1

TABLE OF CONTENTS

Hair loss is not a genetic destination .........................................................4

The third edition ......................................................................................5

How this book is organized ......................................................................7

CHAPTER 1: Introduction ........................................................................11

CHAPTER 2: Genetic destiny...................................................................16

CHAPTER 3: Know your diagnosis ..........................................................36

CHAPTER 4: Pattern hair loss: basic misunderstandings ............................59

CHAPTER 5: Pattern hair loss: getting to the roots ....................................74

CHAPTER 6: Chronic inflammation of the scalp ........................................95

CHAPTER 7: Reversing pattern hair loss .................................................111

CHAPTER 8: Becoming a best responder: hair loss type ..........................131

CHAPTER 9: Becoming a best responder: diet........................................149

CHAPTER 10: The diet-hair loss connection ............................................162

CHAPTER 11: The lifestyle-hair loss connection .......................................190

CHAPTER 12: The microbiome-hair loss connection ................................205

CHAPTER 13: Your next steps (action plan) ............................................218

Thank you ...........................................................................................223

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 Disclaimer
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be confused with medical advice nor used to diagnose or treat any illness, disease, or health problem. If a reader
chooses to implement any recommendations from this book, perfecthairhealth.com, or my.perfecthairhealth.com,
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clear: the information here is not and does not replace any medical, legal, or professional advice. Please use this
information at your own risk. As always, consult your doctor before trying anything you read online (including
content from this book, my.perfecthairhealth.com, and perfecthairhealth.com).

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3
 HAIR LOSS IS NOT A GENETIC
DESTINATION

When I was 16, a classmate told me, “You have a bald spot.” A few months later, I was
diagnosed with male pattern hair loss. I was embarrassed; I didn't understand why it was
happening. Overnight, the diagnosis catalyzed my interest in hair loss science — all to
understand the problem (and try to stop it). Over a decade, I conducted thousands of hours
of research and spent thousands of dollars on Rogaine, shampoos, supplements, topicals,
and low-level laser therapies. My hair loss never slowed down. I knew there had to be
something I was missing.

I spent too much time researching, experimenting, and failing before finally finding a path
toward hair regrowth that worked well for me, and that fit with my treatment preferences.

That’s why I've written this book and built a community dedicated to hair recovery: to help
you learn, avoid frustration, save time and money, and join a group of supportive people.
The answers are out there; they just need to be consolidated to one place. That place is here.

Regrowing your hair takes dedication, hard work, and trust in the paths paved by others.
But for myself (and many members here), the commitment was worth it. I want you to
succeed and realize that hair loss doesn’t have to be your genetic destination.

As you begin to implement these changes, please remember, you are not alone. Up to 50%
of women and 80% of men experience hair loss throughout a lifetime. It’s a commonly
shared problem. But it’s a problem within our power to resolve.

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 THE THIRD EDITION

In 2014, I released the first edition of the Perfect Hair Health book + video. I offered email
support to anyone who messaged me. I worked one-on-one with as many readers as I could.

Two years later, I decided to rewrite and re-release everything. I interviewed readers who
experienced significant hair regrowth. I identified commonalities in their diets, lifestyles,
hair loss therapies, and techniques. I uncovered practices these responders unknowingly did
that others didn’t. Then I compiled my learnings into a second edition (released in 2016).

Since then, this site has come a long way. I’ve published three peer-reviewed papers on
androgenic alopecia. This site has produced dozens of success stories. And as of today, we’ve
grown into a community of thousands.

For the past year, I’ve been quietly working on another update: conducting video interviews,
rewriting the book, updating the demonstration videos, drafting dozens of guides, making
video courses, designing 130+ personalized regrowth regimens, and cataloguing 40+ reader
case studies (2,000-word write-ups and photos detailing past readers’ hair recoveries).

Now I’ve consolidated all of this into a new release: a third edition. And this update comes
with a forum where we can share ideas, hold each other accountable, disseminate new
learnings, showcase progress, interact with success stories, and help everyone maximize
their chances for significant hair recovery. It all starts here, with this book.

As you read on, it might be tempting to skim content, skip chapters, or just ask questions in
our forum. Please don’t do this. I want you to succeed, and your understanding of this
material is integral to your success. With this in mind, I recommend the following:

1. Read this book cover-to-cover. We can’t fix something we don’t understand. This book
dives deep into hair loss science, reveals our treatment options, and provides you with
the information needed to make an educated decision on how to help your hair.

2. Take our regrowth roadmap survey. This questionnaire guides you to a custom-built
hair regrowth regimen — all based on your age, gender, hair loss type, comfortability with
FDA-approved drugs, and time constraints.

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This should provide you with the groundwork to interact with our community. What we
want: members who engage with one another through respect, encouragement, and
evidence-based debates. What we don’t want: someone not reading these materials... then
asking questions in our forum that are answered elsewhere throughout this book and site.

If you need technical support (or have questions unfit for public discussion), you can email
me. While I no longer provide one-on-one email support, I try to respond to everyone.

Otherwise, our forum is an excellent resource center. Have questions about this book? Or
our expert interviews? An ultimate guide? Or even a case study? Each chapter, guide,
interview, and case study has a dedicated discussion thread. In fact, many of our case studies
are active community members. That means you can interact with them directly. Or you can
start a topic, post research, or even make a progress log to start tracking your hair.

Lastly, I want to thank you for reading — and for your support to keep this site running. I
hope this material pays dividends to your health and hair. I look forward to your progress!

All my best,

Rob English
Founder, PerfectHairHealth.com
[email protected]

Key links
These links are complementary to the book and referenced regularly. Please feel free to look
them over!

• Success stories

• Case studies

• Customizable action plan (interactive survey)

• Ultimate guides (hair loss therapies, treatments, chronic conditions, etc.)

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 HOW THIS BOOK IS ORGANIZED

This book and membership site work in tandem to (1) dive deep into hair loss science, and
(2) build you a hair regrowth protocol tailored to your specific needs and preferences.
Chapters 1-5: why we lose our hair. Chapters 6-13: what we’re going to do about it.

Chapter 1: My introduction
All hair loss sufferers remember when they first noticed their hair was thinning. This
chapter uncovers my story, my diagnosis, my attempts to resolve it, and how I spent
thousands of dollars on treatment options that slowed (but never stopped) my hair loss.

Chapter 2: Genetic destiny

Physicians often say that hair loss is genetic and – aside from a hair transplant – we can’t do
much to stop it. This is sometimes true, but it’s not the whole story. While we can have
genes that predispose us to hair loss, we also may have the power to turn those genes on and
off. The latest scientific research — along with my genetic tests, medical diagnosis, family
predisposition to hair loss, before-after photos, and readers’ success stories — shows that
hair recovery is possible (and through many approaches).

Chapter 3: Know your diagnosis

If we want to reverse hair loss, we need to correctly diagnose our hair loss type. Why?
Because different hair loss types stem from different causes (and thereby require different
treatments). Unfortunately, hair loss misdiagnoses are common... leading to subpar
treatments for many sufferers. For instance, while androgenic alopecia may constitute 95%
of hair loss cases in men, this number masks the fact that up to 30% of men with
androgenic alopecia may also have other forms of hair thinning that can (1) accelerate the
hair loss process, and (2) make a one-size-fits-all treatment approach obsolete. This chapter
helps us identify our forms of hair loss, offers next-steps for testing, and reveals the two big
hair loss categories: (1) hair follicle miniaturization, and (2) hair shedding disorders. Once
we can identify our forms, we can go about seeking the best treatments.

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Chapter 4: Pattern hair loss: basic misunderstandings
Androgenic alopecia (pattern hair loss) is one of the most common hair loss types... and
most researchers agree that a hormone called dihydrotestosterone (DHT) causes it. As such,
it’s often recommend that we treat pattern hair loss with drugs to reduce our body’s ability
to produce DHT. In this chapter, we’ll dive into the evidence supporting DHT’s complicated
relationship with pattern hair loss, and what the paradoxes of DHT might tell us about
additional targets for fighting androgenic alopecia.

Chapter 5: Pattern hair loss: getting to the roots

Beyond DHT, there are a lot of other changes that occur in balding scalps. This chapter
catalogues them, then follows the trail of evidence to trace these symptoms, conditions, and
triggers all the way to their roots. In doing so, we’ll create a pattern hair loss flowchart that
attempts to answer some missing pieces of the DHT-pattern hair loss hypothesis. Moreover,
we’ll also speculate additional explanations for (1) the mechanisms behind hair loss, (2)
why most hair loss drugs fail to regrow 100% hair, and (3) what else we can target to return
our scalps to a healthy state and potentially allow for better hair growth.

Chapter 6: Chronic inflammation of the scalp

One of the biggest challenges while fighting hair loss is pinning down the cause of chronic
scalp inflammation. In this chapter, we’ll explore evidence implicating a few unique causes,
along with reported the outcomes achieved by people targeting them. By the end, we’ll have
a clearer idea of things we can target that might help us achieve significant hair regrowth.

Chapter 7: Reversing pattern hair loss

If we want to regrow our hair, we need to restore our scalps to their healthy state before our
hair follicle miniaturization began. This means we need to reverse fibrosis, (maybe)
calcification, and perhaps one of the biggest drivers of androgenic alopecia. In this chapter,
we’ll reveal the science behind why full hair recoveries are possible. We’ll also uncover the
mechanisms we may need to activate in order to make it happen: our innate wound-healing
capabilities. There are several ways this can be done — with and without drugs. We’ll reveal
these methods, as well as the data from one of our peer-reviewed studies on androgenic
alopecia.

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Chapter 8: Becoming a best responder: hair loss type
Remember how our hair loss treatments depend on our type of hair thinning? This chapter
brings this issue to the forefront and the dangers of applying the wrong treatment to the
wrong hair loss form. Using insights from our peer-reviewed data, we’ll leverage these
learnings to reveal powerful multi-pronged treatment approaches for your specific hair loss
case. We’ll also reveal where the line between hair follicle miniaturization (i.e., androgenic
alopecia) and hair shedding disorders blur. We’ve got the case studies to demonstrate just
how difficult a correct diagnosis can be.

Chapter 9: Becoming a best responder: diet

The connection between diet and hair loss is a hotly contested subject in hair loss forums.
Here, we’ll dive into the science behind the diet-hair loss connection. In doing so, we’ll
reveal how supplement companies often mis-cite studies and exploit misinformation to sell
us useless hair care products. Finally, using our data, we’ll reveal a possible intersection
point between diet, androgenic alopecia, and hair shedding disorders... and three things we
can do from a dietary perspective to help our health (and maybe our hair).

Chapter 10: The diet-hair loss connection

This chapter offers a diet designed to (1) improve our innate healing responses, (2) reduce
inflammation, and (3) prevent the conditions that precede hair shedding disorders. We’ll
explain why diets are not one-size-fits-all and how to build your own pro-hair diet out of these
three principles. By the end, you’ll know why vegans, vegetarians, the paleo community, and
beyond are all right (and wrong) about their dietary choices... and what to truly focus on if
we want to maximize our chances of success from any hair loss regimen.

Chapter 11: The lifestyle-hair loss connection

When people think of improving their health, they tend to fixate on diet and exercise... not
realizing that three simple lifestyle changes are often more powerful than any dietary or
exercise overhaul in promoting hormonal health, helping us to heal, and improving our
overall longevity. In this chapter, we’ll reveal these three levers... and how to tailor them to
any lifestyle.

Chapter 12: The microbiome-hair loss connection

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Have you ever wondered why third world countries have such lower incidences of hair loss
when compared to the first world? New evidence implicates that the answer may be, in part,
due to gut health. Out gut microflora influences everything from our metabolism to our
immunity — and it might play a key role in preventing and reversing certain hair loss
disorders. This chapter reveals the science, and how to implement these learnings into your
daily life.

Chapter 13: Your next steps

A summary of everything we just learned an action plan for your next steps. This includes a
customized regrowth regimen, a guide to tracking progress, troubleshooting advice, and
how to make the most out of our entire membership community.

Chapter 14: Thank you

A 220-page book certainly isn’t a quick read. I can’t thank you enough for your support and
your time spent reading this material.

Reversing hair loss isn’t easy, but it’s possible. While we all require individualized treatment
approaches, our regrowth roadmap is meant to fast-track you to a hair loss regimen that is
(1) evidence-based, (2) tailored to your types of hair thinning, and (3) built around your
age, gender, needs, and preferences.

In other words, there are several ways for us to cross the finish line. Whether you want to
leverage FDA-approved drugs or an all-natural approach — our community is here to help.
So, read this book, build your action plan, and remember that you have a support system.

I can’t thank you enough for your time and support, and I look forward to your results.

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 CHAPTER 1:
INTRODUCTION

Chapter summary:

• When I first noticed hair loss, what I decided to do, and the thousands of dollars I
wasted on products that never worked for me.

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INTRODUCTION

My story
Even when I was young, I remembered having thin hair. When I was little, my mother
wouldn’t give me short hair cuts because she said my scalp parts looked too spacey. I never
really cared, but because my styling options were limited, my hair was often on my mind. I
always thought this was normal. I was an otherwise healthy, active, medication-free
adolescent — why would I care at all about thin hair?

Fast forward to high school. Things change when your sex hormones kick in: I’m involved in
athletics, I have a great group of friends, but now there’s this added pressure to be attractive
that forces me to reevaluate characteristics I previously didn’t care about (my weight,
height, skin, hair, etc.).

I’ll never forget one moment in my Junior year. I was sitting in class when the girl behind
me poked the top of my head and said, “You have a bald spot.” I laughed and brushed it off,
but it was psychologically damaging. I hated that other people were aware of my thin hair,
and that I couldn’t keep it to myself. The truth was that I also started noticing my hair was
getting thinner, and so I decided to seek medical advice. I scheduled a consultation with Dr.
Robert Leonard — one of the leading hair loss experts in Massachusetts (this was before he
became the hair guru for celebrities and NFL stars like Rob Ninkovich and Wes Welker).

I walked in, met with his consultation officer, and then had a brief exam with Dr. Leonard
himself. He took one comb through my hair and said, “You’ve got male pattern hair loss on
the crown… You are definitely losing your hair.”

I was devastated. At 17, I was diagnosed with male pattern hair loss. To top it all off, my
father had a full head of hair (and still does to this day). Why was this happening to me?

The initial prescription

I followed up with Dr. Leonard’s associate who suggested three strategies to combat further
hair loss. First, start using Rogaine twice-daily. Second, get a prescription for Propecia
(despite the fact that I was only 17, my diagnosis made me eligible). Lastly, begin low-level
laser therapy.

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This was an expensive regimen. While these therapies are scientifically validated to
potentially improve hair loss, their success is contingent upon their continued use. Rogaine
is effective only while you use it. Propecia is the same story.

What about low-level laser therapy? The cost then was $2,000 for eight sessions. These
recommendations felt not only unrealistic, but also out-of-scope for a 17 year-old (I couldn’t
pay for them with my summer job as a camp counselor).

In any case, I felt I had to do something. So, I talked Dr. Leonard’s team into a low level
laser therapy trial, and I immediately picked up some Rogaine. I also got a prescription for
Propecia. But after reading about the drug’s potential side effects, I threw out the bottle the
next day. (Note: I made a lot of mistakes!)

Stepping forward, backward, or nowhere?

If anything, using Rogaine and doing a mini trial of low-level laser therapy at least eased the
stress involved in having hair loss. I thought to myself, “I’m being proactive, I’m reversing
the problem. In a few months, things will be back to normal.”

Things didn’t go as planned. Firstly, my thinning slowed, but it definitely didn’t stop. After
my laser therapy trial ended, all I had left in the fight was Rogaine. After six months and no
progress, I figured I was still adjusting to the topical. Maybe I needed a full year to see
regrowth? Maybe longer?

Two years later, my hair loss had yet to stabilize. It was still on my mind, but I had bigger
things to think about. I was headed to college to compete in Division 1 athletics. With such
a major upcoming life change, my hair was no longer top-of-mind, and after all, I was doing
everything I felt comfortable doing to slow my hair loss with Rogaine — why think about it
more than I had to?

Abandoning conventional dogma and seeking my own answers

During my first year of college, life went well. I developed a close group of friends. I was in a
relationship. My competitiveness in athletics translated well to academics. This newfound
confidence in my ability to compete at a collegiate level — both athletically and academically
— put a thought into my head: if I expend so much effort being a high performer, why can’t
I translate that energy into solving my hair loss? Surely, there had to be something I was
missing…

As evidenced by my lacking results, I decided Rogaine alone wasn’t going to stop my hair
loss. I also refused to accept baldness as my genetic destination. So I started doing my own

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research. As a student, I had access to medical journals, so I began reading scholarly papers
to better understand why I was losing my hair.

This hobby soon turned into an obsession. Within a few months, I realized that hair loss
wasn’t as clear-cut as most doctors implied. I also realized that most of the online advice in
hair loss forums conflicted with the medical literature. Finally, I realized that if I wanted
unbiased answers, I’d probably need to spend several years educating myself.

I started by scrutinizing our most basic assumptions about the causes of pattern baldness. I
always heard that hair loss is genetic, unpreventable without drugs, and is caused by
something called dihydrotestosterone, or DHT. But is all of this true?

Throughout college and following years, I continued sifting through the available literature
with the understanding that this wasn’t going to be an overnight solve.

After years of research, frustration, experimentation, trial, error, and dead-ends, I finally
experienced hair regrowth. This regrowth was in the absence of Rogaine and all other hair
loss drugs, topicals, and supplements. I didn’t just stop my hair loss; I reversed it.

Why am I writing this book?

Hair loss information is misleading
I’ve researched hair loss for thousands of hours. It took nearly a decade to find a regimen
that fit with my treatment preferences, and that worked for me. I made a lot of mistakes – all
of which I could’ve avoided with a better educational foundation.

I don’t want anybody else to go through this process of researching, second-guessing, and
self-testing. Regardless of your preferences for a natural or conventional approach, you need
a systematic method for trial-and-error. You need to know (1) how strong the evidence is
supporting any treatment, (2) how long to follow that treatment before expecting results,
(3) what to do next if you pass these “results horizons” without success, and (4) how to
maintain results.

The hair loss industry isn’t going away

Hair loss is a massive industry. For two years after college, I worked as an innovation
consultant and market researcher for manufacturers of consumer packaged goods. I can tell
you first-hand: the hair-care industry is here to stay.

14
Standard U.S. retail outlets alone (like CVS or Walmart) sell hundreds of millions of dollars
in hair growth products each year. When you factor in online sales and prescription drugs,
that number skyrockets to the billions.

Because of the financial interests tied to hair loss products (i.e., supplements, topicals,
drugs, and devices) – there’s also a lot of misrepresentation surrounding the science
supporting these products. Cherrypicking data on nutritional supplements… overstating the
side effect profiles from certain hair loss drugs… dismissing data on natural interventions…
the list goes on. This only adds to more confusion for hair loss sufferers.

In my opinion, most of this industry doesn’t need to exist. There are viable, peer-reviewed
alternatives to the never-ending list of hair loss topicals and supplements. There are natural
interventions that do have some clinical support. And for anyone using FDA-approved drugs,
there are ways to amplify their efficacy four-fold while barely increasing your costs (or time).
You just need to be made aware of the information (and ways to implement it).

That’s what this book and site are designed to do: fast-track you to information most
relevant to treating your own hair loss... so we can all maximize our degree of regrowth.

Is regrowing hair difficult to accomplish? Yes.

Does it take dedication? Yes. But if you’re motivated and if it means enough to you, you can
often stop hair loss, see huge improvements, and become a healthier person in the process.

I spent thousands of dollars on products that didn’t address the underlying causes of my
hair loss or help reactivate my dormant hair follicles. I don’t want you to make the same
mistakes I did. So before you make any decisions on treatment options, you deserve to know
all possible paths forward — and then choose accordingly.

In this book, our path starts with education. Specifically, we’re going to scrutinize the
dogma most doctors repeat when we ask them, “Why am I losing my hair?”

There’s an age-old saying, “It’s all in your genes.” Many physicians use this to explain that
hair loss is genetic, that it’s predetermined. But are they right? Yes, absolutely. At the same
time, that doesn’t meant hat hair loss is a genetic destiny. The next chapter explains why.

15
 CHAPTER 2:
GENETIC DESTINY

Chapter summary:

• Physicians often tell us that hair loss is genetic, and aside from a hair transplant,
Propecia, and Rogaine, we can’t do much to stop it.

• This is true in certain contexts. But hair loss is not always genetically predetermined.
While we might have genes that predispose us to hair loss, we may also have the
power to turn those genes on and off.

• The latest research — along with my genetic tests, medical diagnosis, family
predisposition, before-after photos, readers’ photos , and our new study — suggests
this is possible.

• It all starts with epigenetics — a field that’s revolutionizing our understanding of

genes and disease. We now know that “genetic predisposition” no longer means
“genetic destiny”. This applies to many ailments, including hair loss.

• With this knowledge, we can begin to chart our course for hair recovery. It all starts
with how you can best utilize this book, membership site, and our community.

16
GENETIC DESTINY

Hair loss is all in the genes... right?

After my hair loss diagnosis, every medical practitioner I ever consulted told me I was losing
my hair because of my genes. Even my physician said that while drugs like Rogaine or
Propecia may slow or reverse some of my hair loss, there’s not much I can do (short of a
hair transplant) to stop the process. In other words, it’s inevitable. As my former barber
explained to me, “You can’t fight genetics.”

Hearing those words felt defeating. I was up against nature. I was fighting something I
couldn’t control, something that had been decided for me.

But is the assumption that baldness is caused by your genes actually true?

Twenty years ago, the answer was yes. At that time, medical professionals agreed that your
genes — or the DNA your parents pass on to you — determine all of biology (from how tall
you are to how much hair you have). And since genes “run in the family”, if your father had
a heart attack, you’re genetically predisposed to heart disease. If your father lost his hair,
you’re genetically predisposed to baldness.

For instance, studies show a clear relationship between certain genes and hair loss. If we
have this genotype, we’re twice as likely to go bald. If we’re really unlucky and have this
genotype, we’re seven times more likely to bald. If we have both genes? We’re screwed. Or at
least that was the assumption.

Today, researchers are rewriting this assumption. New discoveries are dismantling the
relationship between genes, disease states, chronic conditions... and even our hair.

It all began with The Human Genome Project.

Diving inside our DNA

The Human Genome Project
In 1990, a series of international research teams began working on a multi-year, multi-
billion dollar research collaboration: The Human Genome Project. The objective: to

17
identify and quantify every single human gene. The rationale behind its funding: one major
scientific assumption, and one major scientific promise.

The assumption: our genes are the root cause of our cancers, autoimmune disorders, and
chronic conditions.

The promise: if we map every single human gene, we can identify the genes that trigger
diseases like multiple sclerosis or Parkinson’s. If we know which genes cause disease, we
can develop technologies to “delete” those genes and prevent them from ever happening.

It’s no surprise that the US spearheaded the project’s funding. Over 130 million Americans
— or 45% of the entire US population — suffer from chronic diseases. Chronic conditions
are responsible for seven out of ten American deaths. They account for over 80% of all US
hospital admissions. And every 30 seconds, an American-based doctor amputates a limb as a
consequence to one of the country’s most common ailments: diabetes.

Why wouldn’t a disease-ridden nation support a project with such potential? Why wouldn’t
this nation want to be at the forefront of these discoveries?

The Human Genome Project’s expectations could not have been higher. Whereas mice have
about 20,000 genes, scientists speculated that humans — due to their complexity — would
have seven times that amount — 140,000 genes. Once all the genetic triggers of cancers,
autoimmunity, and even autism were mapped, we’d begin creating technology to “turn off”
those genes and paint a disease-free future.

Thirteen years later, the project was completed. What were the results?

The Human Genome Project’s promises fall flat

The discoveries stemming from the Human Genome Project were puzzling at best, and
disappointing at worst.

For one, scientists uncovered that humans don’t have nearly as many genes as we thought.
In fact, humans have just about 20,500 genes. Shockingly, we have only 300 unique genes
that distinguish us from a mouse.

But the most surprising discovery was that, despite mapping our entire human genome and
identifying some genes linked to disease, nearly all gene variants posed a minimal risk for
disease development. In other words, the root cause of most diseases was not genetic. Some
genes are associated with disease, but most do not cause disease.

18
Intriguingly, researchers also discovered that our genes aren’t so “one dimensional.” Many
genes actually serve multiple functions. They don’t have single-purpose relationships with
specific processes like cancer development or metabolism. This means that if we delete a
disease-linked gene, we might never develop that disease, but we might also impair our
digestion, brain function, or even our immunity. For example, the gene mutation that causes
sickle cell disorder also protects people from malaria. Sickle cell disorder is more common in
malaria-ridden regions, and many researchers now believe this mutation actually helps
sufferers survive into adulthood and reproduce — even if the disease shortens lifespan
overall.

In short, the Human Genome Project failed to fulfill its promise, but it was still undeniably
important. It forced researchers to revise one major scientific assumption...

Genetics do not determine all of biology. Our genes are not always our destiny.

These findings rewrite science, but doctors keep repeating the same dogma
By 2003, the conventional wisdom that genes are the root cause of our cancers, chronic
conditions, and diseases was proven wrong. But doctors never stopped repeating the dogma.
Most continued telling patients their ailments were genetically driven. Why?

In my opinion, the answer is threefold: (1) medical practitioners like issuing answers that
sound definitive; (2) these findings created huge uncertainties and challenged what doctors
told their patients for years; and (3) most patients aren’t scientifically literate. They do better
with simple, blanket explanations.

Think about it. If you’re a cardiologist and your patient asks, “Why do I have heart
disease?”, which answer sounds best?

• “It’s in your genes,” or...

• “We used to think it was your genes, but now we aren’t sure.” or...

• “It’s complicated, and I don’t think you’d understand.”

Of course the first answer sounds the best. A layperson knows about “genes”, but very few
people understand more than, “They’re passed down from your parents to you.” When an
explanation feels beyond someone’s grasp, people often stop asking questions.

Don’t blame your doctor for not wanting to educate you

I don’t think doctors maliciously intend to withhold information. That’s conspiratorial. But
if we look at the pressures they face, it’s no wonder why they default to simple explanations.

19
Doctors work an average of 59.6 hours per week. Most family doctors manage a panel of
2,300 patients. A specialist’s waitlist is months-long and never-ending. On average,
specialists spend just 20.8 minutes per patient. And for new doctors, face-to-face patient
time lasts merely eight minutes. Keeping up with patient demand means longer hours,
shorter patient interactions, and more daily appointments.

When a doctor tells a patient their condition is “genetic”, it’s the shortest answer possible.
It yields the fewest patient inquiries. It’s an answer that gets a patient out of the chair faster.
It’s an answer that gets physicians to their next appointment faster.

Unfortunately, it’s also an answer that can sometimes be misleading. For the majority of
diseases, the Human Genome Project took that “gene” argument off the table. In fact, new
research speculates that 70-90% of disease risk isn’t genetic. It’s environmental.

So the next time a doctor tells you “It’s all in your genes,” ask for more information. And
the next time a doctor says, “Hair loss is genetic,” ask the same question.

My 23andMe DNA test

Earlier in this chapter, we briefly mentioned a few genes associated with hair loss. There are
actually a lot more. I would know. I have almost all of them.

In 2015, I decided to discover more about my genes, so I went and got my entire human
genome sequenced through a service called 23andMe.

This is how it works: 23andMe mails you a vial. You fill that vial with saliva and mail it back
to their lab. 23andMe processes your vial, decodes your DNA, and sends you back the raw
data. The company also provides you with “fun” add-on services — like what percent of
Neanderthal you are, where your mother and father come from, if you have any relatives in
their database, or if you have any life-threatening genetic variants (that one’s not so fun).

I was more interested in finding out what my raw genetic data said about my potential to
develop certain conditions. Specifically, I wanted to know, based on my genes, how likely I
was to go bald.

So I uploaded my 23andMe data into a company called Promethease. Promethease cross-

references your DNA with all the published studies about your genotypes, then sends you
an automated 100+ page report. The report tells you everything from how well you
methylate B-vitamins to how quickly you detoxify drugs to your genetic predisposition for
certain cancers.

20
So, how did my raw DNA compare to all the studies on genotypes and male pattern
baldness?

My genes & hair loss

Here’s a readout of how my DNA stacked up versus all the genotypes linked to hair loss.
Let’s start with the good news: I have one genotype that says I have a reduced risk for
baldness:

So far so good! (For anyone curious, you can read the study about that genotype here.)

Now for the bad news.

I have ten other genotypes linked to hair loss. Each one of them increases my risk for balding.

21
And now for the worst of my genotypes... A 1.6x increased chance for baldness, followed by
a 2x increased chance for baldness...

...followed by an increased risk to go completely bald before 40...

...followed by the worst genotype of them all... a 7x greater risk for baldness.

22
A seven times increased risk for balding! Remember those hair loss genes referenced earlier
in the chapter? I have both. Based on my DNA, I’m screwed.

And then there’s the mounting physical evidence…

Most men in my family are slick-bald

My mother’s father is bald. My mother’s brother is bald. My father’s father was bald. My
father’s brother is bald.

Then there’s my diagnosis. I noticed hair thinning at 16. A few months later, Dr. Leonard
diagnosed me with male pattern hair loss. Here are his notes from our consultation.

A N D R O G E N I C A L O P E C I A D I A G N O S I S ( 2007)

23
 A N D R O G E N I C A L O P E C I A D I A G N O S I S ( 2007)

My photos
Then there are my photos. Let’s start with my baseline photos, going all the way back to
when I was a kid. This was the day we got our first family dog. I’m seven years old.

24
 1996 (B EF OR E)

My hair is parted, so you get an idea of its volume. I’ve never really had thick hair, so even
here you can see some scalp where the hair parts. But I don’t have a bald spot. And I don’t
have signs of pattern thinning.

Here’s a still from a video taken in 2005 — 1.5 years before I was informed about my bald
spot. I apologize for the quality. But, as you can see, my hair is still good!

2005 (B EF OR E)

Now, fast-forward to early 2011 — four years after my official hair loss diagnosis. My friend
and I were hiking in San Luis Obispo when he took a video of me. Here are two stills.

25
 2011 (DUR I N G )

Those photos are after four years of Rogaine use. Just as Dr. Leonard described, I have
“moderate plus thinning at the top” and “increased thinning at the crown.” You can see a
few inches of my scalp from any behind-facing angle. At this point, I have a small bald spot.

Here’s a photo toward the end of 2012 — almost six years on Rogaine. Same thinning,
different angle, different lighting. My thinning is a bit worse. You could see a few inches of
my vertex even from my side profile, which is why I started growing my hair longer.

26
 2012 (DUR I N G )

Yes, I am in a Santa costume. Yes, I am still balding. At this point, I was avoiding side and
back photos like the plague. And this photo wasn’t even in harsh lighting.

So let’s look at the facts:

1. According to my DNA data, I have a genetic predisposition to pattern hair loss

2. At 17 years old, a medical professional diagnosed me with male pattern hair loss

3. My 2011 and 2012 photos show clear thinning at the vertex

All kidding aside — my DNA data, diagnosis, and photos suggest that baldness appears to
be my genetic destiny. But this book isn’t about genetic determinism: it’s about its fallacy.

Now let’s jump ahead to 2014. This is ten months after I dropped Rogaine and started a
drug-free, topical-free, surgery-free approach to combatting hair loss. The lighting is about
the same as the photo in 2012. Here’s my vertex (next page).

27
 2014 (A F T ER )

Next, here’s a photo from August 2016. I replaced a bathroom bulb and cut my hair shorter.
This is the brightest, harshest lighting I could create.

2016 (A F T ER )

28
Finally, here are two photos taken three weeks later. This is the same lighting, but I grew my
hair longer to match the length in the 2011 photos. This is where the density change (and a
few of my grey hairs) is most noticeable.

2016 (A F T ER )

Finally, here are a slew of photos from 2018-2019 highlighting different lightings / hair
lengths. Notably, this is after I’d taken 1.5 years off from any hair loss protocol — to see if
my results from 2013-2016 would hold if I quit the regimen cold-turkey.

Until mid-2018, my hair remained very stable. Since then, I’ve noticed a slight decrease to
hair density. However, it’s hard to say if this is from seasonality... or from me quitting a hair
loss regimen for 18 months. The good news: my n=1 experiment here suggests that the
results from this regimen stick around for a long time... and that unlike minoxidil or
finasteride, all that’s required to maintain our hair gains is a minimal maintenance routine
(more on this later).

These photos were taken throughout 2018-2019 (next page).

29
30
31
Now let’s look at the results of readers who’ve made the same efforts.

READERS’ BEFORE-AFTER PHOTOS: SEE THEM HERE.

Many of our success stories followed the exact regimen I did for hair recovery. But there are
different ways we can all cross the finish line. We’ll discuss these throughout the book.

Is baldness still a genetic destiny?

I’d like to think, just like the Human Genome Project, that we can revise that assumption.
And that for many people, this “revision” can be achieved naturally or conventionally.

Genetic destiny, revised

If most genes are only associated with hair loss, but don’t necessarily cause it... Then what is
the cause?

It turns out that while we can’t change our genes, we do have the power to turn genes “on”
or “off ”. Researchers now believe disease development has less to do with our genes, and
more to do with which genes our body activates or deactivates. This is called gene
expression — or when our cells turn combinations of genes on and off to perform certain
functions.

Today, there’s an entire field exploring factors that influence gene expression: epigenetics.
Epigenetics is the study of how our gene expression changes based on our environment.
Epigenetics has revolutionized our understanding of disease pathology, prevention,
treatment, and reversal.

Everything affects the genes we express — from the air we breathe to the food we eat. This
is why we might carry the gene for a rare cancer, but if we live in an environment that never
activates that gene, we don’t have to develop that cancer.

So, can we apply these principles to hair loss... or use these principles to reverse hair loss?

Yes. Balding and non-balding hair follicles express different genes. If we want to reverse
pattern hair loss, we need to do away with genetic determinism and instead ask ourselves
why these differences exist. The rest of this book is dedicated to answering that question.

32
Hair loss and epigenetics
Hair loss is often chronic and progressive. There’s absolutely a genetic component to it. But
do we have to express the genes associated with hair loss? Not always. In fact, we’ll soon
learn that we can influence our own gene expression to activate genes associated with hair
growth... and deactivate genes associated with hair loss –– all to improve our hair.

Gene expression — and our ability to change it — is the basis for the rest of this book. In
learning this, we’ll come to realize that hair loss isn’t a chronic condition. Rather, it’s often
just a symptom of other conditions that progressively deteriorate the health of our scalps.

Where to begin
If we’re going to reverse our hair loss, we need to understand why we’re losing our hair. As
such, this journey begins with education. I’ll lay out a set of tools to help you identify your
own form of hair thinning. Then, based on your hair loss type, we’ll begin to build a clearer
picture of its triggers and treatments. Finally, we’ll develop your individual action plan.

Think of the rest of this book (and membership site) like a choose-your-own-adventure
guide to treating hair thinning. Here’s what this process looks like:

Step 1: identify your hair loss type. We’ll derive clues as to why we’re losing hair.
How? By examining the presentation of our hair loss. Using examples from the literature
and past readers, we’ll reveal the three most common forms of hair thinning, how they
present differently, and why hair loss misdiagnoses are so common. In most cases, this is
the most critical step in our hair recovery. If we don’t correctly identify our own hair loss
type, we can’t treat it correctly.

Step 2: educate yourself. The better we understand something, the better we can fight
it. In the following chapters, we’ll dive into the science behind each hair loss type (and
how to treat it). Regardless of your specific form of hair thinning, I still recommend you
read through all of the book’s educational materials on each hair loss type. In doing so,
you’ll learn that many of us have more than one hair loss form and don’t know it.

Step 3: regrowth roadmap. It’s tempting to simplify hair loss into “one simple cause,
one simple treatment”. But the truth is far more nuanced. For instance, while the most
common form of hair thinning — androgenic alopecia — is causally linked to one
hormone, many of us also don’t realize that certain underlying chronic conditions can
accelerate its onset. Because of this, the best treatment options will vary wildly across
individuals — all depending on someone’s age, gender, hair loss form(s), comfortability

33
 with drugs, and how much time they’d like to invest daily into resolving this. For these
reasons, I’ve created what I call a regrowth roadmap. This is a five-question survey that,
depending on your answers, provides you with 75+ different hair loss regimens (and
testing recommendations)... all catered to your individual preferences.

When you’ve finished this book (and relevant materials on the membership site), you’ll
have a specific action plan based on your needs and built on the science of hair regrowth. It
all starts by analyzing (and targeting) the following:

1. Scalp Environment. Starting around puberty, our scalps may begin to undergo a series of
changes that precede certain forms of hair loss. New evidence suggests these changes
may kickstart the hair loss cascade. If we want to achieve hair regrowth, we must take
action to return our scalps to their healthy states prior to these changes ever occurring.

2. Diet. Most hair loss is not caused by diet. This is why some morbidly obese, nutrient-
deplete men can retain full heads of hair... while some professional athletes still go bald
despite having full-time nutritionists. At the same time, many forms of hair loss are
exacerbated by a poor diet. Here we’ll reveal a dietary protocol that is not only manageable,
but also avoids bad food choices (while maximizing our chances for hair recovery).

3. Lifestyle. Lifestyle changes that support thyroid function, decrease systemic

inflammation, and promote hormonal balance are often additive to our hair recovery.
Unfortunately, most of us engage in lifestyles that achieve the opposite. By adhering to a
few simple (but powerful) principles, we can seamlessly integrate positive changes into
our lives and become healthier in the process — thus supporting our hair recovery.

4. Microbiome. Our gut flora — or the organisms that live inside our intestines — make up
at least as many cells as we have human cells. They influence gene expression, help us
absorb vitamins and minerals, and constitute up to 70% of our entire immune system.
Unfortunately, our gut health is also largely neglected. Chronic antibiotic use along with
poor diet and lifestyle choices alter the composition of our guts and the very bacteria that
influence the foods we crave and the hormones we produce. Reversing this damage is key
to minimizing systemic inflammation, optimizing our hormones, and even improving
many cases of hair thinning. Here we’ll explain how.

This approach is the same one I used to see hair recovery. It’s also the approach many of our
past readers have used to regrow their hair. All that’s required is your dedication, patience,
and persistence. Now, we’re ready to uncover the science behind our hair.

34
Chapter recap
Some of us have a genetic predisposition to lose our hair. But genetic predisposition does not
mean genetic destiny. The study of epigenetics has helped revolutionize this thinking. It has
taught us that while we can’t change our genes, we can change how they behave... all by
changing our environment.

This has critical implications for diseases and chronic conditions — maybe even hair loss.
Research now shows that balding and non-balding hairs express different genes... but that we
have the power to change this — and in doing so, regrow hair. It all begins with identifying
our hair loss form, the reasons why we’re thinning, and then developing a treatment plan
catered specifically to our needs. The rest of this book is dedicated to doing this.

Want to discuss this chapter?

Have questions about genes, epigenetics, or their relationship to hair loss? Want
clarification on anything you’ve read? There’s a dedicated thread for any and all questions
regarding this chapter. Please access it right here.

Otherwise, it’s time to move onto the first (and most important) phase of treating our hair
loss: identifying our hair loss type. The next chapter is dedicated to achieving this. And
beware: it’s harder than you might think.

35
 CHAPTER 3:
K N OW YO U R D I AG N O S I S

Chapter summary:

• If we want to maximize our chances for reversing hair loss, we first need to identify
our own hair loss type. Beware: this is harder than it may seem.

• For example, I was diagnosed with androgenic alopecia in 2007. This is the world’s
most common hair loss disorder. It accounts for 95% of hair loss cases in adult men.
But in 2017, lab work revealed that I also had an underlying condition that may have
significantly contributed to my hair thinning. In fact, this condition was unrelated to
androgenic alopecia — the diagnosis issued by my doctor ten years prior.

• Unfortunately, this is the story for many hair loss sufferers. Doctors miss a diagnosis,
or misdiagnose the forms of their patients’ hair loss. The reason? They diagnose hair
loss with a visual inspection. They don’t factor in a patient’s health evaluation.

• I am not unique. Of the readers with whom I’ve worked, 30% of men with an
androgenic alopecia diagnosis later tested positive for conditions linked to other forms
of hair thinning. For women, that number is closer to 100%.

