The Ultimate Hair Loss Flowchart: Why We Lose Our Hair

Why do men and women lose their hair to pattern hair loss (AGA)? Why does DHT cause hair loss in the scalp... but hair growth in the chest and face? This article is a systemic, scientific approach to explaining why we go bald, and why drugs like finasteride work wonders for stopping AGA, but not necessarily reversing it.

Written and reviewed by:
Rob English, Medical Editor

Read time: 15 minutes

What Causes Hair Loss?

If you ever google’d “what causes hair loss?”, you’ll find thousands of results saying hair loss is due to…

  • Genetics
  • DHT (dihydrotestosterone)
  • High testosterone

…and a million other one-liner answers.

The reality? These statements are too simple to be right or wrong. For instance:

Yes, our genes might predispose us to hair loss, but gene expression likely matters more than genes alone.

Yes, DHT (a hormone made from testosterone) is linked to hair loss… But only one kind of DHT: scalp tissue DHT. Paradoxically, serum (blood) DHT might protect us against hair loss, and body tissue DHT actually encourages body hair growth.

Yes, hair loss occurs in high-testosterone men… But it also occurs in low-testosterone men. What actually matters is the amount of testosterone converting into scalp tissue DHT – and why.

So how do we distinguish hair loss fact from fiction? As one reader recently wrote in…

“I have been losing my hair for about ten years and I don’t really know where to start because of the overload of information online. What do you recommend are the first steps I can take?”

Unfortunately, there’s no easy answer. So my #1 recommendation is: get informed.

Learn Everything You Can About Hair Loss Science

Don’t just read summary articles. Read peer-reviewed studies. And don’t just read abstracts. Read full papers. Don’t know a term? Look it up. Have a question? Email the author. You’d be surprised how many will get back to you.

The more you know, the better informed you are, the quicker you can sort out the misinformation.

Of course, not everyone can spend years of their life reading pubmed journals. And not everyone can access the full texts from studies. That’s why I wrote this article.

Inside This Article: The Causes Of Hair Loss Mapped Into A Flowchart

This a long post. It’s also a modified excerpt from the new book (this version is more science-heavy). The goals:

  1. Trace the causes of hair loss back to their roots.
  2. Package each piece of evidence into a master flowchart
  3. Use the flowchart as a tool to explain why most hair loss drugs fail to regrow much hair.

This is a systematic, scientific, comprehensive, evidence-based approach to answering why we lose our hair. And in the process, we’ll uncover…

  • The major (known) triggers of hair loss
  • The connection between, calcification, fibrosis, and thinning hair
  • The DHT paradox: why DHT encourages hair loss in the scalp but hair growth in the body
  • How to evaluate any hair loss drug before trying it (like Finasteride or Minoxidil)
  • What we should target if we want to achieve permanent hair regrowth

Any questions? Please reach out in the comments.

Important Note: since writing article, my views on pattern hair loss have evolved. While the following article helps to clarify two rate-limiting recovery factors in pattern hair loss, it fails to dive deep enough into the genetic predisposition of AGA, its potential relationship to mechanotransduction, a concrete explanation for the DHT paradox, and a rationale for the patterning of hair thinning in men and women.

Rather than continuously revise this article and distill what is (very) complex science into lay terms, I instead decided to write a manuscript and submit these ideas to peer-review. The paper was accepted in late 2017. You can read it in full right here, along with a lay person’s breakdown of (some of) its arguments here.

Otherwise, please consider this article a starting point to uncovering additional factors (beyond DHT) involved in androgenic alopecia. And, please disregard my original emphasis on diet, lifestyle, and testosterone:estrogen ratios. While these factors are certainly linked to systemic inflammation and non-androgenic forms of hair loss, the sources of inflammation in AGA are a little less clear, and likely less connected to these factors than I originally implied.

Tracing The Causes Of Hair Loss: Where To Begin?

Let’s start with what our fingers feel and our eyes see: our thinning hair and the skin underneath it.

A Close-Up Of The Balding Scalp

Where is your hair thinning? Temples? Vertex? All over? Using your hands, feel the thinning areas of your scalp. Then feel your non-thinning areas (the sides or back of your head).

Notice anything? In balding sites, our skin feels thicker, less pliable, and significantly less elastic. Touch the green part of your scalp, then the blue. Feel the difference.

Balding Regions Have Thicker, Tighter Skin

Balding Thicker Skin

Next, grab a mirror and look at your head. Do you see any visual differences in your balding versus non-balding regions?

In balding areas, many men’s scalps have a certain “shine” to them. You might see this too. In advanced stages, some balding regions can even look swollen.

Balding Regions Are Shinier, More Swollen

Why do balding parts of the scalp feel tighter, thicker, and look shinier and more swollen?

Balding Shinier Skin

Your balding scalp is tighter, thicker, and shinier because of an overproduction of something called collagen.

Collagen is the fibrous protein that makes up our connective tissues, like our skin. If you ever get a small paper cut, your skin cells make new collagen to repair the wound and make the skin as smooth as it used to be. But if we cut our skin too deeply, our skin can make too much collagen.

But it’s not just too much collagen. It’s disorganized collagen cross-hatchings. This leads to imperfect healing and scar tissue.

Balding Skin Is Tighter, Thicker, And Shinier Due To Excess (Disorganized) Collagen

Interestingly, men with pattern hair loss have four times the amount of collagen fibers at the temples and vertex than men with no hair loss at all. What does that indicate? Balding skin is ridden with scar tissue.

Disorganized (Excess) Collagen Is Also Called Fibrosis

There’s another word to describe the disorganized, over-accumulation of collagen: fibrosis. And while our balding scalps are wrought with excess collagen, our thinning follicles are also surrounded by it! This is called perifollicular fibrosis.

In other words… where there’s hair loss, there’s fibrosis. But does fibrosis cause hair loss?

We can find our answer by studying a rare autoimmune condition that makes people over accumulate collagen and fibrosis. It’s called scleroderma.

The Scleroderma-Fibrosis-Hair Loss Connection

In scleroderma, the body starts to overproduce collagen – sometimes in the lungs, hands, and even the scalp. Regardless of the location, this process results in the same visual symptoms we see in balding scalps: tighter, thicker, 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’s the same skin quality. Same shine, same thickening, same swelling.

But most interestingly, for those who develop scleroderma in the scalp, hair loss soon follows.

That’s a critical piece of information. It confirms that excess collagen and fibrosis occur before hair loss starts. They precede hair thinning. Excess collagen and fibrosis accumulate first, then hair loss comes later.

Scalp Fibrosis Develops Before Hair Loss

Knowing this, we can begin to build our flowchart:

Fibrosis Hair Loss

But how exactly does disorganized, excess collagen (or fibrosis) lead to hair loss?

Fibrosis Restricts Blood Flow To Our Hair Follicles

Body tissues wrought with excess collagen and fibrosis also have lower blood flow. This is even documented in balding regions – blood flow is restricted in thinning areas of our scalps. The more collagen and fibrosis, the more blood flow is restricted.

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.

Lower Blood Flow Lowers Your Tissue’s Oxygen Supply

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. Studies confirm that balding scalp regions are hypoxic.

If a tissue is chronically suffering from low blood flow and low oxygen, hair cannot grow.

In one study, men’s balding regions had just 60% the oxygen levels of non-balding areas. Men with no hair loss had oxygen levels nearly the same all across their entire scalp.

Knowing this, we’ve just added to our flowchart. Excess collagen (fibrosis) decreases blood flow and oxygen, and in doing so, “chokes out” our hair follicles. This leads to hair loss.

Fibrosis Blood Flow Oxygen Hair Loss

Now, are there any other conditions in a balding scalp that might also decrease blood flow and thereby oxygen to our follicles?

Yes. Beneath our scalp skin is another contributing factor: arterial calcification.

Our Scalps Have Become Partially Calcified

It’s not just fibrosis that reduces blood flow and oxygen to our hair. In balding areas, the blood vessels that indirectly support our follicles – in the lower layers of the scalp – may have also become calcified!

Dr. Frederick Hoelzel in the American Medical Association published the connection between scalp calcification, restricted blood flow, and hair loss over 70 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, our scalp bones and blood vessels supporting the follicles are calcified. If an artery is calcified, blood flow is significantly restricted.

What Is Calcification?

According to medical 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.

And finally, it’s also important to note that calcification is not necessarily caused by a calcium-rich diet.

So back to our flowchart. Does calcification cause fibrosis?

Probably not. Most research suggests 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 soft tissue calcification, others just suffer from an overproduction of collagen. So calcification does not have to happen before fibrosis and 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 “thicker, tighter, shinier skin.”

