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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…
- 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 is sometimes linked to lower levels of scalp hair loss, and body tissue DHT 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 – to share some of my ideas on hair loss pathology, formulated over the years.
Inside This Article: The Causes Of Hair Loss Mapped Into A Flowchart
This a long post. The goals are to simplify some elements of hair loss science so we can better understand the benefits (and limitations) of treatments, as well as some angles of attack for pattern hair loss. If you have 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.
Finally, here is a more updated overview: Androgenic alopecia: its causes, treatments, and unknowns.
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
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?
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:
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.
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.”
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:
- Androgens alone don’t cause calcification
- 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:
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 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.
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:
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…
- Activating proteins associated with calcification inhibition
- 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…
- Turn on proteins that encourage calcium buildup
- 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…
- matrix gla protein
- and dozens of others
For the calcification inducers, there’s…
- prostaglandin d2
- transforming growth factor beta 1
- bone morphogenetic protein 2
- bone morphogenetic protein 4
- alkaline phosphatase
- and many more
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:
A Quick Recap:
- 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.
- 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.
- 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:
- Increased DHT
- Increased androgen receptors
- 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:
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
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.
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.
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.
Rob English is a researcher, medical editor, and the founder of perfecthairhealth.com. He acts as a peer reviewer for scholarly journals and has published five peer-reviewed papers on androgenic alopecia. He writes regularly about the science behind hair loss (and hair growth). Feel free to browse his long-form articles and publications throughout this site.
200 thoughts on “A Hair Loss Flowchart: Why We Lose Our Hair (Hypothesis)”
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.
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
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.
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.
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.
Thank you for your reply and Happy New Year!
Here’s an article you may find useful:
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?
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!
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 (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.
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:
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.
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.
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 ?
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.
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.
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).
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.
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.
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 – 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.
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.
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.
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.
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.
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.
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 : youtube.com/watch?v=uTN7DnSaKq0
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.
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.
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).
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..
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 🙂
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?
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:
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.
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.
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).
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) ?
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.
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.
It’s tough to say without more information — since the etiology of hair loss varies from person to person and is often complex, multi-faceted, and not the easiest to identify. There’s a good chance that what you’re experiencing is just the typical onset of pattern hair loss that starts in the years during or after puberty — at least for most men.
Hi rob what do u say about that issue of using a dermaroller can it cause more scarring or can it break fibrosis
Hey Lutaaya — I’m a fan of dermarolling (so long as it’s done correctly). All the evidence suggests that microneedling encourages the breakdown of scar tissue, while simultaneously promoting proper collagen synthesis.
Thank you for all of your research, I’ve learned a lot. I wanted to know whether your research/findings also apply to women with diffuse thinning? I’m a 28 year old female and noticed my hair thinning a few years ago. It is worst on top, especially the top front. It is not a widening part, however. You can see my scalp through my hair along my hairline. At the same time I noticed the thinning I noticed a texture change with my hair becoming dry and unruly – my hair had always been soft and never frizzy. I also shed a lot of hair and have always seemed to shed a lot, i don’t know if it’s worse now or if I just pay more attention now that I notice it’s thinning. The hairs on the top/front are also lighter, less pigmented and thinner. Often when they come out they have white debri covering the root (not just the root but extra white debri). I also have short hairs at the top of my forehead/hair line that I believe we’re once actually part of my hair but my hairline recessed back a little as these hairs miniaturized. I also have what some dermatologists have said is psoriasis and some dermatitis. I’ve had this off and on since I was 15, with it becoming the worst over the past 5 years. Is there any help or insight you can provide? Sorry to have thrown so much at you.
Thanks for reaching out. Based on your pattern of hair loss and your diagnosis of psoriasis, I’m wondering if your hair loss isn’t autoimmune-related, and if hypothyroidism isn’t also a factor in its progression.
I’d suggest reading this article, which might give you some ideas for further testing / treatment specific to your case:
I’d also look into testing for the following:
-SIBO (small intestinal bacterial overgrowth)
-Hypothyroidism (mentioned above)
-PCOS (polycystic ovarian syndrome)
Of nearly all the women with whom I work, at least one of those conditions above are present in addition to hair loss, and research also suggests those conditions might play a causal role in hair loss (and thus the interest in resolving them).
The research in the book is catered to both men and women, but for women specifically — I also recommend looking into everything above.
I’ve read your book, and it was an eye opener. I just have a question regarding the diet. I know that grains are to be avoided. Are stuff like lentils, legumes, chickpeas, beans, and nuts also to be avoided? Basically is it just grains or also cereals, legumes, pulses to be avoided?
Did you ever look imto leptin as a factor?
It seems that leptin resistance is commonly found in plasma as high leptin levels, while low expression of leptin mRNA in bald follicles.
Thanks for your comment. I’ve looked into leptin in the past — though my takeaway was that leptin resistance appears to be further downstream to inflammation, and more likely a byproduct of the factors contributing to hair loss rather than an actual contributor itself. With that said, there’s a strong correlation with leptin resistance, heart disease, and hair loss. I’m open to revising my understandings if you have any additional studies that prove causation!
(sorry for my bad english)
I must say that all the information you give and the work you do seem really interesting and detailed, but I have two unresolved questions:
1) If DHT is not the main explanation for baldness, why do men lose their hair more than women? what would make women less prone to fibrosis and calcification?
2) There are many cases of Male to Female Transgenders on the internet, who recover all hair with a hormone replacement therapy:
What is the link with fibrosis, calcification, and all your theory ?
Thanks for reaching out. I’m writing an article on male-to-female transgender hair regrowth and it should be ready by Monday. In the meantime, here are some quick answers:
1) Women are less prone to hair loss because they have fewer circulating androgens (testosterone and DHT). Androgens are one of the prerequisite for hair loss to occur because they’re part of the step-process that forms calcification / fibrosis. The ratio of testosterone:estrogen also matters. After menopause, estrogen levels plummet in women, and their testosterone:estrogen levels increase — which tend to be a biomarker used to assess atherosclerosis risk. This results in a higher likelihood of calcification and fibrosis progression, and thereby an increased risk for hair loss.
2) Male-to-female transexuals take much more than just estradiol. They also castrate themselves, take DHT inhibitors + androgen receptor blockers, and also take other feminizing exogenous hormones. This has a huge impact on bone structure. We know that hair loss is essentially a two-part equation: 1) structural changes to the scalp that evoke inflammation (ex: muscular development of the muscles lining the scalp, bone growth of the scalp, etc.), and 2) our bodies reaction to that inflammation (ie: whether or not we send DHT as a response to the inflammation). For hair loss to occur, we need both increased tension, and a DHT-inflammatory response. This creates the conditions necessary for calcification and fibrosis to occur, which eventually starve the hair follicles of oxygen, blood, and nutrients — causing them to miniaturize.
When a male transitions to a female, this hormonal manipulation does two major things: 1) it remodels scalp bone structure and atrophies the muscles surrounding the scalp, thus reducing the tension that causes the inflammation in the first place. 2) It reduces the likelihood of DHT being sent as a response to that inflammation, since the liver cannot produce as much DHT anymore because the testes (which produce testosterone, the precursor to DHT) are gone. As a result, transexuals course-correct both sides of the hair loss equation: the scalp tension that causes the inflammation, and the DHT response to that inflammation.
Hi man, thank you very much for this blog. It is amazing!
Let me tell you my case: I always enjoyed VERY GOOD skin and hair, but 1 year ago I started using MINOXIDIL in my face to grow my hair. I used minoxidil for almost 6 months once daily. This minoxidil caused an accelerated aging process: my face became puffy, my skin lost firmness and I started losing hair as well. You can look up online that this same effect has happened with minoxidil in several people.
I am trying to regain my look. I started taking collagen supplements to improve my skin, however this has worsened my hair loss. Now, thanks to your blog, I know why. My theory is that my body is overproducing collagen to counterattack the effects of the minoxidil and heal and this is why I have started to lose my hair. I have read about the benefits of taking Taurine to prevent fibrosis and calcification. I am going to test Taurine and will let you know. It would be nice if you give me your opinion regarding my case. Do you provide (paid) counselling? Thank you.
Sorry, I wanted to say “I started using minoxidil in my face to grow a beard”
Thanks for reaching out. I do Skype consults often, and you can book a session here:
Minoxidil’s effects on skin aging are likely due to its effects on prostaglandins, and specifically prostaglandin E2. It’s possible that minoxidil might’ve increased skin aging. I developed bags under my eyes during my 7 years using Rogaine — all without improvements to my hair. With that said, I’ve also noticed a reduction of under-eye bags by 1) addressing nutrient deficiencies, and 2) quitting Rogaine. It’s taken a while, but in the last few years I’ve seen significant improvement to my facial skin quality. For reference, I wasn’t applying Rogaine to my face — just my scalp.