• This chapter is to prevent your story from becoming mine — so that you can get to
the right treatments faster. First, we’ll dive into hair loss basics. We’ll also uncover
two ways we can lose hair: through hair follicle miniaturization and a hair shedding
disorder. Then, we’ll uncover the presentation, characteristics, and causes of the most
common hair loss types — and compare where our own hair loss might fit in.

• Finally, we’ll use this information to build the foundation of our regrowth roadmap —
our personalized plan for hair recovery.

36
K N OW YO U R D I AG N O S I S

Why the right hair loss diagnosis matters

If we want to maximize our chances for reversing hair loss, we first need to identify our own
hair loss type. Be forewarned: this is harder than it may seem.

You’ve probably heard of the term androgenic alopecia (or pattern hair loss). This is the
most common type of hair loss in adults. It’s so common, in fact, that The American Hair Loss
Association says it’s responsible for 95%+ of hair loss cases in men.

That’s a huge number — and one I don’t dispute. As such, when a male hair loss sufferer
searches online and discovers this statistic, he usually assumes his hair loss must be from
androgenic alopecia. Consequently, he seeks treatments for just androgenic alopecia —
because, after all, there’s a 95%+ chance he has it.

Unfortunately, there’s something this statistic masks. It’s that a huge portion of men with
androgenic alopecia also have other types of hair loss — all due to different causes (and thus
requiring different treatments). If you fall into this category and only try androgenic alopecia
treatments — chances are you’ll miss an opportunity to further improve your hair.

I’m speaking from first-hand experience. In 2007, I was diagnosed with androgenic alopecia.
For the next seven years, I took Rogaine. I didn’t respond well. Then, in 2016, I paid out-of-
pocket for a battery of lab tests which revealed that in addition to androgenic alopecia, I
likely had an underlying condition that contributed to my hair loss — and from a different set
of causes. In other words, I likely had two hair loss types but was only diagnosed with one.
Subsequently, it took me nearly a decade to uncover a regimen that worked.

I am not a unique case. Of readers with whom I’ve worked, nearly 30% of men who were
(1) diagnosed with androgenic alopecia and (2) opted to do more lab testing later discovered
they likely had additional types of hair loss beyond their diagnosis. For females, that
number was closer to 100%. The bottom-line: we’re probably misdiagnosed, a lot.

“But I went to a dermatologist. How could I be misdiagnosed?”

It’s not that a dermatologist has completely misdiagnosed you. Rather, it’s that a
dermatologist may not notice hair loss forms that may compound with androgenic alopecia. If
I had to speculate, I’d say there are two reasons why this happens.

37
1. Many general practitioners are behind on the literature. In 1999, researchers realized
some hair loss forms can disguise themselves as androgenic alopecia yet have entirely
different causes. 25 years later, these findings have made their way into reviews, but not
onto the desks of many primary care physicians. After all, we know how busy they are.

2. Many dermatologists don’t do health evaluations alongside their diagnosis. This

happened to me in 2007, and it happens more than you’d think. There are cases of men
diagnosed with androgenic alopecia who later learn their hair loss is due to a chronic
shingles infection activated by the herpes zoster virus. There are cases of women
diagnosed with androgenic alopecia who later discover that their hair thinning may be
due to the growth of a node on their parathyroid gland. If we only evaluate our health
skin-deep, we’ll only be partially informed.

That’s why I’ve dedicated this chapter to covering the basics behind the major hair loss
types. Later on, we’ll put what we’ve learned to the test and try to identify other readers’
hair loss forms — and finally, your own. This diagnostic work is the first step in our
regrowth roadmap, and a critical part to customizing our own hair loss action plan.

Remember: each type of hair loss has a unique set of causes and a unique set of treatments.
That’s why we can’t apply a one-size-fits-all approach to hair loss, and maybe why some past
treatments you’ve tried have failed.

Diagnostic questions
Different forms of hair loss express at different ages, speeds, and patterns. This means we
can get a good idea of our hair loss type(s) by asking ourselves five questions.

1. When did your hair loss start? Relatively younger (18-40)... or older (40+)?

2. How long have you experienced hair loss? A few months... or a few years?

3. How quickly are you losing hair? Slowly (over years)... or rapidly (within months)?

4. What does your hair loss look like? Recession at the temples / crown... general
thinning throughout the top of scalp... thinning at the sides... all three... or none?

5. What does your shedding look like? When hairs fall out, are they typically long or
short? Do you notice that some hairs look thicker and thinner than others?

As we dive into each hair loss form, reflect on your answers above — and if your own hair
loss aligns with any form or its descriptions.

38
 My answers: I first noticed hair loss at 16 years old. By the time I sought treatment,
I’d seen at least a year of slow, steady thinning. The onset was gradual (over years),
but progressive. I had general thinning (i.e., diffuse) at the top of my scalp — with
the majority of it focused at my crown (i.e., my vertex). For the hairs that shed, I also
noticed different hair diameters

Two categories of hair loss

You’ve probably heard several medical names for different hair loss forms — like frontal
fibrosing alopecia, traction alopecia, alopecia areata, and even retrograde alopecia. However,
this fractionalization doesn’t serve 95% of hair loss sufferers. In reality, we can capture the
vast majority of hair loss cases just by thinking about hair loss in terms of two categories...

• The hair loss forms that lead to hair follicle miniaturization

• The hair loss forms that lead to hair shedding disorders

...and these categories are simply determined by how we lose hair.

A (very) basic summary: how we grow hair

Hair grows out of hair follicles, and these hair follicles are rooted into our scalps’ blood
supply. Together, our hair follicles (and their blood vessel networks) work to fuel the
continuous growth of thick, healthy hair.

H UM A N H A I R F OL L I C L E

39
But hair doesn’t grow forever. It’s limited by something called the hair cycle. This is a
naturally-occurring phenomenon — and a term used to describe the cyclical degeneration
(and regeneration) of every hair follicle on our head. Here’s how the hair cycle works:

For 2-6 years, a hair follicle will grow thick, healthy hair. Then, for reasons not fully
understood, a hair will detach itself from its hair follicle, shed (fall out), and then the hair
follicle will degenerate. Then, in a few months, a new hair follicle will emerge, replace the
degenerated hair follicle above it, start growing a new hair… and a new hair cycle begins.

This several-year cycle repeats indefinitely, everywhere we have hair, and for almost every
hair-bearing species on the planet.

OUR H AIR C YC L E: H AIR C ON STAN TL Y GROWS, SH EDS, AN D REGEN ERATES

In a normal scalp, about 15% of our hairs have already detached from their hair follicle and
are ready to shed. This is why, even in the absence of hair loss, it’s normal to shed 150+
hairs per day. It’s just a part of the natural hair cycle. And once those follicles regenerate,
the hair should always come back... because the hair cycle repeats indefinitely.

Knowing this, there are two ways we can lose hair.

First, the hair follicles can become miniaturized — thus, leading them to produce thinner,
wispier hairs. And secondly, our hair cycle can become disrupted: for instance, a healthy hair
may shed, but a new hair follicle never regenerates to regrow that lost hair.

This is the difference between hair follicle miniaturization and a hair shedding disorder.

40
Hair follicle miniaturization is when our hair follicles decrease in thickness (diameter).
They progressively shrink — thus producing thinner, wispier hairs. This typically occurs
slowly, over a series of years, and in a “pattern”. For men, hair follicle miniaturization can
start at the temples or vertex and progress until the whole top scalp is bald. For women, it
usually just starts as general hair thinning. In hair follicle miniaturization, because the
health of the hair follicle is compromised, this type of hair loss is often considered more
permanent — or harder (but not impossible) to reverse.

H A I R F OL L I C L E M I N I A T URI ZA T I ON : OUR H A I R F OL L I C L ES SH RI N K

41
Now, a hair shedding disorder is different. Hair shedding disorders aren’t when our hair
follicles shrink. Rather, they’re from an interruption in our hair cycle: for instance, when an
old hair sheds but a new hair follicle doesn’t regenerate to replace it. If this happens to
enough hairs, we see decreases to our overall hair density — and in many different patterns.

H A I R SH EDDI N G DI SORDER: A H A I R SH EDS, B UT T H A T H A I R I SN ’ T REP L A C ED

Hair shedding disorders can occur abruptly (within months) or slowly (over years). They
can present as general thinning... or sometimes only in a specific region.

The good news is that compared to hair follicle miniaturization — hair shedding disorders
are considered less permanent. This is because the integrity of each hair follicle isn’t
compromised. Rather, something is just stopping a hair follicle from regenerating. For these
reasons, recovering from a hair shedding disorder involves a different set of treatments.

Different types of hair loss = different causes

It’s amazing to think about, but these subtle differences in how we lose hair can give us
insights into the causes of our hair loss (and steps toward resolving it). We’ll get into that
soon. For now, let’s summarize everything we just learned (next page).

42
As you look at the following chart, reflect back on your own hair loss. Are you thinning in a
pattern? Are you thinning all over? Are you thinning progressively? Did your thinning onset
quickly? Slowly? In bursts? You might not see that your hair loss strictly falls into one
category or another. That’s okay. That’s why we’re doing this exercise.

Next, we’ll dive into one form of hair follicle miniaturization and two forms of hair shedding
disorders. Together these three forms constitute 95% of readers’ hair loss cases. As we
uncover each form and its causes, compare it to your own hair. See where you match up.

We’ll start with a form of hair loss due to hair follicle miniaturization: androgenic alopecia,
also known as pattern hair loss. This is what I was diagnosed with back in 2007.

Hair follicle miniaturization

Androgenic alopecia (i.e., pattern hair loss)
Pattern hair loss is the world’s most common adult hair loss disorder. It affects at least 50%
of women and 80% of men throughout a lifetime. It’s chronic, progressive, and with such a
high prevalence, it’s nearly impossible to walk a city block without seeing someone with it.

The name “pattern hair loss” comes from its presentation. In men, pattern hair loss often
begins at the hairline (temples) or crown (vertex). You might hear it described as a
“receding hairline” or a “bald spot”. Here’s a graph of how it can progress over decades:

43
 N ORWOOD SC A L E (M A L E P A T T ERN H A I R L OSS)

In women, pattern hair loss often starts as even thinning throughout the top of the scalp.
Here you’ll hear the terms “diffuse thinning”, “more scalp showing”, or a “wider hair part”.

L UDWI G SC A L E (F EM A L E P A T T ERN H A I R L OSS)

And here’s what pattern hair loss can look like in real life.

F EM A L E (S OUR C E) MAL E (READER)

In men, as pattern hair loss progresses, it’s normal to eventually see general thinning (like in
females) — because thinning at the temples and vertex start to converge in later stages of its
progression. However, this is less common in early stages. So, if you’re a male with early-stage

44
pattern hair loss and you’re already experiencing general thinning, you may want to pay
extra attention to the rest of this chapter (as this might suggest another form of hair loss).

Causes of androgenic alopecia: male hormones, genetics

The name androgenic alopecia (i.e., AGA) comes from what researchers believe causes the
condition: male hormones (androgens) and genes (genetics). This is why AGA begins
during or after puberty — only after our sex hormones have kicked in.

If these symptoms look or sound similar to your own hair loss, good! Please make note of it.
However, many of us may not have hair loss that fits with these descriptions.

For instance, some men might have an intact hairline or vertex... but diffuse thinning
throughout the top of the scalp. Some men and women might have hair loss extending to
the sides of the scalp (and not just the top). And others might have rapidly accelerating hair
loss — where their hair looks significantly thinner than just 2-3 months prior.

In these cases, it’s absolutely still possible that you have pattern hair loss. But it’s also
possible you have other forms of hair thinning. As such, we need to try to identify them.

Unfortunately, this is where things get complicated. As we’ll soon see, other forms of hair
loss can look identical to pattern hair loss... but rather than being caused by hair follicle
miniaturization, they’re caused by excessive hair shedding.

This brings us to our first hair shedding disorder: telogen effluvium.

Hair shedding disorders

Telogen Effluvium
Telogen effluvium is the most common form of diffuse thinning in women. It’s a disorder
that involves hair shedding — when too many hairs shed, and too few hairs replace them.
This is why it’s named after the “shedding” phase of our hair cycle: the telogen phase.

Telogen effluvium usually onsets suddenly (within months). And one of its tell-tale signs is
excessive hair shedding: clumps of hair in the shower drain... dozens of hairs in your comb...
noticeable hair fall from even light touching. As the hair shedding outpaces new hair
growth, this eventually leads to visibly thinner hair.

Interestingly, while telogen effluvium can present as generalized thinning across the entire
tops of our scalps, it can also affect one region more so than others — like the temples or

45
crown. In these cases, it can look identical to pattern hair loss — making it harder to
diagnosis.

In fact, even if telogen effluvium presents normally (as general thinning), it can be almost
impossible to distinguish from female pattern hair loss. Just see this photo of a female with
telogen effluvium. It looks nearly the same as our female with pattern hair loss.

T E L O G E N E F F L UV I UM ( T E )

Accordingly, one way to identify telogen effluvium isn’t by appearance. It’s by causes.

Causes of telogen effluvium: stress

Telogen effluvium (or TE) is not closely related to male hormones or genetics but rather
physical or mental stress. This is why some doctors refer to it as “shock loss”. There are a
host of causes, but the most common ones from the literature (and from readers) are...

• High fevers / severe infections (i.e., a terrible flu)

• Crash dieting (i.e., a prolonged calorie deficit or rapid weight loss)

• Psychological stress (i.e., anxiety) or physical stress (i.e., sleep deprivation, childbirth)

• Medications (i.e., synthetic retinoids, beta blockers, calcium channel blockers, birth
control pills, antidepressants, and non-steroidal anti-inflammatory drugs like ibuprofen)

This list in itself is stressful (at least to me) — partly because sleep deprivation, anxiety,
restrictive diets, and NSAID’s are part of everyday living for many adults. Not surprisingly,
it’s likely that a majority of us hair loss sufferers have experienced some degree of telogen
effluvium throughout our lives.

The good news is that telogen effluvium is temporary. Once the underlying triggers are
identified and treated, TE often resolves within a year. And if this sounds more like your
hair loss, please make note of it for your regrowth roadmap.

46
However, many of us won’t have hair loss that appears to fit either pattern hair loss or
telogen effluvium. For instance, some of us will have diffuse thinning that has taken years
(not months) to develop. Some of us will have zero stress... but chronic, generalized hair
thinning. Or some of our hair shedding might extend beyond the tops of our scalps and even
to our scalp perimeter (i.e., the sides).

This brings us to the last hair shedding disorder I often see with readers: chronic telogen
effluvium.

Chronic Telogen Effluvium

Remember: telogen effluvium occurs quickly. It onsets in a matter of months — typically
from some sort of stress or trauma — where our hair volume drastically decreases.

But what about diffuse thinning that isn’t rapid? Rather, what about diffuse thinning that is
slow, persistent, and occurs over several years? While this might be pattern hair loss, this
isn’t always the case.

More likely, this sort of hair shedding is known as chronic telogen effluvium (or CTE).
And while the name is nearly identical to TE, its causes are often entirely different.

In my experience working with readers, the most common causes of chronic telogen
effluvium aren’t necessarily stress. Rather, they’re underlying chronic conditions. And since
these conditions can onset slowly, the hair shedding that manifests from these disorders can
also occur slowly... giving way to the “appearance” of pattern hair loss when in actuality,
something under-the-surface is going on.

Just take this example of a female whose hair loss began slowly and diffusely. She seems to
have female pattern hair loss…

C H R ON I C T EL OG EN EF F L UV I UM (C T E)

47
But she actually has chronic telogen effluvium (CTE) — a hair loss disorder that, in her
case, manifested from an underlying condition called hypothyroidism (more on this later).

The silver lining is that just like telogen effluvium, CTE is treatable once its underlying
causes are identified and addressed. This is because CTE is a hair shedding disorder. This
means that while there’s something interfering with our hair cycle, the integrity of each hair
follicle isn’t necessarily compromised.

Causes of chronic telogen effluvium: medications, underlying conditions

Here are just a few reported causes of CTE — from the literature (and past readers):

• Chronic conditions (i.e., hypothyroidism, hyperparathyroidism, and small intestinal

bacterial overgrowth) (more on this later)

• Nutrient deficiencies (i.e., iron, zinc, vitamin B-12, vitamin D) (more on this later)

• Nutrient surpluses (i.e., iodine, selenium, vitamin A) (more on this later)

• Trace element toxicities (i.e. thallium, cadmium) (more on this later)

Unfortunately, these conditions (and issues) are growing more rampant and undiagnosed.

Remember how 1 in 2 Americans has a chronic disease? Well, up to 10% of adults have
hypothyroidism. There’s evidence that 100% of U.S. athletes don’t meet their daily
nutritional demands. In 2015, 18 million Americans drank from water systems containing
hazardous levels of lead and/or copper (putting them at-risk for a heavy metal toxicity).

In fact, I’m one of those at-risk people. I live in an area where 90%+ of lead piping systems
have been replaced. Despite this, when I got my lead levels tested in February 2019, I
discovered my lead levels were in the 81st percentile of the testing database.

The bottom line: many of us are at risk of developing the conditions linked to CTE.

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And remember the lab tests I mentioned earlier in this chapter? The ones ten years after my
hair loss diagnosis? Well, those tests revealed I had subclinical hypothyroidism — which
likely started after my appendix removed in 2006. One symptom of hypothyroidism? Diffuse
thinning. Diffuse thinning was noted in my diagnosis, but since hair follicle miniaturization
was more prevalent, I was only diagnosed with AGA.

For what it’s worth — of the female hair loss sufferers with whom I’ve worked, nearly
100% have tested positive for one of CTE’s underlying associated chronic conditions.
For men, that number is closer to 30% — as pattern hair loss (i.e. male hormones) seems to
drive a higher percentage of hair loss cases in men versus women. In any case, these
numbers are alarming... and indicate a need for further diagnostic work into our health.

How to identify our hair loss form(s)

The are two challenges in identifying our hair loss: (1) different forms can look similar, and
(2) if you’re anything like me or other readers, you may have overlapping hair loss forms.

Couple this with another complication: men and women with pattern hair loss (AGA) tend
to also see increased hair shedding (i.e., telogen hairs) — to the point where this has now
become a part of pattern hair loss’ definition. Now it’s even harder to differentiate pattern
hair loss from TE or CTE — unless our hair shedding is very severe.

As such, the best way to evaluate our hair loss isn’t by simply looking at our scalps. Rather,
it’s by evaluating our overall health (and hair) from three different perspectives:

1. Characteristics. Do you notice visibly thinner hairs (hair follicle miniaturization), or do

you notice hair shedding? Is your hair loss patterned or unpatterned?

2. Presentation. Is your hair loss progressing slowly (years) or rapidly (months)? Is it

chronic and progressive... or does it temporarily improve and then get worse?

3. Causes. Do you suspect you’re suffering from — or have a family history of — any of the
conditions or causes linked to each hair loss form? (Note: this may require testing.)

By evaluating our hair loss by characteristics, presentation, and causes, we can better assess
what’s going on. In doing so, we can select the best path forward to reversing our hair
thinning.

To help with this, I’ve consolidated this information into a graphic — a hair loss form
flowchart. Use this as a tool to vet your own hair loss.

49
Now let’s implement this chart using real photos. The challenge? We won’t have each hair
loss sufferer’s health history. As such, we’ll realize just how easy it is to “misdiagnose”
someone if we limit our diagnostic work to just the visual field.

Guess these hair loss forms!

Example #1: male readers
On the next page, there are three photos from past readers. Which hair loss form does each
person have?

50
 MALE 1 MALE 2 MALE 3

Let’s look at the evidence. These men all have hair loss at the vertex. The loss looks
patterned. This suggests hair follicle miniaturization. Specifically, pattern hair loss (or AGA).

If you guessed AGA, you’re almost correct. Male 1 and 2 have AGA. Male 3 likely has chronic
telogen effluvium (and AGA)... but we’d only know this with a health evaluation.

Male 3 has no familial history of AGA. His two brothers (in their 50’s) have zero hair loss.
Male 3 started losing his hair after beginning a trace mineral supplement. He was concerned
about meeting micronutrient demands and figured more trace minerals would help. He took
the supplement for seven years. After developing brain fog, hair loss, and symptoms of
Alzheimers, his doctor advised him to do a heavy metals test to rule out a poisoning.

The results? Male 3 had arsenic, aluminum, and mercury poisoning. The supplement that
was supposed to improve his health hadn’t been properly third-party tested, and resultantly,
was filled with high amounts of toxic trace elements. And this toxicity manifested as
chronic telogen effluvium in the form of diffuse hair loss at the vertex. You can read his case
study right here. [Note: this is just one of the many reasons why I’m leery about supplements.]

Example #2: female hair loss sufferers

F EM A L E 1 F EM A L E 2 F EM A L E 3

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These female hair loss sufferers have diffuse hair thinning — often seen in female pattern
hair loss (hair follicle miniaturization). At the same time, we know that telogen effluvium
(TE) and chronic telogen effluvium (CTE) can present similarly. Which forms do they have?

Well, female 1 and female 3 don’t have typically pattern hair loss (AGA). Rather, they have
an autoimmune-related hair loss disorder linked to Lupus.

Female 2 does have pattern hair loss (AGA). She suffers from a condition known as
polycystic ovarian syndrome — often characterized by insulin insensitivity, weight gain, a
hormonal imbalance (i.e., higher androgens), and consequently, pattern hair loss.

Example #3: male hair loss sufferers

MALE 1 MALE 2 MALE 3

Male 1 is a past reader. Males 2 and 3 are from this study. They all have diffuse hair thinning
and varying degrees of temple recession. Male 1 has the early signs of the male pattern hair
loss frontal “island”. Male 2 has temple recession and general thinning in the front scalp.
Male 3 has significant frontal thinning, but not in typical male pattern hair loss fashion: his
whole hairline (not just temples) have receded. So which forms do these men have?

Male 2 and 3 have androgenic alopecia (pattern hair loss). But male 1? He likely has pattern
hair loss plus chronic telogen effluvium from a long-standing iron deficiency.

In fact, male 1 and I had worked for over a year — approaching his hair thinning as if it
were exclusively AGA. But it wasn’t until we shifted our focus toward diet and nutrition that
male 1 saw significant hair recovery — and within six months. His case study is here.

Example #4: male and female hair loss sufferers

We won’t dive into these deeply. Just look at these photos and take your guesses. The
answers are on the next page.

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 #1 #2 #3

#4 #5 #6

And the answers…

#1: Male; AGA (reader)

#2: Male; AGA + telogen effluvium (reader)

#3: Male; AGA

#4: Female; chronic telogen effluvium due to hypothyroidism

#5: Female; chronic telogen effluvium due to nutrient deficiencies

#6: Female; AGA

The bottom-line: it’s hard to guess hair loss types (and causes) by appearance alone. We
have to look beyond skin-level... and sometimes beyond the diagnosis of a physician.

Men with early-stage AGA and diffuse thinning: consider more testing
Earlier I mentioned that of the female hair loss sufferers with whom I’ve worked (and who
did testing), nearly 100% discovered they had at least one of the conditions that can
manifest as chronic telogen effluvium (CTE). Of men, that number was closer to 30%.

53
But if we dig into that 30% — the male sufferers who had a CTE-linked condition were
tightly clustered: they were men with early-stage AGA alongside diffuse thinning. Why?

Well, if we look at how male pattern hair loss usually progresses, we see that as it becomes
more severe, the hairline further recedes as the crown further thins. In later stages, these
regions begin to overlap and lead to general hair thinning. So for men with AGA who are
Norwood 3 and beyond, diffuse thinning is expected.

However, diffuse thinning isn’t as expected in early Norwood stages (i.e., Norwood 1-2). So
if you’re a male with early-stage AGA and you have diffuse thinning — it’s possible that
your hair loss might be due to both AGA and CTE. As such, you might want to consider
testing for CTE’s underlying conditions — at least to rule it out for peace of mind.

Interestingly, diffuse thinning in early-stage male AGA sufferers is more common than I
expected. For instance, in our peer-reviewed study on past readers (published in Dermatology
and Therapy), 44% of males with early-stage AGA (i.e., Norwood 1 or 2) also reported diffuse
thinning. That’s a big number... and suggests that maybe AGA isn’t all that’s going on.

My advice: in these scenarios, maybe consider ruling out CTE’s underlying conditions. If I’d
done this back in 2007, I probably would’ve uncovered my hypothyroidism earlier — and I
could’ve augmented my treatment approaches to likely achieve better, faster hair recovery.
Testing information is covered throughout the membership site and in later chapters.

Your next steps...

Catalogue your hair loss form(s), then build a customized action plan
Before moving on, we’re going to “gut-check” a customized hair loss regimen for you. Using
the information in this chapter, guess your hair loss forms. Right now you don’t need to get
this 100% correct, and you don’t need to get more granular than answering:

Do you think you have hair follicle miniaturization, a hair shedding disorder, or both?

Your answer will help give you an idea of your customized hair loss action plan.

Your customized hair loss action plan

Since you’re a member of our community, you have access to this link — which takes you to
a survey that asks you about your age, gender, hair loss form, comfortability with FDA-

54
approved drugs, and the daily amount of time you’d like to invest in regrowing your hair.
Make sure you’re logged in (otherwise, you won’t be able to see that page).

Go and take the survey. Each of your answers will guide you to one of 75+ hair loss action
plans. These are 1,500+ word write-ups catered specifically to your needs and preferences
as a hair loss sufferer. And if you suspect you have a hair shedding disorder, these action
plans also provide you with next steps for testing.

You might be wondering: why take this survey right now? Well, the idea is for you to do this
twice: once after reading this chapter... and once after finishing this book. The truth is that
your understanding of your own hair loss will evolve as you dive deeper into hair loss
science — from its causes to its treatments. You’ll get more benefit from this book (and
action plan) if you see your own understanding evolve.

On top of that, early members of our community really enjoyed taking the survey once
upfront and once later — to see how their regimens changed. So, I’m recommending you try
the same. Then, dive back into this book and see where you stand after you’re finished
reading. The good news: you can take the survey as many times as you’d like!

For now, all that matters is you take the survey, read the write-up, and then return to this
chapter and continue reading.

Still don’t know your hair loss type?

Go to a dermatologist... or leverage our community!
While a dermatologist can make mistakes, the good ones will do a health exam alongside
your hair loss diagnosis... especially if you convey which medications you’re taking, the
abruptness of your hair loss, and anything else that resonated with you in this chapter.

If that option isn’t available, please use our community. Our community is not a surrogate
for medical advice. Our members can’t legally diagnose anything. Having said that, they’re
happy to provide their input about your hair loss based on their own learnings and
experiences.

If this interests you, please go to this forum thread. Read others’ posts to see if your
photos or story are similar to theirs. If you’re still unsure, request a community analysis!

To do this, please reply to that thread and include the following information:

55
 —

[Note: please copy/paste and answer this questionnaire in your reply]

1. What is your age?

2. What is your gender?

3. When did your hair loss start? Relatively younger (18-40)... or older (40+)?

4. How quickly are you losing hair? Slowly (over years)... or rapidly (within months)?

5. What does your hair loss look like? Recession at the temples / crown... general
thinning throughout the top of scalp... thinning at the sides... all three... or none?

6. What is your general diet? Lifestyle? Any food allergies?

7. Are you currently taking any medications? If so, which ones?

8. Is there any other health history that you feel might be relevant? For example,
surgeries surrounding hair loss onset, familial history of hair loss, chronic
conditions, etc.?

9. Please post a quality photo of your hair. Due to megabyte limitations, you may
need to use a third-party photo uploading service (like Imgur).

We have plenty of members who are more than willing to provide their own opinions on
what types of hair loss you might have — and even some insights on how they’d approach
treating it. I might chime in, too.

As always, please remember this is a support community, not a place for medical advice.
Also, please note that all members can read what you submit... so share wisely. If you
upload any lab results, make sure they don’t include sensitive personal information.

56
Chapter recap
Hair grows from our hair follicles. Over 2-6 years, each hair follicle undergoes a natural
process of degeneration and regeneration called the hair cycle. This leads to the shedding
(and regrowing) of hair. This is why (even without hair loss) we can shed 150+ hairs daily.

If a hair follicle shrinks, it’ll produce thinner, wispier hair. If a hair follicle degenerates and
doesn’t regenerate, it won’t regrow the hair that it shed. Thus, we can break down most hair
loss forms into two categories: hair follicle miniaturization and hair shedding disorders.
These can look similar but have different characteristics, presentations, and causes. As such,
we can’t always evaluate hair loss by its “looks”. Sometimes we have to look into our health
history and compare it to the causes of other hair loss forms.

Overwhelmingly, the most common form of hair follicle miniaturization is pattern hair loss
(i.e., androgenic alopecia (or AGA)). Its onset is closely linked to male hormones and
genetics. It occurs slowly as temple recession / crown thinning in most men, and general
hair thinning in most women. Without treatment, it worsens.

Hair shedding disorders like telogen effluvium (TE) or chronic telogen effluvium (CTE) can
often overlap with AGA but are derived from different causes: stress, drugs, dieting, and
underlying conditions. They onset slowly or quickly — often as diffuse thinning. If the
underlying triggers are identified and addressed, TE and CTE can correct on their own.

In my opinion, hair loss misdiagnoses are common. As such, it’s critical to assess our health
alongside our thinning hair. This is especially important for those with diffuse thinning, rapid
onset hair loss, or hair loss that presents as multiple forms.

Generally, this includes individual testing to rule out (or diagnose) any of the following:
hypothyroidism, hyperparathyroidism, nutrient deficiencies, nutrient surpluses, small
intestinal bacterial overgrowth, and trace element toxicities. Testing (and treatment)
information is in our regrowth roadmap.

Anecdotally, nearly 30% of male hair loss sufferers with whom I’ve worked later tested
positive for at least one of these conditions... including those diagnosed with just AGA. For
females, that number is closer to 100%.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help

57
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions which you can access right here.

Up next, we’ll dive into the science behind the most commonly diagnosed form of hair loss:
pattern hair loss (or AGA). Researchers say that it’s genetic and the result of androgens —
specifically, a hormone known as dihydrotestosterone (or DHT); but a closer look into the
data reveals some confusion over these beliefs.

58
 CHAPTER 4:
PATTERN HAIR LOSS: BASIC
MISUNDERSTANDINGS

Chapter summary:

• Experts agree that the hormone dihydrotestosterone — or DHT — is the cause of

pattern hair loss. DHT is higher in men with thinning hair, and men who can’t
produce DHT never go bald.

• Because of this, conventional hair loss drugs (like finasteride) were developed to
reduce our DHT levels, and in doing so, achieve some hair regrowth.

• While finasteride can help slow or stop pattern hair loss, it does not always result in
substantial hair regrowth. DHT is also more complicated than most people think. For
instance, higher DHT leads to hair loss in the scalp, but hair growth in the body and
face. There’s even a certain kind of DHT that’s associated with better hair health.

• These paradoxes suggest there may be more to hair loss than just DHT.

59
PATTERN HAIR LOSS: BASIC MISUNDERSTANDIN GS

Conventional misconceptions
If you’ve ever looked into the causes of pattern hair loss (AGA), the first term people usually
come across is dihydrotestosterone, or DHT. DHT is a hormone that’s made from
testosterone. Hair loss experts are quick to tell you that DHT is the root cause of pattern
hair loss. But is there evidence to support that claim?

There’s actually a lot.

This section covers the science behind the DHT-pattern hair loss connection. First, we’ll
build the case that DHT is the root cause of AGA. Then, we’ll evaluate if hair loss treatments
that reduce DHT are effective. Then, we’ll challenge parts of the DHT-AGA connection to
reveal the complexities (and paradoxes) of DHT’s relationship to our hair.

The case for DHT causing pattern hair loss

I first heard about DHT during my initial hair loss consultation (in 2007) — when I was
diagnosed with pattern hair loss. After some discussion, I learned the following: for reasons
not fully understood, pattern hair loss begins when DHT starts accumulating in our scalp
tissues. Our scalp’s hair follicles become sensitive to DHT and begin shrinking. Over a
series of hair cycles, DHT makes our hair thinner and wispier, until our hair becomes so thin
that it stops growing. The end result: pattern baldness. Here’s a graphical representation:

60
In any case, I wasn’t sold on my doctor’s explanation of how DHT causes pattern hair loss.
So, I went home and started doing more research. I discovered there are three findings that
form the basis of the DHT-hair loss argument:

1. DHT is higher in the scalps of men with thinning hair.

2. If a man is castrated, his testosterone (and DHT) levels plummet permanently. Men
castrated before puberty (i.e., before their DHT levels spike) don’t go bald later in life.

3. Some men lack an enzyme that converts testosterone into DHT in the scalp. Men who
have this genetic condition never develop pattern hair loss.

That’s actually a very compelling argument. DHT levels are higher in balding scalps. Men
who can’t produce DHT don’t go bald. And men who lack an enzyme which converts DHT
in the scalp never lose their hair to pattern hair loss.

Based on this, it seems like DHT causes hair loss. Just look at the extremes. If we never make
any DHT, we never go bald. And if DHT is too high in our scalps, we lose our hair.

The only questions I couldn’t find compelling answers to were...

• Why does DHT increase in balding scalps?

• How does DHT miniaturize our hair follicles?

But I thought to myself, “Who cares?” We know that in the absence of DHT, baldness
doesn’t happen. So DHT must be the culprit. At this point, I agreed with my physicians:

And if DHT is what causes pattern hair loss... maybe taking away DHT will help reverse it.

These data became the basis for many pattern hair loss drugs. So let’s dive into these drugs
— and uncover how effective they are.

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Conventional treatments for AGA: finasteride and minoxidil
To date, there are two FDA-approved drugs for AGA. They are:

• Finasteride (branded as Propecia)

• Minoxidil (branded as Rogaine)

How do they work?

Finasteride prevents DHT conversion

Finasteride is an oral drug that helps prevent testosterone from converting into DHT. This
means idea that less DHT can accumulate in our scalp tissues.

Remember that enzyme that some men lack, which makes them unable to convert
testosterone into DHT in their scalps? That enzyme is called type II 5-alpha reductase.
Finasteride is a type II 5-alpha reductase inhibitor. In other words, it blocks the formation of
this enzyme.

Finasteride’s logic is as follows: by inhibiting testosterone's conversion to DHT, less DHT

can get to our scalp. If less DHT reaches our scalp, we can slow down hair follicle
miniaturization. If enough DHT is blocked, we might even halt hair loss or
experience regrowth.

This type of logic has even led many hair loss sufferers to try an even more potent DHT
reducer known as dutasteride (branded as Avodart). Dutasteride is similar to finasteride.
It’s a 5-alpha reductase inhibitor, but it wasn’t initially intended to treat male pattern hair
loss. Rather, it was developed to reduce the size of enlarged prostate glands. Then, after
realizing dutasteride also reduced DHT levels in the scalp — and possibly even more so than
finasteride — doctors started prescribing it as a hair loss treatment.

Minoxidil improves blood flow, modified prostaglandin activity, and more

Minoxidil isn’t a DHT reducer. It’s a topical vasodilator (it improves blood flow). And
interestingly, no one is sure exactly how minoxidil works. Among the leading theories, it’s
believed that minoxidil provides more blood flow to our hair follicles — which improves the
oxygen and nutrient supply to our hairs. This helps kick hairs out of the telogen (resting)
phase of the hair cycle... and back into the growth phase.

Minoxidil also increases the presence of substances called prostaglandins. Prostaglandins are
made from fats, and they influence the behavior of our immune system. There are good and
bad prostaglandins. The bad ones can induce asthma and prevent hair lengthening. The

62
good ones, however, are associated with healthy hair growth — and more specifically, the
growth (anagen) phase of the hair cycle. Research suggests that in addition to improving
blood flow, minoxidil also increases our “pro-hair” prostaglandins.

To reiterate — minoxidil works differently from finasteride. Whereas finasteride helps to stop
hair follicle miniaturization by reducing DHT... minoxidil helps increase the number of hairs
in the anagen (growth) phase. This is why minoxidil is also a line-of-defense for hair
shedding disorders. However, since increased telogen hairs are also observed in AGA,
minoxidil tends to help improve pattern hair loss as well.

Do these drugs have any side effects?

Yes. As it turns out, type II 5-alpha reductase — the enzyme that converts DHT in our scalps
— plays a number of important roles in the body. Many of these roles aren’t yet fully
understood. But to get an idea of how important type II 5-alpha reductase is, let’s revisit the
men who are severely deficient in this enzyme.

We know these men never lose their hair. Lucky them. When I first read about this
deficiency, I found myself wishing I had it. Then, I read about all its other consequences.

A type II 5-alpha reductase deficiency doesn’t just stop hair loss, it also stops DHT
production in prenatal development. Boys born with this condition are also born with
underdeveloped or ambiguous genitalia. Many parents even raise them as women (believing
they are female) until puberty, when their secondary hormones kickstart some genital
development. Of the men who develop functional genitalia, most of them are infertile.

So this enzyme — and DHT — are critical for proper male development. This is why
pregnant women are advised to literally not touch finasteride’s capsules — since finasteride
and dutasteride can potentially mutate and inhibit the development of male fetus genitalia.

But finasteride and dutasteride aren’t drugs that people take when they’re developing.
They’re drugs people take as adults. Knowing this, can finasteride or dutasteride still cause
problems?

The answer is yes. But it is absolutely critical to contextualize the risk of these side effects ––
so that you don’t inadvertently avoid trying these drugs due to a misguided perception.

Finasteride and dutasteride: side effects

Sexual

63
While DHT and 5-alpha reductase are critical during male development, they’re also
important for sexual health. For instance, men on finasteride for six months had a 30%
decrease in sperm count and changes to sperm volume, concentration, and motility.

On that note, finasteride does come with a risk of sexual side effects. But just how high is
this risk? It’s hard to get a straight answer from people. Depending on your source (i.e., a
physician or a natural health website), you’ll read side effect incidences ranging from 1-40%.
It all depends on which study you decide to reference. Here are two examples:

1. In this year-long study, only 1.8% of finasteride users reported sexual side effects
— compared with 1.3% in the placebo group (i.e., the ones taking sugar pills). When
you go to the doctor, the above study is almost always the one they’ll regurgitate to
quell any of your concerns about finasteride’s sexual side effects. But it isn’t the
whole story.

2. In this year-long study, researchers split finasteride users into two groups: one
informed about the possibility of sexual side effects... and one uninformed when
starting treatment. After one year, 25.4% of informed patients reported erectile
dysfunction versus 5.7% of uninformed patients.

This suggests that many of the sexual side effects from finasteride are psychosomatic — or
in other words, caused by the fact that people “know” they might happen.

At the same time, that study’s incidence of sexual side effects are much higher than what
most doctors suggest. After all, that study showed that by the one-year mark, 15% of
uninformed finasteride users still reported sexual side effects.

To confuse us even more, there are a small number of reports of men taking finasteride for
only a few weeks and then developing unresolved erectile dysfunction. These reports have
created a lot of fear regarding trying this drug. They’ve also led to divide within the medical
community. Why? Because in the multi-year, double-blinded, placebo-controlled clinical
trials that granted finasteride FDA approval, researchers never observed these effects. On
the contrary, those studies found that the magnitude of side effects from finasteride decreased
with continued use, and that after quitting, side effects reversed within three months.

Cognitive
On hair loss forums, some men taking 5-alpha reductase inhibitors have reported
diminished cognition — specifically, “brain fog” and “depression”. Again, this effect hasn’t

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been reported much in clinical studies. However, a lot of people who have felt these effects
have found, in the literature, studies on mice and finasteride that raise alarm bells.

For instance, this study on mice found that mice who were given finasteride long-term —
then “quit” — experienced increased neuro-inflammation and depressive-like behavior.
While that’s not a study on humans, it does fit with a lot of anecdotes collected from Post-
Finasteride Syndrome — a support community for men who reportedly haven’t yet
recovered from finasteride’s side effects (even after stopping the drug).

At the same time, nearly all mouse model studies on finasteride use incredibly high dosages
of the drug – often 100-to-1,000-fold higher than what is prescribed to men. And yes,
dosage matters! Why? Because imagine what would happen if you tried to drink 1,000 times
your daily intake of water. Your bladder would explode, your kidneys would fail, and you
wouldn’t make it to tomorrow. But we don’t go running around telling people not to drink
water over these risks.

Should you take finasteride or dutasteride?

I used to take a hard stance against finasteride, especially when I was younger. This is
because I assigned more emphasis to the drug’s risks than I did its benefits. It’s easy to feel
the same way: those mega-dosed mouse studies and the anecdotes of Post-Finasteride
Syndrome give a terrifying impression. It also didn’t help that the doctors, dermatologists,
and online resources I consulted all gave me conflicting answers. Trying to synthesize it all
(and make a decision) can feel paralyzing.

