Ultimate Hair Loss Flowchart-feature

The Ultimate Hair Loss Flowchart: Why We Lose Our Hair

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.

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. This leads to imperfect healing and scar tissue.

Balding Skin Is Tighter, Thicker, And Shinier Due To Excess 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.

Excess Collagen Is Also Called Fibrosis

There’s another word to describe the 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 excess collagen and 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 excess collagen and fibrosis that reduce blood flow and oxygen to our hair. In balding areas, the blood vessels that support our follicles 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.



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Stop Googling "How To Regrow Hair" Until 3AM

Instead, just sign up for my 10-day course on natural hair recovery.

Inside, you'll get access to my before-after photos, the science behind the DHT paradox, hair treatment mistakes to avoid, reader-submitted photos, and more.

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  • manlikedeso

    Reply Reply January 1, 2017

    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?

    • Rob

      Reply Reply January 2, 2017

      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.


      • Kuba

        Reply Reply January 6, 2017

        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?

        • Rob

          Reply Reply January 6, 2017

          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.


          • Kuba

            January 7, 2017

            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:)

          • Rob

            January 7, 2017

            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.

    • Eileen

      Reply Reply March 5, 2017

      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!

      • Rob

        Reply Reply March 6, 2017

        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.

  • Jolly

    Reply Reply January 1, 2017

    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?

    • Rob

      Reply Reply January 2, 2017

      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!

      • Jolly

        Reply Reply January 2, 2017

        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.

  • Mike

    Reply Reply January 1, 2017

    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.


    • Rob

      Reply Reply January 2, 2017

      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.


  • Jens

    Reply Reply January 4, 2017


    There’s actual evidence that reducing dht levels can lead to hair regrowth, instead of just stopping mpb progression. For example: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4017725/

    How do you explain this?

    • Rob

      Reply Reply January 4, 2017

      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!


      • dante

        Reply Reply January 5, 2017

        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 ?

        • Rob

          Reply Reply January 5, 2017

          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.


      • Jens

        Reply Reply January 5, 2017

        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 (www.ncbi.nlm.nih.gov/pmc/articles/PMC4639964/) 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.

        • Rob

          Reply Reply January 5, 2017

          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.

          • Jens

            January 5, 2017


            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.

          • praz

            January 6, 2017


            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.

          • Rob

            January 6, 2017

            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.


  • praz

    Reply Reply January 5, 2017

    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.


    • Rob

      Reply Reply January 6, 2017

      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.

  • William

    Reply Reply January 7, 2017

    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?

    • Rob

      Reply Reply January 8, 2017

      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).


      • Andrew

        Reply Reply January 31, 2017

        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?

        • Rob

          Reply Reply January 31, 2017

          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.

  • aashi.raut

    Reply Reply February 22, 2017

    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….:(

    • Rob

      Reply Reply February 23, 2017

      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:



  • Stephan Aalsma

    Reply Reply March 5, 2017

    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

    • Rob

      Reply Reply March 6, 2017

      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.

  • raj

    Reply Reply March 27, 2017

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

    • Rob

      Reply Reply March 27, 2017

      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.

      • raj

        Reply Reply March 28, 2017

        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…..

        • Rob

          Reply Reply March 28, 2017

          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.

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