The Leading Theories Of Pattern Hair Loss

Read Time: 20 minutes

Note: This article is technical. If you’re new to hair loss research, it’s best to start here.

Do Any Hair Loss Theories Hold Water?

When it comes to explaining why men and women lose their hair, no theory has all the answers.

Some researchers say that DHT causes hair loss. That’s sort of right. But unfortunately, even the DHT theory cannot explain…

  • …why men start thinning at the hairline and vertex
  • …why women start thinning evenly across the scalp
  • …why men usually don’t lose hair at the scalp sides
  • …why women thin all over, even at the scalp sides
  • …why DHT encourages body hair growth, but scalp hair loss (the DHT paradox)

And while alternative hair loss theories get us closer to the answers, they still have holes.

This article uncovers the leading theories to pattern hair loss. For each theory, we’ll cover:

  1. The Science
  2. The Shortcomings

 

Theory #1: DHT Theory Of Baldness

This is the theory of all hair loss theories. It’s touted by most doctors, surgeons, and researchers trying to quickly summarize why someone’s balding.

The Science

Dihydrotestosterone, or DHT, is a hormone that comes from testosterone.

DHT is higher in thinning regions of men’s scalps. As a result, many researchers say that DHT causes hair loss.

I first heard about DHT when I was diagnosed with pattern hair loss in 2007. Here’s how my doctor described the process:

For reasons not fully understood, hair loss begins when DHT starts accumulating in our scalps. Our hair follicles become sensitive to DHT, then begin shrinking. Over a series of hair cycles, DHT makes our hair thinner and wispier, until our hair becomes so thin that it disappears. The end result: pattern baldness.

Beyond my doctor’s summary, there are three findings which form the DHT-hair loss argument:

  1. DHT is higher in the scalps of men with thinning hair.
  2. If a man is castrated, his testosterone and DHT levels plummet forever. Men castrated before puberty (ie: before their DHT levels spike) never go bald later in life.
  3. Some men have a rare genetic condition where they the lack an enzyme which converts testosterone into DHT in the scalp. Men who have this condition never lose their hair.

That’s a very compelling case… Just look at the extremes. If we never make any DHT, we never go bald. And if DHT is too high in our scalps, we lose our hair.

So what’s wrong with this theory?

The DHT-Hair Loss Theory’s Shortcomings

The DHT-hair loss theory leaves at least four questions unanswered:

  1. If DHT is the problem, then what causes DHT levels to rise in the first place?
  2. Why do our follicles become “sensitive” to DHT?
  3. How does DHT actually shrink our follicles?
  4. Why do men lose their hair in a horseshoe pattern, while women thin all over?

Doctors have a one word answer for all these questions: “Genetics.”

Unfortunately, that’s not only unproven, it’s also misleading.

DHT is just one of many factors associated with hair loss. It’s just one of several hormonal factors. It’s also just one of several biomarkers of a balding scalp – the others being arterial calcification, fibrosis, collagen remodeling, restricted blood flow, and a decreased subcutaneous fat layer.

Even worse, the DHT-hair loss theory doesn’t address DHT’s biggest paradox…

DHT in body and facial tissue encourages hair growth. DHT in scalp tissue discourages hair growth. Why?

Another leading theory takes a stab at answering this.

 

Theory #2: Gravity Theory Of Baldness

Another theory is the Gravity Theory Of Baldness, which came about in an effort to answer the paradox of DHT:

Why does tissue DHT encourage body hair growth and simultaneously discourage scalp hair growth?

The theory’s answer is quite simple: gravity.

The Science

One symptom of a balding scalp is an eroded subcutaneous fat layer.

Subcutaneous fat is an insulating layer of fat. It’s found all over the body – including our scalps (on the sides, back, and top). At the tops of our scalps, the subcutaneous fat rests between the scalp skin and the galea (more on that later):

(source)

When we’re younger, our scalp’s subcutaneous fat is relatively equal on the sides and top of our scalp. But during pattern hair loss, the subcutaneous fat at the top of the scalp starts getting thinner and more eroded.

