and macrovascular complications. This is primar-
to one fifth of all adults with diabetes in the ily because the status of diabetes control in India
world. Overall, the rise of type 2 diabetes in is far from ideal. Based on the available data, the
South Asia is estimated to be more than 150 % mean glycated haemoglobin levels are around 9 %
between 2000 and 2035. which is at least 2 % higher than the goal currently
suggested by international bodies. A balanced
approach to improve awareness about diabetes
Economic and the Societal Impact and its control both amongst patients and the
of the Complications medical fraternity is an urgent need of the hour in
India.
Diabetes is increasingly affecting individu-
als in the region in their most productive years
(refer to Fig. 6.1). This will pose a challenge to Factors Contributing to the Rapid
governments working to improve the economic Increase in Prevalence of Diabetes
situation in their countries. The scenario poses in Asia
huge social and economic problems to most
nations in the region and could impede national Although ageing, urbanisation and associated
and, indeed, global development. More than half lifestyle changes are the major determinants for
of the deaths due to diabetes occur in people the rapid increase, an adverse intrauterine
under 60 years of age and one quarter in people environment and the resulting epigenetic changes
under 50 years of age. India is the largest con- could also contribute in many developing coun-
tributor to regional mortality, with 1.1 million tries. More action is required to understand the
deaths attributable to diabetes in 2015. Despite drivers of the epidemic to provide a rationale for
the huge number of people with diabetes in the prevention strategies to address the rising global
Southeast Asia Region, health-care spending on public health tsunami.
diabetes was estimated to be only USD 6 billion,
accounting for less than 1 % of the global total,
with India estimated to have spent the largest Urbanisation and Socioeconomic
proportion. The health-care spending appears to Transition
be low as government spending on healthcare
is privatised less as predominant healthcare in Diabetes burden in India is contributed by vari-
India. There are an estimated 81,400 children ous factors. Genetic predisposition combined
under the age of 15 living with type 1 diabetes with lifestyle changes, associated with urbanisa-
in the Southeast Asia Region. Approximately tion and globalisation, contributes to this rapid
13,100 children developed type 1 diabetes in rise of diabetes in India. The highest rates of
6 Diabetes in India and Southeast Asia 87
Prevalence of diabetes in adults by age, 2014

India
65
Wo
World
SEA
S EA
60
d
India
55
Source: IDF Diabetes Atlas, Update 2014

50
45
40
Prevalence (%)
35
30
25
20
15
10
5
0
2024 2529 3034 3539 4044 4549 5054 5559 6064 6569 7074 7579
Age (years)
Fig. 6.1 Age-wise prevalence of diabetes
1980 2014
Rank Country Millions of adults with diabetes Rank Country Millions of adults with diabetes
(% of global diabetes) (% of global diabetes)
1 China 20-4 (18-9) 1 China 102-9 (24-4)
2 India 11-9 (11-0) 2 India 64-5 (15-3)
3 USA 8-1 (7-5) 3 USA 22-4 (5-3)
4 Russia 7-1 (6-6) 4 Brazil 11-7 (2-8)
5 Japan 4-7 (4-4) 5 Indonesia 11-7 (2-8)
6 Germany 3-4 (3-2) 6 Pakistan 11-0 (2-6)
7 Brazil 2-7 (2-5) 7 Japan 10-8 (2-6)
8 Ukraine 2-4 (2-2) 8 Russia 10-7 (2-5)
9 Italy 2-4 (2-2) 9 Egypt 8-6 (2-0)
10 UK 2-3 (2-1) 10 Mexico 8-6 (2-0)
12 Indonesia 2-1 (1-9)

13 Pakistan 1-7 (1-6)
14 Germany 5-1 (1-2)
15 Mexico 1-7 (1-6)
16 Italy 4-3 (1-0)
17 Egypt 1-5 (1-4)
19 UK 3-8 (0-9)
24 Ukraine 3-4 (0-8)
Fig. 6.2 Ten countries with the largest no. of diabetes in 1980 and 2014 [3]
urbanisation have been in Singapore, Korea, intermediate rates (30 %) and Bangladesh and Sri
Malaysia, the Philippines and Indonesia (50 %). Lanka have slow rates of urbanisation. The
China, Pakistan, India and Thailand have increase in urban population and ageing are the
2015 more prevalence at the age of 6069 years,

whereas in the Chinese population, it peaks at
Rank
Number of people
Country/territory
with diabetes
7989 years. Indians also have a higher preva-
1 China 109.6 million [99.6133.4]
lence of impaired glucose tolerance at a younger
2 India 69.2 million [56.284.8]
age than the Chinese population. The findings
3 United States of America 29.3 million [27.630.9] from Pakistan and Sri Lanka also show similar
4 Brazil 14.3 million [12.915.8] results.
5 Russian Federation 12.1 million [6.217.0]
6 Mexico 11.5 million [6.213.7]

Anthropometry: Thin-Fat Phenotype
7 Indonesia 10.0 million [8.710.9]
8 Egypt 7.8 million [3.89.0] It is observed that amongst Asians, diabetes

9 Japen 7.2 million [6.19.6] occurs at lower body mass index (BMI) levels
10 Bangladesh 7.1 million [5.312.0]
than in Western populations, and small incre-
ments in weight trigger glucose intolerance in
Fig. 6.3 Prevalence of diabetes in different countries susceptible subjects. Especially Asian Indians
(age 2079 years) [1] have higher odds of developing diabetes, despite
having a significantly lower BMI than the white
main determinants of the global rise in the preva- population.
lence of diabetes. Urbanisation and internal rural Several studies in Asian populations, particu-
to urban migration result in several adverse larly in Asian Indians, have highlighted the met-
impacts: physical activity decreases, diet habits abolically obese phenotype amongst normal
shift towards high-energy foods and body mass weight individuals. This phenotype, character-
index (BMI) and upper body adiposity increase ised by greater abdominal obesity despite a nor-
considerably. The Indian Council of Medical mal BMI, less muscle mass, higher percentage of
Research (ICMR) study done in the 1970s body fat and increased propensity for insulin
reported a prevalence of 2.3 % in urban areas resistance compared with the Western popula-
which has risen to 1219 % in the 2000s. tion, renders higher susceptibility for diabetes in
Correspondingly, in rural areas, prevalence rates Asian populations.
have increased from around 1 to 410 % and even The association of BMI and diabetes is well
13.2 % in one study. Thus it is clear that both in established and is usually modified by ethnicity.
urban and rural India, prevalence rates of diabe- Ethnicity factors that contribute are genetic con-
tes are rising rapidly with a rough urbanrural stitution, lifestyle, living environment and anthro-
divide of 2:1 or 3:1 being maintained through the pometric characteristics. Body composition
last two to three decades with the exception of related to fat distribution is a stronger determinant
Kerala where rural prevalence rates have caught of the metabolic milieu than BMI. The diabetes
up with or even overtaken urban prevalence rates. epidemiology, collaborative analysis of diabetes
The postulates from the ICMRINDIAB study criteria in Europe/in Asia study group noted that
predicted for the burden of diabetes which pro- the overall effect of age on the prevalence of dia-
jected that in 2011, India would have 62.4 million betes differed considerably between the ethnic
people with diabetes and 77.2 million people groups, even in the subjects with the same
with prediabetes. BMI. Asian populations are prone to have more
intra-abdominal fat accumulation and low muscle
mass. Asian Indians, in particular, have the above
Age abnormalities which account for the high preva-
lence of insulin resistance and diabetes at low lev-
As compared to Western populations, Asian els of BMI. The risk of diabetes increases
Indians develop diabetes at a younger age with progressively from a BMI of 23 kg/m2 amongst
Indians. BMI in of 23 kg/m2 is also considered advantageous in certain populations during evo-
overweight for most Asian populations. Asian lutionary selection by repeated famine and feast
Indians have small body size which has been cycles. However, these genes have rendered them
named as thin-fat Indian. Asian Indians have highly predisposed to obesity and diabetes during
thinner limbs, which are suggestive of smaller the modern era of continuous feasting. On the
muscle mass. However, despite their thinness, other hand, the thrift phenotype hypothesis pos-
they are centrally obese, with higher waisthip tulates that intrauterine malnutrition leads to met-
ratio (WHR) and higher subscapulartriceps skin- abolic and structural changes in the beta cells that
fold ratio than their British counterparts. Many are beneficial for early survival, but increases the
studies show that Asian Indians have more body risk of T2D and other chronic disorders in
fat for any given BMI compared with Caucasians adulthood.
and black Africans. Indians also have higher lev-
els of central obesity (measured as waist circum-
ference [WC], WHR, visceral fat and posterior Screening
subcutaneous abdominal fat). This is reflected in
higher plasma nonesterified fatty acid (NEFA) The prevalence of the micro- and macrovascular
and triglyceride concentrations, hyperinsulinae- complications also influences the mortality rate
mia with fasting as well as post-glucose challenge due to diabetes. Unfortunately, more than 50 % of
states and higher insulin resistance. Thus, Asian individuals with diabetes in India remain undiag-
Indians have an unusual thin-fat body composi- nosed, and some may even present with macro-
tion associated with the insulin resistance syn- vascular disease (coronary artery disease and
drome, and this is the now popular thin-fat cerebrovascular disease or stroke and peripheral
Indian concept. vascular disease) and microvascular disease (reti-
nopathy, nephropathy and neuropathy) at the
time of diagnosis.
Smoking and Alcohol Use Data on various complications of diabetes
have also been published by several authors.
Smoking increases the risk of central obesity and However, till recently, most of such data were
insulin resistance and the risk of diabetes is hospital or clinic based and therefore subject to
shown to be higher by 45 % in smokers than referral bias. The Chennai Urban Rural
amongst nonsmokers. The increasing use of alco- Epidemiology Study (CURES) and the Chennai
hol in Asian countries, especially amongst the Urban Population Study (CUPS) provide the first
middle class and rural population, also increases population-based data from India on virtually all
the risk for diabetes and other metabolic diseases complications of diabetes. CURES was a
and deleterious health effects. population-based study involving 26,001 partici-
pants aged 20 years or above based on a represen-
tative population of Chennai. The overall
Genetic Susceptibility prevalence of diabetic retinopathy based on four-
field stereo colour retinal photography was
The genetic burden on Asian Indians makes the 17.6 %. The prevalence of overt nephropathy was
population more susceptible to diabetes. This risk 2.2 % while that of microalbuminuria was 26.9 %.
is further increased due to interaction with envi- Peripheral neuropathy based on biothesiometry
ronmental triggers. Exposure to a high fat diet was detected in 26.1 %.
and lower levels of physical activity trigger the In the CUPS study, coronary artery disease
geneenvironmental interaction. Both the thrifty was evident in 21.4 % of diabetic subjects, 14.9 %
genotype and thrifty phenotype hypotheses of subjects with impaired glucose tolerance and
appear to be the aetiology. The selective presence in 9.1 % of people with normal glucose tolerance.
of thrifty genotypes has been considered to be In the same study, peripheral vascular disease
was present in 6.3 % of diabetic subjects com- awareness levels increased with education,
pared to 2.7 % amongst nondiabetic subjects. only 42.6 % of postgraduates and profession-
Diabetic subjects also had increased subclinical als, which group included doctors and lawyers,
atherosclerosis as measured by intimal-medial knew that diabetes was preventable. The knowl-
thickness at every age point, compared to their edge of risk factors of diabetes was even lower
nondiabetic counterparts. Assuming that 40 mil- with only 11.9 % of the study subjects reporting
lion people in India have diabetes, this translates obesity and physical inactivity as risk factors for
to at least 7 million with retinopathy, 0.8 million diabetes. More alarming was the fact that even
with nephropathy, 10.4 million with neuropathy, amongst known diabetic subjects, only 40.6 %
8.5 million with CAD and 2.5 million with were aware that diabetes could lead to some
PVD. Thus, the burden due to diabetic complica- organ damage. There is another population-
tions is very high in India due to the sheer num- based study which was done to find out the levels
ber of people with diabetes. These figures are in and details regarding awareness on diabetes in
fact very conservative, and it is possible that in urban adult Indian population aged 20 years.
rural areas, the prevalence of complications is The knowledge regarding the causes of diabe-
much higher because of poorer control of diabetes, its prevention and the methods to improve
tes and lack of access to healthcare. the health was significantly low amongst the
Identifying accurate and low-cost screening general population. In the total study group,
methods is a necessary first step in assessing the 41 % were unaware of the health being affected
cost-effectiveness of screening to detect undiag- by diabetes, and only less than 30 % knew about
nosed diabetes. Indian Diabetes Risk Score the complications related to kidneys, eyes and
(IDRS) is more effective and significantly less nerves. Many persons with diabetes (46 %) felt
expensive for screening for undiagnosed T2DM it was a temporary phenomenon. Amongst the
compared to genotyping TCF7L2 SNPs, the diabetic subjects, 92.3 % had sought the help of
strongest genetic marker for T2DM currently a general practitioner to take treatment. Only a
available. Using IDRS screening prior to OGTT small proportion went to a specialist.
reduces costs while still detecting a substantial
portion of NDD individuals. A potential addi-
tional benefit of both the IDRS and genotyping is Current Status of Diabetes Control
their ability to identify individuals who currently in India
do not have diabetes but are at high risk of devel-
oping diabetes in the future. Thus an individual The next challenge in India is that the quality of
with an IDRS score of 60 at baseline was three diabetes care varies considerably depending upon
times more likely to develop diabetes in the the awareness levels, expertise available, atti-
future than low-risk subjects (IDRS <30). tudes and perceptions amongst diabetes care pro-
viders. An estimate based on sales of antidiabetic
pharmaceutical agents shows that on an average
Awareness of Diabetes in India only 1012 % of people with diabetes receive
modern pharmacological treatment in India. In
The awareness of diabetes is a cornerstone of 1998, the DiabcareAsia study was carried out to
the prevention of this disease. CURES reported investigate the relationship between diabetes
that nearly 25 % of the population was unaware control, management and late complications in a
of diabetes. Only around 40 % of the partici- subset of urban Indian diabetes population treated
pants felt that the prevalence of diabetes was at 26 tertiary diabetes care centres. A total of
increasing, and only 22.2 % of the popula- 2,269 patients participated in this study and it
tion and 41 % of known diabetic subjects felt was observed that approximately half of the
that diabetes could be prevented. Though the patients had poor control (HbA1c >2 % points
above upper limit of normal), and the mean diet-related non-communicable diseases like
HbA1c was significantly higher (8.9 2.1 %) T2DM, cardiovascular disease, etc. predomi-
than the levels recommended by the American nantly in urban, but also in rural areas. The
Diabetes Association and the ICMR guidelines in dietary recommendations should be individual-
India. Over 54 % of patients had diabetes-related ised according to the persons ethnicity, cultural
complications. The mean HbA1c levels and fre- and family background and personal prefer-
quency of complications were higher in patients ences and associated comorbid conditions. It
with longer diabetes duration. This study also should be flexible in a variety and preparation
showed that 4 % of patients were on diet therapy, of food choices and timing of meals according
53.9 % were receiving oral antidiabetic agents to the persons daily routine. Both the National
(OHAs), 22 % were receiving insulin and 19.8 % Institute of Nutrition and expert group [2] have
were receiving a combination of insulin and developed some broad Indian guidelines which
OHAs. This study concluded that with increasing recommend reduction intake of carbohydrate,
duration of diabetes, glycaemic control deterio- higher intake of fibre, lower intake of saturated
rates leading to late complications. It also con- fat, optimal ratio of essential fatty acids, slightly
firmed that diabetes care in India leaves much to higher protein intake, lower intake of salt and
be desired and suggested the need for efforts to restricted intake of sugar.
increase awareness amongst health professionals The role of regular physical activity is well
to improve diabetes care in India. established in the management in persons with
type 2 diabetes. A careful assessment of an indi-
vidual should be made by the physician while
Non-pharmacologic Approach incorporating an exercise programme in the man-
for the Management of Diabetes agement. Exercise programme should be indi-
vidualised according to the individual capacity
Lifestyle modifications are the cornerstone of and disabilities. The person with diabetes must
management of diabetes mellitus and include wear appropriate footwear.
the prescription of a healthy diet, regular exer-
cise, the management of stress and avoidance of
tobacco. The aims of dietary management are Clinical Inertia in Diabetes: Failure
to achieve and maintain ideal body weight, eug- to Achieve Tight Control
lycaemia and desirable lipid profile, to prevent
and postpone complications related to diabetes Failure of initiation of or intensification of ther-
and to provide optimal nutrition during preg- apy, when indicated, is termed clinical inertia.
nancy, lactation, growth, old age and associ- Though we have well-defined management
ated conditions, e.g. hypertension and catabolic goals, effective therapies and practice guide-
illnesses. Recently the published STARCH lines, there is often a failure to take appropriate
study shows that Indians consume high carbo- action despite recognition of the problem. This is
hydrate in their diet compared to the Western a common problem in the management of
population. The comparison of macronutrients patients with asymptomatic chronic illnesses.
(i.e. region-wise carbohydrate, fat and protein) The use of soft reasons to avoid intensification
revealed a similar pattern of dietary consump- of therapy and lack of education, training and
tion, that is, high carbohydrate and a lower practice organisation aimed at achieving thera-
range of fat and protein. This study neutralises peutic goals are the common reasons for clinical
the myth that only the south Indian population inertia. Clinical inertia in achieving glycaemic
consumes high carbohydrate in their diet (rice, targets in Indian diabetic subjects could be
idli, etc.). Dietary transition and a sedentary expected to be even more than in the West, where
lifestyle have led to an increase in obesity and it has been reported that 65 % of the patients
diagnosed with diabetes, only 73 % are pre- goals with the potential for long periods of
scribed pharmacologic therapy and only 33 % of hyperglycaemia. Periods of hyperglycaemia
those treated achieve a haemoglobin A1C value long or even short can increase the risk of
of less than 7 % by the ADA goal. This may be micro- and macrovascular complications. The
due to the low rates of awareness of diabetes and current understanding of the complex patho-
its complications in India resulting in poor gly- physiology of the disease and the progressive
caemic control seen in Indians with diabetes. deterioration in glycaemic control over time
Moreover, other factors like poverty, lack of supports the philosophy of earlier intervention
accessibility to health services and inadequate with a more comprehensive initial therapy. The
follow-up are additional factors in developing major classes of antidiabetic agents that may
countries like India. be combined with metformin include sulpho-
Consequently, insulin is delayed until it is nylurea (SU), thiazolidinedione (TZD), dipep-
absolutely necessary. Most patients are initiated tidyl peptidase-4 inhibitor (DPP4-i), insulin
on insulin after a course of multiple oral antidia- and glucagon-like peptide-1 (GLP-1) recep-
betic drugs. Insulin therapy is initiated only when tor agonist. Few studies have investigated the
the HbA1c levels had deteriorated further to effect of metformin-based early combination
around 9 %. Physicians often delay insulin ther- therapy. There are several different types of
apy worrying that the daily injections, modifica- insulin available, but as a minimum, regular
tion of lifestyle due to insulin and dependence on quick-acting human insulin and longer-acting
insulin for life and that patients may feel that NPH insulin should be available to everyone in
insulin therapy indicates the last stage of diabe- all parts of the world.
tes. However, patients who had moved on to insu- In India, which is a resource-limited coun-
lin seemed to have a more positive approach try, all therapies are available and it is a pre-
towards his/her treatment due to the improve- dominantly non-reimbursed market. Usually
ment in quality of life and better control despite sulphonylureas, metformin, alpha glucosidase
the issues outlined above. inhibitors and glitazone form the cornerstone of
therapy with insulin. However, recently gliptins
including the low-cost one as well as SGLT2
Pharmacologic Therapy inhibitors are also available. Biosimilar insulin is
in Diabetes: Is It Different? also available but not popular and premixed insu-
lin is still used widely. Cost and dose play a role
A proactive approach to treating type 2 diabetes in resource-limited environment. Indian usually
is recommended: therapy should be individual- requires lower doses and is more insulin resistant.
ised with early consideration of combination
therapy and ongoing reinforcement of lifestyle
modification messages. Indeed, the conser- Translating Primary Prevention
vative stepwise approach to type 2 diabetes of Diabetes
management involves lifestyle modification,
followed by treatment with a single oral anti- The Indian Diabetes Prevention Programme
diabetic agent, often up-titrated to maximal (IDPP) has been a unique prospective study
recommended doses before combination ther- which has provided several pathways and strat-
apy is introduced. Very often there is a delay egies for the prevention of diabetes in India
between stepping up from monotherapy (e.g. including the importance of the lifestyle modifi-
metformin alone) to combination therapy (e.g. cation and metformin which independently could
metformin plus other OADs, often sulpho- reduce the incidence of diabetes in Asian Indians
nylurea), and this can result in unacceptable with impaired glucose tolerance. Also, these have
delays in achieving and maintaining glycaemic been proposed as the cost-effective benchmarks
amongst high-risk individuals with high degree incident of prediabetes. The mechanistic insights
of insulin resistance and may be useful in other now ascribe these benefits through improvement
developing countries as well. It is important to in insulin sensitivity and beta-cell preservation.
control the persistent IGT as it is demonstrated Prospective, parallel-group, randomised con-
to add to the higher incidence of diabetes with trolled trial across close to 9,000 subjects have
other risk factors for diabetes, such as high BMI, demonstrated that mobile phone messaging is
waist circumference and body fat percentage. In an effective and acceptable method to deliver
a recent collaborative work across South Asia, advice and support towards lifestyle modification
Latin America and South Africa to compare the to prevent type 2 diabetes in men at high risk.
prevalence, awareness, treatment and control Evidence from the DPP, and other prevention tri-
of diabetes and assess the relationship between als conducted in patients with prediabetes, shows
diabetes and prediabetes with known cardio- that appropriate lifestyle modification includ-
vascular and metabolic risk factors, it has been ing physical activity could lead to risk reduc-
demonstrated that propensity for South Asians tion in the incidence of T2DM by almost 58 %.
to develop diabetes and prediabetes at a younger Studies have shown that resistance and aerobic
age and lower body mass index compared with exercise is effective in improving metabolic pro-
individuals from other low- and middle-income file of adults with T2DM. Previous research has
countries. Therefore, it is important that the long- reported improved insulin sensitivity/resistance
term impact and the complications are prevented, and reductions in hyperglycaemia-related medi-
and the health systems and policy makers must cations as a result of exercise training. In par-
make concerted efforts to improve diabetes pre- ticular, supervised resistance training (max. ten
vention and detection in the targeted population. repetitions for >3 days per week) has been shown
Ramachandran A et al. have suggested that it is to lead to significant improvement in insulin
important to develop precise predictors for inci- sensitivity and values of glycosylated haemoglo-
dent diabetes amongst Asian men. The analysis bin, lipid profile and truncal and peripheral sub-
of the data from the combined cohorts of the cutaneous adipose tissue in Asian Indians with
Indian Diabetes Prevention Programmes 1 and T2DM. It has been reported that children and
2 demonstrates that the baseline HbA (1c) was adolescents with type 1 diabetes should complete
highly predictive of future diabetes in Asian a minimum of 3060 min of moderate-intensity
Indian subjects with impaired glucose tolerance physical activity daily. Additional physical activ-
and nearly 60 % of the incidence occurred with ity beyond 60 min/day would be helpful in main-
values 6.0. Diagnostic sensitivity of 6.5 % taining glycaemic profile for T2DM patients. The
for new diabetes was only 51 % using the oral practice of yoga is a traditional Indian practice
glucose tolerance test as the standard for com- that helps therapeutically and promotes physical
parison. The combination of gamma-glutamyl- and mental health. Yoga-based lifestyle modifi-
transferase (GGT) and fasting plasma glucose cation programme helps in the reduction of blood
(FPG) offers a simple and sensitive tool to iden- glucose, HbA1c, triglycerides, total cholesterol
tify subjects at high risk of developing diabetes. and VLDL. Mindfulness eating and yoga exer-
Similarly, several other markers including adi- cise had health benefits on glycaemic control
ponectin, IL-6, retinol-binding protein 4, and in pregnant women with GDM in some studies.
hypertriglyceridaemic waist phenotype have Yogic exercises have enhanced the antioxidant
been proposed to independently associate with defence mechanism in diabetics by reducing
incident diabetes. Prospective, intervention stud- oxidative stress. Unless drastic steps are taken
ies have demonstrated that increased compliance through national prevention programmes to curb
to lifestyle goals especially with the modifica- the escalating trends in all of the countries, the
tion of the diet habits, independent of the physi- social, economic and health-care challenges are
cal activity, could result in the decrease in the likely to be insurmountable.
Organising and Conducting be further streamlined by an individualised

Diabetes Research in the Region approach (Fig. 6.4).
RSSDI (Research Society for the Study of

Diabetes in India) is the largest organisation of Future Directions: Unmet Needs,
diabetes health-care professionals and research- Unanswered Questions
ers in Asia, which was formed in 1972. Currently, and Unquestioned Answers
there are more than 5,500 life members from
across the country representing 29 Indian states There have been rapid epidemiological transitions
and Union territories. Every year, RSSDI organ- translating into a huge disease burden in diabetes
ises the national annual meeting, which not only in the SEA region. Prevention of diabetes through
provides a platform for its members to listen to consistent awareness about the disease in popula-
the leaders in the field of diabetes from within the tion would be a critical step forward which would
country as well as from abroad but also to interact have tremendous implications that halt the prog-
amongst themselves and exchange knowledge ress of disease. One of the global targets for non-
and ideas. Annual meetings of RSSDI have been communicable disease is to halt by 2025 the rise
a regular feature for more than four decades and in the prevalence of diabetes to its 2010 levels. A
are very well attended. RSSDI has a nationwide better understanding for the basis for the gene
presence through its 14 state chapters. All state environment interaction, in which beta-cell dys-
chapters carry on the work of RSSDI at the state function, typically on the background of insulin
and local level. In addition, these chapters carry resistance, is critical for the increase in glucose
out independent activities including CMEs for levels observed in impaired glucose metabolism
member physicians, local research grants and and for the development of the hyperglycaemia of
awareness programmes for public as well as dia- type 2 diabetes, would be explored to target effec-
betes patients. RSSDI regularly publishes a tive therapies. Prevention is of utmost importance,
newsletter, both in print and electronic format, but for the more than 420 million people currently
which serves as an important link between the living with diabetes, managing their disease must
national body and its membership to keep the remain the priority. The recent WHOs report rec-
members informed of various activities, research ommends a multidisciplinary approach with
grants and educational initiatives. The patient education, medication and consistent fol-
International Journal of Diabetes in Developing low-up. For primary prevention, the challenge lies
Countries (IJDDC) is the prestigious indexed in raising awareness, promoting health literacy
publication of RSSDI and is an important and identifying individuals at high risk of diabetes
resource of research work done in the field of dia- for early intervention. For secondary prevention,
betes in India. RSSDI funds research proposals poor access to care, clinical inertia and treatment
from Indian scientists interested in conducting non-adherence are major barriers in evidence-
research in the field of diabetes mellitus. For pro- based practice. Given the phenotypic heterogene-
viding research grants, RSSDI invites proposals ity of diabetes, and thus the pluralistic needs of
from Indian scientists interested in conducting those affected, clinical acumen to identify prob-
original research in the field of diabetes mellitus. lems and sufficient contact time to empower the
Furthermore, limited grants are also available for person to change behaviour and adhere to treat-
the students of medical colleges for smaller proj- ment are key to successful management.
ects. Recently, RSSDI has developed a simple Screening in young-onset diabetes in India for
user-friendly novel approach to decide the appro- CV risk factors and complications would be vital
priate antidiabetic agent to be used in type 2 dia- to curb the impact of the microvascular and mac-
betes through the therapeutic wheel. The best rovascular complications. This has been clearly
choices can be determined from the outer rings of demonstrated in the landmark CINDI and CINDI
the wheel (orange and red), and the choices can 2 trials published recently for the clinic-based
Fig. 6.4 The RSSDI therapeutic wheel
miological, experimental human and animal

survey amongst 4,600 patients for diabetes- studies as well as the data from several mega-
related complications and a retrospective cross- trials have convincingly proved the importance
sectional study of 1,500 patients with newly of tight metabolic control in arresting and pre-
detected young-onset diabetes, respectively. venting the progression of target organ dam-
age. In the last two decades, there is a better
Conclusions understanding of the pathophysiology of type 2
Considering the enormous burden due to dia- diabetes and availability of newer oral drugs
betes in India, it is important to realise the cost- for diabetes; newer insulin and improved deliv-
effective measures of diabetes care like early ery systems should translate to improve diabe-
screening, tight metabolic control, monitoring tes control. However, the survey described
of risk factors and assessing of the organ dam- above indicates the gaps between the guide-
age. The study done for economic analysis in lines and real-life practice. In view of this,
diabetes care in India has also shown that the appreciation and understanding of both patient
cost of providing routine care is only a fraction and physician barriers regarding proper moni-
of the overall cost and is perhaps still manage- toring and judicious use of therapeutic options
able. However, when this is not available or its including insulin therapy for optimising diabe-
quality is poor, the overall direct and indirect tes management should be encouraged in order
costs escalate with disastrous health and eco- to improve control of diabetes in India. Result-
nomic consequences to the individual, his fam- oriented organised programmes involving
ily and society particularly due to the onset of patient education, updating medical fraternity
the micro- and macrovascular complications of on various developments in the management of
diabetes. Published data from several epide- diabetes and providing them the opportunity to
use and analyse these newer treatment options 6. Mohan V, Alberti KGMM. Diabetes in the tropics.
in the form of observational studies are required In: Alberti KGMM, Zimmet P, Defronzo RA, et al.,
editors. International text book of diabetes mellitus.
to combat the diabetes epidemic currently 2nd ed. Chichester: Wiley; 1997. p. 17187.
threatening to affect the lives of millions of 7. Nakagami T, Qiao Q, Carstensen B, The DECODE
people in India. Coordination, patient educa- -DECODA Study Group, et al. Age, body mass
tion and ongoing support are important compo- index and type 2 diabetes-associations modified by
ethnicity. Diabetologia. 2003;46:106370.
nents of quality diabetes care, but most 8. Banerji MA, Faridi N, Atluri R, et al. Body composi-
health-care systems are created to provide tion, visceral fat, leptin, and insulin resistance in
acute and episodic care rather than chronic Asian Indian men. J Clin Endocrinol Metab.
care. The effectiveness of team-based chronic 1999;84:13744.
9. Zargar AH, Wani AI, Masoodi SR, et al. Mortality in
care management is well established but not diabetes mellitusdata from a developing region of
widely implemented. Thus, the challenge lies the world. Diabetes Res Clin Pract. 1999;43:6774.
in designing alternative care models that iden- 10. Mohan V, Shanthirani CS, Deepa M, et al. Mortality
tify people with undetected diabetes, define rates due to diabetes in a selected urban south Indian
population the Chennai Urban Population Study
individual needs, provide interdisciplinary care (CUPS-16). J Assoc Phys India. 2006;54:1137.
and measure effectiveness to make diabetes 11. Rema M, Deepa R, Mohan V. Prevalence of retinop-
prevention and control programmes accessible, athy at diagnosis among type 2 diabetic patients
affordable and sustainable. It is time to evalu- attending a diabetic centre in South India. Br
J Ophthalmol. 2000;84:105860.
ate existing policies to address diabetes and 12. Ramachandran A, Snehalatha C, Satyavani K, et al.
devise a strategy and accountability framework Prevalence of vascular complications and their risk
for short-, medium- and long-term solutions to factors in type 2 diabetes. J Assoc Physicians India.
address the growing unmet needs in diabetes 1999;47:11526.
13. Tripathy BB, Panda NC, Tej SC, et al. Survey for
prevention and control. Immediate action is detection of glycosuria, hyperglycaemia and diabe-
needed to avert this escalating health disaster. tes mellitus in urban and rural areas of Cuttack dis-
trict. J Assoc Physicians India. 1971;19:681.
14. Ahuja MMS, Sivaji L, Garg VK, et al. Prevalence of
diabetes in northern India (Delhi area). Horn Metab
Res. 1974;4:321.
References 15. Gupta OP, Joshi MH, Dave SK. Prevalence of diabe-
tes in India. Adv Metab Disord. 1978;9:14765.
1. International Diabetes Federation. Diabetes Atlas. 7th 16. Murthy PD, Pullaiah B, Rao KV. Survey for detection
ed. 2015 Update. http://www.diabetesatlas.org/ of hyperglycaemia and diabetes mellitus in Tenali. In:
resources/2015-atlas.html. Last accessed on 21 Apr Bajaj JS, editor. Diabetes mellitus in developing
2016. countries. New Delhi: Interprint; 1984. p. 55.
2. Misra A, Sharma R, Gulati S. Consensus dietary guide- 17. Patel JC. Prevalence of hypertension and diabetes
lines for healthy living and prevention of obesity, the mellitus in a rural village. J Diabet Assoc India.
metabolic syndrome, diabetes, and related disorders in 1986;26:68.
Asian Indians. Dia Tec Ther. 2011;13(6):68394. 18. Ramachandran A, Jali MV, Mohan V, et al. High
3. NCD Risk Factor Collaboration (NCD-RisC). prevalence of diabetes in an urban population in
Worldwide trends in diabetes since 1980: a pooled South India. Br Med J. 1988;297:58790.
analysis of 751 population-based studies with 44 mil- 19. Deurenberg P, Deurenberg-Yap M, Guricci S. Asians
lion participants. Lancet. 2016;387:151330. are different from Caucasians and from each other in
their body mass index/body fat per cent relationship.
Obes Rev. 2002;3:1416.
20. Rao PV, Ushabala P, Seshiah. The Eluru survey:
Further Reading prevalence of known diabetes in a rural Indian popu-
lation. Diabetes Res Clin Pract. 1989;7:2931.
4. Sicree R, Shaw J, Zimmet P. Diabetes and impaired 21. McKeigue PM, Shah B, Marmot MG. Relation of
glucose tolerance in India. In: Gan D, editor. Diabetes central obesity and insulin resistance with high
atlas. Belgium: International Diabetes Federation; diabetes prevalence and cardiovascular risk in South
2006. p. 15103. Asians. Lancet. 1991;337:3826.
5. Mohan V, Sandeep S, Deepa R, et al. Epidemiology of 22. Wander GS, Khurana SB, Gulati R, et al.
type 2 diabetes: Indian scenario. Indian J Med Res. Epidemiology of coronary heart disease and risk fac-
2007;125:21730. tors in a rural Punjab population: prevalence and
correlation with various risk factors. Ind Heart 36. Reddy KS, Prabhakaran D, Chaturvedi V, on behalf
J. 1994;46:31923. of the Sentinel Surveillance System for Indian
23. Ramachandran A, Snehalatha C, Dharmaraj D, et al. Industrial Populations Study Group, et al. Methods
Prevalence of glucose intolerance in Asian Indians. for establishing a surveillance system for cardiovas-
Urbanrural difference and significance of upper cular diseases in Indian industrial populations. Bull
body adiposity. Diabetes Care. 1992;15:1348. WHO. 2006;84:4619.
24. Ramankutty V, Joseph A, Soman CR. High preva- 37. Deo SS, Zantye A, Mokal R, et al. To identify the
lence of type 2 diabetes in an urban settlement in risk factors for high prevalence of diabetes and
Kerala, India. Ethn Health Med. 1999;4:2319. impaired glucose tolerance in Indian rural
25. Zargar AH, Khan AK, Masoodi SR, et al. Prevalence population. Int J Diabetes Dev Countries. 2006;26:
of type 2 diabetes mellitus and impaired glucose tol- 1923.
erance in the Kashmir Valley of the Indian subconti- 38. Menon VU, Kumar KV, Gilchrist A, et al. Prevalence
nent. Diabetes Res Clin Pract. 2000;47:135. of known and undetected diabetes and associated
26. Ramachandran A, Snehalatha C, Kapur A, Diabetes risk factors in central Kerala ADEPS. Diabetes Res
Epidemiology Study Group in India (DESI), et al. Clin Pract. 2006;74:289.
High prevalence of diabetes and impaired glucose 39. Chow CK, Raju PK, Raju R, et al. The prevalence
tolerance in India: National Urban Diabetes Survey. and management of diabetes in rural India. Diabetes
Diabetologia. 2001;44:1094. Care. 2006;29:17178.
27. Misra A, Pandey RM, Devi JR, et al. High preva- 40. Raghupathy P, Antonisamy B, Fall CH, et al. High
lence of diabetes, obesity and dyslipidaemia in urban prevalence of glucose intolerance even among
slum population in northern India. Int J Obes. young adults in south India. Diabetes Res Clin Pract.
2001;25:17229. 2007;77:26979.
28. Mohan V, Shanthirani CS, Deepa R. Glucose intoler- 41. Mohan V, Mathur P, Deepa R, et al. Urban rural dif-
ance (Diabetes and IGT) in a selected South Indian ferences in prevalence of self reported diabetes in
population with special reference to family history, India-The WHO-ICMR Indian NCD risk factor sur-
obesity and lifestyle factors- the Chennai Urban veillance. Diabetes Res Clin Pract.
Population Study (CUPS 14). J Assoc Physicians 2008;80:15968.
India. 2003;51:771. 42. Ramachandran A, Mary S, Yamuna A, et al. High
29. Sadikot SM, Nigam A, Das S, et al. The burden of prevalence of diabetes and cardiovascular risk fac-
diabetes and impaired glucose tolerance in India tors associated with urbanization in India. Diabetes
using the WHO 1999 criteria: prevalence of diabetes Care. 2008;31:8938.
in India study (PODIS). Diabetes Res Clin Pract. 43. Rema M, Ponnaiya M, Mohan V. Prevalence of reti-
2004;66:3017. nopathy in non insulin dependent diabetes mellitus
30. Gupta A, Gupta R, Sarna M, et al. Prevalence of dia- in southern India. Diabetes Res Clin Pract. 1996;24:
betes, impaired fasting glucose and insulin resis- 2936.
tance syndrome in an urban Indian population. 44. Dandona L, Dandona R, Naduvilath TJ, et al.
Diabetes Res Clin Pract. 2003;61:69. Population based assessment of diabetic retinopathy
31. Agrawal RP, Singh G, Nayak KC, et al. Prevalence in an urban population in southern India. Br
of diabetes in camel milk consuming RAICA Rural J Ophthalmol. 1999;83:93740.
Community of North West Rajasthan. Int J Diabetes 45. Narendran V, John RK, Raghuram A, et al. Diabetic
Dev Countries. 2004;24:10914. retinopathy among self reported diabetics in southern
32. Ramachandran A, Snehalatha C, Baskar AD, et al. India: a population based assessment. Br
Temporal changes in prevalence of diabetes and J Ophthalmol. 2002;86:10148.
impaired glucose tolerance associated with lifestyle 46. Rema M, Premkumar S, Anitha B, et al. Prevalence
transition occurring in the rural population in India. of diabetic retinopathy in Urban India: the Chennai
Diabetologia. 2004;47:8605. Urban Rural Epidemiology Study (CURES) Eye
33. Mohan V, Deepa M, Deepa R, et al. Secular trends in Study-1. Invest Ophthalmol Vis Sci.
the prevalence of diabetes and glucose tolerance in 2005;46:232833.
urban South India-the Chennai Urban Rural 47. John L, Sundar Rao PSS, Kanagasabhapathy
Epidemiology Study (CURES- 17). Diabetologia. AS. Prevalence of diabetic nephropathy in non insu-
2006;49:1175. lin dependant diabetes mellitus. Indian J Med Res.
34. Basavanagowdappa H, Prabhakar AK, Prasannaraj 1991;94:249.
P, Gurudev KC, Virupaksha S. Study of prevalence 48. Gupta DK, Verma LK, Khosla PK, et al. The preva-
of diabetes mellitus and impaired fasting glucose in lence of microalbuminuria in diabetes: a study from
a rural population. Int J Diabetes Dev Countries. north India. Diabetes Res Clin Pract. 1991;12:1258.
2005;25:98101. 49. Yajnik CS, Naik SS, Raut KN, et al. Urinary albumin
35. Prabhakaran D, Shah P, Chaturvedi V, et al. excretion rate (AER) in newly-diagnosed type 2
Cardiovascular risk factor prevalence among men in Indian diabetic patients is associated with central
a large industry of northern India. Natl Med J India. obesity and hyperglycaemia. Diabetes Res Clin
2005;18:5965. Pract. 1992;17:5560.
50. Vijay V, Snehalatha C, Ramachandran A, et al. practices (DIPPAP-1 study). Int J Diabetes Dev
Prevalence of proteinuria in non-insulin dependent Countries. 1997;17:212.
diabetes. J Assoc Physicians India. 1994;42: 64. Raheja BS, Kapur A, Bhoraskar A, et al. DiabCare
7924. AsiaIndia Study: diabetes care in Indiacurrent
51. Mohan V, Meera R, Premalatha G, et al. Frequency status. J Assoc Physicians India. 2001;49:71722.
of proteinuria in type 2 diabetes mellitus seen at a 65. American Diabetes Association (ADA)
diabetes centre in Southern India. Postgrad Med Recommendations Regarding Glycated Hemoglobin
J. 2000;76:56973. Standardization. American diabetes association
52. Varghese A, Deepa R, Rema M, et al. Prevalence of position statement. Tests of glycemia in diabetes.
microalbuminuria in type 2 diabetes mellitus at a Diabetes Care. 2004;27:S913.
diabetes centre in Southern India. Postgrad Med 66. Dilley J, Ganesan A, Deepa R, et al. Association of
J. 2001;77:399402. A1C with cardiovascular disease and metabolic syn-
53. Ranjit Unnikrishnan I, Rema M, Pradeepa R, et al. drome in Asian Indians with normal glucose toler-
Prevalence and risk factors of diabetic nephropathy ance. Diabetes Care. 2007;30:152732.
in an Urban South Indian population. The Chennai 67. Phillips LS, Branch WT, Cook CB, et al. Clin Inertia
Urban Rural Epidemiology Study (CURES-45). Ann Intern Med. 2001;135:82534.
Diabetes Care. 2007;30(8):201924. 68. Couzin J. Clinical research: deaths in diabetes trial
54. Mohan V, Premalatha G, Sastry NG. Ischaemic heart challenge a long-held theory. Science. 2008;
disease in south Indian NIDDM patients a clinic 884885:15.
based study on 6597 NIDDM patients. Int J Diabetes 69. Kapur A. Economic analysis of diabetes care. Indian
Dev Countries. 1995;15:647. J Med Res. 2007;125:47382.
55. Ramachandran A, Snehalatha C, Latha E, et al. 70. Nagpal J, Bhartia A. Quality of diabetes care in the
Clustering of cardiovascular risk factors in urban middle and high-income group populace: the Delhi
Asian Indians. Diabetes Care. 1998;21:96771. Diabetes Community (DEDICOM) survey. Diabetes
56. Mohan V, Deepa R, Shanthirani CS, et al. Prevalence Care. 2006;29:23418.
of coronary artery disease and its relationship to lip- 71. Kapur A, Shishoo S, Ahuja MMS, et al. Diabetes
ids in a selected population in South India. J Am Coll care in India: physicians perceptions, attitudes and
Cardiol. 2001;38:6827. practices. Int J Diabetes Dev Countries. 1998;18:
57. Premalatha G, Shanthirani CS, Deepa R, et al. 12430. 72.
Prevalence and risk factors of peripheral vascular 72. Chuang LM, Tsai ST, Huang BY, Tai TY. The status
disease in a selected south Indian population the of diabetes control in Asiaa cross-sectional survey
Chennai Urban Population Study (CUPS). Diabetes of 24 317 patients with diabetes mellitus in 1998.
Care. 2000;23:1295300. Diabet Med. 2002;19:97885.
58. Ashok S, Ramu M, Deepa R, et al. Prevalence of 73. Mohan V, Goldhaber-Fiebert JD, Radha V, et al.
neuropathy in type 2 diabetic patients attending a Screening with OGTT alone or in combination with
diabetes centre in south India. J Assoc Physicians the Indian diabetes risk score or genotyping of
India. 2002;50:54650. TCF7L2 to detect undiagnosed type 2 diabetes in
59. Pradeepa R, Rema M, Vignesh J, et al. Prevalence Asian Indians. Indian J Med Res. 2011;133:2949.
and risk factors for diabetic neuropathy in an urban 74. Engelgau MM, Narayan KMV, Herman
south Indian population: the Chennai Urban Rural WH. Screening for type 2 diabetes. Diabetes Care.
Epidemiology Study (CURES-55). Diabet Med. 2000;23(10):156380.
2008;25:40712. 75. Joshi SR, Das AK, Vijay VJ, Mohan V. Challenges
60. Mohan V, Ravikumar R, Shanthirani S, et al. Intimal in diabetes care in India: sheer numbers, lack of
medial thickness of the carotid artery in south Indian awareness and inadequate control. J Assoc
diabetic and non diabetic subjects: the Chennai Physicians India. 2008;56:44350.
Urban Population Study (CUPS). Diabetologia. 76. Misra A, Nigam P, Hills AP, et al. Consensus physi-
2000;43:4949. cal activity guidelines for Asian Indians. Diabetes
61. Deepa M, Deepa R, Shanthirani CS, et al. Awareness Technol Ther. 2012;14(1):8398.
and knowledge of diabetes in Chennai the Chennai 77. Cuff DJ, Meneilly GS, Martin A, et al. Effective
Urban Rural Epidemiology Study [CURES-9]. exercise modality to reduce insulin resistance in
J Assoc Physicians India. 2005;53:2837. women with type 2 diabetes. Diabetes Care. 2003;
62. Murugesan N, Snehalatha C, Shobhana R, et al. 26(11):297782.
Awareness, about diabetes and its complications in 78. Ishii T, Yamakita T, Sato T, et al. Resistance training
the general and diabetic population in a city in improves insulin sensitivity in NIDDM subjects
southern India. Diabetes Res Clin Pract. 2007;77: without altering maximal oxygen uptake. Diabetes
4337. Care. 1998;21(8):13535.
63. Kapur A, Shishoo S, Ahuja MMS, et al. Diabetes 79. Silverstein J, Klingensmith G, Copeland K, et al.
care in India: patients perceptions attitudes and Care of children and adolescents with type 1 diabetes:
a statement of the American Diabetes Association. onset type 2 diabetes in India: CINDI 2. Indian
Diabetes Care. 2005;28(1):186212. J Endocrinol Metab. 2016;20(1):1148.
80. Joshi SR, Bhansali A, Bajaj S, et al. Results from a 94. Sosale A, Prasanna Kumar KM, Sadikot SM.
dietary survey in an Indian T2DM population: a (CINDI). Chronic complications in newly diagnosed
STARCH study. BMJ Open. 2014;4(10):e005138. patients with Type 2 diabetes mellitus in India.
81. Sadikot SM, Nigam A, Das S, et al. Diabetes India. Indian J Endocrinol Metab. 2014;18(3):35560.
The burden of diabetes and impaired fasting glucose 95. Krug EG. Trends in diabetes: sounding the alarm.
in India using the ADA1997 criteria: prevalence of Lancet. 2016;387:14856.
diabetes in India study (PODIS). Diabetes Res Clin 96. Madhu SV, et al. Guideline development group. Int
Pract. 2004;66:29330. J Diabetes Dev Countries. 2015;35 Suppl 1:S171.
82. Research India Diabetes(ICMR-INDAB) study 97. Nanditha A, et al. Diabetes in Asia and the Pacific:
(phase I): Indian Council of Medical Research India implications for the global epidemic. Diabetes Care.
Diabetes 4. Indian J Endocrinol Metab. 2016;39(3):47285.
2014;18:37985. 98. Shen J, Prabhakaran D, Tandon N, et al. A multieth-
83. The Diabetes Prevention Program Research Group. nic study of pre-diabetes and diabetes in LMIC. Glob
The diabetes prevention program. Diabetes Care. Heart. 2016;11(1):6170.
2002;25:216571. 99. Ramachandran A, et al. Combining fasting plasma
84. Lindstorm J, Louheranta A, Mannelin M, et al. The glucose with gamma-glutamyl transferase improves
Finnish diabetes prevention study. Diabetes Care. the sensitivity to predict incident diabetes in Asian
2003;26:32306. Indian men with impaired glucose tolerance. J Assoc
85. Misra A, Alappan NK, Vikram N. Effect of super- Physicians India. 2014;62(11):1822.
vised progressive resistance-exercise training proto- 100. Vinitha R, Johnston DG, Ramachandran A, et al.
col on insulin sensitivity, glycemia, lipids, and body Adiponectin, leptin, interleukin-6 and HbA1c in the
composition in Asian Indians with type 2 diabetes. prediction of incident type 2 diabetes: a nested case-
Diabetes Care. 2008;31(7):12827. control study in Asian Indian men with impaired glu-
86. Thangasami SR, Chandani AL, Thangasami cose tolerance. Diabetes Res Clin Pract. 2015;109(2):
S. Emphasis of yoga in the management of diabetes. 3406.
J Diabetes Metab. 2015;6:10. 101. Ram J, Snehalatha C, Ramachandran A, et al. Retinol
87. Youngwanichsetha S, Phumdoung S, binding protein-4 predicts incident diabetes in Asian
Inqkathawornwong T. The effects of mindfulness Indian men with prediabetes. Biofactors.
eating and yoga exercise on blood sugar levels of 2015;41(3):1605.
pregnant women with gestational diabetes mellitus. 102. Ramachandran A, et al. Improvement in diet habits,
Appl Nurs Res. 2014;27(4):22730. independent of physical activity helps to reduce
88. The DCCT Research Group. The effect of intensive incident diabetes among prediabetic Asian Indian
treatment of diabetes on the development and pro- men. Diabetes Res Clin Pract. 2014;106(3):4915.
gression of long-term complications in insulin 103. Ramachandran A, et al. Hypertriglyceridaemic waist
dependent diabetes mellitus. N Engl J Med. 1993; phenotype as a simple predictive marker of incident
329:97786. diabetes in Asian-Indian men with prediabetes.
89. Okhubo Y, Hideki K, Araki E, et al. Intensive insulin Diabet Med. 2014;31(12):15429.
therapy prevents the progression of diabetic micro- 104. Ramachandran A, et al. Effectiveness of mobile
vascular complications in Japanese patients with phone messaging in prevention of type 2 diabetes by
non-insulin dependent diabetes mellitus. A random- lifestyle modification in men in India: a prospective,
ized prospective six year study. Diabetes Res Clin parallel-group, randomised controlled trial. Lancet
Pract. 1995;28:10317. Diabetes Endocrinol. 2013;1(3):1918.
90. UKPDS Study Group. Intensive blood glucose control 105. Ramachandran A, et al. Predictive value of HbA1c
with SU and insulin compared with conventional for incident diabetes among subjects with impaired
treatment and risk of complications in patients with glucose tolerance analysis of the Indian Diabetes
type 2 diabetes. (UKPDS 33). Lancet. Prevention Programmes. Diabet Med. 2012;29(1):
1998;352:83753. 948.
91. Pung OJ, Sobieraj DM, Engel SS. Early combination 106. Anjana RM, ICMRINDIAB Collaborative Study
therapy for the treatment of type 2 diabetes mellitus: Group, et al. Prevalence of diabetes and prediabetes
systematic review and meta-analysis. Diabetes Obes (impaired fasting glucose and/or impaired glucose
Metab. 2014;16(5):4107. tolerance) in urban and rural India: phase I results of
92. Screening for Diabetes. American diabetes associa- the Indian Council of Medical Research-INdia
tion. Diabetes Care. 2002;25(1):s214. DIABetes (ICMR-INDIAB) study. Diabetologia.
93. Sosale B, Sosale AR, Mohan AR. (CINDI 2). 2011;54(12):30227.
Cardiovascular risk factors, micro and macrovascu- 107. Ramachandran A, Indian Diabetes Prevention
lar complications at diagnosis in patients with young Programme (IDPP), et al. The Indian Diabetes
Prevention Programme shows that lifestyle Indian Diabetes Prevention Programme (IDPP).
modification and metformin prevent type 2 diabe- Diabetes Care. 2007;30(10):254852.
tes in Asian Indian subjects with impaired glucose 110. Snehalatha C, et al. Beneficial effects of strategies
tolerance (IDPP-1). Diabetologia. for primary prevention of diabetes on cardiovascular
2006;49(2):28997. risk factors: results of the Indian Diabetes Prevention
108. Ramachandran A, et al. Persistent impaired glucose Programme. Diabetes Vasc Dis Res. 2008;5(1):
tolerance has similar rate of risk factors as for diabe- 259.
tes results of Indian diabetes prevention programme 111. Unnikrishnan R, Anjana RM, Mohan V. Diabetes
(IDPP). Diabetes Res Clin Pract. 2006;73(1):1003. mellitus and its complications in India. Nat Rev
109. Ramachandran A, et al. Cost-effectiveness of the Endocrinol. 2016. doi:10.1038/nrendo.2016.53.
interventions in the primary prevention of diabetes [Epub ahead of print]. Online ahead of print.
among Asian Indians: within-trial results of the
Diabetes in Latin America
7
Omar Y. Bello-Chavolla
and Carlos A. Aguilar-Salinas
Classication and Unique Aspects areas of Argentina or Uruguay. In urban areas of

of the Pathophysiology of Type 1 Colombia and Mexico, the average proportion of
and Type 2 Diabetes in the Region Native American and European admixture are
5060 % and 3045 %, respectively. In addition,
The Latin America (LA) region is comprised of an ongoing demographic transition has modified
21 countries, including Mexico, six countries in the age structure of Latin American populations
Central America, ten countries in South America, with important increases in the adult (15
and three countries in the Caribbean islands span- 59 years) population and especially for popula-
ning a total population of almost 600 million tions of older populations (aged 60 years and
people. The region is composed of low- and over) [1].
middle-income countries with populations The rapid growth of the number of inhabitants
mainly composed of young adults. Ethnic diver- in the Latin American population observed in the
sity and the preservation of the Amerindian heri- first half of the preceding century was reverted in
tage are unique features of the Latin American the past few decades (2.8 % growth per year in
populations. Meanwhile, the Amerindian compo- 1950, 1.3 % in the early 2000s). This trend
nent is the dominant genetic background in Peru resulted from birth control campaigns, migratory
and Guatemala; its contribution is minimal in movements, and economic phenomena. On the
other hand, a trend for decreasing all-cause mor-
tality started to occur within Latin America
50 years ago. Life expectancy in the region has
increased by 21.6 years on average reaching
73.4 years for the 20052010 period. The varia-
O.Y. Bello-Chavolla, MD, PhD (PECEM) tion of life expectancy is wide within the region,
Department of Endocrinology and Metabolism, ranging from 65.5 in Bolivia to >78 years in
Instituto Nacional de Ciencias Mdicas y Nutricin Chile and Costa Rica. As a result, the percentage
Salvador Zubirn, Mexico City, Mexico of elder population has increased in the last
Facultad de Medicina, Universidad Nacional 50 years. It is expected that, by the year 2050, the
Autnoma de Mxico, Mexico City, Mexico percentage of elders move from 8.8 to 23.6 %.
C.A. Aguilar-Salinas (*) The demographic modifications pose a remark-
Departamento de Endocrinologia y Metabolismo, able challenge for the local healthcare systems.
Instituto Nacional de Ciencias Mdicas y Nutricion,
Vasco de Quiroga 15, Mexico City 14000, Mexico The increase of life expectancy will lead to
e-mail: [email protected] increased number of susceptible cases for having

DOI 10.1007/978-3-319-41559-8_7
102 O.Y. Bello-Chavolla and C.A. Aguilar-Salinas
non-transmissible chronic diseases (i.e., type 2 triglycerides, and abnormal fasting glucose.
diabetes mellitus), which already are the major When three or more of these abnormalities are
health burden within Latin American countries. present, individuals are diagnosed as having the
metabolic syndrome. This condition is associated
with a fivefold increase for having T2D. Several
Type 2 Diabetes metabolic syndrome definitions have been pro-
posed. Using the ATP-III criteria, the age-
Close to 80 % of 415 million T2DM cases live in adjusted prevalence for the region is 28.3 %.
middle- and low-income countries. A significant Population-based data are available for Brazil
proportion of them (41.1 millions) reside in (29 %), Peru (18.1 %), Colombia (34.8 %),
LA. This number is expected to increase to 69.4 in Venezuela (35.3 %), and Mexico (36.8 %). Higher
2040. The International Diabetes Federation (IDF) percentages are found if the IDF definition is
estimated that the age-adjusted prevalence for the applied (for Mexican adults, the prevalence
region was 9.2 % for adults (aged 2079 years) in changes from 36.8 to 49.8 %). The prevalence of
2014. Only North America (10.5 %) and southern the metabolic syndrome traits is different in LA
Asia (10.9 %) had a greater prevalence of diabetes compared to that reported in Caucasian popula-
than LA. Two of the ten leading countries for the tions; low HDL cholesterol, abdominal obesity,
number of cases are located in the region (Brazil and hypertriglyceridemia are significantly more
(14.3 million) and Mexico (11.5 million)) common in LA subjects.
(Table 7.1). In addition, the increment in the num- The clinical expression of T2D has several
ber of cases is expected to be greater in this region peculiarities that have been consistently reported
compared to other areas. in LA populations. Especially among mestizo
According to the Global Burden of Disease individuals, the disease is expressed at an earlier
group, the mean fasting plasma glucose of the age and with a lower body mass index (BMI)
adults living in LA has increased 3.06 mg/dl compared to that reported in Caucasians. The
every decade since 1980 [2]. The end result has premature age of onset increases the social and
been a rapidly increasing prevalence of diabetes. economic burden because of the higher preva-
The epidemic growth is expected to continue lence of chronic complications and premature
since the prevalence of several preceding condi- disability during productive years. In Mexico,
tions of T2D (i.e., obesity and glucose intoler- 22.7 % of people with T2D are under the age 40.
ance) is higher in LA than in other regions. Individuals with early-onset T2D comprise a
According to the latest report by the Food and heterogeneous population [4]. Two thirds of
Agriculture Organization of the United Nations them have BMI >25 kg/m2; these cases had an
(FAO) [3] and the World Health Organization increased prevalence of several metabolic syn-
(WHO), the worldwide prevalence of obesity in drome traits (e.g., hypertension and hypoalph-
2013 was 11.7, whereas the prevalence of obesity alipoproteinemia) and can be controlled using
for the Latin American was reported to be 23.4 %, oral glucose-lowering agents. In contrast, a
distributed in 30.4 % for Central America and large proportion of the lean cases require insulin
21.6 % for South America (Table 7.2). The coun- as part of their treatment. Compared to the over-
tries with the highest obesity prevalence in the all population with T2D, the young T2D popu-
LA region are Mexico, followed by Venezuela, lation had a higher prevalence of underdiagnosis,
Argentina, and Chile. The reported prevalence more school years but a lower socioeconomic
for obesity in Mexican women proves to be level, and higher alcohol and tobacco consump-
higher than the same figure reported for the USA tion. Few young patients undertake preventive
in 2008 (31.8 %). A high percentage of patients measures, with very few receiving statins, ace-
with excess body weight have central fat accumu- tylsalicylic acid, or follow-up with an ophthal-
lation, arterial hypertension as well as abnormal mologist. This group has specific barriers to
concentrations of total cholesterol, HDL and adhere treatment programs (e.g., depression,
7 Diabetes in Latin America 103
Table 7.1 Prevalence of diabetes in Latin America

Annual death Annual Estimated Annual
rate due to treatment cost number of increment of
Number of cases diabetes per subject undiagnosed the number of
Country (2079 years) Prevalence (2079 years) (US dollars) cases cases
Argentina 1,570,200 5.57 15,416 966.44 722,290 29,000
Bolivia 325,220 6.89 4,732 124.63 149,600
Brazil 14,300,000 10.52 129,226 1,031.44 6,164,590 377,000
Chile 1,442,610 12.78 10,459 992.13 755,600 28,000
Colombia 2,067,870 7.26 14,602 482.72 951,220 95,000
Costa Rica 259,350 8.81 1,659 937.20 119,300
Cuba 872,950 8.58 7,560 823.71 401,560 19,000
Ecuador 563,840 6.89 5,492 335.41 259,360 19,000
El Salvador 312,430 9.88 3,233 333.58 143.72
French Guiana 12,610 9.60 5,800
Guatemala 589,140 9.93 7,202 311.52 271,010 27,000
Honduras 239,590 7.16 2,338 209.40 110,210
Mexico 11,500,000 14.4a 80,000a 815.53 3,452,410 323,000
Nicaragua 309,320 11.58 3,001 172.21 142,290
Panama 184,580 8.59 1,399 732.45 84,910
Paraguay 222,220 6.81 2,174 283.14 102,220
Peru 1,108,610 6.81 8,150 307.31 509,960
Puerto Rico 391,870 12.98 108,590
Dominican 405,580 7.36 5,183 419.28 186,570
Republic
Uruguay 157,330 6.02 1,122 922.68 72,370
Venezuela 1,764,900 10.39 13,380 914.01 811,850 61,000
Modified from: Whiting et al. [23]. International Diabetes Federation Atlas 2012
a
Villalpando et al. [93]
work-related stress, and alcoholism) that should the presence of arterial hypertension. Smoking
be intentionally sought. persists as a common risk factor in the patients
On the other hand, the mean BMI of recently with diabetes. Dyslipidemia is one of the most
diagnosed populations is lower in LA patients common comorbidities in T2D, with higher lev-
(e.g., for Mexico, 27.9 kg/m2 in males and els of triglycerides and non-HDL cholesterol
28.9 kg/m2 in females) compared to that reported compared with values of the general population.
in the USA (usually above 30 kg/m2). Mestizo LDL cholesterol (LDL-C) levels >100 mg/dL are
populations are less tolerant to excess body observed in 74.8 % (95 % CI 72.576.9 %) of pre-
weight because fat is accumulated in ectopic viously diagnosed patients [6]. Similar percent-
organs and in the intra-abdominal cavity instead ages have been reported by the Qualidiab network
of the subcutaneous adipose tissue [5]. using data from several South American coun-
T2D coexists frequently with other comorbid- tries [7].
ities. Taking as an example the Mexican popula- A high percentage of women with T2D had at
tion, a high percentage of patients with T2D had least one pregnancy during their lifetimes
at least one cardiovascular risk factor (86.7 %) (94.7 %); this proportion was similar to the one
(e.g., hypercholesterolemia, family history of found in patients without T2D. However, the
cardiovascular mortality, arterial hypertension, number of women who had suffered at least one
and smoking). Nearly half the patients had hyper- abortion was significantly higher in the group
tension, but almost half of them are unaware of with diabetes (OR 1.62, 95 % CI 1.531.83) with
Table 7.2 Average body mass index (BMI) standardized for age by age and country for the years 1980 and 2008
Prevalence of obesity
Men (kg/m2) Women (kg/m2) in adults (%)
1980 2008 1980 2008 2008
Argentina 25.4 27.5 23.8 27.5 29.4
Bolivia 23.0 24.4 23.6 26.9 18.9
Brazil 22.6 25.8 24.1 26.0 19.5
Chile 24.5 27.0 24.0 27.9 29.1
Colombia 22.1 24.9 23.4 26.2 18.1
Costa Rica 23.7 26.5 23.4 27.0 24.6
Cuba 22.7 25.1 23.8 26.6 20.5
Ecuador 23.8 25.6 24.7 27.1 22.0
El Salvador 23.8 26.4 23.7 27.8 26.9
Guatemala 23.2 25.3 22.9 26.8 20.7
Honduras 23.1 25.1 23.0 26.7 19.8
Mexico 24.5 27.4 24.6 28.7 32.8
Nicaragua 24.0 25.8 24.4 27.6 24.2
Panama 23.5 26.3 23.9 27.7 25.8
Paraguay 23.4 25.5 23.5 25.9 19.2
Peru 23.0 24.8 25.1 26.0 16.5
Dominican Republic 22.9 25.2 22.6 26.9 21.9
Uruguay 24.2 26.4 23.3 26.6 23.6
Venezuela 24.6 27.4 24.7 28.1 30.8
Adapted from: Finucane MM, Stevens GA, Cowan MJ, et al., and the Food and Agriculture Organization of the United
Nations. The State of Food and Agriculture 2013
a similar trend found in the risk of stillbirth (OR diagnosed after the age 70; these patients have a
1.99, 95 % CI 1.752.3); these differences were low prevalence of microvascular complications
held significant when adjusted by age. A high and their glucose levels can be kept stable with
percentage of women with T2D during their one or two oral hypoglycemic agents. Both
reproductive years did not use contraceptive groups are represented in similar proportions.
methods (42.5 %); this rate was not significantly Cardiovascular risk factors were common in this
different in women without T2D (38.8 %). A age group; 60 % had hypertension, 88.7 % was
quarter of patients with T2D had a current or pre- taking one or more antihypertensive agents, and
vious history of a urinary tract infection during microalbuminuria was detected in 48.4 % of
the previous year. Additionally, the risk of suffer- cases. These patients have a higher prevalence of
ing an accident is higher for T2D patients (OR geriatric syndromes (falls, motor limitations,
1.42, 95 % CI 1.251.60) with half of the acci- cognitive dysfunction, and polypharmacy) [9].
dents occurring within the patients house. The T2DM patients in Latin America are exposed
risk of accidental falls in patients with T2D is not to endemic and highly prevalent infectious dis-
held significant when stratified by age group [8]. eases (such as tuberculosis, influenza, HIV, and
The elder patient with T2D is a growing group hepatitis C), which represent a serious comorbid-
in the region. Two major profiles are found ity within this group. T2D increases the risk for
among them. The first is composed of T2D having tuberculosis, and it is associated with a
patients with a long exposure to the disease and decreased rate of eradication. The epidemiologic
chronic complications, third-party dependence, transition from infectious to noncommunicable
and requiring a more complex management. The chronic diseases has created a unique environ-
second group is composed of T2D patients ment in Latin American countries where the
interaction of both disease trends increases mor- The information about the epidemiology of
bidity and mortality associated with noncommu- T1DM in this region is scant [12].
nicable diseases [10]. In most high-income countries, the majority
of diabetes in children and adolescents is caused
by T1DM. This statement does not apply for the
Gestational Diabetes LA region. The growth in the number of children
with diabetes is mainly caused by T2D. In
Gestational diabetes is a common obstetric com- Mexico, half of the children with diabetes are
plication in the LA region. Prevalence depends obese, do not have positive titers of GAD anti-
on the sampling approach and the diagnostic cri- bodies, and are controlled with oral glucose-
teria applied. It varies between 4.3 and 30.1 %; lowering agents.
the majority of reports inform percentages close The WHO coordinated a Multinational Project
to 10 %. The use of the recently introduced for Childhood Diabetes (DIAMOND) from 1990
IADPSG criteria results in remarkably higher to 1999 in order to monitor the patterns of world-
percentages [11]. According to the 2015 IDF wide incidence of T1DM in children up to the
Atlas, the age-adjusted prevalence of hyperglyce- year 2000 [13]. The Diabetes and Genetic
mia during pregnancy is 11.5 % (crude 13.2 %) in Epidemiology Unit of the National Public Health
the LA region; it means that close to 0.9 million Institute in Helsinki, Finland served as the coor-
live births are affected by this condition. dinator unit, and 100 centers from 50 countries
Macrosomia is frequently associated with ges- around the world headed by a principal investiga-
tational diabetes. In a multinational survey, the tor were recruited. To be eligible, the center must
prevalence of macrosomia was between 2.8 and have an accurate, well-defined, population-based
9.3 % in the LA region. This percentage was registry. The inclusion criteria considered chil-
greater than that reported in Asia and Africa. dren 014 years with residency in the study area.
Macrosomia is a strong risk factor for having Fifty countries participated in this program.
cesarean section and various adverse perinatal Seventy-five million children fitted the inclusion
outcomes (e.g., fetal distress and cephalopelvic criteria and 19,164 were diagnosed with T1DM
disproportion). from 1990 to 1994, according to WHO classifica-
tion and diagnostic criteria. Ten Latin American
countries (Argentina, Brazil, Chile, Colombia,
Type 1 Diabetes Mellitus (T1D) Paraguay, Peru, Uruguay, Venezuela, Cuba, and
Mexico) participated with 13 centers. The overall
The IDF reported that 542,000 children age-adjusted incidence of T1D varied from
(<15 years) worldwide are affected by this dis- 0.1/100,000 per year in Zunyi, China, and
ease; 86,000 new cases are diagnosed every year. Venezuela to 36.8/100,000 in Sardinia and
Prevalence of T1DM has been increasing in 36.5/100,000 in Finland (350-fold variation
recent years worldwide. An annual increase in among 100 populations around the world). The
incidence of 3 % has been recorded. incidence among populations in South America
The estimated number of cases in LA is ranged from intermediate to very low. The high-
45,100; 7,300 new cases are diagnosed every est incidence rates were among European and
year. Two of the top ten countries with the highest North American populations [14, 15]. The inci-
number of cases are located in the region (Brazil dence rates for T1DM in Latin American coun-
(30,900) and Mexico (13,500)). However, none tries are lower than those described in Spain
of the countries with the highest number of new (12.4/100,000 (11.713.1)) or Portugal
cases per year are located in LA. Readers should (14.6/100,000 (10.619.6)), suggesting that the
be aware that it is likely that these numbers are Amerindian genetic background might be protec-
underestimated due to the lack of national regis- tive against T1DM development. Native unmixed
tries in the majority of the countries of the region. minority groups remain in rural areas of Mexico,
Table 7.3 Incidence of type 1 diabetes in Latin America per 100,000 persons aged 14 years or younger
Incidence (%) (95 % Annual change of Estimate of
Country Study period CI) incidence ascertainment (%)
Puerto Rico 19901999 16.8 (16.017.6) 1.0 (2.7; 0.7) 9097
a
Uruguay (Montevideo) 1992 8.3 (5.411.7) 97
Brazil (Sao Paulo) 19901992 8.0 (5.5311.14) 16 (48.6; 37.2) 7095
Argentina (Avellaneda) 19901996 6.3 (5.711.1) 0.4 (8.8; 10.5) 88100
a
Argentina (Tierra del 19931996 10.3 (5.518.5) 100
Fuego)
a
Colombia (Bogota) 1990 3.8 (2.94.9) 97
a
Colombia (Cali) 19951999 0.5 (0.30.7)
Chile (Santiago) 19901999 3.7 (3.44.0) 7.5 (4.3; 10.9) 100
Cuba 19901999 2.3 (2.22.5) 10.8 (13.4; 25100
8.2)
Mexico (Veracruz) 19901993 1.5 (0.72.9) 100
a
Paraguay 19901999 0.9 (0.81.0) 0.5 (5.7; 4.9)
a
Peru (Lima) 19901994 0.5 (0.40.64) 12.1 (7.5; 35.8)
a
Dominican Republic 19951999 0.5 (0.40.7) 12.6 (11.4; 43.0)
a
Venezuela (Caracas) 19901994 0.1 (0.10.2) 6.8 (24.6; 15.3)
Hispanics in the USA 19901999 11.4 (10.112.9) 51100
Adapted from The DIAMOND Project Group and Gmez-Daz et al.
a
Missing data
Bolivia, Peru, and Guatemala; very low incidence 3,848 T2DM patients (cases) and 4,366 con-
of T1DM has been reported in these groups. trols and have Native American and European
Furthermore, T1DM prevalence seems to be ancestry [16]. The higher susceptibility of the
related to the proportion of Caucasoid popula- admixed Latin American population can be
tions in a certain country (Table 7.3). explained both by the high prevalence of
Caucasian- and ethnic-specific risk alleles.
Fifty-six of the 68 known genetic associations
Genomic Landscape of Diabetes identified in Caucasians were replicated. The
in the Region TCF7L2 and KCNQ1 risk alleles are highly
prevalent in mestizos. In addition, two ethnic-
Type 2 Diabetes specific associations were found. The strongest
novel association was found at chromosome
Amerindian populations have an increased risk 17p13.1, specifically an SLC16A11 haplotype
for having T2D. Populations with Amerindian (OR 1.29 (95 % CI 1.201.38)). Individuals
ancestry comprise 27.663 % of the genetic with the risk haplotype develop T2DM
background of the LA countries. The Slim 2.1 years earlier (p = 3.1 104) and had 0.9 kg/
Initiative in Genomic Medicine for the m2 lower BMI than noncarriers. This frequency
Americas (SIGMA) Type 2 Diabetes of this variant is very small in Europeans and
Consortium was set out to characterize the Africans, moderate in Asians (~10 %), and
genetic factors that explain the higher T2DM high in the Americas native population (50 %).
prevalence registered within this population. This newly discovered risk allele is thought to
The SIGMA consortium genotyped 8,214 be derived from Neanderthal introgression.
Mexicans and Latin Americans, which included Approximately 20 % of the difference in
prevalence of T2DM among people with opportunity to identify the existence of protective
Amerindian and European ancestry can be genotypes or the absence of susceptibility vari-
explained by the presence of the risk allele. ants in the Amerindians. T1DM is a multifacto-
The second risk allele associated with T2DM rial and polygenic disease that exerts a high
in the Latin American population is the p. genetic susceptibility trait with a concordance
E508K variant of the hepatocyte nuclear factor rate in twins of about 3050 %. Genetic variants
1- (HNF-1). It is present in 2.1 % of T2DM of the human leukocyte antigen (HLA) on chro-
patients [17]. The p.E508K variant partially mosome 6p21.3, particularly combinations of
reduces transactivation activity. Although the DR3/DR4, produce the highest risk, which
affected gene is the cause of MODY (maturity- explains nearly 50 % of the genetic contribution.
onset diabetes of the young)-3, the clinical pro- Other non-HLA T1DM susceptibility genes have
file of the patient with the p.E508K variant is been identified also.
undistinguishable from T2D. Cruz-Tapias et al. published a meta-anal-
Several polymorphisms have been studied ysis designed to estimate the risk associ-
among other populations; in Brazilians the ated with variations in HLA class II in some
TCF7L2 rs7903166 (C/T) was associated with autoimmune diseases, including T1DM in
T2DM risk among the southern-Brazilian popu- Latin American countries. Major risk alleles
lation. The frequency of the minor allele was related to T1DM incidence showed to be
38 % in the type 2 diabetes group and 31 % in DQA1*301/*501, DQB1*201/*302/*301, and
nondiabetic subjects, and this allele was signifi- DQB1*401/*402/*405, while the protective
cantly associated with type 2 diabetes risk ones were DQB1*501, DQB1*602/*603, and
(OR = 1.42, 95 % CI 1.151.76 for the dominant DQB1*11/*13/*14/*15. Meanwhile, Gorodezky
model of inheritance). et al. identified HLA haplotypes with a strong
association with T1DM in Mexicans which
included DRB1*0301-DQA1*0501-DQB1*0201
Gestational Diabetes (OR = 21.4), DRB1*0405-DQA1*0301-DQB1*
0302 (OR = 44.5), and the same DQA1/DQB1
Few genetic studies have been focused in women with the HLA haplotype DRB1*0404/*0401
with gestational diabetes in LA. Recently, conferring lower risk, increasing the risk of
Chagoya and coworkers found an association an earlier age at onset (OR = 61.3). Finally, a
between gestational diabetes and two of the most meta-analysis limited to LA patients with T1D
frequently replicated T2D loci: a TCF7L2 haplo- (21 studies, 1,138 cases, and 1,920 controls)
type (rs7901695, rs4506565, rs7903146, found that DRB1*0301 (OR: 9.65; 95 % CI:
rs12243326; P = 2.16 10-06; OR = 2.95) and a 5.6916.36; p < 0.0001), DRB1*1201 (OR: 4.84;
KCNQ1 haplotype (rs2237892, rs163184, 95 % CI: 1.9711.91; p = 0.001), DQB1*0302
rs2237897; P = 1.98 10-05; OR = 0.55). This (OR: 4.58; 95 % CI: 3.366.26; p < 0.0001),
finding is in accordance with the strong relation DQA1*0301(OR: 3.02; 95 % CI: 1.376.65;
that exists between T2D and gestational p = 0.0059) and DQB1*0602 (OR: 0.19; 95 %
diabetes. CI: 0.110.33; p < 0.0001), DRB1*14 (OR: 0.18;
95 % CI: 0.060.55; p = 0.0024), and DQB1*0501
(OR: 0.47; 95 % CI: 0.260.83; p = 0.0097) were
Type 1 Diabetes the most significant alleles associated with
T1D. Despite of the above, Latin American popu-
As recognized by the Diabetes Epidemiology lations and the Amerindian individuals have been
Research International Group, the ethnic diver- underrepresented in the T1DM genetic studies.
sity of the Latin American populations yields an Future GWAS study may consider the inclusion
of ethnic diverse populations composed by both aged 2069 years old. The corresponding rate in
high (i.e., Caucasian) and low (i.e., Amerindians) Peru is 22.4 % [29]. This information is in clear
incidence groups [1820]. contrast with the remarkably lower prevalence of
impaired glucose tolerance (7.9 %, 42.2 million)
reported for the region by the IDF.
Diagnosis of Diabetes A high percentage of T2DM patients remain
and Prediabetes in the Region undiagnosed. For example, in Mexico, half of the
patients with diabetes were unaware of their con-
T2D dition. The undiagnosed proportion of cases in
the region is not different from the rest of the
Prevalence data are available for the majority of developing countries but remarkably higher com-
the countries of the region [2125]. However, the pared to some European countries (nearly 6 %).
design of the surveys is heterogeneous leading to This percentage is even higher in young adults
contrasting conclusions even in the same country (70 %) or low-income groups. Several countries
[26]. Table 7.1 shows the prevalence reported by have implemented screening programs. The strat-
IDF which is derived mainly from population- egies are diverse. For example, Brazil had a mas-
based surveys. Twelve Latin American countries sive screening program in 2001, based in capillary
have prevalence higher than the world average glucose tests (n = 22,069,905). It covered 73 % of
(8.3 %). More than 10 % of the adult population the target population [30]. In Mexico, the adult
is affected in Chile, Puerto Rico, Nicaragua, population who attended for T2D screening in
Venezuela, Mexico, and Brazil. Prevalence is the previous year increased from 10.5 % in 2000
higher in urban settings, native Amerindian to 22.7 % in 2006. However, a major limitation of
communities (>25 % in Canada and the USA), the screening programs is the lack of a systematic
low-income/low-education groups, and popula- inclusion of the detected cases into treatment
tions that have undergone migratory movements programs.
(e.g., 25.7 % in the US/Mexico border). In Incidence data are scant in the region. In the
Mexico, the mean age of onset is 48 years, being Mexico City study, Gonzalez Villalpando and
lower in women. The highest prevalence is found coworkers found an incidence rate of 1.4 cases
in the 5560-year-old group. The time since per 100,000 persons per year in low-income sub-
diagnosis is 9.3 years in males and 8.4 years in jects [31]. Meza and coworkers using a Markov
females [27]. model estimated that incidence rates may vary
There is a lack of data about the prevalence of between five and 25 cases per 100,000 persons
prediabetes in LA [28]. This term encloses three per year among adults aged 3090 years living in
conditions (i.e., impaired fasting glucose (100 Mexico during 2010 [32]. Clearly, an unmet
125.9 mg/dl), impaired glucose tolerance (2 h need in the LA area is the existence of represen-
post-challenge plasma glucose between 140 and tative cohorts of patients with and without diabe-
199 mg/dl), and abnormal HbA1c (5.7 to 6.4 %) tes with a long-term follow-up. Incidence data
associated with an increased risk for having T2D are critical to design and validate public
in the next 10 years. The prevalence of prediabe- policies.
tes in Hispanics living in the USA was 36.8 %
(95 % CI 32.141.7 %) in 20112012 T2DM in Mexico
NHANES. Regrettably, no comparable informa- Mexico has four population-based, nationwide
tion is available in the region because only fast- surveys in which the prevalence of T2D has been
ing glycemia has been registered in the majority measured (National Chronic Disease Survey
of the LA population-based surveys. In the [ENEC] in 1993, National Health Survey [ENSA]
Mexican 2006 National Health and Nutrition in 2000, and the National Health and Nutrition
Survey (ENSANUT, in Spanish), the prevalence Surveys (ENSANUT) performed in 2006 and
of impaired fasting glucose was 19.1 % in adults 2012) [3335]. The surveys (Fig. 7.1) have
Fig. 7.1 Comparison of Prevalence of T2DM in Mexico

T2DM prevalence reported
16 14.4
for the National Health and
14
Nutrition Polls in Mexico
12
Prevalence (%)
for the years 1994, 2000, 9.2 9.2
2006, and 2012, comparing 10
6.7 7.3
the cases with previous 8
medical diagnosis and the 6 4 4.6
cases with both previous 4
medical diagnosis and the 2
cases found by the polls 0
(Adapted from: Hernndez- 1994 2000 2006 2012
vila et al.) Year of ENSANUT
Previous Medical Diagnosis Previous Medical Diagnosis + Cases Found in Poll
proved an increase in prevalence from 6.7 % in and 2.86 per 100 person-years was obtained for
1993 (previously diagnosed (PD) 4.6 % and undi- men and women, respectively, despite taking into
agnosed (UD) 2.1 %) to 7.5 % in 2000 (PD 5.8 % consideration different diabetes-associated risk
and UD 1.7 %) to 14.4 % in 2006 (PMD 7.3 % factors. In addition, Mexico City was among the
and 7.1 % FP). The increases were similar for cities included in the CARMELA study, a multi-
both sexes and for rural and urban areas. The national survey designed to assess the prevalence
growing trend in T2DM prevalence is multifacto- of diabetes, dyslipidemias, and other cardiovas-
rial; aging of the population, the large proportion cular risk factors. Mexico City had the highest
of Amerindian ethnic background, and an prevalence of T2D in the region.
increase in the prevalence of obesity attributable
to changes in the lifestyle are the most obvious T2DM in Brazil
explanations. Results from ENSANUT 2012 According to data from the IDF, Brazil ranks
show that the prevalence of T2DM by PD is 9.2 % fourth among countries with the largest number
in adults over 20 years of age; this implies that of people with T2DM, comprising nearly 14.3
6.4 million Mexican adults have the diagnosis of million cases; the T2DM prevalence in Brazil has
T2DM which shows an overall doubling up from been estimated by the IDF to be 10.52 % in 2012.
the prevalence recorded in the year 2000. A There is significant variability between regions
recent IDF report estimates that 11.5 million ranging from 5.2 % (Brasilia) to 13.5 % (So
(95 % CI 6.213.7 million) Mexican adults are Carlos). The Surveillance of Risk and Protective
affected. Factors for Chronic Diseases Telephone Survey
Several complimentary sources of informa- (VIGITEL, in Portuguese) is a telephone surveil-
tion should be highlighted. The diabetes study of lance system to identify risk and protective fac-
Mexico City is a population-based cohort study tors for noncommunicable chronic diseases in
of subjects from six low-income colonies located subjects aged 18 years or older; through this sys-
within the periphery of the ABC hospital in tem, a trend of increasing prevalence rates for all
Mexico City [36]. The recruitment of adults with- NCCDs has been identified. In 2013, VIGITEL
out T2DM diagnosis started in 1990 reaching reported a prevalence of self-reported T2DM of
1,754 subjects with an average follow-up period 6.9 %. The trend of increasing prevalence has
of 11 years; after the follow-up period, an inci- also been demonstrated for different age groups
dence of 1.42 per 100 person-years for men and as shown in Fig. 7.2, where the prevalence ranges
1.21 per 100 person-years for women was from 8.5 % in the 4554-year group to 17.1 % in
obtained. The resulting incidence was inferior to the 5564-year group and 22.1 % in the groups
those obtained by a similar study undertaken in with 65 years or older. The rates of self-reported
San Antonio, TX, in which an incidence of 2.7 diabetes through VIGITEL have also shown a
Fig. 7.2 Comparison of TRENDS OF T2DM PREVALENCE IN BRAZIL

self-reported T2DM
7.4
prevalence trends from 2006
6.9
6.8
to 2013 in the Brazilian
6.3
6.3
6.2
population as reported by the
5.8
VIGITEL strategy (Adapted
5.5
from Almeida-Pititto et al.)
2006 2007 2008 2009 2010 2011 2012 2013
difference in its distribution: northern Brazil, concentrating in urban areas, along with nutri-
characterized by lower incomes, reports T2DM tional changes and population aging, has contrib-
rates of 3.65.5 %, whereas southern Brazil, with uted to an accumulation of cardiovascular risk
higher incomes, reports rates ranging from 6.7 to factors that have led to a general increase in the
8.2 %. The rates of T2DM have been reported to prevalence of T2DM [3739].
be higher specifically in Japanese Brazilians and
in Native American groups (28 % of Xavantes has T2DM in Central America
T2D). The epidemiologic transition from infectious
Obesity rates in Brazil have similarly been diseases to noncommunicable chronic diseases
escalating across all age groups; serial data from has also changed the epidemiologic landscape
the Household Budget Survey showed that BMI within Central America. The top three countries
>25 kg/m2 have increased from 16 to 50 % in men with the highest prevalence are Nicaragua,
and from 28 to 48 % in women. Likewise, the Guatemala, and El Salvador [40]. The Central
prevalence of BMI >30 kg/m2 has increased from American Diabetes Initiative (CAMDI) 2010 is
8.9 to 12.5 % in men and from 13.1 to 16.9 % in a study by the Pan American Health Organization
women. Other risk factors include physical inac- with the objective to determine the prevalence
tivity and sedentary lifestyle; in Brazil nearly of T2DM and hypertension in people 20 years
41 % of the adult population is not sufficiently or older (n = 10,822) in a sample taken from six
active to achieve health benefits. VIGITEL has Central American populations (urban areas of
reported the prevalence of T2DM risk factors as San Jos, Costa Rica; Santa Tecla, San Salvador,
follows: high frequency of soft drink consump- El Salvador; Villanueva, Guatemala City,
tion (23.3 %), alcohol abuse (16.4 %), cigarette Guatemala; Tegucigalpa, Honduras; Managua,
smoking (11.3 %), and physical inactivity Nicaragua; and the national population of
(33.8 %). The health system provides the full Belize) [41]. Prevalence of previously diag-
range of services for diabetes care and prevention nosed T2DM was similar among males and
but not universally. The federal government cov- females (4.9 vs 5.3 %); the overall prevalence of
ers 5080 % of costs, including basic medicines diagnosed hypertension was higher among
under prescription and testing strips for people women (19.0 %. 95 %-CI = 16.921.4) than
with T1DM. Similar to what has been happening among men (10.9 %, 95 %-CI = 9.612.5).
in other Latin American countries, the epidemio- Overall 5.1 % of participants reported diagnosed
logic transition motivated by populations diabetes while 3.4 % were found to have newly
PREVALENCE OF SELF-REPORTED T2DM IN

CENTRAL AMERICA
10.5 Overall Men Women

7.6
6.9
6.7
6.3
5.8
5.7
5.6
5.3
5.3
5.1
4.9
4.9
4.7
4.6
4.5
4.3
4.2
2.6
2.5
2.5
BELIZE COSTA RICA EL SALVADOR GUATEMALA HONDURAS NICARAGUA TOTAL
Fig. 7.3 Comparative prevalence of the sites studied by Survey of Diabetes, Hypertension and Chronic Disease
CAMDI, comparing the overall prevalence with preva- Risk Factors. Belize, San Jos, San Salvador, Guatemala
lence among men, women, and overall (Adapted from: City, Managua, Tegucigalpa, and Washington, D.C.:
The Central America Diabetes Initiative (CAMDI): PAHO, 2011)
diagnosed diabetes for a total prevalence of T2DM in South America

8.5 %. An additional 18.6 % was reported to After Brazil, the countries with the highest preva-
have prediabetes (IFG and/or IGT). The prevalence are Colombia, Chile, Argentina, and
lence of previously or newly diagnosed diabetes Venezuela. The CARMELA study, conducted in
and prediabetes was comparable in men and seven cities of South America and Mexico, found
women. As shown for all participant sites in no difference in the prevalence between
Fig. 7.3, the prevalence of known and newly Barquisimeto (Venezuela), Bogot (Colombia),
diagnosed T2DM was the lowest in Tegucigalpa Quito (Ecuador), Buenos Aires (Argentina), and
(2.5 % and 2.9 %, respectively); the lowest prev- Santiago (Chile) with a significantly lower preva-
alence of prediabetes was found in Managua lence only for Lima (Peru) [42].
(12.4 %). A population-based, nationwide survey done
In the case of Guatemala for the year 2014, in Peru in 2012 found a T2D prevalence of 7 %
the IDF reports that the prevalence in adults (95 % CI 5.38.7 %). It was estimated that
aged 2079 years was 8.9 % with a total number 763,600 Peruvians may live with diabetes. The
of T2DM cases of 680,000 where nearly 107,500 prevalence of previously diagnosed cases was 4.2
cases are undiagnosed. The number of deaths and 22.4 % for impaired fasting glucose. The
attributable to T2DM in Guatemala during 2014 capital city (Lima) has a higher prevalence com-
was 7,965 implying a cost (both direct and indi- pared to the rest of Peru (8.4 vs 6 %). Peru showed
rect) of 385.4 USD. For Nicaragua in the year a twofold difference in the prevalence of T2DM
2014, the IDF reports a prevalence of T2DM in in the urban population (8.2 %) with respect to
adults aged 2079 years of 10.3 % with a total suburban areas in the mountain and in the
number of T2DM cases of 356,100, where jungle.
98,900 are undiagnosed; the number of deaths In Colombia, several cross-sectional surveys
attributable to T2DM during 2014 in Nicaragua have measured the prevalence of T2D in urban or
was 54.7 with a cost per person with diabetes of rural populations. The highest prevalence
221.3 USD. (8.93 %) was reported in Cartagena in 2006. A
PREVALENCE OF T2DM AND METABOLIC

