Why The Galea Is The Fundamental Cause Of Male Pattern Balding (& Androgens Are Secondary)

IdealForehead

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The Basic Question
One of the most puzzling questions about male pattern baldness that until recently has remained unanswered has been: Why does hair loss afflict us in the Norwood pattern?

Here, as we know it, is the Norwood pattern:

bald.jpg


Hair loss begins at the corners, temples, and crown. Little by little it spreads from these points until the entire top of the head is bald.

For years, scientists have puzzled over the distribution and mechanics of androgenic hair loss as it pertains to scalp anatomy:


image001.jpg



If you look at the basic structure of the head, you will notice a simple difference between balding areas and nonbalding areas:

Balding areas overlie the galea, while nonbalding areas (the NW7 horseshoe) overlie scalp muscles.

The galea aponeurotica (GA) is a fibrous band of connective tissue that connects to numerous scalp muscles. Recent research suggests that the galea is the fundamental cause of male (and female) pattern baldness.

How the Galea Causes Hair Loss
In simple terms, the galea is a site of constant mechanical stress from the muscles that attach to it. This mechanical stress is transmitted to the hair follicles which are attached to it. Mechanical stress triggers epigenetic changes to the hair follicles, which may begin even from the scalp's first development.

An androgenic and inflammatory cascade is eventually triggered as a result of this chronic mechanical tension. Androgen sensitivity genes, androgen receptor genes, and 5-alpha reductase enzymes are upregulated. This cascade causes DHT to accumulate over the galea, which then impairs blood supply, stimulates fibrosis, and miniaturizes hairs, causing baldness to occur.

Androgens are absolutely a critical part of the balding process. But they are thus secondary to the galea in explaining how areas of high and low androgen sensitivity are established and how the inflammatory cascade is triggered.

Mechanical Stress & the Galea
To figure this out, researchers performed Finite Element Analysis, which is a common technique used in mechanical engineering to predict mechanical stresses, eg. for predicting how engine parts or buildings will hold up under stress. Using this technique, they 3D-modeled the scalp and the direction of tension which should be exerted on it by the muscles.

When they studied the tension distribution that resulted, it matched the Norwood pattern, where areas of high stress bald first (corners and crown), and areas of low stress bald last.

Here is a graphical representation of their final finding. The picture on the left is their result. The picture on the right is the standard Norwood pattern. As you can see, they match very well.

intjtrichol_2015_7_3_95_167468_f2-jpg.jpg

(ref)

How Mechanical Stress Leads to Androgenic Baldness
Hair overlying the galea is unique in that the skin from which it grows is mechanically "fused" to the galea, with only a negligibly thin layer of subcutaneous fat cushioning it between:

IntJTrichol_2015_7_3_95_167468_f1.jpg


Not only is this layer of subcutaneous fat quite thin, it atrophies with age. It has been theorized that age-related subcutaneous atrophy may in fact partly be the mechanism by which the balding process "kicks in" at a certain age for different men. (ref) Alternatively, the date of first balding might be pre-determined by the degree to which androgen sensitivity genes are induced by galeal stress during early development.

With minimal cushioning, mechanical stresses that are exerted through the galea are easily transmitted into the skin from which the hair follicles grow.

Integrins, which are proteins that sense mechanical stress, are triggered by the stress, and through chemical mediators, genes are activated in response to stress to accomplish several undesirable things:
  • Androgen receptor production is increased, making the hair cells more sensitive to androgens
  • Androgen sensitivity cofactors are increased, further increasing androgen sensitivity
  • 5-alpha reductase production is increased, leading to more production and accumulation of DHT
  • Androgens upregulate production of transforming growth factor β-1 (TGFβ-1), causing scalp fibrosis
  • Androgens inflame the hair follicles in a feedback loop, causing them to progressively miniaturize over time
One particular focal adhesion protein (Hic-5/ARA55) has been identified which can be triggered by mechanical stress. Once it is triggered, it has been demonstrated to increase androgen sensitivity. Here then is the researcher's proposed pathway by which this all happens:

