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

[IdealForehead]

Where did you get that info from? Because Tsuji stated that they will be able to control density.

Current hair transplantation are density limited based on the natural limitations of the surgical approach. It is impossible for any current transplant to match natural hair density.

You can review the numbers of average natural hair vs transplant density here:

https://www.prohairclinic.com/en/high-density-implantation-dense-packing-hair-transplant

Exceeding 50-60 fue/cm2 leads to higher graft failure for conventional transplants. I'm not sure about Tsuji as it is not my area of expertise, and he doesn't have a final product yet.

Natural density is equivalent to 90-120 fue/cm2, thus you should expect any regular transplant to be roughly half normal density.

 

[H]

All current hair transplantation are density limited based on the natural limitations of the surgical approach. It is impossible for any transplant to match natural hair density.

You can review the numbers of average natural hair vs transplant density here:

https://www.prohairclinic.com/en/high-density-implantation-dense-packing-hair-transplant

Exceeding 50-60 fue/cm2 leads to higher graft failure. That is true regardless of where the follicles come from (eg. Tsuji cloning or the back of your head).

Natural density is equivalent to 90-120 fue/cm2, thus you should expect any transplant to be roughly half normal density.

And this is with multiple operations? We've already discussed how their concept would take multiple procedures to create full density. What do you do for a living humanity needs your to make new galeas...

 

[Iah11]

First of all, if you actually read the post you're replying to you'll see I wrote an entire section on female pattern baldness and why it differs. I cannot reply to every person who does not actually read the thread as I am just repeating myself.

Second my perspective that over a life time balding rates would on average start at zero, exponentially kick in when balding overwhelms the protective hair functions, and level off at a maximum rate is solely conjecture. I am aware of no balding rate studies over the span of life. Either way, this has nothing to do with the principle of galeal tension programming androgen sensitivity.

I am not sure how body hair works as I have not studied it. I have no interest, as I am not concerned with my body hair. But body hair seems almost completely different from all the hair on our head in terms of growth cycles (length), texture, age of development, and that androgens directly stimulate it to grow rather than recede. In these respects, it is very different from the hair on our heads for our entire lives. Whereas the hair on our heads only differentiates into visibly different balding vs non balding hair once the balding process kicks in. Ie. All the hair on our head looks the same until balding starts.

This theory would suggest body and head hair are two very different skin organs with distinct developmental pathways and thus differing responses to stress and androgens altogether. Whereas head hair represents the same organ all over the head which just receives slightly differently epigenetic programming during development from the galeal tension it develops under.

Wait wait wait slow down.

The entire point of this theory is to explain that androgens exert their negative effect scalp hair exclusively due to mechanical stress from the galea.

Now i've told you that there are mutiple aponeuroses in the body (and sites of varying mechanical stress besides i.e. a knee joint vs the chest) yet over the course of your life androgens exclusively have a negative effect on just the scalp hair. And your response is that scalp hair follicles are of a different type to body hair? Lmao well isnt that obvious? Its androgenetic alopecia, the clue is in the "genetic".

The point is your theory attempts to explain the difference in gene expression on the top of the scalp as being kicked off by mechanical stress from the galea but you cant explain why only the top of the head would lose hair after androgen exposure, even though its pretty obvious that hair across the body is subjected to different levels of mechanical stress. Why not at joints? Why not at the lumbar aponeurosis? Or the abdominal?

 

[Kagaho]

All current hair transplantation are density limited based on the natural limitations of the surgical approach. It is impossible for any transplant to match natural hair density.

You can review the numbers of average natural hair vs transplant density here:

https://www.prohairclinic.com/en/high-density-implantation-dense-packing-hair-transplant

Exceeding 50-60 fue/cm2 leads to higher graft failure. That is true regardless of where the follicles come from (eg. Tsuji cloning or the back of your head).

Natural density is equivalent to 90-120 fue/cm2, thus you should expect any transplant to be roughly half normal density.

Keep in mind Tsuji will try to implant proto-hairs, considerably smaller than a thick fue graft

 

[Kagaho]

This guy Iah11 has some really good points. I was thinking about women balding in a different pattern and how the percentege of women balding is much smaller than men.

 

[IdealForehead]

Wait wait wait slow down.

The entire point of this theory is to explain that androgens exert their negative effect scalp hair exclusively due to mechanical stress from the galea.

Now i've told you that there are mutiple aponeuroses in the body (and sites of varying mechanical stress besides i.e. a knee joint vs the chest) yet over the course of your life androgens exclusively have a negative effect on just the scalp hair. And your response is that scalp hair follicles are of a different type to body hair? Lmao well isnt that obvious? Its androgenetic alopecia, the clue is in the "genetic".

The point is your theory attempts to explain the difference in gene expression on the top of the scalp as being kicked off by mechanical stress from the galea but you cant explain why only the top of the head would lose hair after androgen exposure, even though its pretty obvious that hair across the body is subjected to different levels of mechanical stress. Why not at joints? Why not at the lumbar aponeurosis? Or the abdominal?