In terms of your theory on collagen overproduction, the literature suggests that your hair loss and minoxidil use are most likely unrelated, and that any shedding from collagen supplementation is probably the result of some sort of allergenic response to a substance or amino acid within the collagen supplement itself. Collagen intake / supplementation doesn’t lead to the development of excess collagen or fibrosis — but rather, it most likely helps prevent it due to its anti-inflammatory properties. The excess collagen / fibrosis observed in balding scalps is the result of chronic inflammation — which is due to an entirely different set of mechanisms unrelated to collagen intake / supplementation.
Taurine might help prevent the progression of calcification / fibrosis, but in my experience, drugs / diets / nutrients are typically limited to slowing or stopping calcification / fibrosis progression and not necessarily reversing it. For reversal, we likely need a combination of mechanical stimulation + androgen suppression via inflammation reduction, which we can talk about during our consultation.
I do notice more sebum while doing the massage, but I notice even more a while (say couple hours) after the massage. When no massage is performed, scalp is oily but definitely not this much. Why is this?
Hey Rax — how long have you been massaging? Sebum release is one of the most commonly reported effects, and it can take a few months before sebum production begins to downregulate.
Use a good dandruff shampoo! Nizoral, Selsun or Zinc 2% and leave on the scalp for 10 minutes. You might like the results.
What’s up Rob. This will perhaps seem a bit arrogant… But here it goes.
I’ve been skimming through a lot of the information on this page, including questions. Here is the deal for me:
I’m 23 years old and have started to experience MPB. My hair was amazing 3 years ago and it’s gotten quite a lot thinner/I’ve lost some.
Without reading on and spending hours, hours and hours on stopping my hair loss, is there something I could commit to? Could you lay down some sort of general path for me to take? As in buying certain products that would help, living and eating healthily (which I do). There is just so much information out there.
I’m basically asking for a narrowed down version of my options assuming it’s MPB, if I’m not willing to spend 100s of hours on this topic. Can you help me? Perhaps if you could tell me about a way to think in my situation, taking one step at the time to discover different solutions, or something. Since I get that there isn’t an easy fix to it all, I’m curious about what path you think requires the least time.
Perhaps I could even pay you some to help me 1 on 1, if you do those kinds of things, and guide me through my own trial and error process, trying different methods. Perhaps you even have some other solution that wouldn’t take too much effort to type down right below this comment even? I really don’t know.
Thanks in advance Rob. I admire your work. Keep it up.
PS. I don’t have infinite amount of money, but I’m in a place where I need to be efficient to achieve my career goals and make money from what I do. Coming from a place of past depression I’m behind in life and to reach my goals, I am required to put A LOT of time and effort into some other areas rather than this one. This is just a major stress factor to be honest and I really need to deal with it somehow.
Thanks for reaching out. If you’re looking to gain an understanding of the causes of hair loss and the treatment options available, I wrote a book that summarizes my research on hair loss here: https://perfecthairhealth.com/book/
Your treatment options really depend on what you’re comfortable with, and what you define as natural / not natural. Finasteride is a viable and easy option for many hair loss sufferers disinterested in the natural approach, and if you’re comfortable with its potential side effects, it’s a great option for those suffering from the early stages of androgenic alopecia. If you’re not comfortable, the book should outline other options.
I’m happy to help however I can. I want to preface that I always try to approach pattern hair loss from an analytical perspective, and as a result, I have reservations working directly with people who feel desperate to resolve their own hair loss, because of the emotional ramifications that can manifest if our first attempt at solving the problem doesn’t work. I’m not saying you’re this type of person, but it’s important to me that I make that delineation before we begin working together. Typically the people I work with our open to a systematic, comprehensive approach that involves self-testing, tracking, and multiple revisions to a regimen before we begin to uncover what’s really moving the needle for that individual, and what isn’t.
If you’re interested, here is a link to one-on-one consulting:
could you please elaborate on how the feminization of the bone structure due to lower testosterone and higher estrogen levels triggers hair growth, yet having a naturally low t:e ratio has the opposite effect..?
Is there any study that backs up your assumption of low t:e ratio?
I think the comments section of this article should help, but if your question persists after reading the first few comments, let me know and I’m happy to clarify further.
The gist is that a low ratio testosterone:estrogen in men is associated with increased incidences of arterial calcification and atherosclerosis — but that this hormonal imbalance is more reflective of inflammation and underlying thyroid issues, and is thereby indirectly linked to hair loss rather than directly causative. A naturally low t:e ratio in men also likely doesn’t do much to remodel bone or atrophy muscles surrounding the galea.
However, forcibly lowering men’s t:e ratio through 1) castration, and 2) exogenous estrogens will absolutely have an effect on muscular atrophy, and potentially skull bone remodeling (though the data on the latter is more theoretical, and I’m realizing that I should change the strength of my wording on the MTF HRT article). This will likely lead to a reduction in skull tension, and thereby help significantly with hair recovery (along with near-complete DHT attenuation).
In short, comparing naturally low t:e ratios to male-to-female hormone replacement therapy t:e ratios in men is somewhat like an apples-to-oranges comparison. The former is more a marker of systemic inflammation; the latter is a complete hormonal overhaul in an attempt to match a biological male’s hormone profile to that of a female.
You forgot to mention the solution to calcification: magnesium oil.
Hey Fred – I wish it were that simple! Unfortunately for those with androgenic alopecia, magnesium oil very rarely moves the needle for inflammation-mediated scalp calcification, and for hair loss in general. It could be a penetrability problem (calcification observations in AGA extend below the galea aponeurotica). It could also be that the studies on magnesium and calcification dissipation, in vitro, aren’t translating well in vivo (as is the case with many supplements). Or it could be that because the chronic inflammation observed in AGA is likely tension-mediated, then targeting AGA-related scalp calcification with magnesium oil won’t be an effective approach until the tension that’s mediating the inflammation is first relieved. But regardless of the reasoning, I’ve yet to see impressive progress photos from magnesium oil (though I’d love to be wrong).
What do you think about microneedling for inflammation and magnesium oil to apply during each session? Absorption would be much higher but would it be safe?
Very interesting stuff! Thank you for making such a difficult subject quite clear and transparant. I do have one question.
Once we have reversed the calcification and fibrosis in our scalp (by e.g. detumescense and dermarolling) , we can prevent future scalp calcification and fibrosis with a good and descent diet, reducing scalp DHT and AR?
Hey Robby — for the most part, yes. It’s much easier to prevent hair loss than it is to reverse it, so most readers successful with dermarolling, mechanical stimulation (massaging), or both find that they can reduce session frequencies substantially after seeing regrowth and/or tissue remodeling in the scalp. With that said, there will likely always be some maintenance required. For instance, I still massage a couple times per week and maintain a diet / lifestyle in-line with the recommendations on this site.
Hello can u give me break down of where I need to start an what I have to do..
I have very minimally thinning and front right side .. can u advise me how to start
Hey Adam — I’d suggest signing up for the free email course. That should give you a lot of background behind the proposed theories of what causes pattern hair loss, where I think those theories fall apart, and what we should be targeting to reverse hair loss (alongside how I think the best ways are to do it).
I really want to thank you for giving is time to answer our questions! I am a 23 year old scandinavian in the early stages of balding and now i need to do something about it!
I have none in my family that are bald so I am wondering what is going on. I guess my lifestyle with a LOT of stress played its part. I think, apart from what you have mentioned, stress is a killer when it comes to hair. I started lose hair like 1 year ago at the same time as I was stressed and kind of depressed. I went to the doctor becuase i felt that something was wrong. Well, most of my symptoms was linked to the stress. But now when I think about it, I had alot of calcium in my blood and they were worried. I ate D vitamin and drank alot of milk and calcium rich food at the time. Do you think calification can build up that quickly? I thought the stress trigged the balding process, but it might have been a combination…
Another question: When you describe the massaging of the scalp – do you mean that i press like a rounded object as hard so I can and do circlemotions without slipping from the scalp? Or should i just use my fingers?
Thank you Rob!
What were you blood calcium levels? Did you also have low serum vitamin D? I’m asking because blood calcium levels above 10.2 and below-normal serum 25(OH)D (vitamin D) levels often indicate hyperparathyroidism. Did you also have your PTH or TSH tested? If so, what were those numbers?
In cases of hyperparathyroidism, vitamin D supplementation shouldn’t be advised — because it can actually contribute to vascular calcification (since the body lowers vitamin D in the presence of high blood calcium levels as a protective response to calcification).
I would just use your fingers. The video included in any of the book packages is the best advice I can give on mechanical stimulation form / technique.
I forgot to mention – I also have inflammation in my scalp that started around 2 years ago and fungoral is the only thing keeping it in away. I didnt do anything about just until one month ago…
Try Selenium Sulfide 2.5% shampoo. OTC in Canada, Rx in the U.S. Leave on scalp for 10 minutes 3 times a week x1 month then 1-2 times a week. This is a very powerful antifungal shampoo that may also reduce inflammation. Zinc 2% which I also use, has some anti DHT properties but who knows what mechanism there is for the Selenium. It works for me. Oh, my derm also wrote for Clobetasol 0.05% Scalp solution.