Calcification Fibrosis Hair Loss

Now let’s start tracing this chart backwards. We’ve gone as far as calcification and fibrosis. So what triggers both?

Calcification And Fibrosis Precede Hair Loss…

…But What Causes Calcification And Fibrosis?

We can get an idea of what might be causing these conditions if we look at the people most likely to develop arterial calcification and fibrosis: men.

Men are almost twice as likely as women to develop calcified arterial lesions. Why is that? Researchers have long suspected that androgens might be to blame. Read: testosterone and DHT – or dihydrotestosterone.

Why is this so interesting?

Well, most doctors agree that DHT causes hair loss… But none actually know how DHT causes hair loss. If DHT triggers calcification and fibrosis, this explains how DHT causes hair loss. But to confirm this, we need to know if androgens (like DHT) actually precede arterial calcification and fibrosis.

The DHT-Calcification-Fibrosis Connection

Does DHT Cause Calcification And Fibrosis?

Research here is mixed.

On the one hand, 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 (outside of our bodies), increased androgens don’t cause calcification. In these tests, androgens protect against calcification.

This suggests two things:

  1. Androgens alone don’t cause calcification
  2. The test tube studies are missing at least one variable. It must be that increased androgens plus at least one “mystery variable” leads to calcification – but not androgens by themselves.

DHT is the main androgen associated with pattern hair loss. But we also know that DHT alone doesn’t cause calcification and fibrosis… So DHT by itself can’t be the problem.

What does this suggest?

In the scalp, increased DHT plus these “mystery variables” precede both calcification and fibrosis. Knowing this, here’s our new flowchart:

Scalp DHT Fibrosis Calcification

So what could these mystery variables be?

Well, there are two. The first is an increase in androgen receptors. The second is an imbalance of calcification regulators. And explaining both are a bit of a mouthful. So bear with me.

A Crash Course On DHT, Androgen Receptors, And Calcification Regulators

We know that androgens alone don’t cause calcification, and that in the body, androgens must be interacting with other variables to cause calcification and fibrosis. So, what are those variables?

It appears there are two. And in 2016, researchers finally confirmed the first one: androgen receptors.

What Is An Androgen Receptor?

An androgen receptor (AR) is the place inside a cell where androgens – like testosterone and DHT – attach themselves. Think of an androgen receptor (AR) like the landing pad for DHT. Without its landing pad, DHT doesn’t bind to the cell.

Here’s a visual. This is a cell, and the yellow puzzle pieces (labeled AR) are androgen receptors:

Androgen Receptor


Androgen receptors aren’t always active. They typically turn on in the presence of DHT or testosterone, then turn off when these hormones aren’t around.

The Connection Between Increased DHT And Increased Androgen Receptors

In our scalp tissues, increased androgens turn on more androgen receptors, and together, the increased DHT plus the increased androgen receptors results in calcification. Both DHT and androgen receptors must increase (not just one) for calcification to occur.

 Interestingly, DHT plus androgen receptors also increase fibrosis in heart cells.

In other words, increased DHT + increased androgen receptors precede both calcification and fibrosis.

DHT Androgen Receptor Hair Loss

But here’s where things get tricky… Increased androgen receptors aren’t the only other variable. We know this because of DHT’s biggest paradox:

Increased tissue DHT encourages hair loss in the scalp, but encourages hair growth in the face and body.

That means that in our hairy facial and body tissues, calcification and fibrosis don’t occur. Why? Because in our bodies and face, increased DHT instead encourages hair growth – just the opposite of our scalps.

If our flowchart is accurate, this means that in the body and face, when DHT increases, androgen receptors must not increase. Otherwise, our body and facial tissues would also calcify, and hair wouldn’t grow.

But as it turns out, both balding scalps and hair-bearing body and facial tissues have increased DHT and increased androgen receptors… Yet hairy body and facial parts aren’t calcified or filled with fibrosis.

What does all of this mean?

In addition to DHT and androgen receptors, another factor must also be causing calcification and fibrosis. Either something is protecting our body and face from fibrosis and calcification, or something is causing both to happen in our scalps.

Taking this into account, here’s our new flowchart:

DHT Androgen Receptors Mystery Hair Loss

So, what is this new mystery variable? There are several contenders, but diving into all of them would turn this already-monstrous post into a full-blown book.

The reality is, we don’t yet know for sure.

The reason why: 99% of researchers still abide to the DHT-sensitivity argument. They say that “genetics” makes our hair follicles more sensitive to DHT, and that for unknown reasons, DHT accumulates in the scalp and eventually causes hair loss. To my knowledge, there are no current studies even exploring scalp DHT’s connection to calcification (even though when we look at broader research, the connection seems obvious).

On top of that, researchers only recently confirmed (in 2016!) that both an increase in androgens and androgen receptors are needed to cause calcification, not just one. This discovery came from cardiovascular researchers and not hair loss researchers. These fields don’t really talk to each other. Neither is very aware of the other’s work. As a result, our third mystery variable remains a mystery.

But even still, we can make a very strong case for what this variable could be.

Uncovering The New Mystery Variable

Here’s what we know: if we inject regular mice with DHT, they develop calcification. But if we inject DHT into mice who can’t produce androgen receptors, no calcification occurs. Why?

Let’s start by looking at the “engineered” mice who can’t express androgen receptors. When they receive DHT, their bodies respond by…

  1. Activating proteins associated with calcification inhibition
  2. Deactivating proteins associated with calcification induction

In other words, these engineered mice turn on proteins that suppress calcification, and turn off proteins that encourage calcium buildup. The end result: no calcification.

So how do the regular mice – the ones with androgen receptors – respond to a DHT injection? Just the opposite. When these mice receive DHT, their bodies…

  1. Turn on proteins that encourage calcium buildup
  2. Turn off proteins that usually suppress calcium buildup

The result? Calcified arteries.

This is important. Surrounding our bodies and facial hair, we don’t develop the same calcification or fibrosis that we see in balding regions of the scalp. The same isn’t true for our scalp hair. This suggests one thing:

Our new mystery variable is likely, among other things, an imbalance of calcification regulators.

What Are Calcification Regulators?

Calcification regulators are a set of (mostly) proteins with many names and functions. They regulate whether your tissues accumulate or release calcium. We won’t dive into each of them, but if you want to do more research, here are some examples.

For the calcification inhibitors, there’s…

For the calcification inducers, there’s…

Not surprisingly, studies have linked each of these “inducers” to hair loss… but no one’s yet identified their relationships to calcification.

The Hair Loss Triple Threat: Increased DHT + Increased Androgen Receptors + Imbalanced Calcification Regulators

Remember, we need three factors for calcification and fibrosis to occur: increased DHT, increased androgen receptors, plus an imbalance of calcification regulators.

This new flowchart checks out against all the available evidence, including the DHT paradox:

DHT Androgen Receptors Imbalanced Calcification Regulators Hair Loss

A Quick Recap:

  1. Androgen receptors (AR) are the places inside our cells where androgens – like DHT – attach themselves. Androgen receptors often turn on or off depending on whether androgens are near. In order for calcification and fibrosis to occur, we need an increase in androgens (DHT) and an increase in androgen receptors.
  2. At the same time, there must also be an imbalance of calcification regulators. Calcification regulators are a set of molecules, enzymes, and proteins that control whether our tissues store calcium. There are two categories: calcification inducers (promoters) or calcification inhibitors (suppressors). If our body tissues activate too many inducers and too few inhibitors, calcification will accumulate.
  3. Imbalanced calcification regulators explain the DHT paradox – or why DHT encourages hair loss in the scalp but hair growth in the body and face. These regulators stay balanced in hair-bearing body and facial tissues. These don’t calcify. But in the scalp, more inducers than inhibitors activate. The result? Scalp calcification and fibrosis.

We need a combination of all three factors to induce calcification and fibrosis:

  1. Increased DHT
  2. Increased androgen receptors
  3. Imbalanced calcification regulators

Now let’s start tracing this flowchart backwards again.

What could possibly trigger increased DHT, increased androgen receptors, and imbalanced calcification regulators simultaneously?

There are likely two main causes. The first is chronic inflammation. The second is a hormonal imbalance.

Cause #1: Chronic Inflammation

What Is Inflammation?

Inflammation is our bodies’ natural reaction to stressors, like an injury, infection, or toxic chemicals.