IntJTrichol_2015_7_3_95_167468_f3.jpg
(ref)

Once DHT and androgen sensitivity have been triggered in this manner, Norwood pattern miniaturization can then proceeds via three primary mechanisms: dermal sheath thickening, perifollicular fibrosis, and calcification. These processes remodel the tissues – restricting follicle growth space, oxygen, and nutrient supply – leading to the slow, persistent hair follicle miniaturization of androgenic alopecia. (ref)

How Hair Medications/Treatments Can Disrupt This Process
Understanding this cascade, we can then conceptualize our conventional treatments depending on where they intervene.
  • Botox - Supporting this model, scalp Botox relieves mechanical stress on the galea and has been shown to increase hair by 18% after one year, on par with finasteride. (ref)
  • 5-Alpha Reductase Inhibitors - Drugs like finasteride and dutasteride, as well as newer experimental agents like R-equol (see here), can reduce the activity of 5-AR to reduce DHT production. By blocking the DHT from being made, we can disrupt the inflammatory cascade at this level, and the mechanical stress no longer will result in hair loss.
  • Androgen Receptor Antagonists - Drugs like cyproterone, spironolactone, flutamide, & darolutamide work by blocking androgen receptors in the hairs, thus preventing testosterone & DHT from binding. If androgens can't bind to the receptors, again the inflammatory cascade is aborted and hair is preserved.
  • Anti-Histamines - Topical cetirizine or desloratadine can block production of a wide range of downstream inflammatory mediators which are triggered by androgens binding to androgen receptors.
  • PGD2 Inhibitors - Similarly, the newer PGD2 inhibitors like setipiprant/fevipiprant are proposed to be possibly useful for hair loss as they block PGD2 which is a downstream inflammatory mediator provoked by androgen binding.
Other treatments like minoxidil, LLLT, wounding, PRP, and estrogens (ideally ER-beta agonists, see here) may be helpful for undoing the damage of this cascade and promoting new hair growth. But they won't be as effective at actually stopping where the underlying damage is coming from, and thus should be combined with some agents from the above for best effect.

Why Some Men Do Not Bald
Some men, as we know, are simply not prone to balding, and despite likely similar galeal stress, their hair remains pristine with age. Men who do not bald (or are more naturally resistant to balding) within this model can be explained in two possible ways:

(1) Their subcutaneous connective tissue and/or their skin and hair follicles are mechanically structured in a different way from balding men, such that mechanical stress from the galea is not transmitted to the hair follicles and they are thus protected from this stress.

(2) Their hair follicles and dermal papilla cells are genetically resistant to the mechanical stress from the galea, and this stress simply does not induce the same epigenetic changes or inflammatory and androgenic cascade that it does in balding-prone men.

Unfortunately, both of these possible explanations provide us little help, as they are both reliant on genetic differences that are likely pre-ordained from the time of conception.

Hair Transplantation and the Concept of "DHT-Resistance"
Hair from the NW7 zone (ie. outside the galea) is generally described as "DHT-resistant". This "DHT resistance" can be conceptualized to occur in this model as a result of these hairs growing and developing over a life time in an area of the scalp which is free of galeal tension.

By developing in areas without tension, these follicles would be expected to have considerably downregulated genes for androgen sensitivity, androgen receptors, and 5-alpha reductase. This type of downregulation is termed epigenetic change, where due to environmental/developmental factors, these hairs have now become less prone to expressing genes associated with these issues. Those genes have been mostly "turned off".

Some people believe that hair transplants, as long as they are taken from the NW7 zone, should be expected to last for life once transplanted, even in the absence of medications like finasteride. Others believe that if we quantitatively follow these transplanted hairs for decades, we might see them start to miniaturize over time, once they are placed over the galea and newly subjected to its stresses.

Primarily, we would need to understand how quickly after donor zone to galea transplantation, and if at all, the good epigenetic changes induced by developing in the "safe zone" can be undone and epigenetic changes induced by the galeal stress can be manifested. Transplantation studies (ref, ref) would suggest most of the epigenetic differences dictating stress and androgen sensitivity between galeal vs. nongaleal skin are set very early in life, and these switches may be permanent once set, so the protection donor hair gets from developing in a tension free zone may last a lifetime regardless of where or if it is moved.