According to the theory, here’s why:

Our heads are upright for most of the day, creating chronic pressure against the hair follicles and our scalp’s subcutaneous fat layer.

At the start of puberty, men’s androgen levels surge (we get more testosterone and DHT).

The Gravity Theory Of Baldness states that downward force + high androgens kickstart the erosion of subcutaneous fat in the scalp.

For women, the theory states that high estrogen levels preserve the scalp’s subcutaneous fat layer – at least until menopause when estrogen levels plummet.

According to the theory, this is why men start balding into early adulthood, and why women typically don’t lose their hair until later in life.

How Does This Explain The DHT-Paradox?

Well, DHT encourages body hair growth while also encouraging scalp hair loss.

According to the Gravity Theory Of Baldness, DHT will only encourage hair loss if there is constant downward force at that skin site (aka: gravity).

So, the top of men’s heads is under constant gravitational force. But their beards and body hair aren’t under the same force, because they’re angled differently.

And that’s why men don’t go bald at the sides of the scalp or on their bodies or faces. Gravity’s force isn’t directly downward there, so the subcutaneous fat layer doesn’t erode in the presence of androgens like it does at the top of the scalp.

Summarizing The Theory Step-By-Step

Men’s scalps are protected against the downward forces of gravity until puberty, at which point testosterone levels increase and begin to erode the scalp’s subcutaneous fat layer. When this happens, our hair follicle’s subcutaneous “cushion” starts disappearing. The hair has to work harder to continue growing and survive.

Since androgens encourage hair growth in other parts of the body, our body responds to the decrease in the scalp’s subcutaneous fat by sending more androgens there – in the form of DHT.

DHT is supposed to encourage hair growth! But in an effort to encourage hair growth, DHT – a testosterone derivative – also erodes more of the scalp’s subcutaneous fat layer. The process continues until the subcutaneous fat layer nearly entirely dissipates, miniaturizing the hair follicle until it eventually turns dormant.

Gravity, according to the author, explains why men only bald at the top of the scalp, and why DHT encourages body hair growth and scalp hair loss simultaneously.

The Gravity-Androgen-Hair Loss Theory Shortcomings:

If this theory feels incomplete, it’s because it is.

Problem #1: the theory doesn’t actually explain the “pattern” of male pattern hair loss.

While the author explains why men lose hair at the top of the scalp, he doesn’t necessarily explain why the loss occurs in a pattern – or why men generally start thinning at the temples and vertex, then progresses from there.

Problem #2: the Gravity Theory doesn’t explain why men bald differently than women.

Males typically recede at the hairline and thin at the crown, but most women thin all over.

How does the Gravity Theory explain women’s even thinning at the top and sides of the scalp? Technically, any thinning on the scalp sides refute this theory, or at least give evidence of another mechanism.

Problem #3:  like women, men can also lose hair at the sides of the scalp, not just at the top.

Men in advanced stages of hair loss typically lose hair on the sides and even parts of their sideburns.

According to the Gravity Theory, the subcutaneous tissue shouldn’t erode here because it’s not under the same chronic gravitational force. But in advanced stages, men and women definitely experience hair loss in these places.

Problem #4: If this theory were 100% true, we’d also expect DHT to exert the same hair loss effect on other parts of our body that stay upright as long and as often as our heads.

For example, our shoulders. By the logic of the gravity theory, men should never get hairy shoulders. Why? The shoulders are on the same horizontal plane as the tops of our scalps. Our shoulders stay upright just about as long as the tops of our scalps, which means they’re under about the same gravitational pressure.

And at puberty, we’d expect a surge in androgens and the degradation of subcutaneous fat tissue in our shoulders, which means we’d be hard pressed to find any guy who’s balding with hairy shoulders.

Except here is a balding guy with hairy shoulders:

And another:

Hairy shoulders are so common I could start naming friends of mine with them.