For instance, say we stub our toe on a door. Our bodies recognize this injury as a “threat”. Then they activate enzymes, proteins, and hormones to kickstart the healing process. These molecules assess the damage, then determine how much our toe should swell (the pro-inflammatory response) and when to activate repair proteins (the anti-inflammatory response). This is all natural, normal, and healthy.

Chronic inflammation is not healthy. This is when inflammation 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 (read: fibrosis).

Interestingly, increased DHT isn’t just found in balding scalps… It’s also found in inflamed body tissues. There’s even evidence that DHT actually helps regulate inflammation, and that in some tissues, DHT is anti-inflammatory.

This suggests that increased DHT is a part of the inflammatory process. DHT binds to tissues after inflammation occurs. And in our balding regions, if DHT is chronically elevated, our scalps are also probably chronically inflamed.

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

Chronic inflammation is the gun. The DHT-AR-calcification regulator imbalance is the trigger.

But there’s one more “gun” that fires calcification and fibrosis… A hormonal imbalance.

Cause #2: Hormonal Imbalance

Hair loss is closely connected to a hormonal imbalance. Specifically, our testosterone:estrogen ratio.

In women, thinning hair has been linked to higher testosterone:estrogen ratios than non-thinning women. In younger balding men, elevated estrogen levels are also common.

But this is just an association… Where does our T:E ratio fall into our flowchart? Evidence shows that this imbalance happens before calcification and fibrosis.

The T:E-Calcification Connection

Our T:E ratio may actually control which calcification regulators our bodies activate.

Remember: if too many calcification inducers and too few calcification inhibitors are active, calcification occurs.

Our body’s T:E ratio is something that helps “regulate” our calcification regulators. If our T:E ratio is imbalanced, we’re at a higher risk of calcification.

This explains why an imbalanced T:E ratio is so strongly associated with heart disease. In men, lower testosterone levels are associated with higher rates of calcification and stroke. Low testosterone men have a near two-fold increase risk in morbidity. They also suffer from higher arterial stiffness (think: fibrosis). Finally, men with higher estrogen levels are also more likely to develop arterial calcification.

In women, low estrogen levels are associated with higher arterial calcification. Women with polycystic ovary syndrome and high testosterone also have higher rates of arterial calcification. The same is true for women receiving testosterone injections after menopause – the time when their estrogen levels plummet.

So let’s add chronic inflammation and an imbalanced T:E ratio to our flowchart:

Chronic Inflammation Hormonal Imbalance DHT Hair Loss

Now for one final question…

What Triggers Chronic Inflammation And A Testosterone:Estrogen Imbalance?

While there are thousands of factors that contribute to chronic inflammation, an imbalanced T:E ratio, and the conditions that cascade into hair loss, there are four big ones…

Our diet, lifestyle, microbiome, and scalp environment.

For purposes of this article, we’re not going to trace these pillars back any further. The new book covers each pillar in detail – its triggers and what to do about them. For now, here’s the foundation of our hair loss flowchart.

The Master Hair Loss Flowchart

Ultimate Hair Loss Flowchart

This chart is logic-checked against the scientific literature on DHT, hair loss, calcification, fibrosis, and everything in between. It’s a pretty far step from all the one-line answers doctors tell you, like “DHT causes hair loss” or, “You lose hair when you’re stressed.”

But most importantly, this chart is a tool that allows us to evaluate hair loss treatments. So let’s start using it!

Using The Master Flowchart To Evaluate Hair Loss Drugs

Our flowchart explains not only why a drug like Minoxidil is relatively ineffective at reversing hair loss, but also why Finasteride might be great at stopping hair loss but less effective at regrowing hair. (Note: for a quick overview of Minoxidil and Finasteride, read this).

Minoxidil Versus Our Flowchart

Minoxidil works by providing more blood flow to the follicles. Where is “blood flow” implicated on our flowchart?

Almost right at the bottom (after calcification and fibrosis).

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.

Increasing blood flow helps our follicles temporarily. But because Minoxidil doesn’t reverse the calcified, fibrotic condition of 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 tissue DHT from accumulating in our scalps. Where does this take place on our flowchart?

Right before calcification and fibrosis.

Finasteride Minoxidil Hair Loss Flowchart

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

But because calcification and fibrosis are further downstream to DHT, and because calcification and fibrosis are chronic progressive conditions, then reducing DHT won’t actually reverse these conditions! It’ll only slow or stop their progression. This is why Finasteride is great at arresting hair loss, but not at regrowing much 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 you understand a drug’s mechanism (how it works), you can look at the flowchart and evaluate which part of the hair loss 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 arrest hair loss, but since it doesn’t address pre-existing calcification or fibrosis, it’s limited in completely reversing the condition.

Caffeine topicals help boost blood flow to our follicles. But decreased blood flow is the result of calcification and fibrosis buildup, and unless we reverse those conditions and their triggers, the benefits of boosted blood flow will be short-lived.

Hair transplants work by transplanting healthy hair follicles from the back of your head to thinning regions. But since thinning regions are ridden with calcification and fibrosis, transplanted hairs may eventually thin too – which is why so many people experience failed hair transplants.

Every 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.

Calcification And Fibrosis Are The Two Biggest Hurdles To Hair Recovery

If we want to regrow lost hair, we need to restore the environment of the scalp back to its original state – reversing calcification and fibrosis – and restoring blood flow to dormant follicles so they can turn terminal once again. It’s definitely not an easy path forward, but it’s possible.

Beyond Hair: Why Calcification And Fibrosis Matter

If you’re suffering from hair loss and you think that calcification and fibrosis are only happening on top of your scalp, you’re probably wrong.

Calcification and fibrosis can happen in vessels and soft tissues everywhere in our bodies. And in fact, pattern baldness is closely associated with heart disease. As an article from Harvard states:

“Calcium can accumulate in the arterial plaque that develops after an injury to the vessel wall. The plaque is usually soft to begin with, but eventually tends to harden and become calcified.”

If we eliminate the triggers of calcification and fibrosis, we’re not just targeting hair loss… We’re also helping to halt the progression of calcification in other parts of our bodies. We’re positioning ourselves to become healthier, happier, and longer-living.

It’s Easy To Prevent Calcification. It’s Hard To Reverse It.

It’s much easier to prevent calcification and fibrosis than it is to reverse these conditions.

For instance, the right diet can significantly stop the development of calcification, but diet rarely reverses calcification. This is why, in most cases, dietary changes don’t result in significant hair regrowth. So the next time you see an ad claiming “one simple diet trick” can regrow hair, don’t buy into it.

Final Takeaways

Many people try to make hair loss sound like a “one cause, one solution” problem – but this just isn’t reality.

Calcification and fibrosis are the two biggest hurdles to hair recovery.

Drugs like Finasteride decrease scalp DHT, but they do little to reverse any of the calcification and fibrosis already present in our scalps. As a result, most hair loss drugs only slow or arrest hair loss. They don’t necessarily regrow any hair.

Questions? You can reach me in the comments section any time.

190 thoughts on “The Ultimate Hair Loss Flowchart: Why We Lose Our Hair”

  1. Hi Rob,

    I believe that another cause of restriction of hair blood flow could be because of Spinal disc subluxation which pinch the nerves that connect with the arteries going to the scalp. This is a good animation website that shows exactly which vertebrae are responsible for this, I have also seen some people discuss the relationship between scoliosis and hair loss, it could be because of this reason but I am not exactly sure.

    You can see that T1-T3 are responsible for this. What is your opinion on this?

    • Thanks for sharing this. It’s certainly possible. The big challenge is linking the incidence of subluxation to men more than women, and then the “pattern” of hair loss in both men and women. It’s possible that androgens encourage more bone growth for men versus women and that this could more commonly result in subluxation, but I’m not quite sure that this explains all the differences that account for different thinning in men versus women. In any case, I’ll look into this more in the coming days and report back if I find any linking factors.


      • Hey. I have very different question for you.

        So. I am 25 and I am taking steroids about 3 years with my 3 friends. What is interesting , No one from my 3 friends doesn’t have any problems with hair, Just me. I Lost some of my hair when my diet was very poor. In my family these problem was not quite big so I don’t think thats’s my genetics was so bad.

        It’s obvious that I have bigger level of androgens and DHT but other people who taking so much dose of testosterone may have a lot of hairs after many years.

        My question is. Is possible to retrieve hair with bigger level of DHT , androgens? I conclude yes from your article but your response is very important to me. Is possible that scalp massage may help in my case too?

      • There are two things that come to mind here.

        1) Scalp tissue DHT conversion

        When it comes to steroids and hair loss, what matters more isn’t the amount of circulating DHT, but rather the amount of free testosterone converting into scalp tissue DHT. If you’ve read this article, you know that all kinds of DHT and testosterone shouldn’t be feared, and in some cases, DHT and testosterone may even be protective against hair loss and its preceding conditions.