However, the researchers I have cited above have suggested that we need good, decades long studies on the fate of transplanted hairs in human scalps to be clear.

Therapies Attempting to Induce DHT Resistance
Some of the new therapies that are being developed are based on the principle of trying to induce "DHT resistance" to galeal hair follicles by transferring dermal papilla cells from the NW7 zone to them.

It will take decades to see if that "DHT-resistance" holds after years of new stress from the galea. Again, this will depend on the degree to which the positive epigenetic programming our NW7 donor hair gets can retain permanence once the galeal stress begins to exert its pressure on these cells.

Why Female Pattern Hair Loss Looks Slightly Different
Although most site members are male, we do have some women, and I think it's interesting to comment on gender differences in the hair loss pattern within this model.

Female pattern androgenic hair loss follows the Ludwig Pattern. Like with men, this involves balding of the entire galeal region, but with the unique characteristics that it usually starts at the top center of the head and the frontal hairline is usually preserved until the very end:

ludwig-classification-scale.png


The differences in balding distribution can likely explained by two factors.

Firstly, the shape of a woman's head is expected to be different on average from that of a man's, which might lead to different galeal tension patterns. These patterns might be expected to favor the top of the head where many women first notice their loss, rather than the crown, as in men. This would need to be confirmed by further Finite Element Analysis.

Second, and more importantly, women are known to have high levels of aromatase in their frontotemporal scalp. (ref) Aromatase converts testosterone into estrogen. Thus the aromatase in these areas helps protect women's frontal hairlines, corners, and temple points until the very end by clearing out some of the androgen (testosterone) that would otherwise accumulate from galeal stress and damage these hairs.

We know this frontotemporal aromatase is the primary explanation for the gender difference in patterns, as when women are treated with aromatase inhibitors, they develop male pattern (ie. Norwood pattern) hair loss. (ref)

Conclusions
We can therefore understand that although androgens are a critical component of the hair loss process, the problems we experience due to them are initially triggered by galeal tension patterns in the scalp.

On a practical level, this does not change too much in terms of how we should all be treating our hair loss. But I think it's important to understand. It answers a question that has puzzled our species for at least centuries. Furthermore, this understanding can help us better assess possible treatments and therapies and have realistic goals about what is or isn't possible.

Primarily it suggests that at least with current technology, no "simple one time cure" for male pattern or female pattern androgenic hair loss can likely easily exist, and for any of us facing this problem in our teens, 20s, or early 30s, it may likely be a lifelong battle to keep under control. If therapies to confer DHT resistance prove successful and resistant to being undone by the galea, then perhaps it will get easier.

I have always strongly believed people should not wait around for a magic "cure", but rather make practical compromises, and treat the problem with the best agents we have available today.

Fortunately, there have never before been as many agents available for interrupting the hair loss cascade, so we all have plenty of options. Hopefully we'll get better genetic or stem cell therapies in the long run, but until then, as always, it would likely be wise to try to preserve as much hair as is possible.
 
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IdealForehead

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Why are my eyebrows balding? And the nape of my neck?

Within this model, we can presume that androgenic hair loss can occur anywhere mechanical stress is being continually exerted on and transmitted to the hair follicles. Although the primary place this happens for almost all of us is the galea, where almost all men thin or bald with age, it does not mean this is the only place this process can happen.

If there is something unique about your browridge, subcutaneous tissue in this area, or your hair follicles that make them sufficiently sensitive to mechanical stress in this area, then androgenic alopecia could be triggered here as well. The same would apply for your nape and retrograde hair loss.

Almost certainly, since these ought to be lower stress areas in general, androgenic hair loss at the nape and eyebrows would suggest a much more aggressive balding pattern, and you should probably be very careful in how you treat things going forward. I would try to be aggressive if you can handle it.
 