Thanks for all this information about hair fall .Is there any diet known to reduce the calcification and fibrosis in the body .or in the hair follics .. Please inform about such a diet plan If any .
Hey Prince — I wrote a book about this! The information is too large to summarize in an article comment. But you can check out the book on the site, or conversely, you can get much of the information from my other articles.
I am a 85 year old male and lately my bald spot on top of my head is beginning to grow hair.
Before this I only had hair on both sides of my head and in back.
No where else on my body has grown additional hair.
Have heard several reasons for this as I am still taking same medications. No changes there.
However I have a new lady friend and we have started to become lovers again
Could this be the reason as a hormone inbalance now exists.
Or is the testosterole because now there might be body changes because of this,
Thanks for your comment. I’m curious — which medications are you taking? There are reports of 75+ year old men regrowing their hair after injuries — who were also taking medications (likely for arthritis). There might be some sort of synergistic effect between age-related androgenic changes + these medications + injury (or not) that improve hair loss outcomes in individuals your age. With more information, I can better answer your question (for now, I don’t think it has to do with your lady friend).
Do you have any photos of your progress?
I wanted to check if your book and techniques prescribed work for hair loss related to PCOS as well?
Future updates of the book will absolutely include protocols catered toward PCOS-related hair loss. But currently this isn’t included in the book. If you grab a book package, please email me (my email’s inside the book) and I can give you some recommendations based on the women with whom I’ve worked.
Can I pay your book standard package by paysafecard??
Is the only way i have to aviod my parents know i buy that they dont let me im too young 17 years old
Hi Rober — if a “paysafecard” works with my merchant provider (Gumroad), then go for it! But in general, I don’t know why you’d want to hide the payment from your parents. It’s okay to be losing your hair, and want to do something about it.
Hi Rob, thank you for your very interesting article. It has provoked a lot of thought but also confusion with regards to my own hair loss. I have been in menopause for 7 years and have dramatic hair loss (androgenic) that continues despite bioidentical estrogen and progesterone supplements. I am currently on 50mg spironolactone which keeps skin breakouts under control and I have extremely low serum testosterone levels (possibly due to the spiro). Many years ago when I hit puberty I developed extremely oily skin and hair which persisted my entire life, but apart from some white heads and black heads in my teens, I never really had skin breakout. I guess it’s fair to say that I have had excess androgen expression my whole life, but at least in menopause, testing has not shown me to have excess androgens. So the conundrum to me is that I do not have the typical imbalance of dominant testosterone and low estrogen that you would expect to cause hair loss in menopause. Without understanding the cause it is hard to know how to move forward. Any thoughts would be greatly appreciated. Thanks, Nell.
Thanks for reaching out. While there’s overlap in the pathology of hair thinning for men and women (for instance, studies show the presence of perifollicular fibrosis in both males and females), the causes of fibrosis are likely slightly different for each gender.
Of the women with whom I’ve worked, every single woman with hair loss has also had at least one of the following (typically multiple):
-Nutrient deficiencies (typically D3, iron, zinc, and/or B-12)
-SIBO (a symptom of which is often nutrient deficiencies)
-Hyperparathyroidism (generally indicated by high blood calcium, low D3)
-PCOS (polycystic ovarian syndrome)
In my experience, it’s more important to resolve any of the above first — because it often significantly helps with hair recovery (and makes any other additional treatments that much more effective). For a starting point, here’s an article that addresses nutrient deficiencies and SIBO:
Please keep me posted with your hair recovery.
I’ve been reading your articles on your website and the articles I received in my email inbox. There are a lot of interesting info to read.
I’ve got a few questions about Hair loss and I hope I can get simple answers as sometime too much information makes the whole topic confusing.
Many years ago I’ve been on topical treatments for many years with good success but find it hard to keep up with it so gradually stopped it a few years ago. As usual the hair loss process started again.
I’ve started treatment again but this time I prefer ONLY oral supplements as with so many commitments I find it hard to allocate time for topical treatments. I’m currently taking Propecia and Multivitamins. I recently started occasional scalp massages whenever I get the time. I may allocate one day a week for Dermaroller or Dermastamp.
According to your research and the Flowchart:
Hair loss is caused by DHT, Scalp Fibrosis, Scalp Calcification, Scalp Inflammation, etc.
Is Fibrosis and Calcification in the scalp caused by DHT or Inflammation?
Does DHT cause Inflammation in the scalp OR Inflammation cause DHT in the scalp ?
Minimizing or Stopping DHT in the scalp will prevent the formation of Fibrosis and Calcification in the scalp, is that right?
Can the existing Fibrosis in the scalp be reversed or dissolved using Oral Taurine Supplement OR Serrapeptase with Nattokinase Supplement?
If yes, what is the recommended dosage/strength to take for each? What is the possible percentage of success using just the Oral treatments?
Can the existing Calcification in the scalp blood capillaries be reversed or dissolved using Oral Magnesium Orotate Supplement OR MSM Supplement?
If yes, what is the recommeded dosage/strength to take for each? What is the possible percentage of success using just the Oral treatment?
Any recommenations for an effective Scalp Oral Supplements:?
Serrapeptase with Nattokinase
Magnesium Orotate or Chloride
Any recommendations for an effective Scalp Oral Anti-Inflammation Supplement?
Sorry for the long email. Thank you for your kind attention.
Awaiting your COMPLETE reply soon.
I’ll keep the answers reasonably simple, and I’m happy to go into further details in a Skype consultation:
Is Fibrosis and Calcification in the scalp caused by DHT or Inflammation? Scalp inflammation is likely mediated by chronic scalp tension, which upregulates an androgenic response in the scalp (DHT) + signaling proteins associated with fibrosis and calcification onset (transforming growth factor beta 1). Scalp tension –> inflammation –> DHT + TGF-B1 –> fibrosis, calcification –> hair loss
Does DHT cause Inflammation in the scalp OR Inflammation cause DHT in the scalp ? Inflammation likely causes an androgenic response in the scalp (DHT).
Minimizing or Stopping DHT in the scalp will prevent the formation of Fibrosis and Calcification in the scalp, is that right? It should help slow or arrest the progression of fibrosis and calcification, since it appears that both DHT and TGF-B1 are needed for fibrosis and calcification onset.
Can the existing Fibrosis in the scalp be reversed or dissolved using Oral Taurine Supplement OR Serrapeptase with Nattokinase Supplement? You can certainly try those, but in my experience, if we don’t also target chronic scalp tension, fibrosis-preventing supplements only have a small positive effect on our hair.
If yes, what is the recommended dosage/strength to take for each? What is the possible percentage of success using just the Oral treatments? See above.
Can the existing Calcification in the scalp blood capillaries be reversed or dissolved using Oral Magnesium Orotate Supplement OR MSM Supplement? See above.
If yes, what is the recommeded dosage/strength to take for each? What is the possible percentage of success using just the Oral treatment? See above.
Any recommenations for an effective Scalp Oral Supplements:? It depends what your comfortability is with 5-alpha reductase inhibitors. Obviously finasteride is the strongest type II 5-AR inhibitor out there, but its use comes with potential side effects and a life-long commitment to the drug — with hair loss accelerating if you take it for a long time, then decide to stop. See this article:
Any recommendations for an effective Scalp Oral Anti-Inflammation Supplement? See above.
Fascinating read, but I’m not convinced your flowchart explains anything better than the more simplistic DHT>MPB.
My main concern is with inflammation (caused by diet and lifestyle) representing half of the underlying factors. Genetics isn’t even on there, despite baldness running in families?
I’m not aware of any studies showing diet and/or lifestyle as causing MPB. Many athletes and others with excellent diet and exercise regimens go/are bald. You might want to rebalance the chart, and add in genes.
But if you’re certain you’ve hit upon the truth, then why not submit it to a peer-reviewed journal yourself?
Thanks for commenting, and great points. And yes — you’re absolutely right. Inflammation mediated from diet / lifestyle shouldn’t represent half of the underlying factors of MPB (although in general, an inflammatory response might mediate the entire AGA process). And it’s a mistake for me to exclude genetic influence in any of these step-processes.
RE: submitting to a peer-reviewed journal–
I’m in this process currently! I’ve submitted a paper for a new hypothetical AGA pathogenesis model to a journal, and it’s currently in its second (and hopefully final) round of peer review. The paper’s contents are only fractionally represented in the above post — as my understandings of AGA pathology have evolved over the past year. My hope is that the paper will be available within the next couple of months.
All my best,
Hey Rob! I’m curious about the whole calcification/fibrosis theory. It totally makes sense and it seems to fit into all of the other evidence we have with inflammation and DHT nonsense, and so on… But it seems like nobody is talking about this blatantly obvious issue when attempting to regrow hair. How come calcification isn’t mentioned anywhere on hairloss forums. It makes me either skeptical of the theory or rather amazed at the mainstream not accepting it. I want to ask for some literature backing up the calcification/fibrosis model. I can’t seem to find any papers on it. Thanks!