SYNDROME BY ETHNIC BACKGROUND
T2DM Prevalence Metabolic syndrome prevalence
35.8
34.8
35
31.5
31.2
27.3
21.2
18.3
18.1
18.1
17.1
13.4
10.2
DOMINICAN CENTRAL CUBAN MEXICAN PUERTO SOUTH MIXED/OTHER
AMERICAN RICO AMERICAN
Fig. 7.4 Comparative prevalence of T2DM and metabolic syndrome by Hispanic/Latino background, comparing the
overall prevalence among different ethnic backgrounds (Adapted from: Schneiderman et al. [44])
growing trend in the prevalence of the disease medical care are among the particular challenges
was observed in the time period 20092012 that should be overcome in this group [46]. The
based on the number reported by institutions of prevalence is not homogeneous between
the federal government. The magnitude of the Hispanics in the USA (Fig. 7.4). Additional prob-
increment varies from 26 % (in the Amazonas) to lems are faced when they return to their coun-
153 % in Bogota [43]. Still a low prevalence has tries; it is well recognized that glycemic control
been found in rural communities. deteriorates, but, there is scant data on this topic.
In Argentina, the prevalence of T2D changed More studies are required to understand the inter-
from 8.4 to 9.6 % between 2005 and 2009. These action between genetic and environmental risk
numbers are based on patient self-report and a factors that contribute to the increased prevalence
nationwide survey. Argentina, Venezuela, and within these minority groups and between the
Uruguay have more than 90 % of their population ethnic groups living within their country and
living within urban areas. those living in the USA.
T2DM in Hispanics/Latinos Living

in the USA Gestational Diabetes
The Hispanic/Latino population comprises nearly
16 % of the total US population. They are the eth- The gestational diabetes screening programs
nic group with the highest prevalence of T2D applied in the region are under debate. Universal
(22.6 % (95CI % 18.427.5 % in 2012 NHANES)) screening is the recommended approach in
despite that they are not the group with the big- nearly 80 % of the reviewed guidelines. Although
gest mean body mass index (29.7 kg/m2, 95 % CI settings with weak health systems might struggle
29.230.1) [44, 45]. Also, they are the group in to implement a universal screening approach,
which the proportion of undiagnosed cases is selective screening would risk missing up a large
greater (49 %, 95 % CI 40.857.2 %) and the proportion of cases. Selection would be compli-
achievement of treatment goals is the lowest. cated given the nature of some of the most com-
Isolation, language barriers, and lack of access to mon risk factors used to determine the need for
screening. For example, history of previous those with low Amerindian admixture. Temporal
GDM is likely to be missed. Likewise, ethnicity patterns and interaction with environmental fac-
as a risk factor would qualify all patients in tors were postulated as potential explanations for
African, Asian, and Latin American settings as the changes in incidence rates [48, 49].
high risk.
T1DM in Uruguay
The Uruguayan population is, demographically, a
Type 1 Diabetes mixture of Caucasian (Spain, Italy, France,
Portugal, and Lebanon), Negroid (Congo and
There is a lack of national registries and large Angola), and Amerindian (mainly Charras,
cohort studies in the region. Evidence is derived Minuanes, and Guaranies) groups; during the
mainly from single-center studies. Diagnoses and seventeenth and eighteenth centuries, their
treatment of T1D are limited to reference centers. groups were admixed, making it impossible now-
Ketoacidosis remains as a common initial T1D adays to find native unmixed ethnic groups as
manifestation. A Brazilian registry (20082010) opposed to most Latin American countries.
informed that T1D diagnosis was made based on Interestingly, 92 % of the population in
the presence of ketoacidosis in 42.3 %; this per- Montevideo is of Caucasian origin, representing
centage is greater than that reported in the USA one of the cities with the highest T1DM inci-
(29 %) or in some countries of Europe (<20 %). dence according to the DIAMOND study in Latin
Positive titers of anti-GAD antibodies were found America: 8.3 % (CI95 % 5.411.7) [50].
in 64 % of recently diagnosed Brazilian T1D
patients. There is no information regarding the T1DM in Mexico
number of at-risk individuals (based on the pres- Limited information regarding T1DM in Mexico
ence of positive titers of antibodies and/or an has been published. Data collected in the years
abnormal insulin secretion). 19781992 revealed a low incidence that was
A growing challenge is the differential diag- consistent with the figures issued by the
nosis of new-onset hyperglycemia in pediatric DIAMOND project group. The study was con-
populations. Nearly half of children with diabetes ducted under standardized methodology pro-
are obese and resistant to ketoacidosis and could posed by the WHO in an urban area at Boca del
be treated with oral glucose-lowering agents. Rio, a port located on the Gulf of Mexico in
between 1990 and 1993 [51]. The average inci-
T1DM in Chile dence rate was 1.15/100,000 per year (CI95 %
Between 1980 and 1993, a study conducted in a 0.751.9). These results have positioned Mexico
native aboriginal Mapuche population from Chile as the country with the lowest rates of T1D inci-
showed a very low incidence (0.43/100,000 per dence. Nevertheless, Gmez-Daz et al. [52]
year CI 95 % 00.95) of T1DM in children under recently reported remarkably greater incidence
the age of 14 [47]. These data were significantly rates using as source of documentation the regis-
different from that reported for the Caucasian tries of the Mexican Institute for Social Security
Chilean population in the same study (IMSS, in Spanish), the largest social healthcare
(1.58/100,000 CI 95 % 1.112.04; p < 0.0016). provider within the country. Incidence among
Even though Caucasian heritage came mainly children younger than 19 years of age was calcu-
from Spain, incidence of T1DM in this Chilean lated for a 10-year period (20002010); the num-
subgroup was seven times lower than that ber of new T1DM cases increased from 3.4 to 6.2
reported for Madrid or Catalonia. A significant per 100,000 insured cases during the study. The
increase in incidence was observed in the period highest incidence rate was observed in 2006,
20012004 (5.4 vs 8.33/100,000 inhabitants per with 1,029 new cases within a population of
year, p < 0.04). Higher rates were observed in 11,739,112 (8.8 new cases/100,000 insured pedi-
higher-income strata, urbanized counties, and atric subjects). The age groups with the biggest
increment in number of cases were between the lower-than-expected number of cases among
ages of 1014 years (2.1-fold increase between Mexicans, Blacks, and Oriental populations.
2003 and 2010) and 1519 years (1.9-fold Other comparative ethnic studies include the
increase between 2003 and 2010). This study SEARCH study, the Philadelphia Registry, and
revealed a substantial increasing trend in T1DM the Allegheny and Colorado IDDM studies [55].
incidence in Mexican children less than 19 years.
Even though causative factors such as perinatal
infections, weight gain in the first months of life, Complications of Diabetes
and increased maternal age might be related to in the Region
the outcome, it must be considered that inclusion
criteria were different for both studies. Information regarding diabetes-related chronic
complications is scant in LA. Screening proce-
T1DM in Argentina dures for retinopathy, nephropathy, and foot
Four Argentinean centers were included in the problems are performed without proper system-
DIAMOND project. Avellaneda was the most atization. In the 2012 ENSANUT survey, screen-
representative city of Caucasian population; data ing for albuminuria, retinopathy, and foot
were obtained from a retrospective study con- abnormalities were performed in 34.2 %, 38.6 %,
ducted from 1985 to 1988 (obtained from the and 59.3 % of the T2D cases, respectively, during
national census). In addition a prospective survey the previous year. In the same population-based
was conducted from 1988 to 1994; the primary survey, 14.6 % referred having some degree of
sources were preprimary and primary schools visual problems, 13.4 % had lost sensitivity in at
with secondary sources considering pediatric least one part of their bodies, 9.4 % reported hav-
hospitals, private diabetologists, and pediatri- ing had ulcers in legs or feet, 4.9 % were blind,
cians in Avellaneda, its surroundings, and Buenos 3 % had some amputation, 2.3 % had been diag-
Aires City. An annual incidence rate ranging nosed with a diabetic foot, and 1.2 % were on
from 6.89/100,000 per year (CI95 % 4.389.4) in dialysis [56].
1985 to 7.59/100,000 per year (CI95 % 6.41 T2D is the main cause of premature disability,
8.77) in 1990 was observed [53]. blindness, end-stage renal disease (ESRD), and
nontraumatic amputations as well as one of the
Hispanics Living in the USA ten most frequent cases of hospitalization in
Data regarding T1DM prevalence in Hispanics adults.
living within the USA is scarce. Orchard et al. ESRD is a major cause of premature disability
analyzed the NHANES 19992010 sample and premature mortality in the region. Registries
(n = 59,130). The population-based design of the are available in many LA countries, but in few
survey and the small number of cases limited the instances the contributions of diabetes and hyper-
ability of the authors to provide precise estimates tension (main causes of ESRD in all countries)
of the prevalence. The Hispanic population had are estimated separately [57]. The Latin American
half the prevalence of that reported in Caucasians Dialysis and Renal Transplant Registry, founded
and African Americans. The same conclusion in 1991, collected the available evidence in 2010.
was reached when the Mexican American sub- The ESRD prevalence has increased in the region
jects were analyzed as a separate group [54]. from 119 patients per million in 1991 to 660
The T1DM incidence has been compared in patients per million in 2010. The highest preva-
US samples between groups with different ethnic lence was reported in Puerto Rico (1,355 patients
backgrounds. One of the first studies reporting per million) followed by Mexico, Argentina,
incidence was published in 1985 and was con- Uruguay, and Chile (between 777 and 1,136
ducted in southern California between 1978 and patients per million). The higher incidence rates
1981; the observed incidence rates showed an were reported for Mexico (458 patients per mil-
excess of cases in the Caucasian population and a lion year), Puerto Rico, Argentina, Brazil, and
Chile. The most common alternative to replace 0.92.2 % of the adults older than age 50 were
kidney function is hemodialysis (75 % of treated functionally blind. Diabetic retinopathy was
ESRD cases), but large differences exist between responsible of 19 % of the cases in which the
countries and health systems. The kidney trans- cause was recorded. Other common causes were
plant rate increased from 3.7 to 6.9 patients per age-related macular degeneration (26 %) and
million in the 19912010 period. Among coun- glaucoma (26 %). The contribution of diabetic
tries in which the ESRD cause is registered, the retinopathy varied between countries, being the
contribution of diabetes is the highest in Puerto highest (>30 %) in Argentina, Paraguay, and
Rico (66.8 %) and Mexico (61.8 %). The smallest Colombia. Furtado and coworkers collected the
contributions were found for Cuba (26.2 %) and evidence published until 2012 regarding the
Uruguay (23.2 %). prevalence of diabetic retinopathy in the LA
The ESRD incidence reported for Mexico is region. He found 63 studies from 11 countries.
the highest worldwide. This observation is in However, a large proportion of the reports are
accordance with the increased susceptibility for based in relatively small, biased populations
having microvascular complications found in (studied in reference centers).
Hispanics in the USA. This population has a Prevalence of diabetic retinopathy is higher in
threefold increased risk compared to Caucasians. Mexican Americans than in Caucasians, but this
Furthermore, the disease burden of ESRD in the difference was not statistically significant in the
population with diabetes is remarkably bigger in 20052008 NHANES survey. Despite that,
Mexico compared against reported in the Mexican Americans have a significantly higher
USA. The disability-adjusted life years (DALYs) risk for having blindness as a result of diabetic
rate due to diabetic kidney disease is several retinopathy (odds ratio 3.6 (95 % CI 1.0512.56)).
times greater in Mexico (103.1 vs 880.5 per There is scant information about the incidence of
100,000 inhabitants). The same is true for the diabetic retinopathy. The Mexico City Diabetes
annual change of DALYs rate (2.5 vs 6.5 % in the Study found a 3-year incidence of 23 % in 164
19902013 period) and the years of life lost cases [59].
(YLL) (836.2 vs 42.9 per 100,000 individuals). Lower-limb amputations remain as a major
In contrast, the years lost due to disability (YLD) cause of premature disability in the region.
are greater in the USA (44.3 vs 60.2 per 100,000 Diabetes is the cause of 70 % of nontraumatic
subjects). Thus, the distribution of the disease lower extremity amputations. Despite that,
burden is different between Mexico and the population-based information is scant. In the
USA. While in Mexico the burden is caused Mexican ENSANUT 2012 report, 2 % of the
mainly by premature mortality, premature dis- T2D participants had an amputation and 7.2 %
ability is the main contributor in the USA. had at least one ulcer in the lower limbs in the
There is a lack of information about the inci- past. In Costa Rica, the incidence of lower-
dence of diabetic nephropathy and the prevalence limb amputations was 6.02 per 1,000 patients
of the various stages of the disease using as per year among the population treated by a
source of evidence population-based surveys. social security system (20012007). This rate
The prevalence of diabetic retinopathy was is unacceptably high; it is similar to that
estimated at the LA region in 1999. Sixteen informed in other developing countries (13.7
countries and 7,715 patients participated. Any per 1,000 cases per year) and several times
kind of diabetic retinopathy was found in 42 % higher than that reported in Great Britain (2.8
of the cases; 17 % required immediate treatment. per 1,000 cases per year) and the USA (0.8 per
A large percentage had no previous eye exam 1,000 cases per year). Similar rates have
[58]. Other efforts in the region have use as out- informed in Brazil (4.3 %) and for Mexicans
come the functional loss of vision. Using infor- living in the US/Mexico border. In clinic-based
mation from 15 countries and 55,643 patients cohorts, the percentage of amputee subjects is
(20102013), Limburg and coworkers found that remarkably greater (13 % in a cohort from
Chile). In Mexico, 12 % of the hospital admis- The impact of diabetes in health systems
sions among T2D patients were due to lower- should be assessed following the Global
limb ulcers. Burden of Disease group (GBD) approach. It
Cardiovascular events are the major cause considers not only the contribution of the dis-
of mortality in the T2D population. The contri- ease to total mortality but also YLL (years of
bution of T2D among cases with an acute myo- life lost) and YLD (years of life with disability).
cardial infarction is greater than that found in Individual profiles of each one of the countries
Caucasians. In the RENASICA II registry (the of the region are available at the Web page of the
largest registry of acute coronary syndrome in GBD group (www.healthmetricsandevaluation.
LA, n = 4,555), 42 % of cases had T2D [60]. org). For Mexico, diabetes is the third cause of
This percentage is greater than that found in YLL due to premature death; this parameter
the ACCESS (33 %) and the INTERHEART grew 32 % in the time period 19902013. Also it
(7.2 %) studies. The same conclusion was pro- is the leading cause of DALY (with an incre-
posed by the authors of the REACH study [61] ment of 50 % from 1990 to 2013) and the fourth
(1,816 stable outpatients with established vas- cause of YLDs (with a growth of 102 % in the
cular disease). In this report, the prevalence of same time period).
T2D among cases with coronary artery disease, Brazil T2DM accounts for 5.1 % of disability-
cerebrovascular disease, and peripheral artery adjusted life years, according to the Global
disease was 37.2, 37.5, and 56.8 %, Burden of Disease project; when compared to
respectively. other countries, Brazil showed a higher propor-
Based on T2D patients data from the Mexican tion of life years with disability among total
ENSANUT 2006, Reynoso-Novern and disability-adjusted life years for T2DM. Registry
coworkers estimated that 112 cases per 1,000 data suggests that mortality standardized for age
persons with T2D will suffer at least one isch- and gender in people with diabetes was 57 %
emic coronary event within the next 20 years. In higher than that of the general population. The
the same period, there will be 889,433 new cases Brazilian Study on Diabetes Costs (ESCUDI)
of heart failure, 2,048,996 events of myocardial estimated the costs of diabetes care in the public
infarction, 798,188 stroke events, and 491,236 healthcare system by interviewing 1,000 patients
nontraumatic amputations attributable to and a retrospective analysis of their medical
T2D. The expected mortality rate is 539 per records; data suggests that 70.4 % of patients had
1,000 persons with T2D with an average life at least one microvascular complication, 17 %
expectancy of 10.9 years [62]. had at least one macrovascular complication, and
In less than 30 years (19702000), T2DM 16 % had at least one of both. ESCUDI estimated
moved from the fifteenth to the first position that the direct and indirect costs of T2DM were
among the main causes of death. This remark- 1,144 USD per patient at the primary care level,
able change is multifactorial. The coding sys- reaching 2,810 USD at the tertiary level. T2DM
tem of the death certificates was adjusted to is the fifth cause of death in Brazil. The control of
fully represent the contribution of chronic dis- hypertension, tobacco use, and dyslipidemia in
eases (instead of the attribution of death to the recent years has decreased cardiovascular mor-
final event). Recent data indicated that the mortality in T2DM patients from an 11 % increase in
tality rate for T2DM has progressively the 19962000 period to an 8 % reduction from
increased. In 2013, 89,420 of the 717,357 2000 to 2007.
reported deaths (12.46 %) occurred in T2D In Argentina, the crude diabetes mortality
patients. The diabetes mortality rate was 73.95 increased from 19.6 to 21.3 per 100,000 inhabit-
per 100,000 inhabitants. Mortality rates have ants. It is the seventh cause of death (7,701
had a larger increase for men; the average age deaths per year). The main cause of mortality is
at death was 66.7 years [63]. cardiovascular death. Chronic complications are
common. Among patients with more than In a great proportion of the LA countries,
20 years of exposure, 2.6 % had ESRD, 15.7 % three independent sectors (public, social security,
had an amputation, and 6.9 % were blind. and private) provide health services. The public
Diabetes caused in 2005 1,328,802 DALYs; it is sector covers the population not attended by the
the ninth and 11th cause of YLL for women and two other providers. In many instances, the pub-
men, respectively. lic sector offers a basic package of services that
covers the ambulatory care of the main chronic
disease in primary care units at a low cost or free
Coordination and Delivery of charge. The packages usually include generic
of Diabetes Care Services forms of metformin, sulphonylureas, statins, ace-
tyl salicylic acid, and regular NPH insulin. In
Healthcare systems in Latin America have some countries, materials required for self-
evolved in synchrony with the socioeconomic glucose monitoring are provided. Limited or no
and political system [64]. At the end of the 1980s, access to specialists, certified laboratories, and
several countries in Latin America thrived for a reference centers and the lack of coverage for
reduction in poverty and income inequalities. ESRD or other major complications are common
Despite that, big disparities persist in the region deficiencies in this sector. The social security
and within countries. The gross domestic product sector is financed by a fixed contribution by the
(GDP) per capita varies from close to 4,000 USD employee, employers, and the government. A
(Honduras) to 21,000 USD (Chile). In the pro- large proportion of patients with chronic diseases
cess of those reforms, also, the organization and are treated at primary care units. Although
philosophy of their individual healthcare systems patients may have access to specialized services,
changed. Several Latin American healthcare sys- a major challenge is to avoid delays in giving
tems have implemented or are in the process to access to services. Finally, the private sector
implement healthcare reforms. Brazil, Cuba, and offers prepaid medical plans or independent med-
Costa Rica currently have unified healthcare sys- ical services.
tems with parallel subsystem organizations; other The Pan American Health Organization has
countries introduced a government-financed published several documents to help govern-
insurance scheme and healthcare provision to ments and organizations to improve the quality of
attempt a reduction at care inequalities. Despite diabetes care and to provide services to under-
that, four main barriers should be addressed: (1) served communities [66]. Recommendations are
the structural fragmentation of healthcare sys- based in the chronic care model using a patient-
tems, which reduces efforts of mitigating inequal- centered approach. With their support, several
ities in standards of care throughout the region; pilot studies have been implemented in Mexico
(2) the centralized decision-making processes; [67], Chile, and Bolivia with good results.
(3) the lack of regulation within the healthcare However, their impact has not been enough to
system, especially in terms of the quality of change local practices.
health-related services and quality of drugs in Several health systems have launched initia-
health systems; and (4) high costs and low effi- tives to provide specialized care at a low cost.
ciency. The percentage of the GDP allocated to In Mexico, the health ministry started the
cover health expenditures is below 10 % in the UNEMES program, which is a network of pri-
region (being Brazil the highest (9.7 %) and mary care units operated by a multidisciplinary
Venezuela the lowest (3.6 %)). A detailed analy- team (dietitian, psychologist, internist) that
sis of the health systems of the region is beyond applies a standardized intervention against
the scope of this manuscript. Interested readers T2D and other chronic diseases [68]. Some
may consult reference [65] for additional countries (e.g., Brazil and Mexico) have devel-
information. oped Internet-based monitoring systems of the
interventions (SysHiperDia) and policies large percentage of cases do not receive a sub-
focused in T2D [69]. In addition, reforms in stitutive therapy of renal function. Similar
the health insurance coverage have been imple- numbers have been informed several reports
mented to stimulate the adoption of a healthy from Argentina (reviewed in detail in Gonzalez
lifestyle among T2D patients (e.g., in et al. [73]).
Colombia) or to improve the performance of
health providers (e.g., in Chile) [70]. Some
conditional cash transfer programs have been Non-pharmacological Management
linked to preventive health programs.
The direct and indirect costs of T2D treat- More than 80 % of T2D cases are treated by pri-
ment are remarkable [71, 72]. In the region, the mary care physicians in the public and social
annual cost of diabetes healthcare is between security sectors. In many cases, there are sig-
34.6 and 59.9 billion US dollars; it represents nificant delays in getting an appointment, and
close to 12 % of the total healthcare budget. the time spent in each consultation is too short
This proportion is the same than mean percent- to provide proper care. A major problem of the
age worldwide. The average annual cost per region is lack of access to structured and effica-
person is between 1,169 and 2,027 US dollars, cious treatment programs. Providers are not
which is lower to that reported in the USA and properly trained and do not have stimulus to
Europe (5,3749,641 USD). There are large improve the quality of their services and their
differences in the amount of money spent in knowledge regarding T2D. Clinical inertia is a
diabetes healthcare costs between countries. In major challenge in the region. Many health sys-
2010, the biggest budgets were estimated for tems have dietitians involved in the treatment
Mexico (4,836 million USD) and Brazil (4,296 of T2D cases in primary care units, but, only a
million USD). few have multidisciplinary teams. Access to
In 2010, researchers from the National electronic medical records is limited to some
Institute of Public Health in Mexico calculated social security systems. Referral to an endocri-
that the greater direct costs correspond to med- nologist is usually late and limited to cases with
ications (133,143,734 USD), followed by com- chronic complications. There are not enough
plication costs (110,410,928 USD), consult/ endocrinologists in the region. For example,
diagnosis-related costs (59,734.448 USD), and Mexico has close to 800 endocrinologists that
hospitalization costs (39,937,331 USD). are insufficient to treat the 11.5 million cases.
Indirect costs are mainly due to permanent dis- Despite of the above, the services provided by
ability (409,205,846 USD), followed by costs specialists are underutilized due to lack of
due to premature mortality (19,623,029 USD) awareness of the public, their primary care phy-
and costs due to temporal disability (6,372,059 sicians, and the health systems. In many coun-
USD). Thus, more than half of the cost is due tries, diabetes educators are not included in the
to indirect costs; as a result, conclusions are structure of health services. Certified HbA1c
heavily dependent on the methodology applied measurements are not available for a large pro-
to estimate the indirect costs. Out-of-pocket portion of the primary care clinics. Screening
payments are a major challenge in the region. for chronic complications and other preventive
The average annual cost per person was 3,193 actions (e.g., retinopathy screening) are per-
USD; the cost is bigger for cases with chronic formed at lower than expected rates. Table 7.4
complications (2,749 vs 3550 USD). These shows the percentage of cases in Mexico
numbers may be underestimated. The cost of (nationwide) and Argentina (Qualidiab net-
covering diabetes-related ESRD is not prop- work) in which preventive actions are imple-
erly included in these estimations because a mented. Although the representativeness of
Table 7.4 Implementation of preventive actions against diabetes-related chronic complications in Mexico and
Argentina
Preventive action (percentage, 95 % Mexico 2012 (Ref. Argentina Qualidiab 2006
CI) Mexico 2006 [56]) (Ref. [73])
Four or more medical evaluations per 58.8 (58.559.2) 65.4 (64.966.0)
year
HbA1c testing (at least two times per 3.7 (3.63.8) 7.7 (7.38.2) 40
year)
Blood pressure measurements 50.5 (50.250.8) 67.9 (67.468.3) 99
Plasma lipid measurements 27.3 (27.027.6) 79.2 (78.779.7) 61
Microalbuminuria detection 6.6 (6.56.7) 12.6 (11.913.3) 8
Retinopathy detection 12.3 (12.112.4) 8.6 (8.19.0) 45
Diabetic foot detection 9.4 (9.29.5) 14.7 (14.115.2) 55
Follow a dietary and exercise plan 3.7 3.63.7) 6.8 (6.57.4) 2.3
these reports is different, some deficiencies are population that has access to them is small due
shared. Retinopathy screening and foot exams to limited infrastructure or economic reasons.
are not scheduled as needed despite that patients
have frequent contacts with the medical units.
A very small proportion of patients have Rational Selection of Anti-diabetes
received and implemented a dietary/exercise Medications
plan. These deficiencies could be reverted in a
short period of time by quality assurance pro- Multiple diabetes guidelines are available in the
grams and training of the health providers. region. Every country has legal documents that
Some countries have organized support net- regulate local practices. In addition, most national
works coordinated by patients and health profes- diabetes societies have position documents,
sionals. In addition, educational Web pages and which contain the opinions of the local experts.
24-h phone lines are available. However, some of Furthermore, the Latin American Diabetes
these efforts are mainly focused in providing Association (ALAD) published a set of evidence-
information rather than modifying behaviors. based guidelines that take in consideration the
Their impact at community level has not been existing information and local resources. Also,
measured in a systematic manner. Telemedicine the most frequently cited international guidelines
is available in some countries to provide services are widely disseminated among primary care
to communities with limited access. It includes physicians. Despite of the above, a large propor-
medical consultation and screening for some tion of them do not have an in-depth knowledge
chronic complications (e.g., diabetic retinopathy, of any of these documents.
diabetic foot). In some countries (i.e., Argentina) More than 80 % of patients receive pharmaco-
legislation has been modified to give the right to logic treatment for hyperglycemia control. It is
patients to have continuous access to insulin and based mainly in oral glucose-lowering drugs
glucose strips. (generally metformin with or without sulphonyl-
Inequality is a major challenge of the region. ureas). The most recently introduced drugs
Diabetes care is not an exemption. Despite of (DPP-IV inhibitors, SGLT2 inhibitors, GLP1
the above, there are highly qualified reference agonists) are available in the Latin American
centers that provide state-of-the-art care of markets, but, not in the majority of the public or
their patients in the majority of the countries of social security systems. The proportion of
the LA region. However, the percentage of the insulin-treated patients (620 %) [74, 75] is
below the international standards (3050 %). (NPH + regular insulin), administered in two
Insulin is usually administered as a single bed- daily injections; only 9 % received three daily
time dose in combination with oral agents. Insulin insulin injections.
analogs are available in some social security sys- The lack of effectiveness of the diabetes man-
tems. There is no information regarding the pat- agement programs is a multifactorial phenome-
tern of use of insulin based on nationwide surveys non. Explanations are classified as related to the
or registries. In addition, close to 10 % of cases healthcare provider, the service organization, and
are treated with herbal medicine. the patient. Clinical inertia, the lack of decision-
As a result, the achievement of the treatment making tools, and the absence of competence-
goals is lower to that reported in other regions. based training programs are the most common
For example, in the 2012 Mexican ENSANUT barriers for the healthcare provider. With respect
survey, only 25 % of the patients had an HbA1c to the healthcare system, obstacles include atten-
below 7 % despite that the vast majority of them tion processes designed to treat acute conditions,
have more than two medical visits per year and insufficient access to multidisciplinary teams,
were treated with oral agents. Still, 50 % of and other basic services and overcrowded facili-
patients had an A1c above 9 %. According to the ties. Depression, alcoholism, physical limita-
Qualidiab network, 57 % of T2D cases have tions, economic problems, and lack of awareness
fasting plasma glucose above 140 mg/dl in and knowledge of the disease are the most com-
South America [76]. In Brazil, a nationwide mon barriers among patients.
cross-sectional study evaluating 5,750 T2DM
patients in between 2006 and 2011 found mean
HbA1c levels of 8.6 2.2 %, with a median of Translating Primary Prevention
8.1 % where only 48.5 % of patients had HbA1c of Type 2 Diabetes
levels <8 %.
Treatment of comorbidities share the same The region has undergone rapid socioeconomic
problems than that mentioned for the manage- changes moving from a predominantly rural soci-
ment of hyperglycemia. Statins or antiplatelet ety to a westernized lifestyle in less than half a
agents are prescribed in a lower than expected century. Migratory movements to urban centers
percentage of cases. In Mexico, according to the and to the more developed countries exist in a
ATP-III guidelines, 71 % of T2D patients qualify large proportion of the LA countries [79]. As a
for statin therapy; in contrast, less than 10 % of result, dramatic shifts in food availability, food
the cases were treated and controlled at the preferences, and physical activity have happened.
moment of the survey. In addition, nearly 50 % of LA countries, especially Mexico, are among the
T2D cases had high blood pressure; less than biggest consumers of soft drinks and caloric-
10 % are treated and controlled. Similar rates dense processed food. The proportion of the
have been found in Colombia. A large proportion Mexican adult population who does not meet the
of the hypertensive or dyslipidemic cases receive minimum WHO-advised physical activity has
drug therapy, but only a few achieve treatment increased by 6 % between 2006 and 2012. Only
targets. The achievement of treatment goals is 28.8 % of Mexican adults had more than 150 min
below to that reported in the USA [77, 78]. per week of moderate-intensity physical activity.
The Qualidiab network analyzed the efficacy As a result, the adoption of a healthy lifestyle for
of T1D treatment in patients living in several cit- at-risk subjects and T2D cases is a challenging
ies of Argentina and South America. A quarter of process. A growing trend in the region is to
them had a blood glucose level of <80 mg/dl, and reduce the duration of the lactation period due to
41 % had a glucose value >140 mg/dl. Only one- lack of adequate facilities at the work places. As
quarter of the patients could play an active, effec- a result, women do not return to the preconcep-
tive role in DM control and treatment. Half of tion weight leading to an increased risk for hav-
them were treated with a mixed dose of insulin ing T2D. In addition, there is a lack of
T2D-preventive programs applicable for women 10-year period. For Brazil, the estimated cost of
with gestational diabetes. Finally, air pollution the integrated package of preventive actions is
and exposure to several environmental contami- 0.4 USD per year per capita per DALY. However,
nants (e.g., arsenic, lead) are highly prevalent in the individual cost of each public policy is
some areas of the region. These are known risk remarkably different and varies between coun-
factors for having T2D. Each one of these risk tries. A health in all policies approach and a
factors is a target for intervention to prevent coordinating body at the highest social and gov-
chronic diseases. ernmental level are critical to assure the success
Several countries have enforced action plans of the prevention plans.
to mitigate the impact of diabetes. The Pan National and regional (Asociacin
American Health Organization proposed a set of Latinoamricana de Diabetes) nongovernmental
potential actions for the region in accordance associations are active stakeholders in the region
with the recommendations by the World Health [85]. Several academic bodies have published
Organization. Taxes for sugary beverages and pro-action documents; some include critical anal-
caloric-dense industrialized products [80], mass yses of the current approaches and alternative
media campaigns, school-based interventions proposals [86].
[81], various forms of food labeling [82], work-
site interventions, food advertising regulation,
changes in urban settings, and public transporta- Organizing and Conducting
tion [83] are some examples. In some countries Diabetes Research in the Region
(e.g., Mexico, Brazil, Argentina, Guatemala, and
others), these proposals have become public poli- The remarkable impact of diabetes in the region
cies, and they have been integrated in a national has raised the attention of several international
plan against chronic diseases [84]. Still, no suffi- and regional agencies. For example, The
cient evidence has been published to assess the European-Latin American and the Caribbean
impact of these interventions. A PAHO group Health (EU-LAC Health) consortia, funded by
published the estimated impact based on a the European Union, have sponsored calls for
simulation model (the chronic disease prevention projects to develop low-threshold interventions
model) for Brazil, Mexico, and Canada. At the to tackle diabetes and other chronic diseases [87].
individual level, intervention should increase the The Global Alliance for Chronic Diseases, a net-
consumption of fruits and vegetables, decrease work funded by several countries, facilitates the
the fat intake, raise the time devoted to physical interaction between LA researchers and groups
activity, and decrease the mean body mass index, from developed countries to design and validate
cholesterol, and systolic blood pressure of the high-impact interventions in developing coun-
population. According to them, fiscal measures tries [88]. Some national funding agencies (i.e.,
are the public policy with the biggest impact CONACYT) have funded problem-specific calls
(nearly 80,000 life years gained per year). Mass to tackle diabetes-related issues. Although these
media campaigns and school-based interventions efforts are remarkable, an integrated approach is
resulted in half of the effect estimated for taxa- needed to have a significant impact in the short
tion. In Mexico, primary care counseling was the term.
most effective intervention to modify the number Several regional initiatives should be high-
of disability-adjusted life years (DALYs) in the lighted. The CARMEN network addresses health
middle term. Some of these policies may take determinants and health equity [89]. Their prod-
two decades or more to have a significant impact ucts include implementation and evaluation of
on DALYs. The intervention that requires more public policies, social mobilization, community-
time to become cost-effective is the school-based based interventions, epidemiological surveil-
lifestyle modification. The authors assume that lance of risk conditions, and preventive healthcare
the implementation cost will be recovered in a services. The Slim Initiative in Genomic
Medicine for the Americas (SIGMA) Type 2 Research is a critical component to plan and
Diabetes Consortium, a collaboration between implement policies against diabetes. Still, there
the Broad Institute, the University of Southern are several LA countries in which population-
California, and several Mexican institutions based, nationwide epidemiological information
funded by a private source, has identified ethnic- is not available. In addition, there is scant or no
specific risk variants that explain a large propor- information in the region regarding the preva-
tion of the genetic susceptibility for having T2D lence of T2D in pediatric or unserved populations
of the Amerindian communities [16]. Finally, (e.g., Native Americans or migrants). Additional
FunPrecal is a collaborative network between studies are needed about the epidemiology of
several countries of the region with Finnish and gestational diabetes, prediabetes, monogenic dia-
US centers to validate preventive and therapeutic betes, and the majority of chronic complications.
interventions [90]. No incidence data exists in the majority of coun-
Innovation is a common requirement in the tries for many of the diabetes-related outcomes.
call for proposals published in the region. As a National registries and translational research are
result, a growing number of groups are working at an early stage in the region. Few papers had
on nanotechnology, new multidisciplinary informed the use of services or the development
patient-centered treatment schemes [91], tele- of diabetes-related economic models.
medicine, cell-phone-based interventions or new Despite of the above, there are unique research
diagnostic devices, or population-specific prog- opportunities for the study of diabetes in Latin
nostic tests. America. The region has peculiarities that may
be used to generate new local and global knowl-
edge to the field. For example, the ethnic compo-
Future Directions: Unmet Needs, sition of many countries of the region contains a
Unanswered Questions, large proportion of Amerindian heritage, a group
and Unquestioned Answers that has not been sufficiently represented in the
genetic consortia. In addition, the study of the
In summary, three major challenges exist in the interaction between infectious diseases with dia-
region to mitigate the impact of T2D. First, a betes may offer new insights about the effects of
large proportion of the population has preceding diabetes-related abnormalities on the immune
conditions that increase their risk in the midterm. response. Environmental phenomena linked to
Second, half of the patients are undiagnosed, pre- T2D (e.g., migration, exposure to pollutants or
cluding the implementation of preventive actions caloric dense foods and beverages) are rapidly
against chronic complications. Third, the effec- evolving in the region. Public policies against
tiveness of the treatment programs is below the T2D could be tested in a shorter period of time
international standards, resulting in high expen- than in other areas due to the large number of
ditures without changing the rates of premature diabetes-related outcomes occurring in LA.
disability and mortality. The number of prevent- Actions to control the T2D outbreak in LA
able hospital admissions and deaths could be should come from the whole society. Although it
greatly diminished by the implementation of is critical to have the support of the authorities at
nationwide quality assurance programs. Budget the highest level, it is unlikely that governmental
allocation should be based on economic models plans could be sufficient to mitigate the health
and cost-effective interventions. Incentive pro- and economic consequences of the disease.
grams may be helpful to increase productivity Academic institutions, NGOs, and social leaders
and quality of services; those programs should be are crucial for keeping T2D among the top health
adapted to the local culture and needs in order to priorities. Also, they introduce the innovation and
create win-win relationships. A detailed analysis the scientific background of the action plans.
of the potential solutions is beyond the scope of Everybody could contribute. At the end, preven-
this manuscript; interested readers should consult tion and treatment of T2D heavily depend on per-
references [70, 86, 92]. sonal choices that determine peoples lifestyle.
References 11. Chan JCN, Gagliardino JJ, Baik SH, Chantelot J-M,
Ferreira SRG, Hancu N, et al. Multifaceted determi-
nants for achieving glycemic control: the International
1. Saad PM. Demographic trends in Latin America and
Diabetes Management Practice Study (IDMPS).
the Caribbean. In: CEPAL 2010. http://www.cepal.
Diabetes Care. 2009;32:22733.
org/celade/noticias/documentosdetrabajo/6/48786/
12. Collado-Mesa F, Barcel A, Arheart KL, Messiah
Demographic_Trends_in_LAC_PAULO_SAAD_
SE. An ecological analysis of childhood-onset type 1
ED_12_7_09.pdf. Accessed 26 Sept 2015.
diabetes incidence and prevalence in Latin America.
2. Danaei G, Finucane MM, Lu Y, Singh GM, Cowan
Rev Panam Salud Publica. 2004;15(6):38894.
MJ, Paciorek CJ, Lin JK, Farzadfar F, Khang YH,
13. Karvonen M, Viik-Kajander M, Moltchanova E,
Stevens GA, Rao M, Ali MK, Riley LM, Robinson
Libman I, LaPorte R, Tuomilehto J, Diabetes
CA, Ezzati M, Global Burden of Metabolic Risk
Mondiale (DIAMOND) Project Group. Incidence of
Factors of Chronic Diseases Collaborating Group
childhood type 1 diabetes worldwide. Diabetes Care.
(Blood Glucose). National, regional, and global trends
2000;23(10):151626.
in fasting plasma glucose and diabetes prevalence
14. Stanescu DE, Lord K, Lipman T. The epidemiology
since 1980: systematic analysis of health examination
of type 1 diabetes in children. Endocrinol Metab Clin
surveys and epidemiological studies with 370
N Am. 2012;41(4):67994.
country-years and 27 million participants. Lancet.
15. The DIAMOND Project Group. Incidence and trends
2011;378:3140.
of childhood type 1 diabetes worldwide 19901999.
3. Food and Agriculture Organization of the United
Diabet Med. 2006;23(8):85766.
Nations. The state of food and agriculture 2013. In:
16. The SIGMA Type 2 Diabetes Consortium. Sequence
FAO 2013. http://www.fao.org/docrep/018/i3300e/
variants in SLC16A11 are a common risk factor for
i3300e.pdf. Accessed 25 Sept 2015.
type 2 diabetes in Mexico. Nature. 2014;506:97101.
4. Aguilar-Salinas CA, Rojas R, Gmez-Prez FJ,
17. The SIGMA Type 2 Diabetes Consortium. Association
Garca E, Valles V, Ros-Torres JM, et al. Early
of a low-frequency variant in HNF1A with type 2 dia-
onset type 2 diabetes in a Mexican, population-
betes in a Latino population. JAMA.
based, nation-wide survey. Am J Med.
2014;311(22):230514.
2002;113:56974.
18. Lorenzi M, Cagliero E, Schmidt NJ. Racial differ-
5. Del Brutto OH, Mera RM, Atahualpa Project
ences in incidence of juvenile-onset type 1 diabetes:
Investigators. Indices of abdominal obesity may be
epidemiologic studies in Southern California.
better than the BMI to discriminate Latin American
Diabetologia. 1985;28(10):7348.
natives/mestizos with a poor cardiovascular status.
19. Vehik K, Hamman R, Lezotte D, Norris JM,
Diabetes Metab Syndr. 2014;8(2):1158.
Klingensmith G, Bloch C, Rewers M, Dabelea
6. Rojas R, Aguilar-Salinas CA, Jimenez A, Shamah T,
D. Increasing incidence of type 1 diabetes in 017
Rauda J, Avila-Burgos L, Villalpando S, Lazcano
year-old Colorado youth. Diabetes Care.
Ponce E. Metabolic syndrome in mexican adults.
2007;30(3):5039.
Results from the national health and nutrition survey
20. Pettitt DJ, Talton J, Dabelea D, Divers J, Imperatore
2006. Salud Publica Mex. 2010;52(supl1):S118.
G, Lawrence JM, Liese AD, Linder B, Mayer-Davis
7. Gagliardino JJ, de la Hera M, Siri F. Evaluation of the
EJ, Pihoker C, Saydah SH, Standiford DA, Hamman
quality of care for diabetic patients in Latin America.
RF, SEARCH for Diabetes in Youth Study Group.
Rev Panam Salud Publica. 2001;10(5):30917.
Prevalence of diabetes mellitus in U.S. youth in 2009:
8. Aguilar-Salinas CA, Velazquez Monroy O, Gmez-
the SEARCH for diabetes in youth study. Diabetes
Prez FJ, Gonzalez Chvez A, Lara Esqueda A,
Care. 2014;37:4028.
Molina Cuevas V, Rull-Rodrigo J, Tapia Conyer R,
21. Aschner P. Diabetes trends in Latin America. Diabetes
ENSA 2000 Group. Characteristics of the patients
Metab Res Rev. 2002;18 Suppl 3:S2731.
with type 2 diabetes in Mxico: results from a large
22. Atun R, Odorico-Monteiro de Andrade L, Almeida G,
population-based, nation-wide survey. Diabetes Care.
Cotlear D, Dmytraczenko T, Frenz P, Garcia P,
2003;26:20216.
Gmez-Dants O, Knaul F, Muntaner C, Braga de
9. Mehta R, Del Moral ME, Aguilar Salinas
Paula J, Rgoli F, Castell-Florit P, Wagstaf A. Health-
CA. Epidemiologia de la diabetes en el anciano. Rev
system reform and universal health coverage in Latin
Invest Clin. 2010;62:30511.
America. Lancet. 2015;385:123047.
10. Delgado-Snchez G, Garca-Garca L, Castellanos-
23. Whiting D, Guariguata L, Weil C. IDF diabetes atlas:
Joya M, Cruz-Hervert P, Ferreyra-Reyes L, Ferreira-
global estimates of the prevalence of diabetes for
Guerrero E, Hernndez A, Ortega-Baeza VM,
2011 and 2030. Diabetes Res Clin Pract.
Montero-Campos R, Sulca JA, Martnez-Olivares
2011;94:31121.
ML, Mongua-Rodrguez N, Baez-Saldaa R,
24. Wild S, Roglic G, Green A, Sicree R, King H. Global
Gonzlez-Roldn JF, Lpez-Gatell H, Ponce-de-
prevalence of diabetes: estimates for the year 2000
Len A, Sifuentes-Osornio J, Jimnez-Corona
and projections for 2030. Diabetes Care.
ME. Association of pulmonary tuberculosis and dia-
2004;27:104753.
betes in Mexico: analysis of the national tuberculo-
25. International Diabetes Federation. South and Central
sis registry 20002012. PLoS One.
America Region. In: IDF Atlas. 2015. http://www.idf.
2015;10(6):e0129312.
org/regions/south-central-america. Accessed 12 Dec 38. Mendes ABV, Fittipaldi JAS, Neves RCS, et al.
2015. Prevalence and correlates of inadequate glycemic
26. Barcelo A, Rajpathak S. Incidence and prevalence of control: results from nationwide survey in 6,671
diabetes mellitus in the Americas. Pan Am J Publ adults with diabetes in Brazil. Acta Diabetol.
Health. 2001;10(5):3008. 2010;47:13745.
27. ALAD Guidelines 2013. In: ALAD Latinoamerica. 39. Viana LV, Leito CB, Kramer CK, et al. Poor glycae-
2013. http://www.alad-latinoamerica.org. Accessed mic control in Brazilian patients with type 2 diabetes
26 Sept 2015. attending the public healthcare system: a cross-
28. Serrano R, Garca-Soidn FJ, Daz-Redondo A, sectional study. BMJ Open. 2013;3:e003336.
Artola S, Franch J, Dez J, et al. Estudio de cohortes 40. Aschner P, Aguilar-Salinas CA, Aguirre L, Franco L,
en atencin primaria sobre la evolucin de sujetos con Gagliardino JJ, Seclen S, Vinocour M, on behalf of
prediabetes (PREDAPS). Fundamentos y the IDF Diabetes Atlas. Diabetes in South and Central
metodologa. Rev Esp Salud Publica. America: an update. Diabetes Res Clin Pract.
2013;87:12135. 2014;103:23843.
29. Seclen SN, Rosas ME, Arias AJ, et al. Prevalence of 41. The Central America Diabetes Initiative (CAMDI):
diabetes and impaired fasting glucose in Peru: report survey of diabetes, hypertension and chronic disease
from PERUDIAB, a national urban population based risk factors. Belize, San Jos, San Salvador, Guatemala
longitudinal study. BMJ Open Diabetes Res Care. City, Managua and Tegucigalpa PAHO. 2011. http://
2015;3:e000110. doi:10.1136/bmjdrc-2015-000110. w w w . p a h o . o r g / h q / i n d e x .
30. Nucci LB, Toscano CM, Maia ALM, Fonseca CD, php?gid=16710&option=com_docman&task=doc_
Britto MMB, Duncan BB, Schmidt MI, Brazilian view. Accessed 12 Oct 2015.
National Campaign for Diabetes Mellitus Detection 42. Schargrodsky H, Hernndez-Hernndez R,
Working Group. A nationwide population screening Champagne BM, Silva H, Vinueza R, Silva Ayaguer
program for diabetes in Brazil. Rev Panam Salud LC, Touboul PJ, Boissonnet CP, Escobedo J, Pellegrini
Publica. 2004;16(5):3207. F, Macchia A, Wilson E, CARMELA Study
31. Gonzlez-Villalpando C, Dvila-Cervantes CA, Investigators. CARMELA: assessment of cardiovas-
Zamora-Macorra M, Trejo-Valdivia B, Gonzlez- cular risk in seven Latin American cities. Am J Med.
Villalpando ME. Risk factors associated to diabetes in 2008;121(1):5865.
Mexican population and phenotype of the individuals 43. Aschner P. Edemiologia de la diabetes en Colombia.
who will convert to diabetes. Salud Publica Mex. Av Diabetol. 2010;26:95100.
2014;56:31722. 44. Schneiderman N, Llabre M, Cowie CC, Barnhart J,
32. Meza R, Barrientos-Gutierrez T, Rojas-Martinez R, Carnethon M, Gallo LC, Giachello AL, Heiss G,
Reynoso-Novern N, Palacio-Mejia LS, Lazcano- Kaplan RC, LaVange LM, Teng Y, Villa-Caballero
Ponce E, Hernndez-vila M. Burden of type 2 dia- L, Avils-Santa ML. Prevalence of diabetes among
betes in Mexico: past, current and future prevalence Hispanics/Latinos from diverse backgrounds:
and incidence rates. Prev Med. 2015;81:44550. the Hispanic Community Health Study/Study of
33. Olaiz-Fernndez G, Rojas R, Aguilar-Salinas C, Latinos (HCHS/SOL). Diabetes Care.
Rauda J, Villalpando S. Diabetes mellitus in Mexican 2014;37(8):22339.
adults: results from the 2000 National Health Survey. 45. Heiss G, Snyder ML, Teng Y, Schneiderman N,
Salud Publica Mex. 2007;49:3317. Llabre MM, Cowie C, Carnethon M, Kaplan R,
34. Villalpando S, Rojas R, Shamah-Levy T, Avila MA, Giachello A, Gallo L, Loehr L, Avils-Santa
Gaona B, De la Cruz V, et al. Prevalence and distribu- L. Prevalence of metabolic syndrome among
tion of type 2 diabetes mellitus in Mexican adult pop- Hispanics/Latinos of diverse background: the
ulation. A probabilistic survey. Salud Publica Mex. Hispanic Community Health Study/Study of Latinos.
2010;52 Suppl 1:S1926. Diabetes Care. 2014;37(8):23919.
35. Gutierrez JP, Dommarco J, Shamah T, Villalpando S, 46. Cusi K, Ocampo GL. Unmet needs in Hispanic/Latino
Franco A, Cuevas L, Romero M, Hernndez patients with type 2 diabetes mellitus. Am J Med.
M. Encuesta Nacional de Salud y Nutricin 2012. 2011;124 Suppl 10:S29.
Resultados Nacionales. In: Instituto Nacional de 47. Carrasco E, Prez-Bravo F, Dorman J, Mondragn A,
Salud Pblica. 2012. http://ensanut.insp.mx/informes/ Santos JL. Increasing incidence of type 1 diabetes in a
ENSANUT2012ResultadosNacionales.pdf. Accessed population from Santiago of Chile: trends in a period
11 Oct 2015. of 18 years (19862003). Diabetes Metab Res Rev.
36. Burke JP, Williams K, Haffner SM, Villalpando CG, 2006;22(1):347.
Stern MP. Elevated incidence of type 2 diabetes in San 48. Carrasco E, ngel B, Codner E, Garca D, Ugarte F,
Antonio, Texas, compared with that of Mexico City. Bruzzone ME, Prez F. Type 1 diabetes mellitus inci-
Mex Diabetes Care. 2001;24(9):15738. dence in Santiago, Chile. Analysis by counties in the
37. Almeida-Pititto, Loureno Dias M, Franco de Moraes period 20002004. Rev Med Chile.
A, Ferreira A, Reis-Franco D, Goldberg-Eliaschewitz 2006;134(10):125864.
F. Type 2 diabetes in Brazil: epidemiology and man- 49. Gonzlez RN, Torres-Avils F, Carrasco E, Salas F,
agement. Diabetes Metab Syndr Obes Targets Ther. Prez F. Association of the incidence of type 1 diabe-
2015;8:1728. tes mellitus with environmental factors in Chile
during the period 20002007. Rev Med Chile. American population: the REACH registry. Clin
2013;141(5):595601. Cardiol. 2012;35(8):4517.
50. Mimbacas A, Prez-Bravo F, Hidalgo PC, Javiel G, 62. Reynoso-Novern N, Mehta R, Almeda-Valdes P,
Pisciottano C, Grignola R, Jorge AM, Gallino JP, Rojas-Martinez R, Villalpando S, Hernndez-vila M,
Gasagoite J, Cardoso H. Association between diabe- Aguilar-Salinas CA. Estimated incidence of cardiovas-
tes type 1 and DQB1 alleles in a case control study cular complications related to type 2 diabetes in Mexico
conducted in Montevideo. Uruguay Genet Mol Res. using the UKPDS outcome model and a population-
2003;2(1):2935. based survey. Cardiovasc Diabetol. 2011;10(1):1.
51. Aude Rueda O, Libman IM, Altamirano N, Robles C, 63. Barquera S, Campos-Nonato I, Aguilar-Salinas C,
LaPorte RE. Low incidence of IDDM in children of Lopez-Ridaura R, Arredondo A, Rivera-Dommarco
Veracruz-Boca del Rio, Veracruz. Diabetes Care. J. Diabetes in Mexico: cost and management of diabe-
1998;21(8):13723. tes and its complications and challenges for health
52. Gmez-Daz RA, Prez-Prez G, Hernndez-Cuesta policy. Glob Health. 2013;9:3.
IT, Rodrguez-Garca Jdel C, Guerrero-Lpez R, 64. Strengthening health systems: the role and promise of
Aguilar-Salinas CA, Wacher NH. Incidence of type 1 policy and systems research. Geneva, Alliance for
diabetes in Mexico: data from an institutional register Health Policy and Systems Research, 2004. Available
20002010. Diabetes Care. 2012;35(11):e77. at: http://www.who.int/alliance-hpsr/resources/
53. Sereday M, Mart M, Damiano M, Moser Strengthening_complet.pdf.
M. Establishment of a registry and incidence of 65. Atun R, de Andrade LO, Almeida G, Cotlear D,
IDDM in Avellaneda, Argentina. Diabetes Care. Dmytraczenko T, Frenz P, Garcia P, Gmez-Dants O,
1994;17(9):10225. Knaul FM, Muntaner C, de Paula JB, Rgoli F, Serrate
54. Menke A, Orchard TJ, Imperatore G, Bullard KM, PC, Wagstaff A. Health-system reform and universal
Mayer-Davis E, Cowie CC. The prevalence of type 1 health coverage in Latin America. Lancet.
diabetes in the United States. Epidemiology. 2015;385(9974):123047.
2013;24(5):7734. 66. Barcelo A, Luciani S, Agurto I, Orduez P, Tasca R,
55. Orchard TJ, Secrest AM, Miller GR, Costacou T. In Sued O. Improving chronic illness care through inte-
the absence of renal disease, 20 year mortality risk in grated health services delivery networks. Washington,
type 1 diabetes is comparable to that of the general DC: PAHO HQ Library; 2012. PAHO.
population: a report from the Pittsburgh epidemiology 67. Barcel A, Cafiero E, de Boer M, Mesa AE, Lopez
of diabetes complications study. Diabetologia. MG, Jimnez RA, Esqueda AL, Martinez JA, Holguin
2012;53(11):23129. EM, Meiners M, Bonfil GM, Ramirez SN, Flores EP,
56. Flores-Hernndez S, Saturno-Hernndez PJ, Reyes- Robles S. Using collaborative learning to improve
Morales H, Barrientos-Gutirrez T, Villalpando S, diabetes care and outcomes: the VIDA project. Prim
Hernndez-vila M. Quality of diabetes care: the Care Diabetes. 2010;4(3):14553.
challenges of an increasing epidemic in Mexico. 68. Crdova-Villalobos JA, Barriguete-Melndez JA,
Results from two national health surveys (2006 and Lara-Esqueda A, Barquera S, Rosas-Peralta M,
2012). PLoS One. 2015;10(7):e0133958. Hernndez-Avila M, de Len-May ME, Aguilar-
57. Machado-Alba JE, Moncada-Escobar JC, Gaviria Salinas CA. Chronic non-communicable diseases in
H. Quality and effectiveness of diabetes care for a Mexico: epidemiologic synopsis and integral pre-
group of patients in Colombia. Rev Panam Salud vention. Salud Publica Mex. 2008;50(5):41927.
Publica. 2009;26(6):52935. 69. http://www.oment.uanl.mx. Accessed Nov 16 2015.
58. Villena JE, Yoshiyama CA, Snchez JE, Hilario NL, 70. Glassman A, Gaziano TA, Bouillon Buendia CP,
Merin LM. Prevalence of diabetic retinopathy in Guanais de Aguiar FC. Confronting the chronic dis-
Peruvian patients with type 2 diabetes: results of a ease burden in Latin America and the Caribbean.
hospital-based retinal telescreening program. Rev Health Aff (Millwood). 2010;29(12):21428.
Panam Salud Publica. 2011;30(5):40814. 71. Arredondo A, De Icaza E. The cost of diabetes in
59. Gonzlez-Villalpando C, Gonzlez-Villalpando ME, Latin America: evidence from Mexico. Value Health.
Rivera Martnez D, Stern MP. Incidence and pro- 2011;14(5 Suppl 1):S858.
gression of diabetic retinopathy in low income popu- 72. Seuring T, Archangelidi O, Suhrcke M. The economic
lation of Mexico City. Rev Invest Clin. costs of type 2 diabetes: a global systematic review.
1999;51(3):14150. Pharmacoeconomics. 2015;33(8):81131.
60. Jurez-Herrera , Jerjes-Snchez C. Risk factors, 73. Gonzalez L, Caporale JE, Elgart JF, Gagliardino
therapeutic approaches, and in-hospital outcomes in JJ. The burden of diabetes in Argentina. Glob J Health
Mexicans with ST-elevation acute myocardial infarc- Sci. 2014;7(3):12433.
tion: the RENASICA II multicenter registry. Clin 74. Lopez Stewart G, Tambascia M, Rosas Guzmn J,
Cardiol. 2013;36(5):2418. Etchegoyen F, Ortega Carrin J, Artemenko S. Control
61. Cant-Brito C, Chiquete E, Ruiz-Sandoval JL, of type 2 diabetes mellitus among general practitio-
Gaxiola E, Albuquerque DC, Corbaln R, Ramos A, ners in nine countries of Latin America. Rev Panam
Bhatt DL, Steg PG, REACH Latin America Salud Publica. 2007;22(1):1220.
Collaborative Group. Atherothrombotic disease, tra- 75. Legetic B, Cecchini M. Applying modeling to
ditional risk factors, and 4-year mortality in a Latin improve health and economic policy decisions in the
Americas: the case of noncommunicable diseases. characteristics in a community based pediatric weight
Washington, DC: PAHO; 2015. control intervention. Int J Behav Nutr Phys Act.
76. Commendatore V, Dieuzeide G, Faingold C, Fuente 2014;11:17.
G, Lujan D, Aschner P, Lapertosa S, Villena J, Elgart 82. Hamlin R. Front of pack nutrition labelling, nutrition,
J, Gagliardino JJ, DIFAR Academic Committee. quality and consumer choices. Curr Nutr Rep.
Registry of people with diabetes in three Latin 2015;4:3239.
American countries: a suitable approach to evaluate 83. Becerra JM, Reis RS, Frank LD, et al. Transport and
the quality of health care provided to people with type health: a look at three Latin American cities. Cad
2 diabetes. Int J Clin Pract. 2013;67(12):12616. Saude Publica. 2013;29(4):65466.
77. Gakidou E, Mallinger L, Abbott-Klafter J, Guerrero 84. Available at http://www.salud.gob.mx. Accesssed 16
R, Villalpando S, Ridaura RL, Aekplakorn W, Nov 2015.
Naghavi M, Lim S, Lozano R, Murray CJ. Management 85. Available at http://www.alad-latinoamerica.org.
of diabetes and associated cardiovascular risk factors 86. Available at http://www.anmm.org.mx/publicaciones/
in seven countries: a comparison of data from national CAnivANM150/L15-Acciones-para-enfrentar-a-la-
health examination surveys. Bull World Health Organ. diabetes.pdf.
2011;89(3):17283. 87. Available at http://www.eulachealth.eu/es/.
78. Mendivil CO, Mrquez-Rodrguez E, Angel ID, Paz 88. Available at http://www.gacd.org.
G, Rodrguez C, Almada J, Szyskowsky 89. Available at http://www.paho.org/carmen.
O. Comparative effectiveness of vildagliptin in com- 90. Available at: https://funprecal.wordpress.com.
bination with other oral anti-diabetes agents in usual- 91. Hernandez-Jimenez S, Garcia-Ulloa C, Mehta R,
care conditions: the EDGE-Latin America study. Curr Aguilar-Salinas CA, Kershenobich-Stalnikowitz
Med Res Opin. 2014;30(9):176976. D. Innovative models for the empowerment of patients
79. Reich D, Patterson N, Campbell D, Tandon A, with type 2 diabetes: the CAIPaDi program. Recent
Mazieres S, Ray N, Parra MV, Rojas W, Duque C, Pat Endocr Metab Immune Drug Discov.
Mesa N, Garca L, Triana O, Blair S, Maestre A, Dib 2014;8(3):2029.
J, Bravi C, Bailliet G, Corach D, Hnemeier T, 92. Tricco AC, Ivers NM, Grimshaw JM, Moher D,
Bortolini M, Salzano FM, Petzl-Erler M, Acua- Turner L, Galipeau J, Halperin I, Vachon B, Ramsay
Alonzo V, Aguilar-Salinas CA, Canizales-Quinteros T, Manns B, Tonelli M, Shojania K. Effectiveness of
S. Reconstructing native American population his- quality improvement strategies on the management of
tory. Nature. 2012;488:3704. diabetes: a systematic review and meta-analysis.
80. Sarlio-Lhteenkorva S, Winkler J. Could a sugar tax Lancet. 2012;379(9833):225261.
help combat obesity? BMJ. 2015;351:h4047. 93. Villalpando S, Shamah-Levy T, Rojas R, Aguilar-
doi:10.1136/bmj.h4047. Salinas CA. Trends for type 2 diabetes and other car-
81. Jelalian E, Foster G, Sato A, Berlin K, McDermott C, diovascular risk factors in Mexico from 19932006.
Sundal D. Treatment adherence and facilitator Salud Pblica Mx. 2010;52(supl1):S729.
Diabetes in the Caribbean
8
Michael S. Boyne
Introduction ethnic populations. There are English-speaking

(Anglophone) as well as Spanish-, Dutch- and
The Caribbean, also referred to historically as the French-speaking countries (Table 8.1), and there
West Indies, consists of the Caribbean Sea, its are differences in their cultures also. The majority
islands and the surrounding coasts. This large of Caribbean people have West African ancestry
geopolitical area is bordered by the Gulf of as a remnant of the African slave trade and there-
Mexico to the northwest, by the Northern Atlantic fore self-identify as black. Mixed-race and
Ocean to the northeast and by the coastline of European peoples of Dutch, English, French,
South America in the south. There are over 700 Italian and Portuguese ancestry make up a minor-
islands, islets and cays stretching over 4000 km ity. Genetic admixture studies showed rates of
containing a large melting pot of nations and cul- 1015 % for non-African ancestry [1]. Politically,
tures. The climate is mostly tropical, although it most of the Anglophone countries have formed a
is subtropical in the north, but is undergoing sig- socio-economic bloc called the Caribbean
nificant climate change at present. Community (CARICOM). There is moderate
Prior to European immigration in the late geographical mobility, and so several millions live
1400s, the population was estimated to be nearly outside of the Caribbean, mostly in the USA,
a million indigenous people (e.g. the Kalinago, Canada and the UK.
also known as Caribs, and the Arawaks such as The total regional population was 41.9 million
the Tano). These Amerindians were wiped out by in 2014. According to the World Bank, the
disease and genocide although a few remain in the median per capita income was $8995 in 2014
Eastern Caribbean. The influence of the European (http://data.worldbank.org/region/LAC), but the
powers, along with the importation of Africans as range is wide as countries vary from low to high
slaves, followed by Chinese and Indian inden- income (Table 8.1). Tourism is a major source of
tured labourers, as well as Middle Eastern mer- income for many Caribbean nations as the region
chants, has ensured that the Caribbean has diverse has a high literacy rate, tropical weather and rela-
tive political stability.
Life expectancy has been increasing over sev-
eral decades. It increased by 5 years between
M.S. Boyne, MD, FRCPC 1990 and 2013 [2], and it is now 74 years for men
Tropical Metabolism Research Unit, Tropical
and 77 years for women according to the Pan
Medicine Research Institute, The University of the
West Indies, Mona, Kingston 7, Jamaica American Health Organisation (PAHO) (http://
e-mail: [email protected] www.paho.org/hq/index). Hence, the Caribbean

DOI 10.1007/978-3-319-41559-8_8
128 M.S. Boyne
Table 8.1 Populations of Caribbean countries, some of their developmental indicators, and age-adjusted diabetes
prevalence among adults age 2079 years in 2013
Life expectancy at GNI per capita in Age-adjusted
Country Income level Population (2014) birth (years) 2014 (USD) prevalence (%)
Dutch speaking
Aruba HI 103,400 75 24,990 13.6
Curacao HI 155,900 77 14.5
Sint Maarten HI 37,660 76 14.2
Suriname UMI 538,200 71 9470 11.1
English speaking
Anguilla 14,100 12.6
Antigua and HI 90,900 76 13,360 13.3
Barbuda
Bahamas HI 383,100 75 20,980 14.2
Barbados HI 283,400 75 14,960 12.4
Belize UMI 351,700 74 4350 15.9
Bermuda HI 65,180 81 106,140 12.8
British Virgin 28,100 12.6
Islands
Cayman Islands HI 59,170 14.3
Dominica UMI 72,340 77 7070 10.9
Grenada UMI 106,300 73 7850 9.4
Guyana LMI 763,900 66 4170 15.9
Jamaica UMI 2.721 million 73 5220 10.4
Montserrat
St Kitts and Nevis HI 54,940 71 14,490 13.0
St Lucia UMI 183,600 75 7080 8.2
St Vincent and UMI 109,400 73 6560 10.0
Grenadines
Trinidad and HI 1.354 million 70 15,550 13.0
Tobago
Turks and Caicos HI 33,740
Islands
US Virgin Islands HI 104,200 80 13,660 12.1
French speaking
Haiti LI 10.57 million 63 820 6.7
Martinique HI 386,500 14.3
Guadeloupe HI 403,750 79 6.3
St Martin HI 31,530 79
Spanish speaking
Cuba UMI 11.38 million 79 5880 8.1
Dominican UMI 10.41 million 73 6030 11.4
Republic
Puerto Rico HI 3.548 million 79 19,310 13.0
1. Data obtained from the World Bank (data.world.bank.org/country accessed on Nov 29, 2015)
2. Gross national income (GNI) per capita was calculated by the World Bank Atlas method converted to current US
dollars, divided by the midyear population
3. Diabetes prevalence rates from the International Diabetes Federation (http://www.idf.org/diabetesatlas accessed on
Nov 27, 2015) that were estimated by logistic regression models to produce smoothed age-specific prevalence rates
for adults aged 2079 years for 2013. This allows for direct country-to-country comparisons
4. Income level can be high income (HI), upper-middle income (UMI), lower-middle income (LMI) or low income (LI)
8 Diabetes in the Caribbean 129
is rapidly ageing region. Simultaneously, infant expected seroprevalence of HTLV-I in Jamaicans

and child mortality has fallen. with type 1 diabetes (i.e. 17 %). However, this ini-
Coupled with these demographic changes, the tial finding is insufficient to prove a causal associa-
Caribbean is undergoing a rapid nutritional and tion and needs further study. Interestingly, HTLV-I
epidemiologic transition like many regions of the virions use the glucose transporter type 1 (GLUT1)
world [3]. In the 1940s, the most common causes to infect CD4(+) lymphocytes [9].
of morbidity and mortality were infections.
However, over the past 40 years, communicable
diseases account for less than 10 % of the total Type 2 Diabetes
mortality. Atherosclerotic complications, i.e. cor-
onary artery disease and stroke, are now the lead- Role of Lifestyle Factors
ing cause of mortality (accounting for ~7 out of Obesity is rising in the Caribbean as part of the
10 deaths), and diabetes is the third reported global pandemic. The evidence for its role as a
cause in several countries. At the same time, sev- pathophysiologic driver of incident diabetes is
eral Caribbean countries have a double burden of overwhelming, and this is true also for the
infectious diseases (especially HIV/AIDS and Caribbean. The population-attributable risk of
newly emerging diseases such as chikungunya) body mass index for incident diabetes in the
and non-communicable chronic diseases (NCDs), Caribbean is 66 %, and it is 80 % for waist/hip
which are assuming epidemic proportions con- ratio, highlighting the role of adiposity [10]. The
tributing to morbidity and mortality [4]. International Collaborative Study on
Hypertension in Blacks (ICSHIB), which was an
ecological study on the burden of NCDs in the
Classication and Unique Aspects African Diaspora, showed that the prevalence of
of the Pathophysiology of Type 1 obesity increased progressively from West Africa
and Type 2 Diabetes in the Region to the Caribbean and then to North America [11
13]. This geographical gradient in obesity also
Type 1A parallels the gradient in the per capita gross
national product supporting a nutritional transi-
Exposure to human enteroviruses has been impli- tion as the cause. Also worrisome is that the rates
cated as an environmental factor that could trig- of annual weight increase in Jamaicans (1.37 kg/
ger and accelerate the autoimmunity leading to year) are significantly greater than African
type 1A diabetes. In Cuban studies, the presence Americans (0.52 kg/year) and Nigerians (0.31 kg/
of enterovirus RNA in sera from newly diag- year) [14]. Presumably this steep rise in weight
nosed patients with type 1 diabetes was signifi- gain is due to the effects of rapid cultural changes
cantly higher than in healthy controls (27 % vs. in a transitional society, and it does not bode well
3 %) [5, 6]. Also, enterovirus RNA was detected for incident diabetes rates.
in sera of first-degree relatives of islet cell Caribbean women have a disproportionate
antibody-positive patients compared to healthy burden of obesity, as approximately one third of
controls (16 % vs. 0 %). Molecular mimicry or Caribbean women were obese and another third
the hygiene hypothesis are plausible explanations were overweight, and these rates are increasing in
for these phenomena similar to other populations many countries, such as Barbados and Dominica
and regions. [11]. Obesity is about half as common in men.
The human T lymphotropic virus type 1 This sexual dimorphism for obesity is different to
(HTLV-I) virus is endemic in the Caribbean with a other regions of the world where there is parity,
prevalence of 25 % [7]. While endocrine disorders or even greater risk, among men.
such as hypercalcaemia have been reported with The prevalence of diabetes is closely corre-
HTLV-I, there is relatively little data about hyper- lated to the BMI and the amount of intra-abdominal
glycaemia. One study [8] found a higher than fat (as measured by the waist circumference)
130 M.S. Boyne
across the east-to-west gradient of the Diaspora rise in diabetes mortality followed 6 years later.
(Figs. 8.1 and 8.2) [15]. The trends in diabetes However, a notable exception is that Indo-
incidence and mortality paralleled secular Trinidadian men do not have strong correlation of
changes in obesity. As evidence, obesity rates in diabetes prevalence with BMI [17], although this
Cuba plummeted in the early 1990s driven by an may reflect differences in intra-abdominal adi-
economic crisis, but there was a rebound fol- pose tissue deposits.
lowed by an overshoot several years later to its There is a sexual dimorphism in diabetes prev-
current prevalence of ~53 % when the economy alence as women have higher rates [18]. Although
and nutrition improved [16]. The population- much of the variance is due to the higher preva-
wide increase in weight was immediately fol- lence of obesity in women, there is significant
lowed by a 116 % increase in diabetes prevalence residual confounding by other factors, and this
and 140 % increase in diabetes incidence. A 49 % area needs more study. Clinical prediction mod-
els for diabetes in the Caribbean rely on the pre-
dictive ability of obesity using cut points of BMI
14
(30 kg/m2) or central obesity (waist circumfer-
12
Prevalence of diabetes
UK US ence >94 cm in men and 80 cm in women) [19,

10 UK 20]. However, waist circumference is not supe-
US
8
caribbean rior to BMI in Jamaicans in its ability to predict
incident diabetes [21]. Other data however sug-
6 caribbean Men gest that the BMI cut-offs should be lower, i.e.
4 Women
24.8 kg/m2 (men) and 29.3 kg/m2 (women). For
West
2
Africa
West waist circumference, these would be 88 cm and
Africa
0 84.5 cm for men and women, respectively [21].
20 22 24 26 28 30 32 Weight gain in Afro-Caribbean people may
Body mass index (kg/m2) also be modified by the distribution of fat.
Namely, ectopic fat deposits in the liver and
Fig. 8.1 Prevalence of diabetes mellitus (%) in the
African Diaspora according to body mass index (Redrawn within the fascia surrounding the skeletal muscle
from data in Ref. [15]) (i.e. intermuscular adipose tissue or IMAT) may
WBISI Disposition index

2.50
** P <0.01
2.00 **
**
**
1.50
Ratio
1.00
0.50
0.00
Marasmus Kwashiorkor Community Birth weight
survivors survivors controls controls
Fig. 8.2 Ratios after age, sex and BMI adjustment of glu- is a severe acute malnutrition that occurs with moderate
cose metabolism (WBISI and disposition index) of wasting (<60 % weight-for-age) and nutritional oedema.
kwashiorkor survivors, community controls and birth (3) Marasmus is a severe acute malnutrition occurring
weight controls compared to those of marasmus survivors. with severe wasting (<60 % weight-for-age) and no
Notes: (1) ratios represent the relative differences in each oedema. (4) WBISI is the whole-body insulin sensitivity
outcome between the kwashiorkor group and controls index. (5) Disposition index is derived from oral glucose
with the marasmus (comparator) group. (2) Kwashiorkor tolerance testing Data are from Ref. [44]
be independent risk factors for insulin resistance adjusting for body composition, a one-unit
and diabetes. Afro-Caribbean women have large increase in physical activity level (i.e. expending
depots of subcutaneous fat and better adiponectin 590670 kJ or about 20 min of brisk walking
levels than men [22], so the roles of total fat, cen- daily) was associated with a 20-fold reduction in
tral adiposity and fat topology remain to be delin- the risk of diabetes [28].
eated to see if they would explain some of the
excess risk of diabetes in Caribbean women. Role of Developmental Factors
There is a dearth of data about hepatic steatosis in It is well established that low birth weight is asso-
the region. African Americans have greater IMAT ciated with the development of NCDs in later life
compared to Caucasians even after matching for [31, 32]. Birth weight is a crude marker or sum-
the total body fat and skeletal muscle mass [23]. mation of intrauterine growth, which in turn is
Afro-Tobagonian men have high amounts of determined by genetic factors, maternal body
intramuscular fat infiltration as measured by composition, maternal nutrition and placental
peripheral quantitative CT scan. The degree of sufficiency. So, children with low birth weight
IMAT is positively correlated with glycaemia, are more likely to have experienced growth
and this may also be modified by a family history restraint due to intrauterine nutritional restriction
of diabetes. Much of the variability in IMAT may or much less commonly, a genetic predisposition
be genetic, as the residual heritability (due to to low birth weight [33]. However, the associa-
additive genetic effects) was 35 % [24]. IMAT tion of birth weight with type 2 diabetes is J or
may thus be of equal or greater importance than U shaped, i.e. the prevalence of diabetes is
central adiposity [25]. The ectopic deposition of increased in individuals at both extremes of birth
lipids may be higher in obese Afro-Caribbean weight. The mechanisms underlying this rela-
women than in obese white women since African- tionship are not clear. However, both beta-cell
American women have higher rate of fatty acid dysfunction [34, 35] and insulin resistance [34
uptake and higher expression of fatty acid- 36] in childhood and adulthood may occur at the
transporting proteins [26]. extremes of birth weight. Other pathophysiologi-
Physical activity seems to be declining while cal mechanisms involved in low-birth-weight
sedentarism is increasing as part of the epidemio- individuals include hypothalamic-pituitary-
logic transition. The levels of physical activity in adrenal axis activation, visceral adiposity, changes
Barbadian young people are comparable to in adipocytokines and altered appetite. Large-for-
American youth [27], and both are low. There is gestational-age children are more likely to be the
also sexual dimorphism in physical activity as offspring of glucose-intolerant mothers. Thus,
Caribbean women generally report lower levels of they experience intrauterine hyperglycaemia
activity. The importance of this is underscored in causing fuel-mediated teratogenesis, which per se
urban Jamaica where severe or energetic physical may induce insulin resistance and type 2 diabetes
activity was uncommon in men, but non-existent in later life. This was demonstrated in the interna-
in women [28]. The more recent ecological study, tional Hyperglycemia and Adverse Pregnancy
Modelling the Epidemiologic Transition (METS), Outcome (HAPO) study which included more
using accelerometry confirmed that moderate-to- than 1200 Afro-Barbadian mothers [37].
vigorous activity only occurred for 12 min daily Interestingly, fasting glucose was inversely
in Caribbean women and was lower than African related to birth weight in peri-pubertal Jamaican
populations, but similar to American women [29]. boys, but directly associated with girls [38]. This
While men had moderate-to-vigorous activity sexual dimorphism might be due to girls being
about 10 min more than the women [30], they intrinsically more insulin resistant as argued by
were still relatively inactive although they some [39]. However, girls also have an earlier
remained lean. The protective effect of physical onset of puberty (an insulin-resistant state).
activity for incident diabetes is similar to other Earlier menarche and greater breast development
populations in a cross-sectional analysis. So, after in Jamaican children were associated with higher
132 M.S. Boyne
fasting glucose even after adjusting for current incident glucose tolerance more than worsening
BMI or prior growth rates [40]. In fact, fasting insulin resistance [45].
glucose increased by 0.6 mmol/L for each year Other developmentally influenced mecha-
reduction in the age of menarche. nisms can also be in play. Hypothalamic-pituitary-
In Jamaican children, shortness at birth and adrenal axis activation by early life events could
increased current weight are independent predic- account for some of the association with glycae-
tors of insulin resistance, as measured by 2-h mia. Hence, lower birth size and earlier gesta-
insulin levels [41] and increased glycosylated tional age are associated with higher nocturnal
haemoglobin levels [42]. However, data from a cortisol, which in turn is associated with lower
longitudinal birth cohort showed no relationship glucose effectiveness in adulthood [46]. Chronic
of birth size with insulin resistance measured in inflammation of adipose tissue has also been
childhood [38] or in youth [43]. Probably, post- implicated. As an example, faster growth in the
natal growth plays a role in the development of first 6 months of life is associated with higher
insulin resistance. So, children with faster post- serum adiponectin levels in later life [47]. This
natal growth during childhood (i.e. from ages 2 to implies that growth faltering in early infancy may
8 years) had greater insulin resistance, as mea- lead to hypoadiponectinaemia in later life, which
sured by HOMA, in later life [38]. in turn is associated with insulin resistance and
Prenatal factors may play a role in beta-cell glucose intolerance. Finally, there may be an
dysfunction in later life as seen in animal models. interaction with socio-economic status, i.e. young
So, greater maternal weight gain in pregnancy adults whose mothers had lower socio-economic
and smaller birth size are associated with reduced status during pregnancy have more adverse out-
beta-cell function in youth [43]. This phenome- comes associated with low birth size compared to
non is more clearly seen if severe acute malnutri- those from higher status [48]. This may imply the
tion in infancy also occurs. Namely, if children action of other unknown environmental factors
with low birth weight are weaned early onto low- and possibly even endocrine disruptors.
calorie feeds, they are more likely to develop The implication of these observations is
marasmus (typified by severe wasting, i.e. important for Caribbean people. At present the
weight-for-age <60 % but without nutritional average birth weight is ~3.1 kg, but there are a
oedema). Adult survivors of marasmus have significant number of low-birth-weight and mac-
more impaired glucose intolerance (odds ratio rosomic babies, as well as obese mothers. If these
10.9) than age, sex and BMI-matched commu- children have growth faltering in early infancy
nity controls [44]. They have marked beta-cell (the first 6 months of life), or rapid growth in late
dysfunction as measured by an oral disposition infancy/childhood, they are at an increased risk
index, but were only marginally more insulin of type 2 diabetes. Also, when this second gen-
resistant. eration of women later conceive, their offspring
It is therefore possible that intrauterine growth may be exposed to a hyperglycaemic intrauterine
restriction and/or postnatal undernutrition may environment (and thus be born macrosomic) or
impair the development of beta cells during this experience placental insufficiency (and thus be
plastic period of islet development during infancy born small for gestational age). Both conditions
leading to epigenetic changes that decrease insu- would increase the risk of glucose intolerance in
lin and PDX-1 gene expression. This would result the third generation.
in reduced beta-cell mass and glucose-stimulated
insulin secretion in later life. Historically, up to Role of Other Metabolic Factors
5 % of Caribbean populations experienced child- Other metabolic factors may be involved in the
hood severe acute malnutrition up to the 1950s, development of type 2 diabetes, such as
and some of these individuals may contribute to adipocytokines and oxidative stress. In Caribbean
the burden of diabetes today. In Jamaican adults, people, hypoadiponectinaemia is associated with
declining beta-cell function is more of a driver of incident glucose intolerance (OR ~0.93) [49, 50].
Heritability estimates of adiponectin suggest that common. At present, Caribbean clinics are
genetic factors also influence the interindividual swamped with classical type 2 cases.
variation in circulating adiponectin levels and Patients with AKPD have periods in which
therefore the risk of glucose intolerance [51]. they are insulin-requiring resulting in ketosis,
While oxidative stress (e.g. lipid peroxides especially during metabolic stresses, e.g. infec-
such as isoprostanes) [52] and inflammatory tions [57]. At other times, their need for insulin
markers (e.g. sialic acid and highly sensitive decreases such that reasonable glycaemic control
C-reactive protein) [53] may be involved in dia- can be obtained with only lifestyle modification
betic complications in Afro-Caribbean persons, and/or oral antidiabetic agents. Some persons
they may not be involved in the pathogenesis of have insulin resistance and others have experi-
type 2 diabetes [45], but these studies may be enced malnutrition in childhood [58]. It is con-
underpowered. Similarly, glutathione levels are ceivable that they may have reduced beta-cell
marginally lower in patients with type 2 diabetes, mass and glucose-stimulated insulin secretion
but are significantly low in diabetic persons with due to malnutrition in early life similar to the
microvascular complications [54]. marasmic child [44]. Their beta cells appear to be
Chronobiology may play a role in a sex- sensitive to catabolic conditions leading to tran-
specific manner. In Caribbean men, insufficient sient, decreased glucose-stimulated insulin secre-
sleep (i.e. <6 h) or excessive sleep (>10 h) was tion. The precise metabolic triggers (e.g.
associated with diabetes when adjusted for age, glucotoxicity, adipocytokines, non-esterified
BMI and family history of diabetes (OR of 2.7 fatty acids causing lipotoxicity) are not known
and 4.4, respectively). Surprisingly though, in [59].
women sleeping less than 6 h was associated with APKD may be a heterogeneous collection of
a reduced likelihood of diabetes (OR 0.4) [55]. different phenotypes with different degrees of
impaired beta-cell function and autoimmunity
(i.e. anti-GAD65 and anti-IA-2 antibodies) [57].
Atypical Ketosis-Prone Diabetes In an African-American series of AKPD which
(AKPD)/Type 1B Diabetes also contained Afro-Caribbean patients, about
half had no evidence of autoimmunity (A-) with
In 1955, Hugh-Jones published one of the first preserved beta-cell function (+), while 22 %
descriptions of diabetes in the Caribbean where were A--, 17 % were A + - and 11 % were
he observed that type 2 diabetes was more com- A + + [60]. We do not have comparative data in
mon than type 1 diabetes in Jamaica [56]. He also Caribbean persons, but in one study of diabetes in
described an unusual variant which he called Caribbean youth, who were not necessarily
J-type diabetes J standing for Jamaica. In selected on the basis of having ketosis-prone dia-
more recent times, there have been other acro- betes, 30 % were A-+, 41 % were A-- and 39 %
nyms for J- type such as atypical diabetes, phasic were A + - or A + + [59, 61]. As such, some per-
insulin-dependent diabetes, ketosis-prone diabe- sons who have less autoimmunity, i.e. antibody
tes, type 3 diabetes, ketosis-prone type 2 diabetes negative but with preserved beta-cell reserve,
and Flatbush diabetes. This variant was associ- demonstrate a clinical course more in keeping
ated with insulin resistance, phasic dependency with type 2 diabetes despite having periods of
of insulin and a lean phenotype. It most resem- ketosis [62]. Persons with positive autoantibodies
bles type 1B diabetes in the WHO classification. tend to eventually need insulin therapy, while
It is more common in non-white populations, and persons with preserved beta-cell function may
marginal nutritional status may play a role in have periods of insulin independence [57].
some persons. In the Caribbean, there seems to A few candidate genes have been examined to
be fewer cases of AKPD conceivably because explain this variant of diabetes, but no genome-
improved nutrition in the Caribbean over the past wide association studies have been done to date.
several decades is making undernutrition less A missense mutation Gly574Ser in the transcrip-
134 M.S. Boyne
tion factor HNF-1 was thought to be a marker of North Africa region. There is some variation in
AKPD in African-American children [63]. the rates even within countries, depending on the
However, this candidate mutation was not signifi- methods used to diagnose diabetes (fasting glu-
cant in Afro-Caribbean patients [64]. Other cose vs. oral glucose tolerance testing, 1985
investigators working with other ethnic groups WHO diagnostic criteria vs. the 1997 criteria).
found that variants in HNF-1 and HNF-4 are Table 8.1 also gives a breakdown by country
unlikely to be major contributors to the pathogen- where logistic regression models were used to
esis of type 1B diabetes [65], but this is contro- produce smoothed age-specific prevalence rates
versial [66]. for adults aged 2079 years, which can allow for
country-to-country comparisons. Many countries
Maturity-Onset Diabetes of Youth have not carried out national surveys, and their
(MODY) prevalence rates are extrapolated from other
Like most of the world, MODY is rarely seen in Caribbean countries with a similar demographic
the Caribbean. Even though families demonstrat- profile. Clearly it is important for each country to
ing multigenerational inheritance of diabetes and have their data on the burden of disease.
other characteristics consistent with early-onset Naturally, incidence rates of diabetes are also
type 2 diabetes have been identified, evidence of high, although there is some difference based on
autoimmunity or sequence variants in MODY-1 ethnicity. In Jamaica, which is predominantly of
to MODY-6 genes were absent [67]. Insulin pro- African ancestry, the rates are 15 and 20 per 100
moter factor-1 (IPF-1) mutations in familial person-years for men and women, respectively
early-onset diabetes mellitus in Trinidadians [21]. However in Trinidad, where approximately
have been described [68]. 35 % of the population are of Indian ancestry and
another 35 % are of African, the incidence of dia-
betes is higher in Indo-Trinidadians. The rates of
Diagnosis of Diabetes Indo-Trinidadian men were 24 per 1000 person-
and Prediabetes in the Region years compared to Afro-Trinidadian men (13 per
1000 person-years) [17]. This was also similar for
Type 2 Diabetes Indo-Trinidadian women (23 per 1000 person-
years) and Afro-Trinidadian women (14 per 1000
In the 1950s and 1960s, diabetes was uncommon person-years) [17]. On account of the high inci-
in the Caribbean with rates <3 % [6971]. For dence rates, the IDF has been predicted that the
example, in 1958, the prevalence was 1.4 % after prevalence of diabetes in the Caribbean will
screening 2325 adults for glycosuria in Trinidad increase by 3760 % over the period by 2035. The
[72] and 0.73 % among 958 Jamaican adults [71]. epidemic is set to continue as there is a significant
Notably, women with diabetes outnumber men as reservoir of prediabetes. Impaired fasting glucose
far back as 1962 in Trinidad [69], even though occurs in ~3 % [74] and impaired glucose toler-
surprisingly they were not more overweight than ance in 13.7 % [10]. Of note, most surveys did not
the men. perform oral glucose tolerance testing, so most of
By the mid-1970s, PAHO sounded the alarm the regions estimate by the IDF (13.2 %) is actu-
for a looming epidemic of diabetes and NCDs in ally extrapolated from one late-1990s Jamaican
the region [73]. Since then, the prevalence of dia- survey [10]. Remarkably, there are little rural-
betes has increased significantly, and the urban differences [74] although there are differ-
Caribbean, like many developing countries, has ences by income status (lower income having
an epidemic of obesity and diabetes. The higher prevalence). Undiagnosed diabetes is a
International Diabetes Federation (IDF) esti- heavy burden for the region and will increase the
mates that the age-adjusted prevalence in 2013 morbidity, mortality and loss of human capital.
was 9.6 % for the Caribbean which is the second About 25 % of people with diabetes in the
highest in the world after the Middle East and Caribbean are unaware of their status [74, 75].
Youth with Type 2 Diabetes Gestational Diabetes Mellitus (GDM)
Although cases of type 2 diabetes have been The epidemiologic transition would be expected
reported in youth, prevalence data is missing in to increase the risk for gestational diabetes, as
many countries. Anecdotally, these cases have well as the number of women who enter preg-
been increasing with the increasing girth of the nancy with type 2 diabetes. About 413 % of
regions youth. In the US Virgin Islands, the inci- Jamaican women of child-bearing age have dia-
dence of type 2 diabetes in youth age 19 years betes [10, 74]. There has been an apparent
rose significantly between 2001 (5.3/100,000) and increase in the incidence of GDM in Trinidad.
2010 (12.5/100,000) giving an age-adjusted annual Preliminary data show that from 2005 to 2007,
incidence rates of 9.6 per 100,000 [76]. In the prevalence of GDM increased from 1.7 to
Trinidadian schoolchildren, urine screening had a 6.7 % with a mean prevalence of 4.3 % [82].
positive predictive value of 65 % for detecting dia- Unknown genetic factors may play a role. A fam-
betes, and it showed a prevalence of 104/100,000 ily history of early-onset autosomal-dominant
while 75/100,000 had IGT [77]. This would, of type 2 diabetes seems to increase the risk of
course, be an underestimate compared to blood GDM in Jamaican women (12 % vs. 1.5 % in con-
screening. In a small Jamaican study, type 2 diabe- trols, i.e. OR 9.0) which would have implications
tes occurred in a third of cases of diabetes diag- for screening [83].
nosed in youth less than age 25 years [78]. Affected Women with prior GDM are at very high risk
youth were more likely to be female, older at diag- for incident type 2 diabetes. So, among
nosis, obese and have a higher blood pressure Trinidadian women with prior gestational diabe-
when compared to those with type 1 diabetes. tes, 62 % develop diabetes and 17 % had IGT
However, the strongest predictor of type 2 diabetes within 7 years [84]. These data suggest that
was obesity measured by BMI [78]. 1018 % of women convert to diabetes per year,
and the conversion to IGT occurs in another
35 %/year. If confirmed, these rates are extraor-
Type 1 Diabetes dinarily high compared to other regions of the
world [84].
Like many regions, type 1 diabetes is uncommon
in the Caribbean. Precise prevalence and inci-
dence data are sparse in many countries, but data Genomic Landscape of Diabetes
exist for Bahamas and the Eastern Caribbean. in the Region (Local Data, if
The prevalence was very high (31/100,000) in Available, or Best Approximation)
Bahamian youth <age 24 years with an incidence
rate of 10.1/100,000 in those age 014 years [79]. With its unique history of migration and coloni-
Incident rates are 45 per 100,000 person-years sation, it is no surprise that the Caribbean is an
in persons with African ancestry in the Eastern admixed region. Most persons claim African
Caribbean [80, 81] rising to a peak in the US ancestry, and one study using 28 ancestry
Virgin Islands (15.3 per 100,000 person-years) informative markers (AIMs) found that 8490 %
[76, 81] which may reflect their higher degree of had West African ancestry, 1012 % European
genetic admixture. The rates show some seasonal ancestry and 03 % Native American ancestry
variation and a tendency for a secular increase, [1]. Another study using 416 AIMs found Afro-
which augurs for unknown environmental factors Barbadians were ~77 % African, 16 % European
being part of the aetiology such as the accelerator and 7 % Asian [85]. However, Tobagonians had
hypothesis [80]. About half of patients with type the lowest rate of admixture (<6 %) [86].
1 diabetes are type 1A (with anti-GAD65 and/or Spanish Caribbean populations may have more
IA-2 antibodies positivity), and half are type 1B Native American ancestry [87], and this may play
(i.e. autoantibody negative) [61]. a role in the development of incident type 1 diabe-
136 M.S. Boyne
tes in these countries. Genetic susceptibility to Candidate-gene approaches for insulin resis-
type 1 diabetes is determined by a combination of tance have not been very successful. The PC-1
HLA-DQ and DRB1 genes (or a gene in linkage (ENPP1) K121Q polymorphism is not signifi-
disequilibrium with it). In a Cuban sample, a one- cantly associated (Colin A. McKenzie, personal
unit change in European admixture proportion communication, 2015). Variants in peroxisome
was associated with a 5.7-fold risk for type 1 dia- proliferator-activated receptor gamma (PPARG),
betes [88]. The HLA alleles DQA1*0501, *0301 and the obesity-associated gene, FTO, have not
DQB1*0201 and DRB1*0301, *0401 were sus- been well investigated in Caribbean populations.
ceptibility alleles, while DRB1*1501, The Trp64Arg mutation of the beta3-adrenergic
DQA1*0102/3 and DQB1*0602 were protective. receptor has been associated with hyperglycae-
In Afro-Jamaican patients, DRB1*03-DQ2/ mia and obesity in women, but not in men [94].
DRB1*04-DQ8, DRB1*0401-DQ8 and Persons of African ancestry have more fat
DRB1*0408-DQ8 genotypes increase the risk of infiltration of skeletal muscle fat than Europeans.
type 1 diabetes. The DRB1*1503-DQ6 and Since this is a heritable polygenic trait, a
DRB1*03-DQA1*0401-DQB1*0402 haplotypes candidate-gene study examined non-synonymous
were protective alleles. This pattern in the coding variants in carnitine palmitoyltransferase-
Jamaicans is different from the protective and pre- 1B (CPT1B). CPT1B is an enzyme that regulates
disposing haplotypes on European populations skeletal muscle mitochondrial beta oxidation of
[89]. Clearly more work is needed in this area. long-chain fatty acids. The G531L and I66V vari-
For type 2 diabetes, there have been a few ants were associated with ectopic fat infiltration in
studies utilising a candidate-gene approach as the skeletal muscle among 1774 older men from
well as genome-wide association studies, the population-based Tobago Health Study [95].
although some argue that genetic factors play Genome-wide association studies by the
only a minor role among Caribbean populations Genetic Investigation of ANthropometric Trait
[90]. A family history of diabetes in any first- (GIANT) consortium showed several single
degree relative (parent, sibling) or in a grandpar- nucleotide polymorphisms associated with adi-
ent is associated with a two- to fourfold increased posity. Using the phenotype, waist/hip ratio after
risk of diabetes [10, 91]. A family history of dia- adjusting for body mass index, they identified
betes is probably a summary statement for sev- several SNPs (49 loci of which 33 were new), and
eral interactive related genetic, but there is limited the effect size was stronger in women among 20
data on specific genetic factors involved in per- of these SNPs. These SNPs localised to pathways
sons of Caribbean origin. involved in adipogenesis, angiogenesis, tran-
Among the candidate genes, the transcription scriptional regulation, white adipose tissue dif-
factor, TCF7L2, which is involved in beta-cell ferentiation, insulin resistance, adipose
dysfunction, was associated with glucose intoler- inflammation (including adiponectin) and fat
ance in 385 Afro-Caribbean persons living in the topography in the 14,371 individuals of
UK [92]. This seems persistent among nonmigrant non-European ancestry, which also included
populations as among ~1000 Jamaicans, TCF7L2 2437 Afro-Jamaican individuals [96, 97].
was associated with decreased beta-cell function
(as measured by HOMA-%B) (unpublished data).
Mutations in the ATP-sensitive potassium Complications of Diabetes
channel (KCNJ11) in the beta cell are also asso- in the Region
ciated with impaired glucose-stimulated insulin
secretion. The common variant E23K was sig- Health Disparities in Complications
nificantly associated with type 2 diabetes in Indo-
Trinidadians (OR = 1.8) along with a few other People of African ancestry including Afro-
(novel) missense mutations A94P and R369C and Caribbean populations have lower rates of myo-
S118L (in an Afro-Trinidadian) [93]. cardial infarction compared to Caucasians [98,
99], but conversely stroke [100] and renal failure nificant health disparities. In Barbados, diabetes
[101] rates are higher. It is not clear why such accounted for an excess mortality of 42 %, and
disparities exist, but genetic factors [98], coexist- there was a 9 % increase in all-cause mortality for
ing cardiometabolic risk factors [100], access to each 1 % increase in A1c [91]. However, there is
care and intensity of therapeutic control of risk dearth in data in other Caribbean countries about
factors are potential culprits. There is limited specific macrovascular complications and their
data on genetic factors influencing complications mortality. Cardiovascular disease is present in
in diabetic Caribbean people. Persons of African almost 60 % of hospitalised diabetic Jamaicans
ancestry have higher systolic blood pressures, but and is more frequent among women [106]. Silent
lower triglyceride and total cholesterol levels MI may occur in a quarter of Guadeloupian
[99]. Hypertension occurs in 52 % and 35 % of patients especially if they have left ventricular
diabetic Jamaican women and men, respectively hypertrophy [107]. The atrial natriuretic peptide
[10], and there may be less nocturnal dipping of rs5065 (2,238T>C) C allele seems to exert a pro-
blood pressure [102]. Tobacco use is relatively tective effect (24 % vs. 41 %, OR 0.5) in a rela-
low in diabetic persons [10] compared to devel- tively small study in Guadeloupe [108].
oped countries. As a result, these co-morbid car- Diabetes-related mortality is not limited to
diovascular differences may explain some of the older age groups, as 38 % of deaths occurred in
higher rates of stroke and renal failure (which are people under the age of 60 [109, 110]. Mortality
sensitive to blood pressure), and the less athero- in people with type 1 diabetes in the US Virgin
genic lipid profile may reduce the risk of coro- Islands is high, as cumulative survival was 98 %
nary artery disease. Notably, youth with diabetes at 10 years, but fell to 73 % at 20 years. This high
have a more adverse cardiometabolic pattern and incidence rate of T1D in the US Virgin Islands
thus may be more at risk of complications [103], may be partially responsible for the high mortal-
as was also seen in the SEARCH study. ity rate also seen [111].
Mortality and Macroangiopathy Diabetic Foot Disease