Trichosan

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Back in the "old days", barbers used to say if you had loose scalp, you likely wouldn't go bald. I suppose this somehow might pertain to the less pull and stress over the area following in similar theory. My scalp and hairloss however can certify that as a myth.
 

Armando Jose

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We know this frontotemporal aromatase is the primary explanation for the gender difference in patterns, as when women are treated with aromatase inhibitors, they develop male pattern (ie. Norwood pattern) hair loss. (ref)

In the ref, a 5 years old study;"More studies are necessary, but a clear relationship cannot be excluded. To our knowledge, this is the first article, reporting fifteen cases of alopecia induced by aromatase inhibitors.".
"We studied 15 menopausal women aged from 50 to 60 years, with hormone receptor-positive breast cancer, between the ages 50 and 65 years"
Annals of Oncology, Volume 24, Issue 6, 1 June 2013

Waiting confirmation.

And what do you think about hardened and oxidiced sebum plug in scalp and mechanical forces? Have any role in it?
 

IdealForehead

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In the ref, a 5 years old study;"More studies are necessary, but a clear relationship cannot be excluded. To our knowledge, this is the first article, reporting fifteen cases of alopecia induced by aromatase inhibitors.".
"We studied 15 menopausal women aged from 50 to 60 years, with hormone receptor-positive breast cancer, between the ages 50 and 65 years"
Annals of Oncology, Volume 24, Issue 6, 1 June 2013

Waiting confirmation.

And what do you think about hardened and oxidiced sebum plug in scalp and mechanical forces? Have any role in it?

Well yes, pretty much everything I've posted in this thread is relatively new information that wasn't known more than 3-5 years ago. This is all cutting edge hair loss theory and evidence. The scalp tension FEA modelling was published in October 2015, so it's just 2.5 years old now.

Sebaceous activity in the scalp activates in response to the increased androgens which are triggered by the galeal stress. Sebaceous overactivity in turn leads to more inflammation. So yes, excess sebum plays a role.

If you're interested in reading more about the fine level details of how the inflammatory cascade occurs and all these elements fit together, this is the best summary I've found, which was published 2 months ago and is very current along the lines of what we're discussing in this thread:

A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors
 

Bklyn_23

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I’ve heard of the galeal tension theory of balding on here before, but this fleshes it out considerably. Wasn’t there also a case(s) where some surgeon literally severed some of the connective tissue near the galea, increasing its laxity, and the person’s hair loss halted (I think there might have been regrowth too, but I forget). I wonder why no one else has tried that.
 

PeggyPeterson

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Wow...this finding seems so obvious, I’m surprised it hadn’t been researched earlier.

Forgive me if this sounds like a dumb question, if we prove that there is a mechanical factor to Androgenetic Alopecia, would surgically intervention in order to relax the mechanical factors fix this?
 

IdealForehead

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I’ve heard of the galeal tension theory of balding on here before, but this fleshes it out considerably. Wasn’t there also a case(s) where some surgeon literally severed some of the connective tissue near the galea, increasing its laxity, and the person’s hair loss halted (I think there might have been regrowth too, but I forget). I wonder why no one else has tried that.

Wow...this finding seems so obvious, I’m surprised it hadn’t been researched earlier.

Forgive me if this sounds like a dumb question, if we prove that there is a mechanical factor to Androgenetic Alopecia, would surgically intervention in order to relax the mechanical factors fix this?

The trouble with attempting to "cure" this surgically might be primarily that the epigenetic changes which lead to increased androgen sensitivity in the Norwood zones may already be set by the galeal tension pattern very early in life. So those hairs in the Norwood zone may still be more androgen sensitive even if you find a way to take the pressure off later in life.

Furthermore the galea attaches to multiple muscles of the scalp which need to pull on it in order to function. Any surgery to completely "unload" the galea would need to completely alter how the muscles of the forehead and back of the head operate.

Botox provides probably the best practical approach for mechanically unloading the galea as it is a temporary, reversible measure that still leaves the basic function of the galea in tact and only partially reduces its motion. As it is a therapy with no long term studies, no one knows if it will work long term, or if the body will simply acclimate to its application over time and redevelop the same tension-based problems in spite of it. If anyone's looking to experiment, the protocol for scalp botox is briefly described here.