        While there’s limited evidence, I find that those taking steroids aren’t necessarily doomed to lose their hair. But if steroid users experience hair loss while cycling, it probably has less to do with total increased androgens and more to do with increased scalp tissue DHT. Any number of things could increase the conversion of free testosterone to scalp tissue DHT – diet, lifestyle, the microbiome, and scalp environment being four worth mentioning (see the flowchart). And in this case, especially scalp environment. If there’s too much tension in scalp chronically stretching the galea, this encourages an inflammatory response in the scalp skin. Men have higher circulating androgens, and as a result, their bodies utilize more androgens during inflammatory responses / healing. DHT (which is anti-inflammatory in many tissues and healing processes) binds to the affected regions as part of the healing process. But that tension never goes away. The scalp stays inflamed. And without inflammation resolution, the DHT never leaves. Now couple that with the effect of steroids: a massive increase in the amount of total testosterone (especially free testosterone). If this mechanical stress is already present in the scalp before steroid cycling, then that conversion of free testosterone to scalp tissue DHT will explode as you increase androgens exogenously. The end-result: accelerated hair loss.

        The net – if you’re already expressing symptoms of male pattern hair loss before steroid use, or have any predisposition to it due to gene expression, scalp tension, diet, lifestyle, microbiome, etc. – then steroids will accelerate your hair loss. If you have none of these problems, steroids may not affect the hair (in the case of your friends).

        2) In some cases, steroids may increase estrogen and imbalance the testosterone:estrogen ratio.

        If you receive exogenous testosterone via steroids or testosterone replacement therapy (TRT), that doesn’t mean that testosterone stays as testosterone inside your body.

        Testosterone can be converted into estrogen via aromatase enzymes. Aromatase levels shift with age (the older men are, the more likely they are to aromatize free testosterone into either DHT or estradiol – a type of estrogen). Aromatase levels are also partially controlled by our diet, lifestyle, and microbiome.

        If you choose to do steroids or TRT, there’s no way to tell how much of that exogenous testosterone is going to convert into estrogen. But for men on steroids / TRT, oftentimes way more estrogen converts than ever expected. We know how important the testosterone:estrogen ratio is for both men and women. That above article also covers that topic. The net – men with lower testosterone:estrogen ratios tend to experience higher rates of atherosclerosis and arterial calcification… The same calcification implemented in pattern hair loss. So keep these ratios (and your hormones) in check.

        Are you also taking an aromatase inhibitor? It’s highly advised by most doctors prescribing TRT. Otherwise, you risk exacerbating hormonal imbalances.

        RE: massages–

        They help in most cases, but in yours, I think it’s firstly more important to get your hormones back in check. That means diet, lifestyle, and maybe a reevaluation of the benefits of steroids (and an exit strategy) Doing so will decrease shedding and in most cases make the massages several times more effective. I still believe anyone can make significant recoveries from MPB – even steroid users.


      • I took for a while examastane but this medicine also casues hair loss very often. I don’t know why. Examastane is a drug against estradiol. I also took cabaser, medicine against prolactine when I was taking nandrolone. Now I am on a 200mg test per week. It’s low amount of test but bigger than normal. I saw my hairloss when I have big amount of steroids for example trenobolone . Androgenic rate in compare to testosterone is 5:1. Now I am taking low doses of testesterone and I consider what to do now.

        Be on steroids or try paleo diet with massage and dose of supplements.

        So in other words. I am taking steroids now . We know that DHT is not only one problem.
        It’s obvious that my case is because of taking steroids but if taking steroids and decalcification( I mean mainly K2,D3 and massage,pinching) could prevent hairloss or even retrieve hair. I suppose that you can’t give me ultimately response but what you think?
        Many of guys , bodybuiders , old bodybuilders have hair all the time . As far as I know in years of 70′ these poeple have a huge amount of testosterone and no problems with hair. This is very interesting.

        One of my friends which took with me steroids had much worse hairline than me even when he was 17. Now he is 25 and after 3 year of steroids cycle and his hairline is the same as before. It’s weird

        In my family balndess of course exist but my dad ( he is now 50 and have the same hairline like me now at 25)

        Thans for the response. I appreciate that:) Sorry for my English. I am writing from Poland:)

      • You can certainly try the mechanical stimulation exercises + vitamin D3 and vitamin K2. But I still think you may need to reevaluate steroid use. I agree that testosterone and DHT by themselves don’t cause hair loss, which is why some older steroid users at your gym may still have healthy hair. But steroid’s effects on hair health vary from person to person. At this point, the only way you can determine steroid’s impact on your hair is probably by cycling off them and gauging any changes. I don’t have any advice on the best approach to do that.

      • Hey Rob, i’d like to talk with you sometime if possible. I’m going thru the male pattern baldness thing going on since i was 17, and i’m 46 now. But something happened to me at age 41, and well i had lost a 9 yr job as a general manager and i went thru a lot of stress for 5 months and i have to admit i drank 12 beers a day during this time, but basically i got really skinny and started growing thick hair on my whole scalp, even in the front in which i hadn’t seen growth since i was 16. I was low on money, but i ate omnivore as i do now, and i didn’t smoke during my unemployment, and my hair felt so healthy. But i felt like i had lost my identity by losing my job and all the employees/customers relationships, and it was so bad that that i literally felt like there was a pulling on my heart during that period, and i had trouble sleeping. But the front of my scalp hair grew to over 1/4 of an inch and then i got another job and the heart pulling thing had passed and i puffed back up and lost what i had gained in my hair growth. Since then I have tried to recreate what caused my hair growth, but with with little results. I think mucus falls into the inflammation and puffing back up, but going thru this made me hopeful, that the answer is close, because i had next to nothing and the same to lose during that time. But i want to say that you really seem close, and i do like how you are closing the gap in a real way!

    • I think you’ve got something here, not for everyone certainly, but it may explain hair loss on one side of the head. I’m a post-menopausal woman and know hairloss comes with the package however, thank great genes, I had a rocking head of hair to begin with! When I started to lose it my initial thought was “great, no more getting it thinned at the hair dressers” but it never leveled out. Now over 5 years later (and yes I got EVERYTHING checked) one side of my head is about half as thick as the other and no one can explain why. I do supplement with vitamins but really try to get what I need from food. I’ve been using Rogain for around 2 years but really never saw that much of a change until recently but not on the side losing the hair!! I had a thinning temple (L) so I thought I’d try the rogain on it (previously I’d only done the right side) and what do you know it filled in after several months of use. I have actually considered a circulation problem but there really isn’t enough information on it concerning hairloss. The link you gave goes to a under construction site so it wasn’t a help there but your last statement was! Years ago I was in a car accident and fractured T1-T5, now there’s a golf ball sized scar tissue over the area! I’m going to put some serious time into researching this aspect and guinea pig myself on potential treatments. Rob is awesome and has great advice and experience, if I come up with anything I’ll forward to him for consideration. Thanks for your input, I think you help put me on the right road!

      • Eileen – thank you for the kind words. And manlikedeso – thank you for sharing your theories! It’s incredible how through information-sharing we can help everyone better understand the roots of their conditions.

        I appreciate the time you both took to write in. Eileen, keep us posted with your progress! Best of luck and please keep in touch.

    • Hello, I have a similar opinion. About 25 years ago I studied Alexander Technique and combined with meditation I reached something that I describe as Nirvana, or someone has described as Nirvana in the neck. What I noticed is that I have been anxious all my life without realising it, and releasing of my neck was connected with release of anxiety. When my neck released and shoulders dropped, there was a flow of nutrients or hormones or something up and down my neck. I can only guess that there was a restriction of flow and even possibly compression of glands, not just in the neck, but the whole body, because in a sense a pinced nerve in neck probably sends a ‘pinched’ message to another part of body. I have also noticed in a general way that people who stand upright without apparent tightness in neck do not appear to have hair loss, Thank you

  2. Hey Rob, happy new year!
    Such a good article. Here are my questions (or some of):
    1) I agree. Most bald or balding people have ahiny scalps. But how do we know that people with hair haven’t shiny scalps too?
    2) If calcification and fibrosis are the main causes of hair loss, and given that hair loss seldom, if ever, affects the lateral and back sides of the head, why there aren’t calcif./fibros. there?

    • Happy new year! Great questions, and not the most straightforward to answer.