With that in mind, the decision to try these drugs boils down to your personal preferences.
On that note, I don’t care about whether you use these drugs; I care about how you
rationalize that decision.

In other words, if you’re not trying these drugs because, in the past, you’ve been exposed to
misleading information, then that’s not a compelling case. However, if you’re not trying
these drugs because they don’t fit with your world view, or your treatment preferences, or
perhaps you’ve tried them before and experienced side effects so are now looking for
alternative options –– that is completely reasonable.

To help you make these decisions, I’ve written a Finasteride User Guide: an evidence-based
manual of unbiased information regarding the pros and cons of the drug. The goal: to help
inform those interested in finasteride on the facts, not the hype. That way, you can feel better
about the path you’re choosing. Inside, you’ll find:

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 • An objective evaluation of finasteride: pros, cons, side effects, and considerations.

• The model profile of a finasteride user

• If taking, how to reduce your costs of a finasteride prescription by 90%+

• If taking, how to potentially increase finasteride’s efficacy

• If taking, how to reduce the risk of side effects

• If quitting, how to taper off finasteride to reduce risks of withdrawal and hair shedding

You can access the guide right here. And if you have any questions, there’s also a dedicated
discussion thread. You can access that thread here.

What about minoxidil?

Minoxidil doesn’t work by reducing systemic DHT levels. Rather, minoxidil likely works by
improving blood flow, modifying potassium ion channels, and modifying prostaglandin
activity — all of which are suspected to help telogen hairs re-enter their growth (anagen)
phase. As such, minoxidil’s reported side effects are far less concerning than those of
finasteride or dutasteride. Here are a few that people tend to receive attention online.

Skin irritation
The biggest side effect with minoxidil seems to be skin irritation. Between 2% to 6% of
users tend to report it. But interestingly, this might not be due to minoxidil, but rather from
the ingredients that help carry minoxidil into deeper layers of our skin. One “carrier”
ingredient is called propylene glycol. In allergy tests, 80%+ of minoxidil users reporting
skin irritation were actually having a reaction to propylene glycol — and not minoxidil itself.

Rogaine (i.e., the biggest brandname of minoxidil) uses propylene glycol as a carrier agent.
For most people, this won’t cause notable skin irritation. For a few, it might. Interestingly,
some of the ingredients in Rogaine Foam — like butylated hydroxytoluene (BHT) — are
banned in Japan and parts of the E.U. This is because studies have shown that BHT can be
tumor-promoting in animals.

For these reasons, I recommend that anyone interested in using monixidil and worried
about skin irritation to try to find a brand without propylene glycol or BHT. There are dozens
— like Essengen-5 NO PG FAST DRY. I’m not affiliated, nor have I tried Essegen.

Toxicity to cats

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Cats lack the enzyme required to metabolize minoxidil — much like dogs lack the enzymes
required to quickly metabolize substances within chocolate. Resultantly, minoxidil is highly
toxic to cats. From 2001-2014, there were four reported feline deaths from minoxidil
exposure. This doesn’t mean that if you have cats, you can’t use minoxidil. It just means that
you need to take extra precautions for storage, application, and drying to make sure your
cats don’t come in contact with the drug (even through their fur). In other words, don’t
directly apply minoxidil to your feline friends. Apply it to your scalp,

Bags under eyes

I used Rogaine Foam for 6+ years. For the most part, I noticed no side effects. However,
over this period, I did develop chronic bags under my eyes. This effect happens to be
something reported by other minoxidil users online. And similarly to finasteride, this effect
wasn’t something reported in minoxidil’s initial large-scale, long-term clinical trials.

It’s impossible to say whether Rogaine caused these bags under my eyes. What I can say is
that minoxidil has water-retentive properties, and if the drug is liberally applied (as I was
doing) and absorbed beyond the scalp, then it’s possible that these water-retentive effects
may occur in adjacent facial tissues – thereby giving the appearance of slight tissue swelling.
While there’s no hard evidence here, I believe that my eye bags were, in part, a result of (1)
normal aging, and (2) additional water retention resulting from minoxidil use. Since
stopping minoxidil, my eye bags diminished, and I’ve noticed further improvements through
dietary changes (specifically, lowering my salt intake – as salt may also increase water
retention). Others have reported improvements, too!

So, before you quit minoxidil due to concerns over eye bags, try (1) reducing your salt
intake, or (2) switching brands to a formulation without propylene glycol. It’s possible that
both of these things will help!

Heart palpitations
Minoxidil was originally prescribed orally as a blood pressure medication — then later
rebranded as a topical hair loss drug after patients started reporting more hair growth.
However, there is some systemic absorption from topical minoxidil use. As such, a small
percentage of users have reported blood pressure-related effects ranging from dizziness to
heart palpitations. When minoxidil is used as a topical, these effects are incredibly rare.

Should you use minoxidil?

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Similar to finasteride, the clinical evidence suggests that minoxidil is really well tolerated –
particularly in terms of its possible side effects and the magnitude of those side effects. So,
should we use this drug?

Well, like finasteride, minoxidil boils down to personal preference. I quit minoxidil, but not
because of any side effects. Rather, it just didn’t seem to work for me. However, more recent
advents in combination therapies (more on this soon) have made minoxidil a far more
powerful hair loss drug — and if you’re going to make an informed decision on whether to
use it, you should have access to all relevant drug information.

That’s why, just like with finasteride, I’ve created the Minoxidil User Guide. This is an
unbiased, science-based guide to evaluate whether minoxidil is right for you — and if you
choose to use it, how to maximize its efficacy. Inside you’ll find:

• An objective evaluation of minoxidil: pros, cons, side effects, and considerations

• The model profile of a minoxidil user

• If using, how to minimize side effects

• If using, how to increase minoxidil’s efficacy by (potentially) over 400%

• If quitting, ways to taper off minoxidil to maybe reduce risks of excessive hair shedding

You can access the guide right here. And just like with finasteride, there’s also a minoxidil
discussion thread. You can ask questions and access that thread here.

Are finasteride and minoxidil effective?

If elevated DHT causes pattern hair loss, and DHT inhibitors like finasteride reduce scalp
DHT by 50-70%, then how much hair can we grow back when we start taking them? And
what about minoxidil? Does it work, too?

Response and regrowth

When evaluating any hair loss drug’s efficacy, two measurements should come to mind.

The first is response rate — or the percent of people who respond favorably to treatment.
For pattern hair loss, this would be percent of people who see their hair loss slow down,
stop, or even reverse. The second is the amount of hair regrowth. For those taking the
drug, what was the average amount of hair regrown? A little... or a lot?

Finasteride and dutasteride: response rate, amount of hair regrown

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Finasteride and Dutasteride’s response rate is impressively high, estimated to be around
80-90%. That’s a majority of users seeing a slow, stop, or even reversal of hair loss.

But how much hair can we expect to regrow? Most evidence points to a 10% increase in hair
count, along with some thickening of existing hair. That’s not nearly a miracle cure, but it’s
also not terrible either. Yes, most research shows that finasteride is more effective at slowing
or arresting hair loss than it is at reversing it. But there’s also evidence that finasteride’s hair
count increases can hold really well – even over ten-year periods.

Minoxidil: response rate, amount of hair regrown

In short-term trials, about 60% of men believed Rogaine helped them maintain or regrow
some hair. But in multiple year studies, that response rate was less than 30%.

It gets worse when we factor in satisfaction ratings. In one study, 95% of minoxidil users
quit by one year — with 66.5% citing “low effect” as their rationale. And in this five-year
study, only 20-30% of users said they were even satisfied with the drug’s results. At that
point, the only reason some were still using it was because of the drug’s warning label:

“Continued use of ROGAINE® products is needed to maintain hair regrowth. If you stop
using it, the normal hair loss process will start again. You will probably lose your newly
regrown hair within 3 to 4 months and will look the way you looked before using ROGAINE®
products... You'll want to make ROGAINE® products part of your daily routine.”

What this warning label doesn’t say is that, by itself, minoxidil isn’t that effective for pattern
hair loss. Why? Because minoxidil is a drug that helps kickstart more hairs into anagen. But
that doesn’t mean it does anything to stop progressive hair follicle miniaturization — which
is what drives the progression of pattern hair loss. Long-story short, minoxidil might help
early on, but its effectiveness seems to fade.

If you take minoxidil or finasteride, you need to take them for life
Once you stop using finasteride, dutasteride, or minoxidil, any hair gained from those drugs
will fall out within three to twelve months. If you want to maintain your results, it is
generally believed that you have to take these drugs for life.

Now, this might sound daunting and stressful. But in fairness, we do a lot of things on a
daily basis to maintain aspects of health. For example, brushing our teeth.

So, if we frame the use of finasteride or minoxidil in the same way that we frame brushing
our teeth, then keeping up with these treatments may feel a lot less overwhelming. At the
same time, it’s important to know about these limitations prior to starting treatment.

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Finasteride stops future hair loss, but doesn’t reverse all hair loss
Why is it that drugs that reduce DHT — like finasteride or dutasteride — merely result in a
stop in hair loss and slight regrowth but rarely (if ever) full recoveries? If DHT is the cause
of hair loss, then if we stop DHT, shouldn’t our hair come back?

We can actually answer this question with the most extreme form of DHT reduction:
castration. Remember that observational study on boys castrated before puberty — and how
they never suffered from AGA later in life?

Well, that same observational study also followed adult men who were suffering from hair
loss and then got castrated. The result? A permanent plummet in testosterone levels and
DHT production... and a halt in hair loss. But interestingly, not a full reversal of AGA.

What does this mean? That DHT might be causally linked to pattern hair loss... but for
reasons not fully understood, removing DHT only stops pattern hair loss. It doesn’t lead to a
reversal of the disorder.

And what does this mean? It’s time to re-evaluate the DHT-hair loss argument.

Revisiting the DHT-pattern hair loss connection

First, let’s recap what we know so far:
Experts agree that DHT is causally linked to pattern hair loss. This is because: (1) balding
men have higher scalp DHT levels; (2) men who can’t produce DHT never go bald; and (3)
men deficient in an enzyme that converts DHT in the scalp never go bald.

On the other hand, drugs that reduce DHT production — like finasteride and dutasteride —
are mostly limited to slowing or stopping hair loss.

So, could there be more to the DHT-pattern hair loss argument than we think? Maybe.

It turns out DHT is way more complicated than most people think. If we take a look at
DHT’s roles in other parts of the body, it becomes clear why the DHT-hair loss connection
isn’t as cut-and-dry as people like to make it.

The paradoxes of DHT

Paradox #1: tissue DHT versus serum DHT

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What exactly is DHT? We know that DHT is a hormone made from testosterone. We know
that it’s critical to early male development — but in adulthood, we can significantly reduce
the activity of this hormone without noticeable side effects for most men and women.

Interestingly, DHT seems to change its behavior depending on the location in which it is
active. In fact, there are different kinds of DHT, and we can break down the types of this
hormone into two major categories.

Firstly, there’s tissue DHT. This is the kind that binds to tissues like our skin and scalp.
Secondly, there’s serum DHT. This is the kind of DHT that circulates in our blood.

Most people are under the impression that all kinds of DHT — both tissue and serum —
are bad for our hair. But is this true?

Let’s start with tissue DHT. As we already know, tissue DHT is higher in the scalps of
balding men. Scalp tissue DHT is linked to pattern hair loss. In the scalp, where DHT
increases, so does hair loss.

But what about serum (blood) DHT? Well, one study found that serum DHT has no
correlation with pattern hair loss. Another study showed that serum DHT is higher in young
men without hair loss. That’s the opposite of what physicians say about the DHT-hair loss
connection. Based on these studies, serum DHT is either uncorrelated with or protective
against pattern baldness.

So, now we know that serum DHT is not correlated with pattern hair loss, but tissue DHT in
our scalps is. By this logic, tissue DHT in other locations — like our chests and face — must
also be correlated with pattern hair loss. Right? Wrong.

Paradox #2: scalp tissue DHT versus body tissue DHT

Tissue DHT appears to function differently depending on its skin location. For instance,
higher scalp tissue DHT is associated with pattern hair loss. But higher body tissue DHT is
linked to better body hair growth. The same is true for facial hair.

I repeat: the more tissue DHT in your chest and face, the hairier your chest and face.

How can that be? How can tissue DHT encourage both hair growth and hair loss, depending
on its location? In our scalps, there has to be another factor at play. Increased DHT plus
something else must explain why men and women lose their hair.

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There is another factor. In fact, there are several factors that hair loss drugs may not target.
The next chapter discusses them. In my opinion, these factors are what we need to target in
order to see major hair recoveries beyond what we is achieved just with DHT reduction.

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Chapter recap
Doctors say that DHT causes pattern hair loss. This is because: (1) balding scalps have
higher tissue DHT; (2) castrated men don’t produce much DHT and never go bald; (3) men
deficient in an enzyme that converts DHT in their scalps never go bald.; and (4) DHT-
reducing drugs like finasteride and dutasteride have an excellent track record at arresting
pattern hair loss, and regrowing a bit of hair.

At the same time, drugs that lower DHT don’t seem to fully reverse most cases of AGA.
Instead, they tend to slow or arrest its progression.

The bottom-line: when we look more closely at DHT, the evidence indicting DHT as the sole
cause of pattern hair loss feels a little incomplete. After all, DHT promotes pattern hair loss
in the scalp, but hair growth in the body. This suggests that perhaps DHT alone doesn’t
cause hair loss. It must be DHT alongside other factors.

Once we zoom out and look at a balding scalp’s environment, we begin to see other factors
potentially at play. The next chapters uncover more science on pattern hair loss, attempt to
make sense of the DHT paradoxes, explain the pattern and progression of AGA, and build a
flowchart explaining its causes. In doing so, we’ll learn one hypothesis as to why DHT
reducers may fail to recover all of our lost hair.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

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 CHAPTER 5:
PATTERN HAIR LOSS: GETTIN G TO
THE ROOTS

Chapter summary:

• This chapter dives into the features of pattern hair loss beyond just DHT –– its
biological, histological, and morphological markers: where these things intersect with
DHT, and what we might be able to do to fix them.

• Each piece of evidence is packaged into a flowchart that speculates additional

mechanisms behind pattern hair loss and conditions that prevent hair from regrowing.

• This flowchart isn’t just a visual of the hair loss cascade. It’s a tool that may allow us
to evaluate the efficacy and shortcomings of any hair loss treatment. Learn it, know it,
and use it to uncover if a new drug, pill, or therapy will help before you spend a dime.

• It all starts by cataloguing the questions that the DHT = hair loss argument may not
answer. Using these questions as a launching point, we’ll reveal more observations
behind our balding scalps... and potential answers to the DHT paradox.

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PATTERN HAIR LOSS: GETTIN G TO THE ROOTS

A deep-dive into pattern hair loss science

Again, here’s what we’ve covered so far about what causes pattern hair loss:

But as we’ve already discussed, DHT by itself may not be the cause of pattern hair loss. Why?
Because DHT also promotes hair growth in the chest and face. This suggests DHT plus
something else must be triggering hair loss. So, is there any evidence to support this?

Yes. And in this chapter, we’re going to trace the symptoms and conditions of pattern hair
loss all the way to their roots. This is a hypothetical, evidence-based, investigative approach
to uncovering why men and women lose their hair.

We’ll start by identifying five questions the DHT-pattern hair loss theory cannot address.
Then we’ll follow a trail of evidence to answer them — and while building a master
flowchart to help consolidate our thoughts.

We’re building a flowchart, but we’re also creating a guide that enables us to assess the
efficacy of any hair loss drug, supplement, or regimen. By the end, we’ll understand one
possible perspective as to why drugs like finasteride, dutasteride, and minoxidil don’t fully
reverse hair loss, how the DHT paradox actually makes sense, why we lose hair in a specific
pattern, and which conditions we should target to not only stop AGA, but also regrow
dormant hair follicles.

DHT-pattern hair loss argument: unanswered questions

The DHT-hair loss argument is as follows: for reasons not fully understood, DHT begins
increasing in scalp tissues. In response, our genetically sensitive hair follicles begin to

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miniaturize in DHT’s presence. This leads to hair follicle miniaturization and shorter,
thinner hairs... until these hairs stop growing and we’re left with pattern baldness.

This explanation feels incomplete. Why? Because there are five questions that this theory
cannot answer. They are:

• If DHT causes pattern hair loss, how come reducing DHT only stops hair loss... but it
doesn’t fully reverse thinning hair?

• What causes DHT to increase in balding scalp tissues?

• How, exactly, does DHT miniaturize hair follicles?

• Why is DHT linked to scalp hair loss... but also chest and facial hair growth?

• How can we explain the patterning and progression of pattern hair loss?

Most doctors have a one-word answer to our questions: genetics. This is certainly true to an
extent, but it’s also disingenuous. Genes alone can’t explain why the perceived incidence of
hair loss might be rising... or why one genetically identical twin can bald faster than his
counterpart... or why men moving from the third world to the U.S. are anecdotally reporting
pattern hair loss despite no familial history of it… or why 60% of college students in China
(where baldness rates were once very low) are now reporting thinning hair.

So, is it possible to go beyond this “genetic” blanket statement and answer these questions
with the available literature... all while making sense of DHT’s role in AGA?

In my opinion, yes. This is what I set out to do in my 2018 peer-reviewed paper, “A

hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone
paradox and rate-limiting recovery factors.” I know the title is a mouthful. You don’t need to
read it. Rather, we’ll reference aspects of the manuscript to guide us through this chapter.

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The goal: to build an AGA model that helps to not only explains why we go bald, but also
additional things we can target to potentially reverse hair thinning (even beyond DHT).

It all starts by cataloguing the observations we see in balding scalps.

Beyond DHT: what else is happening in balding scalps?

When I first starting reading about AGA, I assumed that increased DHT was the only thing
researchers had observed in balding scalps. I was wrong.

In reality, there are dozens of changes that occur in balding scalps — from skin texture
differences to the genes expressed in each hair follicle. We’re going to catalogue several of
them, and then attempt to trace these changes back to their root causes.

We’ll start with what our eyes can see and our fingers can feel: balding scalp skin.

Balding scalp skin looks shinier

Where is your hair thinning? Temples? Vertex? Grab a mirror and see where you’re balding.
Aside from hair loss, do you notice any differences in your balding and non-balding regions?

In balding areas, our scalps tend to have a certain “shine” to them. In advanced stages, they
can even look swollen. Just look at the green parts of your scalp, then the blue.

Why do balding regions of our scalps look shinier and more swollen?

Balding regions are often ridden with disorganized collagen (i.e., fibrosis)
Balding scalps are often shinier due to structural changes to the skin’s integrity. Specifically,
balding skin can be shinier due to an overproduction of something called collagen.

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Collagen fibers are proteins that make up our connective tissues — like our skin. When we
get a cut, our bodies will make new collagen to repair the wound. Once healed, the skin
looks just like it did prior. This is called ‘perfect’ wound healing: the collagen which fills in
the injury is perfectly organized.

But there’s also a downside to wounding. If we cut our skin too deeply, our bodies can’t
perfectly regulate collagen production during repair. With deeper injuries, the body
overcompensates. It lays down too much collagen in the form of disorganized fibers. If too
many disorganized fibers accumulate, this is called fibrosis (i.e., scar tissue). And one of the
defining characteristics of fibrosis? Shinier-looking skin.

So, is there any evidence of excess, disorganized collagen fibers in balding scalps?

Yes. Balding men have more collagen and four times the amount of elastic fibers at the
temples and vertex than men with zero hair loss. In fact, as hair follicles miniaturize,
disorganized collagen tends to increase around balding hair follicles. And as this collagen
accumulates, it can eventually turn into scar tissue — known as perifollicular fibrosis. In
fact, we can think of disorganized collagen fibers as the “building blocks” of fibrosis.

So, where there’s hair follicle miniaturization, there’s often disorganized collagen (i.e.,
fibrosis). In fact, research suggests that disorganized collagen appears to increase alongside
the progression of pattern hair loss.

But can excess disorganized collagen actually cause hair follicle miniaturization? Or is
fibrosis just a consequence of hair follicle miniaturization? It’s really hard to say. After all,
different research groups will offer different opinions.

In the absolutes, we can glean ideas from studying an autoimmune condition in which
sufferers over-accumulate fibrosis. This condition is called scleroderma. In scleroderma, the
body starts to overproduce collagen — sometimes in the hands, lungs, and even the scalp.
Regardless of the location, the outcome looks similar to balding scalps: shinier-looking skin.

Just look at this photo of a scleroderma sufferers’ hands, and then this photo of a hair
transplant patient’s scalp. Notice the shine around the knuckles and the shine across the top
of the scalp. It almost appears like the same skin quality. Same shine, same swelling. And
importantly, for those who develop scleroderma in the scalp, hair loss soon follows.

This is a critical piece of information. Why? It suggests that disorganized collagen can
negatively affect hair growth. Specifically, it tells us that the over-accumulation of
disorganized collagen (i.e., fibrosis) may lead to hair loss. In other words, disorganized

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collagen fibers may come first; hair loss may come second. If you’ve ever gotten a scar, this
shouldn’t be a surprise. Aside from shinier-looking skin, one defining characteristic of scar
tissue is the absence of hair.

At the same time, there are often cases of pattern hair loss where scarring doesn’t occur
until its end-stages. This has lead many researchers to argue that scarring may be a
consequence (and not a cause) of hair follicle miniaturization. So, I want to emphasize that
opinions here are still split! In any case, we do know that in environments where there is
too much scar tissue, hair cannot grow. As such, we can begin to build our flowchart.

So, if disorganized collagen (i.e., fibrosis) might lead to pattern hair loss, how does this
happen? There are at least two potential pathways:

1. Fibrosis restricts hair follicle growth space

As disorganized collagen (i.e., fibrosis) accumulates around a hair follicle, it expands into
the hair follicle shafts — compromising that hair follicle’s integrity. Specifically, it constricts
the room a hair follicle has to grow hair. Here’s a visual of what this might look like:

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But spacial constriction isn’t the only way disorganized collagen contributes to hair thinning.
As disorganized collagen expands, it also impacts the integrity of our scalp skin.

2. Disorganized collagen reduces a hair follicle’s blood supply

Body tissues wrought with disorganized collagen bundles (i.e., fibrosis) also have lower
blood flow. This is also documented in balding regions. Blood flow is restricted in scalp
regions with thinning hair. The more disorganized collagen, the lower the blood flow.

Knowing this, it’s no surprise that nearly all scleroderma sufferers also have poor circulation
of the extremities (hands, feet, and head). Poorer circulation, less blood flow. But less blood
flow also means less oxygen.

Less blood flow = less oxygen

Blood carries oxygen to our tissues. If our tissues have lower blood flow, they also have
lower oxygen levels. Low tissue oxygen is also known as hypoxia. And again, studies
confirm that balding scalps are more hypoxic versus non-balding scalps.

In fact, balding regions have 40% lower oxygen levels versus non-balding regions. And men
without pattern hair loss have near-equal oxygen levels across their entire scalp. In other
words, balding scalp tissues aren’t getting nearly enough oxygen.

Again, the questions must be asked: are reductions to blood flow (and oxygen levels)
consequences to or causes of hair follicle miniaturization? There’s an argument to be made
on both sides, which I detail here. But for purposes of this flowchart, we can say that in
addition to restricting hair follicle growth space, fibrosis may also decrease blood flow and
oxygen to our hair follicles. In doing so, this excess disorganized collage “chokes out” our
hair follicles, leading to hair follicle miniaturization.

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Now... are there any other conditions in a balding scalp that might also decrease blood flow
and oxygen to thinning hair follicles?

Yes. Deeper in our skin, there may be another possible contributing factor: calcification.

Our skulls may be partially calcified

It’s not just fibrosis that reduces blood flow and oxygen to our hair. In balding areas, there
are anecdotes of deep blood vessels that once supported our follicles becoming calcified.

Dr. Frederick Hoelzel in the American Medical Association published the connection between
scalp calcification, restricted blood flow, and hair loss over 75 years ago. When removing the
brains of cadavers, he discovered...

“Baldness occurred in persons in whom calcification of the skull bones apparently had not
only firmly knitted the cranial sutures but also closed or narrowed various small foramens
through which blood vessels pass most prominently in persons with a luxuriant crop of hair.”

For the layperson: in balding regions, the scalp bones and blood vessel networks running
through the skull to the tissues supporting our hair follicles were calcified. And if an artery is
calcified, blood flow is significantly restricted.

What is calcification?
According to the experts, calcification is “when calcium builds up in places where it doesn’t
usually appear, like the coronary arteries or brain.”

Since elderly people often have more calcification, researchers once thought this process was
a part of normal aging. But it turns out the relationship between age and calcification
doesn’t really exist. Calcification doesn’t have to increase with age. It can be rampant in
young adults and nearly absent in older ones.

We’ll get into the causes of calcification soon, but for now, it’s important to note that
calcification is not caused by a calcium-rich diet.

So back to our flowchart. Does calcification cause fibrosis?

Probably not. Research shows that calcification and fibrosis can occur in the same areas, but
are likely independent of each other. And while some scleroderma patients also suffer from

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soft tissue calcification, others just suffer from an overproduction of collagen. So
calcification does not have to happen before fibrosis or vice-versa.

Knowing this, we’re ready to add calcification into our flowchart. For simplicity’s sake, we’ll
remove the visuals describing a balding scalp — the “shinier skin.”

Balding scalps have reduced blood flow in multiple places...

Before we continue, it’s important to note that in balding scalps, fibrosis and calcification
appear to occur in two different places.

Fibrosis tends to occur around our miniaturizing hair follicles. This restricts growth space
and prevents blood and oxygen from reaching each hair follicle. However, calcification occurs
much deeper: within our skull bones, skull foramina (i.e., the small passageways / holes in
our skull), and the tiny blood vessels that run through that skull foramina.

I know this is a lot to keep track of, so here’s a visual of what’s happening. On the left: a
healthy, hair-bearing scalp. On the right: a balding scalp.

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Here, we can now see two places where blood flow may be reduced. First, see how in the
healthy scalp (left), there are blood vessels running through the skull foramina that help
support the tissues underneath our hair follicles? Well, in balding scalps (right), these
foramina have closed, and the blood vessels that ran through them are now calcified. This
may reduce blood flow to tissues which indirectly support our hair follicles. Secondly, see
how fibrosis accumulates around each hair follicle in a balding scalp? Well, this may reduce
blood flow to the microvascular networks that directly support each hair follicle.

This means that in balding scalps, blood flow may be reduced in (at least) two places.
Fibrosis restricts blood vessel networks directly supporting each hair follicle; calcification
restricts blood flow to the underlying tissues indirectly supporting each hair follicle.

Also note that reduced blood flow occurs above and below the middle layer of our scalp. We’ll
dive into that tissue layer soon. For now, let’s continue tracing this chart backwards.

What might cause fibrosis and calcification?

In our flowchart, we’ve gone as far as explaining fibrosis and calcification’s possible
connection to pattern hair loss. Fibrosis and calcification might directly and indirectly
reduce blood and oxygen to our hair follicles, thus compromising hair follicle integrity and
restricting the growth space of each hair. The end-result? Hair follicle miniaturization (i.e.,
baldness).

So... what might trigger both fibrosis and calcification?

Well, we can uncover what might be causing these conditions if we look at the people most
likely to develop arterial calcification and fibrosis: men.

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Men are almost twice as likely as women to develop calcified arterial lesions. Why is that?
Researchers have long suspected that testosterone and DHT (androgens) might be to blame.
Finally, it looks like DHT is coming into play. So let’s look at the evidence. Can androgens
— like DHT — cause fibrosis or arterial calcification?

A connection between androgens, calcification, and fibrosis

Men and women who take androgens (steroids) significantly increase their risk of arterial
calcification. And in mice, DHT and testosterone injections increase arterial calcification
lesions by 200-400%. The more DHT or testosterone injected, the greater the calcification.
That’s a pretty strong case that androgens cause calcification.

But paradoxically, in studies done in test tubes (i.e., outside of our bodies), an increase in
androgens doesn’t cause calcification. In these studies, androgens often protect against
calcification. The same seems to be true about fibrosis as well.

This suggests two things: (1) androgens alone don’t cause fibrosis or calcification; and (2)
those test tube studies are missing at least one variable. It must be that androgens plus a
“mystery variable” lead to fibrosis and calcification — not just androgens by themselves.

Now let’s apply this knowledge to our scalps. DHT is the main androgen associated with
pattern hair loss. Scalp DHT is higher in men with thinning hair. Men who can’t produce
DHT never go bald. So, in the scalp, increased DHT plus these “mystery variables” must
precede both calcification and fibrosis. Knowing this, here’s our newly updated flowchart.

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Identifying these mystery variables is critical. Why? Because as we recall, DHT is linked to
scalp hair loss... but chest and facial hair growth. Fibrosis and calcification drive hair follicle
miniaturization in our scalps. And fascinatingly, fibrosis and calcification only seem to
appear in balding scalps... but not in hair-bearing areas of the chest and face.

This suggests that, if present, these mystery variables make DHT behave differently. In their
absence, DHT seems to encourage hair growth in the chest and face. In their presence, DHT
may encourage fibrosis, calcification, and hair follicle miniaturization. Maybe if we can
identify these variables, we can glean insights into the DHT paradox.

Specifically, we’re looking for “variables” that (1) are linked to DHT, (2) can cause fibrosis
and calcification, and (2) express in balding scalps, but less so in chest and facial tissues.

So, what could these mystery variables be?

Well, I’ll spare you the fun of spending months cataloguing substances linked to fibrosis and
calcification, cross-referencing them against substances expressed in chest, facial, balding,

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and non-balding scalp tissues, and communicating with researchers / academics to confirm
if the logic makes sense.

The short-answer: there are several variables that (1) increase in the presence of DHT, (2)
encourage the onset of fibrosis and calcification, and (3) are found in balding scalps (and
less so in chest and facial tissues). Unfortunately, covering all of them would turn this
already-dense chapter into a full-blown book.

Instead, we’re going to focus on the most indicted mystery variable: a signaling protein
called transforming growth factor beta 1.

What is transforming growth factor beta 1 (TGF-β1)?

Transforming growth factor beta 1 (TGF-β1) is a protein that our cells release in response to a
stimuli (and helps influence cell functionality). In short, TGF-β1 changes cell behavior.

Transforming growth factor beta 1 (TGF-β1) helps to regulate cell division, growth, and
death. But interestingly, TGF-β1 is probably best-known as a substance that can cause
fibrosis, calcification, and skin-related aging.

TGF-β1 encourages fibrosis and calcification

Studies show that transforming growth factor beta 1 (TGF-β1) encourages the onset of
fibrosis and calcification. Where TGF-β1 goes, fibrosis and calcification follow.

But is this also true in balding scalps?

Yes. This study showed that TGF-β1 actually encourages perifollicular fibrosis. This study
showed that TGF-β1 increases in the presence of DHT. And most importantly, this study
demonstrated that the TGF-β family can over-express in scalps versus bearded regions.

In other words, DHT and TGF-β1 over-express in balding scalps, yet only DHT seems to
over-express in hair-bearing chest and facial tissues. TGF-β1 is linked to fibrosis and
calcification. Balding scalps have fibrosis and calcification. But hairy chests and faces don’t.

What does this suggest? That TGF-β1 is one of our mystery variables.

Excitingly, this also means TGF-β1 is at least a partial explanation for the DHT paradox —
or why DHT encourages hair loss in the scalp... but hair growth in the chest and face.

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We can almost think of this like an equation: DHT + TGF-β1 = hair follicle miniaturization,
fibrosis, and calcification. DHT + no TGF-β1 = no hair follicle miniaturization, no fibrosis,
and no calcification. Yes, this grossly understates the complexity of this relationship. At the
same time, it’s an easy way to catalogue things.

And with that, we can add DHT and TGF-β1 to our flowchart.

To recap: when DHT increases in hair-bearing chest and facial tissues, it doesn’t over-activate
TGF-β1. But when DHT increases in balding scalps, it does over-activate TGF-β1. Together,
DHT + TGF-β1 lead to calcification and fibrosis — which reduce blood and oxygen, restrict
follicle growth space, and lead to follicle miniaturization.

Again, here’s a visual of where these things occur. They’re not all in the same places.

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And again, note the tissue layer between the fibrosis and calcification. It’s interesting that
both of these conditions develop above and below it. Why is that?

To answer this, we’ll need to continue tracing back our flowchart. We’ve just identified a
mechanism for why our balding scalps develop fibrosis and calcification. Our next big
question... what causes that mechanism to occur?

In other words: why does only DHT increase in chest and facial tissues... while DHT and
TGF-β1 increase in balding scalps? What causes these tissues to behave differently?

What causes DHT and TGF-β1 to increase in balding scalps?

To answer this question, we need to evaluate what researchers have already discovered
about DHT and TGF-β1 in other regions of the body. The questions we should ask: are there
any other places where we see DHT and TGF-β1 increase? And if so, why?

Well, DHT and TGF-β1 are not only higher in balding scalps, but also in enlarged prostates
(the small gland that produces men’s seminal fluid (i.e., semen)). In the prostate, there’s
some evidence that DHT may help regulate inflammation... with some studies suggesting
DHT is anti-inflammatory.

What does this mean? That, at least in the prostate, DHT and TGF-β1 may increase in
response to inflammation. And as we’ll soon see, this gives us critical insights into why DHT
and TGF-β1might increase in balding scalps.

What is inflammation?

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Inflammation is the body’s natural reaction to stressors — like an injury, infection, allergen,
or toxin. There are two kinds of inflammation: acute (temporary) and chronic (constant).

Acute inflammation is a typical part of injury repair. For instance, say we stub our toe. Our
bodies recognize this injury as a “threat”. As such, they activate enzymes, proteins, and
hormones to kickstart the healing process. These molecules assess the damage and then
determine how much our toe should swell (i.e., our pro-inflammatory response), when to
activate repair (i.e., our anti-inflammatory response), and when the swelling should dissipate.
This is all natural, normal, and healthy.

Chronic inflammation is not healthy. This is when an inflammatory response never resolves
— like a virus that won’t go away or an ulcer that won’t heal. In these cases, inflammation is
always present, so our tissues never fully repair. This is the type of inflammation associated
with autoimmunity and cancer — and often leads to scarring (i.e., fibrosis).

So... in the prostate, if DHT + TGF-β1 increases as a response to inflammation — do we see

signs of inflammation in balding scalps?

Yes.

Balding scalps do show evidence of inflammation — and quite possibly in the same places
where we see increased DHT and TGF-β1. This suggests that in balding scalps higher DHT
and TGF-β1 is part of an inflammatory response. DHT arrives to the scalp after inflammation.
And in the scalp, if DHT is chronically elevated, the scalp might be chronically inflamed.

There are studies supporting this belief. In balding scalps, chronic inflammation persists
until fibrosis sets in for the inflammation to shift back to the next group of hair follicles —
until all of our hair follicles atop the scalp are surrounded by fibrosis (and we’re left bald).

When we reflect back on the causes of calcification and fibrosis, this makes sense. Studies
show calcification and fibrosis are the end-results of chronic inflammation.

Chronic inflammation is the gun. DHT and TGF-β1 are the triggers. Fibrosis and
calcification are the consequences. Chronic inflammation may cause the arrival of DHT and
TGF-β1, which over time, leads to fibrosis and calcification... a consequence of which is hair
follicle miniaturization (i.e., pattern hair loss).

Knowing this, we can add chronic inflammation to our flowchart.

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What causes chronic inflammation in balding scalps?
Full-disclosure: no one is really sure.

There are many hypotheses — from environmental irritants to faulty immune responses to
latent viruses to reactive oxygen species to microorganisms. But nobody actually knows.
Having said that, there is some evidence indicting one specific variable. In the next chapter,
we’ll uncover that variable, and what we might be able to do about it.

For now, let’s reflect on the flowchart we just created. This chart is a lot to take in, and it’s
certainly incomplete, but it’s also an attempt to go beyond the genetic basis of pattern hair
loss –– so we can begin to speculate on targets outside of DHT. On that note, we can use
this flowchart as a tool to evaluate certain hair loss treatments before we try them.

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Using this flowchart to evaluate pattern hair loss therapies
Our flowchart may explain why drugs like minoxidil are relatively ineffective at reversing
hair loss, and even why finasteride might stop hair loss, but not necessarily fully reverse it.

Minoxidil versus our flowchart

Minoxidil is suspected to work by providing more blood flow to the follicles and modulating
prostaglandin activity. Where does that process take place on this flowchart? Toward the
bottom. Remember: calcification and fibrosis are chronic, progressive conditions. This means
that they don’t go away on their own and they tend to get worse over time. More blood flow
may help our follicles temporarily. But because minoxidil likely doesn’t reverse the calcified,
fibrotic conditions in our scalps, this effect only provides a temporary boost to our hair
follicles. As calcification and fibrosis worsen, minoxidil’s effectiveness fades.

Finasteride versus our flowchart

Finasteride works by preventing the conversion of free testosterone into DHT. It prevents
scalp tissue DHT from accumulating. Where does this take place on our flowchart? Right
before calcification and fibrosis.

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Since finasteride reduces DHT in the scalp, it helps stop the cascade of events that trigger
calcification, fibrosis, and eventually pattern hair loss...

But, because calcification and fibrosis are further downstream than DHT, and because
calcification and fibrosis are chronic progressive conditions, then reducing DHT won’t
likely reverse these conditions! It’ll only slow or stop their progression. This is, in my
opinion, why finasteride stops hair loss but does not necessarily regrow all lost hair.

Try using the flowchart!

We can use this flowchart to explain the results and shortcomings of almost every hair loss
drug on the market. If we understand a drug’s mechanism (how it works), we can look at
the flowchart and evaluate which part of the cascade it addresses. Let’s try it with the drug
spironolactone, a “caffeine” topical, and even a full-on hair transplant.

Spironolactone works by blocking our androgen receptors so that DHT can’t accumulate in
our scalps. This might help stop hair loss, but since it doesn’t address pre-existing
calcification or fibrosis, it’s likely limited in completely reversing the condition. Caffeine
topicals help boost blood flow to our follicles. But, like minoxidil, unless we reverse the
fibrotic, calcified conditions of our scalps and their triggers, the benefits of boosted blood
flow will likely be short-lived. Finally, hair transplants work by transplanting healthy hair
follicles from the back of our heads to our thinning regions. There’s evidence that
transplanted hairs can “eat away” and re-vascularize fibrotic regions of balding scalps.
However, they don’t stop hair loss progression. In other words, they aren’t a fix; they’re only
hair rearrangement.

In my opinion, any treatment’s biggest hurdle is calcification and fibrosis. Without

reversing these two chronic progressive conditions, any drug, supplement, topical, or
therapy targeting hair loss will only be mildly effective.

So, if we want to regrow hair, it’s probably in our best interest try and to restore the
environment of our scalp back to its original state. That might mean we need to target to
reverse calcification and fibrosis — and restore vascularity to dormant follicles so they can
once again grow thicker, longer hairs.

And with that, you may have realized that this exercise may have answered 4 out of 5
questions that we wanted to address.

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DHT-pattern hair loss unanswered questions: answered
Question 1: If DHT causes pattern hair loss, how come eliminating DHT only stops hair
loss... but doesn’t fully reverse full it?

• Genetic model: dermal papillae cell clusters cannot resize in the presence of DHT.

• Our model: fibrosis and calcification. These chronic, progressive conditions might be our
biggest hurdles to hair recovery. Finasteride reduces DHT to help stop the progression
of both conditions, but it can’t reverse the fibrosis or calcification already present. As
such, finasteride typically only stops hair loss. It doesn’t lead to a full recovery.

Question 2: What causes DHT to increase in balding scalp tissues?

• Genetic model: genetic sensitivity to DHT.

• Our model: in balding scalps, DHT arrives as a response to chronic inflammation. While
we haven’t yet identified the source of inflammation, we believe that (1) inflammation
appears to be present in balding regions, and (2) in other tissues, inflammation triggers
the arrival of both DHT and TGF-β1 — two things we see increased in balding scalps.
Thus, chronic inflammation must be one reason why DHT increases in balding tissues.

Question 3: How, exactly, does DHT miniaturize our hair follicles?

• Genetic model: DHT activates TGF-β1 in dermal papillae cell clusters, which damages
them – causing them to shrink in size and thus produce a tinier hair follicle with each
proceeding hair cycle.