(Coronary Heart Disease and Stroke) and Amputations
The leading cause of death in the Caribbean is Diabetic foot disease has major public health
ischemic heart disease, and stroke is the second of consequences for the region. Approximately one
which diabetes is a major cause [104]. Also, dia- of every eight patients in diabetes clinics had a
betes is the leading causes of disability-adjusted major foot complication (amputation, ulcers,
life years. Mortality rates from diabetes have infection). Factors associated with these compli-
increased dramatically, i.e. 63 % from 1980 to cations were neuropathy (OR 9.3), high blood
1990. Diabetes-attributable macrovascular com- pressure (OR 7.9) and longer duration of diabetes
plications are affected by ethnicity. The (OR 1.32) [112]. Diabetic foot disease accounted
population-attributable mortality of Indo- for 30 % of admissions in Barbados and 89 % of
Trinidadians is 2.96.9 times higher than other diabetes-related admissions [113]. In fact,
ethnic groups [98, 105], and most of this is due to Trinidad uses 0.4 % of their gross domestic prod-
diabetes-induced cardiovascular disease. The age- uct solely to treat patients hospitalised for dia-
adjusted death rates due to diabetes in 2000 were betic foot infections [114].
25, 46, 56, 58 and 108 per 100,000 world standard Amputations for diabetic feet are disturbingly
population for Suriname, Bahamas, Barbados, high and are among the highest in the world.
Jamaica and Trinidad, respectively, according to Barbados has the most detailed data where the
PAHO (Health Statistics for the Americas, 2006 1-year incidence of lower extremity amputations
Edition, PAHO). In North America, the rates are was 936 per 100,000 populations (557 per
less than 16 per 100,000, so these data show sig- 100,000 for minor amputations and 379 per
138 M.S. Boyne
100,000 for major amputations) [115]. Women antihypertensive agents lowered the risk by a
had higher amputation rates than those reported half [123]. The risk of retinopathy increased by
for American Indians, and independent risk fac- 30 % for each 1 % increase of A1c [123].
tors were poor footwear (2.7-fold increased risk), Maculopathy was seen in 48 % of Jamaicans
elevated HbA1c (each increase of 1 % led to a with type 2 diabetes 30 years ago [124] and
40 % increase in amputations), peripheral neu- probably remains as high. In a high-risk clinic,
ropathy and peripheral vascular disease [115]. the frequency of diabetic retinopathy was 78 %;
Postamputation mortality rates at 1 and 5 years 30 % had background retinopathy, and 50 % of
are 31 % and 56 %, respectively, which are mostly the eyes had proliferative retinopathy of which
due to sepsis and cardiovascular disease the 34 % had tractional retinal detachments [125].
highest reported worldwide [116]. Besides retinopathy, the burden of glaucoma and
Most of these disparities in the Caribbean are cataracts is also high [91]. These data clearly
probably due to social influences (e.g. inappro- demonstrate the need for retinopathy screening
priate footwear) and healthcare delivery. glycaemic control and blood pressure control in
However, there may be biological factors. For prevention.
example, a persistent inflammatory response in
diabetic ulcers is mostly due to overproduction of
TNF [117]. This persistent inflammation can be Nephropathy
aggravated by low levels of the TNF-receptor as
is seen in persons with the allele, TRAPS In a Jamaican diabetes clinic, about 22 % had
P46L. Interestingly, the allele frequency of eGFR <60 ml/min/1.73 m2, 21 % had moderate
TRAPS P46L in the Barbadian population was albuminuria and 62 % had severe albuminuria
9.5 %, which is 30 times higher than Caucasian [126]. Data from the Caribbean Renal Registry
populations, and could contribute to these high showed that diabetes accounted for ~28 % of the
amputation rates [118]. It is also possible that cases of end-stage renal disease [127]. In many
haemorheological factors, such as increased countries, diabetic persons of African ancestry
plasma viscosity and fibrinogen, may also play a have higher rates of nephropathy. One possible
role in the development of the diabetic foot [119]. explanation is that the increased oxidative stress
seen in Afro-Caribbean persons may be involved
in increased renal damage [52]. Accordingly,
Retinopathy Caribbean patients with microangiopathy have
glutathione deficiency that is probably due to
Some of the best data are from the Barbados Eye reduced synthesis and increased irreversible utili-
Study which showed that the prevalence of reti- sation by non-glycaemic mechanisms [54].
nopathy was approximately 29 % [120]. Most Nephropathy may also be more common in
persons had mild disease while ~8 % had moder- atypical ketosis-prone diabetes [128] for unclear
ate changes, and 1 % had severe retinopathy. reasons.
Clinically significant macular oedema was found
in 9 % of those with diabetes. In the same cohort
after 4 years, the incidence was 32 % in those Hyperglycaemic Crises
with known diabetes at baseline and 21 % in per-
sons with newly diagnosed diabetes [121]. About 60 % of persons admitted with diabetic
Clinically significant macular oedema developed ketoacidosis have type 2 diabetes [129]. The prev-
in 5 %. This increased to 40 % after 9 years and alence of hyperglycaemic crises in the general dia-
the incidence of macular oedema was ~9 % betic population is unknown. Mortality was 7 %
[122]. Increased systolic blood pressure was a for ketoacidosis, 20 % for hyperosmolar hypergly-
risk factor, and over 9 years the relative risk was caemia and 25 % for persons with the mixed keto-
1.3 for every 10 mmHg increase, while using acidosis/hyperosmolar syndrome [129].
Other Complications that the The health of the region is the wealth of
the region in their 2001 Nassau Declaration.
Depression was present in 18 % of type 2 diabetic Subsequently, CARICOM reaffirmed this com-
patients, and older age, Indian ancestry, women mitment in the 2007 Declaration of Port of Spain
and co-morbidities were risk factors [130]. There to begin public health initiatives focused against
are little or no data on other possible complica- NCDs including diabetes. These initiatives would
tions of diabetes such as erectile dysfunction, include primary prevention as well as providing
osteopenia, vascular dementia, dental disease and adequate secondary care. They specifically
reduced lung function in the Caribbean. included antitobacco legislation, promoting
healthy diets that also include indigenous foods
for children, and promote nationwide increases in
Coordination and Delivery physical activity and national commissions to
of Diabetes Care Services coordinate NCD interventions. CARICOM lob-
bied the United Nations to have a high-level
Several studies have shown that cardiometabolic meeting on NCDs which finally occurred in
control of Caribbean diabetic patients is subopti- 1920 September 2011 [138]. This call for a
mal [74] in both private and public sectors [131], coordinated macroeconomic, multisectoral
although this may be improving [132, 133]. In approach is a credit and desperately needed,
fact, less than half attain an A1c goal of <7 %, although there was no significant funding alloca-
and only a small fraction achieve the trifecta of tion by CARICOM, which limited the implemen-
target A1c, blood pressure and lipids [134]. tation of secondary care. Each nation had to find
Patient factors and healthcare system inadequa- the resources to achieve the goals. So, more cul-
cies probably contributed to these issues. turally sensitive incentives to promote healthy
Unfortunately many primary care clinicians are balanced nutrition, opportunities to incorporate
not following any guidelines [135], and, if so, leisure-time physical activities as well as increas-
periodic repetition and reinforcement [136] are ing activity during routine daily living are still
needed to maintain competency. needed. Many countries adopted socialised,
Therefore it is no surprise that the loss of government-subsidised approaches by providing
human capital and the economic costs to the diabetic medications and glucose monitoring
region are staggering. By one conservative esti- supplies. Although many Caribbean countries are
mate, diabetes costs the English-speaking coun- small, access to care is still an issue in inner
tries in 2000 US$218.1 million in direct costs, cities, and rural areas are mountainous and many
US$812.4 million in indirect costs and US$687 times relatively inaccessible. Some countries
million per capita in direct costs along with 5555 have considered mobile clinics to improve access.
diabetes-related deaths [137]. Diabetes and hyper- There have been some efforts to standardise the
tension cost Bahamas 9.1 % of its GDP, Barbados clinical care of persons with diabetes. The
>5 %, Jamaica 6 % and Trinidad and Tobago 8 %. Caribbean Public Health Agency (CARPHA) is
These data are old and are probably a very conser- the new single regional public health agency for the
vative underestimate especially with the ageing of Caribbean, established in 2011 by CARICOM and
the Caribbean and its growing obesity problem. began operation in January 2013. Its predecessor
This growing economic burden is borne by indi- organisation, the Caribbean Health Research
viduals and the governments. Many individuals Council (CHRC), in partnership with PAHO pub-
do not have the required financial resources as lished clinical guidelines for managing diabetes in
many have no retirement savings, pension, lack the Caribbean primary care setting in 2006. The
health insurance, and unemployment is high in metabolic target goals were similar to the IDF
several middle- and lower-income countries. guidelines although there was a more stringent
As a consequence of this threat to Caribbean LDL-cholesterol goal of <1.8 mmol/L. The degree
health and development, CARICOM proposed of uptake and implementation appeared to be inad-
140 M.S. Boyne
equate by the regions clinicians, and proper multi- Table 8.2 Glycaemic indices of some staples commonly
eaten in the Caribbean according to their method of cook-
disciplinary diabetes management teams were not
ing/preparation
well established in many territories, leading to gaps
in holistic care. Newly updated evidence-based Food Boiled Other Preparation
guidelines by CARPHA are to be released in 2016 Cassava 94 (baked)
Breadfruit 47 72 (roasted)
that will try to address areas such as diabetes edu-
Green banana 37 35 (fried)
cation, the central role of diabetes self-management
Ripe plantain 66 90 (fried)
and the prevention of diabetic complications. The
Green plantain 39 40 (fried)
therapeutic approach will be similar to the ADA/
Dasheen 72
EASD guidelines. CARPHA, along with regional
White yam 75 80 (roasted)
universities, is attempting to establish a structured
Lucea yam 74 77 (roasted)
surveillance system for screening and monitoring
Yellow yam 68 80 (roasted)
of NCDs. Systematic screening for risk factors and
Negro yam 73 73 (roasted)
strategies aimed at reducing risk factors for obesity
Sweet potato 46 76 (fried), 82 (roasted)
and type 2 diabetes among schoolchildren are Irish potato 59 70 (fried), 83 (baked)
urgently needed [77, 139]. Eddoes 61
Pumpkin 66
Roti 65 (baked)
Non-pharmacological Management Data adapted from [142, 143]
Nutrition
clinical trial showed that incorporating low-
As mentioned, the nutritional transition towards a intermediate GI indigenous foods into patients
more Westernised diet has helped to drive the meal planning lowered A1c by 0.84 % and also
epidemic. Several surveys have shown energy- improved chronic inflammation (hsCRP), homo-
dense, high-fat, salt are common in the region. cysteine, HDL-C and triglyceride levels [144].
Unfortunately, the Caribbean suffers from a lack
of trained nutritionists and dietetic professionals.
In response to this need, PAHO and the Caribbean Diabetes Education
Food and Nutrition Institute produced a manual
on the nutritional management of obesity, diabe- Diabetes knowledge tends to be poor which
tes and hypertension although it is now outdated, affects their care [145147] but this seems to be
especially with the introduction of so many need slowly improving. Certified diabetes educators
foodstuffs to the market over the decade. are needed although there have been attempts to
Encouragingly, Caribbean patients are inter- fill this void over the past decade by the non-
ested in non-pharmacological management since profit organisation, Diabetes Educators of the
culturally it is deemed more natural. However, Caribbean. Lay persons in communities trained
food security in certain regions poses a threat to in diabetes prevention and care can provide an
this. There is great interest in using locally avail- alternative to traditional point of care of access
able foods like sweet potatoes and yams, but the for diabetes management [148]. Using lay diabe-
glycaemic indices of these foods were not well tes facilitators in Jamaica was associated with an
documented until more recently (Table 8.2) A1c reduction of 0.5 % [149, 150].
[140143]. The mode of cooking can also affect
the glycaemic index (GI). Frying and roasting are
more popular although these methods increase Exercise
the GI compared to boiling. Promoting boiling
can therefore be an important method for control- Physical activity is low especially among women,
ling postprandial spikes. In support, a randomised but there has been increasing interest in recreational
physical activity with more gyms, personal train- Metformin has been used in the region for more
ers, yoga, Pilates and use of public spaces and than 40 years and is the most prescribed agent.
parks for walking. A randomised trial showed Sulphonylureas are commonly used because of
6 months of hatha yoga exercise or conventional their low cost although anecdotally there is a sig-
physical therapy improved fasting blood glucose, nificant amount of symptomatic hypoglycaemia
lipid profile and oxidative stress markers and anti- among the elderly. Most oral agents and insulins
oxidant status in Jamaican patients [151]. are available in the region, and access is determined
by the formulary of the countries. Many clinicians
follow the ADA/EASD guidelines, which are
Nontraditional/Complementary incorporated in the updated CARPHA guidelines,
Techniques and thus use medications (metformin, sulphonyl-
ureas, DPP-4 inhibitors, pioglitazone, acarbose,
There is great interest by patients to use tradi- SGLT2 inhibitors, GLP-1 receptor agonists, basal
tional herbs for glycaemic control [152]. Annatto insulin, NPH insulin, regular insulin, rapid-acting
(Bixa orellana) [153], bitter yam [154], cashews insulin analogues) depending on patient factors
(Anacardium occidentale) [155] and chilli pep- (cost, risk of hypoglycaemia, co-morbid disease,
per (Capsicum frutescens which contains capsa- side effects). In government formularies, metfor-
icin) [156] have mild hypoglycaemic activity. min, sulphonylureas, acarbose, NPH insulin and
Many use guinea hen weed (Petiveria alliacea), regular insulin are used most often.
but it appears to have little hypoglycaemic effect
[157]. This area of natural products remains of
interest for local research. Translating Primary Prevention
of Type 2 Diabetes
Bariatric Surgery Stemming the tide of diabetes requires primary

prevention. Of course, this is the most cost-
Bariatric surgery is an emerging treatment in the effective strategy, and the rise of NCDs threatens
Caribbean but only a very small number of per- the fragile economies of these island nations.
sons have used it. Of these, 85 % had resolution CARPHA instituted the annual Caribbean
of their diabetes, and 15 % were able to reduce Wellness Day (CWD) in 2008, in an effort to
their medication with improvements in quality of strengthen public, private and civil society partner-
life and few complications [158]. ships and to promote multi-country, multisectoral
activities in support of wellness [159]. Culturally
sensitive initiatives are needed but there are few
Tobacco Cessation studies investigating the relationships between the
formation of NCD policy and culture [160].
Tobacco use is relatively low in the Caribbean
compared to other regions, especially among
women. More recently, many countries have Women
passed antitobacco legislation as part of the
CARICOMs drive to reduce the impact of NCDs. Women need special attention as most studies in
the Caribbean identify a higher burden of disease in
women as well as poorer glycaemic control. In the
Rational Selection of Antidiabetes many other regions, women are at a similar or
Medications lower risk of type 2 diabetes than men, even when
obesity is higher in women. This female excess
The CARPHA and national guidelines emphasise may be due to a much greater excess of obesity and
the use of metformin as initial pharmacotherapy. other risk factors in women (e.g. physical activity).
142 M.S. Boyne
However, there may be other factors involved carpha.org/What-We-Do/Research-Training-and-

which need further research. These findings have Policy-Development). The mandate of its
major implications for preventive policies since Research, Training and Policy Development Unit
gender-sensitive messages are needed [18]. is to promote research for health, advise govern-
ments and other stakeholders on research for
health, strengthen national and regional health
Children and Youth research systems, develop mechanisms to support
priority research and promote the sharing of the
The burden of cardiometabolic risk starts early and regions scientific output. Some of its activities
is seen in children. In a recent study [161], about include the administration of research grants, the
one third of Jamaican adolescents were over- hosting of the annual scientific meetings, the deliv-
weight, the girls were less physically active, over ery of training workshops along with the produc-
80 % had 3 risk factors for type 2 diabetes and tion of accompanying manuals (basic and
cardiovascular disease and one third had the meta- advanced research skills, research ethics, grant
bolic syndrome. Thus, interventions are needed to writing and monitoring and evaluation) and the
educate children to reduce their risk. A simple promotion of essential national health research.
measure for risk stratification is the waist circum- The research agenda is packed as it also includes
ference. A waist circumference of 82 cm in young HIV/AIDS and emerging infectious diseases, but
men had better sensitivity to identify insulin resis- nutrition and NCDs including diabetes are priori-
tance than the IDF standard of 94 cm (45 % vs. ties. However, there is no specific set of research
14 %), but the IDF standard of 80 cm for young priorities for diabetes itself. The regions universi-
women remains a reasonable threshold [162]. ties have accelerated their research output for dia-
betes although each investigator acts independently
in determining their research agenda. Investigations
Early Life Interventions into natural products, epidemiological surveys,
behavioural studies, developmental origins and
If cardiometabolic risk can start during foetal complications are more common areas. There is a
life, it raises the issue of optimising the health of paucity of clinical trials for the unique needs of the
women of child-bearing age. Most specifically, region and this needs expanding.
this would involve ensuring a near-normal BMI
prior to entering pregnancy. Interventions that
start in pregnancy involving physical activity and Future Directions: Unmet Needs,
nutrition may actually be too late in the patho- Unanswered Questions,
physiological chain, and thus the effect sizes are Unquestioned Answers
likely to be small, if any. However, prevention of
excessive weight gain in pregnancy, similar to the The preceding description of the state of diabetes
Institute of Medicine guidelines, may be useful. in the Caribbean would highlight that there are
Universal screening for gestational diabetes is several areas that need attention in the future.
not present in all countries, and this should also Some are listed below in no particular order of
be instituted. significance:
Greater efficiencies and synergism of research

Organising and Conduction efforts across the region
Diabetes Research in the Region Greater understanding of the role of obesity
and fat distribution
The Caribbean Public Health Agency is also More understanding of the nature of atypical
responsible for conducting relevant research on ketosis-prone diabetes and how to effectively
public health priorities in the Caribbean (see http:// intervene
Expanding foot care and better vascular type 1 diabetes and islet cell autoantibody-positive
subjects in a population with a low incidence of type
salvage
1 diabetes. Autoimmunity. 2007;40:5405.
Expanding knowledge about the role of early 7. Bartholomew C, Cleghorn F. Retroviruses in the
life factors and possible primary prevention Caribbean. Bull Pan Am Health Organ. 1989;23:
methods appropriate for the region 7680.
8. Smikle MF, Wright-Pascoe R, Barton EN, Dowe G,
Mechanistic understanding of ethnomedicine
Gilbert DT, Choo-Kang E, et al. Autoantibodies,
and relevant clinical studies in promising nat- human T lymphotropic virus type 1 and type 1 dia-
ural products betes mellitus in Jamaicans. West Indian Med
Better systems to collect and track national J. 2002;51:1536.
9. Costa GC, Azevedo R, Gadelha SR, Kashima SH,
data about the NCDs and their complications
Muricy G, Olavarria VN, et al. Polymorphisms at
Greater development of diabetes team GLUT1 gene are not associated with the development
approaches as well as ensuring training of pro- of TSP/HAM in Brazilian HTLV-1 infected individ-
fessionals who can be retained in the region as uals and the discovery of a new polymorphism at
GLUT1 gene. J Med Virol. 2009;81:5527.
there is significant brain drain by migration to
10. Wilks R, Rotimi C, Bennett F, McFarlane-Anderson
the North N, Kaufman JS, Anderson SG, et al. Diabetes in the
Useful models of health reform and funding Caribbean: results of a population survey from Spanish
Devising mechanisms for improved efficien- Town, Jamaica. Diabet Med. 1999;16:87583.
11. Luke A, Cooper RS, Prewitt TE, Adeyemo AA,
cies of health delivery
Forrester TE. Nutritional consequences of the
Gender-sensitive approaches for tailoring African diaspora. Annu Rev Nutr. 2001;21:4771.
public health interventions 12. Luke A, Durazo-Arvizu R, Rotimi C, Prewitt TE,
What social re-engineering is necessary for Forrester T, Wilks R, et al. Relation between body
mass index and body fat in black population samples
primary prevention
from Nigeria, Jamaica, and the United States. Am
To understand the interactions between cul- J Epidemiol. 1997;145:6208.
ture and health policy formation 13. Cooper R, Rotimi C, Ataman S, McGee D,
Health economists are needed to help frame Osotimehin B, Kadiri S, et al. The prevalence of
hypertension in seven populations of west African
some of the regions data into useful advice
origin. Am J Public Health. 1997;87:1608.
for policymakers 14. Durazo-Arvizu RA, Luke A, Cooper RS, Cao G,
Dugas L, Adeyemo A, et al. Rapid increases in obe-
sity in Jamaica, compared to Nigeria and the United
States. BMC Public Health. 2008;8:133.
References 15. Cooper RS, Rotimi CN, Kaufman JS, Owoaje EE,
Fraser H, Forrester T, et al. Prevalence of NIDDM
1. Benn-Torres J, Bonilla C, Robbins CM, Waterman among populations of the African diaspora. Diabetes
L, Moses TY, Hernandez W, et al. Admixture and Care. 1997;20:3438.
population stratification in African Caribbean popu- 16. Franco M, Bilal U, Ordunez P, Benet M, Morejon A,
lations. Ann Hum Genet. 2008;72:908. Caballero B, et al. Population-wide weight loss and
2. Global, regional, and national age-sex specific all- regain in relation to diabetes burden and cardiovas-
cause and cause-specific mortality for 240 causes of cular mortality in Cuba 19802010: repeated cross
death, 19902013: a systematic analysis for the Global sectional surveys and ecological comparison of sec-
Burden of Disease Study 2013. Lancet. 385:11771. ular trends. BMJ. 2013;346:f1515.
3. Wilks R, Bennett F, Forrester T, McFarlane- 17. Miller GJ, Maude GH, Beckles GL. Incidence of
Anderson N. Chronic diseases: the new epidemic. hypertension and non-insulin dependent diabetes
West Indian Med J. 1998;47 Suppl 4:404. mellitus and associated risk factors in a rapidly
4. Sargeant LA, Wilks RJ, Forrester TE. Chronic dis- developing Caribbean community: the St James sur-
eases facing a public health challenge. West Indian vey, Trinidad. J Epidemiol Community Health.
Med J. 2001;50 Suppl 4:2731. 1996;50:497504.
5. Sarmiento L, Cubas-Duenas I, Cabrera-Rode 18. Sobers-Grannum N, Murphy MM, Nielsen A, Guell
E. Evidence of association between type 1 diabetes C, Samuels TA, Bishop L, et al. Female gender is a
and exposure to enterovirus in Cuban children and social determinant of diabetes in the Caribbean: a
adolescents. MEDICC Rev. 2013;15:2932. systematic review and meta-analysis. PLoS One.
6. Sarmiento L, Cabrera-Rode E, Lekuleni L, Cuba I, 2015;10:e0126799.
Molina G, Fonseca M, et al. Occurrence of enterovi- 19. Sargeant LA, Boyne MS, Bennett FI, Forrester TE,
rus RNA in serum of children with newly diagnosed Cooper RS, Wilks RJ. Impaired glucose regulation
144 M.S. Boyne
in adults in Jamaica: who should have the oral glu- uptake in men aged 70 years in relation to size at
cose tolerance test? Rev Panam Salud Publica. birth. Diabetologia. 1998;41:11338.
2004;16:3542. 32. McCance DR, Pettitt DJ, Hanson RL, Jacobsson LT,
20. El Mabchour A, Delisle H, Vilgrain C, Larco P, Knowler WC, Bennett PH. Birth weight and non-
Sodjinou R, Batal M. Specific cut-off points for insulin dependent diabetes: thrifty genotype, thrifty
waist circumference and waist-to-height ratio as pre- phenotype, or surviving small baby genotype? BMJ.
dictors of cardiometabolic risk in Black subjects: a 1994;308:9425.
cross-sectional study in Benin and Haiti. Diabetes 33. Gluckman PD, Hanson MA, Cooper C, Thornburg
Metab Syndr Obes Targets Ther. 2015;8:51323. KL. Effect of in utero and early-life conditions on
21. Sargeant LA, Bennett FI, Forrester TE, Cooper RS, adult health and disease. N Engl J Med. 2008;359:
Wilks RJ. Predicting incident diabetes in Jamaica: the 6173.
role of anthropometry. Obes Res. 2002;10:7928. 34. Li C, Johnson MS, Goran MI. Effects of low birth
22. Boyne MS, Bennett NR, Cooper RS, Royal-Thomas weight on insulin resistance syndrome in caucasian
TY, Bennett FI, Luke A, et al. Sex-differences in adi- and African-American children. Diabetes Care.
ponectin levels and body fat distribution: longitudi- 2001;24:203542.
nal observations in Afro-Jamaicans. Diabetes Res 35. Soto N, Bazaes RA, Pena V, Salazar T, Avila A,
Clin Pract. 2010;90:e336. Iniguez G, et al. Insulin sensitivity and secretion are
23. Albu JB, Kovera AJ, Allen L, Wainwright M, Berk related to catch-up growth in small-for-gestational-
E, Raja-Khan N, et al. Independent association of age infants at age 1 year: results from a prospective
insulin resistance with larger amounts of intermus- cohort. J Clin Endocrinol Metab. 2003;88:364550.
cular adipose tissue and a greater acute insulin 36. Crowther NJ, Trusler J, Cameron N, Toman M, Gray
response to glucose in African American than in IP. Relation between weight gain and beta-cell secre-
white nondiabetic women. Am J Clin Nutr. 2005; tory activity and non-esterified fatty acid production
82:12107. in 7-year-old African children: results from the Birth
24. Miljkovic-Gacic I, Wang X, Kammerer CM, Gordon to Ten study. Diabetologia. 2000;43:97885.
CL, Bunker CH, Kuller LH, et al. Fat infiltration in 37. Metzger BE, Lowe LP, Dyer AR, Trimble ER,
muscle: new evidence for familial clustering and Chaovarindr U, Coustan DR, et al. Hyperglycemia
associations with diabetes. Obesity (Silver Spring). and adverse pregnancy outcomes. N Engl J Med.
2008;16:185460. 2008;358:19912002.
25. Miljkovic-Gacic I, Gordon CL, Goodpaster BH, 38. Boyne MS, Osmond C, Fraser RA, Reid M, Taylor-
Bunker CH, Patrick AL, Kuller LH, et al. Adipose Bryan C, Soares-Wynter S, et al. Developmental ori-
tissue infiltration in skeletal muscle: age patterns and gins of cardiovascular risk in Jamaican children: the
association with diabetes among men of African Vulnerable Windows Cohort study. Br J Nutr. 2010;
ancestry. Am J Clin Nutr. 2008;87:15905. 104:102633.
26. Bower JF, Davis JM, Hao E, Barakat HA. Differences 39. Murphy MJ, Metcalf BS, Voss LD, Jeffery AN,
in transport of fatty acids and expression of fatty acid Kirkby J, Mallam KM, et al. Girls at five are intrinsi-
transporting proteins in adipose tissue of obese black cally more insulin resistant than boys: the
and white women. Am J Physiol Endocrinol Metab. Programming Hypotheses Revisited The EarlyBird
2006;290:E8791. Study (EarlyBird 6). Pediatrics. 2004;113:826.
27. Prochaska JJ, Sallis JF, Griffith B, Douglas 40. Boyne MS, Thame M, Osmond C, Fraser RA, Gabay
J. Physical activity levels of Barbadian youth and L, Taylor-Bryan C, et al. The effect of earlier puberty
comparison to a U.S. sample. Int J Behav Med. on cardiometabolic risk factors in Afro-Caribbean
2002;9:36072. children. J Pediatr Endocrinol Metab. 2014;27:
28. Boyne MS, Gaskin P, Luke A, Wilks RJ, Bennett FI, 45360.
Younger N, et al. Energetic determinants of glucose 41. Bennett F, Watson-Brown C, Thame M, Wilks R,
tolerance status in Jamaican adults. Eur J Clin Nutr. Osmond C, Hales N, et al. Shortness at birth is asso-
2004;58:16668. ciated with insulin resistance in pre-pubertal
29. Luke A, Bovet P, Plange-Rhule J, Forrester TE, Jamaican children. Eur J Clin Nutr. 2002;56:
Lambert EV, Schoeller DA, et al. A mixed ecologic- 50611.
cohort comparison of physical activity & weight 42. Forrester TE, Wilks RJ, Bennett FI, Simeon D,
among young adults from five populations of African Osmond C, Allen M, et al. Fetal growth and cardio-
origin. BMC Public Health. 2014;14:397. vascular risk factors in Jamaican schoolchildren.
30. Dugas LR, Bovet P, Forrester TE, Lambert EV, BMJ. 1996;312:15660.
Plange-Rhule J, Durazo-Arvizu RA, et al. 43. Chin-Harty LA, Royal-Thomas T, Thompson DS,
Comparisons of intensity-duration patterns of physi- Osmond C, Forrester TE, Boyne MS. Role of prena-
cal activity in the US, Jamaica and 3 African coun- tal factors and postnatal growth on insulin sensitivity
tries. BMC Public Health. 2014;14:882. and beta-cell function in Afro-Caribbean youth: vul-
31. McKeigue PM, Lithell HO, Leon DA. Glucose toler- nerable Windows Cohort Study. J Dev Orig Health
ance and resistance to insulin-stimulated glucose Dis. 2015;6:S12. (abstract).
44. Francis-Emmanuel PM, Thompson DS, Barnett AT, 56. Hugh-Jones P. Diabetes in Jamaica. Lancet.
Osmond C, Byrne CD, Hanson MA, et al. Glucose 1955;269:8917.
metabolism in adult survivors of severe acute malnu- 57. Balasubramanyam A, Nalini R, Hampe CS,
trition. J Clin Endocrinol Metab. 2014;99:223340. Maldonado M. Syndromes of ketosis-prone diabetes
45. Boyne MS, Sargeant LA, Bennett FI, Wilks RJ, mellitus. Endocr Rev. 2008;29:292302.
Cooper RS, Forrester TE. Isoprostanes, a marker of 58. Morrison EY, Ragoobirsingh D. J type diabetes
lipid peroxidation, may not be involved in the devel- revisited. J Natl Med Assoc. 1992;84:6038.
opment of glucose intolerance. Diabetes Res Clin 59. Boyne MS. Diabetes in the Caribbean: trouble in
Pract. 2007;76:14951. paradise. Insulin. 2009;4:94105.
46. Thompson DS, Ferguson TS, Wilks RJ, Phillips DI, 60. Maldonado M, Hampe CS, Gaur LK, DAmico S,
Osmond C, Samms-Vaughan M, et al. Early-life fac- Iyer D, Hammerle LP, et al. Ketosis-prone diabetes:
tors are associated with nocturnal cortisol and glu- dissection of a heterogeneous syndrome using an
cose effectiveness in Afro-Caribbean young adults. immunogenetic and beta-cell functional
Clin Endocrinol (Oxf). 2015;82:3528. classification, prospective analysis, and clinical out-
47. Boyne MS, Thompson DS, Osmond C, Fraser RA, comes. J Clin Endocrinol Metab. 2003;88:50908.
Thame MM, Taylor-Bryan C, et al. The effect of 61. Tulloch-Reid MK, Boyne MS, Choo-Kang EG,
antenatal factors and postnatal growth on serum adi- Parkes R, Wright-Pascoe RA, Barton EN, et al.
ponectin levels in children. J Dev Orig Health Dis. Autoantibodies in Caribbean youth with diabetes
2013;4:31723. mellitus. Hum Antibodies. 2008;17(34):5762.
48. Ferguson TS, Younger-Coleman NO, Tulloch-Reid 62. Mauvais-Jarvis F, Sobngwi E, Porcher R, Riveline
MK, Knight-Madden JM, Bennett NR, Samms- JP, Kevorkian JP, Vaisse C, et al. Ketosis-prone type
Vaughan M, et al. Birth weight and maternal socio- 2 diabetes in patients of sub-Saharan African origin:
economic circumstances were inversely related to clinical pathophysiology and natural history of beta-
systolic blood pressure among Afro-Caribbean cell dysfunction and insulin resistance. Diabetes.
young adults. J Clin Epidemiol. 2015;68:10029. 2004;53:64553.
49. Ezenwaka CE, Kalloo R. Caribbean female patients 63. Boutin P, Gresh L, Cisse A, Hara M, Bell G, Babu S,
with type 2 diabetes mellitus have lower serum lev- et al. Missense mutation Gly574Ser in the transcrip-
els of adiponectin than nondiabetic subjects. Neth tion factor HNF-1alpha is a marker of atypical dia-
J Med. 2005;63:649. betes mellitus in African-American children.
50. Bennett NR, Boyne MS, Cooper RS, Royal-Thomas Diabetologia. 1999;42:3801.
TY, Bennett FI, Luke A, et al. Impact of adiponectin 64. Mauvais-Jarvis F, Boudou P, Sobngwi E, Riveline
and ghrelin on incident glucose intolerance and on JP, Kevorkian JP, Villette JM, et al. The polymor-
weight change. Clin Endocrinol (Oxf). 2009;70: phism Gly574Ser in the transcription factor HNF-
40814. 1alpha is not a marker of adult-onset ketosis-prone
51. Miljkovic-Gacic I, Wang X, Kammerer CM, Bunker atypical diabetes in Afro-Caribbean patients.
CH, Wheeler VW, Patrick AL, et al. Genetic deter- Diabetologia. 2003;46:7289.
mination of adiponectin and its relationship with 65. Aguilera E, Casamitjana R, Ercilla G, Oriola J,
body fat topography in multigenerational families of Nicoletti F, Gomis R, et al. Clinical characteristics,
African heritage. Metabolism. 2007;56:2348. beta-cell function, HLA class II and mutations in
52. Mehrotra S, Ling KL, Bekele Y, Gerbino E, Earle MODY genes in non-paediatric subjects with Type 1
KA. Lipid hydroperoxide and markers of renal dis- diabetes without pancreatic autoantibodies. Diabet
ease susceptibility in African-Caribbean and Med: J Br Diabet Assoc. 2005;22:13743.
Caucasian patients with Type 2 diabetes mellitus. 66. Stride A, Ellard S, Clark P, Shakespeare L, Salzmann
Diabet Med. 2001;18:10915. M, Shepherd M, et al. Beta-cell dysfunction, insulin
53. Nayak BS, Roberts L. Relationship between inflam- sensitivity, and glycosuria precede diabetes in hepa-
matory markers, metabolic and anthropometric vari- tocyte nuclear factor-1alpha mutation carriers.
ables in the Caribbean type 2 diabetic patients with Diabetes Care. 2005;28:17516.
and without microvascular complications. J Inflamm 67. Mills JL, Irving RR, Choo-Kang EG, Wright-Pascoe
(Lond). 2006;3:17. R, McLaughlin W, Mullings AA, et al.
54. Lutchmansingh FK, Bennett FI, Badaloo AV, Multigenerational inheritance and clinical character-
McFarlane-Anderson N, Gordon-Strachan GM, istics of three large pedigrees with early-onset type 2
Wright-Pascoe R, et al. Glutathione metabolism in diabetes in Jamaica. Rev Panam Salud Publ Pan Am
persons with type 2 diabetes. West Indian Med J Publ Health. 2010;27:43541.
J. 2012;61:24. (abstract). 68. Cockburn BN, Bermano G, Boodram LL,
55. Cumberbatch CG, Younger NO, Ferguson TS, Teelucksingh S, Tsuchiya T, Mahabir D, et al. Insulin
McFarlane SR, Francis DK, Wilks RJ, et al. Reported promoter factor-1 mutations and diabetes in
hours of sleep, diabetes prevalence and glucose control Trinidad: identification of a novel diabetes-
in Jamaican adults: analysis from the Jamaica lifestyle associated mutation (E224K) in an Indo-Trinidadian
survey 20072008. Int J Endocrinol. 2011;716214. family. J Clin Endocrinol Metab. 2004;89:9718.
146 M.S. Boyne
69. Pyke DA, Wattley GH. Diabetes in Trinidad. West with a family history of autosomal dominant type 2
Indian Med J. 1962;11:226. diabetes. Rev Panam Salud Publ Pan Am J Publ
70. Poon-King T, Henry MV, Rampersad F. Prevalence Health. 2008;23:8591.
and natural history of diabetes in Trinidad. Lancet. 84. Ali Z, Alexis SD. Occurrence of diabetes mellitus
1968;291:15560. after gestational diabetes mellitus in Trinidad.
71. Tulloch JA, Johnson HM. A pilot survey of the inci- Diabetes Care. 1990;13:5279.
dence of diabetes in Jamaica. West Indian Med 85. Murray T, Beaty TH, Mathias RA, Rafaels N, Grant
J. 1958;7:1346. AV, Faruque MU, et al. African and non-African
72. Wright HB, Taylor B. The incidence of diabetes in a admixture components in African Americans and an
sample of the adult population in South Trinidad. African Caribbean population. Genet Epidemiol.
West Indian Med J. 1958;7:12333. 2010;34:5618.
73. Litvak J. Diabetes mellitus: a challenge for the coun- 86. Miljkovic-Gacic I, Ferrell RE, Patrick AL,
tries of the region. Bull Pan Am Health Organ. Kammerer CM, Bunker CH. Estimates of African,
1975;9:31724. European and Native American ancestry in Afro-
74. Cunningham-Myrie C, Younger-Coleman N, Caribbean men on the island of Tobago. Hum Hered.
Tulloch-Reid M, McFarlane S, Francis D, Ferguson 2005;60:12933.
T, et al. Diabetes mellitus in Jamaica: sex differences 87. Moreno-Estrada A, Gravel S, Zakharia F, McCauley
in burden, risk factors, awareness, treatment and JL, Byrnes JK, Gignoux CR, et al. Reconstructing
control in a developing country. Tropical Med Int the population genetic history of the Caribbean.
Health: TM IH. 2013;18:136578. PLoS Genet. 2013;9:e1003925.
75. Ferguson TS, Francis DK, Tulloch-Reid MK, 88. Diaz-Horta O, Cintado A, Fernandez-De-Cossio
Younger NO, McFarlane SR, Wilks RJ. An update ME, Nazabal M, Ferrer A, Roca J, et al. Relationship
on the burden of cardiovascular disease risk factors of type 1 diabetes to ancestral proportions and HLA
in Jamaica: findings from the Jamaica Health and DR/DQ alleles in a sample of the admixed Cuban
Lifestyle Survey 20072008. West Indian Med population. Ann Hum Biol. 2010;37:77888.
J. 2011;60:4228. 89. Heward JM, Mijovic CH, Kelly MA, Morrison E,
76. Washington RE, Orchard TJ, Arena VC, Laporte Barnett AH. HLA-DQ and DRB1 polymorphism
RE, Tull ES. Incidence of type 1 and type 2 diabetes and susceptibility to type 1 diabetes in Jamaica. Eur
in youth in the U.S. Virgin Islands, 20012010. J Immunogenet. 2002;29:4752.
Pediatr Diabetes. 2013;14:2807. 90. Cruickshank JK, Mbanya JC, Wilks R, Balkau B,
77. Batson YA, Teelucksingh S, Maharaj R, Singh V, McFarlane-Anderson N, Forrester T. Sick genes,
Balkaran S, Cockburn B. Screening for diabetes in sick individuals or sick populations with chronic dis-
schoolchildren in Trinidad, West Indies. Paediatr Int ease? The emergence of diabetes and high blood
Child Health. 2013;33:3741. pressure in African-origin populations. Int
78. Tulloch-Reid MK, Boyne MS, Smikle MF, Choo- J Epidemiol. 2001;30:1117.
Kang EG, Parkes RH, Wright-Pascoe RA, et al. 91. Hennis A, Wu SY, Nemesure B, Li X, Leske
Clinical and laboratory features of youth onset type MC. Diabetes in a Caribbean population: epidemio-
2 diabetes in Jamaica. West Indian Med J. 2010; logical profile and implications. Int J Epidemiol.
59:1318. 2002;31:2349.
79. Peter SA, Johnson R, Taylor C, Hanna A, Roberts P, 92. Humphries SE, Gable D, Cooper JA, Ireland H,
McNeil P, et al. The incidence and prevalence of Stephens JW, Hurel SJ, et al. Common variants in
type-1 diabetes mellitus. J Natl Med Assoc. 2005;97: the TCF7L2 gene and predisposition to type 2 diabe-
2502. tes in UK European Whites, Indian Asians and Afro-
80. Jordan OW, Lipton RB, Stupnicka E, Cruickshank Caribbean men and women. J Mol Med.
JK, Fraser HS. Incidence of type I diabetes in people 2006;84:100514.
under 30 years of age in Barbados, West Indies, 93. Boodram LG, Miyake K, Hayes MG, Bell GI,
19821991. Diabetes Care. 1994;17:42831. Cockburn BN. Association of the KCNJ11 variant
81. Tull ES, Jordan OW, Simon L, Laws M, Smith DO, E23K with type 2 diabetes in Indo-Trinidadians.
Vanterpool H, et al. Incidence of childhood-onset West Indian Med J. 2011;60:6047.
IDDM in black African-heritage populations in the 94. McFarlane-Anderson N, Bennett F, Wilks R, Howell
Caribbean. The Caribbean African Heritage IDDM S, Newsome C, Cruickshank K, et al. The Trp64Arg
Study (CAHIS) Group. Diabetes Care. 1997;20: mutation of the beta3-adrenergic receptor is associ-
30910. ated with hyperglycemia and current body mass
82. Clapperton M, Jarvis J, Mungrue K. Is gestational index in Jamaican women. Metabolism.
diabetes mellitus an important contributor to meta- 1998;47:61721.
bolic disorders in Trinidad and tobago? Obstet 95. Miljkovic I, Yerges LM, Li H, Gordon CL,
Gynecol Int. 2009;2009:289329. Goodpaster BH, Kuller LH, et al. Association of
83. Irving RR, Mills JL, Choo-Kang EG, Morrison EY, the CPT1B gene with skeletal muscle fat infiltra-
Kulkarni S, Wright-Pascoe R, et al. The burden of tion in Afro-Caribbean men. Obesity. 2009;17:
gestational diabetes mellitus in Jamaican women 1396401.
96. Shungin D, Winkler TW, Croteau-Chonka DC, Caribbean: an update. Diabetes Res Clin Pract.
Ferreira T, Locke AE, Magi R, et al. New genetic 2014;103:22330.
loci link adipose and insulin biology to body fat dis- 110. Andrade F. Estimating diabetes and diabetes-free
tribution. Nature. 2015;518:18796. life expectancy in Mexico and seven major cities in
97. Locke AE, Kahali B, Berndt SI, Justice AE, Pers Latin America and the Caribbean. Rev Panam Salud
TH, Day FR, et al. Genetic studies of body mass Publ Pan Am J Publ Health. 2009;26:916.
index yield new insights for obesity biology. Nature. 111. Washington RE, Orchard TJ, Arena VC, LaPorte
2015;518:197206. RE, Secrest AM, Tull ES. All-cause mortality in a
98. Beckles GL, Miller GJ, Kirkwood BR, Alexis SD, population-based type 1 diabetes cohort in the
Carson DC, Byam NT. High total and cardiovascular U.S. Virgin Islands. D Diabetes Res Clin Pract.
disease mortality in adults of Indian descent in 2014;103:5049.
Trinidad, unexplained by major coronary risk fac- 112. Ferguson TS, Tulloch-Reid MK, Younger NO,
tors. Lancet. 1986;1:1298301. Wright-Pascoe RA, Boyne MS, McFarlane SR, et al.
99. McKeigue PM, Shah B, Marmot MG. Relation of Diabetic foot complications among patients attend-
central obesity and insulin resistance with high dia- ing a specialist diabetes clinic in Jamaica: preva-
betes prevalence and cardiovascular risk in South lence and associated factors. West Indian Med
Asians. Lancet. 1991;337:3826. J. 2013;62:21623.
100. Chaturvedi N. Ethnic differences in cardiovascular 113. Taylor Jr CG, Krimholtz M, Belgrave KC,
disease. Heart. 2003;89:6816. Hambleton I, George CN, Rayman G. The extensive
101. Earle KK, Porter KA, Ostberg J, Yudkin JS. Variation inpatient burden of diabetes and diabetes-related
in the progression of diabetic nephropathy according foot disease in Barbados. Clin Med. 2014;14:
to racial origin. Nephrol Dial Transplant. 2001;16: 36770.
28690. 114. Cawich SO, Islam S, Hariharan S, Harnarayan P,
102. Chaturvedi N, McKeigue PM, Marmot MG. Resting Budhooram S, Ramsewak S, et al. The economic
and ambulatory blood pressure differences in Afro- impact of hospitalization for diabetic foot infections
Caribbeans and Europeans. Hypertension. 1993;22: in a Caribbean nation. Permanente J. 2014;18:
906. e1014.
103. Tulloch-Reid MK, Boyne MS, Smikle MF, Choo- 115. Hennis AJ, Fraser HS, Jonnalagadda R, Fuller J,
Kang EG, Parkes RH, Wright-Pascoe RA, et al. Chaturvedi N. Explanations for the high risk of
Cardiovascular risk profile in Caribbean youth with diabetes-related amputation in a Caribbean popula-
diabetes mellitus. West Indian Med J. 2009;58: tion of black African descent and potential for pre-
21926. vention. Diabetes Care. 2004;27:263641.
104. Mortality GBD, Causes of Death C. Global, regional, 116. Hambleton IR, Jonnalagadda R, Davis CR, Fraser
and national age-sex specific all-cause and cause- HS, Chaturvedi N, Hennis AJ. All-cause mortality
specific mortality for 240 causes of death, 1990 after diabetes-related amputation in Barbados: a pro-
2013: a systematic analysis for the Global Burden of spective case-control study. Diabetes Care. 2009;32:
Disease Study 2013. Lancet. 2015;385:11771. 3067.
105. Miller GJ, Kirkwood BR, Beckles GL, Alexis SD, 117. Landis RC, Evans BJ, Chaturvedi N, Haskard
Carson DC, Byam NT. Adult male all-cause, cardio- DO. Persistence of TNFalpha in diabetic wounds.
vascular and cerebrovascular mortality in relation to Diabetologia. 2010;53:15378.
ethnic group, systolic blood pressure and blood glu- 118. Quimby KR, Greenidge AR, Hennis AJ, Harrison
cose concentration in Trinidad. West Indies Int DK, Landis RC. Tumor necrosis factor receptor-
J Epidemiol. 1988;17:629. associated periodic syndrome P46L and bilateral
106. Ferguson TS, Tulloch-Reid MK, Younger NO, amputation in diabetes. Rheumatology. 2010;
Boyne MS, Wright-Pascoe RA, Elliott VE, et al. 49:24545.
Cardiovascular disease among diabetic in-patients at 119. Vigilance JE, Reid HL. Glycaemic control influ-
a tertiary hospital in Jamaica. Diab Vasc Dis Res. ences peripheral blood flow and haemorheological
2010;7:2412. variables in patients with diabetes mellitus. Clin
107. Blanchet Deverly A, Amara M, Larifla L, Hemorheol Microcirc. 2005;33:33746.
Velayoudom-Cephise FL, Roques F, Kangambega P, 120. Leske MC, Wu SY, Hyman L, Li X, Hennis A,
et al. Silent myocardial ischaemia and risk factors in Connell AM, et al. Diabetic retinopathy in a black
a diabetic Afro-Caribbean population. Diabetes population: the Barbados Eye Study. Ophthalmology.
Metab. 2011;37:5339. 1999;106:18939.
108. Larifla L, Maimaitiming S, Velayoudom-Cephise 121. Leske MC, Wu SY, Hennis A, Nemesure B, Hyman
FL, Ferdinand S, Blanchet-Deverly A, Benabdallah L, Schachat A. Incidence of diabetic retinopathy in
S, et al. Association of 2238T>C polymorphism of the Barbados Eye Studies. Ophthalmology. 2003;
the atrial natriuretic peptide gene with coronary 110:9417.
artery disease in Afro-Caribbeans with type 2 diabe- 122. Leske MC, Wu SY, Hennis A, Nemesure B, Schachat
tes. Am J Hypertens. 2012;25:5247. AP, Hyman L, et al. Nine-year incidence of diabetic
109. Yisahak SF, Beagley J, Hambleton IR, Narayan KM, retinopathy in the Barbados Eye Studies. Arch
Atlas IDFD. Diabetes in North America and the Ophthalmol. 2006;124:2505.
148 M.S. Boyne
123. Leske MC, Wu SY, Hennis A, Hyman L, Nemesure 139. Batson YA, Teelucksingh S, Maharaj RG,
B, Yang L, et al. Hyperglycemia, blood pressure, and Cockburn BN. A cross-sectional study to deter-
the 9-year incidence of diabetic retinopathy: the mine the prevalence of obesity and other risk fac-
Barbados Eye Studies. Ophthalmology. 2005;112: tors for type 2 diabetes among school children in
799805. Trinidad, West Indies. Paediatr Int Child Health.
124. Moriarty BJ, Dunn DT, Moriarty AP. Diabetic macu- 2014;34:17883.
lopathy in a Jamaican population. Int Ophthalmol. 140. Bahado-Singh PS, Riley CK, Wheatley AO, Lowe
1989;13:3013. HI. Relationship between processing method and the
125. Mowatt L. Diabetic retinopathy and its risk factors at glycemic indices of ten sweet potato (Ipomoea bata-
the university hospital in Jamaica. Middle East Afr tas) cultivars commonly consumed in Jamaica.
J Ophthalmol. 2013;20:3216. J Nutr Metab. 2011;2011:584832.
126. Ferguson TS, Tulloch-Reid MK, Younger-Coleman 141. Riley CK, Bahado-Singh PS, Wheatley AO, Ahmad
NO, Wright-Pascoe RA, Boyne MS, Soyibo AK, MH, Asemota HN. Relationship between the physi-
et al. Prevalence of chronic kidney disease among cochemical properties of starches and the glycemic
patients attending a specialist diabetes clinic in indices of some Jamaican yams (Dioscorea spp.).
Jamaica. West Indian Med J. 2015;64:201. Mol Nutr Food Res. 2008;52:13726.
127. Soyibo AK, Barton EN. Report from the Caribbean 142. Bahado-Singh PS, Wheatley AO, Ahmad MH,
renal registry, 2006. West Indian Med J. 2007;56: Morrison EY, Asemota HN. Food processing meth-
35563. ods influence the glycaemic indices of some com-
128. Ragoobirsingh D, Bennett F, Morrison EY. Kidney monly eaten West Indian carbohydrate-rich foods.
function in phasic insulin dependent diabetes melli- Br J Nutr. 2006;96:47681.
tus in Jamaica. West Indian Med J. 1997;46:224. 143. Ramdath DD, Isaacs RL, Teelucksingh S, Wolever
129. Chung ST, Perue GG, Johnson A, Younger N, Hoo TM. Glycaemic index of selected staples commonly
CS, Pascoe RW, et al. Predictors of hyperglycaemic eaten in the Caribbean and the effects of boiling v.
crises and their associated mortality in Jamaica. crushing. Br J Nutr. 2004;91:9717.
Diabetes Res Clin Pract. 2006;73:18490. 144. Bahado-Singh PS, Wheatley AO, Osagie AU, Boyne
130. Frederick FT, Maharajh HD. Prevalence of depres- MS, Morrison EYS, Ahmad MH, et al. Low to
sion in type 2 diabetic patients in Trinidad and intermediate-glycemic-index Caribbean foods
Tobago. West Indian Med J. 2013;62:62831. reduce glycemia, cardiovascular and inflammatory
131. Wilks RJ, Sargeant LA, Gulliford MC, Reid ME, markers in overweight persons with type 2 diabetes.
Forrester TE. Management of diabetes mellitus in Curr Res Nutr Food Sci. 2015;3:3645.
three settings in Jamaica. Rev Panam Salud Publica. 145. Wint YB, Duff EM, McFarlane-Anderson N, O'Connor
2001;9:6572. A, Bailey EY, Wright-Pascoe RA. Knowledge, moti-
132. Mahabir D, Gulliford MC. Changing patterns of pri- vation and barriers to diabetes control in adults in
mary care for diabetes in Trinidad and Tobago over Jamaica. West Indian Med J. 2006;55:3303.
10 years. Diabet Med. 2005;22:61924. 146. Babwah F, Baksh S, Blake L, Cupid-Thuesday J,
133. Apparico N, Clerk N, Henry G, Seale J, Sealy R, Hosein I, Sookhai A, et al. The role of gender in
Ward S, et al. How well controlled are our type 2 compliance and attendance at an outpatient clinic for
diabetic patients in 2002? An observational study in type 2 diabetes mellitus in Trinidad. Rev Panam
North and Central Trinidad. Diabetes Res Clin Pract. Salud Publ Pan Am J Publ Health. 2006;19:7984.
2007;75:3015. 147. Adams OP, Carter AO. Knowledge, attitudes, prac-
134. Forde H, Marshall M, Cohall D, Nielsen tices, and barriers reported by patients receiving dia-
AL. Assessing predictors for sustainable management betes and hypertension primary health care in
of type 2 diabetes using evidence-based guidelines in Barbados: a focus group study. BMC Fam Pract.
public primary care in a predominantly Afro- 2011;12:135.
Caribbean population. Ethn Dis. 2014;24:46974. 148. Morrison E, Haye I, Amarakoon K, Whitbourne F,
135. Adams OP, Carter AO. Are primary care practitio- Kirlew J, Less L, et al. An interim report of an inter-
ners in Barbados following diabetes guidelines? a vention strategy for diabetes care in Jamaica. West
chart audit with comparison between public and pri- Indian Med J. 2001;50 Suppl 1:559.
vate care sectors. BMC Res Notes. 2011;4:199. 149. Less LA, Ragoorbirsingh D, Morrison EY, Boyne
136. Adams OP, Carter AO. Diabetes and hypertension M, Johnson P. Assessment of a community based
guidelines and the primary health care practitioner in Intervention for diabetes control in adults with type
Barbados: knowledge, attitudes, practices and barri- 2 diabetes mellitus in three parishes in Jamaica: par-
ers a focus group study. BMC Fam Pract. 2010;11:96. ticipant were assigned to interventions using random
137. Barcelo A, Aedo C, Rajpathak S, Robles S. The cost allocations. West Indian Med J. 2008;57 Suppl 1:39.
of diabetes in Latin America and the Caribbean. Bull 150. Less LA, Ragoobirsingh D, Morrison EY, Boyne M,
World Health Organ. 2003;81:1927. Johnson PA. A preliminary report on an assessment
138. Hassell T, Hennis A. The road to the United Nations of a community-based intervention for diabetes con-
High Level Meeting on chronic non-communicable trol in adults with type 2 diabetes. Fam Pract. 2010;27
diseases. West Indian Med J. 2011;60:3846. Suppl 1:i4652.
151. Gordon LA, Morrison EY, McGrowder DA, Young 157. Christie SL, Levy A. Evaluation of the hypoglycae-
R, Fraser YT, Zamora EM, et al. Effect of exercise mic activity of Petiveria alliacea (Guinea Hen Weed)
therapy on lipid profile and oxidative stress indica- extracts in normoglycaemic and diabetic rat models.
tors in patients with type 2 diabetes. BMC West Indian Med J. 2013;62:68591.
Complement Altern Med. 2008;8:21. 158. Dan D, Harnanan D, Singh Y, Hariharan S,
152. Picking D, Younger N, Mitchell S, Delgoda Naraynsingh V, Teelucksingh S. Effects of bariatric
R. The prevalence of herbal medicine home use surgery on type-2 diabetes mellitus in a Caribbean
and concomitant use with pharmaceutical medi- setting. Int J Surg. 2011;9:38691.
cines in Jamaica. J Ethnopharmacol. 159. Samuels TA, Fraser H. Caribbean Wellness Day:
2011;137:30511. mobilizing a region for chronic noncommunicable
153. Russell KR, Omoruyi FO, Pascoe KO, Morrison disease prevention and control. Rev Panam Salud
EY. Hypoglycaemic activity of Bixa orellana extract Publ Pan Am J Publ Health. 2010;28:4729.
in the dog. Methods Find Exp Clin Pharmacol. 160. Samuels TA, Guell C, Legetic B, Unwin N. Policy
2008;30:3015. initiatives, culture and the prevention and control of
154. McAnuff MA, Harding WW, Omoruyi FO, Jacobs chronic non-communicable diseases (NCDs) in the
H, Morrison EY, Asemota HN. Hypoglycemic Caribbean. Ethn Health. 2012;17:63149.
effects of steroidal sapogenins isolated from 161. Barrett SC, Huffman FG, Johnson P, Campa A,
Jamaican bitter yam, Dioscorea polygonoides. Food Magnus M, Ragoobirsingh D. A cross-sectional
Chem Toxicol: Int J Published Br Ind Biol Res study of Jamaican adolescents risk for type 2
Assoc. 2005;43:166772. diabetes and cardiovascular diseases. BMJ Open.
155. Alexander-Lindo RL, Morrison EY, Nair 2013;3:e002817.
MG. Hypoglycaemic effect of stigmast-4-en-3-one 162. Tulloch-Reid MK, Ferguson TS, Younger NO, Van
and its corresponding alcohol from the bark of den Broeck J, Boyne MS, Knight-Madden JM, et al.
Anacardium occidentale (cashew). Phytother Res: Appropriate waist circumference cut points for iden-
PTR. 2004;18:4037. tifying insulin resistance in black youth: a cross sec-
156. Tolan I, Ragoobirsingh D, Morrison EY. Isolation tional analysis of the 1986 Jamaica birth cohort.
and purification of the hypoglycaemic principle Diabetol Metab Syndr. 2010;2:68.
present in Capsicum frutescens. Phytother Res:
PTR. 2004;18:956.
Diabetes in Indigenous Australians
and Other Underserved 9
Communities in Australia
Stephen Colagiuri
Introduction Services Scheme (NDSS) [2], the Australian

Health Survey (National Health Measures
Australias population has just reached 24 million Survey, 20112013) [3], and the AusDiab study
which is relatively small for its large land mass. (19992000) [4]. The Australian Health Survey
The population is diverse with over one in four found that using HbA1c (glycated hemoglo-
being born overseas and includes a unique bin 6.5 %) as the measure, 5.4 % of the popu-
Indigenous population which has lived here for lation over the age of 18 had diabetes, which
thousands of years. It is well recognized that dia- translates to almost 1 million people [3]. Using
betes and other chronic diseases are overrepre- fasting plasma glucose 7.0 mmol/l as the mea-
sented in these diverse groups. This review sure, 5.1 % of Australians aged 18 years and over
examines aspects of diabetes prevalence and care had diabetes. The majority were people known
in three population groups in Australia in which to have diabetes with approximately one newly
health outcomes are of particular concern and are diagnosed case of diabetes for every four already
a significant source of disadvantage: diagnosed cases. Diabetes was more common in
men than women (6.3 % compared with 3.9 %)
Australias Indigenous population of for both known diabetes (4.9 % compared with
Aboriginal and Torres Strait Islander people 3.4 %) and newly diagnosed diabetes (1.4 % com-
People from culturally and linguistically pared with 0.4 %) [3].
diverse backgrounds The 19992000 AusDiab (Australian Diabetes
People living in rural and remote areas and Obesity Lifestyle) study used an oral glucose
tolerance test (OGTT) to estimate that 7.5 % of
Australians over the age of 25 had diabetes,
Diabetes in Australia which equates to approximately 1.2 million peo-
ple [4]. A similar estimate comes from the NDSS,
It is estimated that more than 1.2 million a government-funded national scheme which
Australians are living with diabetes based on data provides registrants with subsidized consumables
from three sources [1]: the National Diabetes for self-monitoring blood glucose, insulin nee-
dles, and insulin pump consumables. The NDSS
has registered 1.2 million people with diabetes
S. Colagiuri, MD
and registers over 250 people every day [2].
Boden Institute of Obesity, Nutrition and Exercise,
University of Sydney, Sydney, NSW, Australia However, it is likely that all three sources
e-mail: [email protected] underestimate the total number of people affected

DOI 10.1007/978-3-319-41559-8_9
152 S. Colagiuri
by diabetes. The Australian Health Survey did not Survey reported prediabetes in 4.0 % of adults
perform an OGTT. The AusDiab study was con- diagnosed on the basis of a fasting plasma glu-
ducted over 15 years ago, and during this time, cose of 6.16.9 mmol/l and 6.0 % based on an
there has been a considerable increase in the pro- HbA1c of 6.06.4 %. These data highlight the
portion of people who are overweight and obese. underestimation of prediabetes when using tests
Both these studies excluded children. Registration which do not specifically identify impaired glu-
with the NDSS is voluntary, and it is likely that a cose tolerance (IGT) [3].
number of people with diabetes are not registered. The greatest risk factor for diabetes is obesity.
While the contribution of many chronic dis- In 20112012, 63 % of Australians aged 18 years
eases to the national burden of disability is and over were overweight or obese, comprised of
decreasing, the diabetes burden continues to 35 % overweight and 28 % obese. The prevalence
increase and is predicted to become the largest of overweight and obesity has increased in
contributor to disability-adjusted life years by Australia over time, from 56 % in 1995 to 61 % in
2017 [5]. In 2011, diabetes was the underlying 20072008. Overweight and obesity vary with
cause of 3 % of all deaths and an underlying or age, with 74.9 % of people aged 6574 years
associated cause of 10 % of all deaths in Australia being overweight or obese compared with 36.4 %
[6]. There are a significant number of diabetes- of people aged 1824 years. More men were
related complications, including heart attacks, overweight or obese than women (70 % vs. 56 %).
strokes, limb amputations, blindness, kidney fail- However, looking at only those people who were
ure, nerve damage, and depression. It is estimated obese, rates are the same for men and women
that annually there are 840,000 hospitalizations (both 28 %). The proportion of people who are
for diabetes, 3500 people having dialysis due to obese has increased across all age groups over
diabetes, and 3500 lower-limb amputations due time, up from 19 % in 1995 to 28 % in 2011
to diabetes [7]. 2012. Between 1995 and 20112012, average
Diabetes impacts the individual, their family, weight increased 3.9 kg in men and 4.1 kg in
and society in general. People with diagnosed women. Rates of overweight and obesity in chil-
diabetes (approximately 5 % of Australians) dren and adolescents aged 517 have remained
account for 12 % of total health care costs in stable at 25 % [10].
Australia. For type 1 diabetes, total direct costs
amount to a minimum of A$570 million
per annum: A$4669 annually for a person with no Australias Indigenous People
complications, rising to A$16,698 per annum
once complications develop [8]. Type 2 diabetes The term Indigenous Australians refers to the
costs at least A$14.6 billion annually, 42 % of Aboriginal and Torres Strait Islander people of
which is attributed to direct medical costs. These Australia, descended from groups that existed
costs are projected to increase to A$30 billion by in Australia and surrounding islands prior to
2025 [9]. The cost pattern is similar in people European colonization in the late eighteenth cen-
with type 2 diabetes with the annual cost increas- tury. The time of arrival of the first Indigenous
ing from A$3500 for people without diabetes Australians is at least 40,000 years ago and may
complications to A$9600 for people with compli- even date back as far as 125,000 years. There is
cations [9]. Australia is fortunate in having the great diversity among different Indigenous com-
NDSS to offset some of these costs. munities and societies in Australia, each with its
In addition to diabetes, intermediate hypergly- own mixture of cultures, customs, and languages.
cemia (prediabetes) is also common. The The Indigenous population of Aboriginal and
AusDiab study found that 16.4 % of adults over Torres Strait Islanders make up approximately
the age of 25 (approximately 2.5 million people) 3 % of the entire population. The age profile
had prediabetes based on a standard 2 h OGTT of Australias Indigenous and non-Indigenous
[4]. More recent data from the Australian Health populations is considerably different with a
9 Diabetes in Indigenous Australians and Other Underserved Communities in Australia 153
larger proportion of young people and a smaller has higher rates of diabetes, significant prema-
proportion of older people (4 % vs. 15 % aged 65 ture mortality, and high rates of complications,
and over) among Indigenous Australians [11]. especially cardiovascular and renal disease.
Life expectancy at birth for Indigenous In addition, the diabetes burden is increased in
Australians in the period 20102012 was populations living in rural and remote areas of
69.1 years for males and 73.7 years for females Australia [14].
compared with 79.7 years for males and 83.1 years The 20122013 National Aboriginal and
for females for non-Indigenous Australians a Torres Strait Islander Health Measures Survey is
gap of 10.6 years for males and 9.5 years for the largest biomedical survey ever conducted in
females [12]. Between 20052007 and 2010 Indigenous Australians and included some 3300
2012, life expectancy at birth for Indigenous individuals aged 18 years and over across
males increased from 67.5 to 69.1 years and from Australia. In addition to collecting data on self-
73.1 to 73.7 years for Indigenous females [13]. reported diabetes, it included measurement of
In 20092013, the age-standardized mortality fasting plasma glucose and glycated hemoglobin.
rate for Indigenous Australians was 985 per The survey showed that 11.1 % of Indigenous
100,000, 1.7 times higher than the 585 per adults had diabetes 9.6 % with previously diag-
100,000 for non-Indigenous Australians. The rate nosed diabetes and 1.5 % with newly diagnosed
ratio was highest for the 3544 years age group diabetes, indicating approximately one newly
where the Indigenous mortality rate was 4.2 diagnosed case for every six diagnosed cases.
times that of the non-Indigenous rate [14]. After taking age differences into account,
Although there have been some improve- Indigenous people were more than three times as
ments, the overall health status of Indigenous likely as non-Indigenous people to have diabe-
Australians remains a concern. Smoking rates tes 3.6 times more likely to have known diabe-
have declined from 51 % to 44 % between 2002 tes and twice as likely to have newly diagnosed
and 20122013 for Indigenous Australians aged diabetes. Indigenous women were significantly
15 and over but remain high with a current 25 more likely than men to have diabetes [15].
percentage point gap between Indigenous and Diabetes prevalence among Indigenous peo-
non-Indigenous Australians. Smoking during ple increased with age. Rates were especially
pregnancy remains high at 50 %. Low birth high among those aged 55 years and over, with
weight rate for babies born to Indigenous moth- around one in every three people in this age group
ers is twice that of non-Indigenous mothers (11 % having diabetes (34.5 %), compared with 12 %
compared with 5 %). It is estimated that 51 % of among non-Indigenous Australians, a gap of 22
low birth weight births to Indigenous mothers is percentage points [15] (Fig. 9.1).
attributable to smoking, compared with 19 % for Although this overall age pattern was similar
non-Indigenous Australian mothers. If smoking to non-Indigenous Australians, diabetes tended to
rates for Indigenous pregnant women were the occur earlier. The prevalence of diabetes for
same as for other Australian mothers, it is esti- Indigenous people aged 3544 years was 9.0 %
mated that the proportion of low birth weight which is similar to that for non-Indigenous peo-
babies could be reduced by 26 % [14]. ple aged 5564 years (8.2 %). Similarly, the prev-
alence for those aged 4554 years was 17.8 %,
similar to that for those aged 6574 in the non-
Diabetes in Indigenous Australians Indigenous population (15.0 %). This pattern was
apparent for both known diabetes and newly
Prevalence diagnosed diabetes [15].
Minges et al. performed a systematic review
The burden of diabetes is not shared equally in of diabetes prevalence in Indigenous Australians
Australia, and no group is more severely affected prior to the 20122013 Australian Aboriginal
than Australias Indigenous population which and Torres Strait Islander Health Survey [16].
154 S. Colagiuri
40
30
%
20
10
0
2534(b) 3544 4554 55 and over
Age group (years)
Aboriginal and Torres Strait Islander Non-indigenous
Fig. 9.1 Diabetes or high blood sugar levels by Indigenous status and age (Sources: 20122013 Australian Aboriginal
and Torres Strait Islander Health Survey and 20112012 Australian Health Survey)
Among 24 studies, sample sizes varied from 152 sharp rise in diabetes prevalence with age with
to 29,687 participants, with 71 % of studies hav- 31.7 % of those aged 35 years and over and
ing a sample size over 500 people. The mean 52.4 % of those 55 years and over having diabe-
sample study age ranged from 21 to 51 years. tes. Of the people with diabetes, 48 (28.7 %) were
Eighteen studies included blood testing with 14 newly diagnosed of whom 24 (50 %) would not
using WHO diagnostic criteria and 4 the ADA have been diagnosed without an OGTT.
criteria, while 25 % presented self-reported data The Australian Health Survey reported that
and 13 % used medical records. The prevalence 4.7 % of the Indigenous population had impaired
estimates of diabetes ranged from 3.5 % to fasting glucose (IFG) indicating an increased
33.1 %. Even when only considering the 16 stud- risk for future diabetes. After taking age dif-
ies with a mean sample age of 3040 years, the ferences into account, Indigenous people were
diabetes prevalence still varied between 6.5 % nearly twice as likely to be at high risk of diabe-
and 26.2 %. Consequently, the authors were tes compared with non-Indigenous Australians.
unable to establish a true single prevalence esti- The prevalence of IFG increased with age with
mate due to the marked heterogeneity of the data. 7.5 % of those aged 55 and over having IFG [3].
These differences may have been the result of The review by Minges et al. included five studies
major differences in the Indigenous populations, which reported an IGT prevalence of 4.721.1 %
the Indigenous communities, or in the way stud- [16]. With the exception of one study, there was a
ies were conducted. greater prevalence of diabetes than IGT. IFG was
The most recent study which included 2 h only assessed in one study of an island population
OGTT testing was the DRUID (Diabetes and in the top end of Australia and reported a preva-
Related conditions in Urban Indigenous people lence of 5.1 %. The DRUID study [17] reported a
in the Darwin region) study [17] which included prevalence for IGT of 12 %. In contrast to diabe-
861 people aged 15 years or older. The overall tes, both IGT and IFG remained relatively stable
prevalence of diabetes was 19.4 %. There was a in the age groups above 25.
Type 2 Diabetes in Young People were compared with 470 type 1 diabetes subjects
Craig et al. determined the incidence of type with similar age of onset. The median observation
2 diabetes in young people <19 years old and period was similar at 21.4 (interquartile range,
their characteristics in the Indigenous group 1430.7) and 23.4 (15.732.4) years for the type
in a prospective population-based study. From 2 and the type 1 diabetes cohorts, respectively. A
2001 to 2006, there were 128 incident cases of significant mortality excess was noted in the type
type 2 diabetes (62 boys, 66 girls). The median 2 diabetes subjects compared with the type 1 dia-
age at diagnosis was 14.5 years (interquartile betes subjects (11 vs. 6.8 %, P = 0.03), with an
range, 13.016.4), and 90 % were overweight increased hazard for death (hazard ratio, 2.0 [95 %
or obese (BMI >85th percentile for age). Mean CI 1.23.2], P = 0.003). Death in the type 2 diabe-
annual incidence was 2.5/100,000 person-years tes subjects occurred after a significantly shorter
(95 % CI, 2.13.0) in 1018-year-olds. Of the disease duration (26.9 [18.136.0] vs. 36.5 [24.4
ethnic groups represented, white Australian 45.4] years, P = 0.01) and at a relatively young age,
comprised 29 %, Indigenous 22 %, Asian 22 %, and there were more cardiovascular deaths (50 vs.
North African/Middle Eastern 12 %, and Maori/ 30 %, P < 0.05). Despite equivalent glycemic con-
Polynesian/Melanesian 10 %. The incidence trol and shorter disease duration, the prevalence of
of type 2 diabetes was significantly higher in albuminuria and less favorable cardiovascular risk
the Indigenous compared with the non-Indige- factors was greater in the type 2 diabetes subjects
nous group (incidence rate ratio, 6.1; 95 % CI, and neuropathy scores, and macrovascular com-
3.99.7; P < 0.001), but incidence rates of type plications were also increased [21].
1 diabetes were similar (15.5 vs. 21.4/100,000,
respectively). Type 2 diabetes accounted for Risk Factors for Diabetes
11 % of incident cases of diabetes in 1018-year-
olds [18]. Obesity
Type 2 diabetes among Indigenous children The National Aboriginal and Torres Strait
and adolescents appears to be increasing in inci- Islander Health Survey showed that four in every
dence, and the burden is much greater than that ten (39.8 %) Indigenous persons were obese, and
experienced by non-Indigenous young people these obese individuals were around seven times
[19]. Indigenous children and adolescents with more likely than normal weight or underweight
type 2 diabetes typically have a family history of individuals to have diabetes (17.2 % compared
type 2 diabetes and are overweight or obese and with 2.4 %) [15].
may have signs of hyperinsulinism such as acan- Daniel et al. reported the risk of having IGT
thosis nigricans [20]. Onset of type 2 diabetes is and diabetes relative to body mass index (BMI)
usually during early adolescence, and patients are among 2626 aboriginal men and women aged
often asymptomatic at presentation. Data on 1594 years. The population was divided into
comorbidities at diagnosis are lacking and may five strata of BMI (<22, 2224.9, 2529.9,
be a reflection of poor screening. 3034.9, and 35 kg/m2). The prevalence of IGT
There is evidence that young-onset type 2 dia- and diabetes, respectively, adjusted for age and
betes is a more lethal phenotype of diabetes and BMI, was 13.9 % and 14.2 % among men and
is associated with a greater mortality, more diabe- 15.7 % and 15.2 % among women. Odds ratios
tes complications, and unfavorable cardiovascular (95 % CI) for IGT and diabetes for increasing
disease risk factors when compared with type 1 BMI strata 22 kg/m2 ranged from 1.7 (1.02.9)
diabetes. Long-term clinical outcomes and sur- to 5.1 (2.410.5) for IGT and from 2.0 (1.23.5)
vival in young-onset type 2 diabetes were com- to 6.1 (3.311.1) for diabetes. For IGT and diabe-
pared with type 1 diabetes with a similar age of tes, across genders, the population-attributable
onset using an ambulatory diabetes center data- risk percentages (95 % CI) for BMI 22 kg/m2
base. Outcomes in 354 people with type 2 dia- were 34.1 % (26.241.9 %) for IGT and 46.4 %
betes with age of onset between 15 and 30 years (38.554.5 %) for diabetes [22].
156 S. Colagiuri
The DRUID study reported the association Busfield et al. studied an Indigenous Australian
between various indices of obesity and diabetes community with a phenotype characterized by
after adjusting for age. Among males, the odds severe insulin resistance. A genome-wide scan
ratios for diabetes in the highest quartile com- for type 2 diabetes susceptibility genes in a large
pared to the lowest quartile were 10.4 (95 % CI multi-generation pedigree from this community
1.290.6) for WHR, 6.0 (1.229.6) for waist cir- identified a region of significant positive linkage
cumference, and 2.0 (0.66.3) for BMI. Among with type 2 diabetes on chromosome 2q with sev-
females, the corresponding odds ratios were eral candidate genes identified in the region [25].
WHR 25.9 (6.0112.0), waist circumference 7.5 Another genome-wide analysis found peaks on
(2.919.2), and BMI 4.8 (2.110.8) [17]. chromosomes 1 and 21. On chromosome 1, the
gene had a strong association with type 2 diabe-
Low Birth Weight tes, hyperlipidemia, and blood pressure in type
Child health, and especially low birth weight, is 2 diabetes in European populations. The gene
considered an important factor in the develop- with a strong association with type 2 diabetes on
ment of diabetes. In 2011, the low birth weight chromosome 21 is involved with regulating insu-
rate for babies born to Indigenous mothers was lin [26]. Further studies are required to replicate
twice the rate for those with a non-Indigenous these findings in other Indigenous and interna-
mother (13 % compared with 6 %) and was sig- tional populations.
nificantly higher in remote areas (15 %) than in
non-remote areas (12 %) [23]. Despite these high Gestational Diabetes
rates, there has been a significant 9 % decline in Ishak and Petocz investigated the prevalence,
low birth weight rates between 2000 and 2011 in trends, and risk factors of gestational diabetes
Indigenous mothers. mellitus (GDM) in Indigenous Australians com-
A major factor in low birth weight is smoking. pared with the non-Indigenous population in a
Fifty percent of Indigenous women smoked dur- retrospective population analysis of 230,011
ing pregnancy in 2011, four times the rate for deliveries from an administrative database in the
non-Indigenous women, and 51 % of low birth state of South Australia between 1988 and 1999.
weight births to Indigenous mothers has been The age-standardized GDM rate for Indigenous
attributed to smoking, compared with 19 % for mothers was more than 2.5 times higher than
non-Indigenous mothers. After adjusting for age that for non-Indigenous mothers (4.3 vs. 1.8 %)
differences and other factors, it is estimated that with no significant trend changes over the time
if the smoking rate for Indigenous pregnant period of the study [27]. However, a more recent
women was the same as for other Australian systematic review of diabetes in pregnancy
mothers, the proportion of low birth weight included 11 studies which reported prevalence of
babies could be reduced by 26 % [14]. GDM in Indigenous Australians. The overall rate
of GDM was higher at 8.4 % compared with
Social Determinants 25 % worldwide [28].
There remains a significant gap between
Indigenous and non-Indigenous Australians in
several parameters which can impact health. These People Living in Rural and Remote
include education attainment rates, employment, Areas
household incomes (43 % of Indigenous adults
were in the lowest quintile compared with 17 % of Australias population is largely concentrated in
non-Indigenous adults), and homelessness [14]. the east and southeast of the country, and most
Australians live in capital cities with the majority
Genetic Studies living in major cities (71 %), 18 % in inner
There have been a limited number of gene- regional areas, 9 % in outer regional areas, 1.4%
related studies including studies on diabetes sus- in remote areas, and 1% in very remote areas.
ceptibility genes in Indigenous Australians [24]. The proportion living in major cities has increased
over the past decade, while the population in very remote areas are between 10 % and 70 % as high
remote areas has fallen [29]. as in major cities. Cardiovascular diseases are
Health outcomes, such as higher rates of death, responsible for nearly a third of the elevated male
are worse outside of major cities related to differ- death rates outside major cities. Male death rates
ences in access to services, risk factors, and the from diabetes are 1.3 times as high in inner
remote environment, although it is not possible to regional areas and 3.7 times as high in very
apportion the generally poorer health outcomes remote areas compared with major cities [31].
outside major cities to these factors [30]. With In 2010, 5.4 % of all deaths that year were
respect to health services, there are lower rates of attributed to diabetes and causes related to diabe-
some hospital surgical procedures, lower rates of tes, although as is well known this will be an
primary care physician consultation, and gener- underestimate. Diabetes-related death rate was
ally higher rates of hospital admission in regional 55 % higher among males than females (39
and remote areas than in major cities. There are deaths per 100,000 males and 25 deaths per
also significant differences in interregional health 100,000 females) [32]. Death rate from diabetes-
behavior and risk factors. People in regional and related causes increased with increasing remote-
remote areas are more likely than their urban ness 28 deaths per 100,000 population among
counterparts to be a daily smoker (outer regional people living in major cities, 32 deaths per
and remote 22 % and inner regional 18 % com- 100,000 population among people living in inner
pared with 15 % in major cities), be overweight or regional areas, and 43 deaths per 100,000 popula-
obese (70 % and 69 % compared with 60 %), be tion among people living in outer regional,
insufficiently active (60 % and 63 % compared remote, and very remote areas.
with 54 %), drink alcohol in harmful quantities Diabetes prevalence is also linked with region
(24 % and 21 % compared with 19 %), and have of residence. Overall in Australia, the age-
high blood cholesterol (37 % and 38 % compared standardized prevalence of diabetes in 2011
with 31 %) [31]. In addition, over half of outer 2012 was 4.2 %. Rates of diabetes were 3.9 % in
regional, remote, and very remote residents live in major cities and 4.9 % in outer regional and
areas classified as the lowest socioeconomic sta- remote areas [3].
tus compared with around one-quarter of people The situation is worse for Indigenous people
in major cities and 77 % in very remote areas. living in remote areas with around one in five
Another contributing factor to the health sta- (20.8 %) having diabetes compared with around
tus of people living in rural and remote areas is one in ten people in non-remote areas (9.4 %).
the higher proportion of Indigenous people and This difference is particularly pronounced for
their generally poorer health outcomes. Most newly diagnosed diabetes, which was five times
Indigenous Australians live in urban areas 35 % as high in remote areas than in non-remote areas
in major cities, 22 % in each of inner and outer (4.8 % compared with 0.9 %) [3]. In addition,
regional areas, and the remaining 21 % in either Indigenous adults in remote areas are less likely
remote or very remote areas. Nevertheless, they to have their diabetes effectively managed
make up a relatively large proportion of the popu- (25.1 % compared with 43.5 %) and two and a
lation living in remote areas of Australia 45 % half times more likely to have chronic kidney dis-
of all people living in very remote areas and 16 % ease (33.6 % compared with 13.1 %).
living in remote areas [30].
Overall, death rates increase with increasing
remoteness. In 2012, the age-standardized rate People from Culturally
was highest in very remote areas (840 per 100,000 and Linguistically Diverse
population), followed by remote (670 per 100,000 Backgrounds
population), outer regional (640 per 100,000
population), inner regional (610 per 100,000 Around 28 % of Australias population was born
population), and major cities (550 per 100,000 overseas with migration from more than 200
population) [31]. Death rates in regional and countries around the world [33]. The proportion
158 S. Colagiuri
of the population born overseas has grown 50 years. For both men and women, odds of type
steadily from one in ten (10 %) in 1947. Between 2 diabetes were higher for all migrant groups
2004 and 2014, Australias overseas-born popu- than the Australian-born reference population.
lation increased from 4.8 million to 6.6 million After adjusting for age and SES, odds were
people. The largest proportion was born in the 6.3 and 7.2 times higher for men and women
United Kingdom (5.2 %) followed by New born in the Pacific Islands, respectively, and
Zealand (2.6 %), China (excluding Hong Kong) 5.2 and 5.0 times higher for men and women
(1.9 %), India (1.7 %), the Philippines (1 %), born in Southern and Central Asia, respec-
Vietnam (1.0 %), Italy (0.9 %), South Africa tively. However, compared with Australian-born
(0.8 %), Malaysia (0.7 %), and Germany (0.5 %) people, age- and SES-adjusted prevalence odds
[33]. The relative proportion of Australian resi- were significantly increased across all groups for
dents born overseas is changing with a decrease males and females including Oceania (2.6 and
in those born in the United Kingdom and an 3.0), Northwest Europe (1.5 and 1.7), Southern
increase in those born in New Zealand, China, and Eastern Europe (2.0 and 2.4), North Africa
and India. Of overseas-born Australians, the big- and the Middle East (4.0 and 4.7), Southeast
gest proportion come from Northwest Europe Asia (3.1 and 4.0), Northeast Asia (1.9 and 2.6),
(including the United Kingdom) (25 %) followed Southern and Central Asia (5.2 and 5.0), America
by Southeast Asia (14 %), Southern and Eastern (2.0 and 2.4), and sub-Saharan Africa (2.7 and
Europe (12 %), Oceania (including New Zealand) 3.1). These sociocultural differences have impli-
(12 %), Northeast Asia (12 %), and Southern and cations for health service planning and delivery,
Central Asia (10 %). This increase in cultural policy, and preventive efforts in Australia.
diversity has implications for health services and Gestational diabetes is a particular problem in
the demographics of health in Australia [30]. mothers from different ethnic groups. A computer-
Culturally and linguistically diverse (CALD) ized database of all births (n = 956,738) between
communities in Australia experience both signifi- 1995 and 2005 in the Australian state of New South
cant health disparities and a lack of access to ser- Wales was used to examine the association between
vices. A systematic review of the literature on the sociodemographic characteristics and the occur-
effectiveness of culturally appropriate interven- rence of gestational diabetes [36]. Between 1995
tions to manage or prevent chronic disease in and 2005, the prevalence of GDM increased by
CALD communities found that the health of 45 %, from 3.0 % to 4.4 %. Women born in South
Australias CALD population is poor in compari- Asia had the highest adjusted odds ratio of any
son to the general population. Hospital admis- region (4.22 [95 % CI 4.014.44]) relative to
sions for CALD people were more than double, women born in Australia. However, all regions
particularly for chronic and disabling conditions, showed increased adjusted odds Northeast and
such as diabetes, traumatic injury, heart and kid- Southeast Asia 3.24 (3.163.34), Europe and North
ney disease, and respiratory problems [34]. America 1.21 (1.161.26), Middle East and North
The prevalence of type 2 diabetes varies by Africa 2.40 (2.302.51), Pacific 2.94 (2.783.11),
ethnicity and socioeconomic status (SES), and other Africa 1.62 (1.461.80), and Caribbean,
migrants experience a disproportionate burden Central, and South America 1.82 (1.652.01).
of disease compared with locally born groups. The rate of progression from GDM to devel-
Abouzeid et al. compared the prevalence odds of oping postpartum abnormal glucose tolerance is
type 2 diabetes among immigrant groups in the greater in certain ethnic groups. In a prospective
Australian state of Victoria with Australian-born study of 101 women who had GDM, ethnicity
residents. The overall prevalence of diagnosed was a major risk factor for the development of
type 2 diabetes in Victoria was 4.1 % in men diabetes during a mean follow-up of 5.5 years
and 3.5 % in women [35]. Of those with type 2 [37]. South Asian women had a significantly
diabetes, over one in five born in Oceania and higher risk of developing abnormal glucose toler-
in Southern and Central Asia were aged under ance (69 %) than women of all other ethnicities.
The prevalence of diabetes and impaired glucose Albumin/creatinine ratio less than 3.5 mg/mmol
tolerance was also very high among other for women and less than 2.5 mg/mmol for men
groups Southeast and East Asian (41 %), Middle Urinary albumin excretion less than 20 mg/L
Eastern (44 %), South European backgrounds Blood pressure less than or equal to
(42 %), and Australian-born women (39 %). 130/80 mmHg
Differences in the clinical characteristics and Normal body mass index (i.e., a BMI score
outcomes of women with GDM from various eth- of between 18.5 and 24.9)
nic groups have also been reported. Wong reported Nonsmoker
a retrospective review of 827 women with GDM
from five ethnic groups (Southeast Asian, South In 20122013, around two in five (38.9 %)
Asian, Middle Eastern, Anglo-European, and Indigenous Australian adults with known diabetes
Pacific Islander). Southeast Asians had the lowest had an HbA1c result of 7.0 % or less. Overall,
BMI and lowest need for insulin therapy and their Indigenous women were more likely than men to
offspring had the lowest rate of macrosomia and achieve this result (47.0 % compared with 28.1 %).
lowest birth weight. In contrast, women from Indigenous people with known diabetes were less
Pacific Islands had the highest BMI and greatest likely than their non-Indigenous counterparts to
need for insulin therapy, and their offspring had have an HbA1c of 7.0 % or less (38.9 % compared
the highest birth weights. This study highlighted with 55.9 %) [15].
the significant differences in clinical characteris- Just over half (56.9 %) met the management
tics of women with GDM [38]. target for triglycerides and 44.4 % met the target
for albumin/creatinine ratio (ACR). However,
Indigenous people with diabetes were less likely
Diabetes Management than non-Indigenous people to meet these targets,
particularly for ACR (44.4 % compared with
In general, information on diabetes management 71.0 %) [15].
and rates of complications in Australia are less Two of the most common problems in
well documented than epidemiological data. Indigenous people are cardiovascular (CVD) and
While there are some data for Indigenous kidney disease. CVD risk factors are prevalent.
Australians, there are few specific data for the The DRUID study found that while people with
other two groups included in this review. diabetes had a greater number of CVD risk fac-
Indigenous Australians have evidence of tors than those without diabetes, these risk fac-
poorer glycemic and metabolic control and high tors were relatively common in young people
rates of diabetes complications and cardiovascu- (aged <35 years) without diabetes with almost
lar mortality. half (45 %) having at least two risk factors and
In the National Aboriginal and Torres Strait only 18 % having none [17]. Six in ten (60.5 %)
Islander Health Measures Survey, the following Indigenous people with diabetes had lower than
goals on the optimal management in those with normal levels of HDL cholesterol compared with
known diabetes were assessed: 32.9 % of those without diabetes (Fig. 9.2). They
were also around twice as likely to have high tri-
Fasting blood glucose between 6.0 and glycerides (45.1 % compared with 20.7 %). A
8.0 mmol/L quarter (25.0 %) had high cholesterol, but only
HbA1c levels less than or equal to 7.0 % around one in ten (9.1 %) of this group were
Total cholesterol less than 4.0 mmol/L aware they had it [15]. Many Indigenous people
HDL cholesterol greater than or equal to with diabetes also had signs of other chronic con-
1.0 mmol/L ditions. Around half (53.1 %) had signs of chronic
LDL cholesterol less than 2.0 mmol/L kidney disease, significantly higher than the cor-
Non-HDL cholesterol less than 2.5 mmol/L responding rate in the non-Indigenous population
Triglycerides less than 2.0 mmol/L (32.5 %) [15].
160 S. Colagiuri
Fig. 9.2 Selected chronic %