As such, the Gravity Theory offers an incomplete explanation as to why DHT encourages hair growth and hair loss depending on the tissue. It doesn’t explain female pattern hair loss. And while the Gravity Theory might explain the relationship between a scalp’s decreased subcutaneous fat, increased DHT, and hair loss, it doesn’t come close to explaining the actual “pattern” of male pattern hair loss – or why recession and thinning starts at the temples and vertex.

The next theory does.

 

Theory #3: The Skull Expansion Theory

The third theory that offers an alternative explanation to the “pattern” of male pattern hair loss is The Skull Expansion Theory.

The theory is as follows: we know that the bones of the human skull continue growing throughout adulthood. We also know – based on observations – that balding men typically have a different head shape than non-balding men. Their forehead has a bulge at the midline, and some would even say their entire heads are larger than the heads of those unaffected by hair loss.

It turns out that DHT – which is elevated in balding scalp tissues – is also a hormone used by the body for bone remodeling.

The Skull Expansion Theory argues, like the Gravity Theory, that the presence of DHT should encourage hair growth, not hair loss. But because DHT also encourages bone growth, then elevated DHT in the scalp also increases skull bone growth. This bone growth expands the size of the skull, and in doing so, moves the follicles further away from the capillary networks that supports them. The resulting reduction of blood flow leads to follicle miniaturization, and subsequently, hair loss.

This theory is versatile in that it explains all the different patterns of hair loss for men. Skull bone growth at the front of the scalp leads to thinning at the temples. Skull bone growth at the back of the scalp leads to thinning at the vertex. If you take a walk around town, you can see for yourself the evidence of the skull expansion theory. Men who are receding at the temples typically have a bulge at the front of their scalp. If you’re suffering from pattern hair loss and you have older photos of yourself, you might even notice the development of this bulge as you began to thin over the years.

The Skull Expansion Theory Shortcomings

The first problem with the Skull Expansion Theory is that there are some men who clearly have experienced skull expansion, but also minimal or no hair loss. This is evident when we look specific cases of frontal bossing — or when the brow line begins to protrude far beyond the forehead.

Not all people with frontal bossing or forehead protrusion experience hair loss.

Moreover, frontal bossing and severe forms of skull expansion are often the result of excessive growth hormone release - sometimes due to a tumor in the pituitary gland. In some cases, the release can be so excessive and so chronic that a person’s hands, feet, face, head, and body continue to grow throughout adulthood.

This is called Acromegaly. Andre The Giant had the condition, but despite his bone growth, he also had pretty good hair.

So did this guy:

There are also cases of men whose skulls haven’t expanded much but have still gone bald.

Take Kelly Slater at 19-years old and then in his forties.

His scalp is very well rounded - there’s no frontal bossing, and minimal (if any) expansion on the sides of his scalp. It looks as if he just shaved his head. He did. But during that period, he also lost a lot of hair.

The second problem is that the Skull Expansion Theory, like the Gravity Theory, doesn’t fully explain the difference in male versus female pattern hair loss, or why women typically thin evenly everywhere while men thin at the temples and vertex first.

With that said, I believe in the association between a bigger head and a balding scalp. Skull expansion is definitely a factor in many pattern hair loss cases. The theory deserves more attention and more research, and its author, Paul Taylor, deserves significant recognition for putting out an idea with more merit than, in my opinion, nearly every other theory. But as far as the skull expansion causing hair loss -- I think this has still yet to be proven.

Which brings us to the last and most specific theory of all.

 

Theory #4: Muscular Tension / Tight Galea Theory

There are a few iterations of the tight galea and muscular tension theories of pattern hair loss, and I believe these theories - while still incomplete - take us closer than any other in addressing all the studied conditions of a balding scalp.

Here are the basic principles behind the theories. If you’re interested in learning more for yourself, I encourage you to read this, this, and this.

Each of those articles is worth your time. In fact, those findings are why I recommend spending so much time massaging the sides, nape, and sutures of your scalp - and not just your thinning areas.