      1) Much of the evidence suggests that excess collagen – or scalp “shininess” – typically precedes pattern hair loss. So if someone has a shiny scalp but isn’t yet suffering from pattern hair loss, it’s likely they will suffer from it in the future. This is especially evident when we look at the way scleroderma results in permanent hair loss when it occurs in hair-bearing areas.

      With that said, I’m sure lower levels of perifollicular fibrosis are less problematic. For instance, the Dalai Lama has a relatively narrow baldness pattern, and the hair-bearing sides of his scalp still have a bit of shine to them:

      2) This is one question that no one has been able to answer, but there are plenty of theories that take a shot:

      I know you’ve commented on that article so have likely already read the material. But I think the galea-based theories are the ones that get us closest to the answer. There’s some interaction with the galea that triggers hair loss, and only (relatively) within that region.

      To get a concrete answer, it’s critical that we get a better understanding of the role of fascia tissue and its relationship to oxygen levels and blood flow. And for that, we need more studies. So as new research comes out, I will continue to keep you updated!

      • Right. I read that article and I’m still not satisfied by the answers it provided.

        Not because it wasn’t a good article – I have a positive opinion of your articles, otherwise I wouldn’t be here following your research. But we should never be too satisfied of our explanations until they are complete.
        Thanks for your answer Rob.

  3. Thanks for all the helpful information. I was wondering if you have any thoughts on the various laser technologies for hair re-growth? The laser combs and laser caps.

    Also, in your research, do you make a distinction between thinning hair and hair loss? If so, what do you see as a distinction in the causative factors and the remedies.


    • Hey Mike,

      Laser therapies show a lot of promise for hair recovery, but the research is still in its infancy.

      For instance, while red light / low-level laser therapy (LLLT) has been used to treat hair loss for over a decade, we still don’t know…

      …the optimal session duration (minutes of use)

      …the best number of sessions per week

      …the most effective infrared or near-red wavelength

      …the best number of laser diodes to use per brush or helmet

      …the exact mechanisms by which LLLT encourages regrowth

      With that said, there’s plenty of evidence that LLLT increases tissue oxygenation, activates heat shock proteins, elicits within tissues a pro-inflammatory response (but only slightly – enough for cell proliferation) via ROS, increases blood flow, and may even inhibit 5-alpha reductase. So there’s likely plenty of benefit in including LLLT / red light into your routine.

      I’ll write an article on this in the next few months to elaborate more.


    • Hi Jens,

      Thanks for sharing. There are a few things here worth mentioning.

      Firstly, I’m in agreement that reducing scalp tissue DHT levels can lead to some hair thickening and/or regrowth. Pumpkin seed oil is a 5-alpha reductase inhibitor and thereby may reduce serum and tissue DHT, and in doing so, produce results similar to Finasteride (another 5-AR inhibitor).

      The problem is that DHT is just one variable in a very complex equation. At this point, results are consistent across dozens of studies: 5-AR inhibitors (whether pumpkin seed oil or Finasteride) may help arrest hair loss and recover some hair. But rarely do they result in incredible hair recovery.

      For instance, just look at the photos that the pumpkin seed oil study highlights – the best-of-the-best responders:

      While the study claims mean hair count increases of 40% for the test group at 24-weeks, this doesn’t manifest visually to a 40% increase in hair volume. The photos aren’t nearly as impressive as the data suggests.

      This all still fits in with the flowchart. Reducing scalp tissue DHT will likely help prevent more fibrosis and calcification from accumulating, and thereby halt hair loss. And for any hairs that are either miniaturizing or on-the-cusp of vellus, then if we arrest future fibrosis and calcification, we can expect some percent of those hairs to thicken / regrow. But this doesn’t result in major recovery. And this is consistent with what we observe in other 5-AR inhibitors like Finasteride. A recent study out of Japan showed ~90% response rate to Finasteride. However, the rate of hair recovery (the amount of hair regrown) was much lower:

      Finally, serum and scalp tissue samples of 5-AR and DHT weren’t measured during the pumpkin seed oil study. While it’s entirely possible that pumpkin seed oil’s main mechanism of action is 5-AR inhibition, it’s only postulation without the actual data. There’s a possibility (though less likely) that pumpkin seed oil’s benefits as an oral supplement may be from another unstudied mechanism of action.

      In any case, I don’t think taking pumpkin seed oil is going to hurt your hair. If you want to include it in your regimen, I don’t see any harm!


      • Hi rob,
        Could the zinc in pumpkin seed be a factor. A lot of people report benefits to hair after eating oysters or zinc supps(including you i guess). Zinc in low-moderate dose actually increases 5-AR and Testosterone. In the treatment group , there was a mild increase(though not significant) in free testosterone. Could the mild increase in T levels be actually beneficial here ?

      • Hey Dante – I totally agree that zinc is critical for hair maintenance and recovery. I’ll look into your question more and get back to you if I find something worth sharing. I know pumpkin seeds are high in zinc, but the absorbability of that zinc is limited due to pumpkin seed’s lectins and binding anti-nutrients. I wonder if pumpkin seed oil has the same problem.

        What’s interesting is that 5-AR inhibiting drugs like Finasteride actually increase circulating levels of testosterone and estradiol by ~15% each:

        So if pumpkin seed oil works by inhibiting 5-AR, then it makes sense to expect an increase in free testosterone while using it.


      • Thank you for your reply,

        Another thing. I’m of course skeptical of detumescence therapy. I’ve spent quite a lot of time researching about it. This study convinced me ( and after reading it I bought your book and started doing the therapy. The study basically says that mechanical stress is a big contributor to MPB, and for me it made sense that massaging and loosening the scalp could actually have a big impact.

        Howewer, I emailed the doctor who was in charge of the study and this is how he replied:


        That therapy could work in theory but I really think that it is not enough to get regrothw or slowing in hair loss.

        The mechanical force that gererates fibrosis of follicles come from the galea and it is not related to the movement of the scalp. The force of occipitofrontalis muscle is continous and very importante even to skull shape, so I think that you spend your time making massages in the scalp.

        I hope you find interesting my information. Feel free to ask me any other cuestion.

        Sincerely, Rafael Tellez ”

        I don’t want to undermine your book, but I guess this made me a bit skeptical.

      • Hi Jens,

        You’re not undermining the book at all. I think it’s healthy to be skeptical!

        I’m very familiar with Rafael Tellez’ study. I’ve also read all the studies it cites. In fact, I wrote an article which dissects that study, in detail, here:

        In short, the galea-hair loss theory is far from complete. And while I think it gets us closer than most theories to explaining pattern hair loss, it leaves many questions unanswered (just a few are addressed in that article). Just search for the term Hic-5 / ARA55 androgen receptor coactivator.

        And based on the author’s email response, I’m not sure he understands the purported mechanisms behind mechanical stimulation and its evidence for hair regrowth. This is probably because he likely just read the Detumescence Therapy paper – and not any other research coming from Dr. Rei Ogawa or dermarolling studies. Mechanical stimulation isn’t simply “movement” of the of the scalp. It’s also acute inflammation generation, stretching, pressing, etc. – all of which have shown (in studies outside of Detumescence Therapy) to promote angiogenesis, downregulate genes associated with the telogen phase, upregulate genes associated with the anogen phase, remodel collagen, and possibly even decrease 5-AR and tissue DHT.

        Beyond that – there are the anecdotal reports of a looser, more elastic, more pliable scalp. I don’t see how it’s possible (in the scalp skin above the galea) to increase the elasticity of the epidermis or dermis without also increasing the elasticity of the galea. We have to also keep in mind that the galea is intertwined with fascia tissue – and that fascia tissue can stretch, remodel, and even detach and wither through certain forms of resistance stretching. All of these things should help increase the elasticty of the galea. So it’s not like the galea’s elasticity is locked in place for all of eternity. The same is true for the occipitofrontalis muscles.

        If you’d like to learn more, I’d encourage you to read through or watch the presentations from the last World Fascia Congress:

        To summarize – mechanical stimulation isn’t just about loosening, and if we think about it only in terms of loosening, we’re likely to undermine all its other mechanisms of action that may encourage hair recovery.

        Lastly, I know you’ve gotten the book so have seen the before-after photos inside. But here are two close-up photos a reader sent me just last week. According to them, they’d committed only to the diet and mechanical stimulation exercises:

        Vertex Hair Regrowth

        I think the evidence in favor of mechanical stimulation and hair regrowth builds every day. It’s just a matter of figuring out the mechanisms, and then how to maximize results for everyone.

      • Hi,

        I also think that the galea theory is flawed, just wanted to hear your opinion about the doctor’s statement.