disease biomarkers in
Indigenous subjects with and 60
without diabetes (Source:
20122013 Australian
Aboriginal and Torres Strait 50
Islander Health Survey
Biomedical Results)
40
30
20
10
0
Abnormal HDL good Abnormal Abnormal GGT Has anaemia
cholesterol triglycerides (liver test)
Chronic disease biomarkers
Does not have diabetes Has diabetes
Thomas et al. examined the management of between Indigenous Australians and Anglo-Celt
144 Indigenous people with type 2 diabetes in patients in an urban Australian community [40].
Australian primary care compared with that in Data from the Fremantle Diabetes Study col-
non-Indigenous patients presenting consecutively lected from 1993 to 1996 (phase I) and from
to the same medical practitioner (n = 449). 2008 to 2011 (phase II) were analyzed. Indigenous
Indigenous Australians had high rates of micro- participants were younger at entry and, at diabe-
and macrovascular disease with 60 % having an tes diagnosis, were less likely to be educated
abnormal ACR compared to 33 % of non- beyond primary level and more likely to be smok-
Indigenous patients (p < 0.01). In addition, they ers. HbA1c decreased in both groups over time
were more likely to have established macrovascu- (Indigenous median 9.6 % [interquartile range
lar disease (adjusted odds ratio 2.7). This excess in 7.810.7 %] to 8.4 % [6.610.6 %] vs. Anglo-Celt
complications was associated with poor glycemic median 7.1 % [6.28.4 %] to 6.7 % [6.27.5 %]),
control, with an HbA1c 8.0 %, observed in 55 % but the gap persisted. Indigenous patients were
of all Indigenous patients, despite the similar fre- more likely to have microvascular disease in both
quency of use of oral antidiabetic agents and insu- phases. The prevalence of peripheral arterial dis-
lin. Smoking was more common in Indigenous ease (ankle-brachial index <0.90 or lower-
patients (38 % vs. 10 %, p < 0.01). However, the extremity amputation) increased in Indigenous
achievement of LDL and blood pressure targets but decreased in Anglo-Celt participants.
was the same or better in Indigenous patients. This While renal disease is common in Indigenous
cross-sectional study confirmed aboriginal ethnic- Australians, there is considerable regional varia-
ity as a powerful risk factor for microvascular and tion in the incidence of end-stage renal disease
macrovascular disease [39]. (ESRD). Cass and colleagues reviewed informa-
Davis et al. used data from the observational tion on 719 Indigenous ESRD patients who com-
Fremantle Diabetes Study to examine disparities menced treatment in Australia during 19931998
in the nature and management of type 2 diabetes using data from the Australian and New Zealand
Dialysis and Transplant Registry who started 2 years of treatment. In these 118, blood pressures
ESRD treatment. Standardized ESRD incidence fell significantly, while ACR and GFR stabilized.
among Indigenous Australians was highest in Rates of the combined end points of renal failure
remote regions, where it was up to 30 times the and natural death per 100 person-years were 2.9
national incidence for all Australians. In urban for the treatment group (95 % CI, 1.74.6) and
regions, the standardized incidence was much 4.8 for the historical control group (95 % CI, 3.3
lower, but remained significantly higher than the 7.0). After adjustment for baseline ACR category,
national incidence. Forty-eight percent of the relative risk of the treatment group versus the
Indigenous ESRD patients came from regions control group for these combined end points was
without dialysis or transplant facilities and 16.3 % 0.47 (95 % CI, 0.250.86; P = 0.013). Treatment
from regions with only satellite dialysis facilities. benefit was especially marked in people with
Because of the location of treatment centers, overt albuminuria or hypertension and in people
there is inequitable access to ESRD treatment without diabetes. The estimates of benefit were
services for a significant proportion of Indigenous supported by a fall in community rates of death
patients [41]. and renal failure.
A number of attempts have been made to Point of care testing (POCT) for HbA1c and
improve clinical systems for addressing the gap urine ACR is increasingly available in Indigenous
in care of Indigenous Australians with diabetes. communities under the auspices of the Quality
McDermott and colleagues assessed changes in Assurance for Aboriginal Medical Services
clinical indicators of adults diagnosed with dia- (QAAMS) Program. Shephard et al. evaluated
betes using audits of clinical records of Torres the QAAMS Program and assessed satisfaction
Strait Islander adults on diabetes registers in 21 with POCT for HbA1c and urine ACR in a medi-
primary care clinics. Over a 6-year period, the cal service in a remote area of Northern Australia
number of adults included on the diabetes regis- for Indigenous people with type 2 diabetes [44].
ter increased from 555 in 1999 to 1024 in 2005. Both doctors and patients reported that the imme-
Mean weight increased from 86.8 to 95.6 kg, and diacy of POCT had contributed positively to the
mean HbA1c level remained unchanged at about identification and management of diabetes,
9 %, but the proportion with HbA1c level <7 % improved doctor-patient relationship, and facili-
increased from 18.4 % to 26.1 % and the propor- tated compliance and self-motivation to control
tion with BP <140/90 mmHg increased from diabetes. At the end of the 12 months, there was a
40.3 % to 66.8 %. This study showed that some statistically significant drop in HbA1c from 9.3 %
improvements can be achieved by introducing to 8.6 % (P = 0.003) with an improvement in the
clinical systems, but important clinical parame- percentage of patients controlling their diabetes.
ters such as weight gain and hyperglycemia The addition of HbA1c as a diagnostic cri-
remain a challenge [42]. terion for diabetes has simplified algorithms
The effectiveness of a systematic treatment for testing and detecting undiagnosed diabetes.
program to modify renal and cardiovascular dis- POCT for HbA1c in this context has particular
ease in an Indigenous Australian community advantages in Indigenous communities. Marley
from the Tiwi Islands with high rates of renal and colleagues compared the Australian glucose-
failure and cardiovascular deaths was reported by based algorithm [45] with an HbA1c-based algo-
Hoy et al. [43]. Adults with blood pressure rithm applied in a remote Australian Aboriginal
140/90, with diabetes and ACR 3.4 g/mol, or community. The HbA1c-based algorithm used
with progressive overt albuminuria were offered an initial POCT HbA1c assessment followed by
the intervention which included attempts to laboratory HbA1c assay if needed. Participants
achieve blood pressure goals and improve control were significantly more likely to receive a defini-
of blood glucose and lipid levels and health edu- tive result within 7 days and to be diagnosed
cation. Two hundred fifty-eight people enrolled with diabetes using the HbA1c algorithm than
in the program, and 118 had complete data for with the glucose-based protocol. The study also
162 S. Colagiuri
highlighted the increased likelihood of follow-up 4. Dunstan DW, Zimmet PZ, Welborn TA, et al. The ris-
ing prevalence of diabetes and impaired glucose toler-
with HbA1c testing; only 42 % of participants
ance: the Australian diabetes, obesity and lifestyle
with an equivocal glucose result underwent an study. Diabetes Care. 2002;25:82934.
OGTT as recommended by the Australian guide- 5. Australia Institute of Health and Welfare Australias
line [46]. Health. Australias health series no 12. Cat no. AUS
122. Canberra: AIHW; 2010.
6. Australian Institute of Health and Welfare (AIHW).
Conclusions Causes of death. 2013. [Online]. Available: http://
Like other countries around the world, Australia www.aihw.gov.au/deaths/causes-of-death/.
is experiencing a steady increase in the number 7. Australian Institute of Health and Welfare (AIHW).
Diabetes: Australian facts 2008. Canberra: Diabetes
of people with diabetes which is placing a con-
Series; 2008.
siderable burden on individuals, their families, 8. Colagiuri S, Brnabic A, Gomez M, et al. DiabCo$t
and the whole society. The impact on Australia: assessing the burden of type 1 diabetes in
Indigenous Australians is particularly heavy Australia. Canberra: Diabetes Australia; 2009.
9. Lee CM, Colagiuri R, Magliano DJ, et al. The cost of
with diabetes prevalence rates, threefold higher
diabetes in Adults in Australia. Diabetes Res Clin
than non-Indigenous Australians. Indigenous Pract. 2013;99(3):385904.
Australians also have increased rates of compli- 10. Australian Bureau of Statistics. http://www.abs.gov.au/
cations, especially renal. Two other groups also ausstats/[email protected]/Lookup/by%20Subject/4338.0~2011-
13~Main%20Features~Overweight%20and%20
experience significant disadvantage people
obesity~10007.
from culturally and linguistically diverse back- 11. ABS. Projected population, Aboriginal and Torres
grounds and people living in rural and remote Strait Islander Australians, Australia, states and terri-
areas. While epidemiological data are available tories, 20112026. ABS cat. no. 3238.0. Canberra:
ABS; 2014.
for these groups, information on diabetes man-
12. ABS. Life tables for Aboriginal and Torres Strait
agement and rates of complications are less Islander Australians, 20102012. ABS cat. no.
well documented. While some programs are 3302.0.55.003. Canberra: ABS; 2013.
being implemented to improve quality of care 13. AIHW. Mortality and life expectancy of Indigenous
Australians 2008 to 2012. Cat. no. IHW 140.
and outcomes, an increased effort is needed to
Canberra: AIHW; 2014.
reduce the care gap in these groups compared 14. AIHW. Aboriginal and Torres Strait Islander health
with other Australians. performance framework 2014 report: detailed analy-
There are many gaps in our knowledge of ses. 2015. Cat. no. IHW 167. http://www.aihw.gov.au/
publication.
diabetes in these populations and unmet needs
15. ABS. Australian Aboriginal and Torres Strait Islander
with respect to prevention, care, and treat- Health Survey: biomedical results, 2012-13. 2014.
ment. Future research will be needed to Cat. no. 4727.0.55.003.
address these gaps and reduce the disparity 16. Minges KE, Zimmet P, Magliano DJ, et al. Diabetes
prevalence and determinants in Indigenous Australian
between these groups and other Australians.
populations: a systematic review. Diabetes Res Clin
Pract. 2011;93(2):13949.
17. ODea K, Cunningham J, Maple-Brown L,
Weeramanthri T, Shaw J, Dunbar T, et al. Diabetes
and cardiovascular risk factors in urban Indigenous
References adults: results from the DRUID study. Diabetes Res
Clin Pract. 2008;80:4839.
1. Australian National Diabetes Strategy 2016-2020. 18. Craig ME, Femia G, Broyda V, et al. Type 2 diabetes
http://www.health.gov.au/internet/main/publishing. in Indigenous and non-Indigenous children and ado-
nsf/Content/nds-2016-2020. lescents in New South Wales. Med J Aust. 2007;186:
2. National Diabetes Service Scheme (NDSS). Data 4979.
snapshots. 2014. [Online]. Available: http://www. 19. Azzopardi P, Brown AD, Zimmet P, Fahy RE, Dent
ndss.com.au/en/Research/Data-Snapshots/. GA, Kelly MJ, Kranzusch K, Maple-Brown LJ,
3. Australian Bureau of Statistics (ABS). Australian Nossar V, Silink M, Sinha AK, Stone ML. Type 2 dia-
health survey biomedical results for chronic dis- betes in young Indigenous Australians in rural and
eases. 201112. Available: http://www.abs.gov.au/ remote areas: diagnosis, screening, management and
australianhealthsurvey. prevention. Med J Aust. 2012;197:326.
20. Sinha A, ORourke S, Yarker J, et al. Type 2 diabetes diverse communities: a systematic literature review.
in children and adolescents in the Indigenous commu- Health Soc Care Community. 2011;19(3):22549.
nities of Far North Queensland. Diabetes Res Clin 35. Abouzeid M, Philpot B, Janus ED, Coates MJ, Dunbar
Pract. 2000;50(Supplement 1):126. JA. Type 2 diabetes prevalence varies by socioeco-
21. Constantino MI, Molyneaux L, Limacher-Gisler F, nomic status within and between migrant groups:
Al-Saeed A, Luo C, Wu T, Twigg TM, Yue DK, Wong analysis and implications for Australia. BMC Public
J. Long-term complications and mortality in young- Health. 2013;13:25260.
onset diabetes type 2 diabetes is more hazardous and 36. Anna V, Van der Ploeg HP, Cheung WN, Huxley RR,
lethal than type 1 diabetes. Diabetes Care. 2013;36: Bauman AE. Sociodemographic correlates of the
38639. increasing trend in prevalence of gestational diabetes
22. Daniel M, Rowley KG, McDermott R, ODea K. mellitus in a large population of women between 1995
Diabetes and impaired glucose tolerance in Aboriginal and 2005. Diabetes Care. 2008;31:228893.
Australians: prevalence and risk. Diabetes Res Clin 37. Girgis CM, Gunton JE, Cheung NW. The influence of
Pract. 2002;57:2333. ethnicity on the development of type 2 diabetes mel-
23. Australian Institute of Health and Welfare. Birthweight litus in women with gestational diabetes: a prospec-
of babies born to Indigenous mothers. Cat. no. IHW tive study and review of the literature. ISRN
138. Canberra: AIHW; 2014. Endocrinol. 2012;2012:3416381; 17.
24. Kowal EE. Genetic research in Indigenous health: sig- 38. Wong VW. Gestational diabetes mellitus in five ethnic
nificant progress, substantial challenges. Med J Aust. groups: a comparison of their clinical characteristics.
2012;197:1920. Diabet Med. 2012;29:36671.
25. Busfield F, Duffy DL, Kesting JB, Walker SM, 39. Thomas M, Weekes AJ, Thomas MC. The manage-
Lovelock PK, Good D, Tate H, Watego D, Marczak ment of diabetes in indigenous Australians from pri-
M, Hayman N, Shaw JTE. A genomewide search mary care. BMC Public Health. 2007;7:30311.
for type 2 diabetessusceptibility gene in indige- 40. Davis TM, Hunt K, McAullay D, Chubb SA, Sillars
nous Australians. Am J Hum Genet. 2002;70: BA, Bruce DG, Davis WA. Continuing disparities in
34957. cardiovascular risk factors and complications between
26. Kowal E, Anderson I. Genetic research in Aboriginal aboriginal and Anglo-Celt Australians with type 2
and Torres Strait Islander communities: continuing diabetes: the Fremantle Diabetes Study. Diabetes
the discussion. Lowitja Institute. 2012. www.lowitja. Care. 2012;35:200511.
org.au/lowitja-institute-publishing. 41. Cass A, Cunningham J, Wang Z, Hoy W. Regional
27. Ishak M, Petocz P. Gestational diabetes among variation in the incidence of end-stage renal disease in
Aboriginal Australians: prevalence, time trend and Indigenous Australians. Med J Aust. 2001;175:247.
comparisons with non-Aboriginal Australians. Ethn 42. McDermott RA, McCulloch BG, Campbell SK,
Dis. 2003;13:5560. Young DM. Diabetes in the Torres Strait Islands of
28. Porter C, Skinner T, Ellis I. The current state of Australia: better clinical systems but significant
Indigenous and Aboriginal women with diabetes in increase in weight and other risk conditions among
pregnancy: a systematic review. Diabetes Res Clin adults, 19992005. Med J Aust. 2007;186:5058.
Pract. 2012;98:20922. 43. Hoy WE, Baker PR, Kelly AM, Wang Z. Reducing
29. ABS. Regional population growth, Australia, 2013 premature death and renal failure in Australian
14, ABS cat. no. 3218.0. Canberra: ABS; 2015. Aboriginals. A community-based cardiovascular and
30. Australian Institute of Health and Welfare. Australias renal protective program. Med J Aust. 2000;172:
welfare 2015. Australias welfare series no. 12. Cat. 4738.
no. AUS 189. Canberra: AIHW; 2015. 44. Shephard MD. Cultural and clinical effectiveness of
31. ABS Australian Institute of Health and Welfare. 2010. the QAAMS point-of-care testing model for diabe-
A snapshot of mens health in regional and remote tes management in Australian Aboriginal medical ser-
Australia. Rural health series no. 11. Cat. no. PHE vices. Clin Biochem Rev. 2006;27(3):16170.
120. Canberra: AIHW. http://www.aihw.gov.au/ 45. Marley JV, Oh MS, Hadgraft NT. Using glycated hae-
rural-health-publications/. moglobin testing to simplify diabetes screening in
32. Australian Institute Health and Welfare (AIHW). remote Aboriginal Australian health care settings.
http://www.aihw.gov.au/diabetes-indicators/deaths/. Med J Aust. 2105;204:2832.
33. ABS. Migration, Australia, 201314. ABS cat. no. 46. Colagiuri S, Davies D, Girgis S, Colagiuri R. National
3412.0. Canberra: ABS; 2015. evidence based guideline for case detection and diag-
34. Henderson S, Kendall E, See L. The effectiveness of nosis of type 2 diabetes. Canberra: Diabetes Australia,
culturally appropriate interventions to manage or pre- NHMRC; 2009. http://www.nhmrc.gov.au/guidelines/
vent chronic disease in culturally and linguistically publications/di17. Accessed Dec 2015.
Diabetes Among Mori and Other
Ethnic Groups in New Zealand 10
Evan Atlantis, Grace Joshy, Margaret Williams,
and David Simmons
Unique Aspects of Diabetes in New Polynesians who arrived mainly between 800 and
Zealand 1200 AD. Pacific peoples largely started arriving
in the 1960s and are mainly Polynesians from
New Zealand, known by the indigenous people Samoa, Tonga, Cook Islands, Niue and Tokelau
(Mori) as Aotearoa, is in the South Pacific to the Islands. Asians are from across the continent and
West of Australia. With a land mass of first arrived in the nineteenth century, with more
270,500 km2 over two major islands (North and rapid increases in immigration in the 1990s.
South Islands), the population was estimated in Although Mori and other minority groups are
2015 to be 4,637,847. In the 2013 census, 74.0 % distributed across the country, the ethnic mix dif-
identified with one or more European identities, fers depending on location, with Auckland
14.9 % (598,605 people) identified as Mori, (population 1.4 million) recognised as the city
11.8 % identified as Asian and 7.4 % identified as with the largest Polynesian population in the
Pacific peoples [1]. European New Zealanders world (approximately 32 %).
are predominantly of British descent arriving
from the mid-nineteenth century. Mori are
Mori Perspective on Health
and Research
E. Atlantis, PhD
Western Sydney University, Historically, mainstream health services and
Campbelltown, NSW, Australia research models have not always benefitted
e-mail: [email protected] indigenous peoples, including Mori [25]. The
G. Joshy, PhD information collected was led by health profes-
Australian National University, sionals (including researchers) who may have
Canberra, ACT, Australia perpetuated colonial values, while the true com-
plexities of Mori values, belief systems and cus-
M. Williams, PhD toms were often not reported accurately [3, 6].
Auckland University of Technology,
Auckland, New Zealand Since the 1960s, in Aotearoa, New Zealand,
e-mail: [email protected] there has clearly been a shift in the way non-
D. Simmons, FRACP, FRCP, MD (*) indigenous health professionals, researchers and
School of Medicine, Western Sydney University, academics have positioned themselves and their
Locked Bag 1797, Penrith, work in relation to working with Mori [2, 49].
NSW NSW 2751, Australia An important starting point includes bicultural

DOI 10.1007/978-3-319-41559-8_10
166 E. Atlantis et al.
strategies developed between Mori and non- concepts may also be helpful for those living
Mori. These strategies are unique to Aotearoa, with chronic health diseases, such as type 2 dia-
New Zealand, because they are an active response betes, in acquiring knowledge and understanding
from the Crown (Government) towards the Treaty and then engaging in activities around health and
of Waitangi, signed in 1840 [12]. It is about hon- well-being. For the individual newly diagnosed
ouring of the Treaty through the acknowledge- with type 2 diabetes, managing their blood glu-
ment and application of the principles partnership, cose concentration through increased physical
participation and protection [5, 912]. Evans and activity and consumption of nutritious food is a
Paewai [13] provided definitions of each princi- priority. The following are concepts often associ-
ple as follows: ated with kaupapa Mori styles of learning that
encompasses collecting and sharing information
(a) Partnership. Mori and non-Mori are all citi- with individuals actively involved in education
zens of New Zealand; Mori are also afforded
tangata whenua (people of the land) status
and/or research projects [6, 17]:
and, as such, might identify with a whnau
(extended family), hapu (subtribe) or iwi Tino rangatiratanga (relative autonomy/self-
(tribal group). determination of Mori culture).
(b) Protection. This applies to the principle of
self-determination and rights to traditional
Taonga tuku iho (cultural aspirations) the
properties or taonga (treasures) such as cul- treasures from the ancestors include cultural
ture, land, language and all that is deemed aspirations Mori hold for their children and
important, including self-determination in messages that guide our/their relationships
matters affecting personal well-being such as
health, welfare, educational policies and
and interaction patterns.
legislation. Ako (reciprocal learning) literally meaning to
(c) Participation. The recognition that Mori, as teach and to learn the teacher or health pro-
individuals and equal partners, should be fessional does not have to be the fountain of
afforded equal access and participation in
societys benefits.
all knowledge.
Kia piki ake i nga raruraru o te kainga (media-
tion of socioeconomic and home difficulties).
These principles provide a framework for Whnau primary concept (a cultural prefer-
identifying Mori ethical and practice issues in ence) that contains both values (cultural aspira-
terms of the rights, roles and responsibilities for tions) and social processes (cultural practices).
health professionals, researchers and Mori com- Kaupapa, the collective vision principle.
munities in Aotearoa, New Zealand.
The dynamics of Mori usually infer whnau Mori research ethics guidelines and aca-
(family) or groups to compete, while individuals demic bodies in health (e.g. New Zealand
cooperate within the whnau (extended families). Research Health Council and Nga Pae o te
Such dynamics emphasise the sense of inclusive- Maramatanga) can now be sourced for learning
ness where people usually feel part of a whnau and sharing information about best practice in the
(family), hapu (subtribe) or iwi (tribes/people) delivery of health services and research with
[1416]. In contrast, some health professionals, indigenous people, in particular, Mori [5, 16,
researchers and academics report that main- 19]. Such knowledge advocates for equal sharing
stream (New Zealand European) perspectives of power and control through the processes of
have a bias towards autonomy rather than towards reciprocity and feedback as a partnership princi-
affiliation and a sense of community within a ple. It also requires consolidation that Mori exist
group [7]. Fundamentally, the collaborative and in a cultural dynamic that is collective and/or
collective methods of learning associated with cooperative [2, 4, 5, 8, 9, 18]. Overall, the goal of
Mori traditions, values and customs would be the kaupapa Mori research approach is to
useful within learning environments for Mori improve the Hauora (health and well-being) of
[2, 4, 17]. The use of kaupapa Mori research each individual within and for the whnau
10 Diabetes Among Mori and Other Ethnic Groups in New Zealand 167
(family), in this instance for those living with Methods

type 2 diabetes. Essentially the core of kaupapa
Mori is the catch cry to be Mori is the norm Eligibility Criteria
where the research approach is for/with/by Mori
and it does not exclude or reject mainstream or Population
other indigenous cultures [2, 4, 17, 19]. This review considered studies in indigenous and
underserved ethnic groups (Mori, Pacific
[namely, Samoa, Cook Islands, Tonga, Fiji, Niue,
Diabetes in Aotearoa, New Zealand Samoa, and Solomon Islands], South Asian
[namely, Bangladesh, India, Sri Lanka, and
The high type 2 diabetes (T2D) prevalence among Nepal] and other Asian ethnic groups) with or
Mori was first reported in 1962 [20]. Immigrants without comparison with European ethnic groups
from the nearby Tokelau Islands were subse- in New Zealand.
quently shown to have an increasing prevalence of
T2D compared with those remaining on the Study Type
Islands [21]. Work was commenced in South This review considered non-experimental (obser-
Auckland, an area with large Mori, Pacific and vational) study designs including before and after
Asian communities, in the 1990s [22] to obtain studies, prospective and retrospective cohort
diabetes epidemiological data linked with a range studies, case control studies and cross-sectional
of diabetes preventative strategies to inform a studies for inclusion.
comprehensive diabetes management and preven-
tion strategy. A local plan (the first such plan pub- Outcomes
lished globally) was developed and reviewed in This review considered studies that reported on
2000, showing progress in some areas but not oth- one or more of the following outcomes: inci-
ers [23]. By 2006, subsequent data showed that dence or prevalence of any type of diabetes
the national epidemic of diabetes was continuing (type 1 diabetes [T1D], T2D or gestational dia-
unabated and now included Asians [24]. betes mellitus [GDM]), biological (namely,
Since 2006, a number of new publications pre-diabetes, metabolic syndrome, obesity) and
have emerged, reporting the prevalence of diabe- lifestyle (namely, smoking, physical inactivity,
tes and its complications. The impression is that and poor diet) risk factors for diabetes; and
the diabetes epidemic continues to make inroads health (mortality and morbidity (namely,
in spite of a range of policies to reduce the obe- complications)).
sity epidemic and improve diabetes care. There
remain few studies describing molecular biologi-
cal differences between Polynesians and Search Strategy and Information
Europeans. This chapter will describe an updated Sources
review on diabetes and its complications among
Mori, Pacific people and Asian vs. European The search strategy aimed to find both peer-
ethnic groups in New Zealand. reviewed published studies and current reports
by the New Zealand Ministry of Health. A two-
step search strategy was utilised in this review.
Objectives An initial search of electronic databases
(MEDLINE/PubMed, EMBASE, Scopus and
This review sought to provide an updated report CINAHL) and the New Zealand Ministry of
on the epidemiology of diabetes including preva- Health website was undertaken using identified
lence, risk factors for complications and severe keywords and index terms (see Appendix 1).
outcomes (e.g. hospitalisation, death) in Mori Next, the reference list of all identified reports
and other ethnic groups in New Zealand. and articles was searched for additional studies.
Studies in English published after 2004 were across studies between 6.5 and >7.0 %, and
considered for inclusion in this review. Where from 5.76.4 % to >6.0 % for pre-diabetes
possible, efforts were made to contact authors (Table 10.1). Only one study used the oral glu-
for missing information. cose tolerance test (OGTT) in a population-
based sample [57]. Similarly, pre-existing
diabetes has been identified through self-report,
Data Collection primary care/general practice records, hospital
chart review and data linkage between pharma-
Data were extracted from papers included in the ceuticals and/or laboratory investigations and
review independently by two reviewers using hospital admissions/national administrative
data extraction tools developed for this review. datasets. Study populations were identified/
The data extracted included specific details about recruited using various methods including com-
the study design, participants and setting and munity screening, clinic databases and popula-
outcomes. tion based health databases (Table 10.1).
Table 10.2 shows the prevalence of diabetes
and pre-diabetes. The prevalence of known dia-
Data Synthesis betes was estimated to be 2.25.0 % among
Europeans vs. 7.012.2 % among Mori, 8.9
Since statistical pooling was not possible 38 % among Pacific people and 9.137.1 %
because of the diverse types of studies reviewed, among Asians. The prevalence of diabetes includ-
the findings were presented in narrative form, ing known diabetes and undiagnosed diabetes by
including tables to aid in data presentation HbA1c screening ranged from 1.1 to 6.1 %
where appropriate. among Europeans but 3.3 to 9.8 % among Mori,
5.315.4 % among Pacific peoples and 4.39.3 %
among Asians. Undiagnosed diabetes alone
Results ranged from 0.4 to 1.1 % among Europeans but
3.66.5 % among Mori, 4.68.1 % among
Figure 10.1 presents a flow diagram summarising Pacific people and 7.47.5 % among Asians. No
the identification of studies included for review. consistent gender differences were found.
Our search strategy identified 292 citations after Three studies (South Auckland, Waikato and
duplicates were removed. Of these, 246 citations Auckland) described the prevalence of diagnosed
were excluded after the first screening of titles diabetes [34, 47, 55] in patients who had been
and/or abstracts for inclusion and exclusion crite- hospitalised with an acute cardiovascular event
ria, leaving 46 citations for a second full text (mean ages 60, 68 and 15+ years, respectively).
screening. After further assessment, 12 citations The prevalence among Mori, Pacific and Asians
were excluded leaving 34 observational studies was approximately double that of European New
for final inclusion in the review. Zealanders (23.339.2 % vs. 11.318.1 %). One,
a nationwide study among people with a mood
and anxiety disorder, aged 16 years, again
Descriptive Data Synthesis showed the greater prevalence of known diabetes
among Mori and Pacific peoples over Europeans
Table 10.1 presents study characteristics of 34 (8.011.3 % vs. 3.6 %) [38].
studies included for review, which were pub- A key theme is that within each study, the
lished in years ranging from 2005 to 2015 [25 prevalence of diabetes is generally highest in
60]. Studies were heterogeneous for age, Pacific people and then Mori, who generally
ethnicity and screening/diagnostic characteris- have a prevalence approximately twice that of
tics. For instance, case definition of diabetes Europeans. Asians also have a high prevalence
using HbA1c diagnostic cutoffs was varied generally between (but sometimes below or
Identification
Records identified through database Additional records identified

searching through other sources
(n = 343) (n = 1)
Records after some duplicates removed

(n = 292)
Screening
Records screened Records excluded

(n = 292) (n = 246)
Full-text articles assessed

Full-text articles excluded
Eligibility
for eligibility
(n = 12)
(n = 46)
Studies included in
qualitative synthesis
(n = 34)
Included
Studies included in
quantitative synthesis
(meta-analysis)
(n = 0)
Fig. 10.1 PRISMA 2009 Flow Diagram for systematic review of publications since 2006, when the last review was
undertaken
above) Mori and Pacific people. These odds impaired fasting glucose were reported among
ratios are consistent with the 2013/2014 New Mori in the Waikato region [57].
Zealand Health Survey. Table 10.3 shows the prevalence of risk factors
There are few studies of pre-diabetes. Two, a for complications among people with diabetes by
national study and a South Auckland study [29, ethnic group. Across the data sources from pri-
32], using HbA1c of 5.76.4 % and 6.17.0 % as mary care (including the national Get Checked
diagnostic criteria, respectively, found that the data) to a mixture of primary care and hospitals
prevalence of HbA1c defined pre-diabetes was and from both national, Waikato, South Auckland,
approximately sixfold higher among non- West Auckland and South Island studies, Mori,
Europeans than Europeans (12.819.9 % vs. 2.1 Pacific people and Asians are more likely to have
2.5 %, respectively). Similarly, high prevalence poor glucose control than Europeans. European
estimates for impaired glucose tolerance and/or and Mori patients with type 1 diabetes were more
Table 10.1 Characteristics of observational studies reviewed

Study identification Study design (follow-up) Participants and setting Outcomes (measures, units)
Agban et al. (2008) [25] Cross-sectional Sample size: N = 7782 Baseline and 2 years for all
(baseline and 2 years Age (years): range in mean outcomes
from cohort study) from 56 to 68 Poor glycaemic control
Gender: male 42 % prevalence (HbA1c >8 %,
Ethnicity: European, Mori, %)
Pacific, Asian (Indian), other HBP prevalence (>130/80,
Asian, Other (Middle Eastern, %)
Latin American/Hispanic and Obesity prevalence
African) (measured BMI 30 for
Eligibility criteria: T2D European, Asian, Indian
patients who had undertaken and Other; BMI 32 for
an annual review in 2002 or Mori and Pacific, %)
2003, and had a follow-up Current smoker prevalence
review 2 years later (self-report, %),
Setting: nationwide data from
primary health care reviews of
patients with T2D collated
within 15 primary care
organisations or diabetes trusts
Brian et al. (2010) [26] Population-based Sample size: N = 1381 (73 %) HbA1c and visual acuity
cross-sectional survey Age (years): 40 measured
using multistage Gender: NR Mean HbA1c (9.9 2.3 %)
cluster random Ethnicity: Fijian Vision threat occurred in at
sampling Eligibility criteria: HbA1c and least one eye of 11.5 %.
visual acuity were measured Diabetes (predominantly
Setting: maculopathy) caused pinhole
Diabetic eye disease was acuity <6/18, <6/60 and
assessed using 90-dioptre lens <3/60 for 3.8 %, 1.1 % and
dilated funduscopy 0.7 % of eyes, respectively.
No person was bilaterally
blind (<6/60) due to diabetes,
but 2.3 % (all on oral
antiglycaemics alone) were
6/60 bilaterally. Compared
with recent diabetes
diagnosis, diagnosis
>10 years ago was predictive
of any (odds ratio [OR] 8.13;
95 % confidence interval [CI]
3.2820.21; P < 0.001) and
vision-threatening (OR 5.25;
95 % CI 1.7116.12;
P = 0.004) eye disease.
Although 80.6 % claimed
regular general diabetes
checkups, only 36.5 %
recalled previous dilated
ocular examination. Four
eyes had received laser
treatment
Table 10.1 (continued)

Brewer et al. (2008) [27] Cross-sectional Sample size: N = 47,904 (408 Diabetes prevalence (HbA1c
(baseline from cohort with prior diagnosis of 7 %, %)
study) and prospective diabetes) All-cause mortality (data
cohort and (median Age (years): 0 linkage, HR with 95 % CI)
2 years) Gender: male 44 %
Ethnicity: European/other,
Mori, Pacific, Asian
(unspecified)
Eligibility criteria: participants
in a Hepatitis Foundation
screening campaign for
hepatitis B (19992001)
Setting: lower half of the North
Island of NZ
Chan et al. (2015) [28] Retrospective cohort Sample size: N = 1,475,347 Age-standardised diabetes
(from 2004 to 2010) Age (years): 0 prevalence (dysglycaemia by
Gender: male 48 % modified ADA and WHO
Ethnicity: European/other, criteria, %)
Mori, Pacific, Asian (Indian),
Chinese, other Asian
Eligibility criteria: residents
who had utilised publicly
funded health services in NZ
and lived in Auckland in 2010
Setting: Auckland metropolitan
region, linked data between a
laboratory repository and
national administrative datasets
for District Health Boards
Coppell et al. (2013) [29] Cross-sectional Sample size: N = 4721 Diabetes prevalence
Age (years): 15 (self-report diagnosed or
Gender: NR HbA1c 6.5 %, %)
Eligibility criteria: NR Pre-diabetes prevalence
Ethnicity: European/Other (HbA1c 5.76.4 %, %)
(Asian, Middle Eastern, Latin
American and African), Mori,
Pacific
Setting: nationwide, 2008/2009
New Zealand Adult Nutrition
Survey
Elley et al. (2008) [30] Cross-sectional Sample size: N = 29,179 Poor glycaemic control
Age (years): range in mean prevalence (HbA1c >8 %, %)
from 56 to 68 HBP prevalence
Gender: NR (>130/80, %)
Eligibility criteria: T2D Obesity prevalence
Ethnicity: European, Mori, (measured BMI 30, %)
Pacific, Asian (Indian), Other Albuminuria prevalence
Asian, Other (ACR 2.5 for men; 3.5 for
Setting: nationwide linked women, %)
hospital records and data Current smoker
obtained from primary health (self-report, %),
care reviews of patients with 5-year CVD risk prevalence
T2D (Framingham risk score
15 %, %)
(continued)

Elley et al. (2010) [31] Prospective cohort Sample size: N = 36,127 Fatal or nonfatal CVD
(median 3.9 years) Age (years): median 59 incidence (data linkage using
Gender: male 49 % ICD-9 and ICD-10 codes,
Eligibility criteria: T2D HR with 95 %CI)
without previous CVD
Ethnicity: European, Mori,
Pacific, Asian (Indian), East
Asian, Other (Middle Eastern,
Latin American/Hispanic,
African, and others)
Setting: nationwide linked
hospital records and data
obtained from primary
health care reviews of
patients with T2D
Ellison et al. (2005) [32] Cross-sectional Sample size: N = 50,819 Diabetes prevalence (HbA1c
Age (years): >20 >7 %, %)
Gender: male 44.6 % Pre-diabetes or diabetes
Ethnicity: European, Mori, prevalence (HbA1c >6 %, %)
Samoan, Cook Island, Asian
(Indian), Chinese
Eligibility criteria: none
specified
Setting: South Auckland.
Screening programme to detect
elevated fasting
hyperglycaemia using HbA1c
Faatoese et al. Cross-sectional Sample size: N = 252 T2D prevalence (prior
(2011) [33] Age (years): range 2064 diagnosis by medical
Gender: male 40 % records, %)
Ethnicity: Mori
Eligibility criteria: Mori
descent
Setting: community screening
for CVD risk factors in Wairoa
Feigin et al. (2006) [34] Cross-sectional Sample size: N = 1423 Diabetes (doctor diagnosed
Age (years): 15 by self-report, %)
Gender: Male 47 %
Ethnicity: European, Mori/
Pacific, Asian/other
(unspecified)
Eligibility criteria: first-ever
cases of stroke 20022003
Setting: Auckland population-
based register
Frederikson and Cross-sectional Sample size: N = 11,977 Maculopathy prevalence
Jacobs (2008) [35] (baseline from cohort Age (years): range 7100 (clinical retinopathy
study) Gender: Male 52 % screening, %)
Pacific (Samoan, Cook Island
Mori, Tongan, Niuean), Asian
(Indian), Chinese, Other
Eligibility criteria: all records of
first screening visits 20022005
for people with diabetes
Setting: Wellington regional
retinal screening programme
for people with diabetes

Grey et al. [36] Cross-sectional Sample size: N = 10,301 Diabetes prevalence
Age (years): range 3574 (electronic medical records,
Gender: male 52 % %)
Ethnicity: Pacific (Samoans,
Tongan, Cook Island Mori,
Niuean) Other Pacific
(including Tokelauan)
Eligibility criteria: none
specified (Fijian excluded)
Setting: primary care practices
in nine Primary Health
Organisations in Auckland and
Northland
Ihaka et al. Cross-sectional Sample size: N = 53 Classification of foot risk
(2012) [37] Age (years): 18 status (podiatric practitioners
Gender: men 53 % category 2, %)
Ethnicity: Mori Obesity, hypertension,
Eligibility criteria: Mori with dyslipidaemia and
diabetes who had not received retinopathy prevalence
a national diabetes assessment (self-report, %)
for >12 months and had
undetected pedal pulses,
absence of sensation, previous
history of peripheral vascular
disease, or ulceration and no
below-knee amputation
Setting: Waitemata district,
Auckland 20072008
Jackson et al. Retrospective cohort Sample size: N = 45,970 Hospital admissions for
(2009) [38] (from 1996 to 2007) Age (years): 0 people with diagnosed
Gender: NR diabetes (hospital records, %)
Mori, Pacific, Asian (Indian),
Chinese, Other Asian
Eligibility criteria: public
hospital discharge with any
mention of T1D or T2D from
1996 to 2007
Setting: counties Manukau
National Minimum Dataset,
2007
Jeffreys et al. Prospective cohort Sample size: N = 74,847 All-cause mortality (data
(2005) [39] (13 years) Age (years): 25 linkage hospital discharge to
Gender: male 50 % death records, %)
Ethnicity: European/other
(non-Mori/non-Pacific),
Mori, Pacific
Eligibility criteria: hospital
discharge diagnosis of diabetes
between 1988 and 2001
Setting: record linkage study of
national hospital discharge
records to death records
(continued)

Joshy et al. (2009) [40] Retrospective cohort Sample size: N = 7900 Hospital renal admission
(from 2003 to 2006) Age (years): NR (hospital records, HR with
Gender: male % NR 95 % CI)
Ethnicity: European, Mori Start dialysis or kidney
Eligibility criteria: renal transplantation (hospital
complication-free adult records, HR with 95 % CI)
diabetes patients registered Death from renal disease
with Waikato regional diabetes (data linkage to death
service, diagnosed with records, HR with 95 % CI)
diabetes before 2003
Setting: Waikato District
Health Board region
Joshy et al. (2009) [41] Cross-sectional Sample size: N = 45,500 Age-standardised diabetes
Age (years): NR prevalence (medical records,
Gender: Male % NR %)
Pacific, Asian
Eligibility criteria: all patients
registered with the practices as
of 1 July 2007
Setting: 10 Rotorua General
Practice Group practices
Joshy et al. (2009) [42] Cross-sectional Sample size: N = 1819 CKD prevalence (eGFR<60,
Age (years): 18 %)
Gender: Male 49 % Microalbuminuria prevalence
Ethnicity: European, Mori, (ACR 2.529.9 for men;
Pacific, Asian 3.529.9 for women, %)
Eligibility criteria: all patients Albuminuria prevalence
with diabetes registered with (ACR 30, %)
the practices as of 1 July 2007
Setting: 10 Rotorua General
Practice Group practices
Joshy et al. (2010) [43] Retrospective cohort Sample size: N = 9043 Age-standardised, all-cause
(from 2003 to 2007) Age (years): 18 mortality rate (data
Gender: male 50 % linkage,/100,000
Ethnicity: European, Mori person-years)
Eligibility criteria: diabetes
patients registered with the
Waikato Regional Diabetes
Service database before 2008,
diagnosed before 2003 and
alive as of 2003
Setting: Waikato region

Kenealy et al. Cross-sectional Sample size: N = 48,444 Fatal/nonfatal CVD
(2008) [44] (baseline from cohort) Age (years): range in mean incidence (data linkage to
and prospective cohort 5366 hospital/mortality data, HR
(median 2.4 years) Gender: male 49 % with 95 %)
Ethnicity: European, Mori, Microalbuminuria prevalence
Pacific, Asian (Indian), East (ACR 2.5 for men; 3.5 for
Asian, Other (Middle Eastern, women, %)
Latin American/Hispanic, Macroalbuminuria
African, others) prevalence (ACR >30, %)
Eligibility criteria: T2D and no Current smoker prevalence
previous CVD (self-report, %)
Setting: people with T2D who Poor glycaemic control
attended at least one diabetes prevalence (HbA1c 10 %, %)
annual review in primary
health care as part of a national
programme from 2000 to 2005;
forms the NZ Diabetes Cohort
Study
Kenealy et al. Cross-sectional Sample size: 65,171 Microalbuminuria prevalence
(2012) [45] Age (years): median 65 (ACR >2.5 men, 3.5 women
Gender: male 51 % to <30, %)
Ethnicity: European, Mori, Macroalbuninuria prevalence
Pacific, Asian (Indian), East (ACR 30<100, %)
Asian, Other (Middle Eastern, Advanced albuminuria
Latin American/Hispanic, prevalence (ACR 100, %)
African, others)
Eligibility criteria: adults in
primary care with T2D, not on
renal replacement therapy
Setting: T2D who had attended
at least one diabetes annual
review in primary health care
as part of a national
programme between 2000 and
2006 in New Zealand; forms
the NZ Diabetes Cohort Study
Kerr et al. (2006) [46] Cross-sectional Sample size: N = 4193 Mortality (data linkage, HR
(baseline from cohort) Age (years): range in mean with 95% CI)
and prospective cohort 5560 Smoking prevalence
(mean 3.8 years) Gender: Male 49 % (self-report, %)
Pacific, Asian, Other
Eligibility criteria: T2D
Hospital admission for MI or
CCF from 1999 to 2001
Setting: the study population
included 4193 individuals with
T2D from South Auckland
who participated in a primary
care audit from 1994 to 1999
(continued)

Kerr et al. (2008) [47] Cross-sectional Sample size: N = 973 T2D prevalence
Age (years): mean 60 (diagnosed, %)
Gender: Male 75 %
Eligibility criteria: patients
admitted for acute CV event
Setting: patients presenting to
Middlemore Hospital Coronary
Care Unit with an acute CVD
event from July 2004 to June
2006. CVD risk factor data
was electronically collected
using acute PREDICT
Kolt et al. (2007) [48] Cross-sectional Sample size: 112 Diabetes prevalence
Age (years): mean 66 (self-report, %)
Gender: male 45 %
Ethnicity: Asian (India, Sri
Lanka, Pakistan, Fiji)
Eligibility criteria: NR
Setting: Auckland-based Asian
Indian community
organisations
Lawrenson et al. Cross-sectional Sample size: N = 26,096 Poor glycaemic control
(2009) [49] Age (years): 20 prevalence (HbA1c >8 %,
Gender: NR OR with 95% CI)
Asian
Eligibility criteria: aged
20 years with T2D
Setting: Hamilton general
practice register linked to
Waikato regional diabetes
service register
Lim et al. (2008) [50] Cross-sectional Sample size: 180 Poor glycaemic control
Age (years): mean 54 prevalence (HbA1c 8.0 %,
Ethnicity: Mori HBP prevalence (treated
Eligibility criteria: household hypertension or 130/85, %)
members with at least one Central obesity prevalence
Mori resident, or Mori with (waist circumference
past GDM or aged 23 years >102 cm for men, >88 cm for
with 2 parents with known women, %)
diabetes Metabolic syndrome
Setting: newly diagnosed with prevalence, (ATPIII
diabetes during a community criteria, %)
screening programme, Te Wai Current prevalence
o Rona Diabetes Prevention (self-report, %)
Strategy Microalbuminuria prevalence
(ACR 2.529.9 for men,
3.529.9 for women, %)
Albuminuria prevalence
(ACR 30, %)
CKD prevalence (eGFR
<60, %)
Retinopathy prevalence
(microaneurysms 5, %)

New Zealand Cross-sectional Sample size: N = 13,309 Diabetes prevalence
Ministry of Health Age (years): 15 (self-report, adjusted rate
(2013/2014) [51] Gender: men and women, the ratios [for age, gender,
proportion is not noted ethnicity])
Eligibility criteria: resident
population aged 15 years
living in permanent dwellings,
aged-care facilities or student
accommodation
Ethnicity: European/Other,
Setting: nationwide, New
Zealand Health Survey
Robinson et al. Cross-sectional Sample size: 5917 Poor glycaemic control
(2006) [52] Age (years): mean 60 prevalence (HbA1c >8.0 %,
Ethnicity: European, Mori, Albuminuria prevalence
Pacific, Asian (Indian), Other (ACR 2.5 for men; 3.5 for
Asian, Other women, %)
Eligibility criteria: patients Current smoker prevalence
with diabetes (self-report, %)
Setting: external audit of Obesity prevalence (BMI
general practice diabetes care >30, %)
carried out in South and West HBP prevalence (systolic
Auckland by the Diabetes Care >140, %)
Support Service At-risk feet (by clinical
review, %)
Dyslipidaemia prevalence
(TC:HDL ratio>4.5)
Robinson et al. Cross-sectional Sample size: N = 62,002 Microalbuminuria prevalence
(2015) [53] (baseline from cohort) Age (years): range in mean (ACR 2.5 for men or 3.5
and prospective cohort 5566 for women, and < 30 for
(median 7.14 years) Gender: male 49 % both, %)
Ethnicity: European/other, Macroalbuminuria
Mori, Pacific, Asian (Indian prevalence (ACR 30, %)
subcontinent or Fijian Indians), Lower limb amputation
other Asian (Southeast Asian, incidence (linked hospital
Chinese) records ICD codes, rate/1000
Eligibility criteria: T2D person years)
Setting: nationwide
Scott et al. Cross-sectional Sample size: 1251 Microalbuminuria prevalence
(2006) [54] Age (years): <26 (ACR >2.5 for males; >3.5
Gender: male 50 % for females, %)
Ethnicity: Mori/Pacific
Islanders, Europeans, Others
Eligibility criteria: attended a
diabetes centre at least once in
the previous 3 years, any
person with diabetes born after
1 January 1978
Setting: 12 paediatric hospital
and adult hospitals across NZ
and forms the all-NZ young
persons diabetes audit,
20032004
(continued)

Scott et al. Cross-sectional Sample size: 4408 Diabetes prevalence (chart
(2007) [55] (baseline from Age (years): mean 68 review, %)
retrospective cohort) Gender: male 65 %
Ethnicity: European, Mori
Eligibility criteria: hospital
discharge diagnosis of all with
acute coronary syndromes
from 1999 to 2002
Setting: Waikato hospital,
Hamilton
Scott et al. Cross-sectional Sample size: N = 12,992 Diabetes prevalence
(2008) [56] Age (years): 16 (self-report, %)
Gender: male 41 % Any 12-month mood and
Ethnicity: European/other, anxiety disorder prevalence
Mori, Pacific (CIDI 3.0/DSM-IV, %)
Eligibility criteria: subsample
with any 12-month mood and
anxiety disorder prevalence
(CIDI 3.0/DSM-IV) for
diabetes prevalence and
subsample with diabetes for
mental disorder prevalence
Setting: nationwide
Simmons et al. Cross-sectional Sample size: 3784 Undiagnosed diabetes, IGT,
(2009) [57] Age (years): 28 and IFG age-standardised
Gender: male 36 % prevalence (OGTT 1998
Ethnicity: Mori WHO criteria, % with
Eligibility criteria: 95 %CI)
nonpregnant adult Mori
Setting: all Mori residents
within the boundaries of the
Waikato District Health Board
and the tribal area of Ngati
Tuwharetoa in the
neighbouring Lakes District
Health Board
Smith et al. Cross-sectional Sample size: 1.4 million Diabetes age-standardised
(2010) [58] Age (years): 0 prevalence (data linkage
Gender: male 46 % records ICD-10-AM
Ethnicity: European/other, system, %)
Mori, Pacific, Asian Age-standardised proportion
Eligibility criteria: health of diabetes cases 1 medical/
events recorded between surgical hospital admissions
January 2006 and December in 2007 (data linkage
2007 for those alive records, %)
Setting: records of subsidy
claims for pharmaceuticals and
laboratory investigations were
linked to records in a national
hospital admissions database to
reconstruct populations of
four District Health Boards
Counties Manukau, Northland,
Waitemata and Auckland

Tomlin et al. Cross-sectional Sample size: 13,281 Poor glycaemic control
(2006) [59] Age (years): 0 prevalence (HbA1c >9.0 %,
Gender: Male 52 % %)
Ethnicity: European, Mori/ Microalbuminuria prevalence
Pacific (ACR >2.5 for males; >3.5
Eligibility criteria: any for females, %)
diabetes High Cholesterol prevalence
Setting: data were collected (6.0, %)
from all 242 practices Smoking prevalence
participating in the South Link (self-report, %)
Get Checked programme,
every practice in the South
Island outside Christchurch
city (the main urban centre)
and 14 practices within
Christchurch
T1D type diabetes, T2D type 2 diabetes, HbA1c glycated haemoglobin, BMI body mass index, NR not reported, ADA
American Diabetes Association, WHO World Health Organization, ACR albumin creatinine ratio, CVD cardio vascular
disease, ICD International Classification of Diseases, ATPIII Adult Treatment Panel, IFG impaired fasting glucose, IGT
impaired glucose tolerance, OGTT oral glucose tolerance test, HR hazard ratio, OR odds ratio, CKD chronic kidney
disease, eGFR estimated glomerular filtration rate, TC total cholesterol HDL high-density lipoprotein, NZ New Zealand,
CIDI Composite International Diagnostic Interview, DSM Diagnostic and Statistical Manual of Mental Disorders
Table 10.2 Prevalence of diabetes and pre-diabetes

Gender European Mori Pacific Asian
Diabetes prevalence and key features
Brewer et al. (2008) [27] 1.1 3.3 5.3 4.3
HbA1c screening/prior
diagnosis; age
5668 years
Chan et al. (2015) [28]a Male 3.0 8.2 11.4 10.8
Prior diagnosis; age 0+ Female 2.2 7.0 11.6 9.3
years
Coppell et al. (2013) [29] 6.1 9.8 15.4
HbA1c screening/prior
diagnosis; age 15+ years
Ellison et al. (2005) [32]a Male 1.0 4.8 8.1 (Cook Island 7.5
HbA1c screening; age Mori)
>20 years 5.1 (Samoan)
Female 0.4 3.6 4.6 (Cook Island 7.4
Mori)
5.4 (Samoan)
Faatoese et al. Male 11.8
(2011) [33] Female 10.0
Prior diagnosis; age
2064 years
Feigin et al. (2006) [34] 11.3 31.4 23.3
Prior diagnosis; age 15+
years; post stroke
Grey et al. (2010) [36] Male 2537
Prior diagnosis; age 26 (Other Pacific)
3574 years Female 2938
32 (Other Pacific)
(continued)

Joshy et al. (2009) [41] 3.1 7.0 8.9 6.7
Prior diagnosis; age not
specified
Kerr et al. (2008) [46] 18.1 31.5 39.2 33.0
60 years; post-acute
CVD
Kolt et al. (2007) [48] Male 34.0
Prior diagnosis; age Female 37.1
66 years
New Zealand Ministry of 2.0 (vs. 2.8 (vs. 1.8 (vs.
Health (2013/2014) [51] non-Mori) non-Pacific) non-Asian)
years: rate ratios
Scott et al. (2007) [55] 17.5 33.0
68 years; post-acute
CVD
Scott et al. (2008) [56] 3.6 8.0 11.3
years; mental health
Simmons et al. Male 6.5
(2009) [57] Female 4.2
Undiagnosed by OGTT;
28+ years
Smith et al. (2010) [58] Male 5.0 12.2 13.9 11.3
Prior diagnosis; age 0+ Female 4.0 10.6 15.0 9.1
years; subsidy claims
Pre-diabetes prevalence
Coppell et al. (2013) [29] 18.1 20.5 24.0
Ellison et al. (2005) [32] Male 2.5 14.7 19.9 (Cook Island 18.3
Mori)
12.8 (Samoan)
Female 2.1 12.8 15.0 (Cook Island 13.3
Mori)
13.3 (Samoan)
Simmons et al. Male 5.4 (IFG)
(2009) [57] 8.5 (IGT)
Female 3.0 (IFG)
9.7 (IGT)
a
Denotes studies which reported data for additional ethnic minority groups not presented
likely to have poor glucose control than those with the Waikato was particularly high (90.0 %) [50].
type 2 diabetes in the South Island [59]. Current smoking was higher among Mori across
Other complication risk factors were more studies (25.034.9 %) than Pacific people
variable between ethnic groups. Mori and Pacific (15.817.8 %), Europeans (8.519.9 %) and
people with known diabetes were more likely to Asians (5.87.7 %). High blood pressure was con-
be obese (60.776 %) than Europeans (43.8 sistently lowest among Asians (17.552 %).
46.6 %) or Asians (24.928.4 %). The prevalence However, the prevalence of high blood pressure
of obesity among Mori with newly diagnosed was higher among Mori and Pacific people than
diabetes in a diabetes prevention programme in Europeans in one national study [25] but lower in
Table 10.3 Prevalence or risk of clinical and lifestyle risk factors for complications and mortality in people with
diabetes
Poor glycaemic control
Agban et al. (2008) (baseline) 23.6 46.6 68.4 40.2
[25]a
Agban et al. (2008) [25] 23.1 44.4 51.9 31.7
(2 years)a
Elley et al. (2008) [30] 23 43 50 36
Kenealy et al. (2012) [45] 6 19 27 12
Lawrenson et al. (2009) [49] 1 (reference) OR 1.78 (95 %CI: OR 1.53
1.33,2.39) (95 %CI:
1.33,1.76)
Lim et al. (2008) [50] 34.4
Robinson et al. (2006) [52]a 22.7 49.5 55.7 44.9
Tomlin et al. (2006) [59] 30.7 (T1D) 51.1 (T1D)
10.4 (T2D) 26.0 (T2D)
High blood pressure
Agban et al. (2008) [25] 27.8 39.8 34.7 27.4
(baseline)
Agban et al. (2008) [25] 23.1 30.5 26.2 17.5
(2 years)
Elley et al. (2008) [30] 67 65 61 52
Ihaka et al. (2012) [37] 49
Lim et al. (2008) [50] 89.4
Robinson et al., (2006) [52]a 32.6 27.6 23.7 24.0
CVD risk/poor metabolic controlb
Elley et al. (2008) [30] 29.6 30.1 18.5 19.6
Ihaka et al. (2012) [37] 55
Lim et al. (2008) [50] 89.4
Robinson et al. (2006) [52]a 27.3 46.3 35.4 34.8
Tomlin et al. (2006) [59] 19.8 (T1D) 17.1 (T1D)
28.9 (T2D) 31.8 (T2D)
Obesity
Agban et al. (2008) [25] 45.1 62.2 62.8 28.4
(baseline)
Agban et al. (2008) [25] 43.8 60.7 60.8 25.3
(2 years)
Elley et al. (2008) [30] 46 73 73 25
Ihaka et al. (2012) [37] 62
Lim et al. (2008) [50] 90.0
Robinson et al. (2006) [52]a 46.6 76.0 73.7 24.9
Current smoker
Agban et al. (2008) [25] 8.5 28.0 16.5 5.8
(baseline)
Agban et al. (2008) [25] 7.8 25.7 14.4 4.2
(2 years)
Elley et al. (2008) [30] 9.6 27.0 16.6 6.1
Ihaka et al. (2012) [37] 25
Kenealy et al. (2008) [44] 11 31 17 6
(continued)

Kenealy et al. (2012) [45] 10.0 28.3 15.8 6.2
Kerr et al. (2006) [46] 11.0 26.9
Lim et al. (2008) [50] 30.6
Robinson et al. (2006) [52]a 13.1 34.9 17.8 7.7
Tomlin et al. (2006) [59] 19.9 (T2D) 25.5 (T1D)
10.9 (T2D) 27.5 (T2D)
Depression/anxiety
Scott et al. (2008) [56] 9.3 (depression) 16.5 (depression) 9.6
17.5 (anxiety) 23.5 (anxiety) (depression)
22.5 (anxiety)
a
b
Includes metabolic syndrome, dyslipidaemia and CVD risk
one national and one South/West Auckland/study microalbuminuria was similar among Mori who
(27.665 % vs. 23.761 % vs. 23.167 % Mori, were newly diagnosed as those with known dia-
Pacific, Europeans, respectively [30, 52]. betes, albuminuria rates were lower (but already
Generally Europeans had lesser CVD risk than higher at European rates) [50].
Mori, but other inter-ethnic group comparisons Other complications have been less com-
were variable. In one study [56], comorbid depres- monly studied. There are only two recent studies
sion and anxiety in people with diabetes were of eye disease: one of maculopathy in those with
higher among Mori compared with European or known diabetes, with the highest prevalence
Pacific ethnic groups. among Pacific people and similar prevalence
One study compared risk factor prevalence in between Europeans, Mori and Asians [35]. The
2002 and among the same patients 2 years later in other showed a very low rate of retinopathy at
primary care [25]. All risk factors improved to a diagnosis among Mori in the Waikato [50]. Foot
greater or lesser extent, but the degree varied by complications were most common among Mori,
ethnic group. The greatest improvements in gly- followed by Europeans, Pacific people and then
caemia occurred in Pacific people and Asians, Asians [53]. Cardiovascular event rates were
and the least improvements in blood pressure 2330 % higher among Mori than Europeans in
occurred in the Mori and Europeans. There was two national samples [30, 44], but not signifi-
limited change in smoking or obesity across eth- cantly higher among Pacific people. Asian car-
nic groups. There remained a very high preva- diovascular event rates were 6 % (nonsignificant)
lence of risk factors across all ethnic groups. to 29 % higher than Europeans.
Table 10.4 shows the prevalence of diabetes Hospitalisation and mortality are integrated
complications and mortality in the studies measures of a range of diabetes, both comorbid
reviewed. One study showed that Mori people and psychosocial characteristics. Hospitalisation
had a substantially increased risk (hazard ratio is also substantially higher among Mori than
was 25) of starting dialysis or having transplant Europeans and Pacific people (who experience
therapy compared with Europeans [40]. Rates of roughly similar rates) whose hospitalisation
microalbuminuria (28.439.0 %) and macroalbu- rates are higher than Asians. Standardised mor-
minura (958.2 %) were highest among Mori in tality rates are significantly higher among Mori
primary care, secondary care and in both T1D than Europeans. However, mortality rates are
and T2D compared with Europeans (1724.9 % lower among Pacific people than Europeans.
and 3.56 % respectively), Pacific people Mortality risk for Asians vs. Europeans was not
(3132.1 % and 9.117.0 %) and Asians statistically significant in the three studies
(2324.1 % and 4.17.0 %). While the rate of reviewed (Table 10.4).
Table 10.4 Prevalence of diabetes-related complications, risk or rate of CVD/mortality

Renal complications
Elley et al. (2008) [30] 27 49 49 30
(albuminuria)a
Joshy et al. (2009) (start 1 (reference) HR 25.2 (95 % CI:
dialysis or transplant) 10.7,59.7)
Joshy et al. (2009) (CKD) Male 25.7 17.9
Female 26.2 20.3
Joshy et al. (2009) Male 24.1 39.0
(microalbuminuria) Female 18.9 28.4
Joshy et al. (2009) Male 5.8 19.2
(albuminuria) Female 6.0 14.8
Kenealy et al. (2008) [44] 20 32 31 23
(microalbuminuria)a
Kenealy et al. (2008) [44] 4 14 15 5
(macroalbuminuria)a
Kenealy et al. (2012) [45] 22.9 32.8 32.1 24.1
(microalbuminuria)a
Kenealy et al. (2012) [45] 3.5 9.0 9.1 4.1
(macroalbuminuria)a
Kenealy et al. (2012) [45] 1.7 8.1 7.8 2.2
(advanced albuminuria)a
Lim et al. (2008) [50] 29.6
(microalbuminuria)
Lim et al. (2008) [50] 7.7
(macroalbuminuria)
Lim et al. (2008) [50] 5.6
(CKD)
Robinson et al. (2006) 27.4 55.2 50.4 36.6
[52] (albuminuria)a
Robinson et al., (2015) 23 33 31 23
[53] (microalbuminuria)a
Robinson et al., (2015) 5 17 17 7
[53] (macroalbuminuria)a
Scott et al. (2006) [54] 17 43.8 (Mori/Pacific)
(microalbuminuria)a
Tomlin et al. (2006) [59] Male 27.8 (T1D) 33.3 (T1D)
35.1 (T2D) 58.2 (T2D)
Female 24.8 (T1D) 47.6 (T1D)
26.0 (T2D) 42.2 (T2D)
Eye complications
Frederikson and Jacobs 12 11 16 (Samoan) 13
(2008) [35]a 14 (Cook
Island Mori)
19 (Tongan)
Lim et al. (2008) [50] 1.9
Foot complications
Ihaka et al. (2012) [37] 100
Robinson et al. 2.13/1000 3.48/1000 1.70/1000 0.68/1000
(2015) [53]a
(continued)

Hospital admissions
Jackson et al. (2009) 19 24 18 13
[38]a
Joshy et al. (2009) 1 (reference) HR 7.0 (95 %CI:
4.6,10.6)
Smith et al. (2010) 27 37 25 21
CVD events/mortality
Brewer et al. (2008) [27] HR 2.56 HR 2.71 (95 %CI: HR 0.53 HR 1.70
(ref. HbA1c 4.0<5.0 %) (95 %CI: 1.90,3.85) (95 %CI: (95 %CI:
0.71,9.19) 0.161.75) 0.10,29.73)
Elley et al. (2010) [31] 1 (reference) HR 1.23 (95 %CI: HR 1.07 HR 1.29
1.14,1.32) (95 %CI: (95 %CI:
0.99,1.15) 1.14,1.46)
Jeffreys et al. (2005) [33] SMR 2.99 SMR 3.44 (95 %CI: SMR 2.23
(ref. not hospitalised (95 %CI: 3.30,3.58) (95 %CI:
diabetes) 2.93,3.04) 2.06,2.41)
SMR 2.98 SMR 3.80 (95 %CI: SMR 2.41
(95 %CI: 3.64,3.97) (95 %CI:
2.93,3.04) 2.21,2.61)
Joshy et al. (2009) 1 (reference) HR 4.1 (95 %CI:
1.5,11.4)
Joshy et al. (2010) Male 551/100,000 1012/100,000
Female 491/100,000 808/100,000
Kenealy et al. [44] 1 (reference) HR 1.30 (95 %CI: HR 1.04 HR 1.06
1.19,1.41) (95 %CI: (95 %CI:
0.95,1.13) 0.91,1.24)
a
Discussion Mori [32] suggests that screening for diabetes in

that area may have had a positive impact on early
The results of this review show that the burden of case finding and management for prevention of
diabetes and related complications remains diabetes-related complications. Despite this, the
greater among Mori and other non-European increased burden of diabetes among Mori/Pacific
ethnic groups as shown in our previous reviews in rates and Asians compared with Europeans has
2000 and 2006 [22, 24]. The prevalence of known continued to rise and is now one of New Zealands
diabetes among those aged 30 years in South most serious health issues, which should inform
Auckland in the early 1990s was 4.2 % in the new national diabetes plan in New Zealand.
Europeans, 7.9 % among Mori and 5.5 % among
Pacific people [42] with approximately 3350 %
undiagnosed [6, 43, 61]. Decades later, these rates Diabetes-Related Policy
have approximately doubled. Glycaemic control
remains poorer among non-European groups and Since the last review [24], diabetes-related policy
many of the other complications and risk factors has positively changed for quality of care, screen-
are especially common among Mori. Renal coming and prevention. For those with diabetes, the
plications rates, particularly microalbuminuria Ministry of Health funded a national programme
and macroalbuminuria, remain substantially (Get Checked) in 2001 that paid general practi-
higher among Mori. Conversely, the low preva- tioners to undertake a diabetes annual review that
lence of retinopathy at diagnosis among Waikato could provide the clinical assessments to inform
the next steps in the management plan of each In 2015, a 5-year plan Living Well with
participating patient. An evaluation in 2007 [62] Diabetes [68] was proposed to ensure that all
reported that many Primary Health Organisations New Zealanders with diabetes, or at risk of devel-
(PHOs), especially those with larger Mori and oping T2D, had access to high-quality, people-
Pacific Island peoples populations, had identi- centred health services.
fied barriers to these population groups using the
programme and had put in place initiatives to
address these barriers. From the numbers and Diabetes Screening
coverage rates reported by DHBs, it appears that
these initiatives were more successful with As non-European populations are at greater risk
Pacific peoples. Although the numbers of Mori of diabetes, they are theoretically more likely to
accessing the programme were increasing, the be screened under the DHB managed health tar-
coverage rates continued to fall short of the target gets programme [69]. This programme was
rate set by District Health Boards (DHBs). In introduced in 2007 but reduced in 2009. One of
2008, poor retention in Get Checked was shown the targets was that 90 % of the eligible popula-
[63] such that in 2005/2006, only 6100 (57 %) of tion would have had their cardiovascular risk
the estimated 10,600 diabetes patients enrolled in assessed within the last 5 years (this would
the Waikato utilised the free check. Younger include a diabetes test).
patients aged <40 years, those of Mori or Asian
origin, and those with type 1 diabetes were less
likely to be retained in the programme with regu- Diabetes Prevention and Prevention
lar checks. A further review in 2011 [64] demon- Research
strated that the Get Checked programme did not
systematically result in improved management or Strategies to prevent diabetes include the Green
outcomes for people with diabetes. As a result, Prescription [70] where a prescription of physical
from July 2012, the Get Checked programme activity to a patient is provided. A recent ran-
was shelved and was replaced by the Diabetes domised controlled trial among Mori and
Care Improvement Package [65]. A key change Europeans with diabetes found that both face-to-
under the new package was placing the responsi- face and telephone delivery of the Green
bility for coordination of diabetes care in the Prescription are associated with improvements in
hands of each DHB, thus allowing DHBs to tailor both weight and HbA1c [71]. Generally, fewer
diabetes care towards their population structure, Mori have participated in the GRx programme
as opposed to a standard national plan under the [72]. This lower participation may have been due
Get Checked programme. to lower referrals from primary care even when
Wider guidance for quality care were released fees, administrative and other barriers have been
by the Ministry of Health in 2014 [66] to comple- removed [70].
ment work from the New Zealand Guidelines Wider family-based [73] healthy eating and
Group. A Virtual Diabetes Register (VDR) cre- activity guidelines [73] are also in place. A com-
ated from six major databases was established by prehensive plan for [74] includes 22 initiatives
the Ministry of Health in 2013 [67]. The six data that target interventions for those who are obese,
sources were: hospital admissions coded for dia- increase support for those at risk of becoming
betes, outpatient attendees for diabetes and dia- obese and introduce broad strategies to make
betes retinal screening, prescriptions of specific healthier choices easier. A limited review of obe-
antidiabetic therapies, laboratory orders for mea- sity (as the main risk factor for type 2 diabetes)
suring diabetes management and primary health prevention strategies over the past 20 years have
(general practitioner) enrolments. There are no indicated that key strategies have largely been
special guidelines for the use of antidiabetes unimplemented [75]. A key success over these
medications among Polynesians. 20 years has been the Energize programme in the
Waikato [76], associated with reductions in child- Strategy has not been followed up, and diabetes
hood obesity. The sister study, Te Wai o Rona: metabolic targets are frequently not met based
Diabetes Prevention Strategy [77], was associ- upon primary care data. Diabetes among all eth-
ated with reductions in weight among Mori with nic groups, particularly Mori, remains a major
and without pre-diabetes in a vanguard study, but public health menace.
research funding was not continued after 3 years. There clearly needs to be more research as to
The coach-supported structured approach to life- why the gap remains between current diabetes
style change has recently been shown to success- outcomes and what should be possible with a
fully limit gestational weight gain across nine national organisational structure that includes a
European countries [78]. Other prevention stud- single payer across primary and secondary care,
ies among Mori (e.g. Ngti and Healthy) show- well-developed primary care including Mori
ing initial promise [79] have not progressed. and Pacific health services, a well-trained work-
force and a raft of policy initiatives to prevent
diabetes and its complications and their wider
Future Directions: Unmet Needs, social determinants. Specific research into the
Unanswered Questions, excess renal disease among Mori is urgently
Unquestioned Answers needed. Current research into the genetic, intra-
uterine/foetal determinants of diabetes and its
The focus of this chapter has been the epidemiol- complications should be broadened within a cul-
ogy of diabetes among Mori and other ethnic turally safe framework. More research into
communities in New Zealand. In spite of sub- appropriate behavioural and self-management
stantial policy initiatives, the prevalence of dia- interventions, building upon global research but
betes, the risk factors for complications, tailoring to local cultural needs, are also crucial
especially poor blood glucose control, and the for those with diabetes. However, the real need is
rates of complications remain substantially for more large scale intervention studies, devel-
higher in these ethnic populations groups com- oped to go to scale, that can transform the current
pared with European New Zealanders. There diabetes healthcare landscape.
have been successful initiatives such as Project We call on the New Zealands Ministry of
Energize, the school based lifestyle programme, Health to make diabetes prevention and manage-
with its high acceptability among Mori and ment among ethnic minority groups a national
Pacific people and has not been extended to too health priority area for urgent action in both dia-
many other areas in the country. The early prom- betes health services development and rollout,
ise from Te Wai o Rona: Diabetes Prevention and both outcomes and translational research.
Appendix: Database Searching Medline Search -8/10/15

Strategies
1 Diabetes mellitus, type 1 or 158,509
diabetes, gestational/ or diabetes
Search Outline mellitus, type 2 or diabetes mellitus
2 Diabetes.ab,ti. 243,850
3 1 or 2 274,256
Concept Search terms
4 New Zealand 20,180
Diabetes Diabetes mellitus, type 1
5 New Zealand.ab,ti. 26,249
Diabetes, gestational
6 4 or 5 35,119
Diabetes mellitus, type 2
7 Pacific Islander.ab, ti. 1069
Diabetes mellitus
8 Mori.ab, ti. 1680
New Zealand New Zealand
9 Samoa 220
Native and unserved Pacific Islander
ethnic groups 10 Polynesia 695
Mori
11 Cook Islands.ab, ti. 88
Samoa
12 Tonga 141
Cook Islands
13 Fiji 437
Polynesia (MESH)
14 Niue.ab, ti. 26
Tonga
15 Melanesia 357
Fiji
16 Solomon Islands.ab, ti. 282
Niue
17 Oceanic Ancestry Group 5709
Solomon Islands
18 Bangladesh 5328
Melanesia (MESH)
19 India 50,204
Oceanic Ancestry Group
(MESH) 20 Sri Lanka 2620
Southeast Asian 21 Nepal 4202
Bangladesh 22 7 or 8 or 9 or 10 or 11 or 12 or 13 70,730
or 14 or 15 or 16 or 17 or 18 or 19
India or 20 or 21
Sri Lanka 23 3 and 6 and 22 220
Nepal 24 Limit 23 to yr = 2005 -Current 156
NB: search terms with/are MESH terms
Scopus Search 14. Thomas DR. Science, values and culture. In:
Department Psychology, editor. Understanding cul-
ture and ethnicity: patterns and policies in plural
TITLE-ABS-KEY (diabetes) AND TITLE- societies. Hamilton: University of Waikato; 1995.
ABS-KEY (New Zealand) AND TITLE-ABS- p. 7687.
KEY (Pacific Islander OR Mori OR Samoa 15. Cram F, Smith L, Johnstone W. Mapping the
themes of Mori talk about health. New Zealand
OR Cook Islands OR Polynesia OR Tonga
Med J. 2003;116(1170):1p following U353. Epub
OR Fiji OR Niue OR Solomon Islands OR 2003/03/28. eng.
Melanesia OR Ocean Ancestry Group OR 16. Mane J. Kaupapa Mori: a community approach.
Southeast Asian OR Bangladesh OR India MAI Rev. 2009;3(1):19.
17. Smith GH. Mori education: revolution and transfor-
OR Sri Lanka OR Nepal) AND PUBYEAR >
mative action. Can J Nativ Educ. 2001;24(1):5767.
2004 AND NOT ALL (trials) OR (RCT) OR 18. Walker R, Amoamo J, editors. Nga tau tohehe: years
ALL (intervention) of anger. Auckland: Penguin; 1987.
Total results: 98 19. Came HA. Doing research in Aotearoa: a Pkeh
exemplar of applying Te Ara Tika ethical framework.
Search date: 12/10/2015
Ktuitui: N Z J Soc Sci Online. 2013;8(12):6473.
20. Prior IAM. A health survey in a rural Mori com-
munity with particular emphasis on the cardiovas-
cular, nutritional and metabolic findings. NZ Med
References J. 1962;61:333.
21. Ostbye T, Welby TJ, Prior IAM, Salmond CE, Stokes
1. New Zealand Census. 2013. www.stats.govt.nz. YM. Type 2 (non-insulin-dependent) diabetes melli-
Accessed 2/12/2015. tus, migration and westernisation: the Tokelau Island
2. Smith LT, editor. Decolonising methodologies: Migrant study. Diabetologia. 1989;32:58590.
research and indigenous peoples. Dunedin: University 22. Simmons D. Diabetes and its complications in New
of Otago Press; 1999. Zealand: an epidemiological perspective. N Z Med
3. Bishop R. Initiating empowering research? N Z J. 2000;113:423.
J Educ Stud. 1994;29(1):175. 23. Simmons D, Kenealy T, Scott DJ. Implementing the
4. Smith LT, editor. Decolonizing methodologies: South Auckland Diabetes Plan: barriers and lessons.
research and indigenous peoples. 2nd ed. Dunedin: NZ Med J. 2000;113:3646.
University of Otago Press; 2012. 24. Joshy G, Simmons D. Epidemiology of diabetes in
5. Hudson M, Milne M, Reynolds P, Russell K, Smith New Zealand: revisit to a changing landscape. N Z
B. Te Ara Tika: guidelines for researchers on Med J. 2006;119(1235):U2003.
health research involving Mori. Auckland: Health 25. Agban H, Elley CR, Kenealy T, Robinson E. Trends
Research Council of New Zealand; 2010. ISBN in the management of risk of diabetes complications
978-9-908700-86-5. in different ethnic groups in New Zealand primary
6. Bishop R, Glynn T, editors. Culture counts: chang- care. Prim Care Diabetes. 2008;2(4):1816.
ing power relations in education. 1st ed. Palmerston 26. Brian G, Fischer-Harder K, Sikivou B, Qoqonokana
North: Dunmore Press Limited; 1999. MQ, Szetu J, Ramke J. Diabetic eye disease among
7. Durie MH. The health of indigenous peoples. Br Med adults in Fiji with self-reported diabetes. Clin Exp
J. 2003;326(7388):5101. Epub 2003/03/08. Eng. Ophthalmol. 2010;38(9):86774.
8. Durie MH, editor. Whaiora: Mori Health develop- 27. Brewer N, Wright CS, Travier N, et al. A New
ment. 2nd ed. Auckland: Oxford University Press; Zealand linkage study examining the associations
1998. between A1C concentration and mortality. Diabetes
9. Hudson M, Milne M, Reynolds P, Russell K, Smith Care. 2008;31(6):11449.
B. Te Ara Tika: guidelines for researchers on health 28. Chan WC, Jackson G, Wright CS, et al. The future
research involving Mori. Auckland: Health Research of population registers: linking routine health data-
Council of New Zealand; 2008. sets to assess a populations current glycaemic sta-
10. Durie MH. The treaty of Waitangi and health care. N tus for quality improvement. BMJ Open. 2014;4(4),
Z Med J. 1989;102(869):2835. Epub 1989/06/14. e003975.
Eng. 29. Coppell KJ, Mann JI, Williams SM, et al. Prevalence
11. Durie MH, editor. Te Mana, te kawanatanga: the poli- of diagnosed and undiagnosed diabetes and prediabe-
tics of Mori self-determination. 1st ed. Auckland: tes in New Zealand: findings from the 2008/09 Audit
Oxford University Press; 1998. Nutrition Survey. NZ Med J. 2013;126(1370):23.42.
12. Orange C, editor. The treaty of Waitangi. Wellington: 30. Elley CR, Kenealy T, Robinson E, et al. Cardiovascular
Bridget Williams Books Limited; 1987. risk management of different ethnic groups with type
13. Evans I, Paewai MK. Functional analysis in a bicul- 2 diabetes in primary care in New Zealand. Diabetes
tural context. Behav Chang. 1999;16(1):2036. Res Clin Pact. 2008;79(3):46873.
31. Elley CR, Robinson E, Kenealy T, Bramley D, Drury 45. Kenealy T, Elley CR, Collins JF, Moyes SA, Metcalf
PL. Derivation and validation of a new cardiovas- PA, Drury PL. Increased prevalence of albuminuria
cular risk score for people with type 2 diabetes: the among non-European peoples with type 2 diabetes.
New Zealand Diabetes Cohort Study. Diabetes Care. Nephrol Dial Transplant. 2012;27(5):18406.
2010;33(6):134752. 46. Kerr GD, Gamble GD, Doughty RN, Simmons D,
32. Ellison TL, Elliott R, Moyes SA. HbA1c screening Baker J. Mortality in individuals with type 2 diabetes
for undiagnosed diabetes in New Zealand. Diabetes and heart disease in a unique New Zealand popula-
Metab Res Rev. 2005;21(1):6570. tion. Diabetes Med. 2006;23(12):13138.
33. Faatoese AF, Pitama SG, Gillies TW, et al. Community 47. Kerr AJ, McLachland A, Furness S, et al. The bur-
screening for cardiovascular risk factors and levels of den of modifiable cardiovascular risk factors in
treatment in a rural Mori cohort. Aust NZ J Publ the coronary care unit by age, ethnicity, and socio-
Health. 2011;35(6):51723. economic status: PREDICT CVD-9. NZ Med
34. Feigin V, Carter K, Hackett M, et al. Ethnic disparities J. 2008;121(1285):2033.
in incidence of stroke subtypes: Auckland Regional 48. Kolt GS, Schofield GM, Rush EC, Oliver M, Chadha
Community Stroke Study, 20022003. Lancet Neurol. NK. Body fatness, physical activity, and nutritional
2006;5(2):1309. behaviours in Asian Indian immigrants to New
35. Fredrikson LG, Jacobs RJ. Diabetes eye screening in Zealand. Asia Pac J Clin Nutr. 2007;16(4):66370.
the Wellington region of New Zealand: characteris- 49. Lawrenson R, Gibbons V, Joshy G, Choi P. Are there
tics of the enrolled population (20022005). NZ Med disparities in care in people with diabetes? A review
J. 2008;121(1270):2134. of care provided in general practice. J Prim Health
36. Grey C, Wells S, Ridell, et al. A comparative anal- Care. 2009;1(3):17783.
ysis of cardiovascular disease risk profiles of five 50. Lim S, Chellumuthi C, Crook N, Rush E, Simmons
Pacific ethnic groups assessed in New Zealand pri- D. Low prevalence of retinopathy, but high prevalence
mary care practice: PREDICT CVD-13. NZ Med of nephropathy among Maori with newly diagnosed
J. 2010;123(1325):4152. Te Wai o Rona: diabetes prevention strategy. Diabetes
37. Ihaka B, Bayley A, Rome K. Foot problems in Maori Res Clin Pract. 2008;80(2):2714.
with diabetes. NZ Med J. 2012;125(1360):4856. 51. New Zealand Ministry of Health. Annual Update of
38. Jackson G, Orr Walker B, Smith J, Papa D, Field Key Results 2013/14: New Zealand Health Survey.
A. Hospital admissions for people with diagnosed dia- 2014.
betes: challenges for diabetes prevention and manage- 52. Robinson T, Simmons D, Scott D, et al. Ethnic dif-
ment programmes. NZ Med J. 2009;122(1288):1321. ferences in Type 2 diabetes care and outcomes in
39. Jeffreys M, Wright C, Mannetje A, Huang K, Pearce Auckland: a multiethnic community in New Zealand.
N. Ethnic differences in cause specific mortality NZ Med J. 2006;119(1235):U1997.
among hospitalised patients with diabetes: a link- 53. Robinson TE, Kenealy T, Garrett M, Bramley D,
age study in New Zealand. J Epidemiol Community Drury PL, Elley CR. Ethnicity and risk of lower limb
Health. 2005;59(11):9616. amputation in people with Type 2 diabetes: a prospec-
40. Joshy G, Dunn P, Fisher M, Lawrenson R. Ethnic tive cohort study. Diabetes Med 2016;33:5561.
differences in the natural progression of nephropa- 54. Scott A, Toomath R, Bouchier D, et al. First national
thy among diabetes patients in New Zealand: hos- audit of the outcomes of care in young people
pital admission rate for renal complications, and with diabetes in New Zealand: high prevalence of
incidence of end-stage renal disease and renal death. nephropathy in Maori and Pacific Islanders. NZ Med
Diabetologia. 2009;52(8):14748. J. 2006;119(1235):U2015.
41. Joshy G, Porter T, Le Lievre C, Lane J, Williams M, 55. Scott AR, Cheng A, Greenacre M, Devlin
Lawrenson R. Prevalence of diabetes in New Zealand G. Implications of hyperglycaemia and ethnicity
general practice: the influence of ethnicity and social in patients with acute coronary syndromes in New
deprivation. J Epidemiol Coummunity Health. Zealand. Diabetes Obes Metab. 2007;9(1):1216.
2009;63(5):38690. 56. Scott K, McGee MA, Schaaf D, Baxter J. Mental-
42. Joshy G, Porter T, Le Lievre C, Lane J, Williams M, physical comorbidity in an ethnically diverse popula-
Lawrenson R. Implications of using estimated glo- tion. Soc Sci Med. 2008;66(5):116573.
merular filtration rate (GFR) in a multi ethnic popula- 57. Simmons D, Rush E, Crook N. Prevalence of undi-
tion of diabetes patients in general practice. NZ Med agnosed diabetes, impaired glucose tolerance, and
J. 2010;123(1310):918. impaired fasting glucose among Maori in Te Wai
43. Joshy G, Colonne CK, Dunn P, Simmons D, o Rona: diabetes prevention strategy. NZ Med
Lawrenson R. Ethnic disparities in causes of death J. 2009;122(1288):308.
among diabetes patients in the Waikato region of New 58. Smith J, Jackson G, Orr-Walker B, et al. A population-
Zealand. NZ Med J. 2010;123(1310):1929. based approach to the estimation of diabetes preva-
44. Kenealy T, Elley CR, Robinson E, et al. An associa- lence and health resource utilisation. NZ Med
tion between ethnicity and cardiovascular outcomes J. 2010;123(1310):6273.
for people with type 2 diabetes in New Zealand. 59. Tomlin AM, Tilyard MW, Dawson AG, Dovey
Diabetes Med. 2008;25(11):3028. SM. Health status of New Zealand European, Maori
and Pacific patients with diabetes in 242 New Zealand health service among Mori in the Waikato and Ngti
general practices. N Z Med J. 2006;119(1235):U2004. Tuwharetoa rohe. Mai J. 2015;4(2):11833.
60. Simmons, D. The epidemiology of diabetes and 71. Williams, M. Te Rongoaa Kakariki: Kanohi-ki-te-
its complications in New Zealand. Diabetic Med. kanohi, e pai ana? Auckland University of Technology.
1996;13:3715. 2014. URL: https://aut.researchgateway.ac.nz/bitstream/
61. Simmons D, Thompson C, et al. Polynesians: prone to handle/10292/8648/WilliamsM.pdf?sequence=6.
obesity and Type 2 diabetes but not hyperinsulinemia. 72. Pringle R. Health and physical activity promotion:
Diabet Med. 2001;18:1938. a qualitative examination of the effect of receiving
62. Ministry of Health and District Health Boards: a Green Prescription (GRx). Hamilton: University
Effectiveness of the Get Checked diabetes pro- of Waikato. Wif Malcolm Insititute of Educational
gram. 2007. URL: http://www.oag.govt.nz/2009/ Research; 2008.
performance-audits/get-checked.htm. 73. Eating and Activity Guidelines for New Zealand
63. Joshy G, Lawrenson R, Simmons D. Retention Adults, Healthy Families NZ. 2015. URL: http://www.
of patients in the Get Checked free annual dia- parliament.nz/en-nz/parl-support/research- papers/
betes review program in New Zealand. NZ Med 00PLLawRP2014041/obesity-and-diabetes-in-
J. 2008;121(1270): U2945. URL: http://www.nzma. new-zealand.
org.nz/__data/assets/pdf_file/0007/17818/Vol-121- 74. Ministry of Health. Childhood obesity plan. 2015. URL:
No-1270-14-March-2008.pdf. http://www.health.govt.nz/our-work/diseases-and-
64. Review of the Diabetes Get Checked Programme. conditions/obesity/childhood-obesity-plan.
Report to ministry of health by Dr Brandon Orr- 75. Swinburn B, Wood A. Progress on obesity prevention
Walker, National Clinical Director for Diabetes. over 20 years in Australia and New Zealand. Obes
2011. URL: https://www.beehive.govt.nz/release/ Rev. 2013;14(Supp 2):608.
diabetes-get-checked-programme-review. 76. Rush E, McLennan S, Obolonkin V, Vandal AC,
65. Upfront: The new face of diabetes care in New Hamlin M, Simmons D, Graham D. Project energize:
Zealand. Best Pract J. 2012; Issue 44. URL: http:// whole-of region primary school nutrition and physical
www.bpac.org.nz/BPJ/2012/may/upfront.aspx. activity programme; evaluation of body size and fit-
66. Ministry of Health Quality Standards for Diabetes ness five years after the RCT. Br J Nutr. 2013;19:19.
Care Toolkit. 2014. URL: http://www.health.govt.nz/ 77. Simmons D, Rush E, Crook N. Development and
publication/quality-standards-diabetes-care- piloting of a community health worker based inter-
toolkit-2014. vention for the prevention of diabetes among New
67. United Nations Public Administration Network, Zealand Mori in Te Wai o Rona: diabetes prevention
New Zealand Health Improves Diabetes Policy strategy. Public Health Nutr. 2008;11:131825.
with Big Data Analytics. 2013. URL: http://www. 78. Simmons D, Jelsma JG, Galjaard S, Devlieger R, van
unpan.org/PublicAdministrationNews/tabid/115/ Assche A, Jans G, Corcoy R, Adelantado JM, Dunne
mctl/ArticleView/ModuleID/1467/articleId/40103/ F, Desoye G, Harreiter J, Kautzky-Willer A, Damm
Default.aspx. P, Mathiesen ER, Jensen DM, Andersen LL, Lapolla
68. Ministry of Health. Living well with diabetes: a A, Dalfra M, Bertolotto A, Wender-Ozegowska E,
plan for people at high risk of or living with dia- Zawiejska A, Hill D, Rebollo P, Snoek FJ, van Poppel
betes 20152020. Wellington: Ministry of Health. MN. Results from a European multicenter random-
2015. URL: http://www.health.govt.nz/publication/ ized trial of physical activity and/or healthy eating to
living-well-diabetes. reduce the risk of gestational diabetes mellitus: the
69. New Zealand Parliament, Parliamentary support, DALI Lifestyle Pilot. Diabetes Care. 2015;38:16506.
Research Papers. Obesity and diabetes in New 79. Coppell KJ, Tipene-Leach DC, Pahau HL, Williams
Zealand. 2014. URL: http://www.parliament.nz/en-nz/ SM, Abel S, Iles M, Hindmarsh JH, Mann JI. Two-
parl-support/research-papers/00PLLawRP2014041/ year results from a community-wide diabetes preven-
obesity-and-diabetes-in-new-zealand. tion intervention in a high risk indigenous community:
70. Williams M, Rush ER, Crook N, Simmons D. the Ngati and Healthy project. Diabetes Res Clin
Perceptions of a Te Rongoa kakariki: green prescription Pract. 2009;85(2):2207.
Diabetes in Eastern Europe
11
Mykolay Khalangot, Vitaliy Gurianov,
Alexander Vaiserman, Ieva Strele,
Vasile Fedash, and Victor Kravchenko
This review is dedicated to relevant diabetes that belong to different socioeconomic and
mellitus-related aspects in several European political communities.
countries that emerged after the breakup of the In this chapter we are trying to analyze some
Soviet Union. After more than two decades of diabetes-related aspects in four lower middle
existence, these countries significantly differ (Armenia, Georgia, Moldova, Ukraine), two
according to their economic standing, demo- upper middle (Azerbaijan, Belarus), and two
graphic parameters, as well as presence, speed, high (Latvia and Russia) income countries in
and orientation of healthcare reforms accordance with the World Bank classification
(Table 11.1). The former Soviet republics that [1] in the former Soviet Union.
prior to 1991 had similar socioeconomic charac- Lower middle-income countries are facing an
teristics and identical healthcare system are now epidemiological transition, with increases in the
independent Eastern European and Baltic states prevalence and mortality related to noncommuni-
cable diseases such as diabetes [2, 3], but the dif-
ferences in life expectancy at birth (Table 11.1)
are not always directly related to economic char-
M. Khalangot, MD, ScD (*)
acteristics. Genetic, ethnic, geographic, and cul-
Shupyk National Academy of Postgradual Medical
Education, Kyiv, Ukraine tural features may also influence health outcomes,
e-mail: [email protected] e.g., the Caucasus region in the former Soviet
V. Gurianov, PhD Union was known for longevity of its population
Bogomolets National Medical University, [4]. Furthermore, diabetes-related mortality data
Kyiv, Ukraine [5] and data on mortality with diabetes mellitus
A. Vaiserman, ScD marked as the cause of death [6], obtained from
Chebotariov Institute of Gerontology, National different independent sources, also does not dem-
Academy of Medical Sciences, Kyiv, Ukraine
onstrate any negative relationship with gross
I. Strele, MD, PhD national income (GNI) per capita (Table 11.1).
Riga Stradins University, Riga, Latvia
Even a positive association between GNI and
V. Fedash, MD, PhD mortality level can be revealed when using cer-
Institute of Physiology and Sanocreatology of ASM,
tain statistical methods (p < 0.001, chi-square test
Chisinau, Moldova
for trend). These data raise doubts about methods
V. Kravchenko, ScD
of recording mortality, as well as about the
Komisarenko Institute of Endocrinology and
Metabolism, National Academy of Medical Sciences, possibility to efficiently influence this outcome in
Kyiv, Ukraine diabetes patients.