The theory is as follows: the parts of the scalp predominantly affected by male pattern baldness are all above the galea. The galea is a fibrous tissue that rests over the entire top of the scalp. It’s a connective tissue that links the muscles above your eyebrow (frontalis) and the muscles behind your ears (occipitalis). There are no muscles on the top of your scalp - just the tendon-like fibrous tissue known as the galea.

(source)

For men, the areas of the galea aren’t really affected by hair loss. It’s just the hair residing over the galea that tends to disappear. So the question is, why?

It turns out that balding scalp tissue actually fuses to the galea.

Above our skull bones, our scalp has five tissue layers - the skin, the subcutaneous fat, the galea, the subgalea, and the pericranium. Again, here's a reference:

(source)

In balding sites, the top three layers fuse together - the skin, subcutaneous fat, and the galea - creating one large, inseparable, fibrotic-ridden unit.

It’s important to note this fusing is unique to balding sites. It doesn’t happen in non-balding areas or at the hair sites on the sides or backs of our heads.

This fusing results in an increased presence of fibrotic tissue, a decrease in scalp skin elasticity, a decrease in the density of the scalp’s subcutaneous fat, and finally, hair loss.

But here's the question no one's yet figured out:

What causes the galea to fuse to the top two layers of our scalps?

There are a few different ideas:

Galea Fusion Theory #1

One idea is that androgens drive greater muscular development, and due to higher androgen levels, men tend to have larger developed muscles surrounding the galea. These muscles are difficult to fully relax. As a result, the muscles are often in contraction and chronically “pulling” on the galea, thereby tightening it.

A galea pulled tight by chronically contracted muscles restricts blood flow to the galea, and in doing so, reduces nutrient flow and oxygen levels of tissues supporting the hair follicles. Over sustained periods, a reduction in tissue oxygen levels can result in chronic low-grade inflammation, which eventually culminates into the development of fibrotic tissue - the same tissue that fuses together the top three layers of the scalp.

Interestingly, the areas where scalp tension is greatest are the vertex and the temples, meaning these areas should be the first to suffer from hypoxia, and the first to go bald.

This idea has existed for years and was partially validated by a study about Botox and hair loss - where Botox was injected at the scalp’s side and back muscles surrounding the galea to disable their movement. The six month results were a reduction in muscle size, a more relaxed galea, modest hair thickening, and partial hair regrowth.

Shortcomings

This idea makes sense for men, but it doesn’t explain the different patterns in male versus female pattern hair baldness.

Galea Fusion Theory #2

We’re back to the Skull Expansion Theory. Androgens increase at puberty and drive, among other things, bone growth. For the most part, our skull bones continue developing throughout our adult lives - and part of this skull bone growth is mediated by DHT. As the skull bones grow, they increase the tension against the galea and its surrounding muscles, which restricts blood flow and reduces oxygen tissue levels (also known as hypoxia), which causes chronic inflammation that eventually culminates in fibrotic fusing of the skin, subcutaneous fat, and galea.

Shortcomings

The same shortcomings as before. This theory gets us very close, but there are still cases of skull expansion without hair loss and little to no skull expansion with hair loss that challenge its completeness. This theory also doesn’t explain the difference in male versus female pattern hair loss - why women thin all over and men thin in a horseshoe-shaped pattern.

Galea Fusion Theory #3

The final idea is that the galea fuses with the scalp’s top two layers because of an increase in scalp androgen sensitivity mediated through mechanical force. This one is a mouthful, so bear with me.

We know that androgens, like DHT, play a role in pattern hair loss because men who are castrated before puberty have very low levels of DHT and don’t go bald later in life. We also know that tissue DHT levels are higher in balding versus non-balding parts of the scalp. This is why people associate DHT with hair loss. There’s definitely a relationship, but whether DHT is the cause of hair loss is still debated (as evidenced above). In any case, this phenomenon begs the question: why do tissue DHT levels increase only in balding areas, and not everywhere in the scalp?

Some researchers believe DHT levels are higher in balding regions because of an idea known as “enhanced androgen sensitivity.” And here comes the mouthful.