• Our model: In addition to genetics, DHT + TGF-β1 cause fibrosis and calcification and
degrade tissue integrity... a consequence of which is hair follicle miniaturization.

Question 4: Why is DHT linked to scalp hair loss... but chest and facial hair growth?

• Genetic model: genetics.

• Our model: DHT alone may actually encourage hair growth (like it does in men’s chests
and faces). But in cases where DHT arrives as a response to chronic inflammation, DHT
also turns on the signaling protein TGF-β1. It’s the arrival of DHT-induced TGF-β1 that
leads to tissue remodeling in our scalps, and thereby hair follicle miniaturization.

Question 5: How can we explain the patterning and progression of AGA?

• Genetic model: genetics.

• Our model: This may have to do with the source of inflammation (more on that soon).

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Chapter recap
When doctors tell you that DHT = pattern hair loss, they’re right. But in that simplification, a
lot of interesting discussion (and hypotheses) are lost. This chapter’s goal was three-fold:

1. To elucidate what might be going on in balding scalps beyond just elevated DHT.
Compared to non-balding scalps, balding scalps have lower blood flow, lower oxygen,
more disorganized collagen fibers, more scar tissue (i.e., fibrosis), more calcification,
more inflammation, more inflammatory prostaglandins (i.e., prostaglandin D2), and
more signaling proteins like TGF-β1.

2. To explain cause-and-effect between these variables. With the flowchart we’ve built,
we can begin to speculate an order of events — and certain things we may need to target
in order to more effectively reverse hair follicle miniaturization: fibrosis and calcification.

3. To offer alternative explanations that expand beyond the genetic side of patter hair
loss. In doing so, we can begin to see some limitations of drugs like finasteride and
minoxidil — and what we may need to target to enhance pattern hair loss reversals.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

Otherwise, it’s time to move onto answering our last big question: in balding scalps, what is
the source of inflammation? In answering this, we’ll reveal a new target to reverse hair
thinning that is as powerful as it is under-utilized.

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 CHAPTER 6:
C HRONIC INFL AMMATION OF THE
SCALP

Chapter summary:

• We just built a flowchart explaining how chronic inflammation may lead to fibrosis
and calcification — two conditions that could prevent better recoveries from pattern
hair loss. These conditions may restrict blood flow, reduce oxygen levels, and even
partially drive hair follicle miniaturization.

• This begs the question: why might balding scalps be chronically inflamed? There are
no hard answers here. But in this chapter, we’re going to provide one perspective.

• This is another deep-dive into the science behind pattern hair loss. As we try to
answer this question, we’ll reveal a potential target for reversing pattern hair loss that
has remained largely ignored (until recently).

• By the end, we’ll have a strong understanding of three targets that may help reverse
hair follicle miniaturization. The better we understand a condition, the better we can
go about resolving it.

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C HRONIC INFL AMMATION OF THE SC ALP

New insights: the purpose of fibrosis and calcification

In the last chapter, we built a flowchart explained one perspective as to why men and women
go bald. The short-answer: DHT arrives to balding tissues as a response to chronic
inflammation. In the presence of inflammation, DHT activates a protein called TGF-β1.
Together, DHT and TGF-β1 respond to chronic inflammation by laying down scar tissue and
calcification. The consequence? Hair follicle miniaturization (i.e., pattern hair loss).

So... what’s the point of fibrosis and calcification? Why did we evolve to deal with
inflammation this way? After all, these conditions are involved in many chronic diseases
from liver cirrhosis to heart disease to multiple sclerosis. And now baldness! This must
mean that fibrosis and calcification are all bad... right?

Wrong.

Fibrosis and calcification aren’t always the evils they’re made out to be
In fact, there’s actually evidence that these conditions aren’t just a consequence of
inflammation... they’re also an adaptive response.

During a tuberculosis infection, our bodies develop calcification deposits in the lungs.
Researchers used to think that this was just a terrible consequence of the inflammation from
the infection. But then in 1970, they discovered that 34% of children who survive
tuberculosis eventually resorbed their lung calcification deposits after the infection died off —
thereby clearing the lungs to allow for normal, uninhibited breathing (as if the disease never
left a mark). Fifty years later, researchers now believe that in tuberculosis, calcification is
actually a protective mechanism. It walls off the infection to prevent its spread to other lung
tissues... and some of us can even reabsorb it after surviving the illness.

This means that fibrosis and calcification can also be protective to our health. In a way, we
can think of them like “last-resort” tools to stop an inflammatory cascade — whether that
inflammation is due to an infection, a virus, or something else.

Reflecting back to AGA, our degree of scalp inflammation may be inversely proportional to
our degree of fibrosis. In other words, fibrosis resolves our inflammation (unfortunately, at
the expense of our hair).

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That means that in balding scalps, identifying the source of inflammation is critical. Maybe
by identifying (and resolving) the source of inflammation, we can stop (or reverse) the
chronic conditions that cause hair follicle miniaturization — just like how calcium deposits
can reabsorb after a tuberculosis infection disappears.

This chapter is dedicated toward uncovering this source of our inflammation. Again, no one
knows why balding scalps are inflamed. But mechanistic evidence implicates a few factors.
In fact, several studies even show that by targeting these factors, we may be able to achieve
hair regrowth that enhances the results demonstrated by finasteride and minoxidil.

Let’s get started.

If inflammation is chronic, its causes must be chronic

Since inflammation in balding scalps is suspected to be chronic, the cause of that
inflammation must also be chronic. Moreover, this cause must be ubiquitous across AGA
sufferers — meaning there’s an equal opportunity for everyone with AGA to experience it.

This is why I don’t buy into the idea that chemical irritants (like haircare products) are a key
trigger of AGA. Yes, they might be a factor for certain individuals. But, throughout the
world, everyone doesn’t experience the same type of chemical irritants. Yet throughout the
world, we can observe people everywhere with pattern hair loss.

Specifically, we’re looking for a cause of chronic inflammation that (1) presents in all (or
nearly all) balding scalps, and (2) helps to explain the arrival of all other observations made
in balding scalps (i.e., the ones we just covered in our flowchart).

With this in mind, let’s start digging for evidence. One place to start? The actual anatomy of
our scalps, or, in other words, our scalp structure.

Anatomical differences in balding versus non-balding scalps

Remember our visual of a balding scalp? Let’s look at where fibrosis and calcification occur.
As we can see, there’s a connective tissue wedged between these two conditions.

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This tissue above calcification and below fibrosis is called the galea aponeurotica. It’s a
dense, fibrous membrane that connects the tops of our scalp with the muscles surrounding
our scalp’s perimeter. It’s anchored by our scalp’s perimeter muscles — almost like a drum
skin pulled taut.

The galea stretches across the top of our scalp — starting at our hairline and ending at the
back of our heads. Interestingly, the galea underlies the exact area where men and women go
bald.

In fact, the galea is what makes AGA-prone hair follicles unique from hair follicles on the
sides and backs of our heads. Whereas scalp hair follicles on our sides overlay muscle, scalp
hair follicles at the top overlay the galea.

This is an important distinction. Why?

Because evidence suggests that in men and women with AGA, the muscles along our scalp
perimeter are chronically, involuntarily contracted. And since these muscles are
connected to the galea, this muscular contraction pulls the galea taut — and tense.

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This may have ramifications for pattern hair loss onset. Specifically, this chronic tension may
give us insights into (1) a source of chronic inflammation, and (2) the patterning and
progression of male and female pattern hair loss.

Here’s how…

A link between muscle tightness, galea tension, and hair loss patterning
Touch the skin on the sides of your scalp (i.e., where you’re not balding). Now touch the
skin where you are balding — like your temples or vertex. What do you notice?

For a lot of men and women with AGA, you’ll notice the skin at the top of your scalp feels
much tighter. And if you have a friend or partner who isn’t balding — go and touch their
scalp (with permission!). Note the difference between the top of their scalp and your own.
Their scalp likely feels much looser. In fact, their skin elasticity at the top of the scalp likely
feels more uniform to the skin elasticity on their scalp sides.

Now place your hand back on the top of your head. Smile wide and raise your eyebrows. Did
you feel your scalp tighten? If so, this is one example of how muscular contraction along our
scalp perimeter can influence scalp tension at the tops of our heads.

Despite smiling to force those muscles to contract, you may have had a few sections of your
scalp that didn’t change tensity — and that maybe already felt tighter (even before smiling
and raising your eyebrows).

Moreover, you might’ve noticed that after relaxing your smile and eyebrows, the top of your
scalp didn’t necessarily return to its “original” laxity. Rather, there might still be a few parts

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that feel tighter than before those muscles contracted. In other words, they’re still trying to
relax.

These subtle (but significant) observations might represent the chronic, involuntary
contraction of specific muscles along our scalp perimeter. The tenser these muscles, the
tighter our scalp tension. But it’s also likely that many of these muscles are so subtly
contracted that most of us aren’t aware of it.

Regardless of our awareness, the outcome is still the same: chronic (and involuntary)
increased tension across the tops of our scalps, which happens to precisely match the
patterning and progression of androgenic alopecia.

Scalp tension may match the pattern of our hair loss

In 2015, investigators modeled balding scalps and found that when our scalp perimeter
muscles contract — even lightly — they create a tensile pattern across our scalps that closely
matches the patterning and progression of AGA.

For men, the tension peaks at the temples and vertex (where men often start losing their
hair). For women, that tension is more evenly distributed across the scalp (matching their
diffuse hair thinning). For an example, just see the similarities between this male’s AGA
progression and the mapping of his scalp tension. The lighter segments represent less
tension... the darker segments represent more tension.

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At the center of the crown, we can see that the hairs still growing fall under a lighter
segment (less tension), but the bald skin is surrounded by a darker segment (more
tension). The same is true with the hairline. Bald temples; more tension. Existing hair; less
tension.

So, what does chronic tension have to do with chronic inflammation?

Well, studies show that if tissue tension remains persistent and unresolved, our bodies stop
perceiving the tension as simply tension... and start perceiving it as inflammation. The end-
result? An increase in DHT, TGF-β1, and, consequently, scarring.

The connection between chronic tension, inflammation, and DHT

In tissues with chronic unresolved tension, our bodies elicit an inflammatory response that
involves (1) DHT, (2) TGF-β1, and (3) scarring. Here are three examples:

1. Men with a tendon-contracting condition called Dupuytren’s contracture express

more inflammation, androgens, and fibrosis (i.e., scarring) in the affected tissues.

2. In Graves’ disease, eyelids retract due to the involuntary contraction of the Mueller
muscle. In biopsies, this muscle shows higher inflammation, androgen activity, and
fibrosis.

3. Prostate tissues — when stretched — induce inflammation and DHT. And when DHT is
expressed under “pressure” in the prostate, it activates TGF-β1. In fact, this is why
researchers believe that pressure may cause prostate enlargement (or benign prostate
hyperplasia) — a condition that early onset pattern hair loss actually helps to predict.

Now, let’s refer back to our flowchart. In balding scalps, the chart argues that chronic
inflammation causes DHT and TGF-β1 to increase. Eventually, DHT and TGF-β1 resolve this
inflammation by laying down scar tissue (i.e. fibrosis) and calcification. As a consequence,
this restricts blood, oxygen, and growth space for our hair follicles — thereby miniaturizing
them. This may partly drive the process of pattern hair loss.

One possible source of inflammation? Chronic tension. And the source of this tension?

The chronic contraction of our scalp perimeter muscles. This pulls the tops of our scalps
tight and creates the exact tension patterning we see in AGA.

Chronic tension may explain the patterning of AGA

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Not only might chronic tension explain the arrival of chronic inflammation in AGA, but it
also might explain AGA’s patterning and progression.

Where scalp tension is highest, inflammation is highest. For men, this tension is highest at
the temples and vertex (where hair loss begins). For women, this tension is spread diffusely
throughout the scalp; hence the “diffuse” thinning. And as our bodies resolve this
inflammation with fibrosis and calcification, we see — as a consequence of tissue
degeneration — the loss of hair in those locations.

Putting the scalp tension theory to the test

You may be thinking, “This sounds like conjecture. We’re using inductive reasoning to draw
similarities between tension-related disorders and pattern hair loss. But where’s the hard
evidence? Where’s the proof that (1) the muscles surrounding our scalps are actually
involuntarily chronically contracted, and (2) relaxing these muscles improves AGA?”

Well, the good news is that both of these points have already been demonstrated — several
times over. And surprisingly, this first happened by accident.

Dr. Freund and the Botox studies

In the 1990’s, a surgeon and university lecturer named Dr. Freund was pioneering a new
treatment for tension headaches. He’d noticed that his patients with tension headache also
had chronically contracted scalp perimeter muscles. Interestingly, Dr. Freund also suffered
from tension headaches — hence his interest in finding a treatment. Specifically, he
wondered if getting these muscles to relax might improve his headaches. So, he decided to
find out.

Dr. Freund ended up injecting botulinum toxin into the muscles surrounding his scalp.
Botulinum toxin is also known as Botox. It’s an injectable neuro-modifier. It preserves the
integrity of a tissue while preventing that tissue from neurally communicating with its
surroundings. In other words, it’s a targeted “muscle relaxer.” If we inject Botox into a
contracted muscle, the muscle relaxes and stays relaxed for 4-6 months... until the Botox is
fully metabolized.

Simultaneously, Dr. Freund was a caucasian male in his 40’s — and like most others of his
age, he was balding. A few weeks after the injections, he began noticing changes.

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Firstly, his tension headaches were gone... but he’d also noticed less hair fall on his pillow
each morning. And within a couple of months, Dr. Freund was certain that (1) his tension
headaches had vanished, and (2) his pattern hair loss had stopped.

After experiencing these results, Dr. Freund set up a clinical study to see if Botox injections
would help other AGA sufferers. Over 48 weeks, he gave 40 male AGA sufferers two rounds
of Botox injections to see if their hair would improve after nearly one year of having a
“relaxed” scalp.

In his study, he decided to use the same hair counting methodologies that the finasteride
studies used for FDA-approval. Those studies showed that finasteride had a response rate of
80% and, in a two-year period, lead to a 10% increase in hair count alongside significant
hair thickening

So, after 48 weeks (less than one year), how did Dr. Freund’s Botox study compare?

Botox results: a 75% response rate... and an 18% increase in hair count
Just by relaxing the scalp muscles with Botox, 75% of subjects saw their hair loss slow, stop,
or reverse. In his paper, he suggested that this response may be similar to finasteride.

More impressively, hair counts, on average, increased by 18%. I repeat, 18%. I was so
impressed with these results that I ended up interviewing Dr. Freund about his study —
which you can watch here. During our interview, he mentioned that some patients in his
practice saw increases of 40-50%. Those numbers are simply astounding.

Best of all, Dr. Freund’s results have been replicated. Since publishing his results, his study
has been validated by other research groups again... and again.... and again.

Obviously, these data on botox injections aren’t nearly as robust as finasteride. For instance,
these studies did not measure hair diameters, they did not compare against control groups,
and their sample sizes are relatively small. That’s not to say the results aren’t real; it just
means we need to keep this in mind and not make any big claims that botox will solve hair
loss for everyone. If you’re interested in more information, please watch my interview with
Dr. Freund or read the transcripts right here.

Tying it all together

If our scalp perimeter muscles are chronically involuntarily contracted, it’s likely that our
galea is chronically stretched — creating tension. This tension may transmit above and below

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its surroundings. Where do we see fibrosis? Above the galea. Where do we see calcification?
Below the galea.

As such, it might be possible that these conditions are simply the end-result of a tension-
driven inflammatory cascade. The consequence is tissue degradation (and pattern hair loss).

Another mechanism: a “pinching” of the scalp’s blood supply

Interestingly, as our scalp’s perimeter muscles contract, they may not only create tension
across the top of our scalps, but they might also constrict the blood vessel networks that run
between these muscles and up to our top-scalps to support AGA-prone hair follicles. In
turn, this may reduce blood and oxygen from reaching our top-scalps.

Interestingly, the same study that showed that balding scalps have 40% lower oxygen levels
also suggested that poorly oxygenated tissues may have a propensity to accumulate higher
levels of DHT, thereby accelerating the balding process. In fact, it’s this mechanism that Dr.
Freund speculated as to why Botox might’ve improved hair loss for his subjects.

This means that in addition to scalp tension, the contraction of our scalp’s perimeter
muscles may also reduce blood and oxygen to balding regions — and that this alone may
increase DHT, fibrosis, and even hair follicle miniaturization. Having covered this, we can
now complete our flowcharts showing the causes of AGA.

Final charts and visuals

These Botox studies are still preliminary, but they’re certainly interesting! Importantly, they
suggest that scalp tension might be a driver of AGA-related inflammation. They also offer an
alternative explanation to the patterning and progression of our hair loss — even across
genders. We can add this information to our flowchart.

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And this visual of the balding process is even more revealing. It shows that reduced blood
flow actually happens in three locations: our scalp perimeters, surrounding the hair follicles,
and deeper near the skull. And the suspected causes? Contracted scalp muscles, fibrosis, and
calcification. The end-result of this chronic, progressive phenomenon? Pattern baldness.

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Now, for one final question…

What causes our scalp perimeter muscles to contract?

If I were to guess, these muscular contractions (and our scalp tension) likely develop
concurrently as we age (from childhood through puberty and beyond). In fact, there are likely
three major contributors — and they all feed off one another.

1. Fascia remodeling. Fascia is the dense, fibrous material that connects, supports, and
holds in place our muscles, tendons, and tissues throughout our body. Fascia has no
nerve endings, so we can’t feel it. But interestingly, fascia is constantly remodeling. We
also store tension in fascia. In the long-run, chronic muscular contractions can influence
nearby fascia remodeling — and in doing so, increase fascia-stored tension — thereby
“locking” scalp tension in place (even if we relax those muscles).

2. Skull bone growth — along with skull suture settlement during and after puberty.
Contrary to popular belief, some of our skull bone sutures do not settle until later into

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 adulthood. This allows for our skulls to continuously remodel (and grow) throughout
much of our adult lives. Interestingly, bone growth is influenced by mechanical force —
meaning that if our scalp perimeter muscles are chronically contracted — it’s likely that
they not only remodel their surrounding fascia but also influence skull bone growth over
a series of years. This may (or may not) influence scalp tension. We don’t yet know.

3. Androgen production — particularly during the shift from adolescence to puberty and
early adulthood. Fascia remodeling, muscular contraction, and bone development are all
partly driven by male hormones. Interestingly, androgenic influence on skull shape (and
its relationship to hair thinning) is partly confirmed by a condition called polycystic
ovarian syndrome (PCOS). PCOS is a driver of female pattern hair loss, and it’s
characterized by (1) increased male hormones, and (2) insulin resistance. While PCOS
can affect women from 16-40, new research shows that its hormonal imbalance (i.e.,
higher male hormones) often starts much earlier than condition develops: often very early
into puberty (during critical phases of bone development). Fascinatingly, women with
PCOS have (1) hair loss patterns similar to male AGA and (2) larger skulls. This suggests
for women with PCOS, higher androgen levels during puberty may not only influence
skull size but also inform the patterning and progression of hair loss. More information
on PCOS be found here.

What about genetics?

If we take a step back, we realize that every single step of this flowchart is regulated by a
combination of genes and hormones. After all, men with lots of DHT (but no genes
associated with AGA) likely won’t go bald; men with these genes (but who’ve been castrated
— and thereby have almost no DHT) likely won’t go bald. So, we need both genes and male
hormones to kickstart the hair loss cascade.

In that same vein, our genetic blueprint and male hormones also influence our magnitude of
muscular development, bone growth, and fascia remodeling. They likely influence whether
we perceive chronic tension as chronic inflammation, how we respond to that inflammation
(i.e., DHT), and whether we develop fibrosis or hair loss in the process.

In short, the “It’s all in your genes” argument is right. But it’s the step-processes beyond
genetics that we’re still learning about.

If you’d like to learn more about this AGA model, you can review my peer-reviewed paper —
which takes a more scientific approach to explaining everything we just covered. Otherwise,
here are some common rebuttals to the hypothesis.

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Is scalp tension actually the cause of AGA?
There are three common rebuttals to the scalp tension-AGA hypothesis: (1) “hair
transplants prove our scalp environment does not influence whether we go bald”; (2) “low
blood flow is a consequence of hair follicle miniaturization, not a cause”; and (3) the reality
that “men transitioning to women can regrow a ton of hair — so AGA must be 100%
hormonal, and therefore scalp tension must have nothing to do with AGA.”

Explaining the counter-arguments to these rebuttal are beyond the scope of this chapter
(and this book). However, I have provided counter-arguments here, here, here, and here.
And if you have questions, you can always reach out in our forum (see the Chapter Recap
for a discussion thread link).

For what it’s worth, I don’t think that scalp tension can explain 100% of AGA cases. I also
don’t think that scalp tension can explain 100% of AGA’s pathophysiology for anyone where
it is present. Yes, the botox studies are encouraging. But even with these studies, the
response rates seem to hover around 80% (rather than 100%). To me, I interpret this as
meaning that scalp tension is likely an accelerator of AGA for the majority of men, but that
AGA can still happen in its absence. Otherwise, we’d expect 100% of people to respond to
the therapy.

The good news? We don’t have to know the exact causes of AGA to improve our hair. In
addition to DHT, we’ve identified two more factors that may limit our hair recovery: fibrosis
and calcification. And just as importantly, we may have identified one source contributing
to their development: the chronic, involuntary contraction of our scalp perimeter muscles.

By targeting all of these things, it’s possible we may see more robust hair recoveries.

Androgenic alopecia research is still filled with uncertainty

It bears repeating: no one is certain what causes AGA. While I believe this flowchart is one
perspective to explaining why we lose our hair, I can guarantee that evidence will emerge in
the coming years that will bolster and refute aspects of the hypothesis, and even force its
reevaluation by me.

I hope this happens, because it’ll demonstrate progress in an underserved field (i.e., hair
loss pathology). Not to mention, that’s how science works. We constantly hypothesize, test,
and reevaluate our own beliefs in light of new evidence — all to develop a better
understanding of the causes of any condition (and how to treat it).

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Is pattern hair loss reversible?
Yes! By now it should be clear that hair loss does not have to be our genetic destination;
while we may be fighting our own genetic predisposition, there are solutions in addition to
drugs that may enhance our hair regrowth.

Pattern hair loss is a chronic, progressive condition. But this is because the conditions that
coincide with AGA — fibrosis and calcification — are also chronic and progressive. If we
want to reverse pattern hair loss, we need to reverse calcification and fibrosis, and in doing
so, return our scalps to their pre-balding state.

But as with most things in life, it takes a bit of work. In order to gain back what we’ve lost,
our first step might be to try to reverse the two chronic, progressive conditions that
finasteride and minoxidil do not target: calcification and fibrosis. Simultaneously, we’ll
need to also target what may contribute to these conditions: scalp tension.

In doing so, we should allow for the return of blood, oxygen, and nutrient flow to dormant
miniaturized hair follicles, as well as the remodeling of our scalp skin (much like what we
discovered with those tuberculosis patients).

Th next chapter will explain what I consider the best approach to do this. The goal is for all
of us to see major hair regrowth by targeting those three factors.

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Chapter recap
The causes of inflammation in androgenic alopecia are still mysterious and poorly
understood. But there is a case to be made that might implicate scalp tension.

This scalp tension may be a consequence of our genetics, androgen levels during puberty
and throughout adulthood, our skull bone development, our fascia remodeling, and the
contraction of our scalp perimeter muscles.

Together, these factors may create an environment that pulls our galea aponeurotic
chronically tight. In some models, these tensile patterns appear to match the onset and
progression of androgenic alopecia. Moreover, this chronic tension may partly explain why
balding scalps experience inflammation, increased DHT, and transforming growth factor-
beta 1 — all of which may contribute to the onset of fibrosis and calcification.

Thus, if we want to reverse pattern hair loss, we may want to look for targets beyond just
DHT reduction: like fibrosis, calcification, and perhaps these scalp muscles. The next
chapter dives into possible strategies to doing this.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

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 C H A P T E R 7:
REVERSIN G PATTERN HAIR LOSS

Chapter summary:

• If we want to regrow hair, we may want to try and restore our scalps to a state before
hair loss began. Some targets of interest: DHT, fibrosis, and scalp tension.

• Interestingly, there are rare case studies of full hair recoveries in the literature –
suggesting that the health of our scalps can be dramatically improved even in later
stages of baldness. In fact, some of these full hair recoveries happened in the absence
of drugs (and by accident). One suspected mechanism? Our innate response to
wound-healing.

• Research shows that targeted and repeated micro-wounding may enhance blood flow,
attenuate or reverse fibrosis, and even stimulate major hair recovery in those with
AGA. And if we combine micro-wounding with methods to reduce chronic tension in
balding scalps, we may be able to achieve cosmetic degrees of hair recovery.

• There are many ways to do this, and some methods are entirely free: targeted soft
tissue manipulation (i.e., massaging). With the right massage technique, we may
influence gene expression, relax chronically contracted muscles, promote micro-
wounding, and change our hair loss outcomes for the better. We’ve even got some
peer-reviewed data to suggest this is possible.

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REVERSIN G PATTERN HAIR LOSS

Addressing calcification, fibrosis, and scalp tension

Now that we’ve revealed additional factors that might be driving AGA, we can try to reverse
them. Specifically, we may benefit from targeting to lower DHT and perhaps reverse both
fibrosis and calcification.

Unfortunately, drugs, supplements, and topicals alone are limited in reversing both
conditions. In fact, even the best drugs seem to only stop their progression.

The shortcomings of drugs, topicals, and supplements

The closest thing we have to anti-fibrotic medications are drugs used for Peyronie’s disease
— a condition where fibrotic material accumulates in the male genitalia.

Clinical studies show that a cocktail of drugs can help stop the accumulation of fibrosis in
Peyronie’s — and thereby stop the disease. At the same time, placebo groups in these
clinical trials tended to fair almost as well as the actual testers — suggesting that much of
the benefit may have just been due to the placebo effect (which is fascinating in itself).

Similarly, vitamin K2 has been shown to reverse drug-induced calcification. However, this is
different from pressure-, infection-, or inflammation-induced calcification. So while vitamin
K2 may help in some cases of calcification, it’s likely not very useful for AGA.

What about topicals? Well, some topicals contain anti-inflammatory / antioxidant

substances that can help reduce the expression of TGF-β1 — and potentially slow down the
progression of fibrosis. But when it comes to AGA, the source of inflammation is a bit
nebulous. Our model builds a case for scalp tension as one driver of inflammation. In this
model is true, a topical is sort of like a bandaid to an underlying problem. Moreover, the
fibrosis and calcification in AGA are deeper than skin-level. It’s unlikely that a topical applied
to our skin is going to penetrate deep enough to have a strong effect on these conditions.

And supplements? Well, there are a lot of people taking herbs and extracts to try to reduce
DHT and TGF-β1 to improve their hair. One of the more well-studied natural DHT-reducers
is called saw palmetto. Unfortunately, while saw palmetto may reduce DHT, it generally
doesn’t lower DHT enough (by itself) to significantly alter hair loss outcomes.

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Interestingly, while finasteride and minoxidil don’t tend to take someone from slick-bald to
a full head of hair, we’ve already seen full hair recoveries without the use of drugs, topicals,
and supplements. And fascinatingly, these recoveries have happened entirely by accident.

A full hair recovery: after an accident (and by accident)

In 1986, the British Medical Journal published a puzzling case study of a 78-year old bald man
who fell asleep in his rocking chair, fell forward, and slammed his head into a roaring coal
fire — severely burning his scalp. When he arrived to the hospital, he refused admission and
surgery... so the doctors sent him home.

In follow-up two weeks later, he mentioned to doctors that his bald patches were regrowing.
Four months after the accident, he came in for his appointment, and to the doctors’
surprise, had regrown his entire hairline... all unintentionally. See these photos (and please
don’t try this at home).

This degree of hair recovery is beyond anything we’ve seen with drugs like finasteride or
minoxidil. It’s an example of someone going from fully-bald to a full head of hair within four
months — all following the aftermath of a burn.

What could possibly explain these results?

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At the time, researchers didn’t know. So, they essentially filed the report into a drawer and
forgot about it. There had been reports of hair regrowth in injury sites dating back to the
1960’s, but again, people wrote these off because they didn’t happen consistently.

However, over the next 30 years, evidence began emerging to explain how this accident
might’ve made this regrowth possible. The mechanism? The activation of wound-healing
pathways. In other words, our bodies’ innate response to temporary stressors — like acute
inflammation. Here’s how this is possible:

A new mechanism for hair regrowth?

Acute inflammation: a weapon to reverse scarring
Our response to acute inflammation depends on injury severity. A paper cut and stab wound
are both acute injuries. A paper cut evokes a small inflammatory response; it probably won’t
scar. But a stab wound evokes a larger response; it probably will scar.

Sounds simple enough. Then came a revelation: in 2009, researchers realized if they created
small wounds on top of scarred skin, the inflammation generated from those wounds could
break down the underlying scar tissue... and improve its appearance.

This led to a realization: micro-wounding may help improve skin scars. It wasn’t long
before anti-aging clinics started applying these principles to patients.

Micro-wounding: a tool for reversing acne scars and wrinkles

Within a few years, dermatologists actually developed a tool to make these micro-wounds: a
microneedler.

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Microneedlers (or dermarollers) are hand-held rollers with hundreds of medical-grade
needles that — when rolled against the skin — puncture its top layers to evoke acute
inflammation. Yes, they hurt. And yes, they look like small medieval torture devices:

MICRONEEDLING DEVICE

Despite the pain, these devices are incredibly effective at resolving scar tissue. Just see the
before-after photos in this study — where repeated microneedling over three months almost
completely eliminated a woman’s acne scars.

To reiterate, since inflammation from microneedling is acute (temporary) and minor (the
needles are 0.5-2.0 mm) — its inflammation doesn’t lead to fibrosis (i.e., scarring). Rather,
it just evokes a small inflammatory response to help metabolize preexisting scars...

Which begs the question, can microneedlers help reverse fibrosis in AGA?

The short-answer: all evidence points to yes.

Microneedling for pattern hair loss: the evidence

After microneedling showed promise in regrowing hair on mice, researchers soon moved on
to testing it on AGA sufferers. Initially, researchers thought microneedling would just help
with topical absorption. So the first AGA study tested if microneedling + minoxidil could
improve hair counts better than minoxidil alone.

The results were outstanding. In twelve weeks, minoxidil plus weekly microneedling
increased hair counts over 400% more than just minoxidil. Just see these photos:

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Next, researchers set-up a small study to see if microneedling improved AGA for non-
responders to minoxidil and finasteride. After six months, 100% of non-responders to
finasteride and minoxidil who added microneedling reported hair improvements of +2 or +3
grades on a 7-point scale. Here are the photos:

This hair improvement is far better than the 10% we’d expect from finasteride. In other
words, microneedling significantly improves the efficacy of topical and oral AGA drugs.

But what about microneedling without other treatments? Is it effective by itself?

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Yes! In follow-ups, this study found that microneedling alone improved hair counts (even
better than minoxidil). In fact, microneedling alone improved hair counts by 15% in just six
months. And those results are now confirmed by other teams, as well.

This is exciting news. These findings show that a small degree of repeated wounding allows
us to leverage our own inflammatory response to break down preexisting scars. Best of all,
these studies demonstrate that micro-wounding is effective at improving AGA!

So... how does micro-wounding help our hair? There are likely several mechanisms.

#1: micro-wounding turns on proteins linked to the growth stage of the hair cycle
Remember: in acute injuries, it’s the set of substances our bodies send to an injury site.
Interestingly, a lot of the growth factors that microneedling stimulates are associated with
the anagen (or growth) stage of the hair cycle. These proteins may, in turn, signal for resting
hairs to turn back on – thereby increasing total hair counts.

#2: micro-wounding downregulates proteins linked to scarring

Micro-wounding may also reduce scar-promoting proteins like TGF-β1 and 2... and increase
the presence of scarless proteins like TGF-β3. In the process of repair, these proteins also
seemingly remodel some of our preexisting scar tissue.

#3: micro-wounding may promote new blood vessel formation

After micro-wounding, as our tissues repair, they produce new blood vessel networks to
help better vascularize an injured region. This is known as angiogenesis — or the formation
of new capillary networks within our skin tissues.

This is important.

In our flowchart, disorganized collagen fibers (i.e., fibrosis) affect the amount of blood and
oxygen reaching our hair follicles. Micro-wounding may combat this in two ways. Firstly, it
may reverse some of that fibrosis by decreasing scar-promoting proteins like TGF-β1 and
increasing scarless-promoting proteins like TGF-β3. And secondly, it may help create new
blood vessel networks to supply our hair follicles with more blood and oxygen in future hair
cycles.

By removing some fibrosis, we might free up hair follicle growth space. By reestablishing
blood flow and oxygen, we encourage hair thickening and regrowth. And it’s through these
mechanisms (among others) that micro-wounding likely helps improve our hair.

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For anyone interested, I’ve written a Microneedling Ultimate Guide. This gives you step-
by-step instructions on microneedling alongside the tools, techniques, and adjunct therapies
to increase your hair count far beyond what we previously thought possible.

You can access that microneedling guide here, or discuss it with our community here.

Microneedling alone is limited in regrowing hair

Unfortunately, microneedling alone doesn’t appear to dramatically reverse hair loss. This
means tha,t by itself, it isn’t a complete solution. Just like other treatments we want to
evaluate, let’s compare microneedling’s mechanisms to our AGA flowchart. What do we
notice?

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The pros: microneedling reduces TGF-β1, fibrosis, and improves blood and oxygen.

The cons: microneedling doesn’t address DHT and chronic inflammation.

This means microneedling, by itself, is not a complete AGA solution.

As such, it likely makes more sense to take a multi-targeted approach. For instance, to (1)
combine microneedling’s effects on wound-healing with (2) something that targets scalp
tension – at least if you’re interesting in tackling pattern hair loss naturally.

Can we combine micro-wounding with Botox?

Yes. That’s certainly one option. After all, Botox may hit “closer” to one source of chronic
inflammation — chronic scalp tension. This is because Botox injections force our scalp

11 9
perimeter muscles out of chronic contraction, and in doing so, may (1) reduce scalp tension,
and (2) improve blood flow to AGA-prone hair follicles.

So, we could combine microneedling and Botox to get the benefits of micro-wounding in
addition to the benefits of scalp tension relief. Hypothetically, this might improve hair loss
better than either method alone. However, this approach comes with one problem...

Botox is expensive
A round of Botox into our scalp muscles costs about $1,500. Botox lasts for 4-6 months, and
Dr. Freund’s study showed that we’d need at least two rounds (1 year) before seeing notable
hair loss improvements. That’s $3,000 just to test a procedure long enough to see results.

Anecdotally, we’ve heard that after 4 or 5 rounds of Botox, our muscles may adjust long-
term to not chronically contracting. Unfortunately, reaching that point is a $7,500+
investment. This just isn’t feasible for the majority of hair loss sufferers. And that means
that this particular strategy for tension relief + micro-wounding is not a viable option for
everyone.

But there is good news. There are other ways to achieve tension relief + micro-wounding. In
fact, there’s even an option that costs nothing. And while it might take a bit of work, these
options have demonstrated significant hair regrowth in certain individuals.

What is this approach? Soft tissue manipulation. In other words, targeted mechanical
stimulation to: (1) reduce scalp tension; (2) promote micro-wounding; and (3) increase the
expression of genes associated with the growth phase of our hair cycle.

Amazingly, this may be possible with hand-based massages. With the correct pressure,
technique, and effort — targeted massages may help remodel our scalp skin, relax
contracted muscles, and regrow significant amounts of hair. Here’s how:

Soft tissue manipulation & hair regrowth: the evidence

It may sound like a jump to suggest that soft tissue manipulation (i.e., massaging) can
achieve the same hair-regrowing effects as microneedling plus Botox. But fascinatingly,
massage therapy shares a lot of overlap with both therapies. Just look at the evidence.

Firstly, massaging may stimulate the same growth factors and collagen remodeling effects as
micro-wounding. Secondly, massage therapy helps halt fibrosis and encourage angiogenesis
(i.e., new blood vessel formation) following injuries. Thirdly, massaging enhances nutrient

12 0
delivery and helps maintain tissue integrity after stress exposure. And fourthly, in burns,
massaging decreases scar thickness and improves skin elasticity.

Essentially, soft tissue manipulation (i.e., targeted pinches / presses) hits many of the
mechanisms as micro-wounding (and perhaps more). And what about tension relief? Can
massaging take our scalp perimeter muscles out of chronic contraction — like Botox?

Evidence suggests yes. Pressure-based massages are commonly used for muscle relaxation.
Interestingly, these same massages can improve tension headaches — likely by taking the
scalp’s perimeter muscles out of chronic contraction. This implies that the right type of
massaging can activate the same mechanisms as microneedling + Botox combined.

However...

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Hitting the same mechanisms as micro-wounding + Botox is a far cry from achieving the
same hair regrowth. After all, saw palmetto and finasteride both reduce DHT. Saw palmetto
doesn’t regrow hair; finasteride does. The difference? Saw palmetto doesn’t reduce as much
DHT as finasteride. They have different magnitudes of effect. Which begs the question...

Can massage therapy actually improve our hair? Are there studies demonstrating its efficacy
on hair regrowth?

The answer might be yes. Full disclosure: I’ve published one of these studies.

Massage therapy for hair regrowth: human studies

Firstly, there’s a case study of a 70-year man who regrew most of his hairline (in 20 weeks)
after implementing twice-daily massages. Then there’s a 2014 study showing that in non-
balding men, 4 minutes of massaging daily increased hair thickness by 10% over six months.

In fact, that same study also measured the effect of skin stretching on dermal papilla cells
(i.e., the cell clusters that act as the “powerhouse” of our hair follicles). It showed that after
72 hours of stretching — thousands of genes were turned on and off. The significance? The
“activated” genes were associated with our hair follicle’s growth phase and the “deactivated”
genes were associated with our hair follicle’s shedding phase.

But what about evidence beyond case studies and non-balding men? Specifically, what about
full-scale studies on men and women with AGA? After all, while massaging may stimulate
angiogenesis, increase growth factors, reduce fibrosis, take our scalp perimeter muscles out
of chronic contraction, and perhaps improve scalp tension — none of that matters if they
don’t improve AGA for most people.

Fortunately, we have data (albeit very limited) that may help answer this question. It’s peer-
reviewed data from our own community that we published in a dermatology journal.

Standardized scalp massages

A history of our community + doing our own study
For the last several years, I’ve been an advocate of scalp massages for androgenic alopecia. I
saw significant improvements using scalp massages for my own hair recovery. And since
2014, I’ve recommended massaging to anyone wanting to improve their hair who isn’t
interested in drugs, surgeries, topicals, or supplements.

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I initially modeled my massage techniques (and the book’s first edition)over twice-daily,
twenty-minute massages and a commitment to trying the massages for at least ten months.
At the time, that was the regimen I’d used to see significant improvements— and I figured
others might benefit from the massage therapy as well. So in 2014, I wrote the first edition
of this book, created a 5-minute demonstration video, and shared it with anyone willing to
participate.

Then I spent two years working with readers, interviewing responders / non-responders,
and revising the massage techniques based on the growing body of evidence on soft tissue
manipulation and hair recovery. Throughout this time, a lot of readers reported major hair
recovery. So in 2016, I incorporated these learnings into the book’s second edition. I re-
released everything — standardizing the massage techniques based on what I’d learned from
our best-of-the-best success stories.

These revised massage techniques were relatively straightforward: twice-daily, twenty-

minute massages spaced twelve hours apart. Each massage session rotated around a specific
scalp region: our front, vertex, or sides/back. And every session consisted of a scalp
“warmup” and then scalp pinches, presses, and stretches. Again, this was all designed based
on the first book’s best responders — alongside the literature on micro-wounding, scalp
skin stretching, and hair.

Overall, readers emailed me to report better hair changes from the new massage techniques.
This was encouraging, but also biased. Email exchanges aren’t a fair reporting sample...
because they don’t provide hard data or objectivity. In fact, a reader is more likely to email
me if they’re either (1) not seeing regrowth, or (2) seeing great hair recovery. What about
everyone else in between?

What about those who’d been committing to the standardized scalp massages but hadn’t yet
reflected on their progress? What about people trying varying massage timings — like 2x10
minutes daily, 1x60 minutes daily, or 40 minutes every couple days? Were their results any
different from my own — or other readers?