DOI 10.1007/978-3-319-41559-8_11
192 M. Khalangot et al.
Table 11.1 Some total and diabetes-related characteristics of the Eastern European countries and Latvia
Total Diabetes related No. of diabetes mellitus
population, Life expectancy deaths (2079), per deaths cases, both sexes,
Country, income GNI per capita, millions at birth, years 100,000 population all ages, per 100,000
level [1] $ (2014) [1] (2014) [1] (2013) [1] 2013 [5] population 2012 [6, 7]
Armenia, LMIC 3,780 3,006 75 32.6 43.12012
Azerbaijan, UMIC 7,590 9,538 71 24.1 7.82007
Belarus, UMIC 7,340 9,470 72 79.6 3.62009
Georgia, LMIC 3,720 4,504 74 32.9 10.42010
Moldova, LMIC 2,550 3,556 69 37.1 10.72010
Russian 13,210 143,8 71 137.2 6.32010
Federation, HIC
Ukraine, LMIC 3,560 45,36 71 45.5 4.92012
Latvia, HIC 15,660 1,990 74 57.9 23.62012
Comments:
GNI per capita (formerly GNP per capita) is the gross national income, converted to US dollars using the World Bank
Atlas method, divided by the midyear population
LMIC lower middle-income countries ($1,0464,125), UMIC upper middle-income countries ($4,12612,735), HIC
high income countries ($12,736 or more)
Life expectancy at birth indicates the number of years a newborn infant would live if prevailing patterns of mortality at
the time of its birth were to stay the same throughout its life
It should be also noted that geographically Federation (IDF) review [5] and presented in
most of Russias territory lies within Asia, and Table 11.2. The first glance at these data causes
this fact inevitably influences some epidemio- many questions and concerns.
logic features of diabetes mellitus.
Thus, the following analysis will be focused Diabetes prevalence among adults in all coun-
on revealing diabetes-related problems, common tries of Eastern Europe except Russia is given
for Eastern Europe, taking into account particu- as a summary of epidemiologic studies con-
larities of separate countries. According to the ducted in other countries, e.g., diabetes preva-
World Bank classification, Latvia is related to lence in Ukraine and Azerbaijan is evaluated,
Central, rather than to Eastern Europe, and based on studies, and performed among rural
together with Lithuania and Estonia makes up a residents of Albania. The same assessments
subgroup of Baltic states. Nevertheless, it is for Belarus are made according to research
included into this review in order to facilitate from Turkey, Poland, Russia, and Bulgaria
possible comparisons, in the light of common [8]. It is surprising that the data from Turkey
Soviet historic background. was not used for Azerbaijan, as the population
of these countries is ethnically related, and
extrapolations for Belarus are not limited by
Classication and Unique Aspects Polish data but are conducted according to
of the Pathophysiology of Type 1 Turkish and Bulgarian data among others [8].
and Type 2 Diabetes in Region The biggest surprise is caused by diabetes
prevalence data from Russia. The only paper,
Diabetes Epidemiology in Eastern referenced by IDF experts [8], is a study about
Europe type 2 diabetes prevalence among several
Siberian ethnic minorities [9]. To project these
Several epidemiologic diabetes-related features results onto all of Russias territory, let alone to
of seven Eastern European countries and Latvia use it for epidemiologic descriptions of other
were taken from the latest International Diabetes counties, is wrong in our opinion. There are
11 Diabetes in Eastern Europe 193
Table 11.2 Some diabetes-related epidemiologic characteristics of the Eastern European countries extracted from the
IDF diabetes atlas sixth edition [5]
Incidence Mean diabetes-
Adult Diabetes Diabetes Diabetes- type 1 related
population Diabetes cases national comparative related diabetes expenditure per
(2079) in (2079) in prevalence prevalence deaths (014) per person with
Country 1000s 1000s (%) (%) (2079) 100,000 diabetes (USD)
Armenia 208,211 5,495 2,64a 2,46 979 n.a. 187
Azerbaijan 642,069 14,634 2,28a 2,45 2,300 n.a. 521
Belarus 711,219 44,525 6.26a 5.07 7,534 5.6 357
Georgia 315,113 9,342 2.96a 2.45 1,481 4.6 383
Moldova 260,604 7,209 2.77a 2.44 1,320 n.a. 287
Russian 10,892,897 1,092,411 10.03 8.28 197,299 12.1 899
Federation
Ukraine 3,485,802 104,358 2.99a 2.45 20,654 8.1 314
Latvia 155,223 9,570 6.17 4.58 1,152 7.5 1,135
n.a. not applicable
a
Estimate of diabetes prevalence based on extrapolation from other countries
recent epidemiologic studies of diabetes preva- (1,043,580 persons) does not significantly dif-
lence in Russia according to glucose tolerance fer from the known number of diabetes patients
test data that included 3,208 randomly selected in Ukraine, which allows to anticipate a signifi-
persons from four Russian regions (Moscow, cantly higher prevalence of diabetes. A recently
Rostov, Ekaterinburg, and Nizhniy Novgorod) started investigation of fasting glycemia and
aged 3070 year. There were 1,757 (55 %) glucose tolerance in rural areas of Ukraine
women and 1,454 (45 %) men included in the revealed that 12 % of persons over 44 years old
study. During the screening process, the gen- have diabetes [12, 13] (Table 11.3).
eral prevalence of diabetes in the above regions
was 1.9 % [CI 95 % 1,482,47] (n = 62 per-
sons), impaired glucose tolerance 2.8 % [CI Diabetes Mortality Trends
95 % 2.293.47] (n = 91 persons). Prevalence in Ex-Soviet Eastern European
of previously undiagnosed type 2 diabetes in Countries
the above population is 1.9 %, which approxi-
mately corresponds to known T2D prevalence; Economic and political crisis of the last Soviet
thus, the actual diabetes prevalence in the stud- years and the first decade of independence led to
ied population was 4.1 % [10]. An error during a significant deterioration of the Soviet health-
interpretation or presentation of data from care system, which in its turn should have led to
Dogadin et al. [9] can be seen, as some of these increase of mortality in post-Soviet countries. It
same results were published in Russian [11] is notable that health systems play a key role in
indicating a 1.1 % prevalence of previously the control and management of diabetes [30], and
undiagnosed diabetes among 18+ years old lower middle-income countries (LMIC) are fac-
residents of Krasnoyarsk (Russia) [11]. Thus, ing an epidemiological transition, with increases
the claim of IDF experts [5] that Russia is a in the prevalence and mortality related to non-
European country with highest number of peo- communicable diseases, such as diabetes [2].
ple with diabetes cannot be confirmed. Deterioration of insulin access for T1D
The extrapolations regarding diabetes preva- patients was of course the most anticipated rea-
lence in Ukraine are not any less doubtful. son for a rise in mortality among diabetics. The
Indeed, the assumption about the number of term insulin supply crisis was sometimes used
adults (2079 years) living with diabetes to refer to problems with free insulin supply in
Table 11.3 Most recent diabetes-related epidemiologic characteristics of the Eastern European countries extracted
from the national informational sources
Diabetes mellitus
incidence in Diabetes mellitus
children and prevalence in
Prevalence of the Prevalencea of the Diabetes adolescents per children and
diagnosed insulin-treated screening data, 100,000 (age adolescents per
diabetes cases, diabetes cases, % (age group, group available, 100,000 (age group
Country, reference (%) (%) population type) years) available, years)
Armenia [14] 2.0 0.3 n.a. 7.9 (014) 38.9 (014)
Azerbaijan [15] 2.0 0.3 n.a. n.a. n.a.
Belarus [1618] 2.9 0.7 n.a. 13.4 (014) 70.1 (014)
Georgia [19, 20] 1.7 n.a. n.a. 10.4 (014) 42.7 (014)
Moldova [21] 2.4 0.4 n.a. n.a. 47.0 (018)
Russian 2.6 0.6 1.9 (3070, 12.0 (014) 72.8 (014)
Federation urban) 15.3 (1517) 186.4 (1517)
[2225]
Ukraine [13, 26, 3.0 0.5 12.7 (45+, 16.4 (014) 86.9 (014)
27] rural)
13.7 (3080, 13.1 (1517) 210.1 (1517)
mixed)
Latvia [28, 29] 4.1 0.9 n.a. 16.2/22.1 (09) 67.3/78.9 (09)
(mal/fem) (mal/fem)
15.0/17.0 247.6/232.2
(1019) (mal/ (1019) (mal/fem)
fem)
Comments:
n.a. not applicable
a
Estimated by authors on the ground of the statistical data referenced
Ukraine [31]. In 2001, Maria Telishevska et al. increase of mortality among young persons from
demonstrated results of a regional (Lviv, West 1985 to 2000 can reflect problems with insulin
Ukraine) study. Its purpose was to reveal causes supply. Using the same source [6] and taking into
of a high death rate among young people with account the number of people of the correspond-
diabetes in Ukraine [32]. It seems that in other ing gender and age in Russia, Ukraine, and
post-Soviet countries this issue was ignored Belarus, we have calculated diabetes mortality
until now. indicators for males (Fig. 11.3a) and females
Recently, chief Russian endocrinologists/ (Fig. 11.3b) aged 1534 years. The data are
diabetologists, Ivan Dedov and Marina approximated by a parabolic relation (with high
Shestakova (2013), reported that adult T1D mor- determination factor for Ukraine R2 = 0.897 and
tality in 2007 and 2012 was 4.81 and 3.26 cases Russia R2 = 0.879 for males; R2 = 0.859 and
per 100,000 persons, respectively, i.e., according R2 = 0.889 for females accordingly). For Belarus,
to the authors, there was a decrease of 28.4 % the model was credible but less convincing, and,
[24]. Unfortunately in this case, there is no T1D for four other counties, mortality during these
patient mortality data for previous years, which years was not assessed or approximated due to a
prevents a more precise tendency assessment. We small number of cases.
thought it would be reasonable to use an elec- It must be noted that WHO mortality database
tronic WHO resource [6] to perform such mortal- [6] only has data about mortality due to diabetes
ity assessment for seven countries (Fig. 11.1). and not about all deceased persons with diabetes.
The age of the deceased (1524 years) allows During the Soviet period, all statistical indicators
us to relate them to T1D with high chances and did not have any protection from manipulations at
that in its turn makes us assume that a multifold different levels. Sometimes a local health manager
No.of deaths - Diabetes mellitus,both sexes, 15-24 years

300
270
Armenia
240 Azerbaijan
210
Belarus
180
Georgia
150
Latvia
120 Russian
Federation
90
Ukraine
60
30
0
1980 1985 1990 1995 2000 2005 2010 2015 2020
Fig. 11.1 Number of death cases due to diabetes mellitus, both sexes, 1524 years (Extracted from WHO mortality
database [6])
3.0
2.5
male
female
2.0
Deaths/100 000
1.5
1.0
0.5
0.0
1965 1970 1975 1980 1985 1990 1995 2000
Year
Fig. 11.2 Age standardized death rate from diabetes mellitus, ages 0 49, Ukraine 19651998. Source: INED/CHDE
[32] (The figure is reproduced from Telishevska et al. [32] with permission of the publisher, John Wiley and Sons)
could demand for another cause of death to be mortality growth marked in countries including
recorded in a person with T1D, for example, Ukraine at the end of the twentieth century
pneumonia (that could have caused a fatal dia- (Fig. 11.2) cannot be absolutely unambiguous.
betic ketoacidosis) or chronic renal failure so that In 60 out of 64 insulin-treated subjects who
statistical indicators could be improved and dia- died in Lviv Oblast in 1998 and the first 8 months
betes remained unmentioned. Decrease of admin- of 1999 and were under 50 years of age, as identi-
istrative pressure that started after 1986 in USSR fied by Maria Telishevska, diabetes mellitus was
could have led to a more honest classification of listed as the underlying cause of death, and so
mortality causes; thus, an assessment of diabetes they would have been recorded in official
statistics as dying from diabetes [32]. Chronic such possibilities were extremely limited during
renal failure was recorded in 44 (69 %) and keto- previous decades, so when explaining the causes
acidosis in 4 (6 %) of the cases. Thus, the main of a multifold growth of diabetes-related mortal-
cause of death in this cohort was not insufficient ity in Ukraine and other post-Soviet countries,
insulin access (confirmed in one out of four lethal seen during the last decade of the twentieth cen-
cases of ketoacidosis) [32] but more likely the tury (Fig. 11.3a, b), we should note the factor of
absence of renal replacement opportunity. But correct data classification and reporting.
a Belarus
3
Russian Federation
Ukraine
2.5
Belarus
Death per 100000 population
Russian Federation
2 Ukraine
1.5
R2 = 0.8973
0.5
R2 = 0.879
R2 = 0.5388
0
1980 1985 1990 1995 2000 2005 2010 2015
b 3 Belarus
Russian Federation
Ukraine
2.5
Belarus
Death per 100000 population
Russian Federation
2 Ukraine
1.5
R2 = 0.8586
0.5
R2 = 0.6617 R2 = 0.8887
0
1980 1985 1990 1995 2000 2005 2010 2015
Fig. 11.3 (a) Changes of annual mortality due to diabetes countries (Crude data extracted from WHO mortality
(male, 1534 years) for three countries. (b) Changes in database [6] with following annual mortality calculation
diabetes mortality (females 1534 years old) for three and model approximation)
Diabetes related mortality indexes in Russian registered patients, i.e., with due account for the
young adults (1534 years old) that we calcu- number of person-years (PY) of observation, and
lated according to WHO mortality database [6] not relative to adult population. Such exact mor-
increased from 0.7 to 1.8 in men and from 0.6 to tality evaluations can be seen in an assessment of
2.0 in women per 100,000 population (1986 and data from a Latvian diabetes register: Mortality
1999, respectively) with a gradual decrease to in a population with diabetes decreased statisti-
almost initial levels by 2010 (0.85 and 0.7). cally significantly from 57.76 per 1,000 PY in
Taking into account recent recommendations 2000 to 45.33 per 1,000 PY in 2012. The age-
about differentiation of diabetes mellitus clinical standardized mortality ratio of the population
types, which use age at diagnosis <35 years as with diabetes to the population of Latvia
one of the two main hallmarks of the T1D [33, decreased from 1.71 (95 % CI 1.621.81) in 2000
34], most diabetes-related death cases in young to 1.23 (95 % CI 1.191.27) in 2012 [35].
adults (1534 years old) can be considered Mortality tendency for men and women with dia-
T1D. These indicators are significantly lower betes in Latvia are shown in Fig. 11.4.
than those, given by Russian authors for 2007 Unfortunately, there is no analysis of mortality
and 2012 (4.81 and 3.26 death cases per 100,000 tendencies of two main types of diabetes (T1D
adult population, respectively) as portrayal of and T2D) according to this registers data.
T1D mortality [24]; however, in the latter case Ivan Dedov [36] points out that the average
the data involves mortality of T1D adults of any life expectancy among men with T2D in Russia
age from all causes. The data about mortality somewhat exceeds the one for the general Russian
dynamics, recently reported by Russian authors, population (according to Russian official health-
are based on information from a diabetes patient care data in 2009 average life expectancy was
register, updated annually since 2007 [24]; there- 62.9 years for men and 75 years for women).
fore, it would be logical to expect an evaluation According to the author, this is associated with a
of mortality cases in relation to the number of thorough health monitoring of T2D patients, who
80.00
70.00 Mortality in male

y = -1.5697x + 69.618 population with
R2 = 0.8884; p<0.001 diabetes
60.00
50.00 Mortality in female

population with
diabetes
40.00
y = -1.009x + 57.249
R2 = 0.9231; p<0.001
30.00 Mortality in general
y = -0.0267x + 15.529 male population
R2 = 0.0351; p>0.05
20.00
10.00 Mortality in general

y = 0.0636x + 12.84 female population
R2 = 0.3843; p<0.05
0.00
2000
2001
2002
2003
2004
2005
2006
2007
2008
2009
2010
2011
2012
Fig. 11.4 Mortality rate differences by gender in a population with diabetes and general population of Latvia 2000
2012, per 1,000 PY (The figure is reproduced from Pildava et al. [35] with permission of the publisher, Elsevier)
frequent the doctor to correct glucose-lowering Gender and Age-Related Aspects

treatment and other risk factors of cardiovascular of Diabetes Patient Mortality: Issues
mortality: arterial blood pressure, lipid metabo- of Recording and Classifying Death
lism, and blood clotting [36]. These reasons can Cases
be accepted only as explanation for the increas-
ing of average age at death of diabetic patients, Using a constantly functioning patient register1
recently recorded by various population registers allows to study the epidemiology of T1D diag-
(in Ukraine [37, 38], Belarus [17], and Russia nosed in adults and to consider gender
[24]). Comparing average life expectancy differences. The aim of this study is to analyze
(according to age at the time of death) of T2D mortality among T1D patients in Ukraine
patients in this case is inappropriate, as the fre- within the gender aspect. We have used a data-
quency of T2D grows with age, i.e., it is wrong to base with 384,080 DM patients with the first
compare average life expectancy in general pop- entry made on 12 February 1998 and the last
ulation at birth with a T2D population, the aver- entry on 28 December 2007. We have grouped
age age at the time of diagnosis in Ukraine was patients according to probable DM type (T1D
57.3 years [38]. That is why, for example, patients age at the time of diagnosis <30 years in case
with Alzheimers disease die later, comparing to of receiving insulin treatment), as well as
the general population not because of a more grouping according to gender and age. General
intensive treatment but due to this illness being assessment of observation duration in age
diagnosed later in life. groups of this cohort was performed using the
Our cross-sectional analysis of nationwide calculation of person-years. We have analyzed
Ukrainian diabetes mellitus patients register dis- the vital status in groups from 15 to 64 years
covered an increase of age at the time of death during the whole observation period, as well as
among T2D patients in 2007, comparing to 2002. for 2003, 2004, and 2005 (for each year sepa-
This increase was much greater for those being rately). Standardization according to age group
treated with oral antidiabetic drugs (OAD) com- and gender was conducted according to official
paring to insulin-treated patients [37, 38]. Age at Ukrainian mortality data in 2003. Odds ratios
death of insulin-treated T2D patients, from 2002 (ORs) and 95 % confidence intervals (CIs)
to 2007, increased by 1.54 (95 % CI 0.812.26) were calculated. In the same way, the relation
years, and those who used OAD by 6.27 (95 % of mortality risk, associated with the male gen-
CI 3.678.87) years. Life expectancy for the gender, was evaluated using ORs in T1D patients.
eral population of Ukraine, which survived until Data about general mortality in Ukraine was
they were 55 years old in 1989, was about taken from the official WHO website 11
22 years (Fig. 11.5). According to WHO life December 2006.
tables, life expectancy for Ukrainians in 5559 We have created a large cohort of T1D patients
age group was 20.4 years in 2006. Life expec- (29,791 persons, Table 11.4). In general, mortal-
tancy at age 60 years for Ukrainians was 17 in ity among men exceeds such among women:
2000 and 18 years in 2012 [39]. In other words, mortality ORs for men and women = 1.37 (95 %
life expectancy for type 2 diabetes patients CI 1.241.5) p < 0.0001. Women with T1D from
achieved in 2007 (age at the time of death = this cohort also have higher average age and
68.68 years for insulin treated and 72.72 years for
OAD treated) remains lower than in the general 1 Such register was functional in Ukraine for some time
Ukrainian population. These data correspond to (20002009), and several studies in the field of T1D [41,
an analysis based on the data from the 42] as well as T2D [4347] were based on its data. Some
Framingham Heart Study, according to which investigations, based on the Ukrainian Diabetes Mellitus
Register, were published in local journals in Ukrainian
diabetic men and women 50 years and over lived
[4851]; therefore, here we are giving a more detailed
on average 7.5 and 8.2 years less than their non- presentation of some of that published data about gender
diabetic equivalents [40]. aspects of mortality among diabetes patients.
years
80
2002
78
76 2007
74
72
70
68
66
64
62
60
Insulin-treated T2D ODA treated Total population
55+, 2006
Year
75
2002
2007
72
69
66
63
60
Insulin-treated T2D ODA treated
Fig. 11.5 Changes in life expectancy of type 2 diabetes and 2007 (N = 2050) according to the analysis of diabetes
patients in Ukraine, estimated by analyzing the average age register. Lower panel presents mean age and 95 % CI of the
at the time of death of those who died in 2002 (N = 1228) insulin-treated and OAD-treated T2D groups [37]
disease duration (p < 0.0001) comparing to men. (40.23 years) average life expectancy of T1D
At the same time, average life expectancy, calcu- patients in Ukraine.
lated according to average age at the time of Stratification of observation period duration
death, did not significantly differ depending on according to age groups is given in Table 11.4. The
gender (p = 0.47). We should note a very low highest number of person-years of observation
Table 11.4 Same characteristics of T1D patient cohorts [48]

Characteristics All Men Women
Number of patients, n (%) 29,721 (100) 15,187 (51.1) 14,515
Total mortality cases, n (%) 1,917 (6.45) 1,119* 798
Mean age, years (SD) 32.54 (11.91) 31.98 (11.45)* 33.12 (12.34)
Mean age at diagnosis, years (SD) 17.74 (7.5) 17.96 (7.46) 17.52 (7.52)
Mean age at death, years (SD) 40.23 (13.04) 40.41 (12.50) 39.98 (13.76)
Mean T1D duration, years 13.91 (11.05) 13.34 (10.83)* 14.52 (11.25)
Follow-up period in age groups: 151,018 76,566 74,452
1524 years, PY
2534 years, PY 246,252 134,602 111,650
3544 years, PY 222,302 114,382 107,920
4554 years, PY 175,750 81,125 94,625
5564 years, PY 62,639 29,122 33,517
6574 years, PY 21,456 9,966 11,490
75 + years, PY 3,126 1,396 1,730
Modified from Khalangot [48]
*P < 0.001 versus women
PY person-years
Table 11.5 Relative mortality rate of T1D patients who are in the Ukrainian register of diabetes in comparison to
general population of Ukraine by age groups (1564 years old)
2003 2004 2005
Age OR 95 % CI OR 95 % CI OR 95 % CI
A women
1524 9.44 6.2114.3 9.6 6.2514.7 8.6 5.3413.8
2534 10.6 8.0813.9 6.64 4.7211.34 8.37 6.2111.3
3544 6.67 5.08.89 5.71 4.187.8 4.14 2.865.99
4554 3.18 2.284.44 4.08 3.065.43 2.5 1.753.56
5564 2.38 1.512.36 2.15 1.383.36
B men
1524 3.21 2.144.83
2534 3.09 2.433.95 3.28 2.594.14 2.41 1.833.16
3544 2.77 2.213.46 2.69 2.153.37 1.95 1.492.54
4554 1.49 1.121.99 1.54 1.172.02
5564
Modified from Khalangot [48]
ORs are shown only in cases when they are significantly different from one
coincides with the age period between 15 and Ukraine somewhat decrease with age and is sig-
64 years, which justifies further analysis of mortal- nificantly higher for women than for men
ity in these age groups. We should mention that (Table 11.5a, b). For women with T1D aged
only a small preponderance of person-years of 1534 years, there is no mortality gender differ-
observation for women starts only at 45 years old ence, usually for the general population of
which differs significantly from the gender-age Ukraine (Table 11.6).
distribution of the general population of Ukraine. Thus, according to a short observation period
Relation of mortality risks for persons with of nearly all Ukraine T1D population, the absolute
T1D in relation to the general population of mortality of young women and men of the
Table 11.6 Risks of all-cause mortality for men relative to women among T1D patients and the general population
Ukraine stratified by age
T1D Total population (Ukraine, 2002)
Age group, years OR (95 % CI) P OR (95 % CI) P
1524 0.197 2.95 (2.813.09) <0.001
2534 0.110 3.49 (3.373.61) <0.001
3544 1.79 (1.502.13) <0.001 3.64 (3.563.73) <0.001
4554 1.60 (1.321.93) <0.001 3.22 (3.173.28) <0.001
5564 1.39 (1.061.82) 0.021 2.61 (2.582.65) <0.001
ORs are shown only in cases when they are significantly different from one [48]
Table 11.7 The relative mortality rate of diabetic patients who are in the register of diabetes in comparison to general
population of Latvia by age groups
Male Female
Age group RR 95 CI RR 95 CI
<20 2.37 1.134.97 2.47 0.936.59
2029 4.47 3.316.02 11.34 7.3417.45
3039 4.33 3.375.03 6.67 5.218.78
4049 2.47 2.232.69 3.42 2.993.89
5059 1.62 1.541.70 2.25 2.122.39
6069 1.34 1.291.38 1.99 1.932.06
7079 1.30 1.271.34 1.65 1.621.69
80+ 1.04 0.991.08 1.12 1.091.15
Data extracted from Pildava et al. [35]
corresponding age turned out to be the same, Investigation of a T1D patient cohort from the
unlike in the general population. And relative mor- UK, which like the Ukrainian diabetic register
tality of young women was several times higher, was created based on data from primary care doc-
comparing to relative mortality among males. tors (7,713 patients, last observation 1999), con-
The comparison of mortality rate indicators of cluded that the risk of death in relation to persons
diabetic patients with the mortality of the general without diabetes is the highest for young T1D
population of Latvia showed that women with patients, and it is greater among young women,
diabetes had higher relative mortality rate than than men [52]. A study from Ukraine [48] con-
men (Table 11.7). For example, in the 20- to firms this conclusion, complementing the fact
29-year-old women group with diabetes, the that the gender difference of mortality among
mortality rate was 11 times higher than that of T1D patients 1534 years old can disappear. This
women in the population of Latvia in the same increase of mortality risk among young women
age group, but in the 3039 age group nearly with T1D has not been sufficiently explained.
seven times bigger. The mortality rate of men One possible explanation can be the following:
with diabetes compared to that of men in the pop- Ischemic heart disease (IHD) in T1D patients is
ulation of Latvia was increased most in the 2029 observed at a younger age [53], and women get it
age group by more than four times [35]. at the same frequency as men [54]. Premenopausal
This way, analysis of diabetic registers in women, due to higher levels of nitrogen oxide
Ukraine and Latvia shows a significantly higher that men, have a more intensive endothelium-
risk of all-cause mortality in young women with dependent vasodilation. Diabetes leads to endo-
diabetes comparing to women without diabetes, thelial disfunction which neutralizes this
than in men with diabetes comparing to women difference between men and women [55]. Data
without diabetes. about the increase of general mortality relative
a Meta-analysis
Armenia
Azerbaijan
Belarus
Georgia
Latvia
Russian Federation
Ukraine
Total (fixed effects)
Total (random effects)
0.1 1 10 100
Relative risk
b Meta-analysis
Armenia
Azerbaijan
Belarus
Georgia
Latvia
Russian Federation
Ukraine
Total (fixed effects)
Total (random effects)
0.1 1 10
Relative risk
Fig. 11.6 Diabetes-related mortality risks (in relation to general mortality for a specific age group in men and women)
for women comparing to men in 1534 (a) and 3554 (b) year age group
risk for women with T1D that were obtained as a (Fig. 11.6a, b) of diabetes-related mortality data
result of analyzing population registers of some comparing to the general mortality in seven
Eastern European and Baltic states can be seen as countries. The data were extracted from WHO
an epidemiologic confirmation of the need to mortality database [6].
continue fundamental research into the reasons Increase of diabetes-related mortality risk (in
of gender differences of the clinical progression relation to general mortality for a specific age
and consequences of T1D. group in men and women) for women comparing
While trying to reveal causes of the described to men in Russia, Ukraine, and Azerbaijan in
phenomenon, we performed a meta-analysis 1534-year age group (Fig. 11.6a) and in Russia,
Ukraine, Azerbaijan, Armenia, and Belarus 55 years [52]; however, the British cohort also
(Fig. 11.6b) in 3554 age group was demon- included children, which could influence the
strated. A generalization of relative risks for this assessment of average T1D duration and age at
age group was performed for all seven countries the time of death. Renal failure is the leading
in order to confirm the assessment in 1534 age cause of death (28.4 %) in Ukrainian T1D patient
group (Fig. 11.6a). During heterogeneity testing cohort [50], whereas according to a British study
(p = 0.45), the homogeneity hypothesis was not of diabetes mellitus patient register containing
rejected; therefore, the Mantel-Haenszel model primary care data, the leading cause of death
was chosen (generalized RR = 3.1 (95 % CI 2.6 among T1D patients was CVD [56]. Similar
3.6). In 3554 age group, the homogeneity results were obtained by a European study,
hypothesis was rejected (p = 0.008); therefore, EURODIAB [57]. Comparison of main causes
the random effects model was chosen (general- of death according to EURODIAB data and
ized RR = 2.0 (95 % CI 1.62.4). Ukrainian Diabetes Register (UDR) data is
Thus, the fraction of death cases from diabe- shown in Fig. 11.7. Apparently, death from renal
tes within the general mortality for females aged failure among T1D patients in Ukraine prevails
1554 turned out to be greater, than the corre- several times over other causes, while in other
sponding number for males. This pattern is more parts of Europe the main cause of death is
prominent in young women. CVD. It was previously noted by epidemiolo-
Thus, it seems that the female gender lowers gists that the main cause of death for T1D
the chances of survival of diabetic women not patients is renal failure [58]; however, these data
only as a result of activating cardiovascular were relevant in 1960s1970s. Todays experts
pathology and not only in the youngest women. believe that the shift in mortality structure toward
EURODIAB has reported an SMR of 2.0 in CVD happened due to intensification of hypo-
12 European countries that followed 28,887 chil- tensive therapy and insulin treatment [59]; there-
dren with T1D (141 deaths during 219,061 fore, the mortality structure of T1D patients that
person-years) with a range of SMR from 0 to 4.7 we have revealed when analyzing UDR can be
among the countries included in the study [52]. assumed to conform to earlier time period of
Life expectancy of T1D patients in Ukraine in clinical practice. An earlier investigation that we
2007, assessed according to age at the time of have previously cited [32] also indicates that
death, did not exceed 40.2 years [48]. In the UK, renal failure is the main cause of death among
according to similar cohort study, this value is young diabetic patients in Ukraine [32].
35% a b c d
30%
25%
20%
15%
10%
5%
Fig. 11.7 Interval estimation of structure (%) of the main within the box and height of boxes, respectively), 95 % CI
death causes among T1D patients, diagnosed before (lines that emerge above and below the boxes) (Data from
30 years of age according to EURODIAB data (white Ukrainian Diabetes Register given according to Khalangot
boxes) and the Ukrainian Diabetes Register (black boxes). et al. [50]; EURODIAB given according to Soedamah-
Death causes: CVD (a); renal failure (b); DKA or coma Muthu et al. [57])
(c); cancer (d). Note: given means (%) SE (the dot
In summary, the performed analysis of diabetes nutrition during in utero development can result
mortality trends in ex-Soviet Eastern European in long-term adaptive changes in glucose-insulin
countries allows to make the following conclusions: metabolism (including reduced capacity for insu-
lin secretion and insulin resistance) that, due to
For 15 years after 1985, the WHO mortality an enhanced ability to store fat, improve survival
databases recorded a multifold diabetes-related under postnatal conditions of nutritional depriva-
mortality growth in several East European coun- tion. However, windows of plasticity close early
tries, including Russia, Ukraine, and Belarus. in life, and postnatal environmental exposures
After the year 2000, there is a gradual reduc- may lead to the selected trajectory of becoming
tion of diabetes-related mortality in these inappropriate, resulting in adverse effects on
countries. adult health. If mismatch exists between the envi-
The analysis conducted in Ukraine indicates ronment predicted in utero and the actual envi-
that the main cause of death for T1D patients ronment experienced in subsequent life (e.g.,
is renal failure. As renal dialysis therapy in excess food consumption), diabetes and other
USSR was scarce, one may assume that post features of the metabolic syndrome will result. To
1985 diabetes-related mortality growth can study this prediction, associations between early-
reflect not just issues with insulin supply, but life conditions and the risk of developing diabe-
also a decrease of administrative pressure, tes mellitus in adulthood have been studied in
when recording the cause of death in corre- Ukraine population. The main findings of these
sponding documents. studies are presented in subchapters below.
Reduction of general mortality, demonstrated
by some diabetes population registers (Latvia), Association Between Prenatal
and an increase of average age at the time of Exposure to the Ukraine Famine
death (Ukraine, Russia, Belarus) allows to of 19321933 and Type 2 Diabetes
assume that the decrease of diabetes-related Nutrition during pregnancy has been proposed as
death cases, recorded by WHO mortality data- an explanation for the occurrence of type 2 diabe-
bases, is a real phenomenon, rather than a reflec- tes later in life, but direct measures are hard to
tion of change of policy toward recording the obtain. To better identify any effects of early
cause of death in corresponding certificates. nutrition, studies of man-made famines can offer
According to data from diabetic registers in distinct opportunities for the unbiased compari-
Latvia and Ukraine, the phenomenon of son of individuals born under such conditions
female gender-related increase of general with unexposed controls [61]. These approaches
mortality in young women was confirmed. We can provide information about specific pregnancy
saw this for the first time when comparing the exposures, especially if the population at risk, the
fraction of those who died due to diabetes timing and degree of exposure and relevant health
within general male and female mortality in outcomes can be accurately defined. For type 2
East European countries according to WHO diabetes in later life, studies of the Dutch famine
mortality databases. of 19441945 Lumey et al. [62], the Chinese
famine of 19591962 Li et al. [63], and three
famines in twentieth century Austria Thurner
Some Aspects of the Pathophysiology et al. [64] all suggest a relation with early-life
of Type 1 and Type 2 Diabetes nutrition. All these studies have a particular
in Ukraine strength: The timing of the famine in relation to
the stage of gestation was particularly well
Association Between Early-Life Events defined in the Dutch study, as was the risk of
and Risk for Diabetes Mellitus adult hyperglycemia in the Chinese study, and a
in Ukraine Population large number of patients receiving antidiabetic
The thrifty phenotype hypothesis proposed by drugs over a long time period was included in the
Hales and Barker [60] suggests that inadequate nationwide Austrian study. However, no study
combines all these strengths. To overcome the by region, date of birth, and sex for comparisons
limitations of previous approaches, the setting of of diabetes prevalence in specific subgroups.
the Ukraine famine of 19321933 was used to The odds of type 2 diabetes by date and region
study the association between early-life nutrition of birth in 43,150 patients with diabetes and
and late-life type 2 diabetes in a large population, 1,421,024 individuals born between 1930 and
in cohorts well defined with respect to the timing 1938 were compared (Fig. 11.8). With adjust-
of the famine in relation the stage of pregnancy ment for season of birth, the OR for developing
and the severity of the famine around the time of type 2 diabetes was 147 (95 % CI 1.371.58) in
birth [65]. individuals born in the first half of 1934 in regions
This study included all patients with type 2 with extreme famine, 126 (114139) in indi-
diabetes diagnosed at age 40 years or older in the viduals born in regions with severe famine, and
Ukraine national diabetes register 20002008 there was no increase (OR 100, 091109) in
and used all individuals born between 1930 and individuals born in regions with no famine, com-
1938 from the 2001 Ukraine national census as pared with births in other time periods (Fig. 11.9).
the reference population. The studied population The associations between type 2 diabetes and
included individuals born before and after the famine around the time of birth were similar in
famine period as controls and those from regions men and women. These findings show a dose-
that experienced extreme, severe, or no famine. response relation between famine severity during
The prevalence odds ratios (ORs) were used as prenatal development and odds of type 2 diabetes
the measure of association between type 2 diabe- in later life and suggest that early gestation is a
tes and early famine exposure, with stratification critical time window of development.
6 6
Births per month
Deaths per month
Prevalence of type 2diabetes
5 5
Births and deaths (monthly number/mean)
Prevalence of type 2diabetes (%)

4 4
3 3
2 2
1 1
0 0
br ry
M ry
ch
M l
Ju y
ne
Se ug ly
em t
N cto r
D em r
em er
Ja ber
br ry
M ry
ch
M l
ay
ne
Se g y
em t
N cto r
D em r
em er
n r
br ry
M ry
ch
M l
Ju y
ne
Se g y
em t
N cto r
D em r
em er
r
ri
ri
ri
pt us
pt us
pt us
O be
ov be
O be
ov be
Ja be
O be
ov be
be
a
a
Au Jul
Au Jul
A Ju
Ap
Ap
Ap
Fe ua
ua
Fe ua
ua
Fe ua
ua
ec b
ec b
ec b
ar
ar
ar
Ju
n
n
Ja
1932 1933 1934

Time (month and year)
Fig. 11.8 Monthly births and deaths in eastern Ukraine census, and prevalence of type 2 diabetes is from the
in 19321934 and prevalence of type 2 diabetes between Ukraine national diabetes register (The figure is repro-
2000 and 2008, by year and month of birth. Ratio of duced from Lumey et al. [65] with permission of the pub-
monthly values to overall mean. Deaths rates are per lisher, Elsevier Science Ltd.)
1,000 population, birth counts are from the Ukraine 2001
2.0 Extreme famine regions

Severe famine regions
Non-famine regions
Odds ratio
1.0
0.5
ne
r
ne
r
ne
r
ne
r
ne
r
ne
r
ne
r
ne
r
ne
r
be
be
be
be
be
be
be
be
be
Ju
Ju
Ju
Ju
Ju
Ju
Ju
Ju
m
em
em
em
em
em
em
em
J
y-
y-
y-
y-
y-
y-
y-
y-
y-
e
e
ec
ec
ec
ec
ec
ec
ec
ec
ec
ar
ar
ar
ar
ar
ar
ar
ar
ar
-D
-D
-D
-D
-D
-D
-D
-D
-D
nu
nu
nu
nu
nu
nu
nu
nu
nu
ly
ly
ly
ly
ly
ly
ly
ly
ly
Ja
Ja
Ja
Ja
Ja
Ja
Ja
Ja
Ja
Ju
Ju
Ju
Ju
Ju
Ju
Ju
Ju
Ju
1930 1931 1932 1933 1934 1935 1936 1937 1938
Time (month and year)
Fig. 11.9 Odds for registered cases of type 2 diabetes half year to the odds for births from July to December,
(20002008) by month and year of birth and famine 1938 (reference group). Error bars show 95 % CIs (The
severity in the region of birth (19321933). Odds ratios figure is reproduced from Lumey et al. [65] with permis-
comparing the odds of type 2 diabetes among births by sion of the publisher, Elsevier Science Ltd.)
Seasonality of Birth in Diabetic Type 1 Diabetes

Patients in Ukraine
Season of birth provides another type of natu- Seasonal pattern of birth in type 1 diabetic patients
ral experiment to examine the association has been repeatedly described around the world
between early-life conditions and later health (see, e.g., [66]). Significant seasonality of birth in
outcomes. Month of birth is a good instrument persons with type 1 diabetes was revealed in
that can help assess the effects of early growth Ukraine population [67]. The data consisted of
on adult health independent of life-course fac- prevalent cases of type 1 diabetes in Ukraine by
tors. This is true because in decades past, there the end of 2003. Cases were restricted to individu-
were important seasonal differences in nutri- als born after 1 January 1960 and diagnosed with
tion, especially in developing countries. The type 1 diabetes before age 30 (n = 20,117). People
food supply (variety, quantity, and freshness of who were born during the same time in general
fruits, vegetables, cereals, and animal protein) population (n = 29,105,560) served as a reference
was varied according to season. These differ- standard. A significant seasonal pattern of type 1
ences in access to high quality food supply can diabetes incidence rates was found (p < 0.001),
potentially influence intrauterine growth with the lowest rates in December and the highest
depending on the month of gestation. Other in April (Fig. 11.10). The rate ratio between the
possible triggering factors for disease progres- extremes was 1.32 (95 % CI 1.271.39). Tests for
sion such as infections, sunlight/photoperiod, seasonal pattern in subgroups defined by sex and
productions of vitamin D and melatonin, and age or by sex and date of birth were all significant
outdoor temperature also tend to change sea- with p-values less than 0.02. No interactions with
sonally. Seasonal patterns of birth for both type sex or age at diagnosis were revealed, while a
1 and type 2 diabetic patients were determined strong interaction with period of birth (p < 0.0001)
in Ukraine population. was demonstrated.
Age 0-9 Age 10-19 Age 20-29 1.3

1.3
1.2
1.2 1.1
1.0
1.1 0.9
Rate ratio
0.8
Rate ratio
1.0
Birth 1980-1974 Birth 1975-1984 Birth 1985-2003 1.3
1.2
1.1
0.9
1.0
0.9
0.8
0.8
J F M A M J J A S O N D J M M J S N J M M J S N J M M J S N
Month of birth
Fig. 11.10 Effect of month of birth on the risk of develop- months. Right-hand panel, analyses subdivided by sex and
ing type 1 diabetes. Left-hand panel, the overall effect with broad categories of date of birth. Men: dark; women: light
the 95 % CI, controlled for sex, age at diagnosis and period (The figure is reproduced from Vaiserman et al. [67] with
of birth. The points are observed rate ratios for single permission of the publisher, Elsevier Science Ltd.)
Type 2 Diabetes mid-March and mid-May and nadirs between

mid-October and mid-December was obtained in
In contrast to the well-described birth seasonality all regions studied (Fig. 11.11). This pattern was
in childhood diabetes persons, the seasonality of substantially uniform for all birth cohorts over
birth in adult type 2 diabetes patients has been the study period.
reported only in few papers. In Ukraine, season-
ality of birth was strongly evident in type 2 diabe- Similar Birth Seasonality in Type 1
tes patients [68]. In this study, cases were and Type 2 Diabetics and Underlying
restricted to type 2 diabetes patients from three Mechanisms Proposed
large Ukrainian regions (Chernigiv: n = 18,594; The results obtained indicate that early-life factors
Kherson: n = 19,738; Rivne: n = 13,882) born linked to seasons are implicated in the subsequent
before 31 December 1959 and diagnosed with development of both type 1 diabetes and type 2
diabetes after age 39. Reference populations diabetes in Ukraine. In the study population, indi-
were based on the Ukraine census 2001 deper- viduals born in April experienced fetal life largely
sonalized data (n = 1,567,917). Seasonality of in the nutritionally marginal months from late
birth was evident in type 2 diabetes patients autumn to early spring and passed the first postna-
(male: peak in 12 April, nadir in 22 November, tal months in a season of relative plenty. These
amplitude 28.9 %, p < 0.001; female: peak in 22 individuals were found to have increased risk of
April, nadir in 15 December, amplitude 36.4 %, diabetes. In contrast, a decreased risk was found
p < 0.001). Similar pattern with peaks between for those born in NovemberDecember. In this
1.4
1.4 a b c d
1.3
1.2
1.3
1.1
1.2 1.0
0.9
Rate ratio (log10 scale)
Rate ratio (log10 scale)

1.1
0.8
0.7
1
1.4
e f g
1.3
0.9 1.2
1.1
1.0
0.8
0.9
0.8
0.7 0.7
J F M A M J J A S O N D J M M J S N J M M J S N J M M J S N
Month of birth Month of birth
Fig. 11.11 Effect of month of birth on the risk of devel- (n = 12,183) (e), Kherson women (n = 13,593) (f), Rivne
oping type 2 diabetes. (a) The overall effect for men (solid women (n = 8,928) (g). In each of the panels, the estimated
line and black squares) and women (dashed line and white patterns subdivided by birth cohort are drawn as thin
circles). (bg) Analyses subdivided by sex and regions. lines; the overall effects are drawn as the thick lines (The
Chernigiv men (n = 6,411) (b); Kherson men (n = 6,145) figure is reproduced from Vaiserman et al. [68] with per-
(c); Rivne men (n = 4,954) (d); Chernigiv women mission of the publisher, Elsevier Science Ltd)
group, fetal development in a nutritionally favor- during the study periods, and, since Ukraine is
able season would have been followed by early a lower middle-income country, the people
infancy in a season of relative shortage (winter- might have experienced the extremes more pro-
spring). Obviously, the first scenario is more high- nounced here than in a more affluent country
risk for diabetes development than the second like Denmark.
one. These results are highly consistent with the Surprisingly, the month-of-birth patterns
thrifty phenotype hypothesis by Hales and obtained for children and young adults
Barker [60]. (029 years) with type 1 diabetes and for middle-
Interestingly, in the very recent research by to-old aged type 2 diabetes patients in Ukraine
Jensen et al. [69], no evidence of seasonality of were quite similar. The finding that type 1 and
birth in adult type 2 diabetes in Denmark was type 2 diabetes share similar seasonality of birth
obtained. The authors have suggested that dif- led to hypothesis that early-life triggers can be
ferences in the effects observed in Denmark common to both phenotypes in Ukraine popula-
and Ukraine can be explained by the differ- tion [70]. These findings are consistent with the
ences in latitude or the standard of living accelerator hypothesis [71] which argue that
between these countries. Indeed, since seasonal type 1 and type 2 diabetes, despite the marked
variation in both nutrition and weather was differences in pathogenesis, are merely poles of a
much more extreme in Ukraine than in Denmark single pathological spectrum.
Correlation Between the Prevalence For patients with a disease duration (DD) of
of Type 1 Diabetes with the Daily up to 15 years (n = 13,677), the daily insulin
Insulin Dose and the Autoimmune dose (DID) was observed to increase linearly
Process Against Glutamic Acid with DD (R = 0.899, p < 0.001), see Fig. 11.12.
Decarboxylase in Adults A further increase in the disease duration in the
range of 1631 years was not accompanied by
The purpose of this diabetes register-based study regular changes in the insulin dose. The regular
in Ukraine [41] was to determine whether the rise of insulin dose, observed with the increase
insulin requirement can change systematically in in the duration of T1D in adults diagnosed
T1D patients and whether this requirement before the age of 30 years, is still an unknown
depends on the same factors that determine its phenomenon.
prevalence. The rate of insulin requirement Furthermore, the differences in the T1D prev-
among adults with type 1 diabetes (T1D) in 24 alence among the 24 Ukrainian regions were
Ukrainian regions was compared. The data obtained (p < 0.001). In the minimal regional
included the prevalent cases of T1D in Ukraine at cluster (MIC), the prevalence rate was 6 (56),
the end of 2006. Only persons aged over 14 years and, in the maximal (MAC) regional cluster, it
at the time of inclusion into the Ukrainian regis- was 9 (89) per 10,000 adults.
ter and diagnosed with diabetes before 30 years Insulin doses standardized according to the
of age were included in this study (n = 26,796). disease duration within the range of 015 years in
As the average duration of the disease was found the minimal prevalence cluster of T1D prevalence
to be 14.86 years, the average daily insulin doses were significantly lower, when compared with the
were calculated for each year of the duration, intermediate and maximal prevalence clusters.
from 0 (<1) to 15 years. The values in the intermediate prevalence cluster
55
Mean daily insulin dose, units
50
45
40
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Disease duration, yrs
Fig. 11.12 Average (Mean SE) daily insulin doses of duced from Khalangot et al. [41] with permission of the
type 1 diabetes mellitus patients depending on the disease publisher, Elsevier Ltd.)
duration in the range of 015 years (The figure is repro-
65
maximal cluster
60
Insulin daily dose (units)
55
intermedial
50
45
minimal cluster
40
35
0 2 4 6 8 10 12 14
Diabetes duration (yrs)
Fig. 11.13 Average daily insulin doses of diabetes mel- cluster, selected according to disease prevalence (The fig-
litus type 1 patients depending on the disease duration (in ure is reproduced from Khalangot et al. [41] with permis-
the range of 015 years) as well as on the territorial sion of the publisher, Elsevier Ltd)
were lower than those in the maximal prevalence results only slightly: OR = 7.91 (2.4425.57),
cluster (Fig. 11.13). p < 0.001.
The median insulin doses were standardized Thus, adult type 1 diabetics living on territo-
according to DD, and the values were lowest in ries with high prevalence of this disease may
the MIC and highest in the MAC populations: require higher daily insulin doses. This phenom-
45.89 (45.2847.19) and 56.59 (53.3357.88) enon may be explained by more intense autoim-
U/24 h, respectively (p < 0.01). Furthermore, the munity in patients residing on these territories.
level of HbA1c in the MAC of T1D patients was Similar comparisons of GADA levels and persis-
observed to be higher than that in the MIC tence in populations that differ significantly
(9.52 2.24 %, n = 240, and 8.57 3.29 %, according to T1D prevalence (e.g., in countries of
n = 111, respectively; p < 0.01). Northern Europe and Japan or Korea) seem very
The glutamic acid decarboxylase 65 antibody desirable to us, but, as far as we know, they have
(GADA) comparisons: A total of 86 T1D patients not been performed yet.
with a mean age of 27.5 years (0.86) and a mean
diabetes duration of 10.3 (0.72) years (SE) were
randomly selected from four regional diabetes Genomic Landscape of Diabetes
registers. The GADA and the plasma c-peptide in Region
levels were also determined. The logistic regres-
sion model was used, and the odds ratio (OR) and For the last two decades, diabetes-related genetic
95 % confidence interval (CI) were calculated. studies in Eastern Europe were conducted mostly
The GADA levels and persistence in the MAC in Russia and concerned in assessing T1D risks
patients (n = 38) were higher than that of the MIC and complications, as well as T2D and some
patients (n = 48): 14.1 4.6 and 3.2 1.2 U/ml, genes associated with genetic polymorphism. In
respectively, mean SE; p = 0.028; OR = 9.66 particular, Dimitry Chistiakov et al. demonstrated
(3.3128.17), p < 0.001. Adjusting for age, gen- that human cytotoxic T lymphocyte-associated
der, and duration of the diabetes affected the antigen-4 gene is strongly associated with and
linked to T1D in a Russian population [72] and Diagnosis of Diabetes

suggest a protective role of the 262 T allele of the and Prediabetes in Region
catalase gene against the rapid development of
diabetic neuropathy in T1D [73]. But association For the last 15 years in Eastern Europe, diabetes
studies of these polymorphisms in KCNJ11 and was diagnosed according to WHO recommenda-
ABCC8 (E23K and ABCC8 exon 31 variants) tions (1999) [79]. The corresponding diagnostic
were only conducted in the regions of Russia criteria in Russia and Ukraine are mentioned in
near Europe [74], but not Siberia. Most recent documents approved by government healthcare
study assessed whether SNPs rs5219 and organizations [80, 81]. Categories of prediabetes,
rs757110 are associated with a predisposition to Impaired fasting glucose (IFG) or impaired glu-
T2DM in Siberians (1,384 T2D patients; 414 cose tolerance (IGT), are known only as given by
healthy individuals, all belong to a Russian eth- WHO (1999) [79]. Stretching of IFG from 6.1
nic group) and found that neither SNP was asso- 6.9 to 5.66.9 mmol/l, as was done by the experts
ciated with the disease [75]. Thus, genomic from the American Diabetes Association (ADA)
landscape of T2D differs significantly between [82, 83] in the process of preventing diabetes
European and Asian parts of Russia. development, is not used. We know of only one
Ukraine as well has some studies, looking at example of comparative assessments of hyper-
genetic aspects of diabetes. In particular, it has glycemia criteria between WHO and ADA: the
been shown that 49A/G polymorphism of screening study involving 2,368 adult residents
CTLA4 gene as in type 1 diabetes mellitus of the Moscow region [84]. The prevalence of
plays an important role in genetic predisposition early disorders of carbohydrate metabolism and
to latent autoimmune diabetes of adults (LADA) T2D are 17.1 and 7.2, respectively, using WHO
in Ukrainian population. 49G/G genotype criteria and 40.0 and 5.9 % by ADA criteria.
CTLA4 is associated with the risk of developing Alexander Dreval et al. [84] believe that refusal
T1D, T2D, and LADA [5]. It is interesting that to undergo oral glucose tolerance test (OGTT)
there were no 49A/G polymorphism of CTLA4 during screening decreases detectability of early
differences between T1D and T2d found in the metabolic disorders by 28.8 and 6.1 % using
study. Just recently, Ukraine saw its first assess- WHO and ADA criteria, respectively. When
ment of neonatal diabetes in patients with onset screening is aimed to diagnose T2D alone, OGTT
of diabetes during the first 9 months of life [76]: can be omitted in subjects with fasting plasma
the incidence of neonatal diabetes in Ukraine glucose level below 4.7 mmol/l. If it is aimed to
over a 36-month period (20122014) was calcu- diagnose both T2D and impaired glucose toler-
lated to be 1 in 126,397 live births. Genetic test- ance, OGTT is not needed in subjects with fast-
ing was undertaken for 42 patients with ing plasma glucose level below 4.2 mmol/l [84].
permanent or transient diabetes diagnosed Screening for T2D and prediabetes in other
within the first 6 months of life (n = 22) or per- Russian cities based on OGTT only in those who
manent diabetes diagnosed between 6 and had IFG levels of plasma glucose revealed the
9 months (n = 20). KCNJ11 and ABCC8 muta- following structure prevalence (%) of blood glu-
tions was the most common cause (52 %) of cose categories according to WHO 1999: isolated
neonatal diabetes. Ukraine has a similar inci- IFG 7.4 (95 % CI 6.78.1); IFG + IGT 1.6
dence of neonatal diabetes as other European (95 % CI 1.21.9); unknown T2D 5.2 (95 % CI
countries [77, 78] and KATP channel gene muta- 4.65.8). Previously known T2D prevalence in
tions are the most common cause. All 11 patients this study population of Chelyabinsk city (Ural
with KCNJ11 and ABCC8 mutations were suc- region) aged 2074 years old was 1.8 (95 % CI
cessfully switched from insulin injections to 1.42.1) % [85]. When using similar design in
oral sulfonylurea therapy with an improvement another study, carried out in Abakan city
in their glycemic control [76]. (Khakassia region), prevalence of screen-detected
T2D, IGT, and IFG were only 1.25 (95 % CI results of multinational, multicenter, observa-
0.941.56); 0.34 (95 % CI 0.180.56); and tional, crosssectional survey assessing diabetes
0.04 %, respectively. Prevalence of known T2D secondary care in Central and Eastern Europe
in Khakassia was 2.13 % [86]. Thus, in Russia (DEPAC Survey) (Table 11.8). A total of seven
known T2D prevalence in different regions does countries, including two Baltic states (Latvia and
not differ significantly and is equal to 1.82.13 %, Lithuania), took part in the DEPAC Survey [87].
whereas screen-detected T2D prevalence has A cohort consisting of 29,721 adult T1D
more substantial regional differences from 7.2 patients can be viewed as full population data on
to 1.25 %. A small OGTT-based study in Ukraine this illness in Ukraine. Inclusion criterion for this
(rural population, age 45+) revealed new T2D cohort was diabetes diagnosis before the age of
prevalence of 12.7 % and normal fasting glucose 30. This hallmark was not used in two other
and tolerance only in 36.6 % of the studied per- cases, which could theoretically increase the pos-
sons [13]. sibility of false allocation of T2D or other dia-
betic type patients to T1D insulin-treated.
Nevertheless, comparing average age and gender
Complications of Diabetes distribution of Ukrainian and DEPAC Survey
in Region patients rather indicates their similarities.
Average HbA1c and BMI levels in Ukraine and
Complication prevalence assessments in a popu- DEPAC Survey did not differ significantly, and
lation of T1D patients based on diabetic register fractions of patients whose HbA1c reached <7 %
data from Ukraine and Russia are compared with in Russia, Ukraine and DEPAC Survey were
Table 11.8 Same characteristics of T1D patients according to cross-sectional data analysis
Characteristics Ukraine [37, 50] Russia [22, 24] DEPAC Survey [87]
Number of patients, n 29,721 294,257 2,497
Gender: females (%) 47.02 n.a. 48.4 (43.050.9)
Mean age, years 34.47 (12.91) n.a. 36.9 (25.242.2)
Mean T1D duration, years 17.32 (11.02) n.a. 13.7 (9.416.6)
BMI, kg/m2 23.16 (4.10) n.a. 24.0 (21.725.7)
Systolic BP, mmHg 125.91 (19.75) n.a. 124 (116133)
Diastolic BP, mmHg 78.15 (10.94) n.a. 76 (6882)
Mean HbA1c, % 8.75 (2.57) n.a. 8.2 (7.79.8)
HbA1c <7 % 18.78 % 26.1 % 23.9 %
Nephropathy (any stage), % 32.14 23.0 27.8 (12.055.4)
Renal failure, % 4.96 9.0 n.a.
End-stage renal failure, % 2.78 n.a. 0.44 (0.02.3)
Amputation (any level), % 2.71 1.2 1.2 (0.04.6)
Foot ulcer, % 4.19 5.6 2.1 (0.77.7)
Retinopathy (any stage), % 55.1 34.7 40.9 (19.087.6)
Blindness, % 3.47 1.54 0.48 (0.03.4)
Insulin analogues, % 9.84 2080 49 (3895)
Data are means or %. (SD or country lowest mean value country highest mean value)
HbA1c data were registered in 8.6 and 13 % T1D cases in Ukrainian and Russian diabetes registers, respectively. BMI
was measured in 25 % of T1D cases (Russian register). Percentage of patients with measurements of protein excretion
according to Russian register data is as follows: microalbuminuria 6.37 %, proteinuria 5.77 % of T1D cases. In case
of the Russian register the diabetic foot category is used and can include foot ulcers and/or amputation cases. Data are
means or %., (SD or country lowest mean value-country highest mean value). Insulin analogues fraction presented as
regional lowest highest value
n.a. not applicable
close. There is no gender, age, or diabetes dura- logues depends on the level of economic prosper-
tion data in the Russian register, and most quanti- ity of the region [24]. It seems that frequent use
tative data are given as category distribution, of these drugs is becoming an issue of image or
which makes a lot of comparisons difficult. It is status of the patient and the healthcare system.
quite unusual that 11.6 % of T1D patients in Some experts are currently criticizing the policy
Russia have insufficient body mass (<18.5 kg/m2) toward government procurement in some post-
and that can indicate a lack of effect from insulin Soviet states, e.g., Kyrgyzstan [3], where an insu-
treatment. It should be noted that the correspond- lin analog, which is not included on the WHO
ing BMI category among T2D patients is only EML, has significantly higher costs and has been
0.2 % [22] according to Russian register data. shown to have little added clinical value [88] is
The data on high prevalence of end-stage renal also purchased.
failure, amputation, foot ulcers, and blindness in Results of a similar cross-sectional review are
Ukraine seems disturbing. But all this indicators also presented for T2D patients (Table 11.9).
seem comparable with highest country mean Among the most significant differences is the
value of DEPAC Survey (Table 11.8). higher percentage of women among T2D patients
Less than 10 % of T1D patients in Ukraine and in Ukraine, comparing to DEPAC Survey. It can-
49 % according to DEPAC Survey data receive not go unnoticed that myocardial infarction is
insulin analogs. In Russia the use of insulin ana- four times less frequent in Ukrainian and Russian
Table 11.9 Same characteristics of T2D patients according to cross-sectional data analysis
Characteristics Ukraine [37, 51] Russia [22, 24] DEPAC Survey [87]
Number of patients, n 105,480 3,705,102 8,231
Gender: females (%) 67.17 n.a. 52.7 (48.171.8)
Mean age, years 66.6 (10.9) n.a. 62.2 (60.564.4)
Mean T2D duration, years 8.98 (7.4) n.a. 10.2 (8.411.1)
BMI, kg/m2 28.64 (4.7) n.a. 30.6 (30.132.6)
Systolic BP, mmHg 144.16 (18.7) n.a. 141 (138149)
Diastolic BP, mmHg 85.97 (10.4) n.a. 83 (8088)
Mean HbA1c, % 8.88 (4.9) n.a. 7.7 (7.58.3)
Total cholesterol (mmol/l) 5.41 (1.2) 5.43 5.39 (5.135.89)
Triglycerides (mmol/l) 2.23 1.8 2.12 (1.932.43)
Nephropathy (any stage), % n.a. 4.9 25.3 (17.639.8)
End-stage renal failure, % 0.26 n.a. 0.44 (0.02.3)
Amputation (any level), % n.a. 1.2 1.2 (0.04.6)
Foot ulcer, % 2.97 2.4 2.1 (0.77.7)
Retinopathy (any stage), % n.a. 15.3 40.9 (19.087.6)
Blindness, % n.a. 0.62 0.34 (0.10.7)
Myocardial infarction, % 3.24 3.7 12.4 (9.116.6)
Stroke or TIA, % 4.46 4.4 7.2 (4.013.3)
Any antihypertensive agents, % 35.99 n.a. 82.5 (75.891.4)
ACE inhibitors, % 25.27 n.a. 66.5 (57.084.1)
Statins, % 3.18 n.a. 48.3 (13.755.5)
OAD + Insulin, % 3.6 n.a. 16 (434)
Insulin only, % 22.5 n.a. n.a.
Data are means or % (SD or country lowest mean value country highest mean value); HbA1c levels registered in 7.4
and 8.4 % T2D cases of Ukrainian and Russian diabetes registers, respectively; BMI measured in 22 % of T2D cases
from Russian registers; percentage of patients with measurements of protein excretion are as follows: microalbuminuria
8 %, proteinuria 13.8 % of T2D cases
T2D patients, then in DEPAC Survey. There are earlier healthcare reports, western Ukraine had
no such significant differences in stroke preva- lower T2D prevalence, compared to Ukraines
lence. That said, the use of statins, any antihyper- average [92].
tensive agents, or ACE inhibitors in Ukraine is
several times less, then in the DEPAC Survey. It
is likely that in this case we are dealing with a Coordination and Delivery
long known paradox Russia and Ukraine have of Diabetes Care Services
highest CVD mortality levels and lowest myocar-
dial infarction mortality levels in Europe: mortal- Assessments of diabetes patient treatment qual-
ity from ischemic heart disease (ICD-9: 410414) ity, based on interviewing, recently performed in
in 1999 in Ukraine was 399.86 and 229.53, several post-Soviet countries by independent
whereas acute myocardial infarction (ICD-9: researchers revealed many specific issues related
410) mortality levels were 18.89 and 6.58 per to accessibility of specialized aid and medica-
100,000 males and females, respectively [89]. tions and also a great degree of treatment dissat-
This is most likely explained by an insufficient isfaction. In particular, British investigators
lifetime diagnostics of myocardial infarction. It is conducted 15 semi-structured interviews with
remarkable that ECG was performed for 81 patients with diabetes and physicians in Russian
(5090) % of DEPAC Survey T2D patients [87]. rural and urban settings, in public and private
Recently, two more possibilities for evaluating sectors. Patients worried about high and rising
diabetes treatment in Ukraine in the framework costs of care, while physicians noted concerns
of an international assessment had been used: about lack of time to treat patients adequately.
EUCCLID a European cross-sectional primary Although all specifically diabetes-related ser-
care diabetes survey in conjunction with the vices are free of charge, patients requiring urgent
EASD study group. In this study, patients will be surgery often face high user fees, either to bypass
randomly selected from a list of all patients waiting lists in state facilities or to be treated
known to the participating GPs with T2D for immediately in a private institution. These hid-
whom the GP is the main diabetes care provider den, out-of-pocket payments impact adversely
[90]. In another investigation, only glycemic con- on equity and act as a barrier to timely care [93].
trol (HbA1c) of type 1 diabetes in clinical prac- The same or close problems are revealed in
tice [91] was compared. Georgia [19], and the reforms of health insurance
Due to a small number of patients from each in Moldova [9496] give us some hope.
country, data are not identified by individual The problem of organizing and financing renal
country names in the final report [90]. However, replacement treatment cannot go unmentioned.
data from individual countries have been seen According to a recent statement from the head of
and discussed at the local level. Ukrainian T2D the Belarus endocrinology service, 126 persons
EUCCLID data was generally close to data from died in 2012 due to diabetes-related causes (177
Table 11.9, occupying lower positions in the persons in 2011). Of these, 82 died as a result of
assessment of treatment quality, comparing to chronic renal failure (115 in 2011), 39 from gan-
other European countries. When assessing grene (56 in 2011), and 5 from coma (6 in 2011)
HbA1c levels in T1D patients in another interna- [18]. Thus, renal failure is considered the main
tional study [91], Ukrainian data were one of the cause of death, which is considered diabetes-
better ones. One possible explanation for this related in Belarus. Coverage indicators of renal
could be the fact that Ukraine was represented replacement therapy in this country (hemodialy-
by one of its Western regions Volyn, which sis, peritoneal dialysis, and kidney transplant) in
belongs to a group of regions with minimal adult 2012 were 432 patients per million population
T1D prevalence. Earlier we have revealed a posi- (189.3) in 2007) [18]. We attempted to clarify the
tive correlation between intensity of insulin meaning of coverage regarding the source of
treatment, HbA1c and GADA levels, and T1D financing of this therapy and to what extent the
prevalence in adults [41, 42]. According to need in such treatment could be satisfied in each
of the mentioned post-Soviet countries. According 1.0

to a 2006 review [97] dedicated to epidemiology
of renal replacement in Central and Eastern 0.8
GN
other
Cumulative survival
Europe, the availability and outcome of renal HTN
replacement therapy in most of these countries 0.6 DM
have become comparable with what is seen in
Western Europe. However, there are still large dif- 0.4
ferences between individual countries. In particu-
lar, there is an urgent need for improvement in 0.2
Belarus and Russia. The best correlation of trans-
plantation/dialysis was noted in the Baltic states 0.0
and the worst in Russia. According to the authors,
0 200 400 600 800
there is no data on Ukraine and Moldova, despite follow-up, days
numerous efforts to collect this data. We can con-
90 1 2
firm that during that period diabetes patients were days year years
discriminated against, when being selected for N at risk
hemodialysis, and peritoneal dialysis was virtu- GN, n=1.179 1.005 649 282
Other, n=1.143 967 644 281
ally unavailable. Since then, there were positive HTN, n=167 141 74 20
changes in Moldova and Ukraine. This type of DM, n=605 490 304 115
treatment became available and covered by insur-
ance (Moldova) or by direct government funding Events
(Ukraine). Recently, a first assessment of renal GN 42 101 147
Other 54 133 177
replacement therapy (RRT) in Ukraine was pub- HTN 5 22 33
lished [98]. According to nephrologic register DM 45 111 149
data, there were 5,985 prevalent RRT patients on
Survival, %
31 December 2012 (131.2 persons per million GN 96.3 89.7 81.3
population). Mean age was 46.5 13.8 years, 56 % Other 95.1 86.1 77.7
men and 74 % received hemodialysis, while peri- HTN 96.8 83.0 65.0
DM 92.3 77.7 64.5
toneal dialysis and kidney transplantation both
represented 13 %. Twelve percent of patients with Fig. 11.14 Kaplan-Meier curves for patient survival
end-stage renal disease had diabetes. In 2012, from day 1, by primary renal disease. GN glomerulone-
1,129 patients started dialysis (incidence 24.8 per phritis, HTN hypertension, DM diabetes mellitus, y years
(Modified from Kolesnyk et al. [98])
million population), with 80 % on hemodialysis.
Mean age was 48 14 years, 58 % men and 20 %
had diabetes. Two years diabetes mellitus patients patients are receiving RRT in Moldova, including
survival on dialysis was 64.5 % (Fig. 11.14). The 80 diabetes mellitus patients (Adrian Tanase;
transplant rate in 2012 was 2.1 per million popula- personal communications data, 2016).
tion. The incidence and prevalence of RRT and In summary, after this review of diabetes clini-
the transplantation rate in Ukraine are among the cal aspects, we can state the following:
lowest in Europe, suggesting that the need for
RRT is not being met. Strategies to reduce the Effect of economic prosperity of the country
RRT deficit include the development and improve- upon T1D treatment is best seen in the usage
ment of transplantation and home-based dialysis of insulin analogs.
programs. Further evaluation of the quality of T2D treatment in Ukraine is characterized by
Ukrainian RRT care is needed. significantly lower use of statins, any antihy-
Peritoneal dialysis recently became widely pertensive agents, ACE inhibitors, comparing
accessible in Ukraine, and diabetes patients even to Central European and Baltic countries.
prevailed among those, who received this treatment Prevalence of myocardial infarction in T2D
[98]. At the time of this chapters preparation, 553 patients in Ukraine and Russia is significantly
lower comparing to Central European and One of the typical reviews of these methods
Baltic countries. that are recommended for treating diabetes and
Financial welfare itself does not always affect its complications [101] does not mention any
the efficacy of diabetes treatment in expected verification of its clinical efficacy. Clearly, it will
fashion or to a sufficient level. be very difficult to perform such verification
Issue of renal replacement therapy of patients using evidence-based medicine.
with diabetic nephropathy is far from being
solved in Eastern Europe. Recently, there is
some progress in providing RRT in Ukraine; Rational Selection of Anti-diabetes
however, its volume and quality is still in need Medications
of improvement.
We have previously mentioned several evaluations
and comparisons of anti-diabetes medications
Non-pharmacological Management use, including the frequency of insulin use (and
its analogs) for diabetes treatment (see section
Current treatment strategies aim at achieving the Complications of Diabetes in Region). Diabetes
best possible control include a non- patient registry-based Ukrainian study revealed
pharmacological approach consisting of lifestyle that glibenclamide treatment of T2D is associ-
interventions using physical exercise and modifi- ated with greater risk of all-cause mortality versus
cation of nutrition intakes in the early stage of gliclazide or glimepiride treatment and cardiovas-
type 2 diabetes [99]. Physical activity, indepen- cular disease (CVD) mortality versus gliclazide
dent of weight loss, has a beneficial effect on dia- treatment [38]. Danish registry-based observa-
betic mortality [100]. Mentions and some tional study showed an increase of all-cause and
descriptions of such lifestyle interventions can be cardiovascular mortality risks in T2D patients
found in patient education literature, as well as in with and without previous myocardial infarction,
guidelines for doctors that exist in Eastern receiving such common insulin secretagogues
Europe. For example, the guidelines of T2D pri- as glibenclamide, glimepiride, and glipizide ver-
mary and secondary care in Ukraine contain short sus metformin, whereas gliclazide versus met-
recommendations on lifestyle modifications with formin had no such risks [102]. Recently, using
dietary advice (calculation of carbohydrate units four different methodological approaches, when
and food glycemic index, saturated fats and fiber analyzing retrospective cohorts of T2D patients,
intake) [81]; however, practical use of these and we discovered an elevated total mortality risk for
other recommendations is difficult due to a lack glibenclamide-treated versus gliclazide and met-
such health workers, as dietologists. The Soviet formin-treated patients, in case of using three of
health system had such medical specialization, this approaches (models). Direct comparison of
and it remains in some post-Soviet countries till gliclazide versus metformin, when using one of
this day; however, the number of such specialists these models discovered a lower mortality risk for
is clearly inadequate, comparing to the number of gliclazide-treated [47]. The advantage of most oral
patients with diabetes. anti-diabetes medications in comparison to gliben-
A similar situation exists in the field of physio- clamide were known, whereas the results of com-
therapy: Rehabilitation and physical training parison of gliclazide and metformin seems new.
experts are not currently a mass category of profes- Unlike insulin, other anti-diabetes medica-
sionals in Ukrainian, as well as other post-Soviet tions are not free for patients in most post-Soviet
healthcare systems. On the other hand, there are countries of Eastern Europe [31, 51, 103, 104].
physiotherapy doctors, who work in large hospi- This establishes a negative relationship between
tals, walk-in clinics, and health resorts, where they the frequency of using cheap drugs and popula-
administer treatment, using various electromag- tions economic situation. Glibenclamide belongs
netic devices, mineral water therapy, massage, etc. to such type of medications, with the greatest
hypoglycemic effect. This makes its chances of oxygen to which tissues are exposed may
leaving Eastern European market quite low. For substantially impact cardio-metabolic health
example, 5 years ago in one region of Central [111114]. Interestingly, living at high altitude
Ukraine, most oral-treated T2D patients received (hypobaric hypoxia) seems to be associated with
glibenclamide [51]. improved glucose homeostasis and a decreased
Thus, treatment algorithms used for glycemic prevalence of T2D [111] and doing interval nor-
control of diabetes patients in Europe are also mobaric hypoxic training is an effective method
practiced in its Eastern European part; however, of improving resistance to hypoxia and correct-
their wide implementation is often limited by ing prediabetic carbohydrate metabolism disor-
economic factors. ders [114].
Translating Primary Prevention Organizing and Conduction

of Type 2 Diabetes Diabetes Research in Region
The lifestyle intervention using physical exercise Diabetes research in the former Soviet Union was
and modification of nutrition is efficient in pre- always carried out in the framework of experimen-
venting type 2 diabetes in patients with impaired tal and clinical endocrinology, with three research
glucose tolerance [99]. Clinical trials confirm and clinical facilities, as centers of this research.
that lifestyle interventions (dietary modification
and increased physical activity) reduce the risk of Kharkov Institute of Endocrinology founded
progressing from impaired glucose tolerance to in 1919 by physiologist Vasyl Danilevsky, in
type 2 diabetes [105]. Assessing T2D risk accord- 1927 insulin production began (mass produc-
ing to FINDRISK scale [106] is quite common in tion of insulin continued for over 50 years). In
Eastern Europe [107]. We should acknowledge 1923, Victor Kohan-Yasniy was the first in the
that todays strategies of primary prevention of country to extract insulin from pancreatic tissue
type 2 diabetes [106] are still not considering the and to administer it to a diabetic coma patient.
fact that Prior to the development of type 2 dia- Back in the 1930s, Semen Henes determined
betes, glucose levels increase into the pre-diabetic that the main objective of treating diabetes
states of isolated impaired fasting glycaemia patients is giving them the opportunity to take
(i-IFG), isolated impaired glucose tolerance up normal amounts of carbohydrates. Together
(i-IGT), or combined IFG/IGT [108]. Physical with O. Reznytska they designed a diet therapy
activity was associated with a lower progression plan for diabetes patients
to diabetes in individuals with i-IGT category, a http://www.ipep.com.ua/.
condition characterized by muscle insulin resis- Kyiv Institute of Endocrinology and
tance. Physical activity did not predict progres- Metabolism was founded in 1965 by endocri-
sion to diabetes in individuals with i-IFG nologist Vasyl Komisarenko. Andriy Yefimov
category, a condition characterized by hepatic headed clinical research in the field of diabetes
insulin resistance [109]. These findings suggest for many years. Prof. Yefimov is considered to
distinct pathophysiological mechanisms of i-IFG be the founder of Ukrainian diabetology.
and i-IGT although the T2D prevention relevance http://www.iem.net.ua/
of these observations requires further clarifica- Endocrinology Research Center (Moscow)
tion. Detecting new phenotypical differences of founded in 1922 by Prof. Vasyl Shervinskiy,
i-IFG and i-IGT that was recently performed in who is considered the founding father of
Ukraine [110] may possibly facilitate this. Russian endocrinology. Human insulin was
Several alternative approaches to diabetes pre- synthesized in 1972 under the leadership of
vention are starting to be investigated in Ukraine. N. Yudaev.
Several studies have indicated that the amount of http://www.endocrincentr.ru/about/diabed/
Future Directions: Unmet Needs, studied today, surviving for more than 70 years,
Unanswered Questions, not diagnosed with diabetes, may have had a
and Unquestioned Answers decreased SDDM prevalence several decades
after the famine episodes. It is assumed that this
One of the unanswered questions that no one unexpected effect can be explained by a situation,
seems to ask is the reason why according to where the carriers of a corresponding genes were
Russian diabetes registers the prevalence of T2D already diagnosed with diabetes.
among women is 2.5 times higher than in men Possibly some recent assessments of SDDM
[115]. The same was noticed in Ukraine [116, prevalence in those Ukrainians who reported
117] but has not been seen in other parts of famine exposure [13] could be an indirect confir-
Europe [118]. Epidemiological studies based on mation of this situation. A recent genotyping of
hyperglycemia screening conducted in Russia those who survived the Leningrad siege [122]
[11, 85] and more recently in Ukraine [13] did also led to unexpected results: In case of UCP3
not confirm the fact of gender differences of the gene, normal allele C and C/C genotype pre-
real T2D prevalence, whereas a British study of vailed in women, whereas mutated allele T,
the trends in diabetes awareness (a self-reported associated with atherosclerosis, T2D, and obesity
doctor diagnosis) showed that diabetes awareness were significantly less common. When explain-
was three time more frequent in women (6 %) ing these results we cannot overlook the possibil-
than men (2 %) [119]. Awareness was lower in ity, that carriers of atherogenic and diabetogenic
rural and less-educated respondents. High body genotype could have greater chances of surviving
mass index predicted diabetes awareness in during famine but could not live till being geno-
women but did not explain gender or socioeco- typed in the twenty-first century due to early
nomic differences. More than half of those development of atherosclerosis. It is clear that
reporting a diabetic diagnosis reported receiving conducting epidemiologic studies in Eastern
no conventional medical treatment, and insulin Europe using individual famine exposure data
use was less frequent than in Western populations can clarify causa relation between undernutrition
[119]. during postnatal development and type 2 diabetes
Thus, in the future we still need to find the rea- risk in adulthood.
son for better diagnostic efficacy of T2D in This review did not attempt to cover all sig-
women compared to men in post-Soviet nificant diabetes research conducted during the
countries. last few years in Eastern Europe or even Ukraine,
Effects of childhood starvation on the risk of Latvia, and Moldova. In particular, some sub-
developing T2D later in life is another topic that stantial clinical and immunological investiga-
should be discussed. The effect of famine on tions in Ukraine [123, 124] remained beyond its
increasing the risk of being diagnosed with dia- reach. Nevertheless, we tried to concentrate on
betes in Ukraine and some other countries was the most familiar to us: issues of diabetes epide-
assessed only based on analysis of large adminis- miology, aspects of diagnostic, and treatment
trative patient databases [65, 120], whereas cur- practice of East European countries that could be
rent prevalence of screen-detected type 2 diabetes compared, as well as some pathophysiologic
(SDDM) among those who survived the famine aspects, the study of which was based on the
during childhood and are still alive today remains analysis of population registers. We can point to
unknown. The developmental origins hypothesis the absence of credible epidemiologic data on
proposes that undernutrition during early devel- diabetes in Eastern Europe or their insufficiently
opment is associated with an increased type 2 adequate interpretation as one of the main con-
diabetes risk in adulthood [121]. If we were to clusion. We can also note a generally significant
assume that this phenomenon is a consequence of range of treatment quality in European countries
a more rapid T2D development in persons with regarding diabetes. The only thing that we can
diabetic genotype, then the population that is count on now is that collaboration with the EU
will lead to gradual improvements of diabetes 13. Khalangot M, Gurianov V, Okhrimenko N,

Luzanchuk I, Kravchenko V. Neck circumference as
care in Eastern Europe and will facilitate new
a risk factor of screen-detected diabetes mellitus:
fundamental research in the field of diabetes. The community-based study. Diabetol Metabol Syndr.
experience of Baltic states gives certain ground 2016;8:12.
for such hopes. 14. Martirosyan H, Petrosyan V, Crape B, Melkomian
DM, Koshkakaryan M, Sahakyan Y, Truzyan
N. Rapid appraisal of diabetes care in Armenia: a
qualitative research. Yerevan: Center for Health
Services Research and Development, American
References University of Armenia; 2012.
15. State Statistical Committee of the Republic of
1. The World Bank Data. Countries and economies. Azerbaijan, Baku 2015. www.stat.gov.az.
http://data.worldbank.org/country. Retrieved 11 Jan 16. Kharchanka A, Roubuts T. Morbidity dynamics of
2015. diabetes in children living in the West region of
2. Narayan KM, Ali MK, Koplan JP. Global noncom- Belarus. Endocr Abstr. 2014;35:P805. doi:10.1530/
municable diseaseswhere worlds meet. N Engl endoabs.35.P805.
J Med. 2010;363(13):11968. doi:10.1056/ 17. Shepelkevich AP. Int J Endocrinol. 2015;4(68):119
NEJMp1002024. 21. (In Russian) www.mif-ua.com/archive/article/
3. Beran D. The impact of health systems on diabetes 40847.
care in low and lower middle income countries. Curr 18. Ocoeoc oaa aeooeco
Biabetes Rep. 2015;15(4):113. oo Pece eapc a copeeo
4. Wilmoth JR, Lundstrm H. Extreme longevity in ae / eee A.. [ p.]. (2012) Ars.
five countries. Eur J Popul/Rev Eur Dmogr. Medica 15(70):611. http://natbookcat.org.by/isgbi/
1996;12(1):6393. marcview.do?id=1067461&position=2.
5. International Diabetes Federation, Diabetes Atlas. 6th 19. Balabanova D, McKee M, Koroleva N, Chikovani I,
ed. Brussels. 2013. http://www.idf.org/diabetesatlas. Goguadze K, Kobaladze T, Robles S. Navigating
6. http://apps.who.int/healthinfo/statistics/mortality/ the health system: diabetes care in Georgia. Health
whodpms/. Pol Plan. 2009;24(1):4654.
7. Turcanu G, Domente S, Buga M, Richardson 20. Georgia Statistical yearbook_2013_eng www.ncdc.
E. Republic of Moldova: health system review. ge.
Health Syst Transit. 2012;14(7):1151. 21. Ministerul Sntii al Republicii Moldova Centrul
8. Whiting DR, Guariguata L, Weil C, Shaw J. IDF dia- Naional de Management n Sntate. ANUARUL
betes atlas: global estimates of the prevalence of dia- STATISTIC AL SISTEMULUI DE SNTATE
betes for 2011 and 2030. Diabetes Res Clin Pract. DIN MOLDOVA ANUL 2013. Chiinu, 2014.
2011;94(3):31121. 22. Dedov II, Shestakova MV, Vikulova OK. National
9. Dogadin SA, Mashtakov BP, Taranushenko register of diabetes mellitus in Russian Federation:
TE. Prevalence of type 2 diabetes in northern popu- status on 2014 (Article in Russian) Caxap
lations of Siberia. Int J Circumpolar Health. ae. 2015;18(3):523. http://endojournals.ru/
2001;60:20510. index.php/dia/article/view/7235.
10. a HC, Co , ooca , 23. Shiryaeva TYu, Andrianova EA, Suntsov YuI. Type 1
Macoa B, Cpo CB, eo . diabetes mellitus in children and adolescents of
Pacpocpaeoc caxapoo aea 2 a Russian Federation: key epidemiology trends (arti-
(o a cpa). Caxap ae. cle in Russian) Caxapae. 2013;(3):2129.
2005;2:78. http://cyberleninka.ru/article/n/raspros http://dx.doi.org/10.14341/2072-0351-813.
tranennost-saharnogo-diabeta-2-tipa-po-dannym- 24. eo , ecaoa MB (2013). Pea
skrininga. peaa opopa Caxap
11. oa CA, paoca EB, Bopaoa ae eepao eeo popa
CB. Pea cpa ee pacopca pepeee opa c coao
a caxap ae. Caxap ae 1, 2004, a aoea 20072012 o.
c. 810. http://cyberleninka.ru/article/n/rezultaty- Caxapae, (2S).Cec [Federal tar-
skrininga-zhiteley-krasnoyarska-na- saharnyy- geted programme Prevention and Management of
diabet. Socially Significant Diseases (20072012): results
12. Khalangot MD, Kravchenko VI, Pisarenko Yu M, of the Diabetes mellitus sub-programme] (article in
Okhrimenko NV, Lerman NG, KovtunVA. Prevalence Russian). http://cyberleninka.ru/article/n/rezultaty-
of diabetes mellitus, impaired glucose regulation, and realizatsii-podprogrammy-saharnyy-diabet- -
their anthropometric risk factors in elderly residents of federalnoy-tselevoy-programmy-preduprezhdenie-i-
rural. Ukraine Endocrynologia. 2014;19(2):11925. borba-s-sotsialno-znachimymi#ixzz3r1FgzdzE.
http://nbuv.gov.ua/j-pdf/enkrl_2014_19_2_7.pdf . 25. Suntsov YuI. Modern antihyperglycemic agents pre-
[Article in Ukrainian]. n.d. scribed in Russia for type 2 diabetes mellitus. (arti-
cle in Russian) Caxap ae. 2012;(1):69. 40. Franco OH, Steyerberg EW, Hu FB, Mackenbach J,
http://cyberleninka.ru/article/n/sovremennye- Nusselder W. Associations of diabetes mellitus with
saharosnizhayuschie- preparaty-ispolzuemye-v- total life expectancy and life expectancy with and
rossii-pri-lechenii-saharnogo-diabeta-2-tipa. without cardiovascular disease. Arch Intern Med.
26. Chernobrov AD, editors. Main indicators of endocri- 2007;167(11):114551.
nological care of Ukraine for 2015: review. Kyiv: 41. Khalangot M, Kravchenko V, Tronko M, Gurianov
V.P. Komisarenko Institute of Endocrinology and V. Correlation between the prevalence of type 1 dia-
Metabolism of the Acad Med Sci, Ukraine Ministry betes with the daily insulin dose and the autoimmune
of Health. Endocrynologia. 2014;19(1) Supplement process against glutamic acid decarboxylase in
1 (data set in Ukrainian). adults. Eur J Intern Med. 2009;20(6):6115.
27. Mankovsky B. The prevalence of undiagnosed type 42. Khalangot M, Tronko M, Okhrimenko N,
2 diabetes mellitus in Ukraine. Diabetologia. Kravchenko V, Gurianov V, Tronko M. Prevalence of
2007;50 Suppl 1:0376. type 1 diabetes correlates with daily insulin dose,
28. The Center for Disease Prevention and Control of adverse outcomes and with autoimmune process
Latvia. http://www.spkc.gov.lv/about-SPKC/. Accessed against glutamic acid decarboxylase in adults. Rijeka,
11 June 2015. Croatia: INTECH Open Access Publisher; 2011.
29. The Central Statistics Bureau of Latvia. http://www. 43. Khalangot M. Current practice of insulin and oral
csb.gov.lv/en. Accessed 11 June 2015. hypoglycaemic agents treatment of diabetes mellitus
30. Atun R, Jaffar S, Nishtar S, Knaul FM, Barreto ML, type 2 patients according to diabetes mellitus regis-
Nyirenda M, et al. Improving responsiveness of ter data analysis in the city of Donetsk, Ukraine.
health systems to noncommunicable diseases. Prim Care Diabetes. 2007;1(4):224.
Lancet. 2013;381(9867):6907. 44. Khalangot M, Hu G, Tronko M, Kravchenko V,
31. Khalangot M, Tronko M. Primary care diabetes in Guryanov V. Gender risk of nonfatal stroke in type 2
Ukraine. Prim Care Diabetes. 2007;1(4):2035. diabetic patients differs depending on the type of treat-
32. Telishevska M, Chenet L, McKee M. Towards an ment. J Womens Health (Larchmt). 2009;18(1): 97103.
understanding of the high death rate among young 45. Khalangot M, Tronko M, Kravchenko V, Kulchinska
people with diabetes in Ukraine. Diabet Med. J, Hu G. Body mass index and the risk of total and
2001;18(1):39. cardiovascular mortality among patients with type 2
33. Shields BM, Peters JL, Cooper C, Lowe J, Knight diabetes: a large prospective study in Ukraine. Heart.
BA, Powell RJ, Hattersley AT. Can clinical features 2009;95(6):454560.
be used to differentiate type 1 from type 2 diabetes? 46. Khalangot M, Tronko M, Kravchenko V, Kulchinska
A systematic review of the literature. BMJ Open. J, Hu G. The joint effects of different types of
2015;5(11):e009088. glucose-lowering treatment and duration of diabetes
34. Royal College of General Practitioners and NHS on total and cardiovascular mortality among subjects
Diabetes. Coding, classification and diagnosis of with type 2 diabetes. Diabetes Res Clin Pract.
diabetes. Secondary coding, classification and diag- 2008;82(1):13947.
nosis of diabetes. 2011. http://www.sdrn.org.uk/ 47. Khalangot M, Kovtun V. Evaluation approach can
sites/sdrn.org.uk/files/nhs%20diagnosis%20classifi- significantly influence oral glucose-lowering drugs
cation% 20report.pdf. total mortality risks in retrospective cohorts of type 2
35. Pildava S, Strle I, Briis . The mortality of diabetes mellitus patients. Curr Diabetes Rev.
patients with diabetes mellitus in Latvia 20002012. 2014;10(5):33642.
Medicina. 2014;50(2):1306. 48. Khalangot ND. Age related and sex peculiarities of
36. Dedov II. Diabetes mellitus a dangerous treat to mortality from diabetes mellitus type 1 (based on
the mankind. [Article in Russian]. Vestn Ross Akad analysis of data of Ukraines diabetes mellitus
Med Nauk. 2012;(1):713. http://europepmc.org/ Register) [Article in Ukrainian]. Problemy starenia I
abstract/med/22550704. dolgoletia. 2008;17(1):7582. http://www.geront.
37. Khalangot MD. Epedemiologic characteristics of kiev.ua/psid-2010/2008_1.pdf#page=75.
diabetes mellitus type1 and 2 according to data from 49. Khalangot MD, Kravchenko VI, Okhrimenko NV,
national population-based patient register. Kovtun VA, Tronko EM. Analysis of mortality, prolif-
[Manuscript in Ukrainian]. Thesis for the Degree of erative retinopathy prevalence, and arterial hyperten-
Doctor of Medical Sciences. V.P. Komisarenko sion among type 1 diabetic patients residing in areas
Institute of Endocrinology and Metabolism AMS of that differ in prevalence of this disease. Endocrinologia.
Ukraine, Kiev; 2009. 2009;14(1):7785. Article in Ukrainian.
38. Khalangot M, Tronko M, Kravchenko V, Kovtun 50. Khalangot MD, Tronko MD, Kravchenko VI,
V. Glibenclamide-related excess in total and cardio- Kovtun VA, Okhrimenko NV, Bolgarska SV. Some
vascular mortality risks: data from large Ukrainian mortality risk factors for type 1 diabetes mellitus
observational cohort study. Diabetes Res Clin Pract. patients in Ukraine evaluated according to data from
2009;86(3):24753. National Register. Endocrinologia. 2010;15(1):62
39. http://apps.who.int/gho/data/view.main.680. 70. Article in Ukrainian.
51. Khalangot MD, Kovtun VA, Okhrimenko NV, 63. Li Y, He Y, Qi L, et al. Exposure to the Chinese fam-
Sokolova LK, Bolgarska SV. Approaches to an ine in early life and the risk of hyperglycemia and
assessment of probable funds required for treatment type 2 diabetes in adulthood. Diabetes. 2010;59:
of patients with diabetes mellitus in Ukraine 24006.
P. ME. ACOC, 3 (89) V/VI 2012|[Article 64. Thurner S, Klimek P, Szell M, et al. Quantification
in Ukrainian]. http://www.umj.com.ua/article/12340/. of excess risk for diabetes for those born in times of
52. Soedamah-Muthu SS, Fuller JH, Mulnier HE, hunger, in an entire population of a nation, across a
Raleigh VS, Lawrenson RA, Colhoun HM. All- century. Proc Natl Acad Sci U S A. 2013;110:
cause mortality rates in patients with type 1 diabetes 47037.
mellitus compared with a non-diabetic population 65. Lumey LH, Khalangot MD, Vaiserman
from the UK general practice research database, AM. Association between type 2 diabetes and prena-
19921999. Diabetologia. 2006;49:6606. tal exposure to the Ukraine famine of 193233: a
53. Krolewski AS, Kosinski EJ, Warram JH, Leland OS, retrospective cohort study. Lancet Diabetes
Busick EJ, Asmal AC, Rand LI, Christlieb AR, Endocrinol. 2015;3:78794.
Bradley RF, Kahn CR. Magnitude and determinants 66. Laron Z, Lewy H, Wilderman I, et al. Seasonality of
of coronary artery disease in juvenile-onset insulin- month of birth of children and adolescents with type
dependent diabetes mellitus. Am J Cardiol. 1 diabetes mellitus in homogenous and heteroge-
1987;59:7505. neous populations. Isr Med Assoc J. 2005;7:3814.
54. Lloyd CE, Kuller LH, Ellis D, Becker DJ, Wing RR, 67. Vaiserman AM, Carstensen B, Voitenko VP, et al.
Orchard TJ. Coronary artery disease in IDDM: gen- Seasonality of birth in children and young adults
der differences in risk factors but not risk. (029 years) with type 1 diabetes in Ukraine.
Arterioscler Thromb Vasc Biol. 1996;16:7206. Diabetologia. 2007;50:325.
55. Steinberg HO, Paradisi G, Cronin J, Crowde K, 68. Vaiserman AM, Khalangot MD, Carstensen B, et al.
Hempfling A, Hook G, Baron AD. Type II diabe- Seasonality of birth in adult type 2 diabetic patients
tes abrogates sex differences in endothelial function in three Ukrainian regions. Diabetologia. 2009;52:
in premenopausal women. Circulation. 2000;101: 26657.
20406. 69. Jensen CB, Zimmermann E, Gamborg M, et al. No
56. Laing SP, Swerdlow AJ, Slater SD, Botha JL, evidence of seasonality of birth in adult type 2 diabe-
Burden AC, Waugh NR, Smith AW, Hill RD, tes in Denmark. Diabetologia. 2015;58:204550.
Bingley PJ, Patterson CC, Qiao Z, Keen H. The 70. Vaiserman A, Khalangot M. Similar seasonality of
British Diabetic Association Cohort Study, II: cause- birth in type 1 and type 2 diabetes patients: a sign for
specific mortality in patients with insulin-treated common etiology? Med Hypotheses. 2008;71:
diabetes mellitus. Diabet Med. 1999;16(6):46671. 6045.
57. Soedamah-Muthu SS, Chaturvedi N, Witte DR, 71. Wilkin TJ. Changing perspectives in diabetes: their
Stevens LK, Porta M, Fuller JH, EURODIAB impact on its classification. Diabetologia.
Prospective Complications Study Group. 2007;50:158792.
Relationship between risk factors and mortality in 72. Chistiakov DA, Savostanov KV, Nosikov
type 1 diabetic patients in Europe: the EURODIAB VV. CTLA4 gene polymorphisms are associated
Prospective Complications Study (PCS). Diabetes with, and linked to, insulin-dependent diabetes melli-
Care. 2008;31(7):13606. tus in a Russian population. BMC Genet. 2001;2(1):6.
58. Dorman JS, Laporte RE, Kuller LH, Cruickshanks 73. Chistiakov DA, Zotova EV, Savostanov KV, Bursa
KJ, Orchard TJ, Wagener DK, Becker DJ, Cavender TR, Galeev IV, Strokov IA, Nosikov VV. The 262T>
DE, Drash AL. The Pittsburgh insulin-dependent dia- C promoter polymorphism of the catalase gene is
betes mellitus (IDDM) morbidity and mortality study. associated with diabetic neuropathy in type 1 diabetic
Mortality results. Diabetes. 1984;33(3): 2716. Russian patients. Diabetes Metabol. 2006;32(1):638.
59. Maahs DM, Rewers M, editors. Mortality and renal 74. Chistiakov DA, Potapov VA, Khodirev DC,
disease in type 1 diabetes mellitusprogress made, Shamkhalova MS, Shestakova MV, Nosikov
more to be done. J Clin Endocrinol Metab. VV. Genetic variations in the pancreatic ATP-
2006;91(10):375759. sensitive potassium channel, beta-cell dysfunction,
60. Hales CN, Barker DJ. The thrifty phenotype hypoth- and susceptibility to type 2 diabetes. Acta Diabetol.
esis. Br Med Bull. 2001;60:520. 2009;46:439.
61. Lumey LH, Stein AD, Susser E. Prenatal famine and 75. Sokolova EA, Bondar IA, Shabelnikova OY,
adult health. Annu Rev Public Health. Pyankova OV, Filipenko ML. Replication of
2011;32:23762. KCNJ11 (p.E23K) and ABCC8 (p.S1369A) associ-
62. Lumey LH, Stein AD, Kahn HS. Food restriction ation in Russian Diabetes Mellitus 2 type cohort
during gestation and impaired fasting glucose or glu- and meta-analysis. PLoS ONE. 2015;10(5):
cose tolerance and type 2 diabetes mellitus in adult- e0124662.
hood: evidence from the Dutch Hunger Winter 76. Globa E, Zelinska N, Mackay DJ, Temple KI,
Families Study. J Dev Orig Health Dis. 2009;1:S164. Houghton JA, Hattersley AT, Flanagan SE, Ellard
S. Neonatal diabetes in Ukraine: incidence, 87. Andel M, Grzeszczak W, Michalek J, Medvescek M,

genetics, clinical phenotype and treatment. Norkus A, Rasa I, Niewada M, Kamiski B, Kraml
J Pediatr Endocrinol Metab. 2015;28(1112): P, Madacsy L, DEPAC Group. A multinational,
127986. multi centre, observational, cross sectional survey
77. Grulich-Henn J, Wagner V, Thon A, Schober E, assessing diabetes secondary care in Central and
Marg W, et al. Entities and frequency of neonatal Eastern Europe (DEPAC Survey). Diabetic
diabetes: data from the diabetes documentation and Medicine. 2008;25(10):1195203.
quality management system (DPV). Diabet Med. 88. Gill GV, Yudkin JS, Keen H, Beran D. The insulin
2010;27:70912. dilemma in resource-limited countries. A way for-
78. Iafusco D, Massa O, Pasquino B, Colombo C, ward? Diabetologia. 2010. doi:10.1007/s00125-
Iughetti L, Early Diabetes Study Group of ISPED, 010-1897-3.
et al. Minimal incidence of neonatal/infancy onset 89. WHO, World Health Statistics. Annual electronic
diabetes in Italy is 1:90,000 live births. Acta File, July, 2001 version. Geneve. Retrieved 30 Jan
Diabetol. 2012;49:4058. 2004.
79. World Health Organization. Definition, diagnosis, 90. Gorter KJ, Wens J, Khunti K, Claramunt XC,
and classification of diabetes mellitus and its com- Topsever P, Drivsholm T, Rurik I. The European
plications: report of a WHO consultation. Part 1: EUCCLID pilot study on care and complications in
diagnosis and classification of diabetes mellitus. an unselected sample of people with type 2 diabetes
Geneva: World Health Org; 1999. WHO/NCD/ in primary care. Prim Care Diabetes. 2010;4(1):
NCS/99.2. 1723.
80. eo .., ecaoa M.B., Macoa M.A. 91. McKnight JA, Wild SH, Lamb MJE, Cooper MN,
eepaa eea popaa Caxap Jones TW, Davis EA, Hofer S, Fritsch M, Schober E,
ae (Meoece peoea).- M., Svensson J, Almdal T, Young R, Warner JT, Delemer
2003.- C.4246. http://www.voed.ru/fcp_sd.htm. B, Souchon PF, Holl RW, Karges W, Kieninger DM,
81. HIIOBAH IHIH POTOO Tigas S, Bargiota A, Sampanis C, Cherubini V,
EPBHHO TA BTOPHHO (CEIAIO Gesuita R, Strele I, Pildava S, Coppell KJ, Magee G,
BAHO) MEHO OOMO POB Cooper JG, Dinneen SF, Eeg-Olofsson K, Svensson
IAET 2 T Approved by Health Ministry of AM, Gudbjornsdottir S, Veeze H, Aanstoot HJ,
Ukraine, 21.12.2012 1118. http://www.moz.gov.ua/ Khalangot M, Tamborlane WV, Miller
docfiles/dod1118_2_2012.pdf. KM. Glycaemic control of type 1 diabetes in clinical
82. The Expert Committee on the Diagnosis and practice early in the 21st century: an international
Classification of Diabetes Mellitus. Follow-up report comparison. Diabet Med. 2015;32(8):103650.
on the diagnosis of diabetes mellitus. Diabetes Care. 92. Kravchenko VI, Tronko ND, Pankiv VI, Venzilovich
2003;26:31607. YM, Prudius FG. Prevalence of diabetes mellitus
83. American Diabetes Association. Diagnosis and clas- and its complications in the Ukraine. Diabetes Res
sification of diabetes mellitus. Diabetes Care. Clin Pract. 1996;34:S738.
2014;37(Supplement 1):S8190. 93. Khlbrandt C, Basu S, Mckee M, Stuckler
84. Dreval AV, Misnikova IV, Barsukov IA, Ponchakova D. Looking at the Russian health care system:
GV, Kuznetsov AV. Prevalence of type 2 diabetes melli- through the eyes of patients with diabetes and their
tus and other abnormalities of carbohydrate metabolism physicians. Br J Diabetes Vasc Dis. 2012;12(4):
depending on diagnostic criteria Caxap ae, 1814.
2010 (1) 116120. http://cyberleninka.ru/article/n/ 94. Richardson E, Roberts B, Sava V, Menon R, McKee
rasprostranennost-saharnogo-diabeta-2-tipa-i-drugih- M. Health insurance coverage and health care access
narusheniy-uglevodnogo-obmena-v-zavisimosti-ot- in Moldova. Health Policy Plan. 2012;27(3):
kriteriev-diagnostiki. 20412.
85. Vaychulis IA, Shaposhnik II, Vaychulis TN. 95. Shishkin S, Jowett M. A review of health financing
Pea cpa caxapoo aea2 a reforms in the Republic of Moldova, Health financ-
px ape eooo oea cpe ing policy paper no. 1. Copenhagen: WHO Regional
paoaeo acee eca. Caxap Office for Europe; 2012.
ae. 2006;9(4):515. http://cyberleninka.ru/ 96. Domente S, Turcanu G, Habicht J, Richardson
article/n/rezultaty-skrininga-saharnogo- E. Developments in primary health care in the
diabeta-2-tipa-i-drugih-narusheniy-uglevodnogo-obmena- Republic of Moldova: essential steps to improving
sredi-rabotayuschego-naseleniya-chelyabinska. access to services. Eurohealth. 2013;19(2):2831.
86. Dogadin SA, Artemenko GP, Tsyplyakova NB, 97. Rutkowski B. Highlights of the epidemiology of
Subrakova NI, Dazidenko LN, Boyko SA, & renal replacement therapy in Central and Eastern
Veselkin DA. Pea cpa caxapoo Europe. Nephrol Dial Transplant. 2006;21(1):410.
aea ee . Aaaa (Peca 98. Kolesnyk I, Noordzij M, Kolesnyk M, Kulyzky M,
Xaac). Caxap ae. 2008;11(2):5558. Jager KJ. Renal replacement therapy in Ukraine:
http://endojournals.ru/index.php/dia/article/ epidemiology and international comparisons. Clin
viewFile/5761/3539. Kidney J. 2014;7(3):3305.
99. Buysschaert M, Hermans MP. Non-pharmacological comparative analysis for cardioprotection.

management of type 2 diabetes. Acta Clin Belg. Fiziolohichnyi zhurnal. 2014;61(3):99117.
2004;59(1):149. 113. Korkushko OV, Shatilo VB, Chyzhova VP, Naskalova
100. Diamond J. The double puzzle of diabetes. Nature. SS, Osmak YeD, Gremiakov AV, Antoniuk-Scheglova
2003;423:599602. IA, Gavalko GV, Naumchuk NS. Organism reaction
101. Kyrylyuk M. Balneotherapy, pelotherapy and phys- to dosed hypoxic hypoxia in the healthy subjects and
iotherapy of diabetes mellitus. iia individuals with prediabetic metabolism distur-
eopooi a eopa xippi. bances Fiziolohichnyi zhurnal. 2016 (in press).
2010;(1):6876. https://scholar.google.com/scholar? 114. Shatilo VB, Korkushko OV, Chizhova VP,
q=+Kyrylyuk+M.+%282010%29+Balneotherapy% Naskalova SS, Gavalko AV, Antoniuk-Shcheglova
2C+pelotherapy+and+physiotherapy+of+diabetes+ IA, Gremiakov AV, Osmak D, Zhuravleva D, Yu
mellitus. B. Efficacy of using interval normobaric hypoxic
102. Schramm TK, Gislason GH, Vaag A, et al. Mortality exercise training in elderly patients with prediabetic
and cardiovascular risk associated with different derangements of carbohydrate metabolism. Problemy
insulin secretagogues compared with metformin in stareniia I dolgoletia. 2015;24:34 (in press).
type 2 diabetes, with or without a previous myocar- 115. Suntsov YuI, Bolotskaya LL, Maslova OV, Kazakov
dial infarction: a nationwide study. Eur Heart IV. Epidemiology of diabetes mellitus and prognosis
J. 2011;32:19008. of its prevalence in the Russian Federation.
103. Perlman F, Balabanova D. Prescription for change: Caxap ae, (1). http://cyberleninka.ru/
accessing medication in transitional Russia. Health article/n/epidemiologiya- saharnogo-diabeta-
Policy Plan. 2011;26(6):45363. i-prognoz-ego-rasprostranennosti-v-rossiyskoy-fed-
104. Khalangot M. Current practice of insulin and oral eratsii.
hypoglycaemic agents treatment of diabetes mellitus 116. Tronko M, Khalangot M, Kravcenko V, et al. Gender
type 2 patients according to diabetes mellitus regis- distribution in Ukrainian adult insulin-treated dia-
ter data analysis in the city of Donetsk, Ukraine. betics depending of age at diagnosis. Endocr Abstr.
Prim Care Diab. 2007;1(4):224. 2006;11:298. http://www.endocrine-abstracts.org/
105. Yung LM, Yung M, Yao X, Chen ZY, Huang Y, ea/0011/ea0011P298.htm.
Leung FP. Exercise, vascular wall and cardiovascu- 117. Khalangot MD, Gurianov VG, Vaiserman
lar diseases. Sports Med. 2009;39(1):4563. AM. Gender differences in prevalence of diagnosed
106. Lindstrm J, Neumann A, Sheppard KE, Gilis- type 2 diabetes and patients body mass index in five
Januszewska A, Greaves CJ, Handke U, Roden Ukraine regions with diverse historical backgrounds.
M. Take action to prevent diabetes the IMAGE BIO. 2012;2:110.
toolkit for the prevention of type 2 diabetes in 118. Gale EA, Gillespie KM. Diabetes and gender.
Europe. Horm Metabol Res. 2010;42:S3755. Diabetologia. 2001;44:315.
107. Schepelkevich AP, Kholodova EA, Salko OB, et al. 119. Perlman F, McKee M. Diabetes during the Russian
Assessment of risk of type 2 diabetes mellitus devel- transition. Diabetes Res Clin Pract.
opment in the republic of Belarus (in Russian). 2008;80(2):30513.
Zdravookhranenie. 2012;11:48. http://rsml.med. 120. Thurner S, Klimek P, Szell M, Duftschmid G, Endel
by/diab/p19.pdf. G, Kautzky-Willer A, Kasper DC. Quantification of
108. Frch K, Borch-Johnsen K, Holst JJ, Vaag excess risk for diabetes for those born in times of
A. Pathophysiology and aetiology of impaired fast- hunger, in an entire population of a nation, across a
ing glycaemia and impaired glucose tolerance: does century. Proc Natl Acad Sci. 2013;110(12):47037.
it matter for prevention and treatment of type 2 dia- 121. van Abeelen AF, Elias SG, Bossuyt PM, Grobbee
betes? Diabetologia. 2009;52(9):171423. DE, van der Schouw YT, Roseboom TJ, Uiterwaal
109. Engberg S, Glmer C, Witte DR, Jrgensen T, CS. Famine exposure in the young and the risk of
Borch-Johnsen K. Differential relationship between type 2 diabetes in adulthood. Diabetes.
physical activity and progression to diabetes by glu- 2012;61(9):225560.
cose tolerance status: the Inter99 Study. Diabetologia. 122. Polyakova IV, Glotov OS, Khoroshinina LP, Turjeva
2010;53(1):708. LV, Ivashchenko TE, Baranov VS. Genotype and
110. Khalangot ND, Kravchenko VI, Okhrimenko NV, allele frequencies of UCP and PPAR gene families in
Pysarenko YuM, Koliasa OS, Kovtun VA, Gurianov residents of besieged Leningrad and in the control
VG, Tronko MD. Anthropometric differences of per- group. Adv Gerontol. 2014;27(3):41824.
sons with various types of screen-detected hypergly- 123. Mankovsky BN, Metzger BE, Molitch ME, Biller
cemia in rural Ukraine. Zurnal NAMN Ukrainy. J. Cerebrovascular disorders in patients with diabetes
2015;21(34):34250. mellitus. J Diabetes Complicat. 1996;10(4):22842.
111. Vogel M, Blaak E, Goossens G. Moderate hypoxia 124. Popova V, Zak K, Gruzov M, Afanasyeva V,
exposure: a novel strategy to improve glucose metab- Simeonova T, Mankovsky B. The prognostic value
olism in humans? EMJ Diabetes. 2015; 3(1):739. of the immunological phenotype of lymphocytes in
112. Serebrovska TV, Shatilo VB. Remote ischemic pre- subjects positive for diabetes-associated autoanti-
conditioning versus intermittent hypoxia training: a bodies. Diabetologia. 2006;49:2801. 233.
Diabetes in Ethnic Minorities
and Immigrant Populations 12
in Western Europe
Oliver Razum and Helmut Steinberg
The issue of diabetes in immigrant, ethnic minor- greater prevalence of microvascular complica-
ities, and underserved communities in Europe tions, especially diabetic retinopathy, and lower
is complex; it is complex due to diverse geo- rates of macrovascular disease in some immi-
graphical and ethnic background of immigrant grant populations. While health-care coverage
populations and differences in health-care sys- is almost universal in Europe albeit delivered
tems across European countries. In addition, the by country-specific systems, immigrant popu-
availability and quality of data differ between lations face different and often additional bar-
countries and, therefore, are not possible to per- riers; often they tend to be less educated and
form systematic comparisons between countries. have difficulty with the native language and dif-
The overarching results demonstrate that immi- ferent cultural and/or religious values that may
grant and underserved populations tend to have interfere with effective diabetes prevention and
a higher prevalence of diabetes when compared treatment. Immigrants who receive medical care
to the native population while not necessar- appear to be provided with the same medications
ily different from populations where they origi- as the natives although there appear to be differ-
nate from. Risk factors for diabetes appear to ences in the utilization of insulin. While there is
be similar between populations, mostly insulin research conducted in specific populations, this
resistance, obesity, and sedentary lifestyle with is often done locally or regionally which ham-
possible genetic differences contributing to the pers the generalization of results. Countries that
increased susceptibility. Some data suggest a have National Health Services (e.g., UK, the
Netherlands, and Scandinavian countries) tend
to have more and possibly more representative
data compared to countries that have statutory
O. Razum
health insurance systems such as Germany. Some
Fakultt frGesundheitswissenschaften, School of
Public Health, Universitt Bielefeld, data originate from small local or regional stud-
Postfach 10 01 31, 33501 Bielefeld, Germany ies where the results are often being published as
e-mail: [email protected] progress reports in the native language that are
H. Steinberg, MD (*) difficult to obtain. Researchers agree that stan-
Division of Endocrinology, Diabetes and Metabolism, dardized large-scale and representative studies
Department of Medicine, University of Tennessee
that allow comparison of different populations
Health Science Center Memphis, 920 Madison
Avenue, Suite #300, Memphis, TN 38163, USA throughout specific countries or even Europe are
e-mail: [email protected] wanting.