Thanks for reaching out. I agree with you — it doesn’t make sense to me why the fibrosis / calcification evidence in AGA isn’t more widely recognized. But it certainly makes sense as the rate-limiting factors to hair recovery, and better fits with the data we have than any other AGA pathogenesis model.
There are links to studies throughout the article, so you can click into any of those for evidence that substantiates any of the claims. Otherwise, I have a paper in its final stages of peer review that attempts to create a new hypothetical AGA pathogenesis model and explain 1) the DHT paradox 2) the rate-limiting recovery factors, and 3) potential treatment targets for better AGA outcomes. If it survives the rest of review, I’ll be sure to share it with readers here.
You’re writing it? Okay, that kinda makes me a bit more skeptical. After all some of these papers that we are basing our data off of could be written by anyone. Like, I’m sure that there is a looooot of information about how this stuff works that non of us understand, we are amateurs. A lot of people on these forums are. We don’t really understand the relationships between hormones and functions as much as an endocrinologist does. We’ve only read a couple papers. I’d say that the best way to solve this is with more research. Which i don’t think may of us have the profession or resources to do so. Also, the H. Choy study. Makes me really suspicious. He or anyone else has never followed up with it. And the results have never been met with anyone trying it on the forums. If anything, I would really like to see some studies on regeneration of tissue with acute inflammation. Thanks Rob!
I think you’re misunderstanding — and discounting — the concept of peer review. Peer-reviewed research means that whenever a research article is submitted to a journal for publication, it needs to survive several steps before reaching publication:
1) Editorial review. This is where an editor (or editors) familiar with the field (generally PhD-level academics) read a submitted manuscript for its argumentative clarity, adherence to submission guidelines, and to gauge whether the assertions in the paper are even plausible. On average, 30-50% of submitted manuscripts fail here.
2) Peer review. If a manuscript survives editorial review, it is then submitted to practicing investigators and academics within its respective field — typically 3-5 peer reviewers — who then read the paper and comment on the plausibility of its arguments, study design, findings, analyses, etc. They leave detailed notes and a recommendation to either reject the paper, make major revisions and resubmit, make minor revisions and resubmit, or accept as-is. This is often a single-blind process where a manuscript submitter has no idea who the reviewers are. Sometimes it’s double-blind. Another 20-30% of manuscripts fail at this stage.
3) Editorial decision. Once all reviewers have sent back their notes and recommendations to the editorial team, those editors then make a decision on the manuscript — then contact the manuscript writer and send them all of the notes from the reviewers. In many cases — if the decision is to make major or minor revisions — the manuscript must be revised and then resubmitted, and go through the entire process all over again.
So amateurs don’t publish in real, accredited academic journals. It’s literally impossible — because their papers won’t survive peer review. Henry Choy’s paper is not in a real, accredited academic journal. It’s in a pay-to-publish journal — where you actually pay the journal to publish your work (and in many cases, there is no peer review). That’s why his research isn’t indexed in pubmed or other databases. His paper deserves significant skepticism, and would not survive peer review.
The manuscript I submitted is indexed in pubmed, and goes through this peer-review process. My manuscript also survived peer review and is accepted for publication. So I don’t consider myself an amateur in this field. And I consider my knowledge in this space far beyond an average hair loss forum reader.
I’d also love to see more research in mechanotransduction, wound healing, and fibrosis resolution. It all takes funding… or a sponsoring university (something I’m currently working on!).
Oh oh actually I have an even greater question. I don’t really know where I should go or what I should read for it. But, I read the study about mechanical tensions on different parts of our scalps influencing chronic inflammation and higher TGF-B1 and fibrosis. But, by Rei Ozawa’s study in the 2014 conference, apply 72 hours of continuous stretching (chronic mechanic stimulation) he upragulated lots of genes that promote hair growth. Why are these two things different, wouldn’t the continuous tension in our scalp actually help inflammation from those data.
Also lastly, with an anecdote, when I was younger, I used to bite the skin on one of my knuckles when i was bored. It soon began to become callous and harden and now years and years later, I’ve scarred my knuckle and it is permanently tougher than the others. This was I’d say Middle school-ish maybe early high school, so I defiantly was not still developing. I’m afraid of inducing this kind of callousing and scarring on my scalp.
The challenge with Rei Ogawa’s research into mechanical stretching is that when a tissue is removed from a body and studied (also known as ex vivo), the studied tissues are almost always compounded with the fact that those tissues are put into a wound-healing environment. This is a huge challenge with science — because it means that not all ex vivo studies — even if done in human tissues — are comparable to what actually happens in vivo.
There’s a lot of in vivo data that mechanical tension (and constant contraction or stretch) can lead to fibrosis. Read these studies:
Clinicopathologic evaluation of the Mueller muscle in thyroid-associated orbitopathy
Induction of COX-2 expression by mechanical tension force in human periodontal ligament cells
Surely Cotsarelis knows what you do. They, his team, are looking for a one product solution?
It appears at this time a remedy or cure is not forthcoming from him since the solution may be one of a multi drug, diet, and mechanical solution until the genetic solution is found. The genetic solution appears to be very complicated. Any comment on Cotsarelis?
I’m of the belief that Cotsarelis and his team haven’t read anything on this site, or if they have, I’m assuming they likely didn’t take the information seriously. I’m not here to undermine any of Cotsarelis’ work (because I think it’s incredibly important). After all, he and his team are responsible for the discovery that at hair follicle sites, PGD2 prevents stem cells from converting into progenitor cells (though I think there are several other factors at play than just PGD2).
When it comes to the current thinkings of hair loss pathology, there are essentially two lines of thought: 1) AGA is genetically predetermined and the problem lies within the hair follicle itself; or 2) AGA is a symptom of tissue remodeling. I tend to believe the latter — because the data overwhelmingly supports that AGA is simply just a symptom of scarring (perifollicular fibrosis and dermal sheath thickening).
People who fall within that first camp tend to adamantly oppose the idea that AGA is symptomatic of scarring, and use evidence of rhesus macaques’ hair transplantation success and the infamous “donor dominance” study as their counterpoints. But a deeper look into all of those studies reveals a series of misinterpretations from these opposers — and in study design flaws — and a lot of challenges surrounding “strip transplantation” and the fact that surrounding tissue sites were transferred alongside the hairs.
The “donor dominance” paper is also often mischaracterized as clear-cut evidence that “transplanted hairs will never thin” — but anyone who actually reads beyond the abstract would realize this is just a gross mischaracterization of the study’s actual findings.
Finally, there’s more recent evidence that when a single human AGA-thinning hair follicle is transplanted into the back of a mouse, it regrows as well (and sometimes even better) than a non-AGA hair from a human scalp. This, alongside the fact that DHT tends to increase hair growth everywhere else in the body, seems to suggest that the DHT-genetic sensitivity argument to hair loss has significant flaws — and deserves reevaluation. Furthermore, no one has yet to explain PGD2’s arrival to balding scalp sites — or its exact role in hair thinning.
I’ve recently refined my opinions of AGA pathology, and I published a paper for a new hypothetical AGA pathogenesis model, if you’re interested:
Is there any research done on a link between symptoms of eczema and hair loss. I am 26 and have been experiencing significant hair loss for the past 2 years. Ive had eczema most my life.
I can recall a time when i was 23-24 and trying to fight eczema on my arm. Majority of my arm had hair except where the eczema was severe, the hair on this portion of the arm was very thin. After applying subscription medicine “Betamethasone valerate 0.1% cream” daily, the eczema went away and as a result i noticed terminal hairs much stronger and thicker than what was there.
Eczema is typically a manifestation of autoimmunity, and autoimmunity is often just representative of chronic, systemic inflammation. Autoimmunity and pattern hair loss both share inflammation in their pathology, but that doesn’t mean that eczema and hair loss are always closely related. It’s my guess that androgenic alopecia and eczema are, for the most part, completely separate conditions, though if you reduce inflammation, you might also reduce both eczema and hair loss.
This is probably why you saw some results with that cream! Please keep us posted if your hair continues to improve, and if you can, take photos to track everything.
And I had amazing results with a stronger corticosteroid, Clobetasol 0.05% Scalp solution. These drugs Betamethsone and Clobetasol all have an anti inflammatory effect by definition but not sure of their benefit without other approaches. We are in the down and dirty approache to AA but seems we are getting closer.
Thank u a lot i will start from tonight
This is an interesting article, but I want to make sure i understand your perspective.
Basically, there are a bunch of chemicals on the scalp that, in a certain balance, lead to calcification. Scalp DHT, along with other factors like testosterone/estrogen rations, promotes an environment where that balance thrives, leading to fibrosis, suffocation of hair follicles, and eventual baldness. Scalp DHT is itself regulated in part by scalp inflammation.