In order for DHT to accumulate in the scalp, DHT needs to attach itself to a receptor site. These receptor sites are known as androgen receptors.

Androgen receptors are located inside our cells. When DHT attaches to a cell’s androgen receptor, that DHT molecule will influence that cell’s functionality. For example, in certain facial and body tissue cells, DHT appears to influence cell function by encouraging hair growth. But for cells surrounding the hair above the galea, DHT appears to encourage hair loss.

How can that be? How can the same hormone encourage both hair growth and hair loss, with the only difference being body location?

It turns out that DHT molecules aren’t the only thing that influences a cell’s function. Certain proteins can also change cell behavior. These proteins are called androgen receptor “coactivators.” These coactivators interact with androgen receptors - the place where DHT binds - and “enhance” the androgen receptor’s function. In other words, these protein “coactivators” increase a cell’s sensitivity to androgens.

One of these coactivators is called Hic-5 / ARA55. This coactivator is highly active in beard tissues and in balding tissues of the scalp, but not so active in non-balding parts of the scalp like the back of the head.

This is important. In tissues with elevated DHT (the tissues that grow facial hair and the tissues in bald parts of the scalp), this protein coactivator is also higher. Some research suggests that this very coactivator regulates androgen sensitivity in human hair follicles. To put it bluntly, if a cell expresses the Hic-5 / ARA55 coactivator, you can bet that DHT will bind to it.

According to the theory, this is why some tissues accumulate DHT and others don’t. At puberty, the Hic-5 / ARA55 coactivator increases in facial, body, and scalp tissues above the galea. As a result, more DHT binds to those cells’ androgen receptors. Paradoxically, in the scalp, more DHT leads to hair loss. In the face and body, more DHT leads to hair growth.

But why? If an increase in Hic-5 / ARA55 explains why certain tissues start accumulating more DHT, then why does an increase in DHT cause hair loss at the scalp but hair growth in the body?

This is where the mechanical force element comes in.

The Hic-5 / ARA55 coactivator is activated by both androgens and mechanical force -- specifically, stretching tension, the kind of tension occurring naturally in the galea.

It also turns out that increased DHT in the scalp also stimulates something called transforming growth factor beta 1 (TFG-β1). TFG-β1 is a signaling protein, and when it’s overexpressed, it leads to perifollicular fibrosis - or scarring surrounding the hair shaft that miniaturizes the hair and leads to hair loss. Chronically elevated levels of TFG-β1 are suspected to cause the fibrotic fusing we observe in the top three layers of balding scalps.

This creates the “perfect storm” hair loss cycle. It goes something like this:

  1. At puberty, an increase in androgens stimulates the expression of Hic-5 / ARA55 coactivators in body, facial, and certain scalp sites. This coactivator makes a cell’s androgen receptor more “sensitive” to DHT - and thereby more likely for DHT to bind to it.
  2. More DHT binds to androgen receptors in body, facial, and scalp tissues… But in the scalp tissues, more DHT also leads to an overexpression of TFG-β1.
  3. Above the galea, the overexpression of TFG-β1 results in perifollicular fibrosis. The hair follicles begin to miniaturize, and over time, this fibrosis begins to fuse together the top three layers of the scalp - the skin, the subcutaneous fat, and the galea.
  4. This “fusion” creates more mechanical tension, especially at the the vertex and temples, and that tension encourages an even higher expression of the Hic-5 / ARA55 coactivator.
  5. The Hic-5 / ARA55 coactivator encourages more DHT to the scalp tissue (increased androgen sensitivity), which increases TFG-β1, which increases perifollicular fibrosis, and then fibrotic fusion of the top three scalp layers (mechanical tension), which activates more Hic-5 / ARA55…
  6. ...and the cycle repeats.

The more Hic-5 / ARA55, the more DHT, the more TFG-β1, the more perifollicular fibrosis, the greater the galea fibrotic fusion, and the more hair you lose… until the entire galea is fused with the top three scalp tissue layers.