DOI 10.1007/978-3-319-41559-8_12
226 O. Razum and H. Steinberg
Heterogeneity of Immigrant ity and also the fact that there are now third and
Populations even fourth generations of immigrant popula-
tions who were born in Europe. While an updated
Immigration in Europe, especially Western and modern concept of ethnicity is appropriate to
Europe, has in principle three origins: reset- better inform about specifics of health-care dis-
tling from colonial territories, need for parities, it makes it difficult to compare old and
additional labor, and asylum policies for new findings in the literature, as well as between
political refugees. This explains a large part countries with differing concepts, unless one has
of the differences in the ethnic backgrounds access to the original definitions and raw data.
of immigrants between European countries
(Table 12.1). For example, the main immigrant
groups in England are from South Asian, Black Diagnosis and Pathophysiology
Caribbean, and East African background,
while the main immigrant groups in Germany The methods of ascertaining the diagnosis of
are from Turkey and Southern Europe, and diabetes in reports have been varied; the diagno-
North African immigrants are found mostly in sis of diabetes or prediabetes has been based on
France, Belgium, and the Netherlands which in self-report or on glucose/HbA1c screening, often
addition also has a large group of Surinamese in high-risk groups, according to the recommen-
Indians. Newer established immigrant popu- dations by the EASD/ADA, or it has been based
lations in Western Europe come from former on reports to registries from participating physi-
communist countries such as Poland, Romania, cians. The majority of subjects suffer from type
or Russia. In some of these countries, Roma 2 diabetes which has been consistently reported
people are an underserved minority who, when to occur earlier (by up to two decades) in minor-
migrating to Western Europe, remain at risk of ity populations. The pathogenesis of type 2 dia-
low access to care and discrimination [9, 32]. betes appears to be related to increased caloric
Recording of ethnicity has not been uniform intake, to (central) obesity, and to insulin resis-
through time and between countries. Early on, tance and beta cell failure, and these do not
ethnicity was assessed based on the country of appear to be different between populations. The
birth or original citizenship or place of birth of excess incidence of diabetes in South Asian
the parents. However, this has changed in some women correlates with more prevalent central
European countries over the last two to three obesity but this is not the case for men [51, 52].
decades due to more modern concepts of ethnic- One study estimates that up to 90 % of Asian
immigrant women may be at risk for diabetes
Table 12.1 Estimated proportion of ethnic/immigrant [21]. The most and the earliest data supporting
minorities in the population of some Western European this statement come from studies in subjects of
countries South Asian ethnicity; more recent studies from
Country Proportion (%) Major ethnic groups Turkey do confirm and extend these results to
France 6.4 North African, South other ethnic minorities [44]. However, when
East Asian waist circumference is used to assess central
Germany 8.5 Turkish, Italian, obesity, the risk for diabetes in South Asians sig-
Greek, Polish
nificantly increases at lower values compared to
Italy 3.2 African, Asian,
African or Caucasian populations. In addition, it
Eastern European
The 4.7 Turkish, North
has been proposed that differences in suppres-
Netherlands African, Surinamese sion of nonesterified fatty acids may act as medi-
United 7.9 African (Caribbean, ators of glucose intolerance in Indian Asian
Kingdom East African), Indian, populations [40]. In minority subjects of African
Pakistani descent as compared to subjects in the country of
12 Diabetes in Ethnic Minorities and Immigrant Populations in Western Europe 227
origin, increased caloric intake from protein and justed diabetes prevalence rates were 5.1 %,
fat has been shown to be associated with higher 11.0 %, and 18.8 % in Dutch, Turkish, and
rates of diabetes [2]. Similar findings have been Moroccan men, respectively; unadjusted diabetes
reported in migrants from South Asia (Pakistan prevalence rates were 2.9 %, 8.4 %, and 16.1 % in
and Sri Lanka) who settled in Norway [54]. This Dutch, Turkish, and Moroccan women, respec-
pattern of increasing food consumption is simi- tively. A different study from Amsterdam [7],
lar to populations in developing countries who Netherlands, that was conducted around the same
move from rural to urban settings with an time compared the prevalence of diabetes
increase in calorie consumption and more seden- between Dutch, Hindustani Surinamese, and
tary lifestyle [45]. African Surinamese groups. Age-adjusted preva-
Few studies have compared genetic determi- lence was 5.5 %, 14.2 %, and 26.7 % for the
nants of type 2 diabetes between immigrant and Dutch, African Surinamese, and Hindustani
native populations. Some studies in South Asian Surinamese groups, respectively. In a univariate
(Indian) populations suggest that genetic differ- analysis, a history of CVD and waist circumfer-
ences may exist [17, 30], but larger studies are ence demonstrated the strongest association with
needed to get better insight into this issue. diabetes. In a multivariate analysis, a history of
CVD, a first-degree relative with diabetes, and
Hindustani Surinamese were the strongest deter-
Prevalence Estimates minants of diabetes. While increased rates of dia-
betes have been found in groups of Indian and
The prevalence of diabetes in minorities is African descent in England and the Netherlands,
affected by ethnicity and country of residence. In it appears that these minorities living in the
one study in the UK [59], standardized preva- Netherlands have almost twice the prevalence
lence rates for diabetes were 1.7, 5.3, and 8.9 % than that observed in England [1]; it is unclear
in white, African Caribbean, and Pakistani/ whether these differences between countries are
Bangladeshi groups. In a more recent study [51], due to differences in the studied populations
incidences of diabetes over an up to 20-year time (e.g., genetic or social/ethnic variability) or due
period were 14 % for European, 33 % for Indian to differences in the environment.
Asian, and 30 % for African Caribbean subjects. Germany has the second highest number of
Based on these findings, it is estimated that by diabetic subjects in Europe (IDF-Atlas 7th edi-
age 80, approximately 50 % of Indian Asian and tion 2015) after the Russian Federation and with
African Caribbean subjects versus approximately Austria and Spain the highest population preva-
20 % of Europeans will have developed diabetes. lence in Western Europe. There are few studies
A study from Oslo, Norway [25], compared the assessing the prevalence and incidence in ethnic
prevalence of diabetes between South Asian and minorities in Germany which is due to privacy
Western subjects in a low-income population; laws as well as the way these data are collected.
diabetes prevalence rates were 27.5 % and 2.9 % Most of these studies are small and likely affected
for South Asian and Western women and 14.3 % by sampling bias. The estimate for diabetes prev-
and 5.9 % for South Asian and Western men, alence in Turkish subjects has been reported in a
respectively. The age-adjusted odds ratios for range from 3 %, which is lower than the prevalence
South Asians versus Westerners were 11.0 for in native Germans, to 14 % which is 50100 %
women and 3.0 for men; adjustment for waist-hip higher compared to native Germans (Icks et al.
ratio reduced these ratios to 7.7 and 2.6 in the Deutscher Gesundheitsbericht Diabetes 2011,
South Asian women and men, respectively. pp 148154; www.diabetesde.org). Most experts
A study from Amsterdam [47], Netherlands, agree that the prevalence of type 2 diabetes is
compared the prevalence of diabetes between likely to be higher than in the native population
Dutch, Turkish, and Moroccan subjects. Unad- [43], where it is assumed to be 7.2 % [18].
Roma, in earlier literature referred to as gyp- observed a 52 %, 42 %, and 38 % prevalence of

sies and travelers, do most likely represent one of any diabetic retinopathy in African/Afro-
the oldest of all migrant minorities in Europe; it Caribbeans, South Asians, and white Europeans,
is well documented that they do have poorer respectively. In the same study, sight-threatening
health and decreased life expectancy. One study diabetic retinopathy was also nearly twice as
from England [39] demonstrated a 4.0 % self- common in both African/Afro-Caribbeans and
reported prevalence of diabetes in the gypsy/trav- South Asians compared to white Europeans.
eler group which was not different from the Diabetic nephropathy was reported in several
native group. In contrast, a study from Hungary studies to progress more rapidly in Asian Indians
[20, 31] reported an 18.4 % prevalence of undiag- [11, 12] with the latter study observing a 40-fold
nosed diabetes, nearly one-and-a-half-fold higher increased risk of end-stage diabetic nephropathy
than the 7.5 % observed in the native Hungarian compared to the native Dutch population.
population. However, more recent studies were not able to
Gestational diabetes seems to be more com- confirm higher rates of complications [19, 56] or
mon among ethnic minorities, e.g., among faster progression of renal disease in minority
Turkish women in Germany (183 per 1,000 groups [38]. While ethnic differences may be
pregnancies compared to 138 per 1,000 pregnan- explained, at least in part, by the higher preva-
cies in German women) [42]. Rates of gestational lence, earlier onset of diabetes, and higher glu-
diabetes have been reported to be elevated also in cose levels, those variables do not appear to
groups of South Asian and African descent completely account for the differences.
whether they lived in Norway [26] or in other Diabetic neuropathy was less common in
countries [27]. This may explain some of the Asian Indians when compared to African or
increased perinatal complications seen in minor- Caucasian groups [56]. Macrovascular disease
ity groups [29]. appears less common with African ethnicities
Children of migrants are often more obese and [56] which is mostly explained by lower rates of
more sedentary suggesting an increased future smoking in this group [33].
risk of type 2 diabetes. For type 1 diabetes, how-
ever, it appears that children born to immigrants
have a lower risk [13, 22, 23]. However, minority Coordination and Delivery
children with type 1 diabetes have worse glyce- of Diabetes Care Services
mic control, more severe hypoglycemic episodes,
and a higher rate of hospitalization [46]. Health care is almost universally available in all
European countries and includes diabetes care
and education, and the patients expenses for
Complications of Diabetes their care including medications are often negli-
gible. All health-care services do have guidelines
Few data are available regarding diabetic compli- for diabetes care that are modeled after ADA/
cations in different ethnic groups. The available EASD recommendations. Nevertheless, for a
data indicate that Asian Indians suffer more from number of reasons that are not all well under-
retinopathy and nephropathy compared to the stood, minorities do not obtain the same benefits
native populations. In subjects in the UK with from the health-care system as their native coun-
early onset of type 2 diabetes (age <40 years), terparts as often evidenced by higher average glu-
South Asians exhibited more retinopathy (17.5 % cose levels and lower attainment of treatment
vs. 7.9 %) and more nephropathy (18.1 % vs. goals for other cardiovascular risk factors such as
7.8 %). In the same study [8], macrovascular dis- hypertension [19].
ease was also more prevalent in the South Asian Data on health-care delivery and utilization in
group (15.7 % vs 9.4 %). These results were con- minorities are scarce, mostly due to lack of
firmed in a larger and more recent study [49] that recording ethnicity in the primary care setting
[5]. One study [15] revealed that Indian patients change the tone of the conversation by removing
with diabetes were less likely to be seen by a pri- humor and adding the interpreters own opinions.
mary care physician, but a later study [36] showed Self-help groups and social clubs are used by
no differences in access to health care for diabe- minority patients to improve self-management of
tes between white and South Asian Indian groups. their diabetes [16], but not all minority groups
However, the latter study showed a tendency find them acceptable.
toward lower control rates of diabetes in the
minority groups. A study from Italy [4] supports
these findings in minorities; while minorities Non-pharmacological Management
with diabetes were cared for in similar propor-
tions as the native population, they were less Diet and exercise are the cornerstone of any dia-
likely to be tested for HbA1cA and had worse betes treatment regimen; it is also the cornerstone
glucose control. of diabetes prevention. Diet and exercise have
A number of barriers to health-care delivery been shown to improve glycemia and lipids in
have been identified [35, 55] (Miriam McHardy ethnic minorities and prevent progression to the
Master Thesis Necessity, Concepts and Feasibility metabolic syndrome [50]. There are no studies
of Culturally Tailored Diabetes Education for comparing the efficacy of these modalities
Migrants in the Netherlands and the United between native and minority populations. As
Kingdom: A Qualitative Study on Experts pointed out above, minority groups face addi-
Views); they include language barriers and lack tional barriers when attempting to change eating
of transportation (drivers license and car), espe- and exercise habits; healthy food items have to be
cially in first-generation immigrants and subjects available, affordable, and useable for established
with low educational status, low health literacy, food patterns. Increasing physical activity can be
and cultural and religious norms [58], as well as difficult for some minority groups, especially
differences in illness perception between patients women who are not permitted to show body parts
and providers [57] (Table 12.2). Even if advice is or exercise in the company of men. Because of
provided in a culturally appropriate context and these additional barriers, it is important to
understanding, implementation of changes can develop and deliver culturally competent diabe-
be a struggle within the routines of already estab- tes care interventions [58].
lished food habits [14].
Efforts to overcome those barriers come from
both the provider (health-care delivery) and the Rational Selection of Antidiabetic
consumer side. For example, case workers and Medications
community links have been shown to improve
diabetes care and outcomes. The use of transla- Drugs for the treatment of diabetes are available
tors [48] can improve communication of certain to all subjects diagnosed with this disease and
issues and concepts but also has the potential to cost is covered completely in most countries.
Most common older and newer diabetes drugs
are available in Europe where the European
Table 12.2 Potential barriers to health-care delivery
Medicinal Agency is in control of approving the
Language applications for marketing by the drug compa-
Different perception of illness nies; however, coverage and reimbursement rates
Low health literacy of drugs are decided separately by the unique
Low educational status regulatory agencies in each country which affects
Cultural norms utilization by the patients. There are no studies
Religious norms comparing efficacy and safety of different anti-
Lack of acceptable healthy food choices diabetic drugs between immigrant and native
Lack of transportation populations, and, therefore, no recommendations
in regard to the first- and second-line choices can part due to barriers that are present in those
be made. In the absence of studies that could pro- groups; in addition, different barriers exist in
vide guidance for drug selection and in the minorities from different origin. Johnson et al.
absence of significant differences in the patho- [28] describe a number of these barriers such as
physiology of diabetes development between lack of access to exercise facilities, family and
immigrant and native populations, drug prescrip- work commitments, cost, language, religious dif-
tion should follow the guidance by ADA/ ferences, and cultural norms; in addition, differ-
EASD. A study from the Netherlands [10] ences in illness perception contribute [57]. Taking
showed underutilization of diabetes drugs in these considerations into account [53], one pre-
Turkish and Moroccan immigrants but not in vention study that adapted the design of the
Surinamese and Antillean immigrants. A study Finnish Diabetes Prevention Study in a culturally
from England [6] provided a more granular list- sensitive way was conducted in Scotland. The
ing of the use of antidiabetic drugs; the utilization study was unable to recruit sufficient numbers of
of oral drugs, predominantly metformin and sul- participants to assess the effect of the interven-
fonylurea, was similar between groups. However, tion on progression to diabetes; the (revised) pri-
minorities were less likely to utilize insulin alone mary question was whether clinically meaningful
or insulin plus oral drugs. The utilization of lipid- weight loss can be achieved. The results of this
lowering and antihypertensive drugs was similar 3-year study, the PODOSA (Prevention Of
between groups. Lower utilization of insulin and Diabetes and Obesity in South Asians), demon-
lipid-lowering agents in migrants was also strated more weight loss associated with a
reported in a study from Italy [34]. The reasons decrease in central obesity and a trend toward
for these differences, especially the lower rate of lower fasting and 2-h post OGTT values; impor-
insulin use, are not clear; this may be due to the tantly, there was less progression to diabetes, and
younger age of immigrants, lower prescription this has to be taken with a grain of salt since the
rates by the providers, or lower acceptance by the study was not powered to view this result with
patient. Additionally, based on the results from a sufficient confidence. A similar diabetes preven-
large Austrian/German registry study, there is a tion study, the DH!AAN study, in Surinamese
difference in the utilization of continuous insulin Asians is currently underway in the Netherlands
infusion therapy between Turkish and German/ [37] (Health Promotion International, Vol. 29 No.
Austrian children [24]. The fact that this under- 4). The results of the PODOSA and the DH!AAN
utilization occurs in the face of universal health- study will be compared with those of a similar,
care coverage points to social and cultural issues currently ongoing study in India, the D-CLIP
in the ethnic minority groups that are not well study [3]. Together, the results will guide devel-
understood. Whether this underutilization of opment of more targeted diet and exercise pro-
insulin pump therapy contributes to worse glyce- grams to prevent diabetes in these populations.
mic control, more severe hypoglycemic episodes,
and a higher rate of hospitalization [46], as
pointed out above, is not clear. Organizing and Conducting
Diabetes Research and Future
Directions
Translating Primary Prevention
of Type 2 Diabetes Diabetes research of ethnic minorities has been
conducted mostly at a local or regional level and
Ethnic minorities are at high risk of developing was more qualitative than quantitative. Results of
diabetes; it is estimated that half of Indian Asian this research point to the increased risk of devel-
subjects may be diabetic by age 80. Therefore, oping type 2 diabetes in a higher proportion of
prevention of type 2 diabetes is of utmost impor- minorities and possibly higher rates of complica-
tance in these groups. Progress has been slow in tions. Results of this research have also identified
a number of barriers to achieving lifestyle changes 3. Anjana RM, Ranjani H, Unnikrishnan R, Weber MB,
Mohan V, Narayan KM. Exercise patterns and behaviour
that are associated with a decreased risk of obe-
in Asian Indians: data from the baseline survey of the
sity, the metabolic syndrome, and diabetes. More Diabetes Community Lifestyle Improvement Program
recent outcome studies demonstrate the feasibil- (D-CLIP). Diabetes Res Clin Pract. 2015;107:7784.
ity of implementing intensive lifestyle changes 4. Ballotari P, Caroli S, Ferrari F, Romani G, Marina G,
Chiarenza A, Manicardi V, Giorgi Rossi P. Differences
that are culturally adapted and lead to promising
in diabetes prevalence and inequalities in disease
outcomes. Results from these ongoing interven- management and glycaemic control by immigrant sta-
tion studies will be available in a few years. tus: a population-based study (Italy). BMC Public
Future research should use the locally/region- Health. 2015;15:87.
5. Baradaran HR, Jamieson J, Gardee R, Knill-Jones
ally acquired information and knowledge to
RP. Scottish survey of diabetes services for minority
design studies that are more representative of ethnic groups. BMC Health Serv Res. 2006;6:130.
national or even Europe-wide ethnic populations. 6. Benhalima K, Song SH, Wilmot EG, Khunti K, Gray
This can be accomplished by large registries that LJ, Lawrence I, Davies M. Characteristics, complica-
tions and management of a large multiethnic cohort of
include data from multiple countries obtained in
younger adults with type 2 diabetes. Prim Care
standardized fashion and/or by sufficiently large Diabetes. 2011;5:24550.
random samples throughout the different coun- 7. Bindraban NR, van Valkengoed IG, Mairuhu G,
tries or, ideally, throughout Europe. This will Holleman F, Hoekstra JB, Michels BP, Koopmans RP,
Stronks K. Prevalence of diabetes mellitus and the
help define the current state of diabetes and its
performance of a risk score among Hindustani
complications in minorities in Europe while Surinamese, African Surinamese and ethnic Dutch: a
accounting for secular changes in the native pop- cross-sectional population-based study. BMC Public
ulation and environment. In addition, larger inter- Health. 2008;8:271.
8. Chowdhury TA, Lasker SS. Complications and
vention studies that include several distinct
cardiovascular risk factors in South Asians and
minority groups (e.g., groups of Turkish, Asian Europeans with early-onset type 2 diabetes. QJM.
Indian, and African descent) should be designed; 2002;95:2416.
results from such a study might identify interven- 9. Correspondent EUR. Commission calls to break cir-
cle of Roma health exclusion across Europe.
tion elements that are generally applicable to
Eureporter. 2014.
achieve improved outcomes as well as elements 10. Denkta S, Koopmans G, Birnie E, Foets M, Bonsel
that require more group specific, ethnic, or local G. Underutilization of prescribed drugs use among
adaptation [41]. The final goal of these efforts is first generation elderly immigrants in the Netherlands.
BMC Health Serv Res. 2010;10:176.
to support the development of culturally compe-
11. Dreyer G, Hull S, Mathur R, Chesser A, Yaqoob
tent health-care systems, health-care systems that MM. Progression of chronic kidney disease in a
provide culturally and linguistically appropriate multi-ethnic community cohort of patients with dia-
services which will reduce racial and ethnic betes mellitus. Diabet Med. 2013;30:95663.
12. Earle KK, Porter KA, Ostberg J, Yudkin JS. Variation
health disparities and improve outcomes.
in the progression of diabetic nephropathy accord-
ing to racial origin. Nephrol Dial Transplant.
2001;16:28690.
13. Ehehalt S, Popovic P, Muntoni S, Willasch A, Hub R,
References Ranke MB, Neu A, Baden-Wuerttemberg
DG. Incidence of diabetes mellitus among children of
1. Agyemang C, Kunst AE, Bhopal R, Anujuo K, Italian migrants substantiates the role of genetic fac-
Zaninotto P, Nazroo J, Nicolaou M, Unwin N, van tors in the pathogenesis of type 1 diabetes. Eur
Valkengoed I, Redekop WK, Stronks K. Diabetes J Pediatr. 2009;168:6137.
prevalence in populations of South Asian Indian and 14. Fagerli RA, Lien ME, Wandel M. Experience of
African origins: a comparison of England and the dietary advice among Pakistani-born persons with
Netherlands. Epidemiology. 2011;22:5637. type 2 diabetes in Oslo. Appetite. 2005;45:295304.
2. Anderson SG, Younger N, Heald AH, Tulloch-Reid 15. Goyder EC, McNally PG, Botha JL. Inequalities in
MK, Simukonda WP, Mbanya JC, Jackson MD, access to diabetes care: evidence from a historical
Balkau B, Sharma S, Tanya A, Forrester T, Wilks R, cohort study. Qual Health Care. 2000;9:859.
Cruickshank JK. Nutrient intakes and dysglycaemia 16. Guell C. Tactics of diabetes control Turkish immi-
in populations of West African origin. Br J Nutr. grant experiences with chronic illness in Berlin.
2011;105:297306. Germany: The University of Edinburgh; 2009. 265 p.
17. Gujral UP, Pradeepa R, Weber MB, Narayan KM, 29. Khalil A, Rezende J, Akolekar R, Syngelaki A,
Mohan V. Type 2 diabetes in South Asians: similari- Nicolaides KH. Maternal racial origin and adverse
ties and differences with white Caucasian and other pregnancy outcome: a cohort study. Ultrasound Obstet
populations. Ann N Y Acad Sci. 2013;1281:5163. Gynecol. 2013;41:27885.
18. Heidemann C, Du Y, Schubert I, Rathmann W, Scheidt- 30. Kodama K, Tojjar D, Yamada S, Toda K, Patel CJ,
Nave C. Prevalence and temporal trend of known dia- Butte AJ. Ethnic differences in the relationship
betes mellitus: results of the German Health Interview between insulin sensitivity and insulin response: a
and Examination Survey for Adults (DEGS1). systematic review and meta-analysis. Diabetes Care.
Bundesgesundheitsblatt Gesundheitsforschung 2013;36:178996.
Gesundheitsschutz. 2013;56:66877. 31. Ksa Z, Moravcsik-Kornyicki , Diszegi J, Roberts
19. Hewitt J. Ethnicity and prevalence of diabetic compli- B, Szab Z, Sndor J, dny R. Prevalence of meta-
cations in elderly patients. In: Gallen I, editor. Pract bolic syndrome among Roma: a comparative health
Diabetes Int. 2004;13942. examination survey in Hungary. Eur J Public Health.
20. Hidvegi T, Hetyesi K, Biro L, Nadas J, Jermendy 2015;25:299304.
G. Screening for metabolic syndrome within a minor- 32. Khlbrandt C, Footman K, Rechel B, McKee M. An
ity ethnic group (adult gypsy people) in Hungary. examination of Roma health insurance status in
Bratisl Lek Listy. 2012;113:7214. Central and Eastern Europe. Eur J Public Health.
21. Hjellset VT, Bjrge B, Eriksen HR, Hstmark 2014;24:7012.
AT. Risk factors for type 2 diabetes among female 33. Leggetter S, Chaturvedi N, Fuller JH, Edmonds
Pakistani immigrants: the InvaDiab-DEPLAN study ME. Ethnicity and risk of diabetes-related lower
on Pakistani immigrant women living in Oslo. extremity amputation: a population-based, case-control
Norway: J Immigr Minor Health. 2011;13:10110. study of African Caribbeans and Europeans in the
22. Hjern A, Sderstrm U. Parental country of birth is a United Kingdom. Arch Intern Med. 2002;162:738.
major determinant of childhood type 1 diabetes in 34. Marchesini G, Bernardi D, Miccoli R, Rossi E,
Sweden. Pediatr Diabetes. 2008;9:359. Vaccaro O, De Rosa M, Bonora E, Bruno G. Under-
23. Hussen HI, Yang D, Cnattingius S, Moradi T. Type I treatment of migrants with diabetes in a universalistic
diabetes among children and young adults: the role of health care system: the ARNO observatory. Nutr
country of birth, socioeconomic position and sex. Metab Cardiovasc Dis. 2014;24:3939.
Pediatr Diabetes. 2013;14:13848. 35. McHardy M. Necessity, concepts and feasibility of
24. Icks A, Razum O, Rosenbauer J, Bachle C, Hungele culturally tailored diabetes education for migrants in
A, Monkemoller K, Muller-Godeffroy E, Heidtmann the Netherlands and the United Kingdom: a qualita-
B, Kapellen T, Scheuing N, Holl RW, D. P. V. I. for tive study on experts views. Hamburg: Hamburg
the, E, The German Federal Ministry For, M. Research University of Applied Sciences; 2014. 134 p.
Competence Network Diabetes. Lower frequency of 36. Nazroo JY, Falaschetti E, Pierce M, Primatesta
insulin pump treatment in children and adolescents of P. Ethnic inequalities in access to and outcomes of
Turkish background with type 1 diabetes: analysis of healthcare: analysis of the Health Survey for England.
21,497 patients in Germany. Diabetes Technol Ther. J Epidemiol Community Health. 2009;63:10227.
2012;14:11059. 37. Nicolaou M, Vlaar E, van Valkengoed I, Middelkoop
25. Jenum AK, Holme I, Graff-Iversen S, Birkeland B, Stronks K, Nierkens V. Development of a diabetes
KI. Ethnicity and sex are strong determinants of dia- prevention program for Surinamese South Asians in
betes in an urban western society: implications for the Netherlands. Health Promot Int. 2014;29:68091.
prevention. Diabetologia. 2005;48:4359. 38. Pallayova M, Rayner H, Taheri S, Dasgupta I. Is there
26. Jenum AK, Mrkrid K, Sletner L, Vangen S, Vange a difference in progression of renal disease between
S, Torper JL, Nakstad B, Voldner N, Rognerud-Jensen South Asian and white European diabetic adults with
OH, Berntsen S, Mosdl A, Skrivarhaug T, Vrdal MH, moderately reduced kidney function? J Diabetes
Holme I, Yajnik CS, Birkeland KI. Impact of ethnicity Complications. 2015;29:7615.
on gestational diabetes identified with the WHO and 39. Parry G, Van Cleemput P, Peters J, Walters S, Thomas
the modified International Association of Diabetes and K, Cooper C. Health status of Gypsies and Travellers
Pregnancy Study Groups criteria: a population-based in England. J Epidemiol Community Health.
cohort study. Eur J Endocrinol. 2012;166:31724. 2007;61:198204.
27. Jenum AK, Sommer C, Sletner L, Mrkrid K, Brug 40. Patel JV, Vyas A, Prabhakaran D, Bhatnagar D,
A, Mosdl A. Adiposity and hyperglycaemia in preg- Durrington PN, Heald A, Hughes EA, Mackness MI,
nancy and related health outcomes in European ethnic Reddy KS, Cruickshank JK. Nonesterified fatty acids
minorities of Asian and African origin: a review. Food as mediators of glucose intolerance in Indian Asian
Nutr Res. 2013;57. doi:10.3402/fnr.v57i0.18889. populations. Diabetes Care. 2005;28:15057.
28. Johnson M, Everson-Hock E, Jones R, Woods HB, 41. Razum O, Spallek J. Addressing health-related inter-
Payne N, Goyder E. What are the barriers to primary ventions to immigrants: migrant-specific or diversity-
prevention of type 2 diabetes in black and minority sensitive? Int J Public Health. 2014;59:8935.
ethnic groups in the UK? Qual Evid Synth Diabetes 42. Reeske A, Zeeb H, Razum O, Spallek J. Differences
Res Clin Pract. 2011;93:1508. in the incidence of gestational diabetes between
women of Turkish and German Origin: an analysis of 51. Tillin T, Hughes AD, Godsland IF, Whincup P,
Health Insurance Data from a Statutory Health Forouhi NG, Welsh P, Sattar N, McKeigue PM,
Insurance in Berlin, Germany (AOK), 20052007. Chaturvedi N. Insulin resistance and truncal obesity
Geburtshilfe Frauenheilkd. 2012;72:30510. as important determinants of the greater incidence of
43. RKI. Gesundheit in Deutschland. In: Koch-Institut R, diabetes in Indian Asians and African Caribbeans
editor, Gesundheitsberichterstattung des Bundes. compared with Europeans: the Southall and Brent
Gemeinsam getragen von RKI und Destatis. Berlin: REvisited (SABRE) cohort. Diabetes Care.
Robert Koch-Institut; 2015. p. 516. 2013;36:38393.
44. Satman I, Omer B, Tutuncu Y, Kalaca S, Gedik S, 52. Tillin T, Hughes AD, Mayet J, Whincup P, Sattar N,
Dinccag N, Karsidag K, Genc S, Telci A, Canbaz B, Forouhi NG, McKeigue PM, Chaturvedi N. The rela-
Turker F, Yilmaz T, Cakir B, Tuomilehto J, Group tionship between metabolic risk factors and incident
T-IS. Twelve-year trends in the prevalence and risk cardiovascular disease in Europeans, south Asians,
factors of diabetes and prediabetes in Turkish adults. and African Caribbeans: SABRE (Southall and Brent
Eur J Epidemiol. 2013;28:16980. revisited) a prospective population-based study.
45. Satman I, Yilmaz T, Sengl A, Salman S, Salman F, J Am Coll Cardiol. 2013;61:177786.
Uygur S, Bastar I, Ttnc Y, Sargin M, Dinag N, 53. Wallia S, Bhopal RS, Douglas A, Bhopal R, Sharma
Karsidag K, Kalaa S, Ozcan C, King H. Population- A, Hutchison A, Murray G, Gill J, Sattar N, Lawton J,
based study of diabetes and risk characteristics in Tuomilehto J, Mcknight J, Forbes J, Lean M, Sheikh
Turkey: results of the Turkish diabetes epidemiology A. Culturally adapting the prevention of diabetes and
study (TURDEP). Diabetes Care. 2002;25:15516. obesity in South Asians (PODOSA) trial. Health
46. Scheuing N, Wiegand S, Bchle C, Frhlich-Reiterer Promot Int. 2014;29:76879.
E, Hahn E, Icks A, Ludwig KH, Mnkemller K, 54. Wandel M, Rberg M, Kumar B, Holmboe-Ottesen
Razum O, Rosenbauer J, Holl RW, Initiative D. Impact G. Changes in food habits after migration among
of maternal country of birth on type-1-diabetes ther- South Asians settled in Oslo: the effect of demo-
apy and outcome in 27,643 children and adolescents graphic, socio-economic and integration factors.
from the DPV Registry. PLoS One. 2015;10:e0135178. Appetite. 2008;50:37685.
47. Schrier AC, Ujcic-Voortman JK, de Wit MA, Verhoeff 55. Wilson C, Alam R, Latif S, Knighting K, Williamson
AP, Kupka R, Dekker J, Beekman AT. Ethnic differ- S, Beaver K. Patient access to healthcare services
ences in the association between cardiovascular risk and optimisation of self-management for ethnic
factors and psychological distress in a population minority populations living with diabetes: a system-
study in the Netherlands. BMC Public Health. atic review. Health Soc Care Community. 2012;20:
2012;12:1090. 119.
48. Seale C, Rivas C, Kelly M. The challenge of commu- 56. Winkley K, Thomas SM, Sivaprasad S, Chamley M,
nication in interpreted consultations in diabetes care: Stahl D, Ismail K, Amiel SA. The clinical characteris-
a mixed methods study. Br J Gen Pract. 2013;63: tics at diagnosis of type 2 diabetes in a multi-ethnic
e12533. population: the South London Diabetes cohort
49. Sivaprasad S, Gupta B, Gulliford MC, Dodhia H, (SOUL-D). Diabetologia. 2013;56:127281.
Mohamed M, Nagi D, Evans JR. Ethnic variations in 57. Yilmaz-Aslan Y, Brzoska P, Bluhm M, Aslan A,
the prevalence of diabetic retinopathy in people with Razum O. Illness perceptions in Turkish migrants
diabetes attending screening in the United Kingdom with diabetes. Qual Study Chron Illn. 2014;10:
(DRIVE UK). PLoS One. 2012;7:e32182. 10721.
50. Telle-Hjellset V, Rberg Kjllesdal MK, Bjrge B, 58. Zeh P, et al. Cultural barriers impeding ethnic minor-
Holmboe-Ottesen G, Wandel M, Birkeland KI, ity groups from accessing effective diabetes care ser-
Eriksen HR, Hstmark AT. The InnvaDiab-DE-PLAN vices: a systematic review of observational studies.
study: a randomised controlled trial with a culturally Divers Equal Health Care. 2014;11:933.
adapted education programme improved the risk pro- 59. Nazroo JY. The health of Britians ethnic minori-
file for type 2 diabetes in Pakistani immigrant women. ties: findings from a national survey. London: Policy
Br J Nutr. 2013;109:52938. Studies Institute, 1997.
Diabetes Among Indigenous
Canadians 13
Sudaba Mansuri and Anthony J. Hanley
Background 2011 National Household Survey [3]. Of those

who identified with Indigenous identity, 60.8 %
Indigenous Peoples of Canada identified as First Nations, 32.3 % identified as
Mtis, and 4.2 % identified as Inuit [3].
According to the Canadian Constitution Act of Indigenous communities are found in all areas
1982, three distinct groups of Indigenous of Canada, including urban, rural, and isolated
Canadians are recognized: First Nations, Mtis, areas. While many Indigenous communities are
and Inuit, with each group having their own set of in close proximity to non-Indigenous cities or
unique languages, traditions, art, and culture [1]. towns, or are otherwise accessible by permanent
First Nations people are currently the largest road, a substantial proportion of Indigenous com-
Indigenous group in Canada [2, 3]. The Mtis are munities are remote or isolated, accessible only
the second largest group, and their history dates by air or water. The largest population of
back to the mid-seventeenth century when Indigenous Canadians is found in Ontario and the
European (predominantly French and Scottish) Western provinces, with eight in ten Indigenous
fur traders married Indigenous (Cree, Ojibway, Canadians living in these provinces [3]. Mtis
Algonquin, and other First Nations) women [3, communities are concentrated in Alberta, British
4]. The third largest Indigenous group is the Inuit, Columbia, Ontario, Manitoba, and Saskatchewan.
who traveled from Western Alaska around 1000 The traditional territory of the Inuit is in the
CE to the Arctic [3, 5]. Arctic regions of Canada (Nunavut, Northwest
Over 1.4 million Canadians are self-identified Territories, and Northern Quebec). Roughly 40 %
with Indigenous identity, accounting for 4.3 % of of First Nations communities are located on fed-
the total Canadian population, according to the erally recognized lands called reserves [3].
However, according to national survey data, off-
reserve Indigenous Canadians are one of the fast-
S. Mansuri, MSc est growing groups in Canada, with 56 % of
Department of Nutritional Sciences, Faculty Indigenous people living in urban areas in 2011,
of Medicine, University of Toronto, up from 49 % in 1996 [3].
Toronto, ON, Canada
Indigenous peoples in Canada speak over 60
A.J. Hanley (*) distinct languages which are grouped into 12 lan-
Departments of Nutritional Sciences and Public
Health Sciences, Faculty of Medicine, University
guage families [6]. According to the 2011 Census,
of Toronto, Toronto, ON, Canada over 200,000 people reported speaking their
e-mail: [email protected] Indigenous mother tongue, and of these people,

DOI 10.1007/978-3-319-41559-8_13
236 S. Mansuri and A.J. Hanley
almost all of them reported speaking their mother reserves, and the residential school system, has
tongue regularly [6]. The most common language led to loss of land, language, and sociocultural
family is the Algonquin family, with over 144,000 knowledge and resources. These effects are
people reporting that their mother tongue still present in Indigenous communities where
belonged to this family. The languages that fall there are poor living conditions, high rates of
under this family include Cree languages, unemployment, low literacy and educational
Ojibway, Innu/Montagnais, and Oji-Cree. The attainment, income inadequacy, and inadequate
Inuit and Athapaskan language families are the community resources [9].
second and third largest language families, with
Inuktitut being the mother tongue among the Inuit
family and Dene being the mother tongue of the Prevalence and Incidence of Type 2
Athapaskan family. Despite the vast diversity in Diabetes
languages among Indigenous Canadians, those
who speak Cree, Inuktitut, and Ojibway account The burden of type 2 diabetes mellitus (DM) is dis-
for almost two-thirds of the languages spoken [6]. proportionately higher in Indigenous Canadians
The age structure of the Canadian Indigenous compared to non-Indigenous Canadians [10,
population is vastly different from the general 11]. Although the prevalence of diabetes was
Canadian population. As a result of higher fertil- extremely rare in this population prior to the
ity rates and shorter life expectancy, the 1950s [12], chart reviews a few decades later
Indigenous population is younger than the non- revealed notably high rates of this condition in
Indigenous population, with the median age of the Mohawk community of Kahnawake, the First
the Indigenous population being 28 years, nota- Nations community of Sandy Lake, and the James
bly lower than the median age of the non- Bay Cree of Northern Quebec [1316]. Data
Indigenous population at 41 years [7]. According from surveillance studies documented a doubling
to the 2011 National Household Survey, of type 2 DM prevalence among Indigenous peo-
Indigenous children aged 14 and under repre- ple in Saskatchewan between 1980 and 1990 [17]
sented 28 % of the total Indigenous population and an increase in prevalence of 45 % between
compared to 7 % of the population of children in 1985 and 1994 among the First Nations popula-
the general population in Canada [8]. Indigenous tion of the Sioux Lookout Zone in Northwestern
youth aged 1524 represented 18.2 % of the total Ontario [18].
Indigenous population and 5.9 % of the youth in The prevalence rates of diabetes among
the general population of Canada [8]. Whereas Indigenous Canadians have been established
Indigenous seniors aged 65 and older made up using a variety of approaches, including self-
only 5.9 % of the total Indigenous population, reported diagnoses in national surveys, adminis-
non-Indigenous seniors represent 14.2 % of the trative data, and more detailed surveys using oral
non-Indigenous population. Among the three glucose tolerance tests (OGTTs). Prevalence
Indigenous groups, Inuit were the youngest, with rates vary considerably according to the method-
a median age of 23 years, First Nations people ology that was used. National data from the
had a median age of 26, and the Mtis had a 20082010 First Nations Regional Longitudinal
median age of 31. Health Survey and the 20092010 Canadian
Since initial contact with Europeans approxi- Community Health Survey found that age-
mately 400 years ago, seismic sociocultural standardized rates of self-reported diabetes
changes in the lives of Indigenous Canadians among the First Nations population were 17.2 %
have significantly impacted their health and for individuals 18 years and older living on-
well-being. The imposition of colonial insti- reserve and 10.3 % among First Nations living
tutions, including the fur trade, the system of off-reserve compared to the prevalence in the
13 Diabetes Among Indigenous Canadians 237
Source Age Age-standardized

Prevalence (%) (95 %
confidence interval)
Non-aboriginal 20092010 12+ 5.0 (4.35.7)
CCHS
First-Nations (on-reserve) 20082010 18+ 17.2 (16.519.0)
RHS
First-Nations (off-reserve) 20092010 12+ 10.3 (3.417.2)
CCHS
Inuit 2006 APS 15+ NA
Mtis 20092010 12+ 7.3 (2.212.5)
CCHS
Fig. 13.1 Prevalence of self-reported diabetes among Longitudinal Health Survey (Phase 2) (First Nations
Indigenous peoples aged 12 years and older, Canada, Information Governance Centre); Social and Aboriginal
2006, 20082010, 20092010 (Source: Public Health Statistics Division, Aboriginal Peoples Survey, 2006: Inuit
Agency of Canada (2011), using data from 2009 to 2010 Health and Social Conditions: Ottawa, ON: Statistics
Canadian Community Health Survey (Statistics Canada); Canada; 2008. Statistics Canada. Public Health Agency of
First Nations Information Governance Centre (2011), Canada. 2011)
using data from the 20082010 First Nations Regional
general population which was 6 % (12 years and Nation, the age-standardized prevalence of type 2
older) (Fig. 13.1) [1921]. DM was 26.1 % [25] over the age of 10.
Administrative data from Manitoba reported Although the administrative data studies men-
a prevalence rate of type 2 DM that was 4.5 tioned above have presented both incidence and
times higher than that in the non-First Nation prevalence rates of type 2 DM [22, 23], there are
population of Manitoba [22]. Similarly, a study still relatively limited data on incidence of type 2
in Saskatchewan also using administrative data DM in Indigenous populations [23, 24]. In the
showed that the prevalence of diabetes was four Indigenous population of Alberta, the incidence
times higher among First Nations women than of diabetes during 19952007 increased at a
among non-First Nations women and 2.5 times slower rate compared to the general population,
higher among First Nations men than non-First even though the overall rates were higher among
Nations men (Fig. 13.2) [23]. According to Indigenous people [24]. There has been one fol-
administrative data from 2007, the prevalence of low-up study using repeat OGTTs, which
diabetes was 13.5 % in Indigenous peoples com- reported a 17 % diabetes conversion rate over
pared to 6 % in non-Indigenous peoples in the 10 years [27].
province of Alberta [24]. In contrast to First Nations, data on diabetes
Over the past three decades, a limited number prevalence and incidence among Mtis and Inuit
of more detailed studies using standardized oral communities are sparser. According to the 2009
glucose tolerance tests (OGTTs) have reported 2010 Canadian Community Health Survey, age-
prevalence rates in Indigenous Canadians to be standardized rates of self-reported diabetes
among the highest in the world (Fig. 13.3) [25, among Mtis were found to be 7.3 % compared to
26]. High prevalence rates were found in two the non-Indigenous population which was 5 %
Quebec communities, with a 48.6 % prevalence (Fig. 13.1) [21]. In a recent report on a population-
rate in Algonquin women of Lac Simon (aged based study in Winnipeg, Manitoba, Mtis aged
15 years and older) and a 16.3 % prevalence in 19 years and older were found to have age- and
women of River Desert (aged 15 years and older) sex-adjusted diabetes rates that were higher
[26]. According to a study in Sandy Lake First (11.8 %) than compared to the provincial
First Nations women

0.25 First Nations men
Non-first Nations women
Non-first Nations men
0.2
Diabetes prevalence
0.15
0.1
0.05
0
80
82
84
86
88
90
92
94
96
98
00
02
04
05
19
19
19
19
19
19
19
19
19
19
20
20
20
20
Year
Fig. 13.2 Age-standardized diabetes prevalence in First Nations and non-First Nations men and women from 1990 to
2005 (Dyck et al. [23])
80
IGT
70 New diabetes
Previous diabetes
60
Prevalence (%)
50
40
30
20
10
0
M F M F M F M F M F M F
1019yr 2029yr 3039yr 4049yr 5059yr >60yr
Age & sex
Fig. 13.3 Age- and sex-specific prevalence of impaired glucose intolerance, newly diagnosed diabetes, and previously
diagnosed diabetes in Sandy Lake First Nation (Harris et al. [25])
prevalence (8.8 %) [28]. An evaluation of diabe- According to the 2006 Aboriginal Peoples
tes in 14,480 Mtis people in Ontario found the Survey, the crude rate of self-reported type 2 DM
age- and sex-standardized prevalence to be in Inuit was 4 % compared to the non-general
11.2 % compared to the general population which population which was 5 % (Fig. 13.1) [30].
was 9 % [29]. Although the prevalence of diabetes in the Inuit
population has previously been documented to be macrovascular complications, including athero-

lower than the other Indigenous groups, recent sclerosis [49] and cardiovascular disease [50],
evidence highlights that it has markedly increased are also evident among Indigenous Canadians
and is now comparable to the general Canadian compared to non-Indigenous Canadians with
population [1, 31]. type 2 DM [51].
In addition to higher overall prevalence and Complications of diabetes in Indigenous peo-
incidence rates compared to the general popula- ples are exacerbated by limited social and eco-
tion, rates of gestational diabetes mellitus (GDM) nomic resources, including inadequate access to
are two- to fourfold higher in Indigenous women. health services due to geographical barriers [10,
The onset of type 2 DM in Indigenous people in 52, 53]. Moreover, complications are likely more
Canada occurs at a much earlier age than in most prominent in Indigenous populations as a result
other populations [25], and pediatric type 2 DM of an earlier age of diabetes onset. This popula-
is a major public health concern [32, 33]. The tion also has a higher prevalence of cardiometa-
increasing incidence of early age of onset of type bolic and lifestyle risk factors for other chronic
2 DM in Indigenous youth over the past several diseases, including smoking, obesity, and hyper-
decades is concomitant with increases in the tension [25, 54].
prevalence of childhood obesity [3439]. One of the most remarkable and worrisome
Potential risk factors of childhood obesity in aspects of the type 2 DM complication profile in
Indigenous school-aged children have included the Indigenous Canadian population relates to the
physical activity, fitness levels, TV watching, and very heavy burden of kidney disease. A study of
dietary factors [36, 38, 39]. According to a recent incidence rates of diabetic end-stage renal dis-
published report from a national surveillance ease in First Nations in Saskatchewan found that
study, the Indigenous Canadian population has even when the higher prevalence of diabetes was
the highest incidence rate and is the largest single taken into account, First Nations with diabetes
ethnic group that contributes to new-onset type 2 were still seven times as likely as non-First
DM [40, 41]. The report highlights that 100/227 Nations with diabetes to have end-stage renal dis-
new diabetes cases belong to Indigenous peoples, ease [45]. Between 1980 and 2000, there was an
and 11 % of these cases account for children eightfold increase in the number of Indigenous
younger than age 10 years [40, 41]. This acceler- patients with diabetic end-stage renal disease [55,
ated onset of both obesity and type 2 DM sug- 56]. Indigenous dialysis patients with end-stage
gests that the origins of these disorders may be renal disease are found to have reduced rate of
traced back to infancy and/or the intrauterine kidney transplantation [57]. The remote location
environment [42, 43]. The early life/intrauterine of Indigenous patients on dialysis does not
risk of type 2 DM will be covered in more detail explain the lower rate of kidney transplantation
below. among this group [58]. Although referral rates
for kidney transplantation assessment are the
same for Indigenous patients as for non-Indige-
Complications nous patients, completion of transplantation doc-
uments and wait-listing for transplantation are
Indigenous peoples in Canada experience a delayed in Indigenous patients [59].
heavier burden of diabetes-related comorbidities Indigenous Canadians with end-stage renal
compared to non-Indigenous peoples [44]. disease are more likely to reside in rural or remote
Indigenous peoples are burdened with a higher locations compared to other dialysis patients. As
prevalence of microvascular complications, such a result, access to hemodialysis units may not
as end-stage renal disease [44, 45], lower extrem- be as readily available. Therefore, peritoneal
ity amputations [46], and retinopathy [4648] dialysis might be very helpful for Indigenous
than their non-Indigenous counterparts with type patients requiring dialysis as it provides the abil-
2 DM. Additionally, higher prevalence rates of ity to undergo dialysis at home without visiting
a medical facility with a hemodialysis unit [60]. Smoking

However, data from three Canadian provinces Cigarette smoking has been associated with an
show that there are less frequent Indigenous users increased risk of type 2 DM in a meta-analysis of
of peritoneal dialysis compared to non-Indigenous 25 prospective cohort studies [67]. According to
patients in Canada [60]. Also, patients who were the meta-analysis, the risk of type 2 DM was
on peritoneal dialysis were more likely to experi- greater for those who smoked >20 cigarettes a day
ence technique failure, compared to non-Indig- than those who smoked <20 cigarettes a day [67].
enous patients; however, adjusted risk for death Smoking prevalence is high in Indigenous popula-
was similar to non-Indigenous patients [60]. tions and has been associated with complications
of type 2 DM [44]. According to national data
from the 20092010 Canadian Community Health
Modiable Risk Factors Survey, the prevalence rates of self-reported smok-
ing among Indigenous peoples aged 18 years and
Individual older were twofold higher than the rates of the
non-Indigenous population [21]. Moreover, rates
Obesity and Body Composition of daily tobacco smoking in Indigenous peoples
Among the modifiable risk factors for type 2 DM, were also 2.22.8 times higher than non-Indige-
overweight and obesity are the most well docu- nous people [21]. According to the 2012 Aboriginal
mented. The standard measure of body weight in Peoples Survey, 52 % of Inuit aged 15 years and
population studies is body mass index (BMI). older smoked cigarettes daily, and another 9 %
According to the 2004 Canadian Community were occasional smokers [68].
Health Survey, the prevalence of obesity (defined In a study on First Nations in Ontario, former
using BMI) was higher among Indigenous smoking was found to be associated with low
Canadians (37.8 %) when compared to non-Indig- beta-cell function, and current smoking was asso-
enous Canadians (22.6 %) [61]. The prevalence of ciated with high beta-cell function, independent
obesity was also higher among Indigenous chil- of diabetes. Additionally, the association of
dren and youth (15.8 %), when compared to their smoking with insulin resistance varied depending
non-Indigenous counterparts [61, 62]. on glycemic status [69]. In another First Nations
When determining the prevalence of over- population, smoking was found to increase inci-
weight and obesity in Indigenous peoples, it is dent diabetes risk in carriers of the HNF1A
salient to consider that the body dimensions of G319S allele. After stratification by baseline
this group, and the Inuit population in particular, smoking status, HNF1A G319S carriers who
are different than other populations [63]. The were active smokers had increased risk of devel-
Inuit are shorter in height and have shorter legs oping diabetes [70].
[63]. As a result, in order to improve the assess-
ment of obesity in Inuit people, measures of body Diet
fat distribution, such as waist circumference, Research on the association of diet with type 2 DM
waist-to-height, and waist-to-hip ratio, should be has received considerable attention. Numerous
employed [6466]. In fact, a meta-analysis of dietary factors such as coffee, fiber, whole grains,
over 300,000 individuals from different popula- and dairy products have been shown to have a pro-
tions around the world found that waist-to-hip tective effect on type 2 DM risk [7174]. While
ratio was a better predictor than waist circumfer- some dietary factors including sugar-sweetened
ence and BMI for diabetes risk [66]. In a study on beverages and high consumption of fat have been
First Nations in Ontario, the 10-year cumulative associated with an increased risk for type 2 DM
incidence of diabetes was associated with high [75, 76]. Additionally, specific nutrients such as
adiposity (defined as higher body mass index, vitamin D have recently been investigated for
percent body fat, waist circumference, or waist- their protective effects against the development
to-height ratio) [27]. of type 2 DM [77].
The nutritional habits of Indigenous peoples Cree from James Bay, higher traditional food
are of significant interest in the context of the consumption was associated with increased n-3
management and prevention of type 2 DM [78]. fatty acids [92]. Overall, however, very limited
Until relatively recently, Indigenous people of data are available regarding traditional food con-
Canada were nomadic hunters and gatherers who sumption and health outcomes among Indigenous
had a traditional diet which consisted of large and peoples.
small animals and birds (including the flesh and The transition to a market-foods diet has been
organs of moose, caribou, rabbit, ducks, geese, accompanied by increasing prevalence of type 2
etc.), freshwater fish, marine fish and mammals, DM in Indigenous populations [10, 25]. A study
and some plant foods and, most notably, berries in a First Nations community in Ontario found a
[79, 80]. In addition, the Iroquoian peoples of the high intake of total and saturated fat, and a diet
Great Lakes and St. Lawrence River region high in GI foods was more common in people
farmed corn, beans, squash, and other crops. A under 50 years of age, where rates of diabetes are
significant body of research has documented a showing their sharpest increase [83]. In another
marked nutrition transition among Indigenous study in the same population, data was obtained
Canadians, in which the nutritional profile of using food frequency questionnaires to determine
Indigenous Canadians has changed from a tradi- dietary patterns in the community. The intake of
tional diet to a market-foods diet that is charac- foods in the junk foods (chips/pop/candy/
terized by a higher intake in fat (especially canned meat) category and fat (especially lard,
saturated fat) and simple and high GI carbohy- consumed or used in preparation) category was
drates and low fiber [78, 8184]. associated with an increased risk of type 2 DM
While the consumption of traditional foods [84]. Similarly, a junk food dietary pattern (high-
has declined in general, Indigenous communities fat and high-sugar foods) identified in the Cree
in some regions, most notably in the Northwest from Northern Quebec was associated with
Territories and Yukon, have maintained a reason- increased diabetes risk [92].
ably high degree of traditional food consumption Another key public health nutrition problem
[81, 85, 86]. Traditional food consumption is affecting Indigenous communities is food insecu-
associated with beneficial impact on micronutri- rity. The prevalence of both individual and house-
ent intake. For instance, days with traditional hold food insecurity is much higher for
food consumption are characterized by increased Indigenous people compared to non-Indigenous
intakes of vitamins D, E, and B6, magnesium, people, with data from a national survey showing
and selenium. In addition, days when Indigenous that 33 % of off-reserve Indigenous Canadians
participants consumed traditional food were were food insecure compared to 9 % of non-
characterized by higher intakes of energy as pro- Indigenous Canadians [93, 94]. After controlling
tein, whereas days when traditional food was not for differences in household sociodemographic
consumed were associated with a higher percent- risk factors (including household income, highest
age of energy as carbohydrate, sucrose, and satu- level of education in household, household type,
rated and polyunsaturated fatty acids [81]. The number of children, etc.), Indigenous households
potential benefits of high-fiber, high-fruit/vegeta- had two to six times greater odds for food insecu-
ble/whole grain, low-fat, low-protein diets in the rity compared to non-Indigenous households [93,
prevention of type DM among Indigenous 94]. In a recent national survey on Inuit, 41 % of
Canadians have been studied [36, 38, 84, 87], and Inuit aged 15 and older lived in households that
the findings have been largely consistent with experienced food insecurity [68].
those from other populations [8890]. With Barriers to food security in Indigenous popu-
regard to traditional foods, the consumption of lations include income inadequacy and environ-
seal oil and salmon has been found to be associ- mental pollution related to the impact of climate
ated with a reduced risk of glucose intolerance in change on traditional food systems [86, 95]. A
Indigenous people of Alaska [91]. In addition, in large number of Indigenous households rely on
social assistance for income [93]. In fact, over [103]. According to a study in a First Nations
66 % of Indigenous households who received community in Ontario, both physical activity and
social assistance were food insecure [94]. In a fitness were associated with lower insulin con-
study of access to traditional and market foods in centrations, suggesting that physical activity/fit-
44 Indigenous communities across Arctic ness may be beneficial to the prevention of type 2
Canada, regional variation affected price and DM [104]. Television viewing was associated
ability to purchase adequate food, with between with childhood obesity in Mohawk children of
40 and 70 % of people saying they could afford Kahnawake [105]. Similarly, in First Nations
enough food [96]. Additionally, Indigenous peo- people aged 1019 years, 5 or more hours of tele-
ple reported inadequate access to fishing and vision viewing/day was associated with a signifi-
hunting equipment, and 46 % of people could not cantly higher risk of overweight than 2 or less
afford to go hunting or fishing [96]. Changes in hours of television viewing/day [36].
the local environment including changes in water
levels have affected harvesting and traditional Intrauterine/Early Life Factors
food acquirement in Indigenous communities High rates of youth-onset obesity and type 2
[97]. Environmental contaminants in Indigenous DM in Indigenous communities suggest that
traditional food resources such as heavy metals, risk factors are operating very early in life, per-
radionuclides, and organochlorines put the health haps even in the intrauterine period. Recent
of Indigenous people at an increased risk [98]. In research arising from the Developmental
order to eradicate food insecurity among off- Origins of Health and Disease (DOHaD) para-
reserve Indigenous populations, government digm has highlighted the importance to chronic
interventions must first address the great burden disease etiology of a number of factors that have
of poverty in this group by increasing income and a significant importance in the context of type 2
social assistance funding for families [93, 95]. DM in Indigenous Canadians [106], including
Overall, the considerable barriers to both tradi- high birth weight, gestational diabetes, and sub-
tional food and healthy market-food access dis- optimal breastfeeding.
cussed above have significant public health High birth weight can have both immediate-
implications for both managing and preventing and longer-term health consequences on infants,
the type 2 DM epidemic currently being experi- including shoulder dystocia, and an increased
enced by Indigenous communities in Canada. risk of type 2 DM [107, 108]. High birth weight
appears to be closely associated with maternal
Physical Activity diabetes and overweight. Consequently, as the
Engaging in physical activity has been well prevalence of maternal obesity and gestational
established to improve blood glucose control and diabetes mellitus (GDM) continues to increase,
has been identified as an important determinant higher birth weight babies will become increas-
in the prevention and management of type 2 DM ingly prevalent as well [109].
[99101]. A recent meta-analysis found that There have been consistent observations of
moderate intensity physical activity including high birth weight in Indigenous Canadian babies
brisk walking was negatively associated with the [110, 111]. The prevalence of high birth weight
risk of type 2 DM [102]. in Cree was 34.3 % compared to 11 % in their
Historically, Indigenous peoples engaged in non-Indigenous counterparts [112]. In a recent
activities such as hunting, fishing, and trapping to study on First Nations women in Northern and in
obtain sustenance [103]. However, as mentioned Southern Quebec, First Nations women were
earlier, because of the nutrition transition, tradi- more likely to have high birth weight babies than
tional activities are less prevalent, and this change non-Indigenous women [113]. Similarly, a study
has had a negative impact on the level of physical reporting singleton births from Cree women liv-
activity among Indigenous peoples and increasing in rural or remote communities in Northern
ing the risk of type 2 DM and its complications Quebec found prevalence rates of 2.4 % for low
birth weight and 36.5 % for high birth weight. In DM [120123]. Specific population groups have
the same study, infants who weighed >4500 g had been shown to possess predisposing alleles to
a 14 % higher prevalence of birth injuries and type 2 DM [124]. Indeed, high rates of type 2 DM
were more likely born to women with GDM in Indigenous communities in Canada suggest an
[114]. Another study on First Nations in Quebec inherited component. Early interest in the search
reported a significant association between macro- for a single Thrifty gene [125] explaining the
somia and postnatal mortality [115]. high type 2 DM burden in Indigenous Canadians
was unsuccessful, due to the fact that type 2 DM
in these communities is very likely caused by the
Population Level cumulative small effects of multiple genes oper-
ating on the background of a detrimental environ-
Environmental/Socioeconomic Risk ment [10, 126]. Nonetheless, a private mutation
Factors in the HNF1 gene (namely, G319S), restricted
Notwithstanding the importance of risk factors to the Oji-Cree population of Northwestern
that occur at the level of the individual, it is Ontario and Northeastern Manitoba, has been
increasingly being recognized that factors that shown to be associated with an increased risk for
characterize the local or broader social, environ- type 2 DM [127]. In fact, by 50 years of age,
mental, and/or geographical environment are HNF1 S319 has specificity (97 %) and positive
playing a critical role in the etiology of type 2 predictive values (95 %) for the development of
DM in Indigenous communities in Canada. These diabetes in the Oji-Cree population [106].
environmental risk factors for type 2 DM have
emerged largely from historic policies of coloni-
zation unique to the Indigenous context [116]. In Clinical Care
particular, the health and social conditions of
Indigenous peoples vary significantly depending For Indigenous people, health-care access and
on residence on-reserve versus off-reserve and in delivery depends on location, with urban and off-
rural versus urban areas [117]. Living in remote reserve Indigenous peoples accessing health care
or rural areas may lead to limited opportunities from provincially funded services. In contrast, as
for education and employment and reduced a part of the set of obligations arising from signed
access to a safe and healthy food supply [20, treaties with the federal government, health-care
117]. Geographic and language barriers may also delivery on-reserves is delivered by federally
result in reduced access to health-care services operated nursing stations and health centers. The
[118]. As well, there is limited availability of cul- First Nations and Inuit Health Branch (FNIHB)
turally appropriate services in Indigenous com- provides health benefits to First Nations and Inuit
munities [20, 119]. These limitations may that are noninsured by provincial insurance plans,
potentially affect the prevalence and distribution including prescription drugs and dental and
of type 2 DM in Indigenous peoples by affecting vision coverage [128, 129]. Physician services
the level of care and treatment available for type and hospital care are provided by the government
2 DM and its complications [117]. of each province or territory [128]. The federal
governments role in Indigenous health occurs
primarily through public health and intervention
Non-modiable Risk Factors strategies [128]. With regard to federal programs
that specifically target diabetes, the Aboriginal
Genetics Diabetes Initiative supports health promotion and
type 2 DM prevention programs which are dis-
Genome-wide association studies (GWAS) of seminated by community diabetes workers [129].
type 2 DM over the past several years have iden- The current health-care delivery system in
tified numerous susceptibility genes for type 2 Indigenous communities consists predominately
of acute and intermittent care management improve diabetes management through the develop-
instead of coordinated chronic disease care [130]. ment of community-based, culturally relevant pri-
As a result of geographical isolation, limited staff mary health-care models. FORGE AHEAD also
and other nonphysician health professionals pro- aims to develop appropriate access to services in First
vide clinical care in these communities [118]. Nations communities [138].
Additionally, hospital admissions for ambulatory
care conditions are much higher in Indigenous
communities [131133], and there is poor com- Primary Prevention
munication between provincially funded hospi-
tals and federal nursing care centers in most There is a great necessity for Indigenous-specific
Indigenous communities [33]. diabetes prevention and intervention strate-
Research has documented suboptimal clinical gies that consider the unique cultures and tradi-
care for diabetes among on-reserve First Nations tions of First Nations, Mtis, and Inuit people.
peoples in Canada. These clinical care gaps are Interventions which include tenets such as
attributable to geographical isolation, limited community involvement, face-to-face interven-
health-care staff, poor chronic disease manage- tions, development of skills to promote behavior
ment, limited surveillance, and high staff turn- change, and the dissemination of educational and
over [134]. Despite the high burden of chronic nutritional knowledge are required to alleviate
disease in the Indigenous population, including the burden of type 2 DM in marginalized com-
type 2 DM, the use of primary health care is munities [139].
lower among Indigenous populations compared In the late 1990s, the government of Canada
to the general population [132]. established the Aboriginal Diabetes Initiative to
National data from the Western provinces help improve the heavy burden of type 2 DM
(British Columbia, Alberta, Saskatchewan, and among First Nations, Inuit, and Mtis [129]. The
Manitoba) on type 2 DM burden and clinical care program has been delivered in three phases. The
gaps found that the age-standardized hospital dis- first phase, ADI Phase 1 (1999), allocated $115 M
charge rate was seven times higher in First over 5 years for health promotion and primary
Nations peoples living on- and off-reserve com- prevention programming. The second phase,
pared to the general population [119]. ADI Phase 2 (20052010), allocated $190 M
There is a higher mortality rate (19.5 per over 5 years to strengthen community-based
100,000) due to type 2 DM in Indigenous health promotion and diabetes prevention activi-
Canadians compared to non-Indigenous Canadians ties. The current phase, ADI Phase 3 (2010
(13.3 per 100,000) [135]. Although there is less 2015), has allocated $275 M for continued
frequent use of primary health services among support of health promotion and diabetes preven-
Indigenous peoples in Northern or isolated com- tion activities and services.
munities [136], the per capita health-care costs of Over the past 25 years, the Sandy Lake Health
Indigenous populations with and without type 2 and Diabetes Project (SLHDP) has been address-
DM are much higher compared to non-Indigenous ing the high rates of type 2 DM in Sandy Lake
populations [137]. Particularly, health-care usage, First Nation in Ontario. The SLHDP has devel-
including physician appointments, hospital visits, oped and implemented a number of community-
and dialysis, is 4060 % higher among First wide interventions including community health
Nations in Saskatchewan with type 2 DM com- promotion events, community surveys to track
pared to the non-Indigenous population without type 2 DM prevalence and risk factors, a grocery
type 2 DM [137]. store program which aims to increase knowledge
Recently, a new program called the Trans of healthy food choices, a community-wide walk-
formation of Indigenous Primary Healthcare ing trail to encourage physical activity, summer
Delivery (FORGE AHEAD) has been initiated in camps for youth, a diabetes radio program, and a
five First Nations communities across Canada to school curriculum [140]. The Sandy Lake First
Nation school diabetes prevention program populations with the necessary resources
developed and evaluated a healthy diet and exer- (health-care services, education, adequate fund-
cise curriculum for 1 year in children in grades ing), so they are able to prevent/control the occur-
35 [141]. After 1 year, there were reductions in rence of type 2 DM with a high-level of skill and
dietary fat, and increases in dietary fiber as well independence.
as an improvement in dietary knowledge, and an
increase in confidence and intention to choose Conclusions
healthy foods [141]. Type 2 DM has been increasing dramatically in
The Kahnawake Schools Diabetes Prevention the Indigenous population of Canada over the
Program (KSDPP) is a community-based, pri- past six decades and has reached epidemic lev-
mary diabetes prevention program based in els in some communities. The high prevalence
Kahnawake Mohawk Territory, Canada, that of type 2 DM and its complications among
aims to improve healthy eating and increase Indigenous populations is a major public health
physical activity in school children. The school issue. Indigenous peoples also have a higher
curriculum is delivered in ten 45-min sessions prevalence for cardiometabolic and lifestyle
every year for all six grades. The curriculum risk factors for other chronic diseases, includ-
focuses on lifestyle, nutrition, and diabetes edu- ing hypertension, obesity, unhealthy eating
cation [142]. The program has also implemented patterns, and smoking. Many of these occur on
a recreation path and a Community Advisory a background of the social determinants of
Board [142]. Results of 8 years of follow-up from health, including poverty, poor housing, low
the program showed early positive effects on a educational attainment, unemployment, and
risk factor (skinfold thickness) for type 2 DM and inadequate community resources. Clinical care
a decrease in consumption of high-fat and high- for diabetes in Indigenous communities is also
sugar foods. Although physical activity, fitness, suboptimal. Despite recent advances with
and television watching improved early on as community-based interventions geared toward
well, they were not maintained at the 8-year fol- increasing physical activity and healthy eating
low-up date [143]. practices in these communities, inadequate
Recently, another school intervention in three environmental and social support for physical
remote First Nations communities in British activity and healthy eating practices remains
Columbia promoted healthy eating and physical an ongoing challenge. Moreover, there is an
activity through action plans by teachers and important need to increase the amount of high-
administrators in Indigenous youth. Although the quality interventions for prevention of type 2
intervention did not find any changes in physical DM in Indigenous peoples. Overall, in order to
activity or overall cardiovascular risk, it did see alleviate the heavy burden of type 2 DM and its
an improvement in aerobic fitness [144]. complications among the Indigenous popula-
Despite recent advances with community- tion, both culturally appropriate primary pre-
based activities geared toward increasing physi- vention programs and clinical care strategies
cal activity and healthy eating practices in these that include the participation of community
communities, inadequate environmental and members are urgently required.
social support for physical activity and healthy
eating practices remains an ongoing challenge.
The results summarized above offer a reason for
optimism regarding the impact and availability of References
type 2 DM interventions targeted for Indigenous
populations. However, challenges include the 1. Public Health Agency of Canada. Diabetes in Canada:
need to implement these programs more broadly facts and figures from a public health perspective.
Ottawa: Public Health Agency of Canada; 2011.
and support their sustainability. In this context, 2. Friesen JW. Rediscovering the First Nations of
there is a greater need to support Indigenous Canada. Chicago: Detselig Enterprises Limited; 1997.
3. Statistics Canada. Aboriginal peoples in Canada: Auditor General of Canada to the House of Commons.
first nations people, Mtis and Inuit: National Report. Ottawa, Canada; 2011.
Household Survey, 2011. Ottawa: Minister of 20. First Nations Information Governance Canada. First
Industry; 2011. 978-1-100-22203-5. Nations regional longitudinal health survey (RHS)
4. Lischke U, McNab DT. The long journey of a forgot- 2002/03: results for adults, youth and children living
ten people: Mtis identities and family histories. in first nations communities. Ottawa: Assembly of
Waterloo: Wilfrid Laurier University Press; 2007. First Nations, First Nations Information Governance
5. Stern PR. Historical dictionary of the Inuit. Lanham: Centre; 2007.
Scarecrow Press; 2013. 21. Statistics Canada. Canadian Community Health
6. Langlois S, Turner A. In: Canada S, editor. Survey (CCHS); 2011.
Aboriginal languages in Canada. Ottawa: Minister 22. Green C, Blanchard JF, Young TK, Griffith J. The
of Industry; 2012. epidemiology of diabetes in the Manitoba-registered
7. Malenfant EC, Morency JD. Population projections First Nation population: current patterns and com-
by Aboriginal Identity in Canada, 2006 to 2031. parative trends. Diabetes Care. 2003;26(7):19938.
Statistics Canada; 2011. 23. Dyck R, Osgood N, Lin TH, Gao A, Stang
8. Statistics Canada. Aboriginal peoples in Canada: MR. Epidemiology of diabetes mellitus among First
First nations people, Mtis and Inuit: National Nations and non-First Nations adults. CMAJ.
household survey, 2011;99 - 011 - X2011001. 2010;182(3):24956.
Canada: Minister of Industry; 2013. 24. Oster RT, Johnson JA, Hemmelgarn BR, King M,
9. Reading CL, Wien F. Health inequalities and social Balko SU, Svenson LW, et al. Recent epidemiologic
determinants of aboriginal peoples health. Prince trends of diabetes mellitus among status Aboriginal
George: National Collaborating Centre for adults. CMAJ. 2011;183(12):E8038.
Aboriginal Health; 2009. 25. Harris SB, Gittelsohn J, Hanley A, Barnie A,
10. Young TK, Reading J, Elias B, ONeil JD. Type 2 Wolever TM, Gao J, et al. The prevalence of NIDDM
diabetes mellitus in Canadas First nations: status of and associated risk factors in native Canadians.
an epidemic in progress. CMAJ. 2000;163(5):5616. Diabetes Care. 1997;20(2):1857.
11. Reading J. The crisis of chronic disease among 26. Delisle HF, Eko JM. Prevalence of non-insulin-
aboriginal peoples: a challenge for public health, dependent diabetes mellitus and impaired glucose
population health and social policy. Victoria: Centre tolerance in two Algonquin communities in Quebec.
for Aboriginal Health Research: University of CMAJ. 1993;148(1):417.
Victoria Press; 2009. 27. Ley SH, Harris SB, Mamakeesick M, Noon T,
12. Chase LA. The trend of diabetes in Saskatchewan, Fiddler E, Gittelsohn J, et al. Metabolic syndrome
1905 to 1934. Can Med Assoc J. 1937;36(4):3669. and its components as predictors of incident type 2
13. Montour LT, Macaulay AC. High prevalence rates of diabetes mellitus in an Aboriginal community.
diabetes mellitus and hypertension on a North CMAJ: Can Med Assoc J = J Assoc Med Can.
American Indian reservation. Can Med Assoc 2009;180(6):61724.
J. 1985;132(10):1110, 2. 28. Martens P, Bartlett J, Burland E, Prior H, Burchill C,
14. Evers S, McCracken E, Antone I, Deagle G. The Huq S, et al. Mtis health status and healthcare utili-
prevalence of diabetes in Indians and Caucasians liv- zation in Manitoba: a population-based study.
ing in Southwestern Ontario. Can J Public Health. Winnipeg: Manitoba Centre for Health Policy; 2010.
1987;78(4):2403. 29. Shah BR, Cauch-Dudek K, Pigeau L. Diabetes prev-
15. Young TK, Szathmary EJ, Evers S, Wheatley alence and care in the Mtis population of Ontario,
B. Geographical distribution of diabetes among the Canada. Diabetes Care. 2011;34(12):25556.
native population of Canada: a national survey. Soc 30. Aboriginal Peoples Survey, 2006: Inuit health and
Sci Med. 1990;31(2):12939. social conditions: supporting data tables. In:
16. Brassard P, Robinson E, Lavalle C. Prevalence of Statistics Canada, editor. Ottawa: Statistics Canada;
diabetes mellitus among the James Bay Cree of 2008.
northern Quebec. CMAJ. 1993;149(3):3037. 31. Egeland GM, Cao Z, Young TK. Hypertriglyceridemic-
17. Pioro MP, Dyck RF, Gillis DC. Diabetes prevalence waist phenotype and glucose intolerance among
rates among First Nations adults on Saskatchewan Canadian Inuit: the international polar year Inuit
reserves in 1990: comparison by tribal grouping, health survey for adults 20072008. CMAJ.
geography and with non-First Nations people. Can 2011;183:E5538.
J Public Health. 1996;87(5):3258. 32. Dean HJ, Mundy RL, Moffatt M. Non-insulin
18. Fox C, Harris S, Whalen-Brough E. Diabetes among dependent diabetes mellitus in Indian children in
Native Canadians in northwestern Ontario: 10 years Manitoba. Can Med Assoc J. 1992;147:527.
later. Chron Dis Canada. 1994;15:926. 33. Harris SB, Perkins B, Whalen-Brough E. Non-
19. Office of the Auditor General of Canada. Chapter 4, insulin dependent diabetes mellitus among First
Programs for First Nations on Reserves, of the 2011 Nations children: new entity among First Nations
Report of the Auditor General of Canada. In: Standing people of northwestern Ontario. Can Fam Phys.
Committee on Public Accounts. Status Report of the 1996;42:86976.
34. Hannon TS, Rao G, Arslanian SA. Childhood obe- 48. Ross SA, McKenna A, Mozejko S, Fick GH. Diabetic
sity and type 2 diabetes mellitus. Pediatrics. retinopathy in native and nonnative Canadians. Exp
2005;116(2):47380. Diabetes Res. 2007;2007:76271.
35. Zdravkovic V, Daneman D, Hamilton J. Presentation 49. Macaulay AC, Montour LT, Adelson N. Prevalence
and course of Type 2 diabetes in youth in a large of diabetic and atherosclerotic complications among
multi-ethnic city. Diabet Med. 2004;21(10): Mohawk Indians of Kahnawake, PQ. CMAJ.
11448. 1988;139:2214.
36. Hanley AJ, Harris SB, Gittelsohn J, Wolever TM, 50. Shah BR, Hux JE, Zinman B. Increasing rates of
Saksvig B, Zinman B. Overweight among children ischemic heart disease in the native population of
and adolescents in a Native Canadian community: Ontario, Canada. Arch Intern Med. 2000;
prevalence and associated factors. Am J Clin Nutr. 160(12):18626.
2000;71(3):693700. 51. Naqshbandi M, Harris SB, Esler JB, Antwi-Nsiah
37. Willows ND, Johnson MS, Ball GD. Prevalence esti- F. Global complication rates of type 2 diabetes in
mates of overweight and obesity in Cree preschool indigenous peoples: a comprehensive review.
children in northern Quebec according to interna- Diabetes Res Clin Pract. 2008;82(1):117.
tional and US reference criteria. Am J Public Health. 52. Health Canada. Diabetes among Aboriginal people
2007;97(2):3116. in Canada: the evidence. Ottawa: Health Canada;
38. Bernard L, Lavallee C, Gray-Donald K, Delisle 2001.
H. Overweight in Cree schoolchildren and adoles- 53. Martens PJ, Martin BD, ONeil JD, MacKinnon
cents associated with diet, low physical activity, and M. Diabetes and adverse outcomes in a First Nations
high television viewing. J Am Diet Assoc. 1995;95(7): population: associations with healthcare access, and
8002. socioeconomic and geographical factors. Can
39. Willows ND. Overweight in Aboriginal children: J Diabetes. 2007;31(3):22332.
prevalence, implications, and solutions. J Aborig 54. Oster RT, Toth EL. Differences in the prevalence of
Health. 2005;2:7685. diabetes risk-factors among First Nation, Mtis and
40. Amed S, Dean HJ, Panagiotopoulos C, Sellers EA, non-Aboriginal adults attending screening clinics in
Hadjiyannakis S, Laubscher TA, et al. Type 2 diabe- rural Alberta, Canada. Rural Remote Health.
tes, medication-induced diabetes, and monogenic 2009;9(2):1170.
diabetes in Canadian children: a prospective national 55. Dyck RF. Mechanisms of renal disease in indigenous
surveillance study. Diabetes Care. 2010;33(4): populations: influences at work in Canadian indige-
78691. nous peoples. Nephrology. 2001;6:37.
41. Amed S, Hamilton JK, Sellers EA, Panagiotopoulos 56. Register COR. Annual report. vol. 1: dialysis and
C, Hadjiyannakis S, Shah BR, et al. Differing clini- renal transplantation. Ottawa: Canadian Institute for
cal features in Aboriginal vs. non-Aboriginal chil- Health Information; 2001.
dren presenting with type 2 diabetes. Pediatr 57. Yeates KE. Aboriginal patients on the road to kidney
Diabetes. 2012;13(6):4705. transplantation: is residence location a barrier?
42. Silverman BL, Rizzo TA, Cho NH, Metzger Kidney Int. 2006;70(5):8268.
BE. Long-term effects of the intrauterine environ- 58. Tonelli M, Hemmelgarn B, Kim AK, Bertazzon S,
ment. The Northwestern University Diabetes in Klarenbach S, Manns B, et al. Association between
Pregnancy Center. Diabetes Care. 1998;21 Suppl 2: residence location and likelihood of kidney trans-
B1429. plantation in Aboriginal patients treated with dialy-
43. Druet C, Ong KK. Early childhood predictors of sis in Canada. Kidney Int. 2006;70(5):92430.
adult body composition. Best Pract Res Clin 59. Tonelli M, Chou S, Gourishankar S, Jhangri GS,
Endocrinol Metab. 2008;22(3):489502. Bradley J, Hemmelgarn B, et al. Wait-listing for
44. Hanley AJ, Harris SB, Mamakeesick M, Goodwin kidney transplantation among Aboriginal hemo-
K, Fiddler E, Hegele RA, et al. Complications of dialysis patients. Am J Kidney Dis. 2005;46(6):
Type 2 diabetes among Aboriginal Canadians: prev- 111723.
alence and associated risk factors. Diabetes Care. 60. Tonelli M, Hemmelgarn B, Manns B, Davison S,
2005;28(8):20547. Bohm C, Gourishankar S, et al. Use and outcomes of
45. Dyck RF, Tan L. Rates and outcomes of diabetic peritoneal dialysis among Aboriginal people in
end-stage renal disease among registered native peo- Canada. J Am Soc Nephrol. 2005;16(2):4828.
ple in Saskatchewan. CMAJ. 1994;150(2):2038. 61. Statistics Canada. Canadian community health sur-
46. McIntyre I, Boughen C, Trepman E, Embil JM. Foot vey, nutrition: general health component, public use
and ankle problems of Aboriginal and non- microdata file guide. Ottawa: Health Statistics
Aboriginal diabetic patients with end-stage renal Division, Statistics Canada; 2005.
disease. Foot Ankle Int. 2007;28(6):67486. 62. Katzmarzyk PT. Obesity and physical activity
47. Maberley D, Walker H, Koushik A, Cruess among Aboriginal Canadians. Obesity (Silver
A. Screening for diabetic retinopathy in James Bay, Spring). 2008;16(1):18490.
Ontario: a cost-effectiveness analysis. CMAJ. 2003; 63. Charbonneau-Roberts G, Saudny-Unterberger H,
168(2):1604. Kuhnlein HV, Egeland GM. Body mass index may
overestimate the prevalence of overweight and obe- of Canadian Arctic indigenous peoples. Public
sity among the Inuitd. Int J Circumpolar Health. Health Nutr. 2008;11(4):34960.
2005;64(4):1639. 79. Johnson-Down L, Egeland GM. Adequate nutrient
64. Weyer C, Funahashi T, Tanaka S, Hotta K, intakes are associated with traditional food con-
Matsuzawa Y, Pratley RE, et al. Hypoadiponectinemia sumption in nunavut Inuit children aged 35 years.
in obesity and type 2 diabetes: close association with J Nutr. 2010;140(7):13116.
insulin resistance and hyperinsulinemia. J Clin 80. Receveur O, Kuhnlein HV. Benefits of traditional
Endocrinol Metab. 2001;86(5):19305. food in Dene/Mtis communities. Int J Circumpolar
65. Warne DK, Charles MA, Hanson RL, Jacobsson LT, Health. 1998;57 Suppl 1:21921.
McCance DR, Knowler WC, et al. Comparison of 81. Kuhnlein HV, Receveur O, Soueida R, Egeland
body size measurements as predictors of NIDDM in GM. Arctic indigenous peoples experience the nutri-
Pima Indians. Diabetes Care. 1995;18(4):4359. tion transition with changing dietary patterns and
66. Ashwell M, Gunn P, Gibson S. Waist-to-height ratio obesity. J Nutr. 2004;134(6):144753.
is a better screening tool than waist circumference 82. Sharma S, Cao X, Roache C, Buchan A, Reid R,
and BMI for adult cardiometabolic risk factors: sys- Gittelsohn J. Assessing dietary intake in a popula-
tematic review and meta-analysis. Obes Rev Off tion undergoing a rapid transition in diet and life-
J Int Assoc Study Obes. 2012;13(3):27586. style: the Arctic Inuit in Nunavut, Canada. Br J Nutr.
67. Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz 2010;103(5):74959.
J. Active smoking and the risk of type 2 diabetes: a 83. Wolever TMS, Hamad S, Gittelsohn J, Hanley AJG,
systematic review and meta-analysis. JAMA: J Am Logan A, Harris SB, et al. Nutrient intake and food
Med Assoc U S. 2007;298:265464. use in an Ojibwa-Cree community in Northern
68. Wallace S. Inuit health: selected findings from the Ontario assessed by 24h dietary recall. Nutr Res.
2012 Aboriginal peoples survey. Statistics Canada. 1997;17:60318.
2014 89-653-X-003. 84. Gittelsohn J, Wolever TM, Harris SB, Harris-Giraldo
69. Daniel M, Cargo MD. Association between smoking, R, Hanley AJ, Zinman B. Specific patterns of food
insulin resistance and beta-cell function in a North- consumption and preparation are associated with
western First Nation. Diabet Med. 2004;21(2): diabetes and obesity in a Native Canadian commu-
18893. nity. J Nutr. 1998;128:5417.
70. Ley SH, Hegele RA, Harris SB, Mamakeesick M, 85. Batal M, Gray-Donald K, Kuhnlein HV, Receveur
Cao H, Connelly PW, et al. HNF1A G319S variant, O. Estimation of traditional food intake in indige-
active cigarette smoking and incident type 2 diabetes nous communities in Denendeh and the Yukon. Int
in Aboriginal Canadians: a population-based epide- J Circumpolar Health. 2005;64(1):4654.
miological study. BMC Med Genet. 2011;12:1. 86. Receveur O, Boulay M, Kuhnlein HV. Decreasing tra-
71. Wolever TM. Dietary carbohydrates and insulin action ditional food use affects diet quality for adult Dene/
in humans. Br J Nutr. 2000;83 Suppl 1:S97102. Mtis in 16 communities of the Canadian Northwest
72. Wolfram T, Ismail-Beigi F. Efficacy of high-fiber Territories. J Nutr. 1997;127(11):217986.
diets in the management of type 2 diabetes mellitus. 87. Wolever TM, Hamad S, Gittelsohn J, Gao J, Hanley
Endocr Pract Off J Am Coll Endocrinol Am Assoc AJ, Harris SB, et al. Low dietary fiber and high pro-
Clin Endocrinol. 2011;17(1):13242. tein intakes associated with newly diagnosed diabe-
73. Tunnicliffe JM, Shearer J. Coffee, glucose homeo- tes in a remote aboriginal community. Am J Clin
stasis, and insulin resistance: physiological mecha- Nutr. 1997;66(6):14704.
nisms and mediators. Appl Phys Nutr Metab = 88. Costacou T, Mayer-Davis EJ. Nutrition and prevention
Physiol Appl Nutr Metab. 2008;33(6):1290300. of type 2 diabetes. Annu Rev Nutr. 2003;23:14770.
74. Tong X, Dong JY, Wu ZW, Li W, Qin LQ. Dairy con- 89. Schulze MB, Hu FB. Primary prevention of diabe-
sumption and risk of type 2 diabetes mellitus: a tes: what can be done and how much can be pre-
meta-analysis of cohort studies. Eur J Clin Nutr. vented? Annu Rev Public Health. 2005;26:
2011;65(9):102731. 44567.
75. Malik VS, Schulze MB, Hu FBCPCN. Intake of 90. Parillo M, Riccardi G. Diet composition and the risk
sugar-sweetened beverages and weight gain: a sys- of type 2 diabetes: epidemiological and clinical evi-
tematic review. Am J Clin Nutr. 2006;84:27488. dence. Br J Nutr. 2004;92(1):719.
76. Bray GA, Popkin BM. Dietary fat intake does affect 91. Adler AI, Boyko EJ, Schraer CD, Murphy NJ. Lower
obesity! Am J Clin Nutr. 1998;68(6):115773. prevalence of impaired glucose tolerance and diabe-
77. Mansuri S, Badawi A, Kayaniyil S, Cole DE, Harris tes associated with daily seal oil or salmon consump-
SB, Mamakeesick M, et al. Associations of circulat- tion among Alaska Natives. Diabetes Care. 1994;
ing 25(OH)D with cardiometabolic disorders under- 17(12):1498501.
lying type 2 diabetes mellitus in an Aboriginal 92. Johnson-Down L, Labonte ME, Martin ID, Tsuji LJ,
Canadian community. Diabetes Res Clin Pract. Nieboer E, Dewailly E, et al. Quality of diet is asso-
2015;109(2):4409. ciated with insulin resistance in the Cree (Eeyouch)
78. Kuhnlein HV, Receveur O, Soueida R, Berti PR. indigenous population of northern Quebec. Nutr
Unique patterns of dietary adequacy in three cultures Metab Cardiovasc Dis. 2015;25(1):8592
93. Willows ND, Veugelers P, Raine K, Kuhle 107. Group HSCR, Metzger BE, Lowe LP, Dyer AR,
S. Prevalence and sociodemographic risk factors Trimble ER, Chaovarindr U, et al. Hyperglycemia
related to household food security in Aboriginal and adverse pregnancy outcomes. N Engl J Med.
peoples in Canada. Public Health Nutr. 2009;12(8): 2008;358(19):19912002.
11506. 108. Boney CM, Verma A, Tucker R, Vohr BR. Metabolic
94. Office of Nutrition Policy and Promotion and Health syndrome in childhood: association with birth
Canada. Canadian Community Health Survey Cycle weight, maternal obesity, and gestational diabetes
2.2, Nutrition (2004): Income-Related Household mellitus. Pediatrics. 2005;115(3):e2906.
Food Security in Canada. Health Canada: Ottawa, 109. Dyck R, Klomp H, Tan LK, Turnell RW, Boctor
ON, 2007. MA. A comparison of rates, risk factors, and out-
95. Power EM. Conceptualizing food security or aborig- comes of gestational diabetes between aboriginal
inal people in Canada. Can J Public Health. 2008; and non-aboriginal women in the Saskatoon health
99:957. district. Diabetes Care. 2002;25(3):48793.
96. Lambden J, Receveur O, Marshall J, Kuhnlein 110. Munroe M, Shah CP, Badgley R, Bain HW. Birth
HV. Traditional and market food access in Arctic weight, length, head circumference and bilirubin
Canada is affected by economic factors. Int level in Indian newborns in the Sioux Lookout Zone,
J Circumpolar Health. 2006;65(4):33140. northwestern Ontario. Can Med Assoc J. 1984;
97. Guyot M, Dickson C, Paci M, Furgal F, Chan 131(5):4536.
HM. Local observations of climate change and 111. Thomson M. Heavy birth weight in Native Indians
impacts on traditional food security in two northern of British Columbia. Can J Public Health. 1990;
Aboriginal communities. Int J Circumpolar Health. 81(6):4436.
2006;65:40315. 112. Rodrigues S, Robinson EJ, Kramer MS, Gray-
98. Kuhnlein HV, Chan HM. Environment and contami- Donald K. High rates of infant macrosomia: a com-
nants in traditional food systems of northern indige- parison of a Canadian native and a non-native
nous peoples. Annu Rev Nutr. 2000;20:595626. population. J Nutr. 2000;130(4):80612.
99. Hu FB, Manson JE, Stampfer MJ, Colditz G, Liu S, 113. Luo ZC, Wilkins R, Heaman M, Smylie J, Martens
Solomon CG, et al. Diet, lifestyle, and the risk of PJ, McHugh NG, et al. Birth outcomes and infant
type 2 diabetes mellitus in women. N Engl J Med. mortality among First Nations Inuit, and non-
2001;345(11):7907. indigenous women by northern versus southern resi-
100. Hu FB, Li TY, Colditz GA, Willett WC, Manson dence, Quebec. J Epidemiol Community Health.
JE. Television watching and other sedentary behav- 2012;66(4):32833.
iors in relation to risk of obesity and type 2 dia- 114. Willows ND, Sanou D, Bell RC. Assessment of
betes mellitus in women. JAMA. 2003;289(14): Canadian Cree infants birth size using the WHO
178591. Child Growth Standards. Am J Hum Biol.
101. Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, 2011;23(1):12631.
Blissmer BJ, Rubin RR, et al. Exercise and type 2 115. Wassimi S, Wilkins R, McHugh NG, Xiao L,
diabetes: the American College of Sports Medicine Simonet F, Luo ZC. Association of macrosomia with
and the American Diabetes Association: joint posi- perinatal and postneonatal mortality among First
tion statement executive summary. Diabetes Care. Nations people in Quebec. CMAJ. 2011;183(3):
2010;33(12):26926. 3226.
102. Jeon CY, Lokken RP, Hu FB, van Dam RM. Physical 116. Kirmayer LJ, Brass GM, Tait CL. The mental health
activity of moderate intensity and risk of type 2 dia- of Aboriginal peoples: transformations of identity
betes: a systematic review. Diabetes Care. 2007; and community. Can J Psychiatry. 2000;45(7):
30(3):74452. 60716.
103. Reading J. Confronting the growing crisis of 117. Tjepkema M. The health of the off-reserve
cardiovascular disease and heart health among Aboriginal population. In: Canada S, editor.
Aboriginal peoples in Canada. Can J Cardiol. 2015; Supplement to health reports. Ottawa: Statistics
31(9):107780. Canada; 2002.
104. Kriska AM, Hanley AJ, Harris SB, Zinman 118. Health Canada. Rural health in rural hands: strategic
B. Physical activity, physical fitness, and insulin and directions for rural, remote, northern and aboriginal
glucose concentrations in an isolated Native communities. Health Canada, 2002. [cited 2000 July
Canadian population experiencing rapid lifestyle 20]. Available from http://publications.gc.ca/pub?id=
change. Diabetes Care. 2001;24(10):178792. 9.689374&sl=0.
105. Horn OK, Paradis G, Potvin L, Macaulay AC, 119. Carriere G, Garner R, Sanmartin C, LHAD. Acute-
Desrosiers S. Correlates and predictors of adiposity care hospitalizations and aboriginal identity in
among Mohawk children. Prev Med. 2001;33(4): Canada, 2001/2001. Ottawa: Statistics Canada;
27481. 2010.
106. Hegele RA. Genes and environment in type 2 diabe- 120. Imamura M, Maeda S. Genetics of type 2 diabetes:
tes and atherosclerosis in aboriginal Canadians. Curr the GWAS era and future perspectives. Rev Endocr
Atheroscler Rep. 2001;3(3):21621. J. 2011;58(9):72339.
121. Billings LK, Florez JC. The genetics of type 2 diabe- 135. Bramley D, Hebert P, Tuzzio L, Chassin M.
tes: what have we learned from GWAS? Ann N Y Disparities in indigenous health: a cross-country
Acad Sci. 2010;1212:5977. comparison between New Zealand and the United
122. Lyssenko V, Laakso M. Genetic screening for the States. Am J Public Health. 2005;95(5):84450.
risk of type 2 diabetes: worthless or valuable? 136. Bhattacharyya OK, Rasooly IR, Naqshbandi M,
Diabetes Care. 2013;36 Suppl 2:S1206. Estey EA, Esler J, Toth E, et al. Challenges to the
123. Medici F, Hawa M, Ianari A, Pyke DA, Leslie provision of diabetes care in first nations communi-
RD. Concordance rate for type II diabetes mellitus in ties: results from a national survey of healthcare pro-
monozygotic twins: actuarial analysis. Diabetologia. viders in Canada. BMC Health Serv Res. 2011;
1999;42(2):14650. 11:283.
124. Chen R, Corona E, Sikora M, Dudley JT, Morgan 137. Pohar SL, Johnson JA. Health care utilization and
AA, Moreno-Estrada A, et al. Type 2 diabetes risk costs in Saskatchewans registered Indian population
alleles demonstrate extreme directional differentia- with diabetes. BMC Health Serv Res. 2007;7:
tion among human populations, compared to other 126.
diseases. PLoS Genet. 2012;8(4):e1002621. 138. FORGE AHEAD program description London, ON:
125. Neel JV. Diabetes mellitus: a thrifty genotype ren- the national diabetes management strategy. 2011
dered detrimental by progress? Am J Hum Genet. [cited 7 Mar 2016]. Available from http://tndms.ca/
1962;14:35362. forgeahead/index.html.
126. Hegele RA, Cao H, Harris SB, Hanley AJ, Zinman 139. Glazier RH, Bajcar J, Kennie NR, Willson K. A sys-
B. The hepatic nuclear factor-1alpha G319S variant tematic review of interventions to improve diabetes
is associated with early-onset type 2 diabetes in care in socially disadvantaged populations. Diabetes
Canadian Oji-Cree. J Clin Endocrinol Metab. Care. 2006;29(7):167588.
1999;84(3):107782. 140. Kakekagumick KE, Naqshbandi Hayward M, Harris
127. Pollex RL, Hanley AJ, Zinman B, Harris SB, Hegele SB, Saksvig B, Gittelsohn J, Manokeesic G, et al.
RA. Clinical and genetic associations with hypertri- Sandy lake health and diabetes project: a community-
glyceridemic waist in a Canadian aboriginal popula- based intervention targeting type 2 diabetes and its
tion. Int J Obes (2005). 2006;30(3):48491. risk factors in a first nations community. Front
128. Health Canada. Fact sheet- First Nations and Inuit Endocrinol. 2013;4:170.
health branch health Canada website 2008 (updated 141. Saksvig BI, Gittelsohn J, Harris SB, Hanley AJ,
2008; cited 26 Feb 2016). Available from http:// Valente TW, Zinman B. A pilot school-based
www.hc-sc.gc.ca/ahc-asc/branch-dirgen/fnihb- healthy eating and physical activity intervention
dgspni/fact-fiche-eng.php. improves diet, food knowledge, and self-efficacy
129. Health Canada. Aboriginal diabetes initiative for native Canadian children. J Nutr. 2005;135(10):
20102015 (updated 2011; cited 26 Feb 2016) 2016. 23928.
Available from http://www.hc-sc.gc.ca/fniah-spnia/ 142. Macaulay AC, Paradis G, Potvin L, Cross EJ, Saad-
pubs/diseases-maladies/_diabete/2010-2015-frame- Haddad C, McComber A, et al. The Kahnawake
cadre/indexeng.php. Schools Diabetes Prevention Project: intervention,
130. Minore B, Boone M, Katt M, Kinch P, Birch S. evaluation, and baseline results of a diabetes primary
Facilitating the continuity of care for first nation cli- prevention program with a native community in
ents within a regional context. 2001. Canada. Prev Med. 1997;26(6):77990.
131. King M, Smith A, Gracey M. Indigenous health part 143. Paradis G, Levesque L, Macaulay AC, Cargo M,
2: the underlying causes of the health gap. Lancet. McComber A, Kirby R, et al. Impact of a diabetes
2009;374(9683):7685. prevention program on body size, physical activity,
132. Shah BR, Gunraj N, Hux JE. Markers of access to and diet among Kanienkeha:ka (Mohawk) children
and quality of primary care for aboriginal people in 6 to 11 years old: 8-year results from the Kahnawake
Ontario, Canada. Am J Public Health. 2003;93(5): Schools Diabetes Prevention Project. Pediatrics.
798802. 2005;115(2):3339.
133. Lavoie JG, Forget EL, Prakash T, Dahl M, Martens P, 144. Tomlin D, Naylor PJ, McKay H, Zorzi A, Mitchell
ONeil JD. Have investments in on-reserve health M, Panagiotopoulos C. The impact of Action
services and initiatives promoting community control Schools! BC on the health of Aboriginal children
improved First Nations health in Manitoba? Soc Sci and youth living in rural and remote communities in
Med. 2010;71(4):71724. British Columbia. Int J Circumpolar Health. 2012;
134. Gracey M, King M. Indigenous health part 1: 71:17999.
determinants and disease patterns. Lancet. 2009;
374(9683):6575.
Diabetes in Native Populations
and Underserved Communities 14
in the USA
Joshua J. Joseph and Sherita Hill Golden
Epidemiology, Classication, 33 %) [1]. Estimates based only on physician