        Been doing the therapy for 3 weeks now and my scalp clearly feels more loose. My diet is pretty good to begin with. I’m Scandinavian and our food culture is so much more advanced than in the States, so there’s not much that I need to change. Will send you before and after photos if this whole thing actually works.

      • Rob

        Those pics looks impressive.

        Am I right in suggesting that diet will give us the correct nutirition values to favour hair growth.

        While stimulation aids nutrient blood reaching follicles more effectively ?

        Reason being.

        JD Moyers recovery was interesting. Because he only used the mechanical stimulation massage ( according to his blog) to test if it worked. He mentions his diet was already balanced with protein and low grains.

        The results were amazing, and he was also laid back in the the process regarding diet and lifestyle .
        Recently I noted in the comment section a few other readers who did the massage on his blog also saw great success.

        I think the biggest obstacle in the massage are peoples dedication and actually giving time to doing them

        I read a forum the other day from 2012, where people were trying DT. Again people saw promising results, where others did it occassionaly.

        One thing im personally noticing is a constant feel of blood flow in the scalp. Feels good.

      • Thank you Praz. That reader is thrilled with his results – and i’m very happy for him. He also was doing the dietary / lifestyle changes, and so there’s a good chance he saw added synergies between those and the mechanical stimulation exercises.

        To give you more background – that reader has been massaging for 16 months. He had some early progress, but for the most part, hair regrowth came very slowly (even with periods of lulls for a couple months). Then in the last six months, progress picked up again. He wasn’t always consistent with the massages – meaning he missed sessions occasionally and sometimes skipped a day. But as you suggested, I think it’s easier to get away with this (and still see regrowth) when you have your diet and lifestyle dialed in.

        In short – it’s certainly possible to see results even with less commitment to the mechanical stimulation exercises. But that degree of results is likely contingent on a person’s diet and lifestyle.


  4. I also heard that pumpkin seed oil , both as supplement and topical is a strong DHT blocker on the same level as Fin. Maybe even better.

    But Lets not forget , alot of people dont see any effects from Finesteride apart from sides.
    Not everyone has decent re-growth. Again this is a chemical stimulant , not natural and attacks the body.

    However this proves that DHT is not the only factor when it comes to MPB. And that is is a by product of a different issue.

    However the industry makes millions out of DHT blockers like Fin, which are very expensive. Even hair transplant and other companies, make a profit from selling Fin.
    Its a cruel industry, which I personally beleive knows the true causes of MPB.

    Another very interesting Book I read recently, explained how bad lifestyle, stress, and hormone inbalance can lead to MPB. And it was interesting how it mentioned Genes. How can Genes which promote hair growth, suddenly turn out to do the opposite later in life ?
    Upregulation and downregulation plays a part which can be takcled on by physical stimulation, mental, and dietary.

    Their are many links to modern diets being the cause of many issues, leading to fibrosis and calcification in people with possible upregulated genes of LL6 (hair loss.)

    In Japan before ww2, many men did not have MPB. unlike they do today. During this period , they ate natural rice, and vegtables. Also high Omega 3s. However after the War they were forced to eat wheat products sold to them by american companies, which lead them to decrease consumption of traditional foods. Wheat at this time was mass produced and possibly contained chemical stimulants due to demand.

    In India hair loss in men has increased recently. Funny thing. Most of them are IT workers who have bad diets, work long hours, and deal with stress. They are also inactive.

    However I beleive mechanical stimulation with lifestyle changes are the biggest factor. Reading JD Moyers road to recovery epmhasis mechanical more than anything else.

    Sorry for the long post.


    • Great points Praz. Hair loss seems to be far more prevalent in first-world versus third-world countries. My hypothesis tends to fall into a lot of what you elude: compromises to diet (soil nutrient depletion, pro-inflammatory foods) and lifestyles (the disappearance of helminths, the rise of vitamin D deficiency) – all of which contribute to a decline in gut health, hormonal imbalances, and likely pattern hair loss.

  5. Almost at the beginning of your article you stated the following: “In balding sites, our skin feels thicker, less pliable, and significantly less elastic.” – Quite the contrary! I’ve only lost hair at the temples and this is by FAR the most pliable part of my scalp. I can hardly grip/manipulate other areas because the skin is so tight and yet they are very densely covered with hair. What do you have to say in response to this?

    • Thanks for reaching out. It’s a great question. I’ve addressed it once before, but in the comments section of a separate post. The question was: “Why are my thinning temples looser than my vertex?” In short, this likely has to do with 1) the position of the galea aponeurotica, 2) where it fuses with the upper layers of the scalp skin, and 3) how far away that fusion point is to skin that will never fuse to the galea.

      There are many theories about MPB etiology. I wrote about the big ones here:

      Check out the final few theories about mechanical force, the galea, and scalp muscle tension. It’s possible that androgen-driven muscle tension (or in our hair loss flowchart article – “scalp environment”) – is a major trigger of the fibrotic cascade beginning at our temples and vertex.

      One of these galea-based theories involves a reinforcing feedback loop between the natural tightness of the galea, the androgen receptor coactivator Hic-5 / ARA55, tissue DHT accumulation in the scalp skin, transforming growth factor beta 1, and the resultant formation of fibrotic tissue that fuses the top three layers of the scalp – the skin, the subcutaneous fat layer, and the galea.

      For men, this process usually begins at the top of the vertex (which is surrounded by the galea), and the temples (which is at the edge of the front part of the galea).

      This distinction is important! For many, the vertex tends to tighten faster than the temples. The entire vertex also rests above the galea – meaning all of the tissue surrounding the galea is subject to fusion.

      Conversely, our temples are right next to our forehead. The forehead has relatively loose skin, and since it doesn’t rest above the galea, the skin and subcutaneous fat next to our temples DON’T fuse with the galea.

      This would explain why the temples remain relatively looser versus the vertex — even in cases where the temples thin before the vertex. The temples feel looser because the skin it resides next to never fuses, which gives the actual temples a bit more give (even when they’re fused).

      In short – skin elasticity is a benchmark for galea fusion, but it often doesn’t translate perfectly to what’s happening under the scalp (galea fusion).


      • Hello,
        so if this is the case should there be any difference to the way the massage is done or just aim to relax the whole scalp?

      • I think a common misconception about the book’s contents is that it exclusively focuses on massaging. While that’s a component of the book, the book is more focused on highlighting ways to reverse scalp calcification and fibrosis as a whole – via mechanical stimulation and other scientifically validated protocols.

        A relaxed scalp might relieve the tension that precedes chronic inflammation, but that alone likely won’t revert much of the accumulated fibrotic / calcified tissue. That’s where acute inflammation and wound healing comes into play (among other things).

        In short – yes, the way you do the massage matters. A massage that only relaxes the scalp skin likely won’t be enough for significant regrowth.

  6. Hi Rob, good day to you.. I am from India….I have prescribed to Minoxidil and Finasteride by Doc. and I have took them almost 2 yrs of time. I shaved of my all hair when I was taking treatement . and found good result but when i stop taking the medicine I am again facing hair Loss problem. So Can you please suggest do I need to continue with that tablets again as i dont want to get habbit of those ones throught the life..Also I have heard of that it does having some negative side effects on your body. Could you please suggest what should I do? I will be glad if you could reply me on this through email. your Article does help me a lot to understand the Hormonal changes in the body. also I like to ask does hypothyroid could be the reason of hair loss as Testosterone and DHT is the main hormones for the cause of hairloss. Please suggest as I do not want to loose my pretty hairs….:(

    • Thanks for your background Aashi. Finasteride is a 5-AR inhibitor, and can reduce scalp DHT levels and thereby help slow, stop, and sometimes even partially reverse the hair loss process. Minoxidil can help boost blood flow to the follicles so both may help in your battle against hair loss. If you took both for two years and didn’t experience any side effects, my guess is that it’s unlikely you’re of the sub-group susceptible to Propecia’s negative sexual side effects. Since I’m not a doctor – I can’t advise you on what to take/not take.

      Hypothyroidism is related to hair loss. I wrote about this here:


    • strong hibiscus infusion does the trick. 100g/liter, powder it with a blender, add water, activate the infusion with an ultrasound cleaner, drink it without sugar and put it directly on your scalp.

  7. Dear Rob, very intereting website, I have never read so many aspects I didn’t know about. My question is, is male pattern baldness (partially) reversible and how is this possible? What do you recommend? (Food, lifestyle etc. wise).