This means that DHT is not directly causing hair to fall out. Rather, its serving as an anti-inflammatory which, under the right conditions, results in a chemical imbalance on the scalp as a ‘side effect’, which then cascades into hairloss. Thus, we should strive to reduce inflammation and optimize hormonal ratios to minimize calcification.
Would you say thats an accurate summary?
Thanks for reaching out. I recently revised a lot of my opinions about this flowchart and the pathology of androgenic alopecia. I cover this in more detail in this paper, which I just published:
I plan on updating this article soon, and explaining the new paper in lay terms to all readers. In the meantime, please check out the paper! You can ask questions about it here:
And just to clarify things — what you summarized in your comment is still mostly right (in regards to my beliefs about hair loss). The paper is just a bit more nuanced, and provides more context behind the arrival of specific, localized inflammation in the scalp regions that experience hair loss.
So, how your theory explain that a hair which is transplanted at the top of the head won’t fall after the transplantation, even if there are fibrosis and calcification in this location?
Hope you understand my question my English is no awesome.
It’s a great question. This is covered in the paper that I recently published:
I also wrote a bit about misconceptions behind hair transplant survival rates here:
In general, we don’t yet have data on long-term (10+ year) survival rates on hair transplantations. Most HT patients also take finasteride indefinitely post-operation. So when we think about how these hairs are transferred along with their follicular units and tissues — they should be protected for at least a few years before they begin to thin. Anecdotally, a lot of readers have also contacted me to tell me their transplants have thinned / fallen out. Dr. Freund also mentions this in a recent interview I had with him. So it’s a well-recognized phenomenon.
Hi Rob, been reading around your site and find your articles fascinating. I have a couple of questions and it’d be great to hear your thoughts.
The first thing is caffeine. I know that applying caffeine topically to the scalp can help hair growth. However caffeine in the body has a number of effects which potentially have a negative impact on hair growth. It acts as a vasoconstrictor which may limit blood flow to hair follicles. It shifts energy production away from thyroid towards adrenal/cortisol energy. I read a study which showed that even though some adaptation occurs in long term coffee drinkers, cortisol levels are always raised above baseline in those who consume caffeine daily. Caffeine also inhibits nutrient absorption. As far as caffeines affect on thyroid, I’ve drank two cups of coffee this morning and my heart rate is still only 57bpm. I strongly suspect that caffeine may be causing thyroid issues for me personally. I’m showing a number of symptoms of hypothyroidism such as dry scalp, some dry itchy patches of skin, thinning hair, generally low energy… What are your thoughts on caffeine’s impact on thyroid and hairloss?
Another thing is the T:E ratio you discuss. I had my T measured about 5 years ago and it was 831ng/dl which is on the high end of the normal spectrum. However my hair has been getting noticeably thinner for the last few years. It’s thinning at an even rate across the top. I lift weights a lot and almost never do cardio besides walking. What I’m getting at is do you think that my T:E ratio could be skewed towards having too much T relative to E and that this could be causing my hairloss? I will say I used to drink a lot of alcohol too and this could be causing a knock on effect on hairloss now from what I see on your blog about inflammation and how it effects hair loss down the road. I’m just mentioning that last bit as a caveat and I’d be really interested to know your thoughts on what I’ve mentioned here.
Anyway thanks for all the information your providing here.
Do you discuss caffeine or T being too high as a cause of hair loss in your book?
Thanks for reaching out. To answer your questions–
As you mentioned, caffeine appears to have different measurable effects when applied topically versus ingested. But while in vitro evidence suggests that topical applications may help improve hair loss outcomes through a few different mechanisms…
…most evidence on oral intake points toward a sustained increase in cortisol production, which is antagonistic to testosterone, our thyroid, and maybe even indirectly — our hair. The increase in cortisol from caffeine consumption can actually be somewhat mitigated by also consuming the caffeine with a little bit of fat and sugar. But in general, I think in terms of the benefits to hair — topical caffeine > oral caffeine, and for certain individuals, caffeine can do more harm than good in terms of thyroid, hormonal, and hair-related health biomarkers.
RE: testosterone:estrogen ratio–
I should clarify a few things here, since I get this question often:
1) T:E ratios vary wildly for each individual and can’t necessarily be compared back to normative data — meaning that if your testosterone levels are 831 ng/dL but you’re exhibiting symptoms of low testosterone (fatigue, brain fog, depression, etc.) — then it’s possible your body used to operate at a higher testosterone level, and the relative drop in testosterone production is part of the pathology of those symptoms (despite still being at the high-end of the scale). So it’s the relative changes for each individual that matter most — and not necessarily the absolute number. This is why some people can sit at 300 ng/dL and feel amazing, while others at 300 ng/dL feel terrible.
2) The T:E ratio is more a tool used to measure systemic inflammation, and as a result, it’s gives us directional insights into thyroid functionality — and thereby hair loss. But it’s not the end-all-be-all of metrics. In fact, it seems more relevant for young men with AGA and menopausal women than it does with other demographics.
3) I’ve recently revised my opinions about the causes of hair loss. I now put less of an emphasis on T:E, and more emphasis on a localized inflammatory response. I just published a paper about this, which you can read here:
Aspects of this are discussed in the book, but I hope these elaborations help!
Hi Rob, very interesting article. I wanted to ask you a question about a factor that I haven’t seen mentioned (maybe it’s my fault). We have to species of demodex(mites) that coexist with us in the hair. One lives primarily in hairs and another one in the sebaceous glands. It’s their natural habitat let’s say. There is always a correlation between the animals and the “plants” that live in every area. Infestation of both species is more common in males than in females, with males more heavily colonizing than females (23% vs 13%) and harboring more D. brevis than females (23% vs 9%).
In the baldness process in which hairs are shrinking does the mites just move away? Can an accumulation of mites? Or a diminish in any of the species have something to do with baldness?
It may sound very simple but without bees there woudnt be polinization and we wouldn’t have flowers.
I know that there is a a link between the animals and their environment and I think that studying the behavior of demodex population in the balding area could give us interesting information. Thanks!
This is a great question. In my latest paper, I theorized how these mites and other microorganisms might contribute to the inflammation in AGA by creating a sebum-feedback loop:
However, I didn’t model their migration. My assumption is that with less access to the sebaceous ducts, these mites migrate elsewhere. It’s absolutely possible that a loss of any commensal species — or a growth in any pathogenic species — may play a role in the baldness process. But the research here is unfortunately limited!
What are your thoughts on using Taurine to combat fibrosis?
I think it’s potentially useful to stave off the progression of fibrosis, but that unless we resolve the tension that mediates the inflammatory process that results in balding — we’ll likely just slow down our hair loss, or at best, keep it in a holding process.
Men go bald at a certain age, typically around 40. Their prostate also acts up and expands at this time. Testosterone levels decrease, meanwhile estrogen increases and they grow breasts.
There is a correlation between prostate issues and hair loss. Most men who have enlarged prostates are also bald. My theory is that estrogen causes these issues.
Side note: I read a post on a forum that coffee increases 5ar activity by 30%.
I’ve always had a thick head of hair but noticed it going south at 17 when I started drinking coffee and monster energy. And my prostate began acting up as well.
I’ve been on fin and Rogaine for 6 months and grew back a significant portion of hair that I’ve lost. It’s ridiculous what those chemicals can do.
Lately I’ve cut coffee, dairy, and grains from my diet and upped my intake of green vegetables. I’ve also dropped fin for a month and experience no shedding. Still on Minox. I’m using scalp elixir by Will Hartfield that contains Rosemary oil, and has been proven to be more effective than even minox. Hopefully I’ve solved the issues by just removing caffeine from my diet.
Caffeine is Satan unless applied topically of course.
First of all, great article !! I really appreciate the care and thought put into it . I recently started the scalp massages (about a week ago)and I have noticed 2 things:
1. My scalp feels a lot more relaxed.
2. I have developed pimples (or boils, I can’t tell really ) in the areas where I had lost hair namely the vertex and the temple.
While the first effect makes sense , the second effect seems strange to me and makes me wonder if I am doing the massage wrong. Moreover, I have observed my scalp getting real oily after massages . Are these two related and will it affect my hair adversely ? I hope you will see this comment and respond.
And keep up the good work man. I really appreciate it. I’d buy your book but I am just a student with no cash lying around. I’ll buy it as soon as I get some moolah XD
Thanks for the kind words. The second effect is commonly reported and is often just a result of too aggressive of a massage technique. Take a break for a few days, and then ease back into things. There’s no need to rush into the 2×20 minutes per day at the beginning. You can build up the duration and intensity over a series of months. And best of luck!
How can I reverse scalp calcification. I have mild thinningand the top of my head is a little domed
The calcification is actually observed deeper — within the blood vessels that run to the hair follicles. And it’s a tedious process! The best bet we have is probably a combination of wounding / mechanical stimulation + anti-androgens + relieving scalp tension. While it might seem irrelevant at first glance, this article will help explain why these things are so important:
Thanks for the great article!