Shortcomings

This theory is the most complicated, and thereby lends itself to serious nitpicking. I won’t get into all of the issues, but these three shortcomings alone warrant more research:

  1. The theory’s argument that TFG-β1 increases more in the scalp than other body sites is unfounded. TFG-β1 is a signaling protein. It’s used in tissues all over the body for processes ranging from inflammatory responses to cell proliferation. While there’s evidence to suggest TFG-β1 inhibits hair growth, I’ve never seen anything that says TFG-β1 is higher in balding scalps than body or facial tissues that bear hair. That needs to be true for the theory to hold. But for now, this statement is just conjecture.
  2. The theory doesn’t explain why, at puberty, androgens stimulate the expression of Hic-5 / ARA55 in soon-to-be hair bearing body and facial tissues, on scalp tissue above the galea where hair is already present, but not on hair-bearing sites on the sides of the scalp. The theory says this coactivator over-expresses above the galea because of the mechanical tension already naturally occurring in the galea... But if this is the reason why the coactivator expresses itself above the galea but not on the sides of the head, then is there also similar tension at every other hair site on the body and face? Here we have a chicken-and-egg problem. Which came first: the tension or the Hic-5 / ARA55 coactivator? And even ignoring this, the theory still doesn’t explain the mechanism behind which androgens activate the Hic-5 / ARA55 coactivator. Basically, the theory consists of a lot of unproven assumptions.
  3. This theory doesn’t explain the different patterns in male and female pattern hair loss!

Problems with the Muscular Tension / Tight Galea Theory

Again, these theories don’t explain the different balding patterns in men versus women. They only explain pattern hair loss for men.

In fact, I haven’t come across an alternative or mainstream theory that addresses these differences. It’s a question we’ve yet to answer.

Otherwise, I tend to agree with the scalp tension and galea theories of hair loss more than others. Scalp tightness and chronic muscular tension can lead to the chronic inflammation that results in the calcification-fibrosis cascade of hair loss.

 

Which Hair Loss Theory Do I Believe?

I don’t adhere to any specific theory.

I think the Gravity Theory, Skull Expansion Theory, and Muscular Tension / Tight Galea Theory all have their flaws and merits. Each theory is capable of explaining most, but not all, of the pattern in the context of male pattern hair loss’ symptoms.

With that said, here's what all these theories miss:

  1. None do a perfect job at explaining why women bald in a different pattern than men.
  2. None of these theories accurately address the DHT paradox - why DHT encourages body and facial hair growth but discourages scalp hair growth.
  3. None of these theories truly take into account the relationship between increased DHT, androgen receptors, imbalanced calcification regulators, and the very strong evidence that calcification and fibrosis precede hair loss by choking the follicles of proper blood, oxygen, and nutrient supply.

What can we glean from all of this?

We need to do more research.

If hair loss research orient their studies to answer...

  1. Why men bald differently than women
  2. Why DHT encourages body hair growth, and scalp hair loss
  3. Why, in advanced stages of androgenic alopecia, men lose hair at the sides and napes of the neck

...then I think those answers will take us closer to a universal cure.

Until then, I believe the best (and safest) hair loss solutions are to target calcification and fibrosis.

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27 Comments

  • Steroid master

    Reply Reply November 2, 2016

    Different person has different sensitivity of skin follicles to testosterone (or DHT), that’s why some people are hairy, some dont.
    When we get older and older, the skin follicles become more and more sensitive to testosterone (or DHT), that’s why the older we are, the more body hair, the more beard, the more hair loss.

    thanks for your detailed outline of different theories about Male pattern baldness, It’s eye-openning.

    I have one question:
    “men who are castrated before puberty have very low levels of DHT and don’t go bald later in life”
    Have anyone 100% checked this? castrated men were scarce, maybe they happened to be those who would not go bald even not castrated?

    Do we need widely castrated men to verify the thoery?