Galeotomies (cuts in the galea) are done in surgical procedures when necessary and could be implemented to reduce tension in theory, but once the galea eventually heals from these cuts, it would be expected to naturally contract (or the muscles attached to it will contract), likely to re-establish over time the same tension level it had before. And cutting the galea would risk severing blood supply to the hair and scarring which can both cause hair loss on their own.

Without knowing the full mechanics of the galea and its associated muscles in a great level of detail, I suppose it would be theoretically possible to "anchor" the galea to the scalp by using mechanical fixation devices like endotines, but more permanent, along its entire perimeter. This could be done like putting down stakes around the edge of a tent or tarp to hold the edges in place.

Once the galea is "fixated" in this way, mechanical stress could no longer be transduced into it by the muscles anywhere within the fixation border. The main body of the galea would then essentially be fused to the skull, and no further distorting forces would be asserted on it or the hair that grows over top of it.

But if the Norwood zones have already upregulated their androgen sensitivity genes long before you do this, circulating androgens may still continue to damage them. I am not sure. It might create new problems and it might not fully solve the fundamental one.

Although hair loss appears to be programmed and initiated by mechanical factors, I think that completely resolving it through a mechanical solution is likely not realistic to hope for. Besides Botox, at the present, the best therapies are still likely traditionally chemicals to interrupt the inflammatory/androgenic cascade and stimulate growth. In the future, perhaps therapies to transfer "DHT resistance" from the occiput to the galeal hairs might allow us to decrease our reliance on the usual chemical agents.
 
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PeggyPeterson

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Botox - Supporting this model, scalp Botox relieves mechanical stress on the galea and has been shown to increase hair by 18% after one year, on par with finasteride. (ref)

Botox provides probably the best practical approach for mechanically unloading the galea as it is a temporary, reversible measure that still leaves the basic function of the galea in tact and only partially reduces its motion. As it is a therapy with no long term studies, no one knows if it will work long term, or if the body will simply acclimate to its application over time and redevelop the same tension-based problems in spite of it. If anyone's looking to experiment, the protocol for scalp botox is briefly described here.

Thanks IdealForehead, Curious to know why Botox for Androgenetic Alopecia isn’t a thing particularly when the study you referenced is 8 years ago and on par with Finasteride less the side affects.

So are any of the emerging treatments in the pipeline incompatible with this mechanical Factor in Androgenetic Alopecia? You were suggesting hair cloning won’t be as effective because it doesn’t address the stress induced by the follicles thus shortening the useful life of the follicle?
 

Rolandconil

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Thanks @IdealForehead

can you explain what botox is for hair? I searched in Google, but there are only beauty procedures for women. How is the procedure used for botox for hair?
also I would like to ask about a head massage, whether massage can stimulate hair growth. in the Russian forum the guy laid out his massage results and they are quite good.
 

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IdealForehead

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Thanks IdealForehead, Curious to know why Botox for Androgenetic Alopecia isn’t a thing particularly when the study you referenced is 8 years ago and on par with Finasteride less the side affects.

So are any of the emerging treatments in the pipeline incompatible with this mechanical Factor in Androgenetic Alopecia? You were suggesting hair cloning won’t be as effective because it doesn’t address the stress induced by the follicles thus shortening the useful life of the follicle?

I'm not sure about hair cloning. We don't have any long term quantitative studies on hair survival rates after transplantation from the Norwood 7 zone to the top of the scalp, so no one actually has any proven data on if the hair will truly last forever, or if it might change over the span of decades to become more galea sensitive if moved to this region.

It may well be that the tension pattern of the scalp is programming our hair loss patterns from our earliest development. Tension patterns may dictate from the beginning of our development which hair follicles will be most capable of expressing androgen sensitivity genes. Genetic switches that are turned on/off at very early developmental stages may be essentially permanent later in life.