    Thanks in advance,
    Stephan Griffith

    • Stephan – thank you for reaching out. To answer your questions – yes, I believe pattern hair loss (both male and female) is reversible – and even through non-pharmaceutical means. There have been incredible case studies of recovery in medical literature. One of the most impressive cases was of a 78-year old bald man who accidentally fell, split his head open on hot coals, and during the healing process, regrew his entire juvenile hairline. My approach to reversing hair loss is scientific and utilizes fields of mechanical stimulation, mechanotherapy, and a diet / lifestyle that minimizes chronic systemic inflammation and optimizes hormonal balance. All specific recommendations are outlined inside the book and video(s) – but those fields make the foundation of the material.

  8. Hi,
    Can you explain how to prevent/reverse fibrosis and calcification naturally in detail??? It would be very helpfull please…….Thanks.

    • Hi Raj – my theories about reversing fibrosis for hair loss are outlined inside the book. Unfortunately, there isn’t a short, straightforward answer to your question.

      At a minimum, the best way to reverse fibrosis / calcification is probably a two-step process: 1) shut down the inputs that trigger calcification and fibrosis. 2) Create a scalp environment that encourages autophagy. Doing both simultaneously is the key to hair regrowth.

      • Hi rob,

        Thanks for the answer. But can you explain that 2 points given by you in an answer in detail?,so that I can implement on myself.
        Hoping for your answer.Thank YOU…..

      • Answering your question is out-of-scope for a blog response due to the answer’s complexity. For example, explaining how to reverse fibrosis and calcification in the book takes up ~100 pages. With that said, the free email course will help you get started. It’s over 10,000 words and highlights (in my opinion) the most promising treatments for fibrotic tissue reversal and pattern hair loss.

  9. Hi Rob,

    Interesting ideas on your website. I tend to be not too concerned about my hair loss but I can’t resist unexpected ideas — such as hair loss being (at least somewhat) reversible with something as simple as scalp massages! IF you look around hard enough you find that many things can be treated with simple methods. And persistence, of course.

    So I’m another guinea pig in this experiment, and thought I’d share something interesting. When I first started pinching my vertex and the ridge(s) I would feel (and hear?) a “crunching” sound when the skin finally folded. No idea if this is common, but I haven’t heard others report it. I no longer experience this, and the skin feels much looser. It’s been maybe 4 months(?) but with a few breaks due to travelling. No other results far but I’ll keep it up for another year or so before making any conclusions/reports.

    • Hey Soren,

      Thanks for your efforts! I look forward to your progress.

      The crunching you mention is actually commonly reported. It’s likely one of two things (or a mixture of both): 1) soft tissue calcification getting broken down, or 2) swollen tissue / fluid due to the acute inflammation generation from the exercises.

      Typically people think they’re experiencing #1, but it’s really #2. And the fact that this noise went away is a good thing. It suggests that whatever the cause, your scalp has been making the proper adjustments so that the same intensity now doesn’t evoke the same response. I’ve certainly heard crunching before. And if you really want to hear crunching, try doing a headstand for a few minutes! When you let your head off the ground after a few minutes, you’ll hear a ring of crunches where the skull and floor meet.


  10. I think you are well onto something with the calcification connection. Consider what a high-sodium diet does: displaces cellular potassium and leeches calcium from bones, teeth etc. displacing them and increasing calcium in the blood (often leading to things like kidney stones). This displaced calcium could lead to calcification in other areas. Sidenote, actor Michael Cane claims he stopped potential hair loss but cutting salt out of his diet. Sorry for the digression. Now, with the high sodium displacing potassium from the cell and displacing calcium, the cells are now potassium deficient (assuming the high-sodium diet is not neutralized with a high-potassium diet, which is not usually the case. Most people get too much salt and not enough potassium). Now, what does minoxidil do other than increase bloodflow through vasodilation? It does something to potassium channels in scalp cells. Can’t remember exactly, but it affects potassium channels. High-sodium diets could definitely affect this as well as feed the calcification process.

    • Thanks Sean! I’ll look into your points on salt / sodium over the next couple of weeks. For me personally, I’ve found keeping a moderate-to-high consumption of salt has helped improve my metabolism. Salts can also help regulate certain aspects of the thyroid. But I’m always open to new ideas. One thing I’ve found lately during my Skype sessions: most hair loss sufferers seem to under-consume potassium regularly, and are likely deficient. So there may be some sort of correlation.

  11. Hi Rob,

    Thanks for the information you provide. I’m Norwood 2/2.5 with a diffuse thinning on top. You can see my hair’s density here :
    Based on your ebook I have simple question:
    I’ve started with the massages in April. But I’m having a hard time trying to loosen up my scalp, especially the frontal part. I’ve made some really minor progress on the vertex. But on the overall, my scalp is very very tight, I don’t have dandruff or sebum after the massages. In your ebook you say “After 3-4 weeks of doing the scalp massages, the elasticity of your scalp skin should begin to drastically change” or “In the first few months, everyone doing the massages should noticed increased elasticity in their thinning regions. If you don’t notice this, you’re probably not going hard enough.”

    On the other side, a few hours after each massage, I still have the sensation of the massage. But my hair is also thinner than before. I remember you saying that if the massages lead to visual thinning, it’s probably because the user is going too hard.
    So my question : where is the truth? Am I going hard enough?

    Thanks a lot for your time.

    • Hey Alex,

      Thanks for reaching out. And great question! The guidelines on dandruff and sebum are meant to act as general rules-of-thumb. I included them in the latest book after reviewing hundreds of readers’ massage video submissions and seeing that a majority weren’t going hard enough to evoke any inflammatory response.

      With that said, there are exceptions to the guidelines, and if you have to pick one guideline to overrule the others, it’s absolutely the one related to visible thinning. That’s something we don’t want to do. So for now, go easier. Don’t worry about scalp elasticity changes. The reality is that some people see major progress with this early on, but for those who’ve had experience with other manual exercises (like the Tom Hagerty exercises), then the changes can take longer to express (likely due the elasticity gains from the previous exercises coming into the massages).

      Bottom line: go easier. Find the right intensity to go a full twenty minute shedding while also minimizing your shedding to 10-15 hairs. If that doesn’t help course-correct, reach out again and we can reevaluate and get you on track.


      • Hi Rob!

        Thanks a lot for your quick answer. I’m currently following your advice.

        There is a thing I don’t understand though, related to MPB:
        I’ve noticed that my hair on the sides and back of my head is as thin as in the top of my scalp. There is more density there compared to the top of my scalp. But I remember that two or three years ago, I had thick hair everywhere. This means I have a general thinning all over my head. Is it a normal for a classic MPB pattern to also thin on the sides and in the back of the head? I’ve always though that the hair on sides and back of the head should not be influenced by MPB.

        Thanks again for your time.

      • Hey Alex — it’s certainly part of the deal for most pattern hair loss sufferers (especially in advanced stages). With that said, typical MPB is diagnosed with that pattern you see on so many men (temple recession and / or vertex balding).


  12. hi rob, i’m facing hair loss sheding its become thining and shining on top, its a mild to moderate class 3, i have take daily supplement now, and after i read study from your post i dont think i’m affect from DHT, what i had to do now, what’s actually supplement that could help..? thanks advice..

    • Hey Caeson – if it’s pattern hair loss, it’s likely DHT-related (along with the other factors mentioned in the article). I actually advocate against most supplementation as the causes of hair loss vary for each individual, and supplementing blindly often leads to a hole in your wallet and no clear results. I’d recommend browsing the site to understand more about what might be affecting your hair personally — a zinc deficiency, skull bone growth, scalp tension, etc. — and then making treatment decisions from there.

      • thanks reply Rob,

        yea i’ m agree there is individual loss vary for each,
        i’m try zinc before but seem like no growing and become thick but the baby hair still there,and i dont have any symptom DHT like, skull bone growth, lush body hair etc…just have shining scalp,less hair and thining…although baby hair were there not going grow thick..

  13. Hey Rob,

    I have a story you will love and this might help the both of us.
    My aunts husband was bald and had been bald for more then 30 years (hair on the sides not a single hair on the top of the scalp!)
    They lived in LA and he had an American lifestyle and diet.
    His age gained up on him and he became ill and the doctors told our family to prepare the final arrangements.
    But as usual his son was searching everywhere for help and someone told him about a drink (Ensure). The friend was just trying to be helpful and had a positive experience with that drink.
    So his son got his father that drink was basically that was the only thing the father was able to eat. To everyone’s surprise he did not pass away according to what the doctors had said.
    He never regained his full strength but he got his old hairline back.
    Ohh yes! I’m talking FULL set of hair like he was 15 again!
    When I came to LA and saw him I did not recognize him. My cousin (the son) pointed at his father and said don’t you wanna say hi to my dad.