    • Rob

      Reply Reply November 3, 2016

      Hey there,

      It’s been well-documented that the majority of testosterone production in men comes from our testes. In fact, some estimates suggest that over 95% of men’s testosterone is produced from the testicles:

      https://www.ncbi.nlm.nih.gov/pubmed/3549275

      Given that relationship, and that DHT is made from testosterone, I’d say that the observational papers suggesting castrated men before puberty never go bald probably hold validity. We could always benefit from deeper analysis and more data, but in general, I think (for now) that relationship is pretty clear.

      • Steroid master

        Reply Reply November 6, 2016

        how can I get full paper from this ncbi website?

        • Rob

          Reply Reply November 7, 2016

          You can either buy the paper or access it through a university.

  • Steroid master

    Reply Reply November 3, 2016

    I saw ad in youtube about Gofybr-get your hair back in seconds.
    Do you think this is another snake oil product?

    • Rob

      Reply Reply November 3, 2016

      If the ad were for getting your hair back in seconds, my guess is that it’s an ad for a topical product that masks thinning hair – like Toppik or Caboki hair fibers. These aren’t necessarily scams – they’re just aesthetic masks to the problem. They don’t regrow your hair, but they certainly give your existing hair a fuller, thicker appearance.

  • Jolly

    Reply Reply November 7, 2016

    Rob, what do you think about the role of genetics? Do some people, because of their genome, develop easily fibrosis or calcification? Because it’s clear in my opinion that even if the gene expression is influenced by diet and environment, there are some people more at risk of hairloss because of genetics.

    • Rob

      Reply Reply November 7, 2016

      Hey Jolly,

      Genetics definitely play a part. While the completion of the Human Genome Project showed that genes don’t determine our destiny – and that gene expression likely plays a large role in disease development – that’s not to say that hair loss isn’t at least partially genetically driven.

      I got a 23andMe test to see how genetically predisposed I was to hair loss. It turns out I have pretty much all of the genes linked to baldness – including the worst ones mapped (polymorphisms to the androgen receptors that increase my chances for baldness 7x).

      So I agree with your statement. And to add to it, I think that certain people (like myself) have to work harder to overcome any genetic disadvantages.

      Best,
      Rob

  • Nicholas

    Reply Reply November 23, 2016

    Hey Rob,
    what do you mean by “chronic muscular tension”? You once told me in the comments of this website that you experimented Tom Hagerty’s scalp exercise, which needs the alternate contraction of the scalp muscles. Is that a different thing? In my actual regime I regularly do that exercise and I hope it’s not damaging my hair, although it doesn’t seem so.

    • Rob

      Reply Reply November 23, 2016

      Hey Nicholas,

      The theory is that the muscles surrounding the galea pull the galea tight and limit blood flow, oxygen, and nutrients required to support the follicles. If you subscribe to this theory, then around puberty our androgens spike and kickstart the development of more defined muscles – including the muscles surrounding the galea. The theory states that due to head shape (and even natural posture), some men subconsciously keep these muscles contracted – which over a series of years leads to hair loss as a result of the constricted blood, O2, and nutrient supply.

      The theory behind the Tom Hagerty exercises is that they allegedly help us to “relax” those muscles that are otherwise in chronic contraction. In doing so, you might restore some blood flow to the hair follicles above the galea and thereby O2 and nutrients as well. Once you gain control of those muscles, you can make a conscious effort to keep them loose throughout the day.

      • Nicholas

        Reply Reply November 24, 2016

        Thank you very much for your answer!

  • Joona

    Reply Reply November 30, 2016

    I remember when I was younger my scalp skin was more “fat” i remember my hairdresser said i not have stress but now my scalp in top very thigh. I dont have still stress but i can not think why that has happened my head is not big… also i remember i had more oily head and forehead now i feel just dry and my hair feels dry too…how explain that? I think it has something to do with my thinning hair in top….just wondering. Also When i do scalp massage my scalp gets very dry and my head full of white dead skin… what i do wrong?

    • Rob

      Reply Reply December 1, 2016

      Hey Joona – the erosion of subcutaneous fat is often closely linked with an increase in androgens (testosterone and/or DHT). At least, that’s the current leading theory.