What do you make of Omega 3 and Ginkgo Biloba which are said not only to improve your health, but also to have a positive effect on your hair? Omega 3 is said to cure inflammation and Ginkgo Biloba is said to improve blood flow. Is it just a flavour of the month or do they can actually do something?
Do you think any of them is a good addition to my diet regarding my beginning hair loss?
Thanks for reading. Omega 3 fatty acids are a bit polarizing in the hair loss world! Within normal amounts, omega 3’s and omega 6’s are potentially great for health. In excess, or if oxidized, they can be extremely problematic. So I’d be very careful supplementing with either.
Gingko Biloba has yet to show any hair regrowth potential in humans — though it does tend to improve blood flow and the speed of hair growth in mice (but almost everything improves hair growth in mice!). If you feel better taking it, I don’t think it’ll hurt.
Thank you for your good work.
Is any issue with the mobilization of sebum throught scalp massage? Sebum or hair fat is good for a healthy hair, but if it is in excess or oxidiced is bad.
Thanks for reading. Sebum is part-fatty acids produced endogenously in the sebaceous glands, part-cellular debris from microorganism byproducts living in the sebaceous gland, part-triglycerides, and part-a few other substances depending on each individual. Generally triglycerides make up nearly half of sebum, and free fatty acids only make up around 15%.
The sebum excreted / produced during a massage shouldn’t be too much of an issue — at least in terms of fat oxidization — and for two reasons: 1) the relatively low amount of sebum we have on our scalps and the lower percentage of fats in sebum itself, and 2) the fact that — aside from some dietary / lifestyle changes — we can’t do much to reduce sebum production, nor would we want to (it’s a protective lubricant for our scalp skin and hair).
Hi Rob – I read your book about 5 months ago and been massaging my scalp ever since with intrigue as to if and how it can work. I am 35 and have been struggling with hair loss for about 18 years, taking finasteride and minoxidil for about the last 12 which have stopped me going bald but certainly not stopped the slow loss. I am yet to notice and hair improvement, if anything it is thinner, but what is interesting is that the balding areas on my scalp which used to feel sore to touch no longer feel that way which I’m hoping is a positive sign. Have you noticed that hair does eventually tend to improve in most cases? Also, with most of the subjects I have seen such as yourself the loss was mild diffuse loss at most, not full on balding. Have you seen proper reversal in people with visible bald patches/receded areas?
Thanks v much
This is a tremendous informative piece, thank you for putting the time into this.
I’m curious my doctor has me supplementing with Collagen, as she says this will help promote hair regrowth. Based on your article do you believe Collagen supplementation could backfire, and potentially lead to fibrosis? I’m curious as to why she would recommend it when excess of collagen is the main concern as you articulate. Thanks!
Hi Rob very nice information on hair loss.. So far the information I am getting is that excess DHT and masturbation is the sole reason of hair loss.. Your research is truly extensive..
I am 32 Year old Male and have been suffering from hair loss. My scalp is too much oily from last year which is causing stickiness on scalp and hair and thereby hair fall.. my family history is also victim of Male Pattern Baldness.. so I am also showing the signs of same. So far I am not bald. But this oily scalp is catalysing it. Can you Please advice me some precautions to stop or prevent this oily scalp prone hair loss..
I’m fascinated by your research and enjoying reading your articles.
I have a few questions but just wanted to share my hair loss history and current situation with you.
I started shedding heavily in my early 20’s and within a few years could see my scalp all along the top. It looked like I was heading for norwood VI fast. My dermatologist prescribed Propecia and the results were astonishing, people could start noticing my hair was darker within a few weeks (I kept it very short) In the coming months I was able to grow my hair longer as it was now thick enough to cover my scalp. It was a major transformation.
I showed some side effects, the most obvious first ones were gynecomastia and weight gain. My libido actually improved as I may already have had problems with my prostate, too much DHT perhaps? I didn’t mind these minor side effects as I could easily hide the man boobs, and having hair again was a game changer. As the years went by, I developed other side effects like brain fog, depression, loss of libido and being socially withdrawn. After 10 years on the drug, I started showing symptoms similar to that of multiple sclerosis.
This was a major wakeup call and I decided to quit it straight away.
My prostate went into shock, as you described in one of your articles, it might have an influx of DHT due to increased receptors there. I suffered from severe lower back pain and difficulty urinating for months before symptoms started clearing. There were times where I thought my life was coming to an end.
Now, five years off the drug and a lot healthier, my hair is thinner but the scalp is still mostly covered so I have more hair now than I did roughly 4 years before starting Propecia. My hairline also moved back about 1cm and got thinner at the crown, but its far way off the claim that my hair would return to pre-propecia state within 12 months.
Based on my experience and looking at your flow chart, I’m not quite sure I fit into it. The fact that I reacted so well and so quickly to a DHT blocker, tells me that my hair loss was due primarily to excess DHT in the scalp and not fibrosis/calcification.
Could it be that there are two groups or flow chart possibilities, one due to fibrosis/calcification and another to excess DHT? Could it be that excess DHT alone can starve a hair follicle of nutrients, if it’s genetically over sensitive?
I see two groups of balding men, the ones who experience hair loss at a steady pace over time, and another group who experience extreme hair loss in their 20’s.
The former group might have slightly elevated levels of DHT and enough to cause fibrosis over time, even though testosterone production goes down. This group might also not react that well to a DHT blocker.
The latter group has excess DHT and testosterone, consistent with losing lots of hair at that age when T production is at its prime. For this group, we might see a DHT blocker works very well. And this group’s hair loss will actually slow down as they get older and T production goes down.
This latter group would also be in line with my experience, I was able to block DHT in my 20’s/30’s when T production was still optimal. Now that I’m in my 40’s and my T production is naturally lower, I don’t lose hair as rapidly as I did back then. This would also go against the fibrosis/calcification theory?
Anyway Rob, apologies for the long post. I hope you can consider this story in your quest to finding all the answers 🙂
All the best
Thanks for reaching out and explaining your situation, and I’m very sorry to hear about the side effects you experienced from finasteride. I’m glad things are better now!
To answer your question re: “Could it be that there are two groups or flow chart possibilities, one due to fibrosis/calcification and another to excess DHT? Could it be that excess DHT alone can starve a hair follicle of nutrients, if it’s genetically over sensitive?”
Yes! Or at least, sort of. I’ve simplified this flowchart to make it digestible to anyone interested in hair loss research. But the reality is that as the inflammatory process kicks off in each hair follicle susceptible to AGA, our tissues appear to respond by producing more PGD2 and PGJ2. These are prostaglandins that decrease hair lengthening and, in the short term, prevent hair from growing. The long-term consequence of this inflammatory process is the onset of fibrosis — which is eventually the roadblock to most AGA therapies. However, for those who lost hair very rapidly — it’s likely their miniaturized follicles are still only in a shortening phase as a result of elevated PGD2 / PGJ2. These prostaglandins appear to be androgen-dependent (or DHT-dependent). So when we take finasteride, we likely reduce their presence in tissue sites. That means hair lengthening can be achieved again — which sounds like your case!
Long-story short: you still fit into the flowchart! It’s just that I wasn’t granular enough with my explanation.
I previously suffered from an eating disorder as a teenager from the age of 17-19. I’m still fairly thin since the disorder but am not underweight, I’m well within my Body mass index.
During my eating disorder my thyroid and kidney function tests were not too good but having recovered my blood test is all normal.
Since I got my eating disorder my hair has become thinner but I have no hair recession.
I eat and drink well now, don’t smoke or drink. My hair still hasn’t improved and my brothers who are older have thicker hair. Do you know what could be the issue still and do you know how I can make my hair thicker again?
Thanks for reaching out. Based on the pattern and history you’ve described, it’s likely that your hair loss is linked more to nutrition-related issues than it is AGA. If you have a chance, I’d check out this article:
I find your research is very intreresting!
I’ve read your book and I’m currently doing the massage sessions but I’m still confused about some aspects of it.
Doing a diet which is rich in zinc and decreasing cortisol levels in order to increase testosterone, doesn’t iscrease also DHT which is a natural product of its metabolism?
Then, is there a relation between vessel calcification and dietary intake of calcium from things like cheese and milk? Limiting their intake could be an effective strategy?
Last, what shampos do you suggest in order to minimize the damage if we feel we don’t want to stop using them yet?
Thank you for your research and website!
I am writing greetings from Turkey. The article is very impressive. The biggest 2 factors of hair loss calcification and fibrosis can we say ? Calcification and fibrosis what should we do to defeat? Please help me. My hair is in very bad shape. I am a 22 year old young girl and to this situation very ı feel bad 🙁 Please write me
Thought you’d find this interesting
What’s up Rob, this might be the best Hairloss Article I have ever read. Seriously.
After studying it thoroughly though, I have one question.
In the beginning you say this: “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 then later on you write: “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.”