    I was in chock! I asked and they told me the whole story and I was super excited and wrote to Abbot Lab. who makes the drink Ensure – but no response:(

    God bless his soul he passed away some years later but I will never forget his hair regain.

    Now you are much more into planing and charting out to find “cause and effect” etc. to finding a cure.
    I on the other hand am so lucky to also be suffering from baldness.

    I had seen and read all over the net and tried so many different ways and everything failed. And I am man enough to say that I have not been able to do the same as and only drink Ensure for 6 months 🙁

    So this is my story and I am 100 % convinced that hailloss of every kind is due to something we eat and that in it self can vary from person to person.

    Can you give your thoughts and maybe this is the final blow to a free cure for everyone 🙂

    • Hey Rasmus,

      It’s much more likely any regrowth your uncle experienced was a result of microbiome / gut flora changes on a liquid-based diet, and much less the result of Ensure. Ensure is highly processed and with vitamin additives — which metabolize differently in their isolated form. In fact, some vitamin additives (like the enrichment process in white grains in the US) may actually contribute to higher levels of systemic inflammation, heart disease, and weight gain. With that said, you can certainly try it. Take photos, and report back if you experience any regrowth!


    • @Rasmus: I’m really interested in this and would love to try this out. Can you share more info about the guy i.e.

      – what else was he eating/drinking – he surely wasn’t just drinking Ensure all day, must have been taking solids/fiber as well
      – was he on any medication?
      – when did he start seeing regrowth and how long it took to get all hair back?


  14. HiRob,
    First up i wanna know are you a derm or plastic surgeon? U have done fabulous extensive research and your interpretation is amazing. Now i have recentlystarted having hair loss. Am 33 now. My grandfather was a person with typical male pattern baldness. None of his children have baldness. Infact all 5 are over 60 years and still have enviable hair. Me, on the other side have the typical balding you had described. Crown aND FRONTAL RECESSION. I have recently had 2 sittings of PR( platelet rich plasma ) injections. Your thoughts on this. Plus i am just curious why am i bald and my dads got great hair :-).

    • Thank you, Bala! I’m not a dermatologist, nor am I a plastic surgeon. But I am a researcher, and I hire medical professionals to help with my research and review the content I write. I’ll write an article about platelet-rich plasma therapy soon and get back to you with a robust answer! And as far as the reasons why you’re starting to lose your hair (despite your father having a full head of hair), I think the latest evidence suggests epigenetic factors (stress, environment, etc.) influence the activation of our predisposition to hair loss more so than ever previously thought:


  15. Hi Rob, I have just started thinning and also just found some of your articles on line. I am intrigued by the research you have done and thank you for offering me some hope for my thinning hair. I have much more of my own research to do, however I did have a question about the information about fibrosis from the “flow chart” article. In it you said that excess collagen is also called fibrosis. My question: is this the very same kind of collagen that hair growth products (like BioSil and Viviscal)say they generate for better skin, hair and nails? If this IS the same kind of collagen, then should we stay away from products like these? That is: Is the product we think we’re talking to help our hair growth, actually causing more collagen build up and therefore fibrosis and hair loss? Thanks for your feedback.

    • Hey Corey,

      Thanks for reaching out. It’s a great question, and I realize I should’ve been clearer in my terminology here. To clarify: collagen and collagen-promoting supplements are not the same as excess collagen. The term “excess collagen” — or in the flowchart, fibrosis — refers to the scarring of connective tissue (or the uneven bundling / hatching of collagen fibers). This is different from regular collagen — which is present everywhere in our skin.

      The difference between collagen and fibrosis is that collagen is the material your skin is made up of; and fibrosis is places that have “excess” collagen. Fibrosis isn’t a result of consuming collagen — it’s the result of long-standing, chronic inflammation — where our skin tissues are under constant damage, and thus in a never-ending state of repair. Eventually, our repair mechanisms make errors, and the result is the formation of disorganized / excess collagen (also known as fibrosis and scar tissue).

      Supplements / foods that support collagen synthesis are good for us! These can help improve the building / breaking down of collagen and thus decrease our changes of fibrosis. They’re also typically high in glycine (like bone broths) — a protein which seems to have systemic anti-inflammatory properties. What truly stops fibrosis is taking away inflammation, so these foods are often a one-two punch.

      I hope this helps! Let me know if anything is unclear.


  16. What i meant to say that in my daily regime can i use any herbal oil (Not during the massage)
    But like after bath or before few hours of bath.
    Will it harm or increase the calcification or oiliness or anything else??

    • In most cases, fat-based topicals are anti-microbial, anti-inflammatory, and should help attenuate the progression of calcification or fibrosis. Just be sure you’re using oils that are cold-pressed and relatively unoxidized.

      In the medium-run, fat-based topicals may actually downregulate sebum production — so their continued use shouldn’t make your hair oilier (though your hair will be oilier after each application — just as a result of the topical itself).


  17. Hi Rob,
    In my case when I was teen I had a big bush on my head(Lots of hairs). Now I can remember myself sitting in a class rubbing my head with a hand and seeing LOTS of hairs on a table, and that started happening after puberty (When I was 15-16years old) but as I had massive bush on my head I wasnt so worried about it until my scalp showed up when I was about 22. I also remember that after puberty I had Gynecomastia (Which happens when you are teen but disappears in some time). I had it till now as Im 24 now but never was so worried about it as Im fit guy and it was just the nipples. My hairs made me to dig into this. That means I always had high Estrogen, I also think my Testosterone is ok because Im pretty hairy on my chest and body. I did read lots of stuff about hair loss and T:E ratio lately. So I started taking Anastrozole. My Gynecomastia is getting little bit better now but I dont see any changes on my hairs yet(I only take it for a week). I lose like 20-40 hairs everyday as Im washing my hairs and that drives me crazy… I also noticed that my eyebrows are thinning and that means that I have Hypothyroidism. But If I had Hypothyroidism I would have overweight as Im eating loads but Im keep loosing weight and having hard time to put some on and that leads me to Hyperthyroidism….(Thyroid problems is also cause of Hair loss)… Any opinion on that? Please help me

    • Hey Dom — Anastrozole is an aromatase inhibitor that competitively blocks the enzymes that help convert androgens into estrogen. So it should lower your estrogen levels. With that said, one of the reported side effects of Anastrozole is hair loss — and the mechanisms of action by which Anastrozole promotes hair loss or hair shedding aren’t yet understood.

      In terms of hypothyroidism — not all people who are hypothyroid gain weight. When I was hypothyroid, I ate plenty and also didn’t put on weight. But I’m not sure your symptoms are due to hypothyroidism or the drugs you’re taking to treat gynecomastia. If I had to guess, there’s likely some overlap between the two.


      • Hey Rob, thanks for quick answer! I dont think Anastrozole got something to do with my hair loss as Im taking it only for a week and I have hair loss for about 2 years already. But as you told me that it causes hair thinning I will defo stop using it and try natural ways to lower my Estrogen. Only thing that comes to my mind is High Estrogen levels, Thyroid problems ( When I google about it I have some symptoms of both Hypothyroidism and Hyperthyroidism), DHT or Hormonal imbalance. I also have Varicocele. Do you think that has to do something with my Hair loss or Hormonal Imbalance (T:E) ?
        Thank you!

      • Hey Dom — it’s certainly possible! Hair loss in young men like yourself is more correlated with high estrogen levels than high testosterone. I’d suggest continued efforts to reduce estrogen — either through diet, lifestyle, or supplementation.

        In terms of varicocele — there are some anecdotes showing that certain supplements are able to resolve this better than even surgery. See this research study:

        As far as getting off Anastrozole — that’s something you and your doctor should discuss together! It’s probably better to hear what he/she has to say, since they have more experience prescribing it and hearing user feedback than me.


  18. Hello Rob,

    So, throughout my lifetime I realized ever since I was a little kid I’ve had a larger forehead, meaning my hairline and temples was extended further back into my scalp/head.
    Though, I’m 20 now. When I went through puberty even from 13 I noticed my hair texture change to unusually soft and luscious my hair seemed super fine, it was thick at the time but it changed, progressively it’s gotten to the point where oddly, not typically a male pattern baldness but I have 10x more hair on my crown than from my sides where most men with male pattern baldness’ hair remain.
    Although, now my temples are thinning aswell but it’s a rather oddly shaped hairline, nothing missing, no bald spots nor patches, I was just wondering what you think..? It’s clearly hair loss but I’m not sure from what.