      Changes to sebum production (the oil to which you’re referring) can manifest in a lot of ways – diet, environment, lifestyle, stress, etc. Accutane is a drug that targets acne reduction by shrinking the sebaceous glands (which produce sebum), and it’s essentially high dose retinol (a form of vitamin A). So vitamin A has been shown to modulate sebum, but there’s just a million other reasons so it’s tough to give you a concrete answer without more information.

      Regarding the massages — I don’t know if you’re doing anything wrong. Dandruff is a commonly reported side effect and it often doesn’t indicate anything negative.

      Best,
      Rob

  • dante

    Reply Reply December 1, 2016

    Hi Rob,
    You mention commonalities between between scleroderma and MPB.
    So, there is a protein called TLR4 which reacts with endotoxin secreted by gram negative bacteria in our gut.
    http://news.feinberg.northwestern.edu/2012/11/fibrosis-_protein/
    Quoting from the study – “when the gene for TLR4 was mutated in mice, the mice became resistant to experimental scleroderma. Agents that block TLR4 are already being developed for inflammation and sepsis in humans. Effective TLR4 inhibitor drugs may blunt and even possibly reverse the fibrosis in scleroderma”
    Guess what antagonizes TLR4 in humans – 5AR derieved steroids. So, there might exist a positive feedback loop where upregulated TLR4 causes DHT buildup and the cycle continues ?
    This points out to the gut microbiome imbalance. This might explain why Danny/Peat insists on taking antibiotics . May be you can explore more on this TLR4 and 5AR connection.

    • Rob

      Reply Reply December 1, 2016

      Dante – incredible find. And thank you for sharing it with me. I’m going to look into this right away.

      One question – could you pass along the information about 5-AR derived steroids being antagonistic to TLR4? If true, your hypothesis about a feedback loop has a lot of merit.

      As far as antibiotics – I’m on the fence, but I understand why Ray Peat sometimes recommends them. Another approach might be reintroducing bacteria that compete with TLR4-promoting microbes. As I learn more I’ll continue to share with you. And thanks again for passing this along!

      • dante

        Reply Reply December 2, 2016

        Hi rob,
        search about tlr4 and 5AR on the raypeat forum. You will find more on the benefits of 5AR there than probably anywhere else.
        I agree with not using antibiotics. Shifting the balance in favor of gram positive might be better

  • Ginger 25

    Reply Reply April 5, 2017

    Dears,

    the solution is simple and not new :

    The DHT is like a fertilizer for hair, yes.

    As the scalp/galea is under tension, the DHT level increases, also due to a cyclic effect of inflammation.

    This DHT simply boost the growth of the Hair, and too much over the Galea resulting in an excess of stimulation : the follicle shrinks because of too much growth rate, tired. That’s simple and obvious but not easy to counteract.
    The root cause is : calcification of blood vessels, resulting in less feedings to capilaries ends, thus brown adipose reduce, thus galea+skin creates tension, that reduce blood flow and increase DHT level (not washed out).

    An organ that is not used, shrink. Scalp must be stimulated (motion, running, cold exposure) and we should eat much less Calcium from Milk and Diaries, also because it perturbates our Gut equilibrium, and lessen the amount of Omega3 manufactured by our microbiots.

    Best Regards

  • Kris

    Reply Reply May 13, 2017

    Hi Rob,
    Thanks for all the work in summarizing all we know and (that we don’t) about hair-loss. Appreciate that you still leave the door open to that one elusive theory of everything about hair-loss.

    Would like to hear your insights on the following:
    1. How come transplanted hair form (back/side areas of scalp) are able to continue growing unaffected by those same factors that caused balding in the vertex and crowning areas? Or has that claim by hair surgeons never been tested?
    2. The blanket reason is almost always genetics or “everyone is different” but I would add one more to the list of things the theories presented above fail to explain and it is quite simply: within males, why do some men bald whereas others don’t ever given similar/normal levels of androgenic hormones?

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