The truth: I didn’t know. All I had were anecdotes from email exchanges. I needed data. I
needed objectivity. I needed to know response rates, recovery rates, and everything in
between. More importantly, I needed to know...

Do standardized scalp massages improve androgenic alopecia?

And one way to answer this question? Design a study using the people trying these
massages for hair regrowth: readers of this book. So, that’s exactly what I did.

12 3
Designing our study: do standardized scalp massages improves AGA?
This was quite an involved process — especially because I wanted to do everything as fairly
and as objectively as possible. This meant having safeguards in place to preserve the
integrity of any data we’d collect. For instance, since I’m the owner of this site, it’s a conflict
of interest for me to do any data analysis. I might be biased in my own interpretations of the
data and its insights (and not even know it).

As such, I did everything I could to legitimize this process. I hired two statisticians,
designed a questionnaire with their help, got approval from an Institutional Review Board,
and when the time came, issued a survey to readers of the second book. The goal: to assess
peoples’ adherence to our standardized massages — along with their ages, gender, hair loss
severity, hair loss regions, diets, topical-, supplement-, and FDA-approved drug-use, and
their perceptions of hair change throughout massage adherence.

The idea was to isolate the massages from any factor that might influence results — like
someone’s age, hair loss gradient, region of thinning, FDA-approved drugs, and even their
use of things like supplements, topicals, and microneedling. If we didn’t control for these
things, it wouldn’t be a fair analysis.

Within a few weeks of launching the questionnaire, we had over 350 responses — and
enough statistical power to start doing valuable analyses. So we closed the survey, and the
statisticians then spent several weeks digging through the data.

Over the next couple of months, one thing became clear: our findings were encouraging. A
large number of people were seeing benefit from our targeted massages, and in addition to
taking the survey, some participants had even sent in photos demonstrating their hair
changes throughout massage adherence (more on this later).

Our findings: scalp massages improve perceptions of hair change

Our most significant finding was that our standardized scalp massages improved
perceptions of hair change. This was true regardless of age, gender, or hair loss severity.

In fact, the data showed that after 40 hours of massaging, most people started reporting
hair regrowth. It didn’t matter if they got there doing 10 minutes per day or 40 minutes per
day. It just mattered that they had accumulated the hours. And even better... the longer they
massaged, the better their results.

12 4
Massaging response rate: how does it compare to minoxidil or finasteride?
To be absolutely clear: we can’t compare massage response rates to any other therapy,
especially FDA-approved drugs. Minoxidil and finasteride have been studies in clinical
settings on thousands of people. Those studies include placebo groups. They also include
objective endpoint measurements (like hair counts, hair thickness, and ratios of growing
versus resting hairs). Conversely, our massage study was a survey where participants self
reported results. That means the data is of much lower quality, and so it would be
disingenuous to make direct comparisons between massaging and these better-researched
therapies.

With that prefaced: minoxidil’s response rate is 30-40%, and finasteride’s response rate is
80%. These numbers are from clinical data and self-assessment surveys. It measures the
percent of people who saw a slow, stop, or partial reversal of their hair loss. So, how does
massaging stack up?

Well, if we define response rate as a reported stop in hair loss or any degree hair regrowth,
massage response rates for those reaching 8 months of effort were 75% and beyond.

Was massage-related regrowth influenced by other AGA treatments?

Encouragingly, no. Our data suggested that the biggest predictor of success from massaging
wasn’t the use of supplements, topicals, or FDA-approved drugs alongside massaging.
Rather, it was simply the time commitment to massaging and adherence to the right
massage techniques (more on this later).

This suggests that the massages work independently of other treatments — and that
improved hair changes happed outside the use of other therapies.

What about regrowth rates (i.e., hair count and hair diameter changes)?
Unfortunately, we couldn’t assess hair count changes. This would’ve required each
participant to go to a dermatologist before and after trying the massages for a hair count
analysis. This would’ve risen the costs of our study to several hundred thousand dollars.

Having said that, the data showed that, on average, the longer someone massaged, the
better their reported hair changes. And if we look at some photos submitted by survey
participants and readers... it seems like the degree of hair regrowth can be quite a lot.

To give you an idea of the range of possibilities, you can see many reader-submitted photos
from over the years. Specifically, if you’d like to better understand the journey of each reader,
feel free to access our case study vault. Here I’ve detailed my time working with 40+

12 5
readers — what worked, what didn’t, the trial-and-error process, what we learned, and their
hair growth along the way.

The long-story short: there are a lot of photos demonstrating success... some of which are of
high enough quality where we can see clusters of new hair emerging from the skin.

Publishing the data in a peer-reviewed scholarly journal

As encouraging as these photos are, they’re anecdotes. In other words, they just show that a
therapy allegedly worked for one person. Nothing more, nothing less.

What matters to me is not the number of people who send in photos. It’s the legitimacy of a
therapy and whether that therapy is supported by data strong enough to withstand the
process of peer-review — the gold-standard for any scientific work.

As such, I wanted to submit our data (and findings) to a well-ranked scholarly journal. So
we spent several months writing our findings into a manuscript. Then we submitted our
paper to a top-20 dermatology journal — Dermatology and Therapy — and then began the
process of peer-review (i.e., where experts in a particular field read your research, examine
your data, and tear into your paper).

In January 2019, we survived peer-review and were accepted for publication. As of today, our
study is available to anyone and everyone. You can read our findings, download the data, and
uncover its insights — all for free. This paper is my thanks back to everyone who committed
to these massages. I’m forever grateful for your time and participation.

Again, it bears repeating that these data are not meant to dissuade you from trying FDA-
approved drugs, or imply that these massages somehow are as effective as using finasteride
and/or minoxidil. But for those looking for a drug-free approach, they may be one option ––
one that has worked for many members of our community.

Beyond the study: what we learned and couldn’t publish

When performing any study, you’re up against limitations. Sometimes it’s paper length.
Sometimes it’s insights from qualitative vs. quantitative data. Sometimes it’s just whatever
is or isn’t considered appropriate for the journal.

Unfortunately, some of the biggest learnings from our study weren’t appropriate for the
paper or journal. We had to stick to what we could quantify.

12 6
That meant I couldn’t share what I considered our most valuable insights: my learnings
from qualitative video interviews with the book’s second edition readers — specifically,
those who’d committed 8 months of effort and hadn’t yet seen results.

For instance, while massage response rates were 75%+ for anyone who’d reached at least 8
months of effort, there were still non-responders. So I reached out to as many of these
people as I could, then had a Skype call with them and asked them to describe their massage
technique.

My findings from these dozens of calls? In 90% of cases, there was a single technique
difference between responders and non-responders. But because our interviews were
“qualitative” rather than quantitative, they weren’t appropriate to include in our paper.

In fact, the same barrier existed for a number of important questions we wanted to answer,
like...

1. Can we predict a responder versus a non-responder?

2. Does diet have any relationship to massage success?

3. Since analyzing the data, are there new massage techniques and best practices?

The answer to all of these questions is yes. And the good news is that I’ve incorporated the
learnings I couldn’t share in the paper throughout the remaining chapters of this book. Rest
assured, you’re getting the most valuable information I have. This is all in an effort to
maximize everyone’s chances — and degree — of hair regrowth.

How do we perform the massages?

This is all covered in our Standardized Scalp Massaging Ultimate Guide.

Inside, we reveal a step-by-step massage guide that goes beyond this book (and our study) —
so that we can hopefully take our results even further. This new guide incorporates
everything I’ve learned (and haven’t yet shared) from our study. Specifically, the optimum
amount of time daily to massage, the exercises that appear to be working best for most
people, and the technique differences that can predict (with 90% accuracy) a responder
versus a non-responder.

I’ve also included a demonstration video detailing each and every massage technique (from
pressure suggestions to pinching strength). Each recommendation is backed by science and
reader insights — all designed to encourage the regrowth of hair.

12 7
Again, that massage guide can be accessed right here. And if you have any questions about
it, please ask them in our discussion thread here.

For now, we return our focus to the science of hair loss — specifically, the insights we’ve
gleaned from massage best responders that go beyond just their massage techniques. That’s
coming up.

12 8
Chapter recap
Fibrosis and calcification are considered two of the most difficult-to-reverse conditions in
medicine. But while drugs, supplements, and topicals are generally limited in their
effectiveness, we have seen reversals accidentally — and perhaps through our own innate
wounding responses. Amazingly, leveraging these same mechanisms has also demonstrated
full hair recoveries in the medical literature.

This is, in my opinion, why micro-wounding (i.e., microneedling) shows promise for hair
regrowth — particularly as an add-on therapy, and perhaps as a standalone intervention.
Having said that, microneedling also has its limitations. It might stimulate angiogenesis,
increase growth factors, reverse some fibrosis, and regrow a little hair. But since it likely
doesn’t address more aspects of AGA’s pathophysiology, it’s likely an incomplete solution.

Thus, a more robust AGA therapy should not only activate our wound-healing responses,
but also target to lower DHT and/or reverse scalp tension. There are a lot of ways we can do
this. For instance, microneedling + Botox can do this effect. However, Botox comes at a
significant expense.

Fortunately, targeted soft tissue manipulation (i.e., standardized scalp massages) might
achieve the benefits of micro-wounding as well as the muscle-relaxing effects of Botox... for
free.

Yes, it takes work. Yes, it takes persistence. But the results achieved by past readers speak
for themselves. We’ve even published data on these methods in a peer-reviewed journal.

In my opinion, these massages are a good option for those completely disinterested in
taking drugs to treat AGA. That said, they likely do work synergistically with other
treatments — meaning you can combine them with other AGA therapies and perhaps see
benefits beyond either therapy by itself. So, if you’re taking any FDA-approved drugs, give
these methods a combined approach. With enough time, you might see great benefit.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

12 9
Otherwise, it’s time to move onto a deeper analysis of our data: what makes a best
responder? As we’ll soon realize, hair recovery is not always about activating the
mechanisms mentioned in this chapter. For many of us, optimizing our chances for hair
recovery is going to require additional interventions. Our data will soon reveal why.

13 0
 CHAPTER 8:
BECOMING A BEST RESPONDER:
HAIR LOSS T YPE

Chapter summary:

• Our study’s findings suggest that hair regrowth from massaging does not depend on
factors like our age, gender, hair loss severity, or the use of microneedling,
supplements, topicals, or FDA-approved drugs.

• However, this isn’t the entire story. Why? Because looking at our best responders, we
see qualitative trends in the data that might help us elucidate greater results.

• In this chapter, we’ll reveal those trends (with the help of our case studies) to show
that getting great results sometimes might require a more robust approach.

• In reading, we may come to some realizations about our own health — and
specifically, where the line between hair follicle miniaturization and hair shedding
disorders begins to blur… and why hair regrowth sometimes involves a lot of factors.

• In doing so, we’ll continue to build our roadmap to hair recovery and begin to take
additional actions that will set us apart and maximize our hair gains. The hope is that
in taking these recommendations, more of us can become best responders to any
therapy.

131
BECOMING A BEST RESPONDER: HAIR LOSS T YPE

Maximizing your chances of hair recovery for any therapy

In the last chapter, we revealed findings from our peer-reviewed study on standardized scalp
massages. Encouragingly, our data showed that perceived hair regrowth from massaging
doesn’t depend on factors like our age, gender, hair loss severity, or use of microneedling,
supplements, topicals, or FDA-approved drugs. The implication? For those of us with
pattern hair loss, if we massage for long enough, maybe we can achieve good results.

But what if we don’t just want good results? What if we want great results?

Specifically, what if we want the hair recovery of the best responders from our community?
Readers like Sam, who wanted to stop his hair loss, but over the course of a year,
experienced such drastic hair changes that he was able to completely change his hair style...

SU C C E SS STORY: + 0 M ONTH S TO + 1 1 MONT HS

How do we maximize our chances for that level of regrowth?

That’s what this chapter is for. We’re going to dive deeper into our study’s data and reveal
how to predict a “great” responder to the massages. Then we’ll apply these findings to our
case studies and their results. In doing so, we’ll attempt to uncover what we can do beyond
massaging to maximize (and fast-track) our chances for success.

Note: these learnings likely apply to any hair loss intervention... not just massaging. So,
regardless of which treatment you pursue, I believe this information is still relevant to you.

13 2
How to predict a best responder to massaging
Our data showed that massaging works as a standalone therapy. In other words, our age,
gender, AGA severity, or the use of topicals, supplements, microneedling, minoxidil, or
finasteride does not influence our results. Massaging benefits men just as much as
women. It works regardless of our pattern hair loss severity. And its effectiveness is
independent of other therapies.

Having said that...

Our data also showed there are two factors that influence our degree of hair recovery from
massaging. And one of these factors involves the pattern in which we lose hair.

Factor #1: diffuse thinners report less benefit from massaging

In our study, participants described their hair loss in two ways: (1) by listing their AGA
severity (i.e., Norwood-Hamilton scale), and (2) telling us where they were losing hair (i.e,
their vertex, temples, and/or diffusely (general thinning across the top of the scalp)).

The data showed that AGA severity did not impact hair regrowth from the massages. In other
words, you could be a Norwood 2 or a Norwood 6 and still see benefits from massaging.

But when we sorted results by hair loss region, we found that diffuse thinners reported
slightly less benefits from massaging versus those with temple and/or vertex thinning. Diffuse
thinners still benefited from massaging... just less so than those without diffuse thinning.

The question is, why? Diffuse thinning is a part of AGA. Massaging targets the causes of
AGA. So why would the pattern of our hair loss — temple, vertex, or diffuse thinning —
matter?

Some diffuse thinners may think they have AGA... but actually don’t
For men approaching Norwood 3 and beyond, temple recession and vertex thinning
eventually extends into one another. This creates diffuse thinning across the scalp. Thus, in
later stages of male AGA, diffuse thinning is normal and expected.

However, that’s not true for all AGA cases.

For instance, men with early-stage AGA (i.e., Norwood 1 or 2) usually won’t express
significant diffuse thinning. Rather, they'll just have temple or vertex recession (like the
Norwood scale suggests). And while it’s certainly possible to be a male, have early-stage

13 3
AGA, and have diffuse thinning — it’s also likely in these cases that you could have a hair
shedding disorder.

The causes of diffuse thinning extend far beyond androgenic alopecia

Hair shedding disorders — like telogen effluvium (TE) and chronic telogen effluvium (CTE)
— are common causes of hair loss among women and the second-most common cause of
hair loss among men. They’re also frequently misdiagnosed as AGA.

The triggers are widespread, but shedding disorders are generally linked to significant stress
and long-standing conditions like hypothyroidism, hyperparathyroidism, small intestinal
bacterial overgrowth, nutrient deficiencies, nutrient surpluses, and trace element / heavy
metal toxicities.

These conditions are likely more common than we think. For instance, over 5% of American
families drink from heavy metal-laden water systems. Hypothyroidism affects up to 10% of
first-world adults. Small intestinal bacterial overgrowth might impact up to 20% of
seemingly “healthy” individuals. And nearly 50%+ of U.S. adults don’t consume enough
vitamin A, D, E, magnesium, or calcium to meet the minimum daily requirements of basic
cellular functionality.

In my opinion, most of us are at risk of having at least one of these conditions. And for those
of us with diffuse thinning? I believe that risk might be higher.

How do these underlying conditions cause diffuse hair loss?

The mechanisms by which these conditions result in diffuse thinning are out-of-scope for
this book. That’s not a cop-out for an explanation. It’s just that each condition is linked to
hair loss for different reasons, and I don’t want to detract from the pacing of this chapter.

However, I’ve written ultimate guides for these chronic conditions — their causes,
connections to hair loss, and treatment approaches. You can access these right here. When
filling out your regrowth roadmap, if you think you may have a hair shedding disorder, those
guides will help you identify (or rule out) each condition. So keep them handy.

Otherwise, since we’ve covered how common these conditions are — it’s also worth
showing a few examples of how condition-related diffuse hair loss can compound with
pattern hair loss such that most doctors simply miss the diagnosis altogether or just mistake
it as AGA.

13 4
• Here’s a photo of diffuse thinning masking as AGA but driven by hyperparathyroidism (at
least according to the surgical group).

• Here’s a photo of hypothyroid-induced thinning that looks similar to female AGA.

• Here are photos of diffuse hair thinning due to nutrient deficiencies.

• Here’s a reader case study of a male with vertex thinning like that of AGA... until a health
history exam revealed the following: (1) no one else in his family has AGA and (2) his
thinning began seven years earlier, shortly after he started supplementing with a natural
mineral product (which he later discovered contained high levels of mercury, arsenic, and
aluminum). In fact, this reader believes his hair loss is linked to heavy metal poisoning.

Long-story short: these conditions are sometimes worth investigating, and they may
manifest in the extremes as diffuse thinning. Without a proper health evaluation, we’re at
risk of mistaking them for AGA. We even wrote about this in our study’s discussion section
— which you can read here.

Now, let’s reflect back to our data…

Our study was a self-assessment questionnaire. Participants evaluated their own hair loss as
AGA. But that doesn’t mean they accurately diagnosed themselves. And the likelihood of a
misdiagnosis skyrockets for people with diffuse hair loss.

This is likely why diffuse thinners reported slightly less benefit from the massages. They
were were applying the wrong treatment to the wrong causes of hair thinning.

Who is at the highest risk of misdiagnosing their diffuse hair loss?

There may be two groups who are at risk of confusing non-AGA-related thinning with AGA:

1. Women (since their hair loss is often diffusely patterned); and

2. Men with early-stage AGA (i.e., Norwood 1 or 2) alongside diffuse thinning.

In fact, this is supported by our data. Diffuse hair loss sufferers in both of these categories
saw less improvement from massaging than those with standard presentations of AGA.

We believe this is because the massages are designed to target pathophysiological aspects
related to AGA. They’re not supposed to target the causes of hair shedding disorders. As
such, trying to treat a hair shedding disorder with massaging is like trying to treat type I
diabetes with treatments for type II diabetes. It just doesn’t work.

13 5
To reiterate, if you have diffuse thinning from AGA, the massages should help. But if you
have diffuse thinning from stress, trauma, medication use, or an underlying chronic
condition? The massages won’t target the causes of your thinning. Therefore, they won’t
work as well.

That’s why we need to develop a regrowth regimen that also addresses the underlying
disorder. More information on this can be found in your interactive survey.

If you think these findings don’t apply to you, think again.

In our study, 93% of women with AGA and 44% of males with early-stage AGA also
reported diffuse thinning. That’s a huge percentage of people in a higher-risk category for a
misdiagnosis, which may suggest that there are many people not treating their hair loss as
robustly as necessary.

If you’d like a real-world example, look no further than Ben M. (a past reader).

Example #1: Ben M.

Ben M. is a male in his early twenties. He first noticed hair loss at his temples and vertex in
the typical form of AGA. Over a series of months, his hair loss became more diffuse. So Ben
eventually found his way to this site, picked up the book, and started trying 2x20 minute
daily massages. Here are his starting photos (long and short hair). Note that he’s in a high-
risk category for a misdiagnosis: male early-stage AGA plus diffuse thinning.

+0 M ON T H S

Over the course of a year, Ben M. reported that the massages seemed to stop the progression
of his AGA. But unfortunately, after 13 months, he hadn’t seen any regrowth. He sent in
photos to show it. Even with longer hair, he still felt he had poor hair density and expressed
concern that the massages might not be working for him.

13 6
 +13 M ON T H S

Accordingly, we started troubleshooting to figure out if anything else was going on.

Ben soon discovered his serum iron levels were low: just 29mcg/dl (normal is 60-170 mcg/
dl). Low serum iron can be the result of a variety of things: low iron consumption, low iron
absorption, low folate levels, a blood infection, a small intestinal bacterial overgrowth,
hypothyroidism, medication interferences… the list goes on. As such, it’s often
irresponsible to start supplementing with iron before doing (1) a deeper health evaluation,
and (2) a full iron panel.

But looking at Ben’s health history, there was one obvious potential cause: his diet. Ben was
a long-term vegetarian. As such, his diet was naturally lower in folate, heme iron, vitamin D,
and several trace elements. So Ben made adjustments (within his comfortability) to eat eggs
and foods higher in nutrients he might be under-consuming. He got a new job to lower his
stress levels and started getting more daily sunlight exposure. I recommended Ben do a full
iron panel (especially if things didn’t improve). Then we lost touch.

Six months later, Ben and I reconnected. He sent in new photos — all to show his progress
from 19 months of massaging + 6 months of the recommended dietary changes.

The results speak for themselves.

+19 M ON T H S

137
Ben’s vertex filled in, his hairline sharpened considerably, and his overall hair density
significantly improved. These improvements occurred between months 13 through 19...
when Ben started treating not only his AGA but also the nutrient deficiencies that might’ve
been contributing his overall diffuse thinning. Read his full case study here.

Example #2: me
In 2006, I started showing signs of vertex thinning and diffuse hair loss. In 2007, a leading
hair transplantation surgeon diagnosed me with male pattern hair loss. Subsequently, I
used minoxidil for seven years. It slowed down my rate of thinning, but beyond that, my
hair kept getting worse. I tried laser therapy along with dozens of different topicals,
supplements, and shampoos — all of which didn’t seem to improve things.

I started seeing hair recovery in 2013 — after I dropped minoxidil, started massaging, and
simultaneously adopted a moderate carbohydrate / nutrient-dense diet avoidant of dairy,
gluten, and other food allergens to which I was likely sensitive.

2011 2016

Fast-forward to 2017: I had recently switched office jobs and my health savings account
from a previous employer was about to expire. I couldn’t put the money toward groceries or
a gym membership, but I could put it toward lab testing. So that’s what I did. I figured I’d
write a few articles detailing any discoveries about my health. I didn’t expect any remarkable
findings. After all, I’d spent the last decade dialing in my diet and lifestyle.

My lab tests
I wanted to be as comprehensive as possible — measuring anything from my thyroid
functionality to the bacterial colonies in my small and large intestine. I also wanted to better
understand my hormones, metabolism, and if I had any nutrient deficiencies. So I did a
thyroid panel, an organic acid metabolite analysis, a urine test for hormone metabolites, a
breath test to measure bacteria in my small intestine, a stool analysis to measure the health

13 8
of my large intestine, and a few other blood draws to determine my heavy metal load and
reactions to food allergens. I also hired a doctor / functional medicine practitioner to help
me interpret the findings.

My results
When I went in to review my findings with the doctor, I didn’t expect any surprises. But for
as healthy as I thought I was — the results shocked me.

My doctor immediately flagged readings from my thyroid and blood panels. I showed high
levels of two biomarkers: reverse T3 and homocysteine. When these markers are elevated,
they imply the presence of hypothyroidism. Yes, the same hypothyroidism that can manifest
as diffuse thinning.

C OM P L ET E B L OOD P A N EL

What is hypothyroidism?
Our endocrine system (and specifically, our thyroid) is the body’s center for hormone
regulation. Our thyroid influences anything from our testosterone and estrogen levels to our
mood. As such, if we have an under-active thyroid (i.e., hypothyroidism), we usually have
lower energy, depression, irritability, sluggishness, and imbalanced hormones.

In the U.S., an estimated 12% of Americans will develop a thyroid disorder. 60% of us won’t
even know we have one. Since thyroid receptors are found all over the body, an under-active
thyroid (if left untreated) will eventually manifest physical symptoms and the tell-tale
symptoms of energy deficiencies: infertility, poor skin quality, eyebrow hair thinning, and
diffuse hair loss across our scalps.

13 9
Given the list of symptoms, I didn’t believe my doctor’s diagnosis. Yes, I’d had one past
symptom of hypothyroidism: diffuse hair loss. But at my 2007 appointment, my
dermatologist identified this as androgenic alopecia. Aside from that, I had no other
symptoms. I had great energy levels, warm hands and feet, no sluggishness, and within-
range levels of testosterone and estrogen (according to my urine metabolites):

DUTC H H ORMON E AN AL YSI S

Moreover, in all of my lab work since 2007, my previous doctor always said my thyroid
function looked normal. Needless to say, I was skeptical. But by the end of my appointment,
my opinion changed.

Hypothyroidism: missing measurements, hidden symptoms

Standard thyroid tests and blood panels don’t include the markers used in my diagnosis:
reverse T3 and homocysteine. My new doctor notified me of this, and when I looked back at
my old tests, I realized she was right. In the last ten years, I’d never had my reverse T3 or
homocysteine tested. Rather, the thyroid tests my general practitioner had ordered only ever
included a few variables: thyroid-stimulating hormone (TSH), free thyroxine (free T4), and
total or free triiodothyronine (total or free T3). And despite 20+ years of research
demonstrating the benefits of using reverse T3 and homocysteine to diagnose thyroid
disease, my previous doctors had never bothered ordering either test.

This half-committed approach to thyroid testing is sort of like a teacher grading 50% of a
student’s test and then giving them an “A” — for ten straight years. The grade looks great!
Unfortunately, it doesn’t represent that student’s understanding of the material. Likewise,
partial measurements of my thyroid may have not only misrepresented my actual thyroid’s
functionality... but perhaps done a disservice to my health.

This became more apparent as my practitioner connected dots between my other minor
concerns and hypothyroidism. In fact, she even identified a potential trigger of

14 0
hypothyroidism using the results of my other lab tests: an unfelt, undiagnosed gluten
intolerance.

A severe gluten intolerance (that I did not know about)

Gluten is a food protein found in rye, barley, and wheat. In the U.S., most of our gluten
consumption comes from pastas and breads. Americans consume a lot of gluten.
Unfortunately, 1% of us have a genetic sensitivity to gluten (called Celiac)... and up to 35%
of us have a non-genetic gluten sensitivity — where our bodies react to the gluten protein by
evoking systemic inflammation... and an autoimmune attack on our thyroid.

The exact mechanisms behind how gluten does this are covered in later chapters. For now,
here’s a (very) quick overview: when we ingest gluten-containing grains, the fiber in the
grain rakes against our intestinal walls and creates micro-tears. This is actually good: it
allows vitamins and nutrients from our food to pass through our intestines and into our
bloodstream — where they are distributed to tissues in-need. Unfortunately, if these micro-
tears become too large, they allow for “larger” molecules to enter the blood that should not
be there. Gluten is one of these molecules. If it bypasses our intestinal walls and enters our
bloodstream, it’s treated by our bodies as a “foreign invader” — and we evoke an immune
response to “attack” it. Unfortunately, a component of gluten looks nearly-identical to our
thyroid. So when our bodies “attack” gluten, they also attack our thyroid. This leads to an
autoimmune thyroid disorder called hashimotos thyroiditis. In fact, this accounts for 90%
of hypothyroid cases.

For what it’s worth, I figured I did not have a gluten sensitivity or hashimotos. Why? Firstly,
my 23andMe test showed I didn’t have Celiac disease. Secondly, in the last decade, I’d tried
dozens of diets — many of them gluten-free. I never felt any different with or without
gluten. And thirdly, to my knowledge, gluten has never given me any digestive distress. I’ve
never felt sick, tired, or irritable after eating it.

Yet, when my lab work arrived, I discovered I was severely gluten intolerant. In fact, my
doctor said that of her non-Celiac patients, my results were of the worst she’d ever seen.

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 G L UT EN R EA C T I V I T Y A N A L Y S I S

These results might not look terrible, but most patients with a severe gluten allergy typically
have just one elevated blood marker. I had four (two of which were out-of-range).

And interestingly, that wasn’t the only evidence of my gluten sensitivity.

Gut-related inflammation: high secretory IgA

My stool analysis showed that my secretory IgA — an immune substance that coats our
intestinal linings — was nearly two-fold higher than the upper-normal range.

S T OOL AN AL YS I S

14 2
Secretory IgA helps regulate the substances which can cross our intestinal walls into our
bloodstream. If secretory IgA is high, it suggests that our body is trying to “protect” itself
from foreign-invading substances. In stool samples, this is often the consequence of a viral
infection, a yeast / bacteria overgrowth, or the ingestion of an allergenic protein.

We need look no further than my Cyrex results to realize the likely culprit: gluten. And
since I’d done all of my tests (blood, stool, urine, and breath test analyses) while eating
gluten (to prepare for my Cyrex reactivity blood draw) — it made perfect sense that my high
secretory IgA was likely linked to my consumption of the gluten molecule.

Was gluten a driver of my hypothyroidism?

It’s not 100% clear, but the data suggests it’s possible. Gluten consumption (alongside its
consequences: increased gut inflammation / permeability) might have been causally linked
to my hypothyroid lab markers during testing.

In fact, the rest of my stool analysis (i.e., a measurement of the health of my large intestine)
showed no issues. Rather, I showed healthy levels of beneficial bacteria, no pathogenic
overgrowths, and no signs of yeast or viral activity.

C OM P R EH EN S I V E S T OOL A N A L YS I S / P A R A S I T OL OG Y X3

And in my breath test to measure bacterial activity in my small intestine (where we absorb
most of the nutrients from our food), I also showed no signs of problems / overgrowths.

14 3
 SMA L L I N T E S T I N AL BAC T ER I AL OVER G R OW T H (BRE ATH TE ST)

Now, let’s reflect back to my original hair loss assessment…

Tying it together: diffuse hair loss, hypothyroidism, and my hair recovery

In 2007, I had diffuse hair loss and vertex thinning. When I saw a dermatologist, I was
diagnosed with pattern hair loss (androgenic alopecia). I tried low-level laser therapy. I used
minoxidil for seven years. This slowed things down, but never stopped or reversed my hair
thinning. I only began seeing hair improvements after I simultaneously started massaging
and tried a diet avoidant of gluten, dairy, and common food allergens (more on this later).

Ten years later, I did a battery of lab tests that required me to reintroduce gluten into my
diet for several weeks — a food protein which I’d mostly avoided for the last few years
(despite feeling fine eating it). Subsequently, my lab tests showed I had hypothyroidism —
and that gluten consumption likely triggered its symptoms.

Now, let’s reflect back to my diet circa 2007. It’s full of gluten. In fact, my diet was full of
gluten ever since I was young. And in 2006 (one year prior to my AGA diagnosis), I had an
appendectomy — a tell-tale sign of severe gut inflammation.

What does all of this suggest?

That in addition to AGA, part of my diffuse hair loss was likely driven by hypothyroidism...
and I didn’t even know it.

Just look at my hair loss description from the dermatologist: early-stage AGA alongside
diffuse thinning. The writing was on the wall. I was at a high-risk of a misdiagnosis! And
when we logic-check this against my hair recovery, it makes even more sense.

When did I see hair recovery? After I started massaging alongside adopting a diet avoidant of
gluten. The main driver of my undiagnosed hypothyroidism? Gluten. That means the results
of my hair recovery were likely not only derived from a more targeted approach to reversing
hair follicle miniaturization (i.e., massaging)... but also stopping the progression of my
hypothyroid-related hair thinning (i.e., by removing gluten).

14 4
If I had known this in 2007, I could’ve better treated my hair loss. I could’ve better
improved my health. So I’m telling you this now...

If you’re at risk for a hair loss misdiagnosis, do more testing

The high-risk categories for a hair loss misdiagnosis are (1) women, and (2) men with early-
stage AGA who also have diffuse hair loss. According to our study, this includes 93% of
women with AGA and 44% of men with early-stage AGA (i.e., Norwood 1 or 2).

If you fall under either category, I can’t stress this enough: do more testing. It may make a
big difference to your hair and health.

If you suspect you’re in one of these at-risk categories or have a shedding disorder, be sure
to say so while filling out your action plan survey. In doing so, you’ll be presented with
symptoms of each underlying condition — so you can see if you match any of those
symptoms... at which point you can follow instructions for testing.

Does this mean that the massages are just “smoke-and-mirrors” — and the therapy’s
best responders are really only treating their non-AGA-related hair loss?
Anything is possible! But I don’t think this is true. Again, our data showed that those with
standard presentations of AGA(albeit self-reported) benefitted more from the massages than
diffuse thinners. This chapter is to explain why this might be the case... and to encourage
anyone in these “risk” categories to do more testing.

To reiterate, we do have plenty of case studies to demonstrate the efficacy of massages for
androgenic alopecia. Remember Sam from earlier in this chapter? He has standard AGA. He
also saw great results from massaging (and within a year).

The same is true of Guillaume. Guillaume has AGA-related temple recession and saw the
steady advancement of his hairline over 2+ years of massaging.

There’s also Peter, who recovered most of his vertex over 7+ months of massaging... or
Adam — who has standard AGA and saw hairline thickening over 7+months... or Trent...
or Calvin... or JD Moyer... or Mike.

14 5
 M I K E : 3- Y E A R H A I R R E C O V E R Y ( M A S S A G I N G )

To reiterate, there are dozens of success stories and case studies. Most of these readers
had AGA, and most saw hair recovery from massaging. So feel free to dig through them!

Any other insights on becoming a “best responder?”

Yes. Aside from the insights gleaned from diffuse thinners, there is one not-yet-discussed
variable that actually predicted better massage results. And this variable didn’t involve any
supplements, topicals, FDA-approved drugs, or microneedling.

Rather, it involved someone’s diet.

Interestingly, readers who reported following a specific type of diet predicted significantly
better hair changes from the massages than any other variable. But just like the insights from
diffuse thinners, interpreting these findings requires context!

As such, we’ll reveal this variable (and its significance) in our next chapter. In doing so,
we’ll reveal three simple things we can do from a dietary (and lifestyle) standpoint that not
only optimizes our health but also our chances for hair recovery.

14 6
Chapter recap
Our data showed that for those of us doing the massages, our degree of hair recovery
doesn’t depend on factors like our age, gender, hair loss severity, or the use of supplements,
topicals, FDA-approved drugs, or microneedling devices.

However, there are two factors that, according to our findings, do influence hair recovery.
The first variable? Our pattern of hair thinning. Specifically, our findings showed that people
with diffuse hair loss tended to report less impressive results from massaging versus those
with temple and/or vertex thinning.

At first glance, this might suggest that the effect of massages on AGA depends on hair loss
pattern, but this isn’t necessarily true. Why? Because a portion of diffuse thinners may not
just have pattern hair loss. Rather, they may also have a hair shedding disorder, and hair
shedding disorders require entirely different hair loss treatments.

There are two groups of hair loss sufferers at the highest risk of misdiagnosing a hair
shedding disorder as AGA: (1) women (since their AGA patterning is almost always
diffuse); and (2) men with early-stage AGA (i.e., Norwood 1-2) alongside diffuse thinning.
In our survey, 93% of women reporting AGA also reported diffuse thinning and slightly
lower (but statistically insignificant) hair change scores. And of men reporting early-stage
AGA, 44% also reported diffuse thinning. Not surprisingly, they also reported less
impressive results from massaging than those with more standard-looking AGA.

This is because while diffuse thinning can be due to AGA, it’s also possible that early-stage
AGA + diffuse thinning may be partially driven by a hair shedding disorder — and caused
by stress, medication use, or an underlying condition. Specifically, hypothyroidism,
hyperparathyroidism, small intestinal bacterial overgrowth, nutrient deficiencies, nutrient
surpluses, and / or trace element / heavy metal toxicities.

Hair shedding from these underlying causes can mask as AGA and even compound (or
accelerate) it. The only way to treat a hair shedding disorder is to treat the conditions that
cause them.

In these cases, massaging hits the wrong target.

In this chapter, we also highlighted two case studies of readers at a high-risk for an AGA
misdiagnosis: Ben M. and me. By diving into these cases, we can see first-hand just how
many ways these shedding disorders can present — and how multi-faceted they truly are.

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The bottom line: if you’re in a high-risk category for a misdiagnosis, I highly recommend
testing for these conditions and seeing a qualified dermatologist. It could make a difference
for your hair and your health.

More information on relevant lab tests can be found in your customized hair loss action
plan. Just make sure to say you have a hair shedding disorder while filling out the survey.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions which you can access right here.

Up next, we’ll reveal the second factor affecting massage effectiveness: diet. And using these
insights, we’ll reveal three things we can do from a dietary perspective to improve the power
of any hair loss treatment. These three things will build the basis for the next three chapters
regarding our diet, lifestyles, and microbiome health — which will help us maximize our
chances for hair recovery. Hint: the best diet for one person will not be what works for
everyone. We’ll soon find out why.

14 8
 CHAPTER 9:
BECOMING A BEST RESPONDER:
DIET

Chapter summary:

• Does diet have any connection to pattern hair loss? The overwhelming majority of
research suggests no, but it is possible that a bad diet might accelerate AGA.

• Interestingly, our study’s findings showed that vegans and vegetarians reported better
hair changes while massaging. At face-value, this seems we could all benefit from
adopting these diets. But digging deeper into the data, this isn’t the whole story.

• We’ll unveil three confounding factors within these finds that explain why vegans and
vegetarians outperformed other massagers. In doing so, we’ll reveal how we can
actually apply these “principles” of diet to any diet out there.

• By the end of this chapter, we’ll finally understand why the diet-hair loss connection is
so contested, why there is no one-size-fits-all diet, and which simple rules we should
follow to maximize our chances of hair regrowth from a dietary and lifestyle
perspective.

• This chapter sets the basis for the rest of this book. Its principles not only apply to
androgenic alopecia but also hair shedding disorders — and the evidence and
recommendations put forth may help improve the efficacy of any hair loss drug or
therapy. So, take the information as it comes and make any adjustments you deem fit
(or none at all).

14 9
BECOMING A BEST RESPONDER: DIET

Does hair loss have anything to do with diet?

Be careful where you ask this question. In natural health forums, you’ll be met with a
resounding, “Yes!” On HairLossTalk, you’ll be downvoted, laughed out of the discussion
thread, and maybe even banned.

For what it’s worth, I understand HairLossTalk’s reactions. There’s a lot of misinformation
about AGA. Most of it is focused on hair loss and its connection to diet.

So, let’s start with the facts.

The authors of this 2017 literature review dove into hundreds of studies and found that
while our nutritional status (and thereby our diet) is definitely connected to hair shedding,
there’s little-to-no data showing a link between diet and androgenic alopecia (AGA). As
such, that review mainly focuses on hair loss due to malnourishment in impoverished
populations.

Unfortunately, many “natural hair loss” marketers use studies from that review to exclaim
that vitamin A is critical for hair regrowth or that you’re definitely losing your hair due to a
biotin deficiency. Then, they market nutritional supplements toward people with AGA.

This is a gross misuse of science. As we’ve already learned, hair shedding disorders and
AGA are not the same! So, we can understand why certain hair loss forums get so hostile
each time the hair loss-diet discussion surfaces. They don’t want AGA sufferers wasting
their time on misleading science, useless supplements, and bogus dietary claims.

At the same time, we shouldn’t silence this debate. Why? Well, for starters, this 2018
literature review summarized that AGA sufferers with an iron deficiency might improve their
AGA by taking iron supplements (and sometimes vitamin C). And this review found that
vitamin D deficiencies were often associated with female pattern hair loss.

Of course, we can argue that these hair loss sufferers (i.e., nutrient deficient AGA sufferers
and women) are in “high-risk” misdiagnoses categories. They may not have strictly AGA —
which would explain why they benefited from iron or vitamin D supplements.

15 0
In general, I tend to agree with that argument. However, I have a hard time applying that
same logic to all reported cases of a dietary change and its effects on AGA.

For instance, this 1930 study on two middle-aged men doing a meat-only diet showed that
at the one-year mark, their gingivitis disappeared, they showed no signs of a nutrient
deficiency, and that one man had reportedly stopped the progression of his AGA.
Interestingly, newer anecdotes from all-meat dieters have reported similar skin and hair
benefits.

Then, there’s Grant Genereux — a middle-aged man with AGA, hair greying, renal disease,
kidney disease, and Alzheimer’s-like symptoms. After trying a diet entirely avoidant of
vitamin A, he stopped the progression of his renal disease, reversed his brain fog, and saw
significant hair thickening along with a partial reversal of his grey hair. He also tested the
diet on gerbils to show its safety… and then wrote three books unveiling the mechanisms by
which a vitamin A-deplete diet might’ve improved his health and hair.

Then, there are readers’ anecdotes. For instance, many best responders from massaging also
followed specific dietary protocols. Take JD Moyer, who spent a decade tweaking his diet,
lifestyle, and supplement protocol to eliminate his asthmatic symptoms. Interestingly, he
also saw great results from the massages (and within a 13-month period).

J D M O Y ER

Then, there’s Patrick — who tried massaging on-and-off for a year (his longest stint was
three months). He was discouraged by a lack of results. But when he restarted the massages
alongside an overhaul of his diet (including more carbohydrates, more protein, and fewer

151
food allergens), he started seeing his temple recession (i.e., AGA) improve... and within a
couple months.