So it is plausible still within this model that hair cloned from the NW7 zone will retain its immunity to scalp tension and androgens, and this immunity may not be reversible due to the early stage at which it was set in life. But I can't say I know for sure one way or another. At the very least, I think such cloned hair could be expected to last decades which would be more than enough to make it worthwhile.

The biggest problem with cloned hair transplantation is that cloning cells poses risks of cancer, which has been a real concern not only in animal studies, but actually in practical human research as well. One stem cell therapy that was being developed by the same company Tsuji is working with for an eye condition had to be put on hold for a few years because of fears it might induce eye cancer.

When you are manipulation thousands of stem cells in a petri dish, genetic errors can occur, and if you transplant cells with those errors back into a person, there is a risk of cancer developing from them. You can read a bit more about that risk here.

Personally, I wouldn't want anyone experimenting on my scalp with these stem cell therapies unless there was at least 5-10 years safety data. I feel much safer with simple anti-androgens, which work just fine.
 
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IdealForehead

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Thanks @IdealForehead

can you explain what botox is for hair? I searched in Google, but there are only beauty procedures for women. How is the procedure used for botox for hair?
also I would like to ask about a head massage, whether massage can stimulate hair growth. in the Russian forum the guy laid out his massage results and they are quite good.

People have claimed massage helps scalp hair for years, and in the context of this theory, perhaps it can. I think it would be unreasonable to expect scalp massage alone to resolve anyone's hair problems, but it certainly couldn't hurt by at least temporarily relaxing the galea and improving blood flow, which might in turn reduce inflammation.

The Botox study was summarized as:

Fifty males with Norwood/Hamilton alopecia classes II to IV had injections to the scalp muscles (divided equally to the frontalis, temporalis, periauricular, and occipitalis) of a total of 150 units of BTX A, followed by a second session 24 weeks later. Assessment included change in hair counts in a 2-cm scalp area, changes in hair loss counts collected by lint roller from the subject's pillow, and patient responses to a questionnaire. The 60-week study period consisted of a 12-week baseline lead-in period and two 24-week treatment periods following each BTX A treatment session.

In the 40 patients who completed the study, mean hair counts increased 18% from baseline to 48 weeks after the initial injection, a statistically significant change. Hair loss was also significantly reduced, by a mean of 39%. The reduction in hair loss and increase in hair counts were not correlated. The treatment response rate was 75%. The subjects noted statistically significant increased hair growth. No adverse events were noted.

https://www.jwatch.org/jd201111100000001/2011/11/10/growing-hair-with-botox
My mom actually gets scalp Botox for migraine headache prevention. I think what you would be looking for is a Botox practitioner who is familiar with using Botox for migraines, since the same principle of relaxing the scalp muscles would apply for both. You could show them the summary article listed above, and instruct them that you want "150 units of Botox to the scalp muscles (divided equally to the frontalis, temporalis, periauricular, and occipitalis) now and again in 24 weeks."

As for the question of why more people don't try this, I'm not sure. The results are quite impressive from that study. It was a small study admittedly so perhaps not as impressive a result as studies that include thousands of men. Beyond that, Botox is expensive and a bit painful to get. We have no long term studies on how well it works beyond a year. But it might be worth a shot if you're not interested in the usual chemical measures.
 
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BaldAsshole

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I have been saying this for a very long time. Androgens are presents in wounds, they are not the main responsible of hair loss, the damage is there before the androgens get overexpressed. Thank you for putting this so well.
 

Iah11

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Doesn't explain DUPA, retrograde alopecia, low incidence of hair loss in hispanics, indigenous people, etc.

Also doesnt address the paradoxical nature of androgens on scalp hair follicles in susceptible vs beard and body hair.

It doesn't address that hairs destined to miniturise still do, even after being transplanted into another site.

Also, the fact that people lose hair not just from the top but on the frontal sides near the eyebrows in androgenetic alopecia, and if its severe enough, nw7 people lose hair way past their crown too. In both these sites, theres no galeal tension. It also doesnt address the monkeys that bald in the horse shoe pattern, even with different mechanical stress patterns.
 
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