and Unique Pathophysiological diagnosis may underestimate diabetes in certain
Aspects of Diabetes Mellitus racial/ethnic groups.
in Minority Populations in the USA As of 2010, approximately 1.9 million indi-
viduals over 20 years of age in the USA devel-
In the USA roughly 25.8 million individuals oped incident diabetes [1]. Compared to NHWs,
(8.3 % of US population) have type 2 diabetes the risk of incident diabetes was 18 % higher in
mellitus (diabetes) [1]. While 18.8 million are Asian Americans, 66 % higher in Hispanic
diagnosed, another 7 million remain undiagnosed Americans, and 77 % higher in NHBs [1].
[1]. The prevalence of diagnosed diabetes in Compared to NHWs, the diabetes incidence was
adults over 20 years of age is highest among non- significantly higher among Mexican Americans
Hispanic blacks (NHBs) (12.6 %), Mexican (87 %) and Puerto Rican Americans (94 %),
Americans (13.3 %), Puerto Rican Americans whereas the risk was similar in Cuban Americans,
(13.8 %), and Native Americans (16.1 %) [1]. Central Americans, and South Americans [1].
The prevalence of diagnosed diabetes is similar The most recent data examining trends for inci-
among non-Hispanic whites (NHWs), Cuban dence of type 1 and type 2 diabetes in the USA
Americans, Central Americans, and South are from the National Health Interview Survey
Americans. It is important to note that diabetes (NHIS), where data from 664,969 adults was
prevalence in Hispanic Americans is influenced analyzed from 1980 to 2012 [3]. The incidence
by the country of origin and primarily driven by per 1,000 persons was 3.2 in 1990, 8.8 in 2008,
the high prevalence in people of Mexican and and 7.1 in 2012, suggesting that the diabetes inci-
Puerto Rican descent [2]. Similarly, diabetes dence has reached a plateau. However, diabetes
prevalence is lowest in Alaska Natives (5.5 %) incidence rates in NHBs and Hispanic Americans
but very high in American Indians (approaching continue to rise significantly more than for
NHWs.
NHIS contains the only estimates of the preva-
J.J. Joseph, MD S.H. Golden, MD, MHS (*) lence of diabetes in Asian Americans in the
Division of Endocrinology, Diabetes, and USA. It revealed that there is significant ethnic
Metabolism, Department of Medicine, Johns Hopkins variation in the prevalence of diabetes, which is
University School of Medicine, highest among Asian Indians (close to 15 %) and
1830 E. Monument Street, Suite# 333, Baltimore,
MD 21287, USA Filipinos (close to 10 %) and lowest among
e-mail: [email protected] Koreans, Vietnamese, and Chinese (37%) in the

DOI 10.1007/978-3-319-41559-8_14
252 J.J. Joseph and S.H. Golden
USA [4], consistent with the known higher Glucose Metabolism and Insulin
diabetes prevalence in individuals living in India, Resistance
South Asia, and the Philippines [5]. In the Insulin resistance is a key contributor to diabetes
Diabetes Study of Northern California, diabetes risk in NHB, Mexican American, Asian
incidence was highest among Pacific Islanders, American, and Native American populations.
South Asians, and Filipinos (19.9, 17.2, and 14.7 Compared to their NHW counterparts and inde-
per 1,000 person-years) compared to other racial/ pendent of adiposity, NHBs, Mexican Americans,
ethnic groups, including other minorities (NHBs, Asian Americans, and Native Americans have
Latinos, and Native Americans) [6]. greater insulin resistance [7]. Studies in non-
Mexican Hispanic Americans have yielded con-
flicting results. Glucose metabolic features differ
Race/Ethnic Differences in Biological among Hispanic Americans from different coun-
Factors tries of origin. This may explain the higher preva-
lence of diabetes in Mexican Americans
Obesity and Fat Distribution compared to those of Cuban American and South
Obesity is one of the strongest risk factors for devel- American descent. Asian Americans have lower
oping diabetes. Racial/ethnic differences in obesity beta-cell insulin secretion compared to NHWs
contribute to the higher risk of diabetes in NHBs [7]. The reduced beta-cell function in Asian
and Mexican Americans; however, NHB women Americans may also explain why they are at high
have greater subcutaneous compared to visceral fat risk for diabetes at lower levels of BMI [8].
than NHW women at a given body mass index
(BMI) and waist circumference and may therefore
develop diabetes at a higher BMI than NHW Individual Racial/Ethnic Differences
women. Among Asian Americans, there is variation in Nonbiological Factors
in the prevalence of overweight and obesity depend-
ing on the country of origin (Table 14.1). Differences Acculturation
in body fat distribution are important contributors to Acculturation in Hispanic American immigrants
diabetes risk in certain Asian populations, for results in an increase in dietary habits that pro-
instance, Japanese Americans and Filipinos have mote obesity [9]. The association of acculturation
more visceral fat at similar levels of BMI and waist with diabetes, however, is mixed and inconsis-
circumference compared to NHWs [4]. tent. Even though acculturation appears to pro-
mote obesity, its association with diabetes may
Table 14.1 Age-adjusted prevalence of overweight and be offset by its positive influence on physical
obesity by Asian American ethnicity from the National activity and access to care, in that screening and
Health Interview Survey [4] intervention occur sooner [9]. Japanese immi-
Age-adjusted Age-adjusted grants to the USA have a threefold higher rate of
overweight obesity diabetes compared to their native Japanese coun-
Race/ethnic group prevalence (%) prevalence (%) terparts [7].
Chinese 21.8 4.2
Filipino 33.0 14.1 Health Behaviors
Asian Indian 34.4 6.0 Physical inactivity is an important risk factor for
Japanese 25.9 8.7 diabetes. NHBs, Native Americans, and Alaska
Vietnamese 19.1 5.3
Natives report less leisure-time physical activity
Korean 27.3 2.8
than NHWs [10]. Mexican American women
Other Asian and 29.2 12.5
Native Hawaiian or
report less leisure-time physical activity than
other Pacific NHW and NHB women [10]. There are sparse
Islander data currently on physical activity in Asian
Golden et al. [1] American populations [4].
14 Diabetes in Native Populations and Underserved Communities in the USA 253
Smoking has also been identified as a risk fac- education, less access to healthcare in NHBs),
tor for diabetes, independent of adiposity. Native racial discrimination, residential segregation,
Americans and Alaska Natives have a higher neighborhood-level poverty, and maternal hyper-
prevalence of smoking than NHWs [10]. NHBs tension [15]. Smaller birth weight is linked to
and NHWs have similar smoking rates, while insulin resistance and diabetes, abdominal pat-
Mexican Americans have significantly lower tern of fat distribution, higher blood pressure,
smoking rates. In Asian Americans there is varia- abnormal lipid profiles, and increased cardiovas-
tion in rates of smoking, with the highest preva- cular disease risk [15]. Studies have also linked
lence among Korean men and the lowest low birth weight with elevated cortisol reactivity
prevalence among Asian Indian men [4]. in childhood and adolescence [15]. And chronic
cortisol exposure can contribute to abdominal
adiposity and insulin resistance [16]. Maternal
Genomic and Epigenetic Landscape psychological stress and fetal overexposure to
of Diabetes cortisol lead to the same metabolic abnormalities
as fetal undernutrition [15].
Results of several genome-wide association stud- Epigenetic changes in the pattern of cellular
ies (GWAS) have linked the following common gene expression may influence how a fetus adapts
gene variants with a 1520% increased risk of to an adverse intrauterine environment which
diabetes: reduced insulin secretion via reduce may increase survival in utero but predispose that
beta-cell mass (CDKAL1, CDKN2A, CDKN2B) individual to enhanced metabolic risk later in life
and beta-cell dysfunction (MTNR1B, TCF7L2, [15]. Further studies are needed to determine
KCNJ11) and increased insulin resistance related how epigenetic changes contribute to the role of
to obesity (FTO) and unrelated to obesity (IRS1, the fetal environment in racial/ethnic differences
PPARG) [11]. While most of the early studies in future risk of obesity and diabetes [17].
focused on individuals of European descent, sev-
eral recent studies have demonstrated that these
susceptibility loci are also present and associated Diagnosis of Diabetes
with increased diabetes risk in ethnic minority and Prediabetes
populations. The limited amount of data in non-
European ancestry populations does not suggest In 2010 the American Diabetes Association
that the genetic architecture of diabetes differs (ADA) updated its clinical practice guidelines to
across race/ethnic groups. Until recently, there include HbA1c criteria for the diagnosis of dia-
were no GWAS analyses in non-European popu- betes and prediabetes. In the context of using
lations; however, several studies have identified HbA1c as a diagnostic criteria in nondiabetic
novel diabetes-associated SNPs in specific race/ individuals, recent studies have suggested that
ethnic groups that are being further evaluated non-glycemic factors may contribute to the
(see Table 14.2). higher HbA1c at similar levels of fasting glucose
Epigenetics represents the interface of envi- seen in NHBs, Hispanic Americans, Asian
ronmental and biological factors and has implica- Americans, and Native Americans, compared to
tions in the predisposition of NHBs to developing NHWs [18]. Suggested factors include variations
diabetes. Low birth weight, fetal undernutrition, in erythrocyte membrane permeability to glu-
and maternal-fetal stress appear to be unique cose, regulation of glucose transport across the
contributors to elevated diabetes and metabolic erythrocyte membrane, glycolytic rates, differ-
risk in NHBs. NHBs have lower birth weight ences in nonenzymatic glycosylation reactions,
than NHWs, which may be related to maternal and deglycation [18].
conditions during pregnancy, including stressful Two recent studies have examined the effect
life events, depressive and anxiety symptoms, glycemia has on HbA1c differences in NHBs
economic inequality (e.g., lower income and and NHWs with diabetes [19, 20]. One study
Table 14.2 Novel GWAS-identified loci associated with type 2 diabetes in non-European populations [1]
New identified
Population SNP Chromosome Associated gene(s) Associated physiological function
South Asians [12] Rs3923113 2 GRB14 Associated with insulin sensitivity
Rs16861329 3 ST6GAL1 Associated with pancreatic beta-cell
function
Rs1802295 10 VPS26A
Rs7178572 15 HMC20A
Rs2028299 15 AP3S2
Rs4812829 20 HNF4A Associated with pancreatic beta-cell
function
East Asians [13]
Loci with strong Rs6815464 4 MAEA
associations Rs7041847 9 GLIS3 Associated with pancreatic beta-cell
development, insulin gene
expression, and glucose
Rs6017317 20 FITM2-R3HDML-
HNF4A
Rs6467136 7 GCC1-PAX4
Rs831581 3 PSMD6
Rs9470794 6 ZFAND3
Rs3786897 19 PEPD
Rs1535500 6 KCNK16 May regulate glucose-independent
insulin secretion in the pancreas
Loci with moderate Rs16955379 16 CMIP
associations Rs17797882 16 WWOX
NHBs [14]
Loci with strong Rs7560163 2 RBM43
associations RND3
Loci with nominal Rs7542900 SLC44A3
associations F3
Rs4659485 2 RYR2
MTR
Rs2722769 11 GALNTL4
LOC729013
Rs7107217 11 TMEM45B
BARX2
Golden et al. [1]
SNP single nucleotide polymorphism
used data from National Health and Nutrition diabetes (compared with NHWs with diabetes) to
Examination Survey III and the Screening for higher fasting glucose and other covariates [20].
Impaired Glucose Tolerance Studies and found In addition, nontraditional glycemic markers,
that NHBs with diabetes had significantly glycated albumin, and fructosamine, which are
higher HbA1c than NHWs with diabetes, which not subject to the effects of erythrocyte turnover
persisted following adjustment for plasma glu- and hemoglobin glycation, were also significantly
cose [19]. A subsequent study, using data from elevated in NHBs with diabetes, compared to
the Atherosclerosis Risk in Communities Study, NHWs with diabetes [20]. Thus, these data sup-
however, came to a different conclusion [20]. This port more hyperglycemia in NHBs with diabe-
study attributed the higher HbA1c in NHBs with tes. As conflicting evidence is evolving about the
contribution of non-glycemic factors to HbA1c criteria for diabetes, recent studies have suggested
levels in minorities with diabetes, caution should that non-glycemic factors may contribute to the
be used in applying HbA1c as the only measure higher HbA1c at similar levels of fasting glu-
to assess diagnosis of prediabetes and/or diabetes. cose seen in NHBs, Hispanic Americans, Asian
Americans, and Native Americans, compared to
NHWs [18]. However, HbA1c is similarly asso-
Diabetes Complications ciated with prevalence and risk of microvascular
and macrovascular complications, and mortality,
Overall, ethnic minorities appear to be dispropor- among NHB and NHWs with diabetes [2527],
tionately affected by microvascular complica- lending credence to true differences in glycemia
tions and mortality associated with diabetes, between the two race/ethnic groups.
likely related to poorer glycemic and cardiovas-
cular disease risk factor control; however, there Cardiovascular Risk Factors
are some notable paradoxes. NHBs with diabetes Hypertension is an important risk factor for dia-
have a lower incidence of cardiovascular disease betic nephropathy/end-stage renal disease
than NHWs with diabetes; however, once they (ESRD) and peripheral arterial disease and likely
have cardiovascular disease, they are more likely contributes to the higher prevalence of these
to die. NHBs have a higher rate of ESRD second- complications in certain ethnic groups. NHBs
ary to diabetic nephropathy but are less likely to have a higher prevalence of hypertension than
die on dialysis than NHWs. NHBs, Native NHWs [10]. Mexican American women have a
Americans and Alaska Natives, and Hispanic higher prevalence of hypertension than NHW
Americans are 2.3, 1.9, and 1.5 times more likely women; however, the prevalence of hypertension
to die from diabetes than NHWs [21]. And while is similar among men in the two race/ethnic
Asian Americans, overall, are 20 % less likely to groups [10]. Native Americans and Alaska
die from diabetes than NHWs, there are varia- Natives have a lower prevalence of hypertension
tions among subgroups, such that Native compared to NHWs and NHBs; however, there
Hawaiians and Filipinos living in Hawaii are 5.7 are regional differences [10]. Studies of blood
and 3.0 times more likely to die from diabetes pressure control and hypertension prevalence
than NHWs living in Hawaii [21]. comparing NHWs to Native Americans and
Asian Americans with diabetes are lacking.
Research to date from clinical trials indicates that
Race/Ethnic Differences in Biological control of reversible risk factors, including hyper-
Factors Contributing tension, is equally effective in lowering the risk
to Complications of nephropathy and cardiovascular disease in
minority and NHW populations [28].
Glycemic Control In a prior systematic review comparing low-
Several systematic reviews and meta-analyses density lipoprotein cholesterol between minority
have shown that ethnic minorities with diabetes populations and NHWs with diabetes, Hispanic
have worse glycemic control than NHWs, which Americans had slightly lower low-density lipo-
likely contributes to the higher risk of micro- protein cholesterol than NHBs and NHWs. In
vascular complications seen in these popula- this review, there were no studies comparing lipid
tions [2224]. The proportion of diabetic ethnic control in NHWs with Native Americans and
minorities with poor glycemic control, defined as Asian Americans with diabetes [29]. While
glycemia above a specific threshold, was signifi- NHBs have lower triglycerides than NHWs [25],
cantly higher among NHBs, Hispanic Americans, which may explain their lower risk of macrovas-
Native Americans, and Asian Americans and cular disease, they generally have a higher preva-
Pacific Islanders [22]. Although discussed more lence of low high-density lipoprotein cholesterol,
in the context of using HbA1c as a diagnostic a strong cardiovascular risk factor [30].
Individual Race/Ethnic Differences relay of information to clinicians, continuous

in Nonbiological Factors (Health QI), healthcare providers (audit and feedback,
Behaviors) Contributing clinician education, clinician reminders, financial
to Complications incentives), or patients (patient education, pro-
motion of self-management, reminder systems)
Self-Monitoring of Blood Glucose (SMBG) [32]. Several prior meta-analyses have exam-
While some studies have shown no differences in ined the impact of these intervention approaches
SMBG by race/ethnicity, several have shown on glycemic control and other metabolic con-
lower rates among NHBs, Hispanic Americans, trol indices in patients with diabetes [3234].
and Asian Americans, compared to NHWs. Two Shojania et al. performed a systematic review and
studies found no difference in SMBG frequency meta-analysis of 58 studies of 66 distinct trials.
in Native Americans compared to NHWs [31]. These studies utilized a median of three quality
There are several barriers to SMBG, including improvement strategies and had a median follow-
inconvenience and intrusiveness, pain, lower up of 13 months. The mean post-intervention
socioeconomic position, education level, social HbA1c difference, compared to pre-intervention,
class, and living in a high poverty area, many of was 0.42 % with greater reductions if baseline
which are disproportionately prevalent in ethnic HbA1c was 8 % [33]. Strategies associated
minority groups [31]. with at least a 0.5 % reduction in HbA1c after
controlling for baseline HbA1c 8 % and study
Physical Activity and Smoking size included team changes (0.67 %) and case
As summarized above, ethnic minorities are less management (0.52 %). In comparative analy-
likely to engage in leisure-time physical activity, ses, interventions that included case manage-
which can contribute to worse glycemic control ment reduced HbA1c significantly more than
and a propensity to developing microvascular interventions that did not include case manage-
complications [10]. ment, and of these types of interventions, the
Native Americans and Alaska Natives have a most effective case management interventions
higher prevalence of smoking that NHWs [10], were those in which the interventionists could
which can contribute to their higher risk of make independent medication changes [33]. This
peripheral arterial disease and amputations. was confirmed in a subsequent meta-analysis of
NHBs and NHWs have similar smoking rates, randomized controlled trials of disease manage-
while Mexican Americans have significantly ment programs improving glycemic control in
lower smoking rates. Therefore, smoking may adults with type 1 and type 2 diabetes [34]. This
not explain ethnic differences in peripheral arte- same study suggested that interventions with
rial disease in these populations. high-frequency patient contact (several times/
month) were more effective than those with low-
frequency contact intervention [34].
Coordination and Delivery of Similarly, interventions that included team
Diabetes Care Services: Health changes reduced HbA1c significantly more than
System Interventions Targeting interventions that did not include team changes,
Minority and Underserved Patients particularly those that included multidisci-
with Poorly Controlled Type 2 plinary, interactive teams [34]. Interventions
Diabetes with team changes remained significant after
controlling for the presence of case management
Evidence-Based General Diabetes [33]. In those studies, adding a new team mem-
Quality Improvement Interventions ber alone was not effective, but rather, adding a
team member with shared care between special-
Quality improvement strategies can target several ists and primary care providers or new team
areashealth systems (case management, team members with an expanded role were most
changes, electronic patient registry, facilitated effective.
A more recent meta-analysis expanded on Table 14.3 Improvement in diabetes-related metabolic

Shojanias prior study by including process out- and process measures in response to patient, provider, and
health system quality improvement interventions in
come measures (proportion taking aspirin, statins, socially disadvantaged populations [35]
and antihypertensives and the proportion screened
# of studies with
for retinopathy, foot abnormalities, and renal dys- Metabolic or process improvement/total # of
function) and additional non-glycemic outcome measure studies examining measure
measures (LDL cholesterol, blood pressure, and HbA1c 8/13
proportion with controlled hypertension or quit- Weight/body mass index 2/9
ting smoking) to evaluate the additional impact Lipids 2/7
of multicomponent diabetes quality improvement Blood pressure 2/4
interventions [32]. Overall, interventions resulted Adherence to annual eye 3/3
in lower HbA1c, LDL cholesterol, and blood exam
pressure in those receiving compared to those Achievement of ADA 2/3
care indicators
not receiving the interventions [32]. These strat-
Adherence to exercise 1/3
egies also improved the likelihood that patients recommendations
received aspirin therapy, antihypertensives, and Improved diabetes 2/2
screening for diabetic complications. Statin use, knowledge
blood pressure control, and smoking cessation Improved physician trust 1/1
were unchanged. For patients with HbA1c 8 %
intervention strategies that lower HbA1c 0.5 %
Table 14.4 Summary of components of successful dia-
included team changes, case management, patient
betes quality improvement interventions in socially disad-
education, and promotion of self-management; vantaged populations
however, for patients with HbA1c < 8 %, facili-
Intervention
tated relay was more effective in lowering level Successful components
HbA1c 0.5 % [32]. The only intervention strat- Patient Interpersonal
egy that was not effective in lowering HbA1c was Utilize social networks
clinician education [32]. These data suggest that Culturally tailored
greater improvements in HbA1c can be achieved Provider In-person feedback (compared to
utilizing QI intervention strategies that target the computerized decision support)
healthcare system and patients. Health system Utilize on-site nurse case managers
Utilize community health workers
Provide medical assistance programs
Diabetes Quality Improvement for prescriptions
Interventions Among Underserved
and Minority Populations interventions with individualized assessment/
reassessment; incorporation of treatment algo-
Glazier et al. conducted a systematic review of 17 rithms, focusing on behavior-related tasks and
studies examining the effectiveness of patient, providing feedback; and high intensity interven-
provider, and health system interventions among tions over a long duration [35]. With one excep-
patients with type 1 or type 2 diabetes in socially tion, interventions targeting racial/ethnic
disadvantaged populations, defined as those of minorities specifically did not involve endocrinol-
low socioeconomic status, or belonging to an eth- ogy subspecialty input on the care team. One
nic/racial minority group [35]. Eight of 13 stud- study of NHBs and Latinos involved nurse imple-
ies showed improvements in HbA1c but less mentation of a detailed protocol and algorithm
impact on body weight, lipids, and blood pres- with endocrinologist supervision which resulted
sure (see Table 14.3). in a significant 3.5 % reduction in HbA1c and
Features of effective interventions included improvement in 8/10 ADA process measures [36].
cultural and health literacy tailoring, led by com- Components of successful interventions from this
munity educators or lay people; 1:1 (versus group) review are summarized in Table 14.4.
Interventions specifically targeting NHBs and Patient Interventions

Latino Americans with diabetes were recently Within Healthcare Organization
summarized in two systematic reviews and meta- In Peeks review of 17 studies of patient interven-
analyses [37, 38]. Table 14.5 below summarizes tions within the healthcare organization that
the types of interventions employed in these stud- sought to improve dietary habits, physical activ-
ies and the effect on process measures and clini- ity, and self-management activities, those that
cal outcomes. were culturally tailored were more effective in
Table 14.5 Quality improvement intervention components in studies of predominantly minority populations
Intervention target(s) Intervention component(s) Summary of outcomes
General patient level interventions
Basch (1999) [39] (100 % Education and counseling Receipt of dilated eye exam
NHB)
Clancy (2003) [40] (78 % Education and stress management Improvement in testing of HbA1c, LDL,
NHB) (MD and RN group visits) microalbumin; use of ACE inhibitors, ASA,
statins, vaccinations, and eye and foot exams
Increased physician trust
Gerber (2005) [41] (66 % Computer training on skills and No significant change in HbA1c, BP, weight,
Latino, 29 % NHB) self-management support in knowledge, self-efficacy
waiting room kiosk
Erdman (2002) [42] (91 % Self-management, lifestyle HbA1c, total cholesterol, LDL (due to
NHB) counseling statins)
HDL
Ziemer (2003) [43] Diet counseling HbA1c
(90 % NHB)
Anderson (2003) [44] (100 % Patient reminders to schedule eye Returning for annual diabetes retinal exam
NHB) exam
DEramo-Melkus (2004) [45] Culturally tailored CBT and HbA1c, weight, BMI, diabetes-related
(100 % NHB) monthly nurse practitioner visits emotional distress
Tang (2005) [46] (100 % NHB) Patient-centered DSME BMI, dyslipidemia
Improved self-management behaviors,
quality of life, difficulty with diet, difficulty
with exercise
Amoak (2008) [47] (100 % Phone calls focusing on aspects Improved psychological adjustment and
NHB) of experience with diabetes exercise
administered by geriatric NP
Skelly (2009) [48] (100 % Teaching and counseling modules No change
NHB) delivered by RN in patients
home
Tang (2010) [49] (100 % NHB) DSME groups HbA1c, BMI, dyslipidemia
Walker (2010) [50] (100 % Educational sessions with patient Improved diabetes knowledge
NHB) navigator follow-up
Carter (2011) [51] (100 % Online DSM Weight, BMI, HbA1c
NHB) Improved diabetes knowledge, diabetes
management practices, physical health status,
mental health status
Ellish (2011) [52] (100 % Eye exam newsletter No change
NHB)
Tang (2012) [53] (100 % NHB) Empowerment-based DSM Blood pressure, serum cholesterol
support Improved self-management behaviors,
quality of life

Culturally tailored patient level interventions
Agurs-Collins (1997) [54] Dieticians and medical staff HbA1c, weight, blood pressure
(100 % NHB) support for weight loss
Anderson-Loftin (2005) [55] Nutrition counseling by RN and BMI, improved food habits
(100 % NHB) DM educator
Brown and Hanis (1999), DSM education and support HbA1c
Brown (2002) [56, 57] (>90 % group by bilingual Mexican
Mexican American) American nurses, dietitians, and
CHWs
Brown (2005) [58] (100 % Extended DSM education No difference in HbA1c
Mexican American) support/education (vs.
compressed education/support)
Corkery (1997) [59] (75 % Diabetes education via bicultural Better program completion rate
Puerto Rican; 25 % other CHWs and diabetes RN educator No difference in knowledge, behaviors, or
Latinos) (vs. diabetes RN educator) HbA1c
Keyserling (2002) [60] (100 % CHW/peer Physical activity and diabetes knowledge
NHB) counselors + nutritionist
Mayer-Davis (2001, 2004) [61, Diet and physical activity Weight, BMI, fasting blood glucose (2001)
62] (82 %NHB) intervention
McNabb (1993) (100 % NHB) Diet and exercise education Weight
[63]
Rosal (2005) [64] (80 % Puerto Diet, physical activity, DSME HbA1c
Rican low-income, Spanish education led by DM nurse, Non-sustained depressive symptoms
speaking) nutritionist, and CHW
No change in physical activity
Self-monitoring
Two Feathers (2005) [65] (64 % CHW lifestyle interventions Improved dietary knowledge and behaviors
NHB; 36 % Latino) and physical activity knowledge
HbA1c
Vazquez (1998) [66] (100 % Nutrition program with Caloric, total fat, total saturated fat, total
Caribbean American Latinos) nutritionists and psychologists energy intake
Carbohydrate intake
Anderson (2005) [67] (100 % Self-management experiments, HbA1c, serum cholesterol, LDL,
NHB) problem-solving, discussing triglycerides, weight
emotional experience living with HDL, SMBG
diabetes delivered by RN and
Improved perceived understanding of
dietician
diabetes, diabetes empowerment, attitudes
toward seriousness of diabetes, positive
attitudes
Murrok (2009) [68] (100 % Dance classes choreographed to Body fat and blood pressure
NHB) gospel music
Bogner (2010) [69] (100 % Individualized program to improve HbA1c
NHB) adherence to oral hypoglycemic
Improved adherence to oral hypoglycemics
and |antidepressants (recognizing
social and cultural context)
DEramo (2010) [70] (100 % Culturally relevant group DSME HbA1c, blood pressure, dyslipidemia
NHB) training, coping skills training, Improved quality of life, vitality, role
and diabetes care intervention physical, bodily pain, perceived provider
support for diet, exercise, diabetes-related
emotional distress
(continued)

Hill-Briggs (2011) [71] (100 % Problem-based DSM training HbA1c
NHB) Improved knowledge, problem-solving,
self-management behavior
Provider level interventions
Benjamin (1999) [72] (40 % Provide based learning methods Improvement in annual eye and
NHB, 36 % Latino) to increase MD use of practice microalbumin exams
guidelines Trends of improvements in annual lipids,
influenza vaccines, and diet/diabetes education
HbA1c
Din-Dzietham (2004) [73] CME and guideline distribution Positive change in prevalence in selected
(100 % NHB) (continuous QI program targeting patterns of care
providers)
Fox and Mahoney (1998) [74] Chart audit and feedback Improvement in HbA1c, self-management
(100 % NHB) behavior, eye exams, and vaccinations
Phillips (2002, 2005) [75, 76] Computerized decision-support HbA1c
(100 % NHB) reminders, bimonthly in-person
individualized feedback
Thaler (1999) [77] (100 % Rapid turnaround HbA1c in one Fasting or random plasma glucose
NHB) group; both groups seen by nurse Frequency of therapy intensification by
practitioner and endocrinologist treatment modality
Ziemer (2006) [78] (100 % Computerized reminders to Improvement in medication titration by
NHB) intensify medications, reminders providers; therapy intensification associated
with HbA1c
Health system
Bray and Thompson (2005), RN case management, DM HbA1c
Bray and Roupe (2005) [79, registry, visit reminders
80] (72 % NHB)
Davidson (2003) [36] (86 % RN-directed care with treatment Improved HbA1c, lipid, annual eye exams,
Latino) algorithms renal tests, foot exams, education, diet
counseling
HbA1c
Fanning (2004) [81] (100 % RN case management (university HbA1c, LDL, blood pressure
NHB) and community settings)
Gary (2004) [82] (100 % NHB) RN case management, CHW Blood pressure, lipid profile
Hopper (1984) [83] (75 % Home health aide Fasting blood sugar (among those offered
NHB) aides)
Eye clinic visits among those who accepted
aides
Hosler (2002) [84] (45 % NHB, Evidence-based guidelines, Improved assessment of HbA1c, lipids, eye
25 % Latino, 7 % Native multidisciplinary DM team, exam, and SMBG, exercise, and diet
American) minority outreach, community assessment
partnerships (CHWs, patient
incentives)
Jaber (1996) [85] (100 % NHB) Pharmacist-led education HbA1c and fasting glucose
Miller (2003) [86] (100 % Rapid turnaround HbA1c HbA1c
NHB) Frequency of pharmacological diabetes
therapy

Philis-Tsimikas (2004) [87] RN case management with 100 % compliance with ADA standards for
(72 % Latino) treatment algorithms + CHW performing HbA1c, lipids, foot exams, and
urine microalbumin
HbA1c, cholesterol, blood pressure
Improved DM knowledge and self-efficacy
Multi-target interventions (patients and healthcare system)
Cook (1999) [88] (88 % NHB) Patient education, nurse case HbA1c
management, multidisciplinary BMI
diabetes team (including
endocrinologist), treatment
algorithms
Anderson-Loftin (2002) [55] Culturally competent, dietary HbA1c, fasting blood glucose, frequency of
(100 % NHB) self-management intervention acute care visits
with dietician and nurse case Improved dietary habits
manager
Bray and Thompson (2005) RN case management (APN) with HbA1c

[79] (100 % NHB) supervising physician (unclear if
endocrinologist), DM registry,
visit reminders, patient education
and self-management support,
provider decision-support tools
Mahotiere (2006) [89] (100 % Provider QI interventions focused proportion of beneficiaries with diabetes
NHB) on system changes surrounding receiving biennial lipid profile
the physician visit combined with
patient interventions
Gary (2009) [90] (100 % NHB) Nurse case management and ED visits and blood pressure
CHW using evidence-based HDL
clinical algorithms with feedback
to PCPs
Rith-Najarian (1998) [91] Podiatric screening and patient Amputations
(100 % NHB) education, provider guidelines,
multidisciplinary team, DM
registry and tracking system, flow
sheets
lowering HbA1c than general QI interventions self-management [38]. In a meta-analysis of

(0.69 % versus 0.1 %) [37]. Also, peer support eight studies, interventions resulted in a signifi-
and 1:1 interventions were more effective than cant 0.83 % reduction in HbA1c [38].
online and computer-based approaches. In a sys-
tematic review and meta-analysis looking exclu- Provider Interventions
sively at randomized controlled trials of patient In Peeks review, provider interventions includ-
interventions targeting NHBs, most of which ing education, continuing medical education,
were culturally adapted and included peer pro- computerized decision support, in-person feed-
viders, two of 22 increased patient attendance at back, and problem-based learning improved
screening visits, and 20 of 22 promoted diabetes process measures [37]. The majority of these
studies were conducted in NHBs with diabetes. feedback to primary care physicians [90]. Finally,
Interventions involving computerized decision- one study focusing exclusively on Native
support reminders and chart audit and individu- Americans in the Indian Health Service included
als feedback resulted in improved HbA1c and provider guidelines, a multidisciplinary team,
treatment modification [7476, 92]. diabetes registry/tracking system, and flow sheets
[91]. Compared to podiatric screening and patient
Healthcare Organization Interventions education, the multi-target intervention resulted
Healthcare organization interventions in minor- in a significant reduction in amputation rate [91].
ity populations have included systems for rapid
turnaround HbA1c, circumscribed appointments,
support staff (e.g., nurse case management, com- Non-pharmacological Management
munity health worker, pharmacist), and increased of Diabetes in Minority
follow-up through home visits or telephone/ and Underserved Populations
mail contact [37, 38]. In Peeks review, 14 stud-
ies with interventions targeting the healthcare Lifestyle intervention is the mainstay of non-
organization resulted in a mean HbA1c reduc- pharmacological management of diabetes. The
tion of 0.34 %. Ricci-Cabello et al. included five American Diabetes Association recommends ini-
healthcare system intervention trials in NHBs in tial management of diabetes with 6 months of
their systematic review and meta-analysis and diabetes self-management education (DSME) to
found the two most highly effective interventions support lifestyle modifications to achieve modest
in improving HbA1c, and frequency of therapy weight loss. The physical activity and dietary
intensification included rapid turnaround HbA1c recommendations are >150 min of moderate-
[77, 86]. intensity physical activity, and medical nutrition
therapy emphasizing a variety of nutrient-dense
Multi-target Interventions foods in appropriate portion sizes focused on
Multi-target interventions target all aspects and reduced energy intake for individuals with a BMI
components of healthcare delivery, including 25 kg/m2 with proper macronutrient distribu-
patients, providers, and the healthcare system. tion [93]. In addition to physical activity and
Five of these studies have targeted NHBs with dietary management, novel factors for diabetes
diabetes and used various approaches. Three management have emerged including dietary pat-
studies showed an improvement in HbA1c [55, terns, dietary composition, intensity of physical
79, 88]. All of these interventions included activity, and weight loss with both nonsurgical
patient education and self-management support and surgical approaches.
and nurse case management, two included
treatment algorithms [79, 88], and two involved
collaboration with a physician in treatment deci- Dietary Patterns
sions (one an endocrinologist [88] and one an
unspecified physician [79]). While two additional Mediterranean Diet
multi-target interventions showed improvement The largest analysis of the Mediterranean diet
in process measures and non-glycemic clinical was the Prevention with Mediterranean Diet
outcomes [89, 90], they did not improve glyce- (PREDIMED) study. The trial enrolled 7,447
mic control. One study involved patient interven- persons in Spain at high cardiovascular risk with
tions and provider-focused QI interventions either diabetes or three cardiovascular risk fac-
focusing on system changes surrounding the phy- tors. Participants were randomized to one of
sician visit [89] and the other involved nurse case three diets: a Mediterranean diet supplemented
management and community health workers with extra-virgin olive oil, a Mediterranean diet
using evidence-based clinical algorithms with supplemented with mixed nuts, or a control diet
(advise to reduce dietary fat) and were followed [100]. These findings lend credence to improved
for 4.8 years for the development of the pri- glucose metabolism with vegetarian dietary pat-
mary end point of major cardiovascular events. terns. In individuals with diabetes, a small (n = 99)
Mediterranean diet with extra-virgin olive oil multiethnic (NHW 44 %, NHB 44 %, Hispanic
and Mediterranean diet with nuts were associated American 4 %, and Asian American 8 %) clinical
with 30 and 28 % reductions in major cardiovas- trial of a low-fat vegan diet or American Diabetes
cular events [94]. Among participants with dia- Association diet for 72 weeks revealed greater
betes in the Mediterranean diet groups compared reductions in HbA1c and cardiovascular risk fac-
to control, there was a 29 % reduction in major tors in the low-fat vegan group [101].
cardiovascular events. The Mediterranean diet
also reduces HbA1c. In 215 overweight Italian DASH Diet
individuals with newly diagnosed diabetes, The Dietary Approaches to Stop Hypertension
Mediterranean diet vs. low-fat diet was associ- (DASH) diet encourages the intake of fruits, veg-
ated with a 0.6 % and 0.4 % lower HbA1c at 1 etables, whole grains, and low-fat dairy products
and 4 years, respectively, with a 37 % reduction in combination with sodium restriction [102].
in antidiabetic medication use [95]. In 259 Israeli The DASH diet was initially studied in a multi-
participants, a low-carbohydrate Mediterranean ethnic trial with 65 % ethnic minorities (35 %
diet versus a traditional Mediterranean diet or NHW, 60 % NHB, 5 % other minority groups)
American Diabetes Association diet was associ- and significantly lowered blood pressure among
ated with greater reductions in HbA1c and cardio- all participants with twofold greater reductions
vascular risk factors [96]. Notably, the majority among racial/ethnic minorities [102]. Further
of the improved glucometabolic findings with studies revealed that components of the DASH
the Mediterranean diet remained significant diet may also improve insulin sensitivity [103].
with adjustment for weight loss. Although, the The DASH diet is recommended for all
Mediterranean diet has not been assessed in a Americans including those with diabetes [93].
clinical trial among US ethnic minorities, obser-
vational findings in the Multiethnic Study of
Atherosclerosis (MESA) (42 % white (NHW), Dietary Composition
12 % Chinese American (CA), 26 % NHB, 21 %
Hispanic American) reveal that participants with Glycemic Index/Glycemic Load
greater adherence to a Mediterranean dietary pat-
tern had lower insulin and glucose independent Carbohydrates are the chief dietary component
of racial/ethnic group [97]. These results suggest influencing insulin secretion and postprandial
a likely beneficial effect of the Mediterranean glycemia [104]. The glycemic index measures
diet on improved glucose metabolism among US the effect of carbohydrates on postprandial blood
racial/ethnic minorities with diabetes, although glucose, and the glycemic load takes into account
intervention trials in these populations are needed. the glycemic index and the amount of carbohy-
drate consumed. Several studies with multiethnic
Vegetarian Diet participants using low-glycemic index eating pat-
The Adventist Health Study 2 assessed the role terns have demonstrated HbA1c decreases (0.2
of vegan and vegetarian diets in the USA. Among 0.5 %), but these are not unanimous [105]. One
73,308 NHB and NHW participants with no his- difficulty is that fiber intake was not consistently
tory of cancer or cardiovascular disease, there controlled, thereby causing difficulty in interpre-
was a 12 % reduction in all-cause mortality over tation. Results of low-glycemic index/glycemic
5.8 years [98], 3050 % lower diabetes preva- load diets on cardiovascular disease risk factors
lence [99], and 4060 % lower diabetes incidence including low-density lipoprotein and total cho-
in the vegetarian versus non-vegetarian groups lesterol are mixed [105].
Low-Carbohydrate/Low-Fat Dietary [110]. Clinical trials have provided strong evi-

Approaches dence for the HbA1c lowering value of resistance
training in NHW older adults with type 2 diabe-
Low-carbohydrate versus low-fat diets have been tes [111]. There are limited data on glycemia in
extensively examined in diabetes management. A response to exercise in NHB, Hispanic
2012 meta-analysis of 23 clinical trials of low- Americans, and Native Americans with diabetes.
carbohydrate versus low-fat diets including stud- Among individuals without diabetes in the
ies of participants with and without diabetes HERITAGE Family Study, a 20-week trial of
revealed that both diets reduced glucose in a sim- thrice weekly exercise in NHB and NHW, NHB
ilar manner [106]. We will focus on data from had a greater increase in fasting glucose with
two recent low-carbohydrate versus low-fat diet exercise compared to NHW, although there were
trials in overweight or obese patients with diabe- reductions in fasting insulin in both groups [112].
tes. First, a 12-month multiethnic trial (59 % A multiethnic (52.7 NHW, 43.5 % NHB, 3.8 %
NHB, 3 % Hispanic American, 38 % NHW) of Hispanic American) randomized clinical trial
obese (BMI 35 kg/m2) adults was randomized examining the effect of aerobic exercise, resis-
to low-carbohydrate (LC) (<30 g/day) or a tance training or combined aerobic exercise, and
calorie-restricted low-fat diet (LF) (500 calorie resistance training on HbA1c levels in 221 par-
reduction with <30 % calories from fat). Among ticipants with diabetes found that aerobic exer-
54 participants with diabetes, HbA1c decreased cise alone or resistance training alone had no
by 0.7 % in the LC group versus 0.1 % in the LF effect on HbA1c, only the combined group
group (p = 0.02) with no significant weight-loss revealed significant reductions in HbA1c
differences [107]. Second, a 12-month multieth- (0.34 %, p = 0.03) and improvements in cardio-
nic trial (64 % NHB, 16 % Hispanic American, respiratory fitness over 9 months [113]. They
15 % NHW, and 3 % Asian) of 105 overweight lacked the power to examine racial/ethnic differ-
participants with diabetes randomized to a LC ences. Potential components of improved glucose
versus LF diet revealed no significant difference metabolism with physical activity are skeletal
in weight (3.4 %) or HbA1c change (0.02 % muscle mitochondrial mass, mitochondrial func-
LC versus 0.24 % LF, nonsignificant) [108]. A tion, and aerobic capacity [114, 115]. The racial/
major strength of these studies is the inclusion of ethnic differences of aerobic capacity with physi-
ethnic minorities, but a weakness is the inability cal activity were tested in a 6-month trial of aero-
to stratify by race due to power limitations, so it bic exercise training in NHB and NHW
is unclear whether there are racial/ethnic differ- postmenopausal women. The NHW women had
ences. Based on these studies, the potentially a greater increase in cardiorespiratory fitness
greater HbA1c reduction with LC vs. LF diets with sustained resting metabolic rate, whereas in
appears to be independent of weight loss. NHB women, resting metabolic rate declined
over the course of the trial, suggesting a perturba-
Physical Activity and Exercise tion in mitochondrial function [116, 117]. A
Exercise interventions improve glycemic control study of exercise capacity and all-cause mortality
in diabetes in majority of NHW studies [109]. A in NHB and NHW men with diabetes found that
meta-analysis examining the effects of exercise exercise capacity is a stronger and more graded
interventions (mean 3.4 sessions/week with predictor of mortality for NHW than for NHB
49 min/session) on glycemic control in individu- men [118]. The high-fit compared to low-fit
als with diabetes revealed mean HbA1c reduction NHW and NHB men had a 67 % and 46 % reduc-
of 0.66 % (p < 0.001) in people with diabetes, tion in mortality risk, respectively [118]. These
even with no significant change in BMI [109]. studies reveal that there is a benefit to physical
Higher levels of exercise intensity are associated activity in US racial/ethnic minorities, but the
with greater improvements in HbA1c and fitness type (aerobic vs. resistance) and intensity of the
physical activity need to be further characterized. (control group) and followed a median of
A recent meta-analysis of step counters to 9.6 years for the development of the primary out-
improve physical activity and HbA1c in individu- come of a composite of death from cardiovascu-
als with diabetes underscores this point. Data lar causes, nonfatal myocardial infarction,
from 11 randomized clinical trials using step nonfatal stroke, or hospitalization for angina.
counters (pedometers) revealed that step counter They found no association between the lifestyle
use is associated with a significant increase in intervention and primary outcome (HR: 0.95,
physical activity (1,822 steps/day), but no change p = 0.51). Notably, the hazard ratios for Hispanic
in HbA1c [119]. Americans, NHBs, NHWs, and Native Americans
were 0.66 (95 % CI: 0.411.05), 1.34 (95 % CI:
Weight Reduction: Bariatric Surgery/ 0.911.96), 0.94 (95 % CI: 0.801.11), and 0.74
Lifestyle Interventions (95 % CI: 0.311.76), suggesting possible vari-
Elevated body mass index and adiposity are the ance by race/ethnicity, especially for Hispanic
most important predictors of diabetes [120122]. Americans (HA) compared to NHBs. The authors
Obesity is also an independent predictor of clini- and others note that differences in rates of cardio-
cal cardiovascular disease [123125]. Mortality protective medication use and power issues due
for diabetes, myocardial infarction, and stroke to lower than expected cardiovascular disease
was similar for each of these conditions, but event rates may account for the null finding.
when any two are combined, the risk is multipli- There was also a suggestion of heterogeneity of
cative [126], reinforcing the importance of response to intervention based on the history of
improving weight in individuals with elevated cardiovascular disease at baseline (p = 0.06).
weight. The underlying relationship between There were a number of positive outcomes of the
obesity, cardiovascular disease, and diabetes has study including reduced hepatic steatosis, body
been reviewed and is potentially mediated weight, healthcare costs, and microvascular out-
through the adipokines released from visceral fat comes including diabetic nephropathy and reti-
[127130]. In this section we will review the data nopathy, as well as increased physical fitness,
on nonsurgical and surgical interventions to pro- physical function, glucose control, and quality of
mote weight loss in diabetes and improve glyce- life [132134]. Given the benefit in these second-
mia with the goal of long-term reduction in ary outcomes from a diabetes management per-
morbidity and mortality. spective, there are many important reasons to
encourage overweight and obese individuals with
diabetes to enroll in a lifestyle intervention pro-
Lifestyle, Diet, and Behavioral gram with the goal of weight loss [134].
Interventions In a multiethnic (59 % NHB, 32 % NHW, 2 %
Hispanic American) randomized comparison of a
The largest analysis of a lifestyle intervention in commercially available portion-controlled
individuals with diabetes was Look AHEAD weight-loss intervention with a diabetes self-
[131], a multiethnic (63 % NHW, 16 % NHB, management education program, the portion-
13 % Hispanic American, 5 % Native American, controlled group lost greater weight (7.3 kg vs.
1 % Asian or Pacific Islander, and 2 % other 2.2 kg) with a larger reduction in HbA1c (0.7 %
minorities) randomized controlled lifestyle inter- vs. 0.4 %) [135]. Finally, a recent systematic
vention trial with 5,145 overweight or obese par- review and network meta-analysis of 33 studies
ticipants. Participants were randomized to either (4,774 participants) evaluating behavioral pro-
intensive lifestyle intervention that promoted grams in diabetes management revealed that in
weight loss through decreased caloric intake and comparison with usual care among ethnic minor-
increased physical activity (intervention group) ity participants, behavioral programs lowered
or received diabetes support and education HbA1c by 0.42 % compared to usual care [136].
Surgical Interventions STAMPEDE are also seen in other studies of

LVSG and RYGB at a rate of 715 % per year
Bariatric Surgery for Individuals [137]. Given the current popularity of LVSG,
with BMI 35 kg/m2 longer-term comparative effectiveness data on
Bariatric surgery procedures are associated LVSG are needed. However, bariatric surgery
with diabetes remission due to hormonal experts believe the effect of LVSG on weight
changes and weight loss [137]. Hormonal loss and comorbidity improvements seems to be
changes include reduction in ghrelin and somewhere between those of RYGB and LAGB
increases in glucagon-like peptide-1 (GLP-1) [151]. Five-year outcomes from RYGB among
and glucose-dependent insulinotropic peptide mostly NHW participants found that shorter
(GIP). Lower levels of ghrelin postsurgically diabetes duration, lower HbA1c, younger age,
decrease appetite stimulation through a decrease higher serum insulin levels, and nonuse of
in stimulation of orexigenic neurons neuropep- insulin were associated with higher remission
tide Y/agouti-related peptide. Postsurgically rates [152].
levels of glucagon-like peptide-1 and glucose-
dependent insulinotropic peptide increase exert- Bariatric Surgery for Individuals
ing effects on the enteroinsular axis with potent with BMI <35 kg/m2
insulinotropic activity. The long-term weight Controversy exists regarding bariatric surgery for
loss occurs due to decreased food (energy) con- treatment of diabetes with BMI <35 kg/m2. There
sumption caused by the reduction in appetite are limited data to assess the benefit of bariatric
and anatomical constraints. The surgical proce- surgery for individuals with BMI 3035 kg/m2.
dures currently performed include laparoscopic Short-term data from the STAMPEDE trial in the
adjustable gastric banding (LAGB), laparo- 36 % of the participants having a BMI <35 kg/m2
scopic vertical sleeve gastrectomy (LVSG), revealed similar benefits as participants with
Roux-en-Y gastric bypass (RYGB), biliopan- BMI 35 kg/m2 [143], and two systematic
creatic diversion, and biliopancreatic diversion reviews draw similar conclusions [153, 154], but
with duodenal switch (Fig. 14.1). In the USA, there remain no high-quality longer-term data on
RYGB was the most commonly performed pro- remission rates and complications. Thus, the cur-
cedure but with wide adoption of LVSG; LVSG rent ADA guidelines do not recommend bariatric
has surpassed RYGB and is performed in one surgery treatment for individuals with diabetes
half of bariatric surgical procedures [139]. The and BMI <35 kg/m2 [155]. The complication
type of procedure is important for individuals rates are important including near-term (30-day)
with diabetes as diabetes remission varies and longer-term mortality rates which vary
greatly across procedures. Meta-analyses and depending on procedure, center, and surgical
reviews report remission rates of 48 % (29 expertise. Morbidities of bariatric surgery includ-
67 %) for LAGB, 84 % (7790 %) for RYGB, ing vitamin deficiencies, mineral deficiencies,
72 % (5588 %) for LVSG, and 99 % (97 and post-bariatric surgery hypoglycemia second-
100 %) for biliopancreatic diversion with duo- ary to insulin hypersecretion require long-term
denal switch [140, 141]. Recent analysis of the management [156]. Further understanding of
two most popular procedures have shown dia- non-trial-based 1-year complication rates (mor-
betes remission rates ranging from 27 to 75 % bidity and mortality) are important as part of the
for LVSG versus 4293 % for RYGB [142]. In risk/benefit criteria for all individuals with diabe-
the STAMPEDE trial, diabetes remission rates tes regardless of BMI.
at 1 and 3 years of follow-up were 12 and 5 %
with intensive medical therapy alone, 42 and Morbidity and Mortality
38 % in RYGB group, and 37 and 24 % in the While glycemia is important in diabetes, the goal
LVSG group (Table 14.6). The diminishing in diabetes management is to maximize longevity
rates of diabetes remission over time noted in and quality of life. This involves control of
Gastric Volume Reduction Procedures
a Gastric Band Lower esophageal Sleeve b

sphincter Gastrectomy
Stomach
Pylorus Sleeve
pouch
Resected
Pylorus stomach
Gastric Volume Reduction and

Malabsorptive Procedures
Stomach Lower esophageal
pouch sphincter Stomach pouch
Gastrojejunal
anastomosis Gastroileal
Pylorus anastomosis
Biliopancreatic
limb
Roux limb Alimentary
Duodenum limb
Biliopancreatic Jejunojejunal
limb anastomosis
Ileoileal
anastomosis
Common
channel
Roux-en-Y Cecum Biliopancreatic
c d
Gastric Bypass diversion
Fig. 14.1 Anatomic modifications as created in the four angle of His. (c) The Roux-en-Y gastric bypass involves
most common bariatric surgery procedures. (a) Gastric creation of a 15- to 20-mL gastric pouch, a 150-cm Roux
banding involves placement of an adjustable gastric band limb, and a 50-cm biliopancreatic limb. (d) The biliopan-
around the proximal part of the stomach. The band is fixed creatic diversion procedure includes a distal gastrectomy
in position by inserting plication sutures anteriorly. The with long Roux-en-Y reconstruction, where the enteroen-
band can be adjusted/tightened over time by injecting terostomy is placed 50 cm proximal to the ileocecal
fluid into the subcutaneous port connected to the band. (b) valve. Both the volume of the gastric remnant and the
Sleeve gastrectomy involves reducing gastric volume by length of the alimentary limb can be modified to suit the
7580 % by resecting the stomach alongside a 30 F endo- patients weight loss goal (Vest et al. [138])
scope beginning 3 cm from the pylorus and ending at the
glycemia, but also cardiovascular risk factors treatment (ILMT) plus RYGB versus ILMT
with a focus on blood pressure and lipids. In the alone had a twofold greater achievement of the
multiethnic Diabetes Surgery Substudy, partici- primary composite outcome of HbA1C <7 %,
pants randomized to intensive lifestyle medical LDL <100 mg/dl, and systolic BP <130 mmHg at
Table 14.6 Glycemia, diabetes remission, cardiovascular risk factors, and cardiovascular events in diabetes bariatric
surgery studies
Publication Population characteristics/ Summary of primary
year Study/site/size ethnicity Study design/interventions findings
2012, 2014 STAMPEDE Uncontrolled type 2 Randomized in a The primary end point at
trial [143, 144] diabetes (HbA1c 9.7 %) non-blinded fashion to years 1 and 3 was reached
and moderate obesity intensive medical therapy in 12 and 5 % IMT alone
(BMI 36.6 kg/m2 (IMT) alone, IMT plus group (HbA1c 7.5 and
(2743 kg/m2)) with a Roux-en-Y gastric bypass 8.4 %) vs. 42 and 38 % in
diabetes duration of (RYGB) or IMT plus gastric bypass group
8.5 years laporoscopic vertical (HbA1c 6.4 and 6.7 %)
USA 74 % NHW sleeve gastrectomy and 37 and 24 % in the
(LVSG) and followed for LVSG group (HbA1c 6.6
150 and 137
a primary end point of and 7.0 %)
participants
HbA1C <6 %
(years 1 and 3)
2013 STAMPEDE Subset of participants Evaluated at 1 and 2 years At 2 years, HbA1c was
trial substudy with a diabetes duration for assessment of 8.4 % for IMT vs. 6.7 %
[145] of 8.4 years and BMI beta-cell function for RYGB and 7.1 % for
36 kg/m2 (mixed-meal tolerance LVSG with greater
USA 72 % NHW testing) and body insulin sensitivity,
composition beta-cell function, and
60 participants
reduction in truncal fat
in the RYGB group,
but not in the LVSG
group
2012 Prospective Secondary outcome: RYGB surgery (n = 88) Diabetes remission rates
Utah Obesity BMI 35 kg/m2 and at years 2 and 6 were 75
Study [146] diabetes (FBG <126 mg/ and 62 % in RYGB and 7
dl, HbA1c <6.5 % and no and 8 % in control group
use of antidiabetic 1, and 6 and 6 % in
medication) control group 2. Of note,
USA 96 % NHW Control group 1 (n = 93): 13 % of participants in
sought but did not have control groups underwent
269
surgery Control group 2 bariatric surgery over the
participants
(n = 88): randomly 6 years of follow-up
selected from a
population-based sample
not seeking weight-loss
surgery. Diabetes
remission: FBG <126 mg/
dl, HbA1c <6.5 %, and no
use of antidiabetic
medication
2013 The BMI 35 kg/m2 Observational cohort Among participants who
Longitudinal study assessing RYGB had diabetes at baseline,
Assessment of or laparoscopic adjustable 216 RYGB participants
Bariatric gastric banding (LAGB) (67.5 %) and 28 LAGB
Surgery at 3 years for weight loss participants (28.6 %)
(LABS) [147] and diabetes remission experienced remission at
USA NHW: 86 % Diabetes remission: 3 years
774 NHB: 11 % FBG <126 mg/dL or
participants Hispanic American: 5 % HbA1c <6.5 % both
(33 % of total without use of
cohort) antidiabetic medication

Publication Population characteristics/ Summary of primary
year Study/site/size ethnicity Study design/interventions findings
2014 Courcoulas Diabetes and BMI Participants were Partial and complete
et al. (2014) 3040 kg/m2 randomized to RYGB remission of diabetes
[148] (n = 24), LAGB (n = 22), were 50 % and 17 %,
or lifestyle weight-loss respectively, in the RYGB
program groups (LWLI) group and 27 % and 23 %,
(n = 22) respectively, in the LAGB
USA NHB: Partial diabetes group (P < .001 and
remission: subdiabetic P = .047 between groups
hyperglycemia (HbA1c for partial and complete
<6.5 % and fasting remission), with no
glucose 100125 mg/dl remission in the LWLI
with no antidiabetic group. Significant
medications reductions in use of
antidiabetic medications
69 participants 33 % RYGB Complete diabetes
occurred in both surgical
14 % LAGB remission: normal HbA1c
groups
and FBG with no
17 % LWLI
antidiabetic medications
Diabetes duration:
RYGB: 7.4 years
LAGB: 6.1 years
LWLI: 5.7 years
2015 Ng et al. 593 patients with Retrospective analysis of NHB patients showed less
(2015) [149] diabetes weight change and % expected weight loss
USA BMI 46.2 kg/m2 comorbidities outcomes than Caucasian and
with LAGB and RYGB in Hispanic patients. DM
1,684 patients 8 % NHB (37 % diabetes)
a prospective database remission rates did not
68 % NHW (36 % over 1 year vary by ethnicity 70 %
diabetes) (RYGB) and 50 %
14 % Hispanic American (LAGB)
(30 % diabetes)
2013 Diabetes HbA1c 8 % and BMI Subjects underwent At 1 year the primary end
Surgery Study 3039.9 kg/m2 ILMT plus RYGB point occurred in 49 % of
[150] (n = 60) versus ILMT subjects in the surgery/
USA and 52 % NHW alone (n = 60) with a ILMT vs. 19 % in the
Taiwan primary composite ILMT group
outcome of HbA1c <7 %,
120 28 % East Asian
LDL <100 mg/dl and
participants 9 % NHB systolic BP <130
7 % Hispanic American
3 % Native American
Surgical Treatment and Medications Potentially Eradicate Diabetes Efficiently trial (STAMPEDE) trial
1 year (Table 14.6). This finding suggests analyses are underpowered to report mortality
improved cardiovascular risk factor control with among diabetes participants alone. No studies
RYGB. Prospective data on cardiovascular events have focused on cardiovascular events and mor-
in participants with diabetes are limited to the tality in racial/ethnic minorities.
Swedish outcome study, with a 44 % reduction in
CHD events at 13 years. Both retrospective anal- Ethnic Differences
yses including analysis by Adams et al. [157] and Limited data are available to assess the effects of
prospective analysis in the SOS [158] have shown bariatric surgery in US racial/ethnic minorities.
long-term reductions in mortality, but these The major US trials STAMPEDE, Diabetes
Surgery Study, LABS, and Courcoulas et al. drug therapy [161]. The emerging fields of phar-
(Table 14.6) were multiethnic but lacked the macogenomics and precision medicine have the
power to examine racial/ethnic differences in dia- potential to transform the specificity of medica-
betes remission. There is conflicting data regard- tion selection based on genetic alterations. An
ing weight-loss post-bariatric surgery in NHW example of the potential clinical utility of this
versus racial/ethnic minorities with some studies approach is found in maturity-onset diabetes
showing greater weight loss in NHW and a of the young (MODY) caused by HNF1-alpha
smaller number of studies showing equivalent mutations. Individuals with MODY are often
weight loss [149]. Some of the variation in find- misdiagnosed with type 1 or type 2 diabetes,
ings may be due to majority/minority status of but the diagnosis is clinically important because
participants or variations in African or Hispanic patients can often be managed with sulfonylurea
origins. A study in South Florida, USA (a major- treatment alone [162]. Other monogenic forms
ity Hispanic region) with NHBs, Hispanic of MODY and neonatal diabetes have been iden-
Americans (less Mexican Americans), and tified and have resulted in targeted treatment or
NHWs revealed similar outcomes for weight-loss did not require treatment with excellent long-
post-RYGB and LAGB among HA and NHWs, term outcomes [163].
with decreased weight loss among NHBs [159].
A retrospective analysis by Ng et al. (Table 14.6)
revealed NHB patients had less % excess weight Repaglinide
loss than NHW and HA patients [149]. Among
539 patients with diabetes, diabetes remission Antidiabetic medication metabolism may be
rates did not vary by ethnicity [149]. A second affected by variant alleles. Cytochrome P450
retrospective analysis examining metabolic superfamily member CYP2C8 is an enzyme
effects of bariatric surgery in 4,088 nondiabetic involved in the metabolic inactivation of several
multiethnic adults (17 % NHB, 23 % Hispanic drugs. The CYP2C8*2 is a common variant allele
American) in the Kaiser-Permanente system in NHB, with a frequency of 18 % vs. 0.4 % in
(USA) showed racial/ethnic variation with whites. This common variant allele causes
decreased metabolic syndrome remission in reduced CYP2C8 function and thus has the
NHB or Hispanic American vs. NHW partici- potential to alter therapeutic levels of repaglinide
pants independent of weight loss [160]. Racial/ [161, 164]. It is currently unclear which other
ethnic differences in response to bariatric surgery antidiabetic medications are affected by similar
remain a high-priority area for further research mechanisms.
given the potential for improved diabetes control
and remission.
Metformin
Rational Selection of Antidiabetes Recently, a large retrospective analysis of elec-

Medications in Minority tronic health record database revealed a greater
and Underserved Populations HbA1c response to metformin among NHB
patients (0.90 %) when compared with European
Pharmacokinetics and pharmacodynamics of American patients (0.42 %) irrespective of base-
drugs are potentially affected by race/ethnic- line HbA1c [165]. Genetic ancestry explains only
ity, thus resulting in variability in response to a small proportion of the variation in HbA1c lev-
drug therapy. One of the most important sources els among NHB, and HbA1c is similarly predic-
of variability in drug exposure is potentially tive of cardiovascular events among NHB and
genetic differences in variant alleles effecting NHW, so the response may translate into
the expression of enzymes that metabolize or improvement in clinical outcomes [165]. Further
transport drugs or in the expression of targets of evidence comes from a US Veteran Affairs study
where NHB patients treated with metformin had lower blood glucose and promote significant
a trend toward lower all-cause mortality (HR weight loss may be an attractive option specifi-
0.89, p = 0.29) compared to NHW [166]. cally among NHBs, Hispanic Americans, and
Native Americans. In a multinational study (92 %
white and 6 % black (includes some NHBs)), lira-
Sodium-Glucose Co-transporter 2 glutide and exenatide reduced weight by 3 kg at
(SGLT2) Inhibitors 26 weeks with reductions in HbA1c of 1.12 and
0.79 %, respectively [173]. They have also been
Racial/ethnic minorities have worse control of associated with reductions in blood pressure
cardiovascular risk factors in diabetes [167]. [174]. Unfortunately, these medications have
NHB compared to NHW has a higher prevalence been understudied in US racial/ethnic minority
of hypertension, poorer rates of control, and populations [175], where they may be of even
higher long-term morbidity and mortality associ- greater benefit.
ated with hypertension [168]. HA, particularly
Mexican Americans, also has poorer rates of
blood pressure control compared to NHW [169, Weight-Loss Medications
170]. Thus, antidiabetic medications that lower
blood pressure may be of greater benefit in racial/ Currently, less than 2 % of patients with obesity
ethnic minorities. The sodium-glucose co- use anti-obesity drugs [176]. Even though the
transporter 2 (SGLT2) inhibitors lower blood rates of obesity are higher in US racial/ethnic
glucose by preventing reabsorption of glucose in minorities [172], visits made to physician offices
the proximal tubule of the nephron, which leads by NHW patients compared to nonwhites
to elimination of glucose and an osmotic diuresis. (OR,1.55; 95 % CI, 1.082.24) were more likely
The osmotic diuresis results in lower systolic to involve an anti-obesity drug prescription [176].
(36 mmHg) and diastolic blood pressures This differs from earlier trends showing the high-
(13 mmHg) and mild weight loss (13 kg) est usage among Hispanic American women
[171]. These changes in blood pressure and [177]. Pharmacological agents approved for
weight could potentially help to ameliorate the weight management can be useful adjuncts to
disparities in blood pressure control. Long-term lifestyle change for patients who have been
follow-up of SGLT2 inhibitor trials are ongoing unsuccessful with diet and exercise alone and
to evaluate the effect of SGLT2 inhibitors on car- have been recently reviewed by Apovian et al.
diovascular events. [178]. See Table 14.7 for 1-year weight loss
among patients that complete therapy.
GLP-1 Receptor Agonists