So first you say Fibrosis and Calcification are independent of each other, and then later on mix them together again, by adding Fibrosis to the result of “more inducers activate than inhibitors”. I couldn’t quite grasp how DHT + Increase in ARs + Imbalance in Calcification Regulators leads to Fibrosis.
Maybe I just overread something, but that seems a little odd….
Thank you for your invaluable work though,
What are your thoughts on these counter arguments to detumescence therapy?
Your article is just awesome. I’ve realised that whatever you’ve said is happening with my scalp too. My is extremely tight, there is barely any elasticity. My hairs, specilally in the temple area and over forehead seems like they are being pulled out from the inside. And also The density and the thickness of my side hair is much lower than the top and crown area, which is quite unusual.I’m 17 & 1/2. A year ago, I had hair all over my head, all of these problems were not there. But I’ve noticed that my hair is receeding very quickly. Hair has gone out from my temple area. Also from my forehead. Im very worried that Im losing hair at such a young age… Can u please tell my what I can do to effectively prevent hair loss and regrow my lost hair?
I have some questions too.
1)Will onion juice help in regrowing hair??? I’ve seen on the internet that a lot of people had success using onion juice. And if it is good, how often should I apply? Currently doing every 4 days . And will i have the effectiveness if I shampoo after rinsing the juice?
2)I’ve heard that scalp massage using hair brush significant reduces calcification, is it true?
3) I think Im very deficient in Vitamin D, not only im losing my hair, but my teeths are also getting severly demineralized day by day…. so what’s the best time to vitamin d from sunlight? A lot of the doctors seem to advice getting sun during the morning or afternoon because the sun is toxic for our body during the noon. But the internet says the opposite, going out in the Noon, as UV ray is very low during the day and afternoon time. So what time should I go out for getting the sun? And how long should I stay at the sun? My skin colour is a lighter shade of brown…neither brown not white… Im thinking of staying under for the sun for 5 mins interval like 5min sun+5 min shade for+5min sun+5 min shade+5 min sun for avoidint tan.
4) I use a shampoo called Biosol which contains ketokonazol 2% & Zync Pyrithione… The shampoo feels good, doesnt lather and deosnt dry out the scalp …. is there any side effects of ketokonazol? Also the bottle says to keep the shampoo in conctact with the scalp for 3-5 mins… so should I do as the bottole says? Or should I rinse after applying thoroughly… Lastly , can I keep using the shampoo forever??I mean will tghe ingredients be harmful for long term usage?
Also can you give me your email or Facebook so that I can contact you?
Your research is unbelievable! I have been researching on my own for months and everything you say seems right on–especially the questions you pose against the volumes of (often contradicting) information on hair loss–especially in regard to DHT.
I am a 52 y.o. woman, definitely in peri-menopause, and started a low dose fem hrt (0.5 mg of norethindrone acetate and 2.5 mcg (0.0025 mg) of ethinyl estradiol) at the end of February this year. I started experiencing a massive shed in July–about 4.5 months later–that lasted over 2 months. At that point, I went into what is my normal shedding season–September–and it seems I have lost nearly half of my hair! It SEEMS to be slowing down, but I am not sure. Also, I have significant regrowth. I think I want to get your book and the Skype option because I have a lot of questions I want to ask as well as share details about my specific experience that I think might be interesting to you as a researcher. I have had a scalp biopsy and the findings were “subtle” for AGA, but that “clinicopathologic correlation was required” in my case. My derm did not want to hear my history–she only wanted to prescribe spironolactone! I don’t do well with drugs, and this one comes with too many potential side effects. I want to do the natural route.
My question for you today is regarding the hrt. My pre-hrt blood test in February showed estrogen, progesterone, and testosterone to be non-existent. First of July, blood tests revealed that testosterone was high (at 49 from <3)); free test was up from 0.3 to 3.1 estradiol was the same (<5.0); progesterone was up from <0.1 to 0.3; and DHEA was up a little (at 61.9 from 56.5. My internist and derm both say that hrt does not cause hair shedding, but my research says that any significant change in hormone levels can cause it. I am extremely sensitive to medications. Could my hrt have caused my shedding 4.5 months later?
Thanks for reaching out. Female pattern hair loss is often grouped in with androgenic alopecia (AGA), but in many cases, it’s a completely different condition. For instance — hypothyroidism, hyperparathyroidism, small intestinal bacterial overgrowth, PCOS, certain nutrient deficiencies / surpluses, and medication use can all cause rapid hair loss / hair shedding — but these forms of hair loss are often 1) entirely unrelated to androgens, and 2) morphologically different from AGA (for instance, all of the above typically don’t lead to scarring, whereas AGA does lead to scarring).
There are certainly cases where HRT in peri-menopausal / menopausal females also coincides with hair shedding. Whether this is the result of HRT or just associative as the body undergoes broader hormonal shifts is unclear.
If your testosterone is high, it’s certainly possible that your hair loss could be androgen-mediated, and in some ways, related to HRT. To clarify — you experienced no hair loss pre-HRT? And you’ve been on HRT for 4.5 months and are now experiencing hair loss? Both oral drugs you’re taking shouldn’t (according to the literature) raise free or total testosterone. However, if nothing else has changed besides you taking these drugs, and your testosterone is that high, it’s certainly possible that you’re disproving this. There were some theoretical concerns about oral contraceptives raising testosterone in some women, but early studies tended to quell the fears:
I’d tell your doctor that elevated testosterone in women is associated with female AGA, and given that you’ve seen an increase in both testosterone and hair thinning following HRT, there has to be some sort of interaction occurring. Are you taking any other medications?
Rob, Thank you for responding! I am on no other medications.
Regarding prior hair loss, I believe I was losing some volume and more hair overall prior to starting FemHrt but I was not seeing anything like the excessive shedding I experienced that began about 4.5 months after starting the RX. As I mentioned, I believe it is slowing down now, but the loss is still higher than normal. If the RX has just triggered a telogen effluvium that will resolve within 3-6 months after it began, I am OK with that, but if the FemHrt is causing this ongoing hair loss, I will have to re-evaluate my use of the RX.
One interesting note is that one month after I started the drug, my hair loss completely normalized for 4 months. Then suddenly, it accelerated as I described. Frustrating.
I am having blood work repeated next week, and will be able to verify hormone levels for my Dr. the week after.
I have read your book, and am on day 24 of the massages. I am relieved to have a drug-free option for my hair loss. Also, I have identified several areas that I needed to address regarding my other habits, and look forward to discussing those with you on our Skype session. I just really want to know about the HRT, so I will continue to research it. If contraceptives can cause hair loss, it seems reasonable to me that HRT can as well, especially for someone like me, who normally needs a “pediatric dose” of medications.
By the way, according to my scalp biopsy, there is no evidence of scarring or inflammation, and the percentage of catagen/telogen follicles were normal.
Thank you Rob, and I am sorry for “James’s” comment You are definitely not a “shill”. In my opinion, the price I paid for your book was more than worth it just for the free content you had already posted on the internet. You have done years and years of research, and have taken the time to formulate and share extremely helpful info, and I am grateful!
One more thing: I just looked again at my most recent blood work and realized that my estrogen levels were the same AFTER starting HRT as they were BEFORE–less than 5.0 pg/mL. “Normal” for postmenopausal women is <6.0-54.7. With my testosterone so high (at 49 up from <3.0), this seems definitely out of balance. Maybe it is not that my T is abnormally high (because normal for postmenopausal women is 25.8-134.8), but my E is too low? I would still like to know HOW it got that high, but I now want to know why the HRT didn't budge my estrogen.
Shilling a book at end makes me suspicious of this.
You’re allowed to feel however you want (though I disagree with your word choice). I’d recommend reading the source material of this article (i.e., the cited studies), then building a counterargument using evidence that appears contradictory to any of its claims. Otherwise, there’s just no room for learning / healthy debate, and your feelings will likely persist.
Hi Rob, thanks for the information, you really try to get to the root cause of the problem.
I wanted to know your opinion on the results of Dr. Choy´s paper of detumescence therapy. They argue about 90% recovery in 100% of the subjects of the study. In your experience with the many cases that you have seen firsthand, how much recovery can be achieved? and in how much time could the maximum recovery be accomplished?
Hi Rob, thanks do much for all your hard work on this. I am 21 and have recently been experiencing a receding hair line and shedding.
This seems to be happening very rapidly, I’ve identified a few factors that fit me into your flow chart.
1. I take concerta, which is known to reduce blood flow to scalp.
2. I also have yeast overgrowth in my body and now on my scalp which I beleive is causing the chronic inflammation.
3. I’ve also noticed increased body hair which make me think my DHT has increased systematically
What are the chances I can recover my hair loss in my hair line if I can eliminate the inflammation of my scalp?
It’s hard to say with certainty, but it sounds like your hair loss might be related to AGA and non-AGA related factors. Non-AGA related factors include inflammatory problems like fungal infections. At the end of the day, the right treatment for you will depend entirely on your own comfort levels with 1) treatment time commitments, 2) financial constraints, and 3) your comfortability with FDA-approved AGA drugs and their potential side effects.