P A T RI C K (+1 M ON T H ) P A T RI C K (+2 M ON T H S)

Were Patrick’s results a function of the “cumulative” effect of massaging (like in Calvin’s
case study)... or does this suggest a potential synergy between diet and massaging?

It’s hard to say. But, we may be able to use the data from our study to find out...

Do the massages work better alongside certain diets?

Our data demonstrated that finasteride, minoxidil, topicals, and supplements don’t enhance
our degree of hair regrowth from massaging. But fascinatingly, there was a variable that did.
It was diet. Specifically, those following a vegan and vegetarian diet.

Massagers adhering to veganism or vegetarianism reported better hair changes than those
doing a standard American diet (even after controlling for total massage effort).

This confused me. After all, I tried a vegan / vegetarian diet for over a year to see if it would
help my hair. I noticed the opposite results: more hair shedding, more hypothyroid-like
symptoms. Many readers have reported the same.

So, why were vegans / vegetarians in our data reporting slightly (but statistically significant)
better regrowth from massaging? I had to know. So, after completing our study, I reached

15 2
out to some vegans/vegetarians in our dataset. I wanted to learn what I was missing. Was
there really a synergy between veganism / vegetarianism and massaging, or were we
misinterpreting the findings due to a confounding factor?

I figured the interviews might provide clarity. And fortunately, they did.

Vegans and vegetarians report better results from massaging... but why?
Of the vegans / vegetarians reporting great hair changes from massaging, the overwhelming
majority also made efforts to address any nutrient deficiencies that might’ve arisen from
their diet. That meant greater efforts to supplement with zinc, vitamin B-12, vitamin D, and
iron — or to eat more vegan-friendly foods containing those nutrients / vitamins.

This wasn’t by my recommendation; they did this on their own accord.

In other words, these vegans / vegetarians proactively tackled any nutrient deficiency that
might’ve occurred from going vegan / vegetarian. And this led me to another question...

Was this also the case for great responders following other diets?

So, I reached out to more massage participants to find out — and this time, ones adhering to
different diets: paleo, standard American, and even Ray Peat / Danny Roddy. The results
remained consistent: most great responders tried to offset any potential dietary-driven
nutrient deficiencies by supplementing or consuming more of certain foods. In other words,
these responders did everything they could become nutrient replete.

And therein lies the confounding factor.

Massage efficacy likely doesn’t improve from simply going vegan / vegetarian. Rather, vegan /
vegetarian massagers just happened to be more likely to try to ensure they weren’t deficient
in any certain nutrient or vitamin. And when we expanded our lens to look at other best
responders following other diets, these responders did the same!

We’ve just derived our first insight from the diet-hair loss connection. If we want to
maximize our chances for hair recovery, we need to become nutrient replete.

Rule #1: become nutrient replete

This is a perfect example of why, in some cases, we must look beyond quantitative data. At
face-value, supplementation does not improve massage-related hair regrowth. But in the

15 3
context of someone’s diet, supplementing with certain nutrients or consuming certain foods
to offset potential dietary-driven deficiencies do improve massage efficacy. It’s not about
being vegan or vegetarian; it’s about being nutrient replete.

The next question is: why? The answer may have to do with supporting the mechanisms of
massaging.

Remember how massaging generates acute inflammation... and how repeated acute
inflammation promotes growth factors that may encourage angiogenesis, help reverse
fibrosis, and remodel our scalp tissues? Well, being nutrient replete helps this happen.

Studies show that nutrient repletion enhances our recovery from inflammation. After an
injury, vitamin C helps synthesize new (healthy) collagen... glucose helps create new blood
vessel passageways... and zinc improves bacterial clearance and helps to activate stem cells.

In other words, being nutrient replete supports our ability to heal. And since micro-
wounding / acute inflammation is a major mechanism of massaging, this is probably why
people who were nutrient replete reported better hair changes. That means that massage
success has less to do with any diet... and more to do with getting all of our nutrients.

That means we can adhere to any particular diet... so long as we take measures to avoid any
nutrient / vitamin deficiencies associated with each of them. Encouragingly, that means
there is no “best” diet for hair regrowth. It all depends on the individual.

We can take this a step further. As long as we follow a diet that (1) maximizes our recovery
from inflammation, and (2) minimizes conditions linked to shedding disorders — we’re
doing everything we can (from a dietary perspective) to help our hair (more on this later).

So, regarding diet, is there anything else we can do in order to maximize our recovery from
wounds and minimize the onset of conditions linked to hair shedding disorders? And if so,
do these dietary practices align with the findings from our best responders?

Yes and yes. There are two more things we can do to promote hair regrowth from dieting —
and this stands for any hair loss therapy we pursue. This brings us to our second insight...

Rule #2: avoid a prolonged calorie deficit

Another common thread among our best-of-the-best responders: they all avoided a chronic
calorie deficit. In other words, they made sure they ate enough on a daily basis.

15 4
This may seem simple enough, but for people doing intermittent fasting or low-carb diets
like Atkins or a ketogenic diet, accidental under-eating is a widespread problem.

In fact, this happened to me when I tried a low-carb (ketogenic) paleo diet. Here’s how:

Our bodies use macronutrients for energy: fat, protein, and carbohydrates. If we want to do
a low-carb diet and don’t want to lose weight, we need to eat the same amount of calories we
burn daily. So, if we reduce our carbohydrate intake, we must increase our fat and protein
intake to avoid a calorie deficit. Sounds simple enough, but in reality, this is hard to do.

The problem is that fat is incredibly satiating — more so than carbohydrates. As we increase
the amount of fat we consume, we’re more likely to feel fuller faster than when we were
eating more carbohydrates. This subtle shift can spur a chronic caloric deficit, and thereby
weight loss.

This is why low-carb diets are so effective for people who want to lose weight. Studies
actually show that it doesn’t matter which diet you follow for weight loss — they’re all just
as effective. It’s just that on lower-carb diets, it’s easier to under-eat, so weight loss feels
more effortless. The same is true for intermittent fasting: the practice makes it very easy to
under-eat.

But there’s a dark side to low-carb diets (alongside chronic under-eating). It reduces our
output of thyroid hormone. In other words, a low-carb diet + a calorie deficit can drive us
toward a hypothyroid state as our body “readjusts” to its caloric deficit and attempts to
decrease the amount of basal energy it expends on a daily basis. Moreover, low-carb diets
(and caloric deficits) increase cortisol levels — a common biomarker for stress.

As we’ve already learned, hypothyroidism and chronic stress may increase our risk of hair
shedding disorders — specifically, telogen effluvium and chronic telogen effluvium. This
explains why so many people (including myself) have reported increased shedding during and
after their transition to low-carbohydrate diets.

To reiterate: you can still succeed on a low-carbohydrate diet. You just need to take extra
precautions to avoid a calorie deficit.

As such, entering your daily food ingestion into a calorie tracker like FitDay.com will help
you reduce your risk of chronically under-eating and likely improve your hair loss outcomes
for any drug or therapy mentioned in this book.

15 5
These two principles (becoming nutrient replete and avoiding a calorie deficit) apply to
everyone. But there’s something else we should be doing to minimize our systemic
inflammation from foods and reduce the onset of conditions commonly linked to hair
shedding disorders. And interestingly, this one is more person-specific...

Rule #3: avoid inflammatory or allergenic foods

Trust me when I say that we’re all consuming allergenic foods on a consistent basis. But
before we get into that, here’s why we should avoid them.

Since the 1940’s, we’ve known that allergens (e.g., pollen) prolong our recovery from acute
injuries. However, recent studies have finally clarified how: allergen exposure increases
inflammation and the arrival of TGF-β1 — which, as we’ve learned, can encourage scar
tissue development. This is also true for allergenic foods. Ingestion of common allergens
(i.e., dairy, gluten, etc.) increases inflammation and prolongs our wound recovery time.

But... does this actually lead to hair loss?

Not directly. But as we’ve learned from my personal lab results, allergens like gluten can
exacerbate hypothyroidism — a condition that not only leads to diffuse hair loss but also
delays wound-healing. So that’s one mechanism by which a food allergen may contribute to
hair thinning. And importantly, research shows that a gluten-free diet can help reverse many
hypothyroid symptoms. That means that for sensitive individuals, a food allergen may
indirectly contribute to hair thinning — and removing that food allergen may improve the
condition causing hair thinning (and thus improve their hair loss).

Again, it’s not that allergenic foods directly cause hair loss. Rather, it’s that food allergens (1)
delay the wound-healing process — which worsens the efficacy of massaging or other
therapies, and (2) worsen thyroid functionality — which worsens hair shedding disorders.

In other words, if we’re trying to holistically treat our hair loss, we should definitely avoid
food allergens — regardless of the hair loss type from which we suffer.

Sadly, this is easier said than done. In today’s world, food allergens have reached pandemic
levels. We’re consuming more than ever... and we don’t even know it.

Food allergy prevalence: high. Food allergy intake: high.

Let’s just look at the suspected number of Americans suffering from food allergens... and
the amount of allergens ingested per person.

15 6
For starters, it’s estimated that 65% of adults have a dairy / lactose intolerance. Knowing
this, how much dairy does the average American consume daily? Three-quarters of a pound.

Likewise, it’s possible that up to 35% of Americans have a gluten sensitivity (many of them
undiagnosed). So how much wheat does the average American eat yearly? 130+ pounds.

One average American, two common food allergens, hundreds of pounds devoured, every
single year. Knowing this, it’s no wonder why 50% of U.S. adults have a chronic disease.
We’re constantly inflaming ourselves with our food choices.

And beyond gluten and dairy, other estimates suggest that almost 11% of U.S. adults have
allergies to foods like soy, nuts, and shellfish. The worst part is that this number is probably
much higher, but our reactions are so subtle that we’re not yet aware of how the
inflammation presents: dermatitis, rosacea, acne, bowel discomfort... the list goes on.

Take me, for example. I had no idea I was gluten intolerant until doing lab testing — which
showed how gluten consumption was likely a partial trigger to my hypothyroidism — and
thereby my diffuse hair shedding.

How many of us are allergic to foods and don’t know it? How many others just haven’t done
the right testing? I wondered this as I interviewed our survey participants for our study.

In the end, it became clear that while some great responders didn’t worry about dieting,
others did extensive experimentation — eventually finding a diet that worked best for their
bodies (and lifestyles). I specifically remember one reader who spent years identifying his
food intolerances and building a diet to avoid them. Here’s a quote he left on the site:

I’ve [been] vegetarian for 22 years and it really improved my life a lot. For the last 5 years, I’ve
been pretty much vegan. In the last year or so, I’ve been as much raw vegan as possible and
that’s when my hair began to improve noticeably. The BIG things to avoid even as vegan are:
gluten, alcohol, sugar, caffeine I can’t emphasize enough what poisons these are. All of the
above cause inflammation. For me, these turn my hair thin and grey very quickly. If I stay on
the raw vegan diet with lots of vegetables and some fruit, my hair recovers and looks thicker.
So much so that people comment on it. Sorry veganism didn’t work for you. It certainly
works for me.

He’s not wrong. Veganism didn’t work for me. In fact, it was disastrous. I went hypothyroid
and shed significant amounts of hair. At the same time, I’m different from this reader. We
have different allergens, systems, and nutrient demands. As such, I can’t apply what works
for myself to him (or anyone else). It’s an apples-to-oranges comparison.

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Long-story short: our food allergens vary wildly and, consequently, so do our optimal diets.
That means a diet that minimizes your own systemic inflammation might, ironically,
exacerbate inflammation in others. And this is why the “best” diet for hair growth is
individualized.

Can we uncover our own food allergens?

Yes. I used to recommend an elimination diet — where someone keeps a daily food log
journal tracking their energy levels, skin health, hair health, and bowel movements... then
eliminates a food group (i.e., wheat, cruciferous vegetables, dairy, etc.) for several weeks,
reports the changes, reintroduces that food, and see if there’s a change in how they feel. It
takes a long time, but for many people, they find foods that work well for them.

Unfortunately, I no longer think this is a viable approach. The reason being: I did this in the
past, with gluten, and recorded absolutely zero changes on, off, and back on wheat. Yet lab
tests showed I was highly reactive to gluten.

That means there’s really only one way to properly test our allergens: lab work. The
frustrating part about this is that insurance often doesn’t cover this — which puts the
financial burden of allergen testing on each of us.

There are a hundred different tests available, but if you’re going to go down this road, one
options is an MRT Mediator Release Test for Food Sensitivities test. This is likely not
necessary for most people, but if you’re not price sensitive, it may be worth pursuing.

Rather than using antibody measurements, the above test measures our white blood cell
activity in the presence of 170 of the most common food proteins and chemicals. That
means we don’t need to necessarily eat these foods regularly to develop antibodies just to
show a positive reactivity test (like I had to do with gluten). Rather, we can just test for an
allergic reaction — with allegedly the same (if not better) accuracy — and then begin to
build a diet personally optimized for our health.

The above test is offered through True Health Labs — a lab testing company that not only
provides out-of-pocket lab testing without doctor’s orders, but also guarantees the lowest
online prices for any test within their array. I’ve partnered with them (at no cost to you) to
make any lab tests you’d like easier. You’re more than welcome to shop around, and if you
find lower prices, tell me! Otherwise, they’re the best resource I’ve found.

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How to create a diet following these three principles
The easiest way to adhere to these rules is to track your micro- and macro-nutrients using
FitDay.com, to do food allergy testing, and then to build a diet that avoids those allergens
but also allows you to remain micro- and macro-nutrient replete.

Again, if you decide to go that route (which I recommend for anyone who can afford it), you
can do your allergy testing here. By testing, you’ll know whether things like nightshades,
gluten, dairy, lactose, casein, nitrates, rice, eggs, soy, and dozens of other food proteins /
groups are potentially problematic for you.

Unfortunately, this approach is cost-prohibitive. And for those of us who don’t want to
spend additional money on allergy testing, there is another way.

For instance, while each person’s food sensitivities may vary, we can build a diet that avoids
the most common allergens for the majority of people. Simultaneously, we can find a diet
that is also nutrient replete and avoidant of a calorie deficit.

In doing so, we can consume a diet that may promote less systemic inflammation, improves
recovery from micro-wounds, minimizes or reduces our risk of autoimmunity, helps to quell
the conditions associated with hair shedding disorders.. and better our odds of hair recovery.
We’ll uncover that diet in the next chapter.

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Chapter recap
There is very little (if any) evidence linking diet as an interventional tool for pattern hair
loss. Having said that, a poor diet may exacerbate hair loss. And on that note, our study’s
findings suggest the best diet for health (and maybe our hair) is one that (1) maximizes our
ability to recover from wounds, (2) minimizes our systemic inflammation, and (3)
eliminates dietary factors that contribute to conditions that cause hair shedding disorders.

Knowing this, we can improve our odds of hair recovery by following three dietary rules:

1. Become nutrient replete.

2. Avoid a prolonged calorie deficit.

3. Avoid inflammatory / allergenic foods.

In a best-case scenario, we could all do lab testing to uncover our nutrient deficiencies,
surpluses, and allergens, as well as build a diet catered to our needs. Unfortunately, not all
of us have the ability to do this. That’s okay. In the next chapter, we’ll uncover a diet that
should get 75% of us most of the way there (without expensive lab work).

Looking ahead: going beyond our diets

Our diet is just one lever to maximize our ability to recover from wounds, minimize
systemic inflammation, and reduce any underlying conditions that can spur hair shedding
disorders. There are two other levers that may assist us: our lifestyles and our microbiome.

The rest of this book focuses on optimizing our health so that we can maximize our hair
recovery. Using the insights from our study, we’ll uncover small (but powerful) changes we
can make to our diets, lifestyles, and gut health so that we can not only improve our
outcomes for hair regrowth... but also become a healthier person in the process.

Note: not all best responders made these changes. And in all reality, our preliminary data
suggested that the massages can work even in the absence of changes to diet, lifestyle, or
gut health. So, if these recommendations feel overwhelming to you, that’s okay; you don’t
have to try them. They’re certainly there if you’re an over-achiever, and they’re certainly
there if you need to troubleshoot down the line.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help

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disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

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 C H A P T E R 10 :
THE DIET-HAIR LOSS CONNECTION

Chapter summary:

• The best diet for our hair is likely one that is (1) is nutrient replete, (2) avoids a
calorie deficit, and (3) avoids inflammatory / allergenic foods. Unfortunately,
designing such a diet involves lots of self-testing, expensive lab work, and constant
tracking through a food monitoring app. If this sounds unappetizing to you, I totally
understand.

• This chapter provides you with an evidence-based overview of the diet-hair loss
connection. We’ll build a diet that not only hits all of the above marker but also
attempts to avoid the most common allergens for the majority of people.

• We’ll uncover the biggest dietary offenders: grains, certain vegetable oils, heavy
goitrogen consumption, and a methionine:glycine imbalance. We’ll explain how each
of these dietary choices can lead to problems with our health (and maybe our hair).

• Then, we’ll formulate a diet that excludes these offenders and includes nutrient-dense,
pro-thyroid foods. Dish ideas, macro-nutrient, and micro-nutrient evaluations
included.

• These recommendations are designed to help anyone with their health — regardless of
the treatments they decide to pursue for their hair loss. Further dietary
recommendations (and tweaks) can be found in your regrowth roadmap — right after
you’ve completed the survey to help guide you to the right hair loss action plan.

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THE DIET-HAIR LOSS CONNECTION

A diet focused on hair recovery

In the last chapter, we revealed data suggesting that for most hair loss treatments, we can
optimize our chances of hair regrowth by...

• Maximizing our ability to recover from wounds

• Minimizing our systemic inflammation

• Preventing the conditions that cause hair shedding disorders

We can support these principles by utilizing three levers: our diet, lifestyle, and gut health.
This chapter focuses on just diet.

Again, the best diet for hair regrowth is going to be person-specific. It’ll involve using a
tracking software like FitDay.com to make sure you’re getting all of your micronutrients. It’ll
involve food nutrient and allergy testing to determine if you have any nutrient deficiencies,
nutrient surpluses, or food allergies. And it’ll involve eating enough food to remain at a
healthy weight (rather than a caloric deficit). Depending on the person, any diet can work —
from veganism to paleo to the standard American diet — so long as it abides by these three
principles:

1. Becoming nutrient replete

2. Eliminating allergenic / inflammatory foods

3. Avoiding a prolonged calorie deficit

For those who don’t want to go through the hassle of personal testing, there is a diet that
should get most people most of the way there. This diet provides a complete micro- and
macronutrient profile, minimizes allergenic foods for the majority of the population, and is
avoidant of a calorie deficit. This chapter uncovers that diet.

A diet to maximize our chances of hair recovery

Again, this diet should work for 75% of us with pattern hair loss (AGA) or hair shedding
disorders. The goal: to minimize allergens / inflammation, maximize our nutrient
absorption / intake, and keep us out of a calorie deficit.

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This diet is based on the latest literature, our learnings from best responders, and our
published data. It’s a diet that’s meant to act synergistically with the massages (or any hair
loss treatment) not only to improve our overall health but also to increase our chances of
major hair recovery.

Rather than just list the diet, a better place to start is to cover the foods worth avoiding.
Some of these foods may come as a surprise, but the evidence suggests that they’re
completely unnecessary to maintaining our health. In fact, removing them might even do
things like increase fertility, correct long-standing hormonal imbalances, and resolve the
systemic inflammation that heightens our risk of heart disease, shedding disorders, and a
plethora of conditions.

#1: Grains are not your friend

The first (and maybe biggest) culprit of first-world dietary inflammation is grains.

Grains today are not the grains of yesterday

There’s a debate as to how long ago humans started eating a lot of grains. Some say grains
came into our diets 10,000 years ago. This is the earliest we’ve found evidence of humans
domesticating grain varieties — so that we could eat them on a large scale.

One of the arguments “anti-grainers” make is that grains haven’t been in our diets long
enough for us to adapt to eating them. Consider the millions of years of evolution that made
us the humans we are today. If we just started mass-consuming grains 10,000 years ago,
that might not be enough time for our genes to adjust to the food source.

But more recent findings suggest grains have been in our diets for 100,000 years. That’s the
earliest we’ve found grain remnants in the knapsacks of indigenous peoples. While the same
logic holds true — 100,000 years is just a blip on our evolutionary timeline — it makes the
argument, “Grains aren’t a natural part of our diets,” much harder to make.

In reality, it doesn’t matter when we started eating grains or if they’re natural to our
evolutionary diets. The truth is that grains today aren’t what they used to be, and most grain
varieties of today are doing more harm than good. This section covers why.

1. The current state of grains: an influx of genetic modifications

The grains we eat today aren’t what they used to be 10,000 years ago. In fact, they’re not
even the same grains from 25 years ago.

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To make crops more resilient to herbicides, pesticides, and insects, many agro companies
insert altered genetic coding into foods like corn, wheat, soy, and other widely sold high-
yield crops. By genetically modifying the crop, agro companies reduce the total yield lost
from chemical damage and insects.

Grains that are genetically modified are more common than you think. In 2011, 88% of corn
and 94% of soy sold in the US was genetically modified. It’s getting tougher to track GMO
foods because of labeling legislation. And it may be to the detriment of our health.

GMO’s reduce fertility and are linked to premature death in animals

Genetic modification allows for grains (and foods like soy) to have their own insecticides
built into them. With current research estimating that the average American eats 193
pounds of genetically modified food each year, how does this impact human health?

Recent GMO research points to potential long-term health implications for humans, and
we’re only beginning to scratch the surface of the environmental implications.

One recent long-term GMO study from Russia researched hamsters being fed genetically
modified food for two years over three generations. By the third generation, most of the
hamsters were infertile, grew more slowly, and had alarmingly high infant mortality rates.
Another study showed that rats on a GMO-corn diet developed early-life liver and breast
cancer, with 70% of the female rats dying prematurely (versus 20% in the control group).

You might be wondering how this relates to hair loss. Hair loss has been around for
thousands of years, and GMO’s really just took off around 1996. So, what’s the big deal?

GMO’s hurt our hair by hurting our thyroid and promoting inflammation
Genetically modified foods have altered protein structures. Modified soy and corn contain
proteins that can evoke a toxic or allergenic-like response in humans. When we ingest
anything toxic or allergenic, our body’s first response is usually inflammation of the affected
areas, which means GMO’s can partially drive low-level systemic inflammation.

Studies have also shown that overconsumption of GMO’s can — through tumor generation
— disrupt hormonal balance and result in reproductive disorders and infertility. These are
failures of the endocrine system, which is largely powered by our thyroid.

Again, a diet that acts synergistically with any hair loss treatment should increase our
wound-healing capabilities, decrease systemic inflammation, and avoid allergenic foods.
GMO’s encourage just the opposite. Thus, they have no place in a pro-hair diet.

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A huge source of GMO’s in your diet comes from grains. So, eliminate them. But don’t stop
there. It’s also estimated that 75% of processed foods contain genetically modified
ingredients. So eliminate processed foods, soy, and sugar beets from your diet. It seems as
though eating these foods from U.S. sources is just not worth the health risks.

If we only buy organic non-GMO grains, then what’s the big deal?
Unfortunately, GMO’s are not the only issue with grains. There are other offenders — like
gluten, lectins, and phytates — that make grains a less-than-optimal food source.

2. Gluten
We covered gluten earlier, but now we’re going to dive deeper into its science. Gluten is a
type of protein found in wheat, barley, and rye. Gluten intolerance was once thought to be
rare, but with more recently developed testing markers, it turns out that possibly 35% of the
population could be gluten-sensitive.

Gluten in the blood can lead to an autoimmune attack on our thyroid

How can gluten consumption lead to an attack on our thyroid? It begins not with gluten,
but rather a constituent of gluten — called gliadin. Gliadin is a set of proteins that closely
resembles our thyroid gland.

When we digest grains, the fibrous parts of grains rake against our intestinal walls. This
creates micro-tears along our cell lining and allows for certain nutrients and minerals to
leach into our bloodstream. It might sound bad, but this “raking” is actually a part of the
normal digestive process. When we consume fiber within a normal range, that fiber not only
feeds our gut bacteria but also creates small tears in our intestinal walls to allow for some
permeability of nutrients and minerals into our bloodstream.

Problems arise when we eat too much fiber, and thereby damage our intestinal walls beyond
normal ranges. When this occurs, vitamins and minerals still get through to our blood... but
so does unwanted bacteria, viruses, parasites, and larger protein molecules that would’ve
otherwise stayed in our digestive tract. Gliadin is one of those proteins.

Because grains are so high in fiber, excessive grain consumption increases the permeability
of our gut and intestines, which means more interaction between your blood stream and the
foods we digest. When we eat gluten-containing foods, gliadin can (and will) enter the
blood stream. Because gliadin is not supposed to be there, our body reads gliadin as an
invader and produces antibodies to attack it.

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Unfortunately, because gliadin is so structurally similar to the thyroid gland, our body
inadvertently also attacks our thyroid tissue. These events suppress the thyroid and can lead
to a type of hypothyroidism called Hashimotos, which is classified as an autoimmune
disorder since the thyroid is being attacked by your own antibodies. It is estimated that
Hashimotos is responsible for ~90% of U.S. hypothyroid cases.

But gliadin’s (and thereby gluten’s) involvement in autoimmune disease doesn’t stop there.
Gliadin antibodies (the same ones our bodies produce to attack our thyroid) have also been
implicated in type 1 diabetes.

The only way to stop gliadin from entering our bloodstream is to (1) restore our gut lining
so that it can’t pass through into the bloodstream... or (2) completely cut out gluten. I’d
recommend the latter. Why? Because new testing methods suggest that gluten’s effects on
our immune system can last up to six months even after we stop eating it.

Aside from the 1% of people with celiac disease, gluten is only an issue if our intestinal
lining is damaged enough to allow for gliadin to enter our bloodstream. So beyond fiber, do
grains — in any other way — contribute to beyond-normal damage to our intestinal walls?

Yes. Grains can damage our intestinal linings beyond normal ranges — and all through
another one of its compounds called lectins.

3. Lectins: mostly indigestible, often inflammatory

Lectins are natural protein toxins that are mostly indigestible to humans. They’re found in
the seeds of fruits. From an evolutionary standpoint, they serve to protect the seed from
digestion when an animal eats an entire fruit, so that it can pass through the digestive track
unharmed and have a chance to sprout one day. Lectins are also abundant in grains and
legumes.

Eating too many lectins damages our intestinal walls

Unfortunately, lectins contribute to damaging the lining of your intestines, but in a different
way than fiber. Whereas fiber physically damages the cells of our intestinal wall, lectins
prevent those cells from healing. Again, that’s the exact opposite of what we want in terms
of improving our ability to recover from inflammation.

This prolonged damage can lead to something known as “leaky gut”, which is another term
to describe an overly permeable intestinal tract. If we have a leaky gut, then not only will the
vitamins and nutrients from our foods make their way into our bloodstream, but so too will

167
unwanted bacteria, viruses, parasites, and indigestible proteins that our gut would normally
keep out.

A high lectin, high fiber diet can result in higher gut permeability, more chronic systemic
inflammation, more autoimmunity, and a greater risk of the conditions associated with hair
shedding disorders. On top of that, high lectin intake is also associated with a handful of
other inflammatory GI tract diseases. So, keep the lectins to a minimum.

So... if lectins inhibit our intestinal lining’s ability to repair itself, do they also enter our
bloodstream?

Yes. And once lectins are in our bloodstream, they can create even more problems.

In the blood, lectins bind to thyroid hormones and hinder thyroid function
Once in your bloodstream, lectins bind to thyroid stimulating hormone (TSH) receptors and
block our production of thyroid hormone. This suppresses the thyroid, contributes to
hormonal imbalance, and spurs systemic inflammation.

To summarize, lectins are associated with both diminished thyroid functionality and
systemic inflammation. And the only way to reduce lectins is to reduce their consumption.

That often means removing grains, but sometimes, it means limiting other sources of lectins,
too. Nut- and seed-products (like coffee, chocolate, or almond milk) also contain lectins.
And while it’s nearly impossible to go zero-lectin, it’s also worth being cognizant of your total
lectin load — and making dietary choices accordingly (more on this later).

But the problems with grains don’t stop there. On top of contributing to leaky gut, grains
contain compounds that also interfere with the absorption of the vitamins and minerals our
bodies need to function.

4. Phytates: inhibitors of critical minerals

Phytates (phytic acid) are found primarily in grains, nuts, and cocoa. When a food with
phytic acid is eaten, phytic acid binds to a variety of minerals inside that food that our
bodies would otherwise absorb in the absence of phytic acid. By binding to these minerals,
these minerals become indigestible.

For example, phytic acid has been shown to significantly reduce the mineral absorption of
manganese, zinc, chromium, and iron in the gastrointestinal tract.

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How does this impact your hair? Proper mineral absorption is vital to thyroid health. For
instance, weakened zinc metabolism or a zinc deficiency is closely associated with
hypothyroidism, and a poor-functioning thyroid can precede a hair shedding disorder.

This doesn’t mean you should start supplementing with zinc. Rather, it means you should
avoid foods (like grains) that promote high gut permeability, inhibit nutrient absorption,
potentially hurt your thyroid, and in doing so, generate chronic systemic inflammation.

One final note: grains and fortification

Beyond these concerns, there’s evidence that grain fortification (i.e., adding vitamins and
minerals to refined grains) might be linked to higher incidences of disease. Fortified grains
are stripped of their germ and bran then fortified with B-vitamins, iron, and other nutrients
that a grain loses when its germ and bran are removed. For the last twenty years, the U.S.
has mandated that refined (white) grains be fortified. Ironically, evidence suggests that
when a country introduces fortification, inflammatory gut disorders and heart disease spike.
If you’re interested, please read Richard Nikoley’s article on the evidence.

Summarizing the negative impact of modern-day grains

Beyond grains, what other dietary changes can we make to optimize thyroid health, reduce
chronic inflammation, and prevent the calcification and fibrosis cascade that contributes to
hair loss?

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#2: Minimize inflammatory polyunsaturated fats
“Common knowledge” on fats is wrong
Just as we may reevaluate our stance on grains, it’s imperative that we also reconsider how
certain fatty acids generate chronic inflammation within the body.

If you asked your doctor about fats, he or she would probably say something along the lines
of, “Fats are bad, especially saturated. Saturated fats clog your arteries and kill you. The only
safe fats are unsaturated fats, like those that are liquid at room temperature — like canola
and other vegetable oils.”

This couldn’t be further from the truth. It’s disappointing that most doctors don’t bother to
read the latest research and evidence suggesting the exact opposite of that advice. In fact,
the dogma that saturated fats are “bad” is about thirty years outdated.

Saturated fat isn’t the enemy

For many years, people looked at heart disease and pointed the finger at saturated fats.
These assumptions were driven from the research of Ancel Keys, a professor of human
nutrition and public health. He published an infamous paper titled the Seven Countries
Study, which found an association with increased heart disease and increased saturated fat
consumption from dairy and animal products. The study gained significant amounts of
traction, and Keys’ findings went on to drive the USDA dietary recommendations that
stands today (yet is now finally being revised).

What you may not know is that his original study was composed of 22 countries, not seven.
Keys actually omitted the countries that would have made his study’s findings inconclusive.
He cherrypicked his data points and drew misguided conclusions about the dangers of
saturated fats. This led to the dissemination of bad information, which eventually
culminated into the widespread belief that saturated fats are, for lack of a better term, evil.

Saturated fats are actually really good for your body, your thyroid, and your hair.

The real enemy: polyunsaturated fats – specifically, omega-6’s

Ironically, polyunsaturated fats are often revered as healthy. They’re the oils you can buy at
health stores in the form of cold-pressed flax seed oil, hemp seed oil, or fish oil.

The most well-known polyunsaturated fats are omega 3’s and omega 6’s. These are
considered essential fatty acids because your body can’t produce them, so they have to be
incorporated into the diet. They’re required for certain functions of the body, such as

17 0
proper cognitive performance, nerve function, and bodily development. Most plant foods
have at least some trace amounts of essential fatty acids.

Scientists used to think that high amounts of these fats were healthy, but recent research
suggests a different story. It’s actually the ratio of polyunsaturated omega-6 to omega-3
consumed that matters more than the total amount of polyunsaturated fats in the diet.

Several studies have found that an excess of omega-6 fatty acids promotes the “pathogenesis
of many diseases, including cardiovascular disease, cancer, and inflammatory and
autoimmune diseases, whereas increased levels of omega-3 PUFA (a low omega-6/omega-3
ratio) exert suppressive effects.”

In one article, researcher Chris Kresser summarizes the history and science behind the
detrimental effects of excess omega-6 fatty acids.

“In the U.S. the average person’s tissue concentration of [omega]-6 fat is 75%. Since we get
close to 10% of our calories from [omega]-6, our tissue contains about as much [omega]-6
as it possibly could. This creates a very inflammatory environment and goes a long way
towards explaining why 4 in 10 people who die in the U.S. each year die of heart disease.”

The optimal ratio of omega 6-to-3 is suggested to be somewhere between 4:1 and 1:1.
What’s the average ratio of the standard American diet? Somewhere between 10:1 and 20:1,
with many Americans showing ratios as high as 25:1. How could we be consuming so much
omega-6?

Post Industrial Revolution, everyone started eating more omega-6

Up until the Industrial Revolution, the ratio of omega-6 to -3 in our diets wasn’t really an
issue. The spike in omega-6 consumption came from the widespread emergence of cooking
oils in the form of soy, olive, safflower, canola, and other vegetable oils.

There have been entire books published on efforts trying to reverse public confusion on fats.
If you still have doubts, I encourage you to dig deeper into the available research on
polyunsaturated fats and the mechanisms behind the inflammation created from excess
omega-6. For the purposes of this book, this is as far as we’ll take this:

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What about our hair?
To close the book on the Ancel Keys’ fabricated findings, it turns out that arterial plaque is
mostly made out of polyunsaturated fats. Remember, that’s the kind of fat our bodies don’t
create. The only way we can get it is to eat it.

Excess omega-6 fatty acids promote systemic inflammation within the body. Inflammation
reduces our ability to recover from wounds and exacerbates the conditions that precede hair
shedding disorders. Therefore, in order to reduce inflammation and prevent future hair loss,
we may want to reduce our overall omega-6 consumption.

Quelling Inflammation by reducing omega-6 fatty acids in our diets

Interested in the omega 6-to-3 ratios of certain cooking oils? Just read this article or look at
the ratios yourself, then stop cooking with these vegetable oils. In fact, stop cooking with
any oil that isn’t solid at room temperature. Otherwise you’ll find yourself at risk for
another detriment to liquid-based cooking oils: oxidization.

Oils that are liquid at room temperature oxidize with heat from cooking
You might look at the omega 6:3 ratio on flaxseed oil and think it’s a safe oil because the
ratio looks balanced. That’s only partially true. Flaxseed oil can still cause inflammatory
problems. Why? Because by the time you ingest it, its polyunsaturated fats will likely be
oxidized.

Oxidation occurs when unstable fatty acid molecules — namely, polyunsaturated fats — are
exposed to oxygen. Polyunsaturated fats have a unique molecular structure: a carbon-carbon
double bond. Conversely, saturated fats have a carbon-carbon single bond. This single bond
is much more stable in the presence of oxygen.

In polyunsaturated fats, when enough oxygen is present, the carbon-carbon double bond
degrades and becomes a carbon-oxygen bond. A byproduct of this reaction? Free radicals —
highly unstable molecules that bind with anything in sight and are believed to accelerate the
progression of cancers, arterial calcification, and age-related disease.

The more polyunsaturated fats, the more likely an oil will become oxidized. And the more
oxygen present, the more free radicals are generated during that process.

Unfortunately, UV light and high temperatures catalyze this entire process and can increase
oxidation of vegetable oils over ten-fold. But even vegetable oils that have never been
cooked can be problematic, as oxidation is impossible to prevent unless an oil is never
exposed to oxygen.

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This makes even cold-pressed oils high in polyunsaturated fats (like flaxseed) an issue.
While cold-pressing improves the quality of the oil, it doesn’t prevent oxidation. That oil
still has to be shipped to you from far away, traveling in large containers with fluctuations in
heat and storage. By the time you ingest it, the chance of it being oxidized is so high that
you’re better off avoiding it altogether.

Oxidized oils generate free radicals inside our bodies, which accelerate aging, form
carcinogenic compounds, and damage DNA. In fact, research speculates that free radicals are
what cause the injuries (read: inflammation) that eventually lead to atherosclerosis and
arterial calcification.

This is generally the problem with most omega 3 supplements (like fish oil). By the time
you ingest that supplement, it’s often already rancid and dangerous.

Omega 6:3 matters – eat more fish, eliminate vegetable oils

To wrap this up, oxidized polyunsaturated fats are highly inflammatory. Chronic systemic
inflammation reduces our ability to recover from micro-wounds, precipitates hormonal
imbalances, and exacerbates the underlying conditions that can lead to hair shedding
disorders. So, minimize your omega-6 intake, get your 6:3 ratio back between 1:1 and 4:1,
stop consuming rancid oils / supplements, and stop encouraging systemic inflammation.

You can do this by tossing the vegetable oils, reducing your use of cooking oils (in general),
and consuming a few ounces of shellfish, mackerel, sardines, and / or wild salmon 2-3 times
a week. This will help your omega 6:3 ratio tremendously.

Which oils should we cook with?

I used to cook a lot with red pail oil and coconut oil — which are high in saturated fats, low
in omega 6, and solid at room temperature. This is because saturated fats are far more
resistant to oxidation. They also make up about 50% of our cell membrane structures,
increase immune functionality, and help with the proper absorption of the fat-soluble
vitamins A, D, E, and K.

However, I recently stopped cooking with oils altogether. I didn’t like the flavor of coconut
oil or red palm oil (even when refined). Moreover, non-stick pans make cooking without oils
way easier nowadays. Any stir-fry — from vegetables to meats — can be cooked without
fusing half of your meal to the bottom of your pan. And the best part is that you can always
add in oils for flavoring (like olive oil) after cooking... and thereby avoid heavy oxidation.

But, there’s more we can do from a dietary perspective to reduce systemic inflammation.

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#3. Minimize (but don’t eliminate) goitrogens
Goitrogens are found in cruciferous vegetables (and certain fruits)
Goitrogens are chemical compounds founds in cruciferous vegetables like kale, broccoli, and
brussels sprouts... but they’re also found in soy and in the skin of peaches, strawberries, and
a handful of other fruits.

Goitrogens inhibit iodine absorption

Goitrogenic compounds compete with the thyroid gland and inhibit our absorption of a
critical trace element: iodine. Iodine is classified as an essential nutrient and is naturally
found in soil, seawater, fish, and some dairy. Without iodine, our thyroid cannot generate
the hormones necessary for optimal health.

Up to 40% of the world is at risk of an iodine deficiency. An iodine deficiency is associated

with hashimotos, hypothyroidism, and certain reproductive diseases and cancers – mainly
because of its impact on thyroid functionality.

But how, exactly, does this relate back to our hair? Well, goitrogenic compounds inhibit the
absorption of iodine from the thyroid, and in scenarios of iodine deficiency, the thyroid
starts underperforming. This culminates into hypothyroidism — one of the conditions we’d
like to avoid to help stave off a hair shedding disorder.

Should I completely remove goitrogens?

For most of us, no (and for two reasons).

Firstly, it’s hard to entirely remove goitrogens due to their widespread prevalence in foods.
And secondly, some foods that contain goitrogens are also nutrient-dense and contain
beneficial substances that may outweigh the risks of low goitrogenic consumption.

Example: cruciferous vegetables like broccoli. Yes, broccoli contains high amounts of
goitrogenic compounds. However, broccoli also contains substances which help with heavy
metal chelation, activate endogenous (i.e. within-the-body) antioxidants, reduce
inflammation, and even improve estrogen excretion (thus contributing to better hormonal
balance — which is especially important for younger men with AGA). This is probably why
broccoli consumption, over many years, is associated with a lower risk of death from heart
attacks and cancers. As such, we’re faced with a dilemma.

Can we reap the benefits of cruciferous vegetables while minimizing their potential risks?

Yes, we just have to be wise about how we eat them.

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Want to eat cruciferous vegetables?
Just try to adhere to these three things:

1. Avoid “green” smoothies

2. Boil / steam any goitrogenic vegetables

3. Eat these vegetables in moderation

Firstly, we want to avoid raw, green smoothies. Despite the fad of raw juicing and
smoothies, blending raw vegetables together and drinking them isn’t necessarily healthy.