Table 14.7 Odds of reducing body weight by % catego-
Racial/ethnic disparities exist in obesity preva- ries at 1 year with lifestyle intervention and adjunctive
lence in the USA with NHBs and Hispanic medication among those who complete treatment
Americans having a higher prevalence of over- >5 % >10 %
weight (BMI 25 kg/m2) and obese (BMI Weight Weight
Medication loss loss
30 kg/m2) individuals compared to NHWs
Phentermine/topiramate 74.5 % 49.1 %
[172]. Asian Americans have a lower prevalence 7.5/46 mg daily
of overweight (BMI 25 kg/m2) and obese (BMI Phentermine/topiramate 85.1 % 64.3 %
30 kg/m2) individuals compared to NHWs 15/92 mg daily
[172], but this is confounded by evidence that Lorcaserin 10 mg twice daily 65.8 % 35.2 %
Asian Americans have increased risk of diabetes Naltrexone/bupropion 65 % 39 %
at a lower BMI due to greater visceral adiposity 32/360 mg daily
[155]. Given these disparities medications that Liraglutide 3.0 mg daily 73 % 41 %
Translating Primary Prevention Asian American). Over the course of 2.8 years,
of Type 2 Diabetes in Minority the lifestyle intervention and metformin interven-
and Underserved Populations tion reduced diabetes risk by 58 % and 31 %,
respectively, compared to placebo [180]. For
Prevention is important for the individual person, every kilogram of weight loss, there was a 16 %
as well as for the US healthcare system. Diabetes reduction in risk, adjusted for changes in diet and
is associated with higher lifetime medical expen- activity [182]. Study participants are being fol-
ditures despite being associated with reduced life lowed long term in the DPP Outcomes Study, in
expectancy with twofold greater annual per cap- which the original lifestyle intervention group
ita medical spending than for nondiabetic indi- was offered lifestyle reinforcement semiannually
viduals which accounts for 20 % of US healthcare and the metformin group received unmasked
dollars [179]. The American Diabetes Association metformin. At 10 years of follow-up, progression
recommends patients with prediabetes be referred to diabetes was reduced by 34 % in the lifestyle
to an intensive diet and physical activity behav- group and 18 % in the metformin group com-
ioral counseling program targeting 7 % weight pared with placebo [183]. At 15 years of follow-
loss and increasing moderate-intensity physical up, diabetes incidence was reduced by 27 % in
activity (such as brisk walking) to at least the lifestyle intervention group and by 18 % in
150 min/week. They also recommend metformin the metformin group with cumulative incidences
especially for individuals with BMI >35 kg/m2, of diabetes of 55 % for lifestyle, 56 % metformin,
aged <60 years, and women with prior gesta- and 62 % placebo [184]. There were no overall
tional diabetes mellitus [93]. These recommen- differences in an aggregate microvascular out-
dations are based on randomized controlled come between treatment groups, although those
diabetes prevention trials [180, 181]. Clinical tri- whom did not develop diabetes had a 28 % lower
als of lifestyle intervention including the Diabetes prevalence of microvascular complications [184].
Prevention Program (DPP) (physical activity/
dietary modification) aimed at reducing incident
diabetes in at-risk individuals have proved suc- Current Landscape
cessful in US racial/ethnic minorities [180]. The
DPP [180] compared standard lifestyle recom- Given the initial short-term success of the DPP
mendations plus placebo twice daily to standard [180], funding agencies have sponsored many
lifestyle recommendations plus metformin at a culturally specific interventions using the DPP as
dose of 850 mg twice daily or an intensive pro- a general guide. A systematic review and meta-
gram of lifestyle modification (aimed for 7 % analysis of twenty-eight US-based studies apply-
weight loss through a low-calorie low-fat diet and ing the findings of the DPP revealed an average
at least 150 min of physical activity per week) in 4 % weight loss at 12 months [185]. Change in
overweight (BMI >24 kg/m2) individuals at risk weight was similar regardless of whether the
for diabetes (impaired fasting glucose and 2-h intervention was delivered by clinically trained
post 75-g glucose load). The program had a professionals or lay educators. Additional analy-
16-lesson curriculum covering diet, exercise, and ses limited to 17 studies with a 9-month or greater
behavior modification designed to help the par- follow-up assessment showed similar weight
ticipants achieve these goals. The curriculum was change. Every additional lifestyle session
taught by case managers on a one-to-one basis attended increased weight loss by 0.26 %. The
during the first 24 weeks after enrollment and authors conclude that costs associated with dia-
was flexible, culturally sensitive, and individual- betes prevention can be lowered without sacrific-
ized. The mean body mass index was 34.0 kg/m2 ing effectiveness by using nonmedical personnel
at baseline, and the trial contained 45 % racial/ and motivating higher attendance at program ses-
ethnic minority participants (20 % NHBs, 16 % sions [185]. The effectiveness on community-
Hispanic American, 5 % American Indian, 4 % based interventions based on the DPP is
controversial, and the long-term impact of these randomized comparative effectiveness trial of a
interventions given the lower magnitude of lifestyle intervention based on the DPP delivered
weight loss compared to the DPP remains by community health workers (or promotoras),
unknown [186]. metformin, and standard care in Hispanic women
[192]. This trial will be the first US study to test
the comparative effectiveness of metformin and
Non-Hispanic Blacks lifestyle intervention versus standard care among
prediabetic Hispanic adults in a real-world set-
Twenty-one DPP translations focused on NHBs ting [192].
led to half of the weight loss reported in the DPP
immediately post-intervention [187]. A YMCA
translation of the DPP lifestyle intervention American Indian/Native Alaskan
among multiethnic (57 % NHB, 35 % NHW, 3 %
Hispanic American, 2 % others) low-income The Special Diabetes Program for Indians
nondiabetic adults found that persons attending Diabetes Prevention (SDPI-DP) demonstration
nine or more lessons had a 5.3 kg (95 % CI = 2.8, project implemented the DPP lifestyle interven-
7.9 kg) greater weight loss at 12 months than did tion among 36 healthcare programs serving 80
those with standard care alone [188]. Interestingly, American Indian/Alaskan Native tribes [193].
this study found no difference in cardiovascular With similar eligibility criteria, the crude diabe-
risk factor control [188]. A 24-month lifestyle tes incidence of SDPI-DP (4.0 % per year) was
weight-loss program (75 % NHW, 25 % NHB) close to that of the American Indians in the
delivered by community health workers with a lifestyle intervention group of the DPP clinical
goal of 7 % weight loss vs. usual care found that trial (4.7 % per year) and lower than that of the
the intervention group experienced significantly American Indians in the placebo group of DPP
greater decreases in fasting glucose (4.35 mg/ (12.9 % per year), strongly suggesting the
dL), insulin (3.01 U/ml), insulin resistance (0.97), feasibility of translating the DPP intervention
body weight (4.19 kg), waist circumference across a wide range of Native American commu-
(3.23 cm), and BMI (1.40) over 2 years [189]. nities [193].
Other interventions including a community
health advisor-based diabetes prevention inter-
vention in urban NHB communities have not Asian American
shown weight reduction at 1 year [190].
Efforts to translate the DPP findings with Asian
American populations are limited to short-term
Hispanic American pilot studies in different ethnic subgroups that
were generally associated with weight loss
In Project HEED (Help Educate to Eliminate [194197].
Diabetes), participants were randomized to a In summary, a recent US report revealed that
peer-led lifestyle intervention (81.5 h sessions) while most diabetes prevention programs were
versus control for 12 months. The participants moderately successful at reducing the risk for
were majority Hispanic American (90 %), low- developing diabetes consistent with prior analy-
income undereducated women. The intervention ses [198], only four studied primarily NHB or
group lost more weight than the control group Hispanic American subjects [199]. These four
and maintained weight loss at 12 months (7.2 analyses are constrained by lack of standardiza-
versus 2.4 lb, P < 0.01) [191]. Unfortunately, tion in the implementation and documentation
one quarter of participants progressed to dia- making it difficult to assess their costs and long-
betes at 1 year [191]. Promotora Effectiveness term effectiveness [199]. The results of the
Versus Metformin Trial (PREVENT-DM) is a SDPI-DP study in American Indian and Native
Alaskan tribes are promising, but the lack of a specialty referrals through a gatekeeper may lead
comparison group and high loss to follow-up to more appropriate referral patterns [202, 214],
temper conclusions about its long-term effective- restrictions on specialist referrals differentially
ness [200]. Further research in all racial/ethnic applied to patients who are poor, uneducated, or
subgroups is critical to determine the most effica- have low literacy can adversely affect health out-
cious and cost-effective community-based trans- comes [1]. Therefore, incorporating endocrinol-
lations for diabetes prevention. ogy subspecialty care into the infrastructure of
multi-target diabetes QI interventions may
improve the clinic outcomes for minority and
Research Gaps and Future underserved patients with diabetes.
Directions
Approaches to Healthcare Delivery Surgical Interventions for Non-

in Minority and Underserved pharmacological Management
Populations of Diabetes
A high level of evidence supports the effective- Given the high prevalence of diabetes among
ness of culturally tailored patient-targeted inter- racial/ethnic minorities, there remains a critical
ventions in lowering HbA1c in minority need for further research to understand differ-
populations with diabetes; however, there is less ences in weight loss and metabolic effects includ-
evidence for the role of healthcare system and ing diabetes remission post-bariatric surgery in
multi-target interventions in improving the qual- an appropriately powered prospective manner.
ity of diabetes care in this population [38]. A Given the variance in prevalent diabetes rates
recent study observed a trend since 2001 for most within ethnicities based on ancestry, there will
interventions to occur in primary care settings need to be significant consideration given to the
and since 2008, for many to occur in non-clinical size of prospective trials. For instance, within
settings [34]; however, endocrinologists are an Hispanic Americans, the prevalence is lower
integral part of the clinical management of among Cubans (9.3 %) and Central and South
patients with diabetes and may not be integrated Americans (8.5 %), whereas the prevalence is
into these care settings. In reviewing general dia- higher in Mexican Americans (13.9 %) and
betes QI interventions not specific to minority Puerto Ricans (14.8 %), suggesting possible dif-
populations, many successful diabetes QI inter- ferences in etiology or risk factors which may
ventions involved endocrinologists who assisted limit the generalizability of subgroup findings to
with medical management either within an the whole. The same is true for Native American
endocrinology clinic [201, 202] or outside of an populations with an overall prevalence of 15.9 %,
endocrinology clinic [203209]. Among studies ranging from 6.0 % among Alaskan tribes
of diabetes disease management programs, sev- to 24.1 % among those living in Southern
eral have included endocrinology input/consulta- Arizona [175].
tion as part of the care management team [206,
209212].
Minority and socially disadvantaged patients Diabetes Prevention
with diabetes have less access to subspecialty
care than majority and more socioeconomically Significant barriers remain to primary prevention
advantaged patients. In one study, diabetic adults of diabetes in the US racial/ethnic minorities
with only a primary or secondary education had including US work and leisure-time culture.
more contacts with their general practitioner and Americans work long hours, and for those in
dieticians but fewer visits with endocrinologists lower SES groups, they often are required to
or diabetes nurses [213]. While management of work more than one job in order to make enough
money to support themselves and family. Among prevention program, which is bolstered by a tax
low socioeconomic status groups, there is a link on soda, which serves to increase public aware-
between longer working hours and incident dia- ness of the caloric/glycemic content of soda.
betes [215]. Americans live far from their work- In most trials, participants lose weight for the
places, and physically active modes of first 6 months and then begin slow and steady
transportation (biking, walking) are uncommon weight regain. Notably, in trials this sometimes
(<4 % of Americans) [216]. During the work corresponds to a decrease in intensity of the inter-
commute, Americans are exposed to fast-food vention as well. Clearly, the nexus of cost versus
restaurants that prioritize food calorie-dense food length/intensity of interventions is important.
[217]. Neighborhood fast-food exposure is asso- Interventions need to be long enough and trans-
ciated with poorer diets [218] and increased missible enough so that participants can develop
energy intake [219]. Predominantly racial/ethnic and commit to lifelong healthy habits for diabe-
minority neighborhoods have greater fast-food tes prevention and improved cardiometabolic
restaurant density compared to predominantly health. Currently in the USA, there is a large
NHW neighborhoods [220]. Long work hours degree of short-term dieting and meal replace-
and commutes may leave less time for sleep and ments, but in our opinion the most effective
other health-restorative behaviors. Poor sleep approach is education surrounding healthy
quality and sleep insufficiency occur with greater dietary choices and food preparation.
frequency in NHB [221223] and have been Understanding methods to promote further
associated with insulin resistance [224, 225], weight loss beyond 6 months remains important
hyperglycemia, and incident diabetes in NHW and may lead to further long-term reductions in
populations [226, 227]. In the Insulin Resistance diabetes incidence. Second, type 2 diabetes is
and Atherosclerosis Study, short sleep duration likely inclusive of more specific diseases with
showed a nonsignificant protective effect on inci- polygenetic inheritance, gene environment, and
dent diabetes in NHBs [228]. This finding is con- environment interactions. The genetic influence
trary to findings in NHWs and Hispanic may be different among various ethnicities,
Americans in the same study which showed a which may change how we consider not only tar-
significant association between short sleep dura- geted interventions but also translation of tar-
tion and incident diabetes, consistent with the geted interventions. The Human Genome Project
prevailing literature [228]. Leisure-time activities and the current trends toward personalized medi-
are becoming increasingly sedentary involving cine using genomic and pharmacogenomic data
sitting, television viewing, and screen time [229]. may cause large shifts in how we categorize,
In the face of these barriers, instituting health- diagnose, and treat diabetes. It is possible that for
ful habits for diabetes prevention remains populations where the key issue is genetic or epi-
difficult. Primary prevention of diabetes in US genetic, changes causing insulin resistance, phys-
racial/ethnic minorities would benefit from being ical activity, or metformin may be an excellent
multilevel and multifaceted and requires buy-in option, whereas for someone with insulin secre-
from multiple stakeholders. An attractive model tory deficits, these may not represent promising
is the chronic care model promoting self-man- options, and a sulfonylurea or early provision of
agement skills and tracking systems in the indi- insulin may be efficacious. On the individual
vidual patient and coordination/promotion of patient level, we have already seen the success of
care partnerships between health systems, com- these approaches with MODY, as discussed pre-
munity resources, and public policy [230]. In this viously. Given the rising incidence of diabetes in
model all the pieces are equally important from minority and underserved populations, it will be
the patient to public service officials. Examples critical to identify and implement the most effec-
of this include a patient being educated regarding tive treatment and healthcare delivery interven-
diabetes prevention in the office and then being tions to improve outcomes in these high-risk
supported in the community by a diabetes populations in the USA.
References studies identifies eight new loci for type 2 diabetes in

east Asians. Nat Genet. 2011;44(1):6772.
14. Palmer ND, McDonough CW, Hicks PJ, Roh BH,
1. Golden SH, Brown A, Cauley JA, Chin MH, Gary-
Wing MR, An SS, et al. A genome-wide association
Webb TL, Kim C, et al. Health disparities in endo-
search for type 2 diabetes genes in African
crine disorders: biological, clinical, and nonclinical
Americans. PLoS One. 2012;7(1):e29202.
factors an Endocrine Society scientific statement.
15. Kuzawa CW, Sweet E. Epigenetics and the embodi-
J Clin Endocrinol Metab. 2012;97(9):E1579639.
ment of race: developmental origins of US racial
2. Daviglus ML, Talavera GA, Avils-Santa ML,
disparities in cardiovascular health. Am J Hum Biol
Allison M, Cai J, Criqui MH, et al. Prevalence of
Off J Hum Biol Counc. 2009;21(1):215.
major cardiovascular risk factors and cardiovascular
16. Anagnostis P, Athyros VG, Tziomalos K,
diseases among Hispanic/Latino individuals of
Karagiannis A, Mikhailidis DP. The pathogenetic
diverse backgrounds in the United States. JAMA.
role of cortisol in the metabolic syndrome: a hypoth-
2012;308(17):1775.
esis. J Clin Endocrinol Metab. 2009;94(8):
3. Geiss LS, Wang J, Cheng YJ, Thompson TJ, Barker
2692701.
L, Li Y, et al. Prevalence and incidence trends for
17. Slomko H, Heo HJ, Einstein FH. Minireview: epi-
diagnosed diabetes among adults aged 20 to 79
genetics of obesity and diabetes in humans.
years, United States, 19802012. JAMA. 2014;
Endocrinology. 2012;153(3):102530.
312(12):1218.
18. Dagogo-Jack S. Pitfalls in the use of HbA1(c) as a
4. Narayan KMV, Aviles-Santa L, Oza-Frank R,
diagnostic test: the ethnic conundrum. Nat Rev
Pandey M, Curb JD, McNeely M, et al. Report of a
Endocrinol. 2010;6(10):58993.
National Heart, Lung, And Blood Institute
19. Ziemer DC, Kolm P, Weintraub WS, Vaccarino V,
Workshop: heterogeneity in cardiometabolic risk in
Rhee MK, Twombly JG, et al. Glucose-independent,
Asian Americans in the U.S. Opportunities for
black-white differences in hemoglobin A1c levels: a
research. J Am Coll Cardiol. 2010;55(10):96673.
cross-sectional analysis of 2 studies. Ann Intern
5. Chien AT, Chin MH, Davis AM, Casalino LP. Pay
Med. 2010;152(12):7707.
for performance, public reporting, and racial dispari-
20. Selvin E, Steffes MW, Ballantyne CM, Hoogeveen
ties in health care: how are programs being designed?
RC, Coresh J, Brancati FL. Racial differences in
Med Care Res Rev MCRR. 2007;64(5
glycemic markers: a cross-sectional analysis of
Suppl):283S304.
community-based data. Ann Intern Med. 2011;154(5):
6. Karter AJ, Schillinger D, Adams AS, Moffet HH, 3039.
Liu J, Adler NE, et al. Elevated rates of diabetes in 21. Minority H. Office of Office of Minority Health.
Pacific Islanders and Asian subgroups: the Diabetes 2012.
Study of Northern California (DISTANCE). 22. Kirk JK, Bell RA, Bertoni AG, Arcury TA, Quandt
Diabetes Care. 2013;36(3):5749. SA, Goff DC, et al. Ethnic disparities: control of gly-
7. Dagogo-Jack S. Ethnic disparities in type 2 diabetes: cemia, blood pressure, and LDL cholesterol among
pathophysiology and implications for prevention US adults with type 2 diabetes. Ann Pharmacother.
and management. J Natl Med Assoc. 2003;95(9):774. 2005;39(9):1489501.
77989. 23. Kirk JK. Disparities in HbA1c levels between
8. Torrens J. Ethnic differences in insulin sensitivity African-American and Non-Hispanic white adults
and beta-cell function in premenopausal or early with diabetes: a meta-analysis. Diabetes Care.
perimenopausal women without diabetes: the Study 2006;29(9):21306.
of Womens Health Across the Nation (SWAN). 24. Kirk JK, Passmore LV, Bell RA, Narayan K,
Diabetes Care. 2004;27(2 SRC - GoogleScholar): DAgostino RB, Arcury TA, et al. Disparities in A1c
35461. levels between Hispanic and non-Hispanic White
9. Perez-Escamilla RJ. Acculturation, nutrition, and adults with diabetes. Diabetes Care. 2008;31(2):
health disparities in Latinos. Am Nutr P S. 2011;93(5 240.
SRC - GoogleScholar):1163S7. 25. Selvin E, Ning Y, Steffes MW, Bash LD, Klein R,
10. Kurian AK, Cardarelli KM. Racial and ethnic differ- Wong TY, et al. Glycated hemoglobin and the risk of
ences in cardiovascular disease risk factors: a sys- kidney disease and retinopathy in adults with and
tematic review. Ethn Dis. 2007;17(1):14352. without diabetes. Diabetes. 2011;60(1):298305.
11. McCarthy MI. Genomics, type 2 diabetes, and obe- 26. Selvin E, Steffes MW, Zhu H, Matsushita K,
sity. N Engl J Med. 2010;363(24):233950. Wagenknecht L, Pankow J, et al. Glycated hemoglo-
12. Kooner JS, Saleheen D, Sim X, Sehmi J, Zhang W, bin, diabetes, and cardiovascular risk in nondiabetic
Frossard P, et al. Genome-wide association study in adults. N Engl J Med. 2010;362(9):80011.
individuals of South Asian ancestry identifies six 27. Matsushita K, Blecker S, Pazin-Filho A, Bertoni A,
new type 2 diabetes susceptibility loci. Nat Genet. Chang PP, Coresh J, et al. The association of hemo-
2011;43(10):9849. globin a1c with incident heart failure among people
13. Cho YS, Chen C-H, Hu C, Long J, Hee Ong RT, Sim without diabetes: the atherosclerosis risk in commu-
X, et al. Meta-analysis of genome-wide association nities study. Diabetes. 2010;59(8):20206.
28. Lakkis J, Weir MR. Pharmacological strategies for 41. Gerber BS, Brodsky IG, Lawless KA, Smolin LI,
kidney function preservation: are there differences Arozullah AM, Smith EV, et al. Implementation and
by ethnicity? Adv Ren Replace Ther. 2004;11(1): evaluation of a low-literacy diabetes education com-
2440. puter multimedia application. Diabetes Care.
29. Lopes AA. End-stage renal disease due to diabetes 2005;28(7):157480.
in racial/ethnic minorities and disadvantaged popu- 42. Erdman DM, Cook CB, Greenlund KJ, Giles WH,
lations. Ethn Dis. 2009;19(1 Suppl 1):S147. El-Kebbi I, Ryan GJ, et al. The impact of outpatient
30. Sumner AE, Zhou J, Doumatey A, Imoisili OE, diabetes management on serum lipids in urban
Amoah A, Acheampong J, et al. Low HDL- African-Americans with type 2 diabetes. Diabetes
cholesterol with normal triglyceride levels is the Care. 2002;25(1):915.
most common lipid pattern in west Africans and 43. Ziemer DC, Berkowitz KJ, Panayioto RM, El-Kebbi
African Americans with metabolic syndrome: impli- IM, Musey VC, Anderson LA, et al. A simple meal
cations for cardiovascular disease prevention. CVD plan emphasizing healthy food choices is as effective
Prev Control. 2010;5(3):7580. as an exchange-based meal plan for urban African
31. Kirk JK, Graves DE, Bell RA, Hildebrandt CA, Americans with type 2 diabetes. Diabetes Care.
Narayan KMV. Racial and ethnic disparities in self- 2003;26(6):171924.
monitoring of blood glucose among US adults: a 44. Anderson RM, Musch DC, Nwankwo RB, Wolf FM,
qualitative review. Ethn Dis. 2007;17(1):13542. Gillard ML, Oh MS, et al. Personalized follow-up
32. Tricco AC, Ivers NM, Grimshaw JM, Moher D, increases return rate at urban eye disease screening
Turner L, Galipeau J, et al. Effectiveness of quality clinics for African Americans with diabetes: results
improvement strategies on the management of dia- of a randomized trial. Ethn Dis. 2003;13(1):
betes: a systematic review and meta-analysis. Lancet 406.
Lond Engl. 2012;379(9833):225261. 45. DEramo-Melkus G, Spollett G, Jefferson V, Chyun
33. Shojania KG, Ranji SR, McDonald KM, Grimshaw D, Tuohy B, Robinson T, et al. A culturally compe-
JM, Sundaram V, Rushakoff RJ, et al. Effects of tent intervention of education and care for black
quality improvement strategies for type 2 diabetes women with type 2 diabetes. Appl Nurs Res ANR.
on glycemic control: a meta-regression analysis. 2004;17(1):1020.
JAMA. 2006;296(4):42740. 46. Tang TS, Gillard ML, Funnell MM, Nwankwo R,
34. Pimouguet C, Le Goff M, Thibaut R, Dartigues JF, Parker E, Spurlock D, et al. Developing a new gen-
Helmer C. Effectiveness of disease-management eration of ongoing: diabetes self-management sup-
programs for improving diabetes care: a meta- port interventions: a preliminary report. Diabetes
analysis. CMAJ Can Med Assoc J J Assoc Med Can. Educ. 2005;31(1):917.
2011;183(2):E11527. 47. Amoako E, Skelly AH, Rossen EK. Outcomes of an
35. Glazier RH, Bajcar J, Kennie NR, Willson K. A sys- intervention to reduce uncertainty among African
tematic review of interventions to improve diabetes American women with diabetes. West J Nurs Res.
care in socially disadvantaged populations. Diabetes 2008;30(8):92842.
Care. 2006;29(7):167588. 48. Skelly AH, Carlson J, Leeman J, Soward A,
36. Davidson MB. Effect of nurse-directed diabetes care Burns D. Controlled trial of nursing interven-
in a minority population. Diabetes Care. 2003;26(8): tions to improve health outcomes of older African
22817. American women with type 2 diabetes. Nurs Res.
37. Peek ME, Cargill A, Huang ES. Diabetes health dis- 2009;58(6):4108.
parities: a systematic review of health care interven- 49. Tang TS, Funnell MM, Brown MB, Kurlander
tions. Med Care Res Rev. 2007;64(5 suppl):101S56. JE. Self-management support in real-world set-
38. Ricci-Cabello I, Ruiz-Prez I, Olry de Labry-Lima tings: an empowerment-based intervention. Patient
A, Mrquez-Caldern S. Do social inequalities exist Educ Couns. 2010;79(2):17884.
in terms of the prevention, diagnosis, treatment, con- 50. Walker EA, Stevens KA, Persaud S. Promoting dia-
trol and monitoring of diabetes? A systematic betes self-management among African Americans:
review. Health Soc Care Community. 2010;18(6): an educational intervention. J Health Care Poor
57287. Underserved. 2010;21(3 Suppl):16986.
39. Basch CE, Walker EA, Howard CJ, Shamoon H, 51. Carter EL, Nunlee-Bland G, Callender C. A patient-
Zybert P. The effect of health education on the rate of centric, provider-assisted diabetes telehealth self-
ophthalmic examinations among African Americans management intervention for urban minorities.
with diabetes mellitus. Am J Public Health. Perspect Health Inf Manag AHIMA Am Health Inf
1999;89(12):187882. Manag Assoc. 2011;8:1b.
40. Clancy DE, Cope DW, Magruder KM, Huang P, 52. Ellish NJ, Royak-Schaler R, Higginbotham
Salter KH, Fields AW. Evaluating group visits in an EJ. Tailored and targeted interventions to encour-
uninsured or inadequately insured patient population age dilated fundus examinations in older African
with uncontrolled type 2 diabetes. Diabetes Educ. Americans. Arch Ophthalmol Chic Ill 1960.
2003;29(2):292302. 2011;129(12):15928.
53. Tang TS, Funnell MM, Noorulla S, Oh M, Brown 65. Feathers J. Racial and Ethnic Approaches to
MB. Sustaining short-term improvements over the Community Health (REACH) detroit partnership:
long-term: results from a 2-year diabetes self- improving diabetes-related outcomes among African
management support (DSMS) intervention. Diabetes American and Latino adults. Am J Publ Health P.
Res Clin Pract. 2012;95(1):8592. 2005;95(9 SRC - GoogleScholar):155260.
54. Agurs-Collins TD, Kumanyika SK, Ten Have TR, 66. Vazquez IM, Millen B, Bissett L, Levenson SM,
Adams-Campbell LL. A randomized controlled trial Chipkin SR. Buena Alimentacion, Buena Salud: a
of weight reduction and exercise for diabetes man- preventive nutrition intervention in Caribbean
agement in older African-American subjects. Latinos with type 2 diabetes. Am J Health Promot
Diabetes Care. 1997;20(10):150311. AJHP. 1998;13(2):1169.
55. Anderson-Loftin W, Barnett S, Sullivan P, Bunn PS, 67. Anderson RM, Funnell MM, Nwankwo R, Gillard
Tavakoli A. Culturally competent dietary education ML, Oh M, Fitzgerald JT, et al. Evaluating a
for southern rural African Americans with diabetes. problem-based empowerment program for African
Diabetes Educ. 2002;28(2):24557. Americans with diabetes: results of a randomized
56. Brown SA, Hanis CL. Culturally competent diabetes controlled trial. Ethn Dis. 2005;15(4):671.
education for Mexican Americans: the Starr County 68. Murrock CJ, Higgins PA, Killion C. Dance and peer
Study. Diabetes Educ. 1999;25(2):22636. support to improve diabetes outcomes in African
57. Brown SA, Garcia AA, Kouzekanani K, Hanis American women. Diabetes Educ. 2009;35(6):
CL. Culturally competent diabetes self-management 9951003.
education for Mexican Americans: the Starr County 69. Bogner HR, de Vries HF. Integrating type 2 diabetes
border health initiative. Diabetes Care. 2002;25(2): mellitus and depression treatment among African
25968. Americans: a randomized controlled pilot trial.
58. Brown SA, Blozis SA, Kouzekanani K, Garcia AA, Diabetes Educ. 2010;36(2):28492.
Winchell M, Hanis CL. Dosage effects of diabetes 70. DEramo MG. The effect of a diabetes education,
self-management education for Mexican Americans: coping skills training, and care intervention on phys-
the Starr County Border Health Initiative. Diabetes iological and psychosocial outcomes in black
Care. 2005;28(3):52732. women with type 2 diabetes. Biol Res Nurs P.
59. Corkery E, Palmer C, Foley ME, Schechter CB, 2010;12(1 SRC - GoogleScholar):719.
Frisher L, Roman SH. Effect of a bicultural commu- 71. Hill-Briggs F, Lazo M, Peyrot M, Doswell A, Chang
nity health worker on completion of diabetes educa- Y-T, Hill MN, et al. Effect of problem-solving-based
tion in a Hispanic population. Diabetes Care. diabetes self-management training on diabetes con-
1997;20(3):2547. trol in a low income patient sample. J Gen Intern
60. Keyserling TC, Samuel-Hodge CD, Ammerman AS, Med. 2011;26(9):9728.
Ainsworth BE, Henrquez-Roldn CF, Elasy TA, 72. Benjamin EM, Schneider MS, Hinchey
et al. A randomized trial of an intervention to KT. Implementing practice guidelines for diabetes
improve self-care behaviors of African-American care using problem-based learning. A prospective
women with type 2 diabetes: impact on physical controlled trial using firm systems. Diabetes Care.
activity. Diabetes Care. 2002;25(9):157683. 1999;22(10):16728.
61. Mayer-Davis EJ, DAntonio A, Martin M, 73. Din-Dzietham R, Porterfield DS, Cohen SJ, Reaves
Wandersman A, Parra-Medina D, Schulz R. Pilot J, Burrus B, Lamb BM. Quality care improve-
study of strategies for effective weight management ment program in a community-based participatory
in type 2 diabetes: Pounds Off with Empowerment research project: example of Project DIRECT. J Natl
(POWER). Fam Community Health. 2001;24(2): Med Assoc. 2004;96(10):131021.
2735. 74. Fox CH, Mahoney MC. Improving diabetes preven-
62. Mayer-Davis EJ, DAntonio AM, Smith SM, tive care in a family practice residency program: a
Kirkner G, Levin Martin S, Parra-Medina D, et al. case study in continuous quality improvement. Fam
Pounds off with empowerment (POWER): a clinical Med. 1998;30(6):4415.
trial of weight management strategies for black and 75. Phillips LS, Hertzberg VS, Cook CB, El-Kebbi IM,
white adults with diabetes who live in medically Gallina DL, Ziemer DC, et al. The Improving
underserved rural communities. Am J Public Health. Primary Care of African Americans with Diabetes
2004;94(10):173642. (IPCAAD) project: rationale and design. Control
63. McNabb WL, Quinn MT, Rosing L. Weight loss pro- Clin Trials. 2002;23(5):55469.
gram for inner-city black women with non-insulin- 76. Phillips LS, Ziemer DC, Doyle JP, Barnes CS, Kolm
dependent diabetes mellitus: PATHWAYS. J Am P, Branch WT, et al. An endocrinologist-supported
Diet Assoc. 1993;93(1):757. intervention aimed at providers improves diabetes
64. Rosal MC, Olendzki B, Reed GW, Gumieniak O, management in a primary care site: improving pri-
Scavron J, Ockene I. Diabetes self-management mary care of African Americans with diabetes
among low-income Spanish-speaking patients: a (IPCAAD) 7. Diabetes Care. 2005;28(10):235260.
pilot study. Ann Behav Med Publ Soc Behav Med. 77. Thaler LM, Ziemer DC, Gallina DL, Cook CB,
2005;29(3):22535. Dunbar VG, Phillips LS, et al. Diabetes in urban
African-Americans. XVII. Availability of rapid American and white Medicare beneficiaries with
HbA1c measurements enhances clinical decision- diabetes mellitus in New York City. Health P.
making. Diabetes Care. 1999;22(9):141521. 2006;31(4 SRC - GoogleScholar):26388.
78. Ziemer DC, Doyle JP, Barnes CS, Branch WT, Cook 90. Gary TL, Batts-Turner M, Yeh H-C, Hill-Briggs F,
CB, El-Kebbi IM, et al. An intervention to overcome Bone LR, Wang N-Y, et al. The effects of a nurse
clinical inertia and improve diabetes mellitus control case manager and a community health worker team
in a primary care setting: Improving Primary Care of on diabetic control, emergency department visits,
African Americans with Diabetes (IPCAAD) 8. and hospitalizations among urban African Americans
Arch Intern Med. 2006;166(5):50713. with type 2 diabetes mellitus: a randomized con-
79. Bray P, Thompson D, Wynn JD, Cummings DM, trolled trial. Arch Intern Med. 2009;169(19):
Whetstone L. Confronting disparities in diabetes 178894.
care: the clinical effectiveness of redesigning care 91. Rith-Najarian S, Branchaud C, Beaulieu O, Gohdes
management for minority patients in rural primary D, Simonson G, Mazze R. Reducing lower-extremity
care practices. J Rural Health Off J Am Rural Health amputations due to diabetes. Application of the
Assoc Natl Rural Health Care Assoc. 2005;21(4): staged diabetes management approach in a primary
31721. care setting. J Fam Pract. 1998;47(2):12732.
80. Bray P, Roupe M, Young S, Harrell J, Cummings 92. Ziemer DC, Tsui C, Caudle J, Barnes CS, Dames F,
DM, Whetstone LM. Feasibility and effectiveness of Phillips LS. An informatics-supported intervention
system redesign for diabetes care management in improves diabetes control in a primary care setting.
rural areas: the eastern North Carolina experience. AMIA Annu Symp Proc AMIA Symp AMIA Symp.
Diabetes Educ. 2005;31(5):7128. 2006:1160.
81. Fanning EL, Selwyn BJ, Larme AC, DeFronzo 93. American Diabetes Association. Standards of medi-
RA. Improving efficacy of diabetes management cal care in diabetes 2014. Diabetes Care. 2014;37
using treatment algorithms in a mainly Hispanic Suppl 1:S1480.
population. Diabetes Care. 2004;27(7):163846. 94. Estruch R, Ros E, Salas-Salvad J, Covas M-I,
82. Gary TL, Batts-Turner M, Bone LR, Yeh H-C, Wang Corella D, Ars F, et al. Primary prevention of car-
N-Y, Hill-Briggs F, et al. A randomized controlled diovascular disease with a Mediterranean diet. N
trial of the effects of nurse case manager and com- Engl J Med. 2013;368(14):127990.
munity health worker team interventions in urban 95. Esposito K, Maiorino MI, Ciotola M, Di Palo C,
African-Americans with type 2 diabetes. Control Scognamiglio P, Gicchino M, et al. Effects of a
Clin Trials. 2004;25(1):5366. Mediterranean-style diet on the need for antihyper-
83. Hopper SV, Miller JP, Birge C, Swift J. A random- glycemic drug therapy in patients with newly diag-
ized study of the impact of home health aides on dia- nosed type 2 diabetes: a randomized trial. Ann Intern
betic control and utilization patterns. Am J Public Med. 2009;151(5):30614.
Health. 1984;74(6):6002. 96. Elhayany A, Lustman A, Abel R, Attal-Singer J,
84. Hosler AS, Godley K, Rowland DH. An initiative to Vinker S. A low carbohydrate Mediterranean diet
improve diabetes care standards in healthcare orga- improves cardiovascular risk factors and diabetes
nizations serving minorities. Diabetes Educ. control among overweight patients with type 2 dia-
2002;28(4):5819. betes mellitus: a 1-year prospective randomized
85. Jaber LA, Halapy H, Fernet M, Tummalapalli S, intervention study. Diabetes Obes Metab.
Diwakaran H. Evaluation of a pharmaceutical care 2010;12(3):2049.
model on diabetes management. Ann Pharmacother. 97. Abiemo EE, Alonso A, Nettleton JA, Steffen LM,
1996;30(3):23843. Bertoni AG, Jain A, et al. Relationships of the
86. Miller CD, Barnes CS, Phillips LS, Ziemer DC, Mediterranean dietary pattern with insulin resistance
Gallina DL, Cook CB, et al. Rapid A1c availability and diabetes incidence in the Multi-Ethnic Study of
improves clinical decision-making in an urban pri- Atherosclerosis (MESA). Br J Nutr. 2013;109(08):
mary care clinic. Diabetes Care. 2003;26(4):115863. 14907.
87. Philis-Tsimikas A, Walker C, Rivard L, Talavera G, 98. Orlich MJ. Vegetarian dietary patterns and mortality
Reimann JOF, Salmon M, et al. Improvement in dia- in adventist health study 2. JAMA Intern Med.
betes care of underinsured patients enrolled in proj- 2013;173(13):1230.
ect dulce: a community-based, culturally appropriate, 99. Tonstad S, Butler T, Yan R, Fraser GE. Type of veg-
nurse case management and peer education diabetes etarian diet, body weight, and prevalence of type 2
care model. Diabetes Care. 2004;27(1):1105. diabetes. Diabetes Care. 2009;32(5):7916.
88. Cook CB, Penman A, Cobb AB, Miller D, Murphy 100. Tonstad S, Stewart K, Oda K, Batech M, Herring RP,
T, Horn T. Outpatient diabetes management of medi- Fraser GE. Vegetarian diets and incidence of diabe-
care beneficiaries in four Mississippi fee-for-service tes in the Adventist Health Study-2. Nutr Metab
primary care clinics. J Miss State Med Assoc. Cardiovasc Dis. 2013;23(4):2929.
1999;40(1):813. 101. Barnard ND, Cohen J, Jenkins DJ, Turner-McGrievy
89. Mahotiere TJ. A program to reduce the disparity in G, Gloede L, Green A, et al. A low-fat vegan diet
the rate of biennial lipid profiles between African- and a conventional diabetes diet in the treatment of
type 2 diabetes: a randomized, controlled, 74-wk 114. Petersen KF, Dufour S, Befroy D, Garcia R, Shulman
clinical trial. Am J Clin Nutr. 2009;89(5): GI. Impaired mitochondrial activity in the insulin-
1588S96. resistant offspring of patients with type 2 diabetes. N
102. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Engl J Med. 2004;350(7):66471.
Svetkey LP, Sacks FM, et al. A clinical trial of the 115. Kelley DE, He J, Menshikova EV, Ritov
effects of dietary patterns on blood pressure. N Engl VB. Dysfunction of mitochondria in human skeletal
J Med. 1997;336(16):111724. muscle in type 2 diabetes. Diabetes. 2002;51(10):
103. Shirani F, Salehi-Abargouei A, Azadbakht L. Effects 294450.
of Dietary Approaches to Stop Hypertension 116. Swift DL, Johannsen NM, Lavie CJ, Earnest CP,
(DASH) diet on some risk for developing type 2 dia- Johnson WD, Blair SN, et al. Racial differences in
betes: a systematic review and meta-analysis on con- the response of cardiorespiratory fitness to aerobic
trolled clinical trials. Nutrition. 2013;29(7-8): exercise training in Caucasian and African American
93947. postmenopausal women. J Appl Physiol.
104. Brand-Miller JC. Postprandial glycemia, glycemic 2013;114(10):137582.
index, and the prevention of type 2 diabetes. Am 117. Santa-Clara H, Szymanski L, Ordille T, Fernhall
J Clin Nutr. 2004;80(2):2434. B. Effects of exercise training on resting meta-
105. Evert AB, Boucher JL, Cypress M, Dunbar SA, bolic rate in postmenopausal African American
Franz MJ, Mayer-Davis EJ, et al. Nutrition therapy and Caucasian women. Metabolism. 2006;55(10):
recommendations for the management of adults with 135864.
diabetes. Diabetes Care. 2014;37(Supplement_1): 118. Kokkinos P, Myers J, Nylen E, Panagiotakos DB,
S12043. Manolis A, Pittaras A, et al. Exercise capacity and
106. Hu T, Mills KT, Yao L, Demanelis K, Eloustaz M, all-cause mortality in African American and
Yancy WS, et al. Effects of low-carbohydrate diets Caucasian men with type 2 diabetes. Diabetes Care.
versus low-fat diets on metabolic risk factors: a 2009;32(4):6238.
meta-analysis of randomized controlled clinical tri- 119. Qiu S, Cai X, Chen X, Yang B, Sun Z. Step counter
als. Am J Epidemiol. 2012;176 suppl 7:S4454. use in type 2 diabetes: a meta-analysis of random-
107. Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, ized controlled trials. BMC Med. 2014;12(1):36.
McGrory J, et al. The effects of low-carbohydrate 120. Hu FB, Manson JE, Stampfer MJ, Colditz G, Liu S,
versus conventional weight loss diets in severely Solomon CG, et al. Diet, lifestyle, and the risk of
obese adults: one-year follow-up of a randomized type 2 diabetes mellitus in women. N Engl J Med.
trial. Ann Intern Med. 2004;140(10):77885. 2001;345(11):7907.
108. Davis NJ, Tomuta N, Schechter C, Isasi CR, Segal- 121. Narayan KMV, Boyle JP, Thompson TJ, Gregg EW,
Isaacson CJ, Stein D, et al. Comparative study of the Williamson DF. Effect of BMI on lifetime risk for
effects of a 1-year dietary intervention of a Low- diabetes in the U.S. Diabetes Care. 2007;30(6):
carbohydrate diet versus a low-fat diet on weight and 15626.
glycemic control in type 2 diabetes. Diabetes Care. 122. Neeland IJ, Turer AT, Ayers MCR, Powell-Wiley
2009;32(7):114752. TM, Vega GL, Farzaneh-Far R, et al. Dysfunctional
109. Boul NG, Haddad E, Kenny GP, Wells GA, Sigal adiposity and the risk of prediabetes and type 2 dia-
RJ. Effects of exercise on glycemic control and body betes in obese adults. JAMA J Am Med Assoc.
mass in type 2 diabetes mellitus: a meta-analysis of 2012;308(11):1150.
controlled clinical trials. JAMA. 2001;286(10):1218. 123. Rabkin SW, Mathewson FA, Hsu P-H. Relation of
110. Haddad E, Wells GA, Sigal RJ, Boul NG, Kenny body weight to development of ischemic heart dis-
GP. Meta-analysis of the effect of structured exercise ease in a cohort of young North American men after
training on cardiorespiratory fitness in Type 2 diabe- a 26 year observation period: the Manitoba Study.
tes mellitus. Diabetologia. 2003;46(8):107181. Am J Cardiol. 1977;39(3):4528.
111. Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, 124. Hubert HB, Feinleib M, McNamara PM, Castelli
Blissmer BJ, Rubin RR, et al. Exercise and type 2 WP. Obesity as an independent risk factor for cardio-
diabetes: the American College of Sports Medicine vascular disease: a 26- year follow-up of participants
and the American Diabetes Association: joint posi- in the Framingham Heart Study. Circulation.
tion statement. Diabetes Care. 2010;33(12): 1983;67(5):96877.
e14767. 125. Wilson PWF, DAgostino RB, Sullivan L, Parise H,
112. Boul NG, Weisnagel SJ, Lakka TA, Tremblay A, Kannel WB. Overweight and obesity as determi-
Bergman RN, Rankinen T, et al. Effects of exercise nants of cardiovascular risk: the Framingham experi-
training on glucose homeostasis: the HERITAGE ence. Arch Intern Med. 2002;162(16):186772.
Family Study. Diabetes Care. 2005;28(1):10814. 126. Di Angelantonio E, Kaptoge S, Wormser D, Willeit
113. Church TS, Blair SN, Cocreham S, Johannsen N, P, Butterworth AS, Bansal N, et al. Association of
Johnson W, Kramer K, et al. Effects of aerobic and cardiometabolic multimorbidity with mortality.
resistance training on hemoglobin A1c levels in JAMA. 2015;314(1):52.
patients with type 2 diabetes. JAMA J Am Med 127. Desprs J-P, Lemieux I. Abdominal obesity and met-
Assoc. 2010;304(20):2253. abolic syndrome. Nature. 2006;444(7121):8817.
128. Kahn SE, Hull RL, Utzschneider KM. Mechanisms 143. Schauer PR, Bhatt DL, Kirwan JP, Wolski K,
linking obesity to insulin resistance and type 2 dia- Brethauer SA, Navaneethan SD, et al. Bariatric sur-
betes. Nature. 2006;444(7121):8406. gery versus intensive medical therapy for diabetes
129. Rosen ED, Spiegelman BM. Adipocytes as regula- 3-year outcomes. N Engl J Med. 2014;370(21):
tors of energy balance and glucose homeostasis. 200213.
Nature. 2006;444(7121):84753. 144. Schauer PR, Kashyap SR, Wolski K, Brethauer SA,
130. Lau DCW. Adipokines: molecular links between Kirwan JP, Pothier CE, et al. Bariatric surgery versus
obesity and atherosclerosis. AJP Heart Circ Physiol. intensive medical therapy in obese patients with dia-
2005;288(5):H203141. betes. N Engl J Med. 2012;366(17):156776.
131. The Look AHEAD Research Group. Cardiovascular 145. Kashyap SR, Bhatt DL, Wolski K, Watanabe RM,
effects of intensive lifestyle intervention in type 2 Abdul-Ghani M, Abood B, et al. Metabolic effects of
diabetes. N Engl J Med. 2013;369(2):14554. bariatric surgery in patients with moderate obesity
132. Lazo M, Solga SF, Horska A, Bonekamp S, Diehl and type 2 diabetes: analysis of a randomized control
AM, Brancati FL, et al. Effect of a 12-month inten- trial comparing surgery with intensive medical treat-
sive lifestyle intervention on hepatic steatosis in ment. Diabetes Care. 2013;36(8):217582.
adults with type 2 diabetes. Diabetes Care. 146. Adams TD, Davidson LE, Litwin SE, Kolotkin RL,
2010;33(10):215663. LaMonte MJ, Pendleton RC, et al. Health benefits of
133. Group LAR, et al. Effect of a long-term behavioural gastric bypass surgery after 6 years. JAMA.
weight loss intervention on nephropathy in over- 2012;308(11):1122.
weight or obese adults with type 2 diabetes: a second- 147. Courcoulas AP. Weight change and health outcomes
ary analysis of the Look AHEAD randomised clinical at 3 years after bariatric surgery among individuals
trial. Lancet Diabetes Endocrinol. 2014;2(10):8019. with severe obesity. JAMA [Internet]. 2013 [cited 5
134. Wing RR. Implications of Look AHEAD for clinical Dec 2015]. Available from: http://jama.jamanetwork.
trials and clinical practice. Diabetes Obes Metab. com/article.aspx?. doi:10.1001/jama.2013.280928.
2014;16(12):118391. 148. Courcoulas AP, Goodpaster BH, Eagleton JK, Belle
135. Foster GD, Wadden TA, LaGrotte CA, Vander Veur SH, Kalarchian MA, Lang W, et al. Surgical vs med-
SS, Hesson LA, Homko CJ, et al. A randomized ical treatments for type 2 diabetes mellitus: a ran-
comparison of a commercially available portion- domized clinical trial. JAMA Surg. 2014;149(7):707.
controlled weight-loss intervention with a diabetes 149. Ng J, Seip R, Stone A, Ruano G, Tishler D, Papasavas
self-management education program. Nutr Diabetes. P. Ethnic variation in weight loss, but not co-
2013;3(3):e63. morbidity remission, after laparoscopic gastric
136. Pillay J, Armstrong MJ, Butalia S, Donovan LE, banding and Roux-en-Y gastric bypass. Surg Obes
Sigal RJ, Vandermeer B, et al. Behavioral programs Relat Dis. 2015;11(1):94100.
for type 2 diabetes mellitus: a systematic review and 150. Ikramuddin S, Korner J, Lee W-J, Connett JE,
network meta-analysis. Ann Intern Med. Inabnet WB, Billington CJ, et al. Roux-en-Y gastric
2015;163(11):848. bypass vs intensive medical management for the
137. Malkani S. An update on the role of bariatric surgery control of type 2 diabetes, hypertension and hyper-
in diabetes management. Curr Opin Endocrinol lipidemia. JAMA. 2013;309(21):22409.
Diabetes Obes. 2015;22(2):98105. 151. Hutter MM, Schirmer BD, Jones DB, Ko CY, Cohen
138. Vest AR, Heneghan HM, Schauer PR, Young JB. ME, Merkow RP, et al. First Report from the
Surgical management of obesity and the relationship American College of Surgeons Bariatric Surgery
to cardiovascular disease. Circulation. 2013;127(8):945 Center Network: laparoscopic sleeve gastrectomy
59. doi: 10.1161/CIRCULATIONAHA.112.103275. has morbidity and effectiveness positioned between
139. Spaniolas K, Kasten KR, Brinkley J, Sippey ME, the band and the bypass. Ann Surg. 2011;254(3):
Mozer A, Chapman WH, et al. The changing bariat- 41022.
ric surgery landscape in the USA. Obes Surg. 152. Still CD, Wood GC, Benotti P, Petrick AT, Gabrielsen
2015;25(8):15446. J, Strodel WE, et al. Preoperative prediction of type
140. Buchwald H, Avidor Y, Braunwald E, Jensen MD, 2 diabetes remission after Roux-en-Y gastric bypass
Pories W, Fahrbach K, et al. Bariatric surgery: a sys- surgery: a retrospective cohort study. Lancet
tematic review and meta-analysis. JAMA. Diabetes Endocrinol. 2014;2(1):3845.
2004;292(14):172437. 153. Maggard-Gibbons M, Maglione M, Livhits M,
141. Tice JA, Karliner L, Walsh J, Petersen AJ, Feldman Ewing B, Maher AR, Hu J, et al. Bariatric surgery
MD. Gastric banding or bypass? A systematic for weight loss and glycemic control in nonmorbidly
review comparing the two most popular bariatric obese adults with diabetes. JAMA. 2013;309(21):
procedures. Am J Med. 2008;121(10):88593. 225061.
142. Trastulli S, Desiderio J, Guarino S, Cirocchi R, 154. Parikh M, Issa R, Vieira D, McMacken M, Saunders
Scalercio V, Noya G, et al. Laparoscopic sleeve gas- JK, Ude-Welcome A, et al. Role of bariatric surgery
trectomy compared with other bariatric surgical pro- as treatment for type 2 diabetes in patients who do not
cedures: a systematic review of randomized trials. meet current NIH criteria: a systematic review and
Surg Obes Relat Dis. 2013;9(5):81629. meta-analysis. J Am Coll Surg. 2013;217(3):52732.
155. American Diabetes Association. Standards of medi- 169. Egan BM, Zhao Y, Axon RN. US trends in preva-
cal care in diabetes 2015. Diabetes Care. lence, awareness, treatment, and control of hyperten-
2015;38(Supplement_1):S12. sion, 19882008. JAMA. 2010;303(20):204350.
156. Lee CJ, Clark JM, Schweitzer M, Magnuson T, 170. Guo F, He D, Zhang W, Walton RG. Trends in preva-
Steele K, Koerner O, et al. Prevalence of and risk lence, awareness, management, and control of
factors for hypoglycemic symptoms after gas- hypertension among United States adults, 1999 to
tric bypass and sleeve gastrectomy: postsurgical 2010. J Am Coll Cardiol. 2012;60(7):599606.
hypoglycemic symptoms. Obesity. 2015;23(5): 171. Oliva RV, Bakris GL. Blood pressure effects of
107984. sodiumglucose co-transport 2 (SGLT2) inhibitors.
157. Adams TD, Gress RE, Smith SC, Halverson RC, J Am Soc Hypertens. 2014;8(5):3309.
Simper SC, Rosamond WD, et al. Long-term mortal- 172. Ogden CL, Carroll MD, Kit BK, Flegal
ity after gastric bypass surgery. N Engl J Med. KM. Prevalence of childhood and adult obesity
2007;357(8):75361. in the United States, 20112012. JAMA. 2014;
158. Sjstrm L, Narbro K, Sjstrm CD, Karason K, 311(8):806.
Larsson B, Wedel H, et al. Effects of bariatric sur- 173. Buse JB, Rosenstock J, Sesti G, Schmidt WE,
gery on mortality in Swedish obese subjects. N Engl Montanya E, Brett JH, et al. Liraglutide once a day
J Med. 2007;357(8):74152. versus exenatide twice a day for type 2 diabetes: a
159. Khorgami Z, Arheart KL, Zhang C, Messiah SE, de 26-week randomised, parallel-group, multinational,
la Cruz-Muoz N. Effect of ethnicity on weight loss open-label trial (LEAD-6). Lancet. 2009;374(9683):
after bariatric surgery. Obes Surg. 2015;25(5): 3947.
76976. 174. Wang B, Zhong J, Lin H, Zhao Z, Yan Z, He H, et al.
160. Coleman KJ, Huang Y-C, Koebnick C, Reynolds K, Blood pressure-lowering effects of GLP-1 receptor
Xiang AH, Black MH, et al. Metabolic syndrome is agonists exenatide and liraglutide: a meta-analysis of
less likely to resolve in hispanics and non-hispanic clinical trials. Diabetes Obes Metab. 2013;15(8):
blacks after bariatric surgery. Ann Surg. 2014;259(2): 73749.
27985. 175. Ferdinand KC, Nasser SA. Racial/ethnic disparities in
161. Yasuda S, Zhang L, Huang S-M. The role of ethnic- prevalence and care of patients with type 2 diabetes
ity in variability in response to drugs: focus on clini- mellitus. Curr Med Res Opin. 2015;31(5):
cal pharmacology studies. Clin Pharmacol Ther. 91323.
2008;84(3):41723. 38. 176. Xia Y, Kelton CML, Guo JJ, Bian B, Heaton
162. Pearson ER, Starkey BJ, Powell RJ, Gribble FM, PC. Treatment of obesity: pharmacotherapy trends
Clark PM, Hattersley AT. Genetic cause of hypergly- in the United States from 1999 to 2010: pharmaco-
caemia and response to treatment in diabetes. Lancet therapy treatment of obesity. Obesity. 2015;23(8):
Lond Engl. 2003;362(9392):127581. 17218.
163. Fajans SS, Bell GI. MODY: history, genetics, patho- 177. Khan LK, Serdula MK, Bowman BA, Williamson
physiology, and clinical decision making. Diabetes DF. Use of prescription weight loss pills among US
Care. 2011;34(8):187884. adults in 19961998. Ann Intern Med. 2001;134(4):
164. Garca-Martn E, Martnez C, Ladero JM, Agndez 2826.
JA. Interethnic and intraethnic variability of 178. Apovian CM, Aronne LJ, Bessesen DH, McDonnell
CYP2C8 and CYP2C9 polymorphisms in healthy ME, Murad MH, Pagotto U, et al. Pharmacological
individuals. Mol Diagn Ther. 2006;10(1):2940. management of obesity: an endocrine society clini-
165. Williams LK, Padhukasahasram B, Ahmedani BK, cal practice guideline. J Clin Endocrinol Metab.
Peterson EL, Wells KE, Gonzlez Burchard E, et al. 2015;100(2):34262.
Differing effects of metformin on glycemic control 179. Zhuo X, Zhang P, Barker L, Albright A, Thompson
by race-ethnicity. J Clin Endocrinol Metab. TJ, Gregg E. The lifetime cost of diabetes and its
2014;99(9):31608. implications for diabetes prevention. Diabetes Care.
166. Gosmanova EO, MANGOLD TA, RAWLS WN, 2014;37(9):255764.
WALL BM, et al. Effect of metformin-containing 180. The Diabetes Prevention Program. Reduction in the
antidiabetic regimens on all-cause mortality in veter- incidence of type 2 diabetes with lifestyle interven-
ans with type 2 diabetes mellitus. Am J Med Sci. tion or metformin. N Engl J Med. 2002;346(6):
2008;336(3):2417. 393403.
167. Ford ES. Trends in the control of risk factors for car- 181. Pan X-R, Li G, Hu Y-H, Wang J-X, Yang W-Y, An
diovascular disease among adults with diagnosed Z-X, et al. Effects of diet and exercise in preventing
diabetes: findings from the National Health and NIDDM in people with impaired glucose tolerance:
Nutrition Examination Survey 19992008*: cardio- the Da Qing IGT and Diabetes Study. Diabetes Care.
vascular risk factor control. J Diabetes. 2011;3(4): 1997;20(4):53744.
33747. 182. Delahanty LM, Pan Q, Jablonski KA, Aroda VR,
168. Lackland DT. Racial differences in hypertension: Watson KE, Bray GA, et al. Effects of weight loss,
implications for high blood pressure management. weight cycling, and weight loss maintenance on dia-
Am J Med Sci. 2014;348(2):1358. betes incidence and change in cardiometabolic traits
in the diabetes prevention program. Diabetes Care. pacific islander communities: the PILI ohana proj-
2014;37(10):273845. ect. Transl Behav Med. 2014;4(2):14959.
183. Diabetes Prevention Program Resea. 10-year follow- 195. Islam N, Zanowiak J, Wyatt L, Kavathe R, Singh H,
up of diabetes incidence and weight loss in the Kwon S, et al. Diabetes prevention in the New York
Diabetes Prevention Program Outcomes Study. City Sikh Asian Indian community: a pilot study. Int
Lancet. 2009;374(9702):167786. J Environ Res Public Health. 2014;11(5):546286.
184. Long-term effects of lifestyle intervention or metfor- 196. Leake AR, Bermudo VC, Jacob J, Jacob MR, Inouye
min on diabetes development and microvascular J. Health is wealth: methods to improve attendance
complications over 15-year follow-up: the Diabetes in a lifestyle intervention for a largely immigrant
Prevention Program Outcomes Study. Lancet Filipino-American sample. J Immigr Minor Health.
Diabetes Endocrinol [Internet]. 2015 Sep [cited 2012;14(3):47580.
2015 Oct 7]; Available from: http://linkinghub.else- 197. Islam NS, Zanowiak JM, Wyatt LC, Chun K, Lee L,
vier.com/retrieve/pii/S2213858715002910 Kwon SC, et al. A randomized-controlled, pilot
185. Ali MK, Echouffo-Tcheugui JB, Williamson intervention on diabetes prevention and healthy life-
DF. How effective were lifestyle interventions in styles in the New York City Korean community.
real-world settings that were modeled on the diabe- J Community Health. 2013;38(6):103041.
tes prevention program? Health Aff (Millwood). 198. Dunkley AJ, Bodicoat DH, Greaves CJ, Russell C,
2012;31(1):6775. Yates T, Davies MJ, et al. Diabetes prevention in the
186. Kahn R, Davidson MB. The reality of type 2 diabe- real world: effectiveness of pragmatic lifestyle inter-
tes prevention. Diabetes Care. 2014;37(4):9439. ventions for the prevention of type 2 diabetes and of
187. Samuel-Hodge CD, Johnson CM, Braxton DF, the impact of adherence to guideline recommenda-
Lackey M. Effectiveness of diabetes prevention pro- tions: a systematic review and meta-analysis.
gram translations among African Americans: Diabetes Care. 2014;37(4):92233.
African Americans and DPP translations. Obes Rev. 199. Chou C-H, Burnet D, Meltzer D, Huang E. The
2014;15:10724. effectiveness of diabetes prevention programs in
188. Ackermann RT, Liss DT, Finch EA, Schmidt KK, community settings [Internet]. 2015 [cited 15 Dec
Hays LM, Marrero DG, et al. A randomized com- 2015]. Available from: http://198.246.124.29/diabe-
parative effectiveness trial for preventing type 2 dia- tes/pdfs/data/2014-report-acknowledgments.pdf.
betes. Am J Public Health. 2015;105(11):232834. 200. Knowler WC, Ackermann RT. Preventing diabetes
189. Katula JA, Vitolins MZ, Morgan TM, Lawlor MS, in American Indian communities. Diabetes Care.
Blackwell CS, Isom SP, et al. The healthy living 2013;36(7):18202.
partnerships to prevent diabetes study. Am J Prev 201. Gaede P, Vedel P, Larsen N, Jensen GV, Parving
Med. 2013;44(4):S32432. H-H, Pedersen O. Multifactorial intervention and
190. Faridi Z, Shuval K, Njike VY, Katz JA, Jennings G, cardiovascular disease in patients with type 2 diabe-
Williams M, et al. Partners reducing effects of diabetes. N Engl J Med. 2003;348(5):38393.
tes (PREDICT): a diabetes prevention physical 202. Moore SH, Martin DP, Richardson WC. Does the
activity and dietary intervention through African- primary-care gatekeeper control the costs of health
American churches. Health Educ Res. 2010;25(2): care? Lessons from the SAFECO experience. N
30615. Engl J Med. 1983;309(22):14004.
191. Parikh P, Simon EP, Fei K, Looker H, Goytia C, 203. de Sonnaville JJ, Bouma M, Colly LP, Devill W,
Horowitz CR. Results of a pilot diabetes prevention Wijkel D, Heine RJ. Sustained good glycaemic con-
intervention in East Harlem, New York City: project trol in NIDDM patients by implementation of struc-
HEED. Am J Public Health. 2010;100 Suppl tured care in general practice: 2-year follow-up
1:S2329. study. Diabetologia. 1997;40(11):133440.
192. Perez A, Alos VA, Scanlan A, Maia CM, Davey A, 204. Hirsch IB, Goldberg HI, Ellsworth A, Evans TC,
Whitaker RC, et al. The rationale, design, and base- Herter CD, Ramsey SD, et al. A multifaceted inter-
line characteristics of PREVENT-DM: a community- vention in support of diabetes treatment guidelines: a
based comparative effectiveness trial of lifestyle cont trial. Diabetes Res Clin Pract. 2002;58(1):
intervention and metformin among Latinas with pre- 2736.
diabetes. Contemp Clin Trials. 2015;45:3207. 205. Legorreta A, Peters A, Ossorio C, Lopez RJ, Jatulis
193. Jiang L, Manson SM, Beals J, Henderson WG, D, Davidson MB. Effect of a comprehensive nurse-
Huang H, Acton KJ, et al. Translating the diabetes managed diabetes program: an HMO prospective
prevention program into American Indian and study. Am J Manag Care. 1996;2:102430.
Alaska native communities: results from the special 206. Sadur CN, Moline N, Costa M, Michalik D,
diabetes program for Indians diabetes prevention Mendlowitz D, Roller S, et al. Diabetes management
demonstration project. Diabetes Care. 2013;36(7): in a health maintenance organization. Efficacy of
202734. care management using cluster visits. Diabetes Care.
194. Kaholokula JK, Wilson RE, Townsend CKM, Zhang 1999;22(12):20117.
GX, Chen J, Yoshimura SR, et al. Translating the 207. Majumdar SR, Guirguis LM, Toth EL, Lewanczuk
diabetes prevention program in native Hawaiian and RZ, Lee TK, Johnson JA. Controlled trial of a
multifaceted intervention for improving quality of of the evidence: eating out and diet. Obes Rev.
care for rural patients with type 2 diabetes. Diabetes 2012;13(4):32946.
Care. 2003;26(11):30616. 218. Moore LV, Diez Roux AV, Nettleton JA, Jacobs DR,
208. California Medi-Cal Type 2 Diabetes Study Group. Franco M. Fast-food consumption, diet quality, and
Closing the gap: effect of diabetes case management neighborhood exposure to fast food: the multi-ethnic
on glycemic control among low-income ethnic study of atherosclerosis. Am J Epidemiol. 2009;
minority populations: the California Medi-Cal type 170(1):2936.
2 diabetes study. Diabetes Care. 2004;27(1): 219. Roux AVD, Smith AE, Gore LD. Associations of
95103. fast food restaurant availability with dietary intake
209. Polonsky WH, Earles J, Smith S, Pease DJ, and weight among African Americans in the Jackson
Macmillan M, Christensen R, et al. Integrating med- heart study, 20002004. Am J Public Health.
ical management with diabetes self-management 2011;101(S1):S301.
training: a randomized control trial of the Diabetes 220. Block JP, Scribner RA, DeSalvo KB. Fast food, race/
Outpatient Intensive Treatment program. Diabetes ethnicity, and income. Am J Prev Med.
Care. 2003;26(11):304853. 2004;27(3):2117.
210. Gaede P, Lund-Andersen H, Parving H-H, Pedersen 221. Hicks RA, Lucero-Gorman K, Bautista J, HICKS
O. Effect of a multifactorial intervention on mortal- GJ. Ethnicity, sleep duration, and sleep satisfaction.
ity in type 2 diabetes. N Engl J Med. 2008;358(6): Percept Mot Skills. 1999;88(1):2345.
58091. 222. Lauderdale DS. Objectively measured sleep charac-
211. Shea S, Weinstock RS, Starren J, Teresi J, Palmas W, teristics among early-middle-aged adults: the
Field L, et al. A randomized trial comparing tele- CARDIA study. Am J Epidemiol. 2006;164(1):
medicine case management with usual care in older, 516.
ethnically diverse, medically underserved patients 223. Gangwisch JE, Heymsfield SB, Boden-Albala B,
with diabetes mellitus. J Am Med Inform Assoc. Buijs RM, Kreier F, Pickering TG, et al. Sleep dura-
2006;13(1):4051. tion as a risk factor for diabetes incidence in a large
212. Ko S-H, Song K-H, Kim S-R, Lee J-M, Kim J-S, US sample. Sleep. 2007;30(12):1667.
Shin J-H, et al. Long-term effects of a structured 224. Buxton OM, Pavlova M, Reid EW, Wang W,
intensive diabetes education programme (SIDEP) in Simonson DC, Adler GK. Sleep restriction for 1
patients with Type 2 diabetes mellitus a 4-year week reduces insulin sensitivity in healthy men.
follow-up study. Diabet Med J Br Diabet Assoc. Diabetes. 2010;59(9):212633.
2007;24(1):5562. 225. Broussard JL, Ehrmann DA, Van Cauter E, Tasali E,
213. Chin MH, Zhang JX, Merrell K. Specialty differ- Brady MJ. Impaired insulin signaling in human adi-
ences in the care of older patients with diabetes. Med pocytes after experimental sleep restriction A ran-
Care. 2000;38(2):13140. domized, crossover study. Ann Intern Med.
214. Martin DP, Diehr P, Price KF, Richardson WC. Effect 2012;157(8):54957.
of a gatekeeper plan on health services use and 226. Cappuccio FP, DElia L, Strazzullo P, Miller
charges: a randomized trial. Am J Public Health. MA. Quantity and quality of sleep and incidence of
1989;79(12):162832. type 2 diabetes: a systematic review and meta-
215. Kivimki M, Virtanen M, Kawachi I, Nyberg ST, analysis. Diabetes Care. 2009;33(2):41420.
Alfredsson L, Batty GD, et al. Long working hours, 227. Knutson KL, Ryden AM, Mander BA, Van Cauter
socioeconomic status, and the risk of incident type 2 E. Role of sleep duration and quality in the risk and
diabetes: a meta-analysis of published and unpub- severity of type 2 diabetes mellitus. Arch Intern
lished data from 222 120 individuals. Lancet Med. 2006;166(16):1768.
Diabetes Endocrinol. 2015;3(1):2734. 228. Beihl DA, Liese AD, Haffner SM. Sleep duration as
216. McKenzie B. Modes less traveledbicycling and a risk factor for incident type 2 diabetes in a multi-
walking to work in the United States: 20082012. ethnic cohort. Ann Epidemiol. 2009;19(5):3517.
US Census Bur N Y [Internet]. 2014 [cited 15 Dec 229. Matthews CE, Chen KY, Freedson PS, Buchowski
2015]. Available from: https://www.census.gov/con- MS, Beech BM, Pate RR, et al. Amount of time
tent/dam/Census/library/publications/2014/acs/ spent in sedentary behaviors in the United States,
acs-25.pdf. 20032004. Am J Epidemiol. 2008;167(7):87581.
217. Lachat C, Nago E, Verstraeten R, Roberfroid D, Van 230. Bodenheimer T, Wagner EH, Grumbach K.
Camp J, Kolsteren P. Eating out of home and its Improving primary care for patients with chronic ill-
association with dietary intake: a systematic review ness. JAMA. 2002;288(14):17759.
Index
A Ancestry informative markers (AIMs), 135

Abdominal Ankle-brachial index, 160
fat distribution, 253 Antidiabetes medications, 13, 263
obesity, 88, 102 among Polynesians, 185
Abnormal Caribbean, 141
ACR, 160 China and Western Pacific Region, 7476
fasting glucose, 102 Eastern European countries, 216217
glucose tolerance, 40, 158 ethnic/immigrants populations, Western Europe,
lipid profiles, 253 229230
Aboriginal Diabetes Initiative, 243, 244 Latin America, 119120
Acarbose, 22, 74, 75, 141 in USA
Acarbose Cardiovascular Evaluation (ACE) study, 75 American Indian/Alaskan Native, 273
ACE inhibitors, 214, 215 with Asian American, 273274
Acetyl-CoA, 9, 10 current landscape, 272273
Acetyl-CoA carboxylase (ACC), 9, 10 DPP, 272
Acetyl salicylic acid, 102, 117 GLP-1 receptor agonists, 271
ACR. See Albumin/creatinine ratio (ACR) HEED, 273
ACT NOW (ACTos NOW for the Prevention of metformin, 270271
Diabetes), 22 NHBs, 273
Acute coronary syndrome, 116, 178 repaglinide, 270
Acute insulin response to glucose (AIRg), 65 SGLT2 inhibitors, 271
Acute insulin secretory response weight-loss medications, 271
glucose, 12 Antihyperglycemic therapy, 3
to intravenous glucose, 11 Antihypertensive agents, 104, 138, 214, 215
ADA. See American Diabetes Association (ADA) Antiretroviral therapy (ART), 15, 40
Adiposity, 12, 39, 40, 53, 74, 88, 129, 131, 136, 240, Argentina, diabetes in
252, 253, 265, 271 complications, 114
Aerobic exercises, 93, 264 implementation of preventive actions,
Aerobic fitness, 40, 245 118119
African-Americans in the Atherosclerosis Risk in mortality, 116
Communities study, 11 T1DM
AGI. See Alpha glucosidase inhibitors (AGI) diagnosis, 114
Albumin/creatinine ratio (ACR), 159161, 171, incidence, 105, 106
174177, 179 T2DM, prevalence, 102, 103, 111, 112
Alpha glucosidase inhibitors (AGI), 4, 74, 75, 92 Aspirin therapy, 257
American Diabetes Association (ADA), 18, 24, 70, 91, Atypical ketosis-prone diabetes (AKPD), 133134
92, 140, 154, 211212, 226, 228, 230, 253, AusDiab (Australian Diabetes and Obesity Lifestyle)
257, 262, 263, 266, 272 study, 151, 152
Amputations, 18, 114, 212, 213, 239, 256, 262 Australia, diabetes, 151152. See also Indigenous
for diabetic feet, 137138 Australians, diabetes
leg, 52, 68 incidence, 69
limb, 152 obesity rates in, 49, 50
lower-limb, 115, 152, 177 populations, 151
nontraumatic limb, 14, 116 Australian Health Survey, 151, 152, 154

DOI 10.1007/978-3-319-41559-8
286 Index
B hyperglycaemic crises, 138

Baltimore Longitudinal Study on Aging (BLSA), 11 nephropathy, 138
Bariatric surgery, 141, 265270 osteopenia, 139
Beta-cell dysfunction, 11, 67, 74, 94, 131, 132, 136, 253 reduced lung function, 139
Beta-cell function, 24, 6567, 75, 132, 133, 240, 252 retinopathy, 138
Bisphenol A (BPA), 67 stroke, 137
Blood glucose vascular dementia, 139
control of, 43, 72, 161, 186, 242 demographic changes in, 129
daily testing of, 57 developmental factors
fasting, 37, 38, 141, 159 hypothalamic-pituitary-adrenal axis
levels, 71, 120 activation, 132
self-monitoring of, 151, 256 intrauterine growth restriction, 132
SGLT2 inhibitors lowers, 271 low birth weight, 131132
test strips, 14 prenatal factors, 132
Blood pressure, 68, 74, 139, 160, 257, 263, 267, 271 socio-economic status, 132
adults with, 161 European immigration, 127
control of, 43, 72, 255 future directions, 142143
diastolic, 271 GDM, 135
high, 120, 137, 180, 181, 253 genome-wide association studies, 135136
measurements, 119 health-care delivery system, 139140
systolic, 121, 137, 138 life expectancy, 127
in type 2 diabetes, 156 metabolic factors, 132133
Body mass index (BMI), 37, 65, 88, 102, 104, 112, 129, MODY, 134
130, 155, 156, 159, 240, 252 non-pharmacological management
Brazil, diabetes in, 7, 120, 121 bariatric surgery, 141
adults, 86 diabetes education, 140
complications, 114 exercise, 140141
healthcare system, 117 nontraditional/complementary techniques, 141
prevalence, 88 nutrition, 140
type 1 diabetes tobacco cessation, 141
diagnosis, 113 prediabetes, 134
incidence, 105, 106 research, 142
type 2 diabetes total populations, 127, 128
average BMI, 104 tourism source, 127
diagnosis, 108110 type 1A, 129
disability-adjusted life years, 116 type 1 diabetes, 135
prevalence, 102, 103 type 2 diabetes, 129131
diagnosis, 134
primary prevention, 141142
C youth with, 135
Cancer, 54, 68, 69, 74, 76, 203, 263 Caribbean Health Research Council (CHRC), 139
CANOE (CAnadian Normoglycemia Outcomes Caribbean Public Health Agency (CARPHA), 139142
Evaluation), 22 Caribbean Wellness Day (CWD), 141
Cardiovascular disease (CVD), 3, 36, 49, 53, 68, 7476, Central America, diabetes in, 3, 251
91, 137, 138, 142, 155, 157, 159, 161, 216, age-adjusted diabetes prevalence, 1, 2
239, 253, 255, 263, 265 CDPC, 21
Caribbean Community (CARICOM), 127, 139, 141 T2DM, 110111
Caribbean, diabetes in Central obesity, 39, 53, 59, 64, 89, 130, 226, 230
ageing region, 127, 129 Certified diabetes educator (CDE), 59
AKPD/type 1B diabetes, 133134 Chennai Urban Population Study (CUPS), 8990
antidiabetes medications, 141 Chennai Urban Rural Epidemiology Study (CURES),
Community (CARICOM), 127 89, 90
complications Childhood diabetes
amputations, 137138 obesity, 53, 58, 74, 186, 239, 242
coronary heart disease, 137 T2DM diabetes, 19
dental disease, 139 Childhood metabolic syndrome, 67, 69
depression, 139 Chile, diabetes in
diabetic foot disease, 137 healthcare delivery system, 117
erectile dysfunction, 139 life expectancy, 101
health disparities, 136137 obesity prevalence, 102, 103
Index 287
T1D, 105, 106 kidney disease, 115

T1DM lower-limb amputations, 115116
complications, 114 microvascular, 115
diagnosis, 108, 113 premature disability, 114
China and Western Pacific (WP) Region, diabetes in retinopathy, 115
antidiabetes medications, 7476 MENA Region, T2DM, 49, 52
diagnosis, 7071 Continuous subcutaneous insulin infusion (CSII), 75
epigenome-wide association study, 6667 Coronary artery disease, 89, 116, 129, 137
future directions, 7677 Coronary heart disease, 68, 137
genome-wide association studies, 66 Cultural barriers, 19, 58
health care delivery system, 76 Culturally and linguistically diverse (CALD), 158
JADE programme, 76 CVD. See Cardiovascular disease (CVD)
morbidity and mortality, 6768
number of peoples affected by, 64, 65
pathophysiology, 6566 D
prevalence, 64, 65 Daily insulin dose (DID), 209210
prevention and control strategies Depression, 52, 102, 120, 139, 152, 182
early detection and prevention, 74 Developmental Origins of Health and Disease
National Plan and NCD prevention, 72 (DOHaD), 242
tobacco control, 72, 74 Diabetes. See also specific countries
primary prevention of T2DM, 7172 cause of death in poverty countries, 25, 26
risk factors clinical inertia, 9192
beta-cell dysfunction, 67 complications, 152, 228
endemic infections, 67 global burden of, 14
socioeconomic determinant, 67 type 1 diabetes (see Type 1 diabetes
WPDD Plan for Action (20062010), 72, 73 mellitus (T1D))
young-onset and comorbities, 6970 type 2 diabetes (see Type 2 diabetes mellitus
Cholesterol (T2DM))
HDL, 8, 24, 55, 102, 159 Diabetes Care Improvement Package, 185
high blood, 157 Diabetes Epidemiology Collaborative Analysis of
LDL, 55, 103, 139, 159, 255, 257, 263 Diagnostic Criteria in Asia (DECODA)
non-HDL, 103 data, 64
total, 93, 102, 137, 159, 213 Diabetes prevention program (DPP), 1625, 93, 180,
Community Diabetes Prevention Centers (CDPC), 272, 273, 275
2122, 25, 26 Diabetes self-management education (DSME), 262
Complications in diabetes, 152, 228 Diabetic foot, 114, 119, 137138
Argentina, 114 Diabetic ketoacidosis, 113, 138, 195
Brazil, 114 Diabetic kidney disease, 68, 76, 115
Caribbean Diabetic nephropathy, 115, 138, 211, 216, 228,
amputations, 137138 255, 265
coronary heart disease, 137 Diabetic retinopathy, 70, 71, 89, 114, 115, 119, 138,
dental disease, 139 225, 228
depression, 139 Diacylglycerol (DAG), 9
diabetic foot disease, 137 Diet, 3, 11, 15, 24, 39, 40, 52, 55, 57, 59, 65, 75, 88, 91,
erectile dysfunction, 139 93, 140, 229, 240242, 262263, 265, 272
health disparities, 136137 Dietary Approaches to Stop Hypertension (DASH) diet,
hyperglycaemic crises, 138 263
nephropathy, 138 Dietary composition, 263265
osteopenia, 139 Dietary fiber, 16, 20, 245
reduced lung function, 139 Dietary Guidelines for Americans, 21
retinopathy, 138 Dietary pattern, 5556, 241, 262263
stroke, 137 Dipeptidyl peptidase-4 inhibitor (DPP4-i), 92
vascular dementia, 139 Disability-adjusted life years (DALYs), 115
ethnic/immigrants populations, Western Europe, 228 District Health Boards (DHBs), 185
Indigenous Canadians, 239240 DPP. See Diabetes prevention program (DPP)
Latin America DREAM (Diabetes Reduction Assessment with Ramipril
blindness, 114 and Rosiglitazone Medication), 22
cardiovascular disease, 116 DRUID (Diabetes and Related conditions in Urban
DALY and YLDs, 116 Indigenous people in the Darwin region)
ESRD, 114115 study, 154, 156, 159
288 Index
E G
Eastern European countries, type 1 and 2 diabetes in Genetic Investigation of ANthropometric Trait (GIANT)
anti-diabetes medications, 216217 consortium, 136
complication prevalence assessments, 212214 Genome-wide association studies (GWAS), 66, 156, 243,
diabetes care services, 214216 253, 254
epidemiological studies, 192194, 218 Gestational diabetes mellitus (GDM), 41, 228
genetic studies, 210211, 218 Caribbean, 135
i-IFG and i-IGT, 217 in ethnic women, 158159
life expectancy at birth, 191192 in Indigenous Australians, 156
mortality in Indigenous Canadians, 239, 242243
gender and age-related aspects, 193204 Latin America
and GNI per capita, 191192 diagnosis, 112113
non-pharmacological management, 216 genetic studies, 107
and prediabetes, diagnostic criteria, 211212 IADPSG criteria results, 105
primary prevention, 217 macrosomia, 105
research, 217 prevalence, 105
total population, 191192 Get Checked programme, 184185
in Ukraine population Gliclazide, 216
birth seasonality, 206208 Glitazone, 92
daily insulin dose, 209210 Glucose transporter type 1 (GLUT1), 129
early-life conditions and risk, 204 Glutamic acid decarboxylase 65 antibody
famine, prenatal exposure, 204206, 218 (GADA), 210
GADA in adults, 210 Glycaemic index (GI), 67, 140
prevalence, 192194 Glycated haemoglobin (HbA1c), 24, 37, 41, 64, 70,
Electromagnetic devices, 216 86, 9193, 108, 118, 120, 138, 151, 152,
Electronic medical records, 118, 173, 270 159162, 168, 169, 185, 210, 212, 214, 226,
Endocrinology Research Center, 217 253271, 274
End-stage renal disease (ESRD), 3, 52, 68, 114, Glycemic control, 14, 55, 57, 112, 155, 160, 211, 214,
115, 117, 118, 138, 160161, 215, 217, 228, 230, 255, 256, 262, 264
239, 255 Green Prescription, 185
Enterovirus RNA, 129 Gross domestic product (GDP), 3, 25, 64, 117, 137
Ethnic/immigrants populations in Western Europe, Gross national income (GNI), 191192
diabetes in
antidiabetic medications, 229230
complications, 228 H
diagnosis, 226227 Healthcare expenditures, 2, 3
future directions, 231 Help Educate to Eliminate Diabetes (HEED), 273
health-care delivery system, 228229 Hemodialysis, 115, 214, 215, 239, 240
heterogeneity, 226 Hepatitis C virus (HCV), 5455
non-pharmacological management, 229 High-density lipoprotein (HDL) cholesterol, 8, 24, 55,
pathophysiology, 226227 102, 159
prevalence, 227228 HIV/AIDS, 19, 34, 40, 129, 142
prevention of type 2 diabetes, 230 Human capital investment, 13
research, 230231 Human Genome Project, 275
Ethnicity, 11, 16, 19, 34, 36, 38, 50, 63, 65, 71, 88, 113, Human T lymphotropic virus type 1 (HTLV-I) virus, 129
134, 137, 158, 160, 168, 170178, 226228, Hyperglycemia and Adverse Pregnancy Outcome
252, 256, 265, 268270 (HAPO) study, 131
Exercise, 11, 15, 17, 1921, 24, 56, 57, 91, 93, 119, Hypertension (HTN), 7, 8, 14, 24, 53, 58, 64, 91,
140141, 216, 229, 230, 245, 264265. See 102104, 110, 111, 114, 116, 137, 139, 140,
also Physical activity 161, 228, 239, 245, 253, 255, 257, 271
Hypoadiponectinaemia, 132
Hypoglycemia, 57
F
Fatty acids, 9, 65, 131
Finnish Diabetes Prevention Study (FDPS), 1516 I
First Nations and Inuit Health Branch (FNIHB), 243 IDF. See International Diabetes Federation (IDF)
Food and Agriculture Organization of the United Nations IDPP. See Indian Diabetes Prevention Program (IDPP)
(FAO), 102 Impaired fasting glucose (IFG), 9, 12, 24, 37, 111, 154,
Food glycemic index, 216 211212
Index 289
Impaired glucose tolerance (IGT), 912, 15, 16, 22, 24, complications, 239240
25, 33, 36, 71, 74, 75, 93, 111, 135, 152, 154, diet, 240242
155, 159, 211212 environmental/socioeconomic risk factors, 243
India and Southeast Asia, diabetes in genetics, 243
awareness, 90 health-care access and delivery, 243244
clinical inertia, 9192 incidence and prevalence of, 236239
control measures, 9091 intrauterine/early life factors, 242243
economic and social impact, 86 obesity and body composition, 240
factors physical activity, 242
ageing, 8688 primary prevention, 244245
alcohol, 89 smoking, 240
anthropometry, 8889 Insulin and glucagon-like peptide-1 (GLP-1) receptor
genetic susceptibility, 89 agonist, 92
lifestyle changes, 86 Insulin-dependent diabetes mellitus (IDDM). See Type 1
micro-and macrovascular complications, 89 diabetes mellitus (T1D)
screening methods, 8990 Insulin pump therapy, 230
smoking, 89 Insulin resistance, 811, 55, 65, 67, 74, 88, 89, 9294,
urbanisation, 8687 131133, 136, 142, 156, 204, 217, 225, 226,
future directions, 9495 240, 252, 253, 273, 275
non-pharmacologic approach, 91 Insulin secretagogues, 75
pharmacologic therapy, 92 Insulin secretion, 8, 9, 11, 12, 16, 40, 55, 75, 204
prevalence, 8588 abnormal, 113
primary prevention, 9293 beta-cell, 252
research, 94 carbohydrates, 263
RSSDI therapeutic wheel, 94, 95 glucose-stimulated, 132, 133, 136
Indian Council of Medical Research (ICMR) study, Insulin sensitivity index (IS), 65
88, 91 Insulin signaling pathways, 9, 10
Indian Diabetes Prevention Program (IDPP)-1, 23 Insulin therapy, 75, 92, 95, 133, 159
Indian Diabetes Prevention Program (IDPP)-2, 23 Intensive lifestyle intervention (ILI), 16
Indian Diabetes Prevention Program (IDPP), 16, 18, Intermuscular adipose tissue (IMAT), 130, 131
25, 92 International Collaborative Study on Hypertension in
Indian Diabetes Risk Score (IDRS), 90 Blacks (ICSHIB), 129
Indigenous Australians, diabetes in, 162 International Diabetes Federation (IDF), 1, 2, 7, 33, 63,
age profile, 152153 102, 192193
CALD communities, 157159 International Journal of Diabetes in Developing
death rates in remote and rural areas, 156157 Countries (IJDDC), 94
life expectancy, 153 Isolated impaired fasting glycaemia (i-IFG), 217
management Isolated impaired glucose tolerance (i-IGT), 217
blood assessment, 159
ESRD, 160161
POCT for HbA1c, 161162 J
for triglycerides, 159, 160 Joint Asia Diabetes Evaluation (JADE) programme, 70
type 2 diabetes, 160 Juvenile onset diabetes. See Type 1 diabetes mellitus
urine ACR, 161 (T1D)
mortality rate, 153
vs. non-Indigenous Australians, 152153
prevalence, 153154 K
risk factors Kahnawake Schools Diabetes Prevention Program
gene-related studies, 156 (KSDPP), 245
gestational diabetes, 156 Kaupapa Mori research approach, 166167
low birth weight, 156 Kharkov Institute of Endocrinology, 217
obesity, 155156 Kidney disease, 49, 158, 159, 239
social determinants, 156 Kidney transplantation, 115, 174, 214, 215, 239
type 2 diabetes in young people, 155 Kyiv Institute of Endocrinology and Metabolism, 217
Indigenous Canadians, diabetes in
age structure, 236
languages, 235236 L
population, 235 Laparoscopic adjustable gastric banding (LAGB), 266
type 2 diabetes Laparoscopic vertical sleeve gastrectomy (LVSG), 266
290 Index
Latin America, diabetes in Green Prescription, 185

admixed populations, 106 GRx programme, 185
anti-diabetes medications, 119120 Te Wai o Rona: Diabetes Prevention Strategy, 186
complications diabetes screening, 185
blindness, 114 eligibility criteria
cardiovascular disease, 116 outcomes, 167
DALY and YLDs, 116 population, 167
ESRD, 114115 search strategy and information sources, 167168,
kidney disease, 115 187188
lower-limb amputations, 115116 study designs, 167
microvascular, 115 Get Checked programme, 184185
premature disability, 114 health and research, perspective on
retinopathy, 115 bicultural strategies, 165167
demographic modifications, 101 kaupapa Mori research approach, 166167
future directions, 122 partnership, participation and protection, 166
gestational diabetes Living Well with Diabetes, 185
diagnosis, 112113 objectives, 167
genetic studies, 107 observational studies reviewed, characteristics of,
IADPSG criteria results, 105 168, 170179
macrosomia, 105 population, 165
prevalence, 105 prevalence of
health-care delivery system, 117118 complication risk factors, 169, 180182, 184
life expectancy, 101102 CVD/mortality risk, 182184
non-pharmacological management, 118119 known and undiagnosed diabetes, 168169,
prediabetes, 108 179180, 184
research, 121122 pre-diabetes, 169, 179180
total populations, 101 type 2 diabetes, 167
type 1 diabetes publications, systematic review of, 168169
diagnosis, 113114 Virtual Diabetes Register, 185
genetic studies, 107108 Massage, 216
incidence, 105106 Maturity-onset diabetes of youth (MODY), 134
prevalence, 105 Mediterranean diet, 262263
type 2 diabetes Metabolic stress, 6567, 133
Amerindian populations, 106107 Metformin, 4, 16, 2225, 74, 92, 117, 119, 141, 216,
BMI for age by age and country, 102, 104 230, 270273, 275
diagnosis, 108112 Mexico, diabetes in, 7, 101, 121, 127
elder patient, 104 ESRD incidence, 115
genomic studies, 106107 implementation of preventive actions, 118119
prevalence, 102, 103 T1D, 105, 106, 113114
primary prevention, 120121 T2DM, 102, 103, 108109, 120
risk factors, 103 UNEMES program, 117
women, 103104 YLL, 116
Life expectancy, 34, 36, 68, 101, 116, 127, 153, 191, Microvascular disease, 89, 160
197199, 203, 228, 236, 272 Middle East and North Africa (MENA) Region,
Low-density lipoprotein (LDL) cholesterol, 55, 103, 139, T2DM, 59
159, 255, 257, 263 complications, 49, 52
cultural factors
dietary pattern, 5556
M healthcare quality, 57
Macrovascular diseases, 56, 89, 160, 225, 228, 255 health literacy, 5657
Maculopathy, 138, 182 poor adherence, 57
Magnesium, 241 sedentary lifestyle, 56
Malonyl-CoA, 9 smoking, 56
Mori and other ethnic groups, New Zealand epidemiology, 50
data collection, 168 ethnicity of, 49, 50
data synthesis, 168 future directions, 58
Diabetes Care Improvement Package, 185 improving strategies
diabetes prevention and prevention research clinical care, 59
Energize programme, 185186 diabetes education, 59
Index 291
guidelines, 59 in Arab countries, 54, 58

National Diabetes Prevention Program, 58 body mass index, 37, 65, 74, 88, 102, 104, 112, 129,
pesticide usage, 59 130, 135, 155, 156, 159, 240, 252
screen for diabetes, 58 in Caribbean, 129
treating hepatitis C infection, 59 central, 39, 53, 59, 64, 89, 130, 226, 230
obesity rates, 49, 51 childhood, 53, 58, 74, 186, 239, 242
prevalence, 52 China and WP Region, 6467
prevalence rates, 49, 50 high-fat and high-caloric diet, 40
prevention, 5758 Indigenous Australians, 155156
risk factors Indigenous Canadians, 240
chronic hepatitis C infection, 5455 Latin America, 102, 109
genetics, 5354 in MENA region, 5253
obesity, 5254 nutritional management, 140
pesticide exposure, 55 rates, 49, 50, 110, 130
physical activities, 54 USA population, 252
total populations, 49 in women, 141
Mineral water therapy, 216 young-onset, 242
Modelling the Epidemiologic Transition (METS), 131 Oral antidiabetic agents (OHAs), 91
Multiple daily injections (MDI), 75 Oral glucose tolerance test (OGTT), 40, 64, 151, 152,
Multivariate analysis, 227 154, 168, 211212
Orlistat, 22
Overt albuminuria, 161
N Oxidative stress, 55, 75, 93, 132, 133, 138, 141
National Aboriginal and Torres Strait Islander Health
Measures Survey, 159
National Diabetes Services Scheme (NDSS), 151 P
National Health Interview Survey (NHIS), 251252 Pathobiology of Prediabetes in a Biracial Cohort
Nephropathy, 52, 57, 89, 90, 114, 138, 228, 255 (POP-ABC) study, 11
Non-communicable disease (NCD), 33, 102, 138, Peripheral artery disease, 116, 160, 255, 256
140143 Peripheral neuropathy, 52, 89, 138
Nonesterified fatty acid (NEFA), 89 Peripheral vascular disease, 14, 89, 138, 173
Non-hispanic blacks (NHBs), 273 Persistent organic pollutants (POPs), 67
Non-insulin-dependent diabetes (NIDDM). See Type 2 Physical activity, 1, 3, 8, 9, 15, 16, 1822, 24, 3940,
diabetes mellitus (T2DM) 49, 53, 54, 5658, 65, 88, 89, 91, 93, 120,
Non-pharmacological management 121, 131, 139142, 166, 185, 216, 217, 239,
Caribbean 242, 244, 245, 252, 256, 258, 262, 264, 265,
bariatric surgery, 141 272, 275
diabetes education, 140 Physiotherapy, 216
exercise, 140141 Pioglitazone, 2224, 141
nontraditional/complementary techniques, 141 PODOSA (Prevention Of Diabetes and Obesity in South
nutrition, 140 Asians), 230
tobacco cessation, 141 Point of care testing (POCT), 161
ethnic/immigrants populations, Western Europe, 229 Polymorphisms, 107, 136, 210, 211
India and Southeast Asia, 91 Population-based Tobago Health Study, 136
Latin America, 118119 Prediabetes, 910, 15, 17, 18, 21, 23, 50, 52, 55, 58, 63,
USA 64, 122, 152, 226
DASH, 263 in Asia, 7071
DSME, 262 with cardiovascular and metabolic risk factors, 93
PREDIMED, 262 Caribbean, 134135
vegetarian diet, 263 double, 24
Nontraditional/complementary techniques, 141 Eastern Europe, 211212
Normal glucose tolerance (NGT), 11, 16 initial transition to, 1112
Latin America, 108112
progression to type 2 diabetes, 1011, 25
O USA, 253255
Obesity, 7, 8, 10, 12, 18, 19, 34, 3639, 57, 139, 152, Prevention with Mediterranean Diet
218, 225, 230, 231, 265, 271. See also Type 2 (PREDIMED), 262
diabetes mellitus (T2DM) Primary Health Organisations (PHOs), 185
abdominal, 88, 102 Psychosocial stress, 67, 253
292 Index
R historical perspective, 34
Race/ethnic difference future directions, 44
biological factors healthcare access and complications, 4243
complications, 255 prevalence, 33
insulin resistance, 252 risk factors
obesity and fat distribution, 252 adiposity, 39
nonbiological factors age, 3436
acculturation, 252 diet, 40
complications, 256 environmental influence (migration), 38
health behaviors, 252253 ethnicity, 36
Randomized controlled trials (RCTs), 17 family history, 3436
Registered dietitian (RD), 59 gender, 3436
Renal replacement therapy (RRT), 68, 214216 HIV/AIDS impact, 40
Research Society for the Study of Diabetes in India obesity, 3839
(RSSDI), 94 physical activity, 3940
Retinopathy, 138, 182, 184, 228 urbanisation, 3638
Rosiglitazone, 22, 23 Sulfonylureas, 22, 75
Roux-en-Y gastric bypass (RYGB), 266 Sulphonylureas (SU), 92, 117, 119, 141
RSSDI diabetic therapeutic wheel, 94, 95
T
S T2DM. See Type 2 diabetes mellitus (T2DM)
Salt intake, 91 Te Wai o Rona: Diabetes Prevention Strategy, 186
Sandy Lake Health and Diabetes Project (SLHDP), 244 Thiazolidinedione (TZD) drugs, 4, 22, 25, 92
Screen-detected type 2 diabetes (SDDM), 218 Total cholesterol, 93, 102, 137, 159, 213
Selenium, 241 Transformation of Indigenous Primary Healthcare
Self-monitoring of blood glucose (SMBG), 256 Delivery (FORGE AHEAD), 244
Sexual dimorphism, 129131 Treaty of Waitangi, 166
Slim Initiative in Genomic Medicine for the Americas Tuberculosis, 13, 19, 104
(SIGMA) Type 2 Diabetes Consortium, Type 1 diabetes mellitus (T1D)
121122 in Caribbean, 135
Smoking, 3, 56, 59, 67, 68, 72, 74, 89, 103, 110, 153, in Eastern European countries
156, 160, 167, 180, 182, 228, 239, 240, 245, birth seasonality, 206208
253, 256, 257 complication prevalence assessment, 212213
Socioeconomic status (SES), 67, 157, 158, 257, 275 daily insulin dose, 209210
Sodium-glucose co-transporter 2 (SGLT2) inhibitors, 92, early-life conditions and risk, 204
119, 141, 271 epidemiological studies, 192193, 218
South America, 120, 158, 251, 252, 274 GADA in adults, 210
incidence of type 1 diabetes, 106 genetic studies, 210211, 218
T2DM mortality, gender and age-related aspects,
diagnosis, 111112 193204
prevalence of obesity, 102, 104 health care costs, 152
South Asians, diabetes in, 16, 167, 226229, 252, 254 in immigrants children, 228
abnormal glucose tolerance in women, 158 Latin America, 105106
epigenome-wide association study, 66 diagnosis, 113114
normal glucose tolerance, 65 genetic studies, 107108
risk for diabetes in, 226227 incidence, 105106
Special Diabetes Program for Indians Diabetes prevalence, 105
Prevention (SDPI-DP), 273 Type 2 diabetes mellitus (T2DM), 33
STOP-NIDDM (Study to Prevent Non-Insulin- in Caribbean, 129131
Dependent Diabetes Mellitus), 22 children and youth, 142
Stress, 57, 91, 103, 253 diagnosis, 134
Stroke, 14, 49, 68, 89, 116, 129, 137, 152, 214, 265 early life interventions, 142
Sub-Saharan Africa (SSA) region, diabetes in, 7 lifestyle factors, 129131
clinical manifestations, 4041 women, 141142
control and prevention, 4344 youth with, 135
economic cost, 4142 in Eastern European countries
epidemiology anti-diabetes medications, 216217
current trends, 34 birth seasonality, 207208
Index 293
complication prevalence assessment, 213214 U

early-life conditions and risk, 204 Uruguay, 101, 115
epidemiological studies, 192194, 218 T1DM, 105, 106, 113
famine, prenatal exposure, 204206, 218 T2DM, 102, 103
genetic studies, 210211, 218 USA, in diabetes
mortality, gender and age-related aspects, adults with diabetes, 86
197199 antidiabetes medications
non-pharmacological management, 216 American Indian/Alaskan Native, 273
and prediabetes, diagnostic criteria, 211212 with Asian American, 273274
primary prevention, 217 DPP interventions, 272273
SDDM, 218 GLP-1 receptor agonists, 271
global epidemic of, 2, 4, 13 HEED, 273
health care costs, 152 metformin, 270271
among Indigenous Canadians NHBs, 273
complications, 239240 repaglinide, 270
diet, 240242 SGLT2 inhibitors, 271
environmental/socioeconomic risk factors, 243 weight-loss medications, 271
genetics, 243 classification, 251252
health-care access and delivery, 243244 complications, 255
incidence and prevalence of, 236239 diagnosis, 253255
intrauterine/early life factors, 242243 dietary composition
obesity and body composition, 240 glycemic index/glycemic load, 263
physical activity, 242 lifestyle intervention, 265
primary prevention, 244245 low-carbohydrate/low-fat diets, 264
smoking, 240 physical activity, 264265
Latin America weight reduction, 265
Amerindian populations, 106107 epidemiology, 251252
BMI for age by age and country, 102, 104 GWAS, 253, 254
diagnosis, 108112 HbA1c, minority populations, 274
elder patient, 104 health system interventions
genomic studies, 106107 evidence-based general diabetes, 256257
prevalence, 102, 103 healthcare organization interventions, 262
primary prevention, 120121 intervention level, 257
risk factors, 103 metabolic/process measure, 257
women, 103104 multi-target interventions, 262
pathophyisology, 810 patient interventions, 258261
prediabetes provider interventions, 261262
annual rate, 10 types of, interventions, 258261
IGT and IFG, 9 non-pharmacological management
initial transition to, 1112 DASH, 263
progression, 1011 DSME, 262
prevention PREDIMED, 262
CDPC, 2122 vegetarian diet, 263
costs of, 25 primary prevention, 274275
Da Qing study, 15 race/ethnic difference (see Race/ethnic difference)
DPP, 16 surgical interventions
DPP lifestyle intervention, 17 Bariatric surgery, 266, 267
FDPS, 1516 BMI 35 kg/m2, 266
IDPP, 16 BMI 35 kg/m2, 266
knowledge among health professionals, 1718 ethnic differences, 266269
lifestyle modification, 1517 morbidity and mortality, 266270
medications, 2224 non-pharmacological management, 274
primary, 1214 T2DM, Hispanics/Latinos Living, 112
strategies in community, 1821
risk factors, 78
unique vulnerabilities in developing countries, V
1415 Vegetarian diet, 263
in worldwide estimation, 7 Virtual Diabetes Register (VDR), 185
in young Indigenous Australians people, 155 Vitamin B6, 241
294 Index
Vitamin D World Health Organization (WHO), 43, 70, 77,

deficiency, 56 102, 121
production of, 206
against T2DM development, 240
Vitamin E, 241 X
XENDOS (XENical in the Prevention of Diabetes in
Obese Subjects) study, 22
W
Western Pacific Diabetes Declaration (WPDD) Plan for
Action, 72, 73 Y
World Diabetes Day Resolution by the United Nations Years lost due to disability (YLD), 115, 116
General Assembly, 43 Yoga, 93, 141

Sam Dagogo-Jack Eds. Diabetes Mellitus in Developing Countries and Underserved Communities

Uploaded by

Copyright:

Available Formats

Sam Dagogo-Jack Eds. Diabetes Mellitus in Developing Countries and Underserved Communities

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Sam Dagogo-Jack Eds. Diabetes Mellitus in Developing Countries and Underserved Communities

Uploaded by

Copyright:

Available Formats

What is the book about?

What is the book about?

What populations are most affected by diabetes?

What populations are most affected by diabetes?

Diabetes Mellitus in

ISBN 978-3-319-41557-4 ISBN 978-3-319-41559-8 (eBook)

Library of Congress Control Number: 2016959999

Springer International Publishing Switzerland 2017

Printed on acid-free paper

This Springer imprint is published by Springer Nature

No other disorder exerts a more pervasive and catholic global burden on

Memphis, TN, USA Sam Dagogo-Jack

1 The Global Burden of Diabetes: An Overview . . . . . . . . . . . . . . . . 1

12 Diabetes in Ethnic Minorities and Immigrant

S.R. Aravind, MBBS, DNB, FRCP, FDRC, DHA, FRSSDI Columbia

Vitaliy Gurianov, PhD Bogomolets National Medical University, Kyiv,

Helmut Steinberg, MD Department of Medicine, Division of Endocrinology,

Sam Dagogo-Jack, MD, is Professor of

Introduction [5]. Whatever the causes, the estimates are con-

Springer International Publishing Switzerland 2017 1

King, Aubert & Herman, 1998

Introduction again with the fastest increases occurring in

Springer International Publishing Switzerland 2017 7

Fig. 2.1 Projected

415 Africa 141%

million Middle East & North Africa 104%

South East Asia 82%

South and Central America 65%

Western Pacific 40%

North America & Caribbean 37%

Fig. 2.2 The major

evolution of individual pathophysiological following features: (1) baseline fasting plasma

Fig. 2.4 Criteria for

200 mg/dl (11.1

HbA1c < 5.7% 5.7 6.4% HbA1c > 6.5%

Fig. 2.5 Human

modification is a more compelling approach to general public, through demonstrative education

government leadership should collaborate to face-to-face counseling sessions in group for-

popularity of informal retail markets (espe- to incorporate some element of self-monitor-

Fig. 2.7 Diabetes

Community Diabetes Prevention Centers

Medications for Diabetes placebo [50]. The STOP-NIDDM (Study to

Limitations of Medications Table 2.4 Desirable characteristics of an ideal drug for

Costs of Preventing T2DM agencies) would need to be explored and mobi-

Lower respira- Ischaemic

The effective translation of diabetes pre- Diabetes Prevention Centers, to serve as a

Overview Diabetes prevalence in adults is in general

Springer International Publishing Switzerland 2017 33

Epidemiology of Diabetes in Africa The burden of diabetes in sub-Saharan Africa is

IDF 2013 2035 Increase

Prevalence (%) estimates of

Fig. 3.4 Prevalence of 0

rural [ ] and urban [ ]

studies in Africa, using

randomly selected samples

Adiposity Available data strongly links the current epide-

Average GNI per capita

Average indirect cost per person with diabetes

Average total cost per person with diabetes

Future Perspectives of Diabetes