On that note, I’ll be sure to write more articles catered toward finding the right treatment. In the meantime, I’d recommend checking out a few more articles on this site to understand more about AGA pathology, and what to target to potentially improve AGA outcomes.
You mentioned in a previous comment, to take care of the ‘trigger’ to AGA if at all magnesium oil was to be effective. Then can you please tell me what is that trigger and how to deal with it? And any other ways to deal with fibrosis and calcification?
I’ve subscribed to your emails but didn’t get any confirmation mail yet. Please look into it.
Hi there, this was a very interesting read. I’d just like to point out something about minoxidil though; it doesn’t just increase blood flow, it also promotes PGE2 and PGE2 is an Estrogen Receptor Beta agonist. ER-Beta receptors have been shown to be active in the stem cells which create the progenitor cells missing in pattern hair loss. That may be part of the reason certain estrogens are able to keep hair follicles in the anagen phase longer.
[…] suggests that in AGA, fibrosis may cause hair loss, and through a few mechanisms: firstly, through the constriction of space for a hair follicle to […]
Hey, i want to know why we call the hairs of the back healthy hair ? It’s because they have less dht receptors ? Resistant to baldness ? Genetical reason ? Or all the follicular units have the same genetic and the same sensibility to the dht ?
Thx for the answer..
This is another attempt to talk about MPB and add no solutions.
Rob talks about excess DHT, but stressed excess calcification & fibrosis. To the readers one can drastically reduce DHT levels. The way to do this isn’t mentioned.
As far as calcification/fibrosis again nothing is mentioned except Vit K which is bit ridiculous. So until Rob gets a game plan, & I don’t see any, it’s a bunch of nonsense by another health expert. Yes, we’ve seen 100 of them selling this supplement or book.
When I read this, I thought Rob the expert had some real suggestions.
I may research the calcification/fibrosis angle & present real solutions. Not some ineffective herb or vitamin or dietary change.
The article was written to reveal some under-appreciated aspects of androgenic alopecia’s pathology. The article sets out to do exactly what its title says: explain why we lose our hair. If you’re looking for advice, therapies, or treatments – this isn’t the right article. Yet there are dozens of others on this site that can provide insights here.
As far as referring to me as “Rob the expert” – I can’t help but feel, based on the way the rest of your message reads, that this is a dig at me. It’s easy to take swings at people anonymously online. It’s harder to actually recognize their work. For reference, here are the last two peer-reviewed papers I’ve published on androgenic alopecia:
As far as me presenting “some ineffective herb or vitamin or dietary change” – this is a bit disingenuous and at-odds with the very argument you originally stated: that I presented no solutions.
I don’t recommend herbs or vitamins to treat androgenic alopecia. The flowchart presented here shows us just how limited these things are in actually reversing the rate-limiting recovery factors of the condition. If you decide to implement any of the advice from this article, I hope you can read between the lines and understand what I’m really saying: for people to stop buying into supplements that do absolutely nothing for their hair. In doing so, you (and everyone else) can save yourself thousands of dollars.
Good luck with your research!
Hi Rob, and anyone else who may wish to add a comment:
I’m about to go down the Dermapen (Microneedling) route for my scalp. A large basis for the touted effectiveness of microneedling is that it brings collagen and growth factors to the micro-injury sites, and that it supposedly a “good thing” for hair loss, as well as for, say, fine lines in the face.
After reading this article, I see increased collagen in the scalp as a “bad thing” (paraphrasing here!).
What is your opinion of microneedling the scalp for hair loss in light of this? I am fairly sure I have confused the mechanism of collagen so far as microneedling vs its detrimental impact in hair loss as per your article. Perhaps they are two different mechanisms, with different effects?
Best Regards, Matt.
It’s a great question, and it’s been raised a few times here… mainly due to my lacking clarity as I tried to simplify the article into lay terms. When I reference “excess collagen”, what I really mean by this is disorganized collagen. Disorganized collagen is fibrosis (or scar tissue). Microneedling seems to help diminish this type of scarring while simultaneously promoting the formation of more organized collagen. In AGA, more organized collagen is generally a good thing – because one of the rate-limiting recovery factors of AGA is disorganized collagen in the form of perifollicular fibrosis and collagen-like streamers residing underneath the hair follicles.
Long story short: microneedling probably helps to remove some of the bad collagen and promote some of the good collagen.
ive been suffering from hair loss for the past two year . i am 23 years and i was having thick hair as of 21 . my hair now fall many times when i just comb . multiple strands of hair fall out (300) everyday. my hair even falls when i rub my hands through my hair. im really scared and my scalp can noticeably seen in day light. please what should i do to stop this situation..
First I’m sorry for my bad english 🙂 Thank you very much for all these informations.
I’m interested in reversing hair loss but also the fact that I have too much body hair. Is it the same method for both?
Have you considered the role of vitamin K2 in preventing calcification.
Vitamin K2 mk7 activated proteins such as matrix GLA protein which prevents calcification in soft tissues and is understood to actually reverse the calcification process.
Vitamin K2 works with vitamins D3 and A to properly support calcium blood levels and directing calcium to desirable places in the body (bones, teeth etc.) and away from undesirable places (soft tissues, joints etc.)
Male pattern baldness corrolates with hypertension because both are a symptom of calcification.
Thanks for reaching out. I’ve seen research demonstrating that vitamin K2 can reverse calcification induced from drugs like Warfarin, and mechanistic research demonstrating a potential role for preventing soft tissue calcification in humans. Unfortunately, in the last five years, I’ve interacted with (probably) 40+ people who’ve tried mega-dosing with vitamin K2 alongside adjunct vitamins/minerals to improve their pattern hair loss, and I’ve yet to see any improvements with anyone using this approach.
In cases of nutrient deficiencies or poor diets, vitamin K2 (alongside becoming nutrient replete) will likely help to slow down the progression of AGA. But as far as a preventive tool, I have my reservations. This article might be of interest to you:
Hi rob, if scalp clar and fib, are in part responsible for hair loss then why aren’t there more females with hair loss?
Thanks for reaching out. The current estimates are that female pattern hair loss affects 50% of women throughout a lifetime. So, the incidence seems pretty high to me!
In terms of comparing these statistics against males (80% of whom will experience male pattern hair loss), the difference may just boil down to significantly less androgen production throughout adulthood.
Hi Rob, thank you for all this information and these explanations, it is very clear and everything is summarized here.
What do you think of the Growband product by Hairguard, some explanations perfectly match what you explain. It is certainly not miraculous but it must be able to help, by stimulating the bloodflow and relaxing the hair scalp apparently that fights fibrosis and calcification.
This product is incredibly overpriced, but there seems to be a logic behind it.
Thanks for this super useful article.
I am very healthy on my diet, do sports, etc. So, I ask myself, how come it could be that I have calcification and fibrosis? You see, I am having the thining hair or the top and can already see my scalp.
You mention in the article the excess of collagen. I have been taking collagen supplements for a couple of years maybe, and probably that´s the time when my hair started to thin, more aggressively in the last year. Would you think that the collagen supplements has something to do in this process?
Not sure if you have an article about preventing calcification and fibrosis (or even reversing), but it would be a great addition.
Thanks once again,
I am finally made an effective hair growth technique which is made possible by multiple factors.
1. Magnesium oil on scalp for 30 minutes before bath.
2. Using Eclipta Alba & Phyllanthus Niruri Tinctures (Topical at Night)
3. Scalp massage after bath.
4. A very good green diet.
Hello Rob. I concerned about my hair and I was reading your article and it’s great. Rob why is it that many homeless people with poor diets a unhealthy lifestyle have no issues with hair loss?
first of all I must say: I am very happy to have found your site, your precious information declined in scientific papers and via email. Thank you.
I wrote you an email, sorry to be redundant, but I thought it would be useful to post my experience/doubts for everyone who read. Hope you find the time to answer and feel free to choose where to answer 🙂
I have some question cause I think that most of the articles are partly destinated to a male audience.
I’m a woman of 33, I know for sure that I have (severely) abused my hair in the past with aggressive dyes and pulled hairstyles, I have had periods in my 20s with itchy and discomfort scalp, since many months overcome by the application of natural oils, super gentle shampoos and LOTS of massages. Sometimes I feel some annoyance in the scalp but can’t find why.
I had some truly relief and visible results using minoxidil 5% (not the one on the market but a galenic preparation with nigellamed, progesterone, latanoprost, 17-alpha-estradiol, estrone, melatonin ..) but i quit after a year scared to be totally slave of that drug. And I lost all my gained hair density.
Considering that I can exlude many health problems like Pcos, lack of vitamins, intestinal disorder… can I really reconduct my thinning state to chronic inflammation? And what’s the discriminant that can explain the success of the galenic preparation? Maybe the anti-inflammatory plus estrone recipe?
Many thanks in advance for your advices.