For starters, when we blend vegetables into a smoothie, they become liquid. Liquids stay in
our mouths for just a few seconds before we swallow them. That’s a problem for a food
that’s designed to be chewed — like a cruciferous vegetable.

When we chew solid food, we release enzymes from our saliva to help us break down that
food for absorption. One enzyme, salivary amylase, helps us break down carbohydrates.
Another, lingual lipase, helps us break down fats. While other salivary-based enzymes help
us stave off viruses and pathogenic bacteria, as well as increase our vitamin B-12 absorption.
Some salivary enzymes might even help chelate heavy metals and trace elements.

When we slam down a raw green smoothie, we bypass this entire step of the digestive
process. The end-result is a lot of digestive distress, less absorption of nutrients, potentially
more heavy metals / gut lining damage... and much more goitrogenic exposure due to the
sheer ease and volume of consumption from drinking versus chewing.

So: stop raw-juicing and smoothie-making. Start chewing your food. Our bodies know what
they’re doing! Let them work they way they should.

Secondly, if we’re going to eat cruciferous vegetables, we should just cook them. In doing
so, we’ll help reduce the number of goitrogenic compounds.

For instance, this study showed that boiling brussels sprouts for 30 minutes deactivates
90% of goitrogens in the food. Yes, we’ll lose some vitamins and nutrients during the
cooking process, but we’ll also retain many of its minerals and vitamins.

Steaming or boiling should do the trick — and when it comes to cruciferous vegetables other
than brussels sprouts, less “hardy” vegetables probably require less boiling time. For
instance, if we boil broccoli for 30 minutes, it would likely turn to mush. As such, I typically
just boil my broccoli for ten minutes (sometimes less).

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Lastly, if we’re going to eat cruciferous vegetables, we should eat them in moderation.
Avoiding green smoothies is a great start. Limiting your (cooked!) cruciferous vegetable
consumption to just 1.5 cups per day is even better. And if you’re at risk of (or have) an
iodine deficiency or hypothyroidism... reduce that amount even more.

The bottom-line: cruciferous vegetables can be eaten as part of a healthy, happy, hair-friendly
diet. Just avoid the smoothies, boil your vegetables, and eat them in moderation.

Can’t I just supplement with iodine while eating goitrogenic foods?

You can, but this isn’t always the right approach. A better approach is to probably act on
these three pieces of advice above, rather than trying to course-correct your goitrogen
consumption with more iodine. This is because at a certain point, thyroid iodine uptake
becomes nearly impossible in the presence of too many goitrogens.

On top of that, nutrients behave differently in concentrated forms or when separated from
the adjuncts found inside the foods containing them. With iodine specifically, evidence
points in the direction that supplementation might not always be helpful.

For instance, supplemental iodine can trigger an autoimmune attack and exacerbate the
symptoms of hypothyroidism. Another study found that 78% of those with autoimmune
hypothyroidism actually reversed the disorder with iodine restriction. That means that
amounts of iodine beyond normal levels can potentially exacerbate hypothyroidism.

Beyond that, it turns out our ratio of selenium and iodine also matters. Selenium is found in
high amounts in fish, and adequate amounts of selenium ensure that iodine reacts normally
inside our bodies. Depending on the amount of selenium present, it’s also protective against
the mercury in salmon, tuna, and other seafood. Blindly supplementing with iodine and not
also selenium might imbalance our selenium:iodine ratio, and maybe even contribute to the
hair shedding disorders we’re trying to avoid.

At the end of the day, I don’t recommend supplemental iodine... and until we know more
about iodine’s cofactors, I think it’s best to just get iodine from foods. So if you’re looking to
safely increase iodine levels, instead just eat quality seafoods, supplement with kelp, or
decrease your overall goitrogenic load.

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#4. Stop eating only muscle meat, and start eating nose-to-tail
Protein balance matters
Consuming adequate amounts of protein is critical for our health. However, what’s often
overlooked is the type of protein that people ingest, and how an overload of certain types of
proteins can lead to chronic systemic inflammation.

Amino acids are the building blocks of proteins. There are 20 of them. Our body can make
certain amino acids on an as-needed basis, but there are some amino acids that must be
consumed from our diets. These are called essential amino acids.

Most people are under the impression that, “All protein is equal, just make sure you’re
getting enough.” But this isn’t true. For instance, every cut from an animal has its own
specific amino acid profile, and not all profiles are created equal.

For most Americans, animal meat is the major source of protein. However, most Americans
also only ingest one kind of animal meat: muscle. Think ground beef, rib-eye steak, t-bone
cuts, filet mignon, and chicken breast. Rarely — if ever — do most people eat the rest of
what an animal has to offer (liver, kidneys, brains, sweetbreads, and / or bones).

Eating only muscle meat may contribute to systemic inflammation

When you’re only consuming one type of amino acid profile (specifically, the profile of
muscle meat), and you consume it very often, you’re laying the groundwork for systemic
inflammation. Here’s how.

Muscle meats are very high in the amino acid methionine (a type of essential amino acid
that our body can’t create). Once inside our bodies, methionine can convert into an amino
acid known as homocysteine.

If you’ve read my case study from an earlier chapter, you’ll already know that one of my
blood tests revealed high levels of homocysteine. High homocysteine is associated with
elevated blood coagulation, atherosclerosis, and heart disease. In fact, many physicians use
serum homocysteine to gauge a patient’s risk for heart attack.

The more methionine ingested, the more it gets converted into homocysteine, and the
higher our risk for heart disease. But that’s not all that methionine does. High consumption
of methionine also depletes glycine: an amino acid present in skin, bones, and other body
tissues.

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Glycine seems to exert the opposite effect of excess methionine. Glycine helps to quell
inflammation by suppressing free radicals and other triggers of arterial inflammation.
Unfortunately, glycine is also an amino acid that we barely consume.

In mice, restricting methionine has actually been shown to extend life expectancy by
30-40%. But even more interestingly, glycine supplementation has been shown to do the
same thing — and inhibit the negative effects of excess methionine.

And perhaps most relevant, increased glycine (through gelatin supplementation) has been
shown to increase human scalp hair thickness by ~10% in six months.

Remember the importance of our omega-6:3 ratio? The same idea applies here. By balancing
out our methionine:glycine ratio, we can reduce diet-driven inflammation and help better
support any hair loss treatment.

How do we decrease our methionine:glycine ratio? By eating more glycine-rich foods.

Glycine is high in the animal parts we forget to eat

What are the sources of glycine? Unsurprisingly, glycine is found in the parts of the animal
we don’t generally eat. Abundant sources of glycine are found in bone broths / stocks,
gelatin, collagen, connective tissues, and animal skins. If you’re eating muscle meats, you
should absolutely eat these too.

The importance of glycine:methionine plays out in nearly every “animal protein is bad for
you” study. Of all the research that finds a correlation between meat consumption and heart
disease or cancer, when we look closer at the data, we almost always see that the
populations studied ate predominantly processed muscle meats and rarely (if ever) organs,
bones, and other glycine-rich animal parts. In essence, these studies would be better off
(and maybe more accurate) in stating that chronic, excess methionine consumption is
associated with disease — which is something we already know.

To summarize: if you’re a meat-eater, start eating “nose-to-tail” and stop focusing on muscle
meats alone. Eating nose-to-tail means rotating your animal foods to include muscles, bone
broths, skins, and organ meats. Doing so will decrease arterial inflammation, increase your
odds of living longer, and maybe even increase your chances of keeping (or regaining) hair.

Nutrition Data does a great job of presenting the different nutritional and protein profiles of
foods. If you’re ever interested, you can look on their site and see for yourself.

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Recap of dietary recommendations
Based on what we now know, if we want to reduce inflammation, increase thyroid health,
and reduce our risk of the conditions that precede hair shedding disorders, we should:

1. Eliminate (most) grains from our diet

2. Reduce our omega 6:3 ratios by removing vegetable oils and eating more fish

3. Minimize goitrogens by minimizing the consumption of raw cruciferous vegetables

4. Eat “nose-to-tail” to balance our glycine and methionine ratios

Here’s a summary chart to keep things organized:

So... what does a diet like this look like? And how can we implement it? Fortunately, this is
much easier than it may seem.

An anti-inflammatory, nutrient-replete diet

A diet that helps support our health (and hair) is a diet that helps us (1) become nutrient
replete, (2) avoid any food allergens, and (3) avoid a prolonged calorie deficit. If we can do
these three things, we’ll reduce our systemic inflammation, improve our hormonal profile,
prevent the conditions that precede shedding disorders, and (hopefully) maximize our
chances of hair recovery.

The following diet eliminates most grains, reduces our consumption of goitrogens, provides
a balanced omega 6:3 ratio, corrects any amino acid imbalances from over-consuming
muscle meats, and gives us the micro and macronutrients we need to live a happy, healthy
life. It requires zero supplementation — since we’re getting what we need from food.

Our objective here is to ingest adequate amounts of the fat-soluble vitamins A, D, E, and K,
consume the right kinds of fats to properly assimilate those vitamins and nutrients, take in a
healthy amount of protein with an anti-inflammatory amino acid profile, and receive the
right levels of water-soluble vitamins, nutrients, and trace minerals.

17 9
If you’re familiar with different diets, this may look similar to a moderate carbohydrate
paleo diet — with the absence of the foods we listed above (plus some modifications).

Foods I eat
Here are my own guidelines for my personal diet, plus a list of foods I consume regularly.
This is meant as a guide, not a bible. Moreover, it’s probably worth mentioning that I’m
6’4”,195 pounds, and relatively active — so I eat around 3,000 calories per day. You may
need to adjust this diet up or down based on your own height, weight, and activity level.

Meats / seafood
Summary: I eat most meats and seafood — as long as they meet the quality standards
discussed in this chapter. I try to rotate my meats so that I never over-consume one type of
amino acid profile. When I eat muscle meat, I try to enjoy it with a cup of bone broth or
collagen / gelatin mixed with water. I generally have eight to twelve ounces of meat or
seafood per day, along with 10-20 grams of protein per day from bone broth / stock /
collagen / gelatin (though it’s not the end of the world if you can’t do this). Once weekly, I
eat a few ounces of raw oysters. Otherwise, I’d probably need to supplement with zinc.

• Daily Amount: 8-12 ounces per day, plus 10-20 grams of protein from bone broths

• Options (among others): Ground Beef, Bison, Lamb, Chicken Liver, Bone Broths / Stocks, Crab,
Raw Oysters, Wild Scallops, Chicken / Duck Eggs, Wild Salmon, Bacon, Mackerel, Sardines, Sea Bass

Carbohydrates
Summary: Depending on my activity level, I eat around 150-250 grams of carbohydrates per
day. Even with moderate exercise, this keeps me out of ketosis (more on this later). Like
meats and seafoods, I try to rotate my carbohydrate sources daily to vary taste and nutrient
profiles. I also eat white rice 4-5 times per week. Of all the grains, it’s the least problematic
in regard to the issues highlighted in this chapter. (Note: rice grains are sometimes linked to
high levels of arsenic. However, as long as you consume white rice and rinse it a few times
before boiling, arsenic levels shouldn’t be too concerning. After years of eating white rice 4-5
times per week, I had my arsenic levels tested and they were fine. Also, white rice tastes
great when cooked within bone broths/stocks.)

• Daily Amount: 150-250 grams per day

• Options (among others): White Potatoes, White Rice, Most fruits

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Roots / Vegetables / Fungi / Nuts
Summary: I try to eat 3-7 servings of roots, vegetables, fungi, or nuts each day. These come
in the form of mixed green salads, greens mixed in with rice bowls, leafy greens on lettuce-
wrapped burgers, stir-fries with parsnips and/or mushrooms, handfuls of nuts (for calcium),
and steamed / boiled broccoli or cauliflower. You’ll notice some of these foods contain
goitrogens. To reiterate: we should minimize goitrogens, but we don’t need to necessarily
eliminate goitrogens entirely.

• Daily Amount: 3-7 servings per day

• Options (among others): Mixed Greens, Carrots, Garlic, Onion, Parsnips, Zucchini, Broccoli
Sprouts, Steamed / Boiled Broccoli, Cauliflower, Mushrooms, Squash, Brazil Nuts, Macadamia Nuts

Seasonings / supplements
Summary: I enjoy salt and am not very restrictive when it comes to spices. In terms of
supplements, I’ll sometimes take animal collagen / gelatin mixed with water If I’m eating
muscle meat and don’t have access to bone broths or stocks. The brand I often use is Great
Lakes Collagen (I am not affiliated), since they do heavy metals testing. But other collagen
or gelatin supplements will do, so long as they test and aren’t actually selling bone meal
(which is really just ground up bones).

• Daily Amount: as needed

• Options (among others): Collagen / Gelatin, Himalayan Salt / Sea Salt, Raw Apple Cider
Vinegar, Ground Pepper, Most spices

Liquids
Summary: I stay clear of soft drinks and sodas. I mainly drink water. With that said, I do
drink coffee (black) in the mornings, and sometimes black / green teas in the early
afternoon. I drink tap water that I filter through a Berkey System (again, I am not affiliated).

Daily Amount: as needed

Options (among others): Water (through a Berkey filter, never bottled), Coffee, Black or Green Tea,
Herbal Teas

Oils
Summary: I’ve recently stopped cooking with cooking oils. The reality is that today’s non-
stick pans make non-oil stir-frying easy. If I use oil, it’s often olive oil for flavoring after
cooking. If I had to choose a cooking oil, I prefer refined coconut oil over regular coconut oil

181
(refined is absent of the distinct “coconut” flavor). For salads, I’ll often add cold-pressed
olive oil as a dressing. Again, I try not to cook with oil (to minimize oxidation).

• Daily Amount: sparingly while cooking, or moderately for flavoring

• Options (among others): Refined Coconut Oil, Lard, Ghee / Clarified Butter, Olive Oil
That’s my diet. And here are my macro and micro-nutrient breakdowns for a typical day of
food (from FitDay.com). Please keep in mind that I’m 6’4’’ and 195 pounds. I’m relatively
active. As such, I tend to eat ~3,000 calories per day. But everyone is different. On this day,
I happened to have eaten oysters — so my zinc is higher than normal.

DAI L Y MAC RON UTRI EN T I N TAKE

DAI L Y VI TAMI N / MI C RON UTRI EN T I N TAKE

18 2
And here’s a dietary summary:

DI ET SUMMARY

My meals
These meals are by no means comprehensive, but here are a few food dishes that I enjoy
eating. My hope is that this clarifies the diet, and spurs some of your own dish ideas.

Spiralized Zucchini / Squash + Meats / Seafoods — You can buy a spiralizer for
under $15 and use it to turn zucchini, squash, or any other vegetable into thin
strings that resemble pasta. Stir fry it in salt, spices, add in olive oil after cooking,
and pair it with any meat or seafood for a delicious and filling meal.

Mashed Potatoes — Skin white potatoes, boil them, and then mash them in with
ghee, olive oil, coconut oil, or lard and add salt and pepper.

Lettuce-Wrapped Burgers — Instead of making yourself a hamburger with buns,

wrap it in large lettuce leafs and enjoy it grain-free. Feel free to experiment with
toppings: onion, garlic, or whatever else you may have in the fridge / house.

White Rice Cooked In Bone Broth / Stock + Meats / Seafood + Vegetables — If

you’ve got a rice cooker, this is easy to make and a great way to consume more bone
broth. Instead of cooking your rice in water, cook it in bone broth. Then add in a
duck egg and stir it all together while adding a teaspoon of apple cider vinegar for

18 3
 flavor. Add in ground beef, sautée it with salt and spices, stir-fry in mushrooms /
vegetables, and you’ve got yourself a great meal.

Sushi — I don’t usually make this at home, but when going out with friends, it’s a
great option that adheres to many of our suggestions throughout this chapter.

Eggs And Bacon — No explanation needed.

Dietary suggestions
To maximize the diet’s effectiveness in reducing inflammation and (hopefully) improving
health outcomes, I also take into consideration the following suggestions:

Eat organic, pasture-raised, grass-fed animals

The quality of your meat, dairy, and eggs matters! Pasture-raised, grass-fed animals have
lower levels of inflammation, and their meat has better omega 6:3 ratios. If you consume
these animals, you’ll be consuming a better ratio in your own diet. Organic-certified farms
don’t use genetically modified ingredients, antibiotics, or hormones when raising the
animals, which helps ensure you’re not consuming substances that are thyroid-inhibiting.

If you don’t have access to these types of meats, it’s not the end of the world. Just opt for
them whenever they’re accessible.

Take note of fruits and meats in the same meal

Fruit and meat are great foods, but depending on your needs, they may need to be eaten
separately. The vitamin C in fruit increases iron absorption from meats, and high iron
accumulation can interfere with thyroid health and inflammation. This is particularly
relevant for men with hair loss and women post-menopause, but is less relevant for
populations at a higher risk of anemia (i.e., younger females with hair loss with healthy
menstrual cycles). This is covered in more detail in later chapters.

Be careful with dairy

As we’ve already covered, dairy is one of the most commonly ingested allergenic foods. So
be careful with consuming it regularly! I used to think I could tolerate a lot of dairy, but I
definitely have an upper limit. For instance, if I eat six ounces of cheese and drink raw goat
milk daily, it’s only a matter of time before I develop acne (another form of diet-driven
inflammation).

18 4
So, if you can’t stomach dairy, don’t eat it. But if you’re one of the 35% of human beings
that can tolerate lactose, if you don’t suspect a casein allergy, and if you’re not concerned
that 60-80% of estrogens from our diet come from dairy — then feel free to eat it. After all,
dairy can be a great source of calcium, fat-soluble vitamins, and micronutrients.

Be careful with nuts

Brazil and macadamia nuts are included in this diet as a means to help us get more calcium.
Having said that, nuts are also one of our potentially problematic foods — since nuts often
have high levels of phytate and lectins. We can do things to mitigate this issue — like
soaking nuts overnight and not eating exclusively raw nuts.

However, if any of this concerns you — or if you (1) have a condition that precedes a hair
shedding disorder, (2) already get enough calcium from other foods, or (3) suspect you have
a nut sensitivity — you don’t need to include these in your diet. For what it’s worth, this is
one of those cases where allergen testing might help.

Don’t go ketogenic for prolonged periods

We’ve already covered aspects of this — but oftentimes with paleo-related diets, people will
consume high amounts of fat and protein but fewer carbohydrates. Depending on your
activity level, consuming fewer than 50-100 grams of carbohydrates per day can result in
something called ketosis. This is a state when your body runs out of glycogen stores and
begins producing ketone bodies from fat reserves for energy.

Ketosis is highly effective for weight loss. It’s even the basis of the Atkins Diet and many
low-carbohydrate Paleolithic diets. But because higher-fat diets are so satiating, its followers
have a higher propensity to consistently under-eat. Again, this is great for weight loss... but
can also result in hypothyroidism and promote more hair shedding. When I was
experimenting with a low-carb paleo diet, this happened to me. My hair started shedding,
my temperature dropped to the mid-95’s, I accidentally lost a lot of weight, and I caught the
flu for the first time in five years. In short, my thyroid health plummeted.

With that said, ketogenic diets also have many health benefits. They’ve been successfully
used to fight certain types of cancers, reverse epilepsy, and even manage Alzheimer’s
disease. A lot of research is still underway, but until things are better understood, I’d be
careful with ketosis and (at a minimum) track that you’re not in a calorie deficit.

Because of concerns over accidental caloric deficits, some question whether ketosis is
sustainable long-term. One idea is that ketogenic diets are sustainable for long periods only
if there is access to thyroid hormones through animal foods. Animals’ thyroid glands, when

18 5
consumed, can boost our own thyroid function. If you’re ketogenic and hypothyroid, then
eating animal thyroid appears helpful. But, if you’ve got a normal-functioning thyroid and
eat animal thyroid, you can develop the opposite — hyperthyroidism (an overactive
thyroid). Hyperthyroidism has its own laundry list of symptoms and associated conditions,
one of which is fine and brittle hair.

For this reason, animal thyroid gland is nearly impossible to buy in U.S. grocery stores. If
you’re in the U.S. and eating a ketogenic diet, you’ll likely need a prescription for thyroid
medication to keep your thyroid optimized. So, unless you’re resolving a different health
problem, I’d be careful trying ketosis as a diet while trying to improve your hair.

Don’t want to follow this diet? That’s okay!

One of the biggest challenges for people on this diet is the limited carbohydrate sources
(white rice, white potatoes, etc.). I agree! While these foods certainly work well for me (and
other readers), I don’t want you to feel like you have to eat them. It’s just that many people
have low-grade allergies to other carbohydrate sources — like nightshades or sweet potatoes
— so I don’t include those in the base diet plan. But there’s a possibility that you’re not one
of those people and might do great with those foods.

Again, this diet is just one way to (1) become nutrient replete, (2) avoid allergenic foods,
and (3) avoid a calorie deficit. Feel free to experiment with other food choices or diets, so
long as you do your best to adhere to those three principles.

To help you out with this, here are a list of diets, their potential nutrient deficiencies, and
their most common potential allergens. Just look out for these things and find alternatives
where you can — an augmented chart, inspired by examine.com (next page).

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 P OP UL A R DI ET S: C ON C ERN S A N D SOL UT I ON S

Can’t I just supplement with whatever I’m missing in my diet?

Maybe, but I don’t recommend it.

For starters, supplement companies in the U.S. (and elsewhere) have essentially zero
regulation so long as they put a notice on their bottles that “These statements are not
evaluated by the FDA and therefore should not be construed as health advice. Consult your
doctor before trying this product.”

What this really does is just absolve supplement manufacturers of any risk. This allows
them to produce cheaply manufactured supplements from unreliable ingredients suppliers
on websites like Alibaba... then charge obscene markup prices.

This leads to two huge problems: (1) variance in the listed versus actual ingredients, and (2)
heavy metal contamination. The reality is that, without third party testing, we don’t have a
clue what we’re getting inside our supplements; and if those supplements contain unlisted
trace metals, we’re actually doing more harm than good. For a perfect example of how well-
intended supplementation actually caused hair loss and heavy metal poisoning, please read
this case study.

187
Beyond that, we’re still only at the precipice of understanding how nutrients and vitamins
separated from their adjunct ingredients behave when ingested. And there’s also evidence
that over-consuming certain nutrients like selenium and vitamin A — both of which are
included in leading hair loss supplements — can cause hair thinning.

For these reasons, I recommend avoiding supplementation — unless you (1) have a risk of
deficiency, (2) trust your supplier, and (3) track your nutrient status as you supplement.

Going beyond diet

Diet isn’t the only lever we can use to improve our health and hair. Another lever that’s
potentially just as important (if not more): our lifestyles. In fact, by leveraging just a few
simple lifestyle changes, we can improve our hormone health and help our hair potentially
even more so than with diet alone. This is all coming up in the next chapter.

18 8
Chapter recap
Diet is not a miracle cure for hair loss. Having said that, we can still adopt a diet that may
maximize our chances of benefiting from any hair loss treatment. This diet can be utilized
regardless of food limitations: whether you’re vegan, vegetarian, paleo, or anything in
between. All you need to do is make food choices that (1) make you nutrient replete, (2)
avoid a calorie deficit, and (3) avoid any systemic / allergenic foods.

This will vary for everyone, and a diet that works for you might not work for everyone else.
Having said that, the diet in this chapter is designed to get the majority of us most of the way
there.

In fact, it’s the same diet that I currently follow. And after experimenting with dozens of
diets for the last decade — from the Gerson Therapy diet to veganism to vegetarianism to
low-carb paleo and beyond — I find this diet works best for my system (and for many others
who’ve committed to it).

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

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 C H A P T E R 11 :
THE LIFEST YLE-HAIR LOSS
CONNECTION

Chapter summary:

• Despite all the experimentation most people do with diet, it’s not the only powerful
tool for improving hormonal health, reducing systemic inflammation, and improving
health outcomes. Another major lever? Our lifestyle choices.

• We’ll uncover three lifestyle choices most of us are doing wrong — to the detriment of
our hormonal health (and maybe even our hair).

• Then we’ll reveal easy-to-make changes that (1) maximize our ability to recover from
wounding, (2) minimize our systemic inflammation, and (3) help minimize (or
reverse) the conditions that can precede hair shedding disorders.

• Just like our diets, implementing these lifestyle choices depends on our individual
needs. To help you with this, be sure to take the quiz in your regrowth roadmap —
which will provide additional lifestyle recommendations based on your age, gender,
and hair loss type.

• Note: many best responders from this book have made these lifestyle changes. So
learn from the paths they’ve paved — and read on to uncover the science behind each
change.

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THE LIFEST YLE-HAIR LOSS CONNECTION

A lifestyle built for our health (and hair)

In the last chapter, we built a diet that (1) maximizes our ability to recover from wounding,
(2) minimizes systemic inflammation, and (3) helps to reduce the onset of conditions that
can precede hair shedding disorders. Now it’s time to do the same, only with a different lever:
our lifestyles.

In this chapter, we’ll introduce three simple, easy-to-implement lifestyle changes designed
to maximize our health (and hair). In fact, these lifestyle changes are also relatively easy
ones to which we can commit.

Updates from the previous book

In past versions of this book, I built cases for lifestyle changes designed to optimize thyroid
health, balance our hormones, and cut down on costs related to cosmetics. Two of these
changes were to (1) stop shampooing, and (2) start taking cold showers. I summarized
literature explaining the benefits of both practices (and why they were worth trying).

Most readers didn’t love these two recommendations. Some had a hard time transitioning to
no-shampoo — and noted greasier hair for 6-8 weeks (until their sebum production settled),
which made them uncomfortable in public. Other readers disliked taking cold showers.
Consequently, these two recommendations discouraged many readers from also trying many
other recommendations in this book. It all seemed too overwhelming.

I understand this. It’s one reason why I created the regrowth roadmap — to tailor our
regimens to each of our ages, genders, time constraints, and comfortabilities. Moreover, one
of the founding principles of this site is to always reevaluate our assumptions about hair
loss (and its treatments)... and to revise our opinions in light of new evidence, no matter the
cost.

Sticking to these principles, I recently reevaluated (as best as I could) my five years of
anecdotes from readers trying no-shampooing and cold showers. While these two changes
seemed to benefit readers’ wallets and endocrine systems, only two readers considered these
changes integral to their success. In other words, no-shampooing and taking cold showers
doesn’t seem to make a difference between hair regrowth and no hair regrowth — at least for
the majority of readers.

191
So, as long as you’re not over-shampooing (i.e., 1+ times per day) and taking prolonged,
very hot showers (or regularly exposing your testes to hot water), you’re like fine skipping
those two lifestyle changes. As such, I’ve removed them from this chapter.

However, if our goals are to optimize our wound-healing capabilities, minimize

inflammation, and prevent the conditions that precede hair shedding disorders — then
lifestyle changes are still one of our most powerful levers. All we need to do is focus our
efforts on three principles:

1. Sleep

2. Sunlight

3. Blood donation (or iron panel testing) — depending on your gender

These changes are not only manageable for most of us, but they also move the needle
further than anything else I’ve come across — at least in terms of the above goals. So let’s
break these down one-by-one.

#1. Sleep: the ultimate hormone regulator

When men want to “double” their testosterone or women want to address a hormonal
imbalance, their minds often fixate on two tools: diet and exercise.

However, even the best diet and exercise regimen pales in comparison to one simple lifestyle
change: getting enough sleep. Here’s the science behind how sleep might be the best
weapon we have against inflammation (and accelerated aging) — and how it’s sadly
overlooked and undervalued in the first-world.

Every mammal on earth needs sleep

Sleeping is an unusual state. It requires an animal to remain at rest, unconscious, and in one
place for an extended period of time. If we consider sleep’s opportunity cost, that’s time not
spent hunting, reproducing, or avoiding predation: all things critical to survival.

Given the importance of these activities, I always presumed that over millions of years of
evolution, mammals would’ve evolved to select against sleeping long hours. After all, the
less we sleep, the more things we can do to improve our survival.

But evolution hasn’t de-prioritized sleep... for every single mammalian species on the planet.
And for us humans, this one activity is supposed to constitute 33% of our lifetime.

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Unfortunately, the modern world is narrowing that activity from 8 hours per day (33%) to
six hours (25%) or worse. And while that dip might look relatively small, it has huge
ramifications on our brain health, hormonal health, and maybe even our hair.

“Wakefulness is low-level brain damage. Sleeping restores that damage.”

It’s a statement from one of the world’s top sleep scientists, and it’s true. While we’re
awake, free radicals inflame our brain. Our built-in repair mechanism? Sleep. Sleeping
activates anti-inflammatory signaling proteins that reduce free radicals, repair brain injury,
and (while awake) allow us to remain attentive, process memory, and perform bodily
“background tasks” — things we do that we don’t ever notice.

One of those background tasks? Regulating our endocrine system — and specifically, our
hormones. When we stop sleeping, this system is one of the first to fall apart.

Two hours of nightly sleep deprivation can age us by 10 years

We’ve all probably heard that we need about 8 hours of sleep per night. What most of us
haven’t heard are the consequences of not hitting that benchmark.

In men, a shift from 8 to 6 hours of sleep lowers testosterone levels by ten years. In other
words, you’ll have the hormonal profile of someone tens years older than you just from a
week’s worth of sleeping six hours per night.

The mechanism has to do with a region of the brain called the hypothalamus — which
regulates our pituitary gland and significantly influences the degree of testosterone our
testes produce. As our waking hours stretch, we experience more oxidative damage to our
pituitary gland. With less sleep, we activate fewer repair mechanisms to resolve this
damage. This lowers our testosterone production, and in prolonged cases (4+ days), may
even shrink the size of our testes.

Knowing this, it’s no surprise why men’s testosterone levels today are 22% lower than they
were 30 years ago. With the advent of smart phones, brighter screens, and the internet,
we’re likely to stay up longer and later than ever before.

Likewise, in women, chronic sleep deprivation increases cortisol, decreases estrogen, and
dysregulates menstruation. The end-result for both genders: irritability, diminished
cognition, and often the tell-tale symptoms of severe hypothyroidism.

In fact, studies show that just a 25% reduction in sleep each night can increase cytokines
and signaling proteins linked to systemic inflammation — the same inflammation we want

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to avoid if we’re to improve our health (and hair). Unfortunately, this sleep deprivation can
carry long-lasting consequences... particularly if we never course-correct.

The consequences of sleep deprivation over a lifetime

From a wound-healing perspective, sleep-deprived volunteers heal slower than non-deprived
volunteers. From a quality-of-life perspective, sleep-deprived individuals have poorer thyroid
functionality, higher rates of autoimmunity, increased weight gain, and a larger incidence of
metabolic syndrome. From a longevity perspective, women sleeping 5-7 hours per night
significantly increase their risk of a coronary event versus those who get 8 hours.

How much sleep are we actually getting?

The average American sleeps just 6.8 hours per night. That’s down from nearly 9 hours in
1910. Worryingly, 40% of Americans sleep less than six hours per night... regardless of their
income or number of children. In other words, 40% of us are sleep-deprived due to bad
habits. I used to be one of them — until my daughter was born. Now I’m not sleep-deprived
due to bad habits; I’m just sleep-deprived because I’m a parent.

On that note, about half my friends claim they can thrive off of 4-5 hours nightly. Lucky
them. But looking into the data, I have my doubts they’re being honest with themselves.

Yes, there is a gene which allows people to function on 6 hours per night of sleep. How
many people in the population have it? Less than 1%. This means either 50% of my friends
are in that 1% pool... or the ones claiming they feel great are probably just sleep-deprived,
surviving off stimulants, and have the hormonal profiles of a 104-year-old.

The bottom-line: most of us aren’t sleeping enough. And regardless of how you feel now,
over a lifetime, you may pay a price.

We all need 7-8 hours of sleep per night

The minimum amount of sleep adults need to maintain functionality is 7 hours. Anything
less, things start to fall apart — even with just one bad night of sleep.

Moreover, sleep quality matters. There are several stages of sleep. Each stage activates
different levels of brain activity. All stages are important, but our deeper stages (i.e., rapid
eye movement and beyond) are where we see the majority of mechanisms activate that aid
in tissue repair. This typically happens 90+ minutes into sleeping — which is why we can’t
take several short naps throughout the day and expect to feel the same as when we get one
long night of sleep.

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So, if we’re doing any hair loss therapy involving wound-healing — we’re going to want to
activate these mechanisms... and we’re going to want to hit these sleeping windows.

How can we improve our sleep time and quality?

Our ability to activate these repair mechanisms depends entirely on our ability to enter deep
sleep. And interestingly, a common activity many of us engage in may prevent this from
happening: drinking alcohol.

Ever fall asleep after a night of drinking and, the next morning, feel like you dreamt a lot?
Interestingly, research suggests this is just an illusion. Studies now show that as we
metabolize alcohol, we inhibit our ability to enter deep sleep (where dreaming occurs). With
the general rule-of-thumb of “one drink processed every 45 minutes”, it’s only by morning
time that we’ve actually metabolized enough alcohol to finally reach deep sleep (and start
dreaming). So why do we feel we’ve dreamt a lot? Because by the time we wake up, our
dreams have only just started happening.

This phenomenon is also related to a condition called delerium tremens. It’s characterized
by psychosis and hallucinations, and it’s caused by chronic alcohol consumption (and its
withdrawal). Fascinatingly, studies show that the brain activity of those with delerium
tremens aligns with that of someone in deep sleep. The conclusions of researchers? When
alcohol is drunk so regularly, our brains become so deprived of deep sleep that they force it
to happen while we’re awake. The consequence? Wakeful hallucinations (dreaming). And
the cure? A good night’s rest.

Knowing this, my first recommendation is that if you’re going to drink heavily, do it earlier
in the day (so you can process the alcohol by the time you’re ready to go to bed). Beyond
that, there are three more principles to help us improve our sleep time and quality:

1. Consistency. Go to bed (and wake up) at roughly the same time each night and day.

2. Length. 7-8 hours of night is what we all should hit, and consistently.

3. Quality. Keep your room dark. Avoid light pollution. Don’t drink alcohol before bed.
Sleep with your phone in the other room. If your partner snores, tell them to figure it
out. In other words, do whatever it takes to ensure your 7-8 hours per night are restful.

If you do these three things consistently, you can expect reductions in inflammation, better
hormonal balance, and a substantially improved ability to heal from wounds — all of which
are key components to massaging, microneedling, and other hair loss therapies.

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#2. Get sunlight whenever possible
We need vitamin D for hormone synthesis and immune functionality
Something often overlooked in health is the importance of sun exposure. Our bodies
naturally produce vitamin D when we are exposed to the sun. We can find vitamin D in food
sources like dairy or in supplements, but the best way to receive vitamin D is naturally.

Because of the connection between skin cancer and sunburns, people often stay out of the
sun more than they should. The truth is, while individual tolerances vary from person-to-
person, sun exposure is central to our thyroid function, hair health, and even longevity.

What happens when we are vitamin D-deficient?

In premenopausal women, insufficient sun exposure (and thereby low vitamin D) is
associated with an increased risk of autoimmune thyroid disorder. In fact, research shows
the lower your vitamin D, the worse your thyroid disorder. That same study also revealed
that 92% of Hashimotos sufferers (the autoimmune form of hypothyroidism) have
significantly low serum vitamin D markers.

On top of that, low levels of vitamin D have also been associated with decreased immunity,
osteoperosis, heart disease, and certain cancers. Dr. Michael Holick of Boston University has
dedicated his entire career to this research; if you’re interested, you can read more here.

Beyond sleep, if you decide to make only one other change to your life, try to get into the
sun everyday.

How much is enough Vitamin D?

It’s hard to say. Considering most of us work indoors during daylight hours, and considering
we evolved (more or less) in the sun and naked, it’s postulated that most of today’s first
world countries aren’t even close to optimal levels. What does this suggest? Expose yourself
to the sun as much as possible (without burning). But how can we make this change and live
(and work) a normal life?

A few years ago, I decided to reorient my schedule around one goal: to get adequate sun
exposure. It wasn’t easy. I live in San Francisco (which gets some sun throughout the year),
but I also work a full-time job outside of this book. I’m inside an office forty hours per week,
and I generally commute 90 minutes total each day. When I leave my apartment each
morning, there’s little to no sun. When I arrive home each night, there’s little to no sun.
This means I had to somehow get daily sun exposure during working hours.

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What did I do? I started packing a lunch. Then, I stopped scheduling meetings during my
lunch break. I started jogging / walking everyday at noon to maximize my sun exposure, I
wore shorts and went shirtless. I ended up getting 30-45 minutes of near full body sun
exposure.

But I didn’t stop there. Each weekend day, I made an effort to hike or exercise wherever the
sun was shining. Sometimes that meant driving 45 minutes out of the city. Sometimes that
meant going to the beach with friends. Whatever the case, it didn’t matter to me — so long
as I was getting daily sun exposure between the hours of 10am and 3pm (the hours in which
our bodies can produce their own vitamin D3).

Can’t I just supplement with vitamin D?

It’s tough to say. On the one hand, if you’re severely vitamin D deficient or lack access to
regular sunlight, supplementation will likely help. It certainly did for Jared.

On the other hand, we still don’t fully understand how isolated forms of vitamins react in
our bodies. For example, 15 years ago doctors used to recommend supplementing with
vitamin D3 alone. But today, research reveals that vitamin D3 requires several adjunct
vitamins and minerals to prevent toxicity — three of which are vitamin A, vitamin K2, and
magnesium. If you’re supplementing with vitamin D3 and not also receiving proper amounts
of vitamin A, K2, and magnesium, your risk for arterial calcification may actually increase.

But is the same true for sun exposure? Can we get too much vitamin D from the sun and
increase our risks?

Not really. Our bodies have a built-in mechanism that prevents vitamin D toxicity through
sun exposure. It’s called a sunburn. After a long enough exposure, the sun’s heat on our
skin “photo-degrades” our precursors for vitamin D3 synthesis. This stops our bodies from
overproducing vitamin D3 — which is especially important if we’re lacking in vitamin D3’s
adjuncts and cofactors.

On top of that, the benefits of sunlight exposure extend beyond vitamin D3 synthesis. It
turns out that sunlight may also stimulate the production of nitric oxide — a known
vasodilator — in our blood vessels, which significantly lowers our blood pressure and
improves blood flow. Improved blood flow through nitric oxide release is actually one of the
mechanisms purported in low level laser therapies for hair regrowth. Knowing this, it’s no
surprise that the wavelengths utilized in LLLT devices are the same ones available to us via
the sun during summertime. Essentially, these LLLT devices just give us our summertime
density for hair.

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So, get outside, get into the sun, and reap benefits beyond vitamin D supplementation.

Avoid sunscreens
Finally, I suggest you stop using sunscreens. Firstly, sunscreens block UVB light, and UVB
light is the spectrum we need to synthesize vitamin D3. The more UVB blocked, the less
vitamin D3 created, the less benefit you reap from the sun.

Secondly, studies show that sunscreen users are actually more likely to burn than non-
sunscreen users! Why? It’s simple: sunscreen gives us a false sense of “long-lasting” sun
protection... but most sunscreen users never reapply. After an hour or so, sunscreen’s
effectiveness wanes, but sunscreen users continue to sit in the sun without reapplying —
assuming they’re still protected. The end result? They get burned, and often badly. Non-
sunscreen users are able to gauge the sun’s intensity more easily — as they can literally feel
its heat on their skin (when you apply sunscreen, this sensation slightly dissipates). As a
result, they’re more aware of when they’re starting to burn, and thereby more likely to cover
up before a burn becomes a problem.

If you feel like you’re burning, cover up or sit in the shade. When I’m outside and my skin
starts to feel too hot, I cover-up with a large hat or a sarong (light towel). The outfit combo
makes me look ridiculous, but who cares?

With that said, please be cognizant about your sun exposure. Know your limits.

Final sunlight takeaways

If you have the choice, always opt for sunlight exposure over a vitamin D3 supplement. Get
sunlight exposure between the hours of 10am-3pm when our bodies are capable of
synthesizing vitamin D3 from the sun. Aim for 15-45 minutes per day, with as much skin
exposed as possible, but adjust this depending on your comfort level and your likeliness to
burn (don’t overdo it). If you can’t reorient your schedule or don’t have access to sunlight,
take a supplement, but don’t abuse the supplement, and be sure to also supplement with
vitamin K2 and magnesium.

Finally, when you do get sun exposure, delay showering for as long as possible. Why?
Research suggests that sebum (yes, the same substance our hair can overproduce) likely
contains precursors we need to synthesize vitamin D3. Moreover, it may take up to 24-48
hours for our bodies to actually reabsorb our skin’s sebum and utilize its precursors to make
vitamin D3.

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If true, this explains why indigenous tribal groups have higher serum vitamin D3 levels than
Hawaiian surfers. These indigenous groups shower less frequently, whereas Hawaiian
surfers are constantly wading in water and washing away the sebum that would otherwise
have helped them make vitamin D3.

It should be no surprise that body soap also washes away our skin’s sebum. So, after a day
in the sun, delay showering! And when you do shower, maybe reduce your use of body soap
(so the surfactants don’t wash away the excess sebum).

Lastly — and it bears repeating — I don’t suggest you bake in the sun for six hours each day.
With most work schedules, that’s not really possible anyway. However, getting 15-45
minutes of sun exposure daily will help lift your levels significantly — so shoot for whatever
is manageable and without overdoing it.

If you’d like to read more about vitamin D and its connection to hair loss (and hormonal
health), I wrote an article that you can read here.

#4. Males: donate blood. Females: get a full iron panel

The dangers of excess iron
Iron is an important trace mineral , but too little or too much iron can have devastating
effects on our health (and hair).

Have you ever wondered why a significant portion of women often begin losing their hair
after menopause? Part of the reason is likely a decline in their estrogen levels — as tissue
estrogen appears to be protective against female hair loss in the scalp. However, there’s also
something to be said about iron accumulation.

Women’s menstrual cycles not only serve a reproductive purpose, but also result in low-level
blood loss over the course of their periods. With this blood loss, excess iron and calcium
that have made their way into the bloodstream from the diet is excreted. The end-result:
menstrual cycling helps keep a female’s iron levels low.

Interestingly, women with healthy menstrual cycles also have a significantly lower risk of
heart disease. Yet this protection stops with menopause. During menopause, we see a stop in
the menstrual cycle and, consequently, a reduction in estrogen levels and a stop in a
woman’s own built-in ability to deplete iron. The consequence? A sudden surge in retention
of iron in the blood... and something called iron overload.

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Iron overload in both men and women negatively affects the endocrine system and is linked
to infertility, hypothyroidism, diabetes, liver disease, osteoporosis, and hair loss. Excess iron
has also been linked to higher cancer rates because it is believed to increase free radical
damage, according to the Journal of the National Cancer Institute.

Excess iron generates oxidative stress (inflammation)

As excess iron accumulates in the blood, it activates reactive oxygen species which increase
oxidation (and thereby inflammation) in our blood vessels. Unfortunately, this inflammation
can extend beyond just our arterial walls. One study found that iron overload also damages
pancreatic cells and may be a major driver of insulin resistance. Another showed that iron
overload may drive part of the weight gain linked to metabolic disease. Another indicated
that iron overload can lead to fibrosis (i.e., scar tissue) in the hearts of mice.

Long-story short: if we want to maximize our ability to recover from wounds, minimize our
systemic inflammation, and minimize our chances of developing the conditions that cause
hair shedding disorders... we should take care to prevent an iron overload.

Iron overload is predominantly a male problem

While women have menstruation, men have no natural mechanism to rid their bodies of
excess iron. With our standard American diet chock full of fortified grains (i.e., added iron),
iron overload is now a concern for most men and post-menopausal women.

Don’t think you have iron overload? One study found that 13% of older men and women
had dangerously high levels of iron in their systems. Granted the age ranges were 67-96, the
study is still important because it sheds light on something that most people don’t think
about: the incidence of iron overload in Americans. There’s even a debate over whether the
medically established “normal” ranges of iron are too high (remember, their testing averages
are from people on a standard American diet — which furthers the argument that
subclinical iron overload may even be more prevalent than we currently presume).

If we have (or are at risk of) iron overload, then reducing our iron levels can have a
significant impact on improving insulin sensitivity and reducing overall systemic
inflammation. Therefore, depleting ourselves of excess iron can improve our health (and if
we have an associated shedding disorder, even our hair). The question is: how do we do it?

Blood donations: a tool to correct iron overload

The easiest way to help correct iron overload is to donate blood.

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Donating blood every two months (the minimum allowance between donations) will slowly
reduce iron levels and help prevent further accumulation. Donating blood is completely free,
and if you’re eligible, I recommend donating as often as possible. You’re not only helping
your own health and hair, but you’re also saving other people’s lives.

What if I can’t donate?

If you can’t donate, there are still other options. Firstly, there are health centers that allow
for therapeutic blood letting. I’d suggest looking into that option.

Otherwise, I’d recommend that if you’re at-risk of iron overload, you significantly pair back
your consumption of red meats and organ meats. Limit red meat consumption to 1-3 times
weekly, and completely eliminate organ meat consumption (we can get those nutrients
elsewhere). Instead, eat more white meats like chicken.

Next, consider food pairing. Pairing high iron meals with a cup of coffee or tea can reduce
iron absorption by 60-75% — but only for the type of iron found predominantly in plants
and grains (non-heme iron). If you want to reduce the absorption in iron found in meats,
you’ll need to inhibit heme iron. Calcium can inhibit both heme and non-heme iron
absorption. So, anytime you’re eating meat, have some dairy (but only if you’re not allergic).
And if you’re enjoying non-animal foods rich in iron, enjoy them with coffee or tea.

Interestingly, vitamin C (found in fruits) enhances iron absorption. So avoid having vitamin
C-rich foods (i.e., strawberries, oranges, etc.) while consuming iron-rich foods.

Coffee, tea, and calcium will help reduce the accumulation of excess iron in the body. And if
you’re concerned about your iron levels being too high (or low), feel free to get a full iron
panel, available here. In most parts of the U.S., you don’t need a requisition form and can
order the test yourself.

Otherwise, you get a partial (and free) iron test each time you donate blood. All blood
donation centers test your iron levels before allowing you to donate, and if you’re too low,
they’ll ask you to come back another time. Conversely, if your iron is too high, it’s a good
thing you’re there!

Females: if you’re losing hair, do a full iron panel (no matter what)
This is especially important for women with female hair thinning regardless of their age: a
significant driver of hair loss in women tends to be nutrient deficiencies, one of which is
commonly iron. So, get a full iron panel! Doing so is important, because we can’t always

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determine cause-and-effect from the partial iron readings we get during free blood draws.
More information on this is included in your regrowth roadmap action plan.

Any other lifestyle changes worth mentioning?

Yes, but I’m worried about overwhelming people into paralysis by analysis. Here’s why:

In 2000, a grocery store ran an experiment to see how the number of available product choices
might affect a customer’s propensity to make a purchase. On separate days of the week, the
store set up two displays of jellies: one display with 6 flavors; the other with 24 flavors. The
researchers hypothesized that with more choices, people would be able to find a flavor that
better suited them and thereby make more purchases.

They were wrong. Consumers exposed to 24 flavors were one-tenth as likely to buy any jelly
at all — compared to those exposed to 6 flavors. The implication? That if we face too many
choices, we diminish our ability to (1) pick a favorite choice, and (2) follow through with
“purchasing” that choice. Today, this same phenomenon now plays out in online dating.
When faced with an endless number of future partners, people become more indecisive, less
committal, and less willing to “choose” just one person.

That same logic applies to habit-forming, or making changes to our diets and lifestyles.

If I only provide three simple (but powerful) lifestyle changes: good sleep, consistent
sunlight, and regular blood donations (if applicable) — my hope is that you’ll be more likely
to follow through with them. This is exactly why I removed my earlier recommendations of
quitting shampoo and taking cold showers. Yes, I could provide you with a dozen more
changes that would probably improve our health (and maybe our hair). But in doing so, I’d
increase the risk of people not following through with any choice at all.

So, here are two more levers. But please do what is reasonable for you. Don’t feel compelled
to commit to the whole list. After all, research shows even lists can be stressful:

• Stay active, not sedentary. Evidence shows that daily walking improves fat and
carbohydrate metabolism, reduces systemic inflammation, and decreases the risk of the
conditions that commonly precede hair shedding disorders. In fact, chronic sitting might
potentially contribute to enlarged prostates in men due to the pressure sitting puts on the
prostate — which may explain why the condition is less common in more active men.
Unfortunately, 25% of American adults are nearly completely sedentary. It’s not 100%
your fault. The modern world has a built-in infrastructure which minimizes movement...

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 and we often have to do everything we can to fight against it to stay healthy. If you’re
curious about solutions in terms of exercise (and beyond) — I’ve written a three-part
article series on hair loss, activity levels, and exercise — which you can start here.

• Take control of stressful relationships. And not just personal, but professional. Studies
consistently show that when we feel out of control of a chronic stressor — be it a significant
other or a working environment — our stress levels (i.e., cortisol) stays elevated. This
leads to more systemic inflammation, and as a consequence, more obesity, metabolic
syndrome, cancers, and underlying conditions that cause hair shedding. Despite the
challenges in leaving these situations, setting healthy boundaries with these common
stressors can often make huge differences to your cortisol production, your systemic
inflammation, and your outlook on life.

Again, put yourself in a position to take action rather than feel overwhelmed from decision
paralysis by analysis. Stick to those three pieces of advice, and nothing more (unless you
truly have the bandwidth to do them without stress).

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Chapter recap
Here’s what we’ve learned in this chapter — captured in a single flowchart.

Use this to your advantage, and above all, don’t feel overwhelmed by its information. All of
these changes are within your control. And if you don’t make any of these changes, that’s
fine too. There are still plenty of people regrowing their hair from the massages — with zero
augmentations to their dietary or lifestyle choices.

Coming up
When it comes to maximizing our ability to recover from injuries, minimizing our systemic
inflammation, and minimizing the conditions that precede shedding disorders, there’s one
more major pillar worth mentioning: our microbiome. The bacteria in our microbiomes
helps us metabolize foods, regulate inflammation, and maintain hormonal balance. These
microbes also constitute 70% of our immune functionality. And believe it or not, poor gut
health may be one of the major factors that contributes to hypothyroidism, chronic
inflammation, and even hair shedding. The following chapter reveals how we can work with
our gut to improve our immune system, keep our hair, and live a healthier life. And in diving
into this chapter, we’ll finally have enough understanding to explain why people have seen
their hair loss halt with extreme diets (like all-meat and vitamin A-deplete diets).

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

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 C H A P T E R 12 :
THE MICROBIOME-HAIR LOSS
CONNECTION

Chapter summary:

• Our microbiome controls everything from the foods we crave to the way we fight
infection. And in the first world, the absence of certain microbes could explain why its
populations have more allergies, autoimmunity, and chronic conditions than those in
the third world.

• We examine two potential “microbial” contributors to hair loss: (1) the first world’s
absence of helminths, and (2) increased gut permeability. Each of these is linked to
chronic inflammation, hormonal imbalance, and the hair loss cascade. Resolving leaky
gut isn’t easy, but the solutions are simpler than you may think. In fact, you may
already be doing them.

• We’ll uncover revolutionary new pilot treatments for autoimmune-based hair loss
disorders — like alopecia areata. Promising treatments may reside in “fixing” our gut
health... and researchers are getting very creative with how to do this.

• Warning: much of the research supporting this chapter is still ongoing. While there’s
significant evidence supporting helminths and their benefits to reversing
autoimmunity, helminthic therapy is still an experimental treatment. So, please don’t
go and contract helminths in the name of hair health. I certainly didn’t.

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THE MICROBIOME-HAIR LOSS CONNECTION

Hair loss (and its absence) in the third world

My sister works in development and does a lot of international traveling. She’s spent time in
Senegal, Ghana, Haiti, India, China, Myanmar, Thailand, Nicaragua, Brazil, Vietnam, and has
also worked alongside many of these country’s communities.

When our family gets together over the holidays, she shares her stories and photos. Her
trips are inspiring. But on a personal level, her photos intrigued me for a different reason. In
all of my sister’s photos, almost none of these communities’ indigenous men were bald.
Most didn’t even have signs of thinning hair.

I also learned that many of these communities also lacked the same degree of heart disease
and autoimmunity crippling the first world. When my sister lived in Myanmar, she even had
a hard time explaining to people her cashew allergy — mainly because locals didn’t have a
word for “allergy” (since allergies there didn’t really exist). How is that possible?

How can entire communities of people — some of whom suffer from malnourishment, lack
access to clean drinking water, and walk around barefoot next to sewage — have full heads
of hair and significantly lower rates of allergies and autoimmunity?

This question was the driver behind my early years of hair loss research. Spoiler alert: it’s
still unanswered. But now that we’ve built a solid understanding of the causes of pattern
hair loss and hair shedding disorders — we can finally attempt to answer it.

Why might the third world have better hair than the first world?
At first, the answer seems obvious: genetics. But, as we’ve mentioned earlier, genes alone
can’t explain why the perceived incidence of hair loss is on-the-rise… or why one genetically
identical twin can bald faster than his counterpart… or why people moving from the third
world to the U.S. now report hair loss — despite no familial history of it... or why 60% of
college students in China (where baldness rates were once very low) now report thinning
hair.

The implications from these studies: (1) indigenous populations seem to retain more hair
than first world populations, (2) people who move from the third to the first world report

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more hair loss, and (3) third world countries that develop into first world countries report
hair loss earlier than ever before.

But why? Is it their diet? Lifestyle? Something else?

That’s what we’ll uncover in this chapter. We’ll try to answer this question by exploring how
shifts in diet and lifestyle might explain why the first world has more hair loss than the
third world, and why developing pockets of the third world might begin to experience more
hair loss.

Then, we’ll dive deeper and reveal how diet and lifestyle (while still influential) probably
can’t explain everything. Rather, there’s another (often overlooked) variable present in third
world countries and lacking in developed nations. This variable may not only explain the
third world’s lower incidence of autoimmunity and allergies but also its lower rates of hair
loss.

What is it? Differences in these populations’ gut microbiomes.

But before we get there, let’s explore what the third world often does better than the first —
despite a relative lack in resources: better diets and lifestyles.

Diet and lifestyle: does it explain better hair in the third world?
The American diet versus the third world diet
When we think about the standard American diet, we think about processed foods, sugar,
dairy, and grains – particularly, gluten-containing grains. Interestingly, many third world
nations don’t include gluten-containing grains as part of their dietary staples. For instance,
while data is limited on grain consumption in the developing world, my sister’s host
families in Senegal and Ghana almost entirely excluded wheat from their diets. This was
also the case in the rural communities in which she lived in East Asia.

Wheat (both white and whole) is a staple of the American diet. It’s found in cereals, pastas,
breads, beer, and even nutrition bars. And as we’ve learned, up to 35% of us have a low-
grade intolerance to it. The more gluten consumption, the more permeable our guts, the
more antibody activity toward gluten, gliadin, and our thyroid, the worse our thyroid
functionality, and the higher our chances for hypothyroidism — a disease which presents in
up to 10% of first-world adults. And that’s just looking at gluten. When we factor in the
effects of sugars, dairy, and beyond, these systemic inflammatory markers amplify (as do our
chances for the conditions that cause hair shedding disorders).

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So, one possibility is that Americans’ overconsumption of processed foods, gluten, sugars, and
dairy might ramp up systemic inflammation and increase our propensity for conditions
linked to hair shedding. Another possibility is that these foods (especially when eaten
throughout childhood) encourage more rapid growth — thereby influencing bone
remodeling, scalp structure, scalp tension, and our onset of pattern hair loss... sort of like
what we see in women with early-onset PCOS (i.e., larger skull sizes).

But, these are just hypotheses. Is there any hard evidence linking a change in the third
world’s diet and a higher incidence of hair loss (from hair shedding or pattern hair loss)?

It’s tough to say. But one documentary did attempt to make this case. Only it wasn’t about
gluten, sugar, or dairy. It was about another American dietary staple: meat.

“The China Study” film: is first world’s hair loss caused by meat?
Americans eat more meat than almost all other countries. In the film Forks Over Knives (a
documentary about “The China Study” and the benefits of a plant-based diet), the narrators
anecdotally state that increased meat consumption is associated with hair loss. They suggest
that alongside the introduction of Western foods in China came an increase in hair loss.
They also suggest that current generations of Hawaiian men experience more hair loss now
than ever before... ever since they deviated from their indigenous plant-based diet.

This terrified me. After watching the film, I became a vegetarian for over a year, and I even
tried two stints of veganism in hopes of preventing more hair loss. As we’ve previously
learned, this didn’t work for me (but again, it might work for you).

Since then, the film’s assertions about hair loss has been rebuked due to confounding
variables in the analysis. For instance, Hawaii’s increase in meat consumption also came
alongside an increase in processed foods (i.e., fortified grains, vegetable oils, etc.) — which
have shown to be problematic for our health and hair.

Nonetheless, the film brings up a great point: in any country, an increase in processed foods
tends to precede more disease states. So, maybe the reason why the first world suffers
disproportionately from hair loss is because, collectively, what we put in our bodies is junk.

That’s a fair argument, and I can buy into it in terms of diseases that lead to hair shedding
disorders. I can also stretch my imagination to say that maybe poor dieting can accelerate the
onset of pattern hair loss for those who are genetically predisposed... if we consider a
possible link between processed foods, sugars, child growth rates, bone remodeling, skull
shape, scalp tension, and androgen activity. But again, I’m not quite ready to stretch this far.

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So... what other evidence is there?

The American lifestyle versus the third world’s lifestyle

The third world lives entirely different lives than the people of developed countries. For
instance, in many indigenous communities, there aren’t office jobs. There’s farm and labor
work. So, unlike Americans, these communities aren’t (on a daily basis) sitting down for
12-15 hours, staring at bright screens, or sleeping just 6.8 hours per night. In other words,
they’re moving regularly, and they’re outdoors — getting regular sunlight.

So, when taking this into consideration, maybe it’s not only diet... but also a different
lifestyle that contributes to the first world’s higher incidence of hair loss. Again, nobody
knows.

These connections are anecdotal. Where’s the real evidence?

Unfortunately, I don’t know of any researchers working toward answering this question. As
such, we’re limited in the conclusions we can draw. We need to rely on anecdotes and
research from related fields to form a logical, rational hypothesis. We also need to be honest
with ourselves and recognize that science does not yet have an answer to these questions.

If diet and lifestyle were the only difference between the first and third world, I wouldn’t
have bothered dedicating an entire chapter to this topic. However, there’s another thing we
haven’t yet mentioned…

Our microbiome — the billions of microorganisms crawling around our skin and in our
intestines. These organisms influence our immunity, our ability to process nutrients, our
personalities, and maybe even our propensity to lose hair. To understand why, we need to
first understand just how powerful of a lever the microbiome is at influencing our health.

When I first wrote about the microbiome-hair loss connection (in 2014), the research was
lacking. Today, these ideas are rapidly evolving… with some research teams even looking
toward the microbiome for potential treatments.

It all starts with the “Old Friends Hypothesis”.

The “Old Friends Hypothesis”

Many of you are probably familiar with the Hygiene Hypothesis. It’s the idea that frequent
and recurrent exposure to dirt, colds, flus, and infections helps build up our immune system

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— especially when we’re younger. This idea came about after scientists discovered that
younger siblings from families with 3+ children had fewer allergies, which they
hypothesized to be the result of the younger children’s frequent exposure to parasites,
viruses, and bacteria from playing and surrounding themselves with older siblings.

The Old Friends Hypothesis is an extension of the Hygiene Hypothesis and takes this
concept a step further. It’s built off a simple fact: crawling on our skin and in our guts, we
host at least as many microorganism cells as we do human cells. Research shows that these
non-human cells help our bodies — from our gene expression and immunity to the amount
of hormones we produce to our overall mood and health. In fact, 70% of our immune
system is derived within our digestive tract — where most of our cells aren’t even human.
And so the Old Friends Hypothesis is simply that these non-human cells create a symbiotic
(i.e., beneficial) relationship with our bodies. These microbes, parasites, viruses, and
bacteria help us metabolize nutrients and keep bad bacteria at bay.

But the biggest takeaway of the hypothesis? If the presence of these microorganisms benefits
our bodies... then their absence may actually hurt us. And in the first world — where we are
overly sterile, pop antibiotics like candy, constantly wash our hands and bodies, and live a
life of shoes, clothing, walls, and other barriers to the outside world — maybe we’re sicker
simply because we’re lacking the microbes that once helped us regulate our health.

There’s actually great evidence supporting this belief — and how our absence of certain
microorganisms may even be linked to hair loss.

Example #1: lactobacillus reuteri

Lactobacillus reuteri is a microorganism that lives in our gut. It was once prevalent in ~40%
of first world humans, but in the last 40 years, that number is now closer to 10-20%.

Fascinatingly, lactobacillus reuteri seems to help regulate our vitamin D synthesis,

cholesterol levels, testosterone production... and possibly even the shine and texture of our
hair. Its mechanisms seem to be that the bacteria helps dampen our immune response to
stressors — and in doing so, reduces our levels of pro-inflammatory substances that usually
wreak havoc on our tissues. The end-result: healthier-looking skin, reduced disease states,
significant boosts to testosterone (in male mice), better thyroid functionality, and thicker
shinier hair. You can read more about its benefits right here.

Example #2: fecal transplants

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Ever heard of clostridium difficile? It’s a pathogenic bacteria that creates a lot of
inflammation in our guts (and can kill us in cases of recurrent colonization). In fact, this
bacteria kills nearly 30,000 Americans each year — mainly because it very quickly becomes
resistant to antibiotic treatment. As such, practitioners desperate to save their patients have
sometimes resorted to “alternative” treatments in an attempt to overcome antibiotic
resistant-c. difficile infections. One such alternative treatment: a fecal transplant.

This is when a healthy “donor” patient provides stool samples that are packaged into
supplements for an “infected” patient to insert or ingest. Since our stools contain much of
the bacteria from our own guts, this type of therapy is an attempt to transfer the gut
microbiome of a health individual into that of a sick individual.

It may sound gross, but if you’re facing certain death from recurrent c. difficile, you’re
willingness to try anything skyrockets. And, fascinatingly, these fecal transplants are
incredibly effective. One study showed that fecal transplants can cure 93% of c. difficile
infections. But the craziest part? Many “cured” patients end up matching the body mass
indexes of their donors... and sometimes even taking aspects of their personality.

It’s crazy to think about, but it goes to show us how powerful our microbiome can be in
terms of its influence on our immunity, hormonal balance, health, and even our cognition.
Healthy donors have a gut biome composition that can fight off c. difficile colonizations. But
ingesting donor’s bacteria, while life-saving, also might lead you to taking on aspects of that
donor’s health (and mood). For these reasons, I’m incredibly excited for the future of this
therapy.

So, is it also possible that fecal transplants allow us to take on aspects of someone’s “hair”?

Maybe. In this study, two patients infected with c. difficile tried fecal transplants.
Simultaneously, both had a condition called alopecia areata — an autoimmune form of hair
loss where our bodies begin to “attack” our hair follicles — sometimes leading to full-body
hairlessness.

Fascinatingly, after the fecal transplant, both patients reported hair regrowth in places that
had been bald for years. One patient showed a near-full hair recovery in his scalp The
implication: our gut bacteria may regulate our autoimmunity and the conditions preceding
hair shedding disorders. In order words, our guts can directly influence our hair.

So... back to the Old Friends Hypothesis. Aside from lactobacillus reuteri, is there anything
else our guts might be missing? Maybe an organism that once co-evolved with us... but due
to our first world living, is no longer present in our systems?

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Yes. Believe it or not, there’s a parasite that is nearly entirely eradicated from the first
world... and researchers are now realizing the benefits of hosting them. They’re called
helminths. These small intestinal-dwelling parasites influence anything from our immune
response to our food sensitivities... and even our ability to fight off autoimmunity and grow
hair. Here’s how:

Helminths: a possible missing link

Helminths, better known as hookworms, are tiny parasites that live in the small intestines
of their host. Helminths can enter the body through skin contact when walking barefoot in
soil with larvae in it, but, for the most part, they’re not passed freely from person-to-person.

Helminths possess a unique survival capability. Normally, when a parasite enters our bodies,
our immune system fights back by treating the parasite like an infection — inflaming the
affected region, inducing a fever, attacking the parasite, and eventually killing it. But when a
helminth enters our body, none of this really happens.

Instead, helminths modulate our t-cells (immune cells), tricking them into thinking these
parasites are non-threatening, so that our immune system doesn’t attack them. In fact,
helminths stay alive in our small intestines by continuously doing this — muting the
sensitivity of our own t-cells so that we no longer react to small stressors (namely, the
hookworms themselves). And, interestingly, this “trick” also leads to broader changes to our
own immune response.

Our bodies encounter small stressors everyday, and many of these are at or below the
inflammatory threshold of hookworms. To name a few: gluten, peanuts, shellfish, pollen,
dairy, and any other common first-world allergy. When a helminth modulates our own t-
cells to ensure its survival, it also modulates our reaction to these environmental stressors.
In the presence of helminths, we react to these stressors with less inflammation.

And the benefits of helminths may extend beyond allergies and to autoimmunity.

Helminths may explain lower allergies and autoimmunity in the third world
It is estimated that 40% of the world’s population has a helminth infection. Interestingly, in
the U.S., this number is closer to 0% . Hunter-gatherers and early Native Americans almost
universally carried helminthic parasites. Most of third world is infected with helminths, and
in the majority of cases, there are no symptoms at all. There’s even evidence that we co-
evolved inter-dependently with helminths, and that we might be more protected from
autoimmune conditions with an infection than without one.

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Today, scientists are even testing to see if introducing these worms can improve symptoms
of autoimmunity. It’s a treatment known as Helminthic Therapy — when a patient chooses
to self-infect with hookworms in hopes of treating their autoimmune condition. The
research is still in its infancy, but studies have shown serious promise. There have been
accounts of autoimmune disease remissions for allergies, Multiple Sclerosis, IBS, Crohn’s
Disease, and Ulcerative Colitis — to name only a few.

Is there a connection between helminths and hair loss?

Again, this is a stretch... but it’s certainly possible. How? Well, it seems like helminths
might help stave off (or reverse) the conditions that precede hair shedding disorders.

Once inside the small intestine, hookworms survive for three to five years by feeding off a
constant low-level supply of blood. So long as someone isn’t overly infected, a moderate
amount of hookworms will not only mute our inflammatory responses to small stressors,
but, more importantly, deplete our blood iron levels and prevent iron overload. As we
learned, iron overload is associated with inflammation, suppressed thyroid function,
hormonal imbalance, and the inflammatory cascade that can result in excessive hair
shedding. As such, depleting our iron to appropriate amounts is critical for anyone trying to
minimize inflammation and prevent future hair loss. Remember the theories behind why
most women begin losing their hair only after menopause? Helminths might possess the
same blood-cleansing benefits as menstruation.

This also means that helminths probably ingest some of the 1% of calcium that dissolves
into our bloodstream. This could help prevent calcification from occurring in other areas of
the body – like your arteries and capillaries near and around your scalp. In a way, helminths
are a natural form of blood letting - not dissimilar to blood donation. The fact that blood
donors typically have lower rates of heart disease should be enough to convince you of those
benefits. Keep iron and calcium at healthy levels in the blood, and you might prevent the
calcification and fibrosis that precede heart disease (a condition closely linked to pattern hair
loss).

Helminthic therapy and hair regrowth

If you’re interested in better understanding the topic, I encourage you to read An Epidemic of
Absence by Moises Velasquez-Manoff. The author details the theories behind helminthic
therapy and even his own experience self-infecting with helminths. He’s also a sufferer of
alopecia universalis — a more advanced form of the autoimmune disorder alopecia areata.
When he tried hookworm therapy, he even noted the growth of hair for the first time in

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decades. Most importantly, Velasquez-Manoff provides a historical perspective about the
implications of eradicating helminths and what to do if you’re interested in therapy.

Again, since I am not a medical professional, you need to consult your doctor if you’re
considering trying helminthic therapy (or anything else in this book). I cannot condone or
encourage the use of helminths. I’ve never tried helminthic therapy, and while I tend to view
these parasites in the same vein as a probiotic, experimentation here needs to be done under
the supervision of a doctor. As the research unfolds, I will continue to revise and update my
understanding of helminths and hair loss. For now, the ideas connecting hair loss and the
absence of helminths remain theoretical until studies validate (or invalidate) a true
association.

How can we improve our gut health?

The third world may have helminths (alongside a diet and lifestyle better aligned with our
evolutionary past), but those of us living in the first world can still make simple changes to
optimize our gut health and microbiome. In doing so, we can help reduce systemic
inflammation and become a healthier person in the process.

Microbial balance: keeping bacteria where it needs to be

When it comes to gut health, there are entire books on which bacteria belong in the gut,
which don’t, which help you metabolize nutrients, which steal nutrients, and which
supplements you should take to rebalance any microbial imbalances you might have.

This is not that kind of book, and for one simple reason. Beyond the presence of good and
bad bacteria, there’s something that matters more than your microbial make-up: our ability
to keep bad bacteria out of the bloodstream and good bacteria in our digestive tract. What
regulates this ability? Our gut permeability.

Resolving leaky gut should be our first priority for gut health
We’ve talked about leaky gut in earlier chapters. It’s when your intestinal walls become so
inflamed and torn that large, unwanted protein molecules slip through the walls’ cracks and
make their way into the bloodstream. In the case of gliadin (from gluten), this creates an
autoimmune attack on the thyroid. And we already know that lectins in our bloodstream
can bind to thyroid hormones and inhibit the ability for our endocrine system to function.
But what about bacteria?

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Bacteria in the blood increases inflammation
When our guts become too permeable, it’s not just protein molecules that get through… it’s
also bacteria.

There’s mounting evidence of a connection between blood levels of bacteria and heart
disease. For one, studies show that prolonged bacterial infections (and higher rates of
bacteria in the blood) increase arterial plaque. Secondly, for certain blood bacterial
infections, our bodies fight the infection by calcifying the bacteria. And finally, there are
bacterial strains that once inside our bloodstream can settle into our heart valves and cause
a life-threatening heart infection. Long story short, if we want to live long, keep our hair,
and keep arterial calcification and fibrosis at bay, we have to maintain a healthy blood-gut
barrier and keep good bacteria in and bad bacteria out.

How do we do that? We resolve leaky gut, and in doing so, optimize gut permeability.

This sounds difficult. I mean, we’re already trying to reverse hair loss. Now we need to fix
leaky gut? While it might seem like a daunting task, every single recommendation in this
book isn’t just about hair health, it’s also about gut health. If you’re taking into
consideration these recommendations, you’re already taking steps to resolve leaky gut.

Our dietary and lifestyle recommendations already target leaky gut

You’ll see that this book’s diet is relatively low in fiber. That’s no accident. There’s evidence
that too much fiber can aggravate our intestinal tract and create the conditions required for
leaky gut to occur. The same is true for lectins.

Not getting enough sunlight? New research suggests that the more vitamin D deficient you
are, the more susceptible your the intestinal wall is to damage. Based on this, it’s not
surprising that vitamin D deficiency is implicated in most autoimmune conditions.

And what about sleep? Well, it’s been known for almost twenty years that adequate sleep
helps regulate the proliferation of commensal bacteria... while sleep deprivation can
exacerbate bad bacterial overgrowths in the small intestine and beyond.

We could list dozens of more examples, but the main point is this: every single dietary and
lifestyle change from this book is designed to help prevent or reverse leaky gut... and in doing
so, promote the proliferation of our gut’s beneficial microflora, improve nutrient

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assimilation, and most importantly... minimize the conditions that precede hair shedding
disorders. The end-goal? To improve your immunity, your health, and even your hair.

The end of this book

There you have it: the major triggers that manifest pattern hair loss and hair shedding
disorders, as well as recommendations on how to stop the hair loss cascade from happening.
With that comes the end of this chapter and the major recommendations of this book.

In the next (and final) chapter, we’ll uncover how to boil this 60,000+ word book and
100,000+ word membership site into simple, actionable hair loss advice tailored to your
individual needs… all in under 60 seconds.

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Chapter recap
Hair loss seems less prevalent in the third versus first world; difference in genetics, diets,
and lifestyles likely don’t fully explain why. But, there’s another reason why pockets of the
third world seem more protected from pattern hair loss and hair shedding disorders: their
microbiome — specifically, how the commensal and symbiotic microorganisms in the gut
may influence someone’s propensity to keep their hair.

There are several examples why, but the evidence covered in this chapter revolves around l.
reuteri, fecal transplants, and helminthic therapy. Together, these treatments may make for
powerful weapons in the fight against autoimmune forms of hair loss... and even hair
shedding disorders.

Want to discuss this chapter?

Have questions about any of the research presented in this chapter? Want clarifications? We
want to keep things as organized as possible, and posting public questions will help
disseminate the information to everyone — so we can all benefit. As such, there’s a dedicated
thread for any and all chapter questions that you can access right here.

Otherwise, it’s time to recap everything we’ve learned... and begin building a customized
action plan catered to your age, gender, hair loss type, comfortability with drugs, time
availability, and your specific needs.

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 C H A P T E R 13 :
YO U R N E X T S T E P S ( AC T I O N P L A N )

Chapter summary:

• After reading a (nearly) 250-page book on hair loss, you may feel overwhelmed. What
do you do next? How do you build your own action plan? How can you streamline
your access to the content most relevant to you?

• This chapter does the heavy lifting for you: providing you with next steps for building
a plan, using the membership site, interacting with our forum, and even working one-
on-one with me (if that’s something that interests you).

• By the end, you’ll have a custom-made regrowth regimen tailored to your needs,
information on how to navigate the rest of this site, and the tools to interact with our
community.

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YO U R N E X T S T E P S ( AC T I O N P L A N )

Condensing this book into your own action plan

This book contains a lot of information, and taking it in at once can feel overwhelming.
After all, diagnosing your hair loss type, learning about hair loss science, uncovering your
treatment options, and building an action plan can feel like an Atlas task... especially after
reading 220+ pages of material. In fact, such a task might discourage you from pursuing any
hair loss action plan at all.

That’s exactly what I don’t want. This is why I’ve built an interactive questionnaire and a
membership site to streamline this process for you. Here, we’ll uncover the four next steps
you can take toward your journey to hair recovery. It starts with a summary of the book’s
materials that are most relevant to you. It’s followed by a custom-made action plan tailored
to your individual needs. And it ends with action-oriented next steps, troubleshooting
guides, and one way for us to interact.

1. Build a regrowth regimen (with the help of our survey)

I spent the last year trying to find a way to personalize the information on this site — so
that any hair loss sufferer can have instant access to a treatment plan most relevant to them.
The only way to do this? Spend the time building custom regrowth plans based on peoples’
individual needs. So, I designed a five-question interactive survey. Then I wrote 75+
individual hair loss action plans — all catered to someone’s age, gender, hair loss type,
comfortability with FDA-approved drugs, and daily time constraints. These plans condense
everything you just read into a regrowth regimen tailored specifically to you.

You can take that survey (and discover your action plan) right here.

If you’ve read this book cover-to-cover, you’ve probably already taken this survey (at the end
of the “Know Your Diagnosis” chapter). But now that you’ve finished the book, your
answers may have changed.

For instance, maybe after reading our “Becoming A Best Responder” chapters, you suspect
you may have androgenic alopecia + a hair shedding disorder. Maybe after reading our
ultimate guides on minoxidil and finasteride, you’ve decided for / against including those
treatments. In any case, it’s likely worth it to take the survey one more time. After all, as we

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deepen our understanding of hair loss, we also deepen our perspectives on how we might
treat it.

Again, that survey link is right here. Depending on your responses, you’ll find specific
dietary and lifestyle tweaks, treatment do’s and don’ts, and even next steps for lab tests
should you suspect a hair shedding disorder. This is all to maximize our chances of hair
recovery — and to streamline you to the information most relevant to your hair loss case.

2. Start a progress log

There’s no better way to hold yourself accountable than by announcing your regrowth
regimen to our community. In fact, I’d highly recommend starting a progress log. This
allows you to organize your thoughts in one place, begin photo-tracking your hair, and get
advice from fellow community members. Best of all, as our members glean insights into
what is and isn’t working, we can disseminate those learnings through our community.

Again, you can start your own progress log right here.

How to format your progress log

A great way to keep things organized is to copy, paste, and answer the following questions
in your progress log.

Post topic: [First name] [last initial], [Age], progress log

(1) What is your gender? [Male, female, other]

(2) How old were you when you started losing your hair? [Age]

(3) Which type(s) of hair loss do you suspect you have? [Androgenic alopecia, a
hair shedding disorder, both androgenic alopecia and a hair shedding disorder,
autoimmune hair loss, etc.]

(4) What is your hair loss protocol? [Try to get specific. Include details about your
daily regimen and supplements, topicals, and / or dietary / lifestyle changes. Include
any other health information you think is relevant, when you started the protocol,
and your plan moving forward.]

(5) Post photos of your hair loss. [Please see this photo-taking guide for directions
on how to take effective progress photos with relative ease.

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Here’s an example topic / post:

TYLER L., 40, progress log

(1) What is your gender? Male

(2) How old were you when you started losing your hair? 28

(3) Which type(s) of hair loss do you suspect you have? Androgenic alopecia

(4) What is your hair loss protocol? I’m trying the scalp massages + microneedling.
I’m following the massage protocol outlined here, however, I skip the massages on
weekends due to my travel schedule. I combine the massages with microneedling
once every 12 days as outlined here. I use a Derminator 2.0 at a 1.5mm needle depth.

I’m a lifelong vegetarian and track my micro- and macro- nutrients through
FitDay.com. I’ve adopted two of the lifestyle changes in the book (getting more sleep
and more sunlight), but I don’t plan on donating blood because my iron panels
showed low-normal iron levels. I take a daily curcumin supplement.

I started this protocol on April 13th, 2019. I will update my progress log with photos
once per month. If I don’t see progress after six months, I plan on adding in minoxidil.
If you have any questions or advice, please reach out!

(5) [Tyler’s photos should try to adhere to the standards set here].

3. Dig into our case studies

Some say the best way to learn is through failure... and I agree. I’ve learned more about my
body from testing (and failing) my way through dozens of different diets and hair loss
regimens. At the same time, sometimes we want to learn from someone else’s trials, errors,
failures, and triumphs.

Enter our 20+ case studies. These are 2,000+ word write-ups detailing years of my email
exchanges, trials, errors, and learnings from working with past readers. You’ll see how
someone’s regimen evolves every step of the way... with each case study teaching us 3+ key
takeaways to carry into our own regimens.

And if you’re looking for inspiration, dig into our success stories. These pages contain
dozens of before-after photos of past and present readers of this site — all to showcase their
hair changes to inspire us to continue with our current regimen.

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4. Leverage our community
For years, readers have left comments on this site’s articles asking for a forum — with the
intent to centralize our site’s community. Finally, this forum is here... and I’d love for you to
use it.

The organization of the forum is simple and intuitive. Any chapters / courses / guides / case
studies / interviews featured in the learning dashboard have their own dedicated discussion
threads. Otherwise, there’s a general discussion forum where you can post anything you’d
like (so long as it’s respectful). For instance, you can use our “General Discussion” section
to post new studies or research articles you find interesting. You can create a “Progress Log”
(as mentioned above). Or you can post things that are “Off Topic” to our hair — from
general health inquiries to personal discoveries to current events and beyond.

Above all, I encourage you to share your trials, errors, learnings, and successes — so that we
can all help each other achieve significant hair recovery.

5. Want personalized help? Let’s work together.

This book, site, and community should answer most of questions you may have about the
hair regrowth process. However, I also understand that others might desire one-on-one
support.

While I no longer provide one-on-one email support, I do offer 60-minute Skype calls —
where we can speak face-to-face through video chat and uncover more about your hair loss,
health history, what you’ve tried, what’s worked, what hasn’t, and then start toward
building a regrowth regimen custom-made to you. You’re also welcome to ask me anything
— from what I’m currently researching to questions about general health to troubleshooting
advice. I want to help however I can.

You can access my schedule (and book a call) right here.

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 T H A N K YO U

Chapter summary:

• A thank you for reading (and how to contact me).

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T H A N K YO U

Thank you for your time

I want to thank you for taking the time to read this book, and for your contribution to keep
this site running. My hope is that you now have a better understanding of hair loss: its
science, misconceptions, causes, and the levers we can target to resolve it.

I encourage you to reach out to me at any time if you truly don’t find answers to your
questions in this book, on this site, or in our community. While I can’t guarantee a
response, I try my best to answer everyone. My goal here is for you to succeed and save
time, energy, and money. I’d like to help however I can. I truly appreciate that you’ve
allowed me to share this research with you.

All my best,
Rob English
Founder, PerfectHairHealth.com
[email protected]

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