All our tissues in our entire body develop from a single cell.

One single cell.

And over the course of our development, multiple genetic, hormonal, and mechanical pressures exert themselves to shape various progeny of that first progenitor cell into the various organs of our body.

Tissues develop in progressively forking pathway where at each fork, something induces change to create a new tissue type.

Some tissues diverge earlier in development, and some diverge very late in development.

The question developmental biologists attempt to answer is: how and why does each fork occur?

This theory explains how the Norwood 1-7 fork of scalp hair development occurs. Nothing more.

Here is a simple diagram of how our tissues fork starting from the bottom as a single celled zygote into the various organs of our body at the top:

Our hearts and our biceps are both made of muscle. But it is very different muscle with very different properties. They both come from our mesoderm, but the fork that generates the difference occurs very early on, and so although they are both muscles, they are not the same. The same can be said for the difference between body hair and head hair.

Pubic hair, chest hair, *** hair, beard hair, etc. have completely different texture, age of growth, rate of growth, density, triggers for growth/maturation compared to head hair. The only thing body hair shares with head hair is they are both hairs (just like heart and biceps are both muscles). Otherwise, they are plainly different in many many capacities. Like our biceps are different from our heart. They are both muscles, but they are developmentally divergent muscles with very different characteristics.

By contrast, the hair on our head all appears essentially identical in terms of texture, growth, length, density, and pattern of growth. If you pluck a hair from a healthy head anywhere on the head and compare it to another hair somewhere else on the head, they will be likely indiscriminable under a microscope. You could not tell the difference. Because they are developmentally almost identical to one another.

This theory posits that: (1) the hair that exists on our head is sensitive to mechanical stress, and (2) mechanical stress induces androgen sensitivity in the Norwood pattern via the galea.

This theory offers no suggestions about the characteristics of body hair, as that would be like trying to draw conclusions about how to treat heart disease by studying a bicep. They are different organs that arise from different developmental pathways, with different growth stimulants and triggers, and displaying different natures altogether.

The notion that hair on your head develops androgen sensitivity in the Norwood pattern due to mechanical stress does not imply that all hairs anywhere in the body must have the same mechanical sensitivity.

This just helps to explain one tiny fork among the thousands that occur in our development to lead to making our adult bodies the way they are.

 

[IdealForehead]

This guy Iah11 has some really good points. I was thinking about women balding in a different pattern and how the percentege of women balding is much smaller than men.

Idealforehead i know you're a really valuable poster, but it looks like you are trying too hard to justify this galea theory man

just sayin

Did you actually read the original post where I explained why women bald in a different pattern? It mostly has to do with the aromatase in their scalp. Women bald in the Norwood male pattern when treated with aromatase inhibitors.

Women balding to a lesser extent that men is expected as women have low androgen levels to begin with.

I am not sure how you think I haven't addressed this or how this doesn't fit into the theory.

 

[IdealForehead]

@PeggyPeterson asked what I think this research would suggest will lead to in terms of new treatments, and the answer in my opinion is: likely nothing major.

What I think many people are missing is this theory is useful only for understanding why the Norwood pattern develops. It also provides information for understanding how the feedback loops of balding operate and how tension can be an ongoing mediator of balding, which is why Botox can slow it. It is valuable for someone who wants to understand why the body works the way it does. But it does not change the fundamental process or how we can realistically treat it.

I discussed earlier how galeal anchoring could be done to deload the galea. But as I explained there, even this would not undo the years of androgen sensitivity programming that has already taken place. Doing so might slow or halt the balding rate like Botox, but it also might impair facial expressions, and it would not likely stop the process altogether.

One new target this theory might offer would be via topical chemicals that disrupt the mechanically induced androgen upregulation process. eg. Inhibitors of the focal adhesion protein (Hic-5/ARA55) which is responsible for translating mechanical stress into androgen sensitivity. This could conceivably disrupt some of the tension-mediated feedback mechanisms of androgenic alopecia, but it would be extremely experimental and could cause other unknown risks without knowing how these proteins work in the rest of the body. And again, it wouldn't undo already established androgen sensitivity patterns once they are set.

The prospect of "infusing" galeal zone hairs with cloned dermal papilla cells from the Norwood zone is probably the most promising upcoming technology for men/women who still have sufficient hair to save. I think this will be the most important technology we see in our lives for keeping the hair we have. Tsuji's approach likely represents the best hope in our lives for men with already advanced balding.

But all this goes way beyond galeal theory. Again, galeal theory just answers the "why" of the Norwood patterning. It doesn't tell us what to do about it.

And this is with multiple operations? We've already discussed how their concept would take multiple procedures to create full density.

Sorry H, it appears my memory was foggy as it has been 6 months since I read Tsuji's research, and as Kagaho has pointed out, I have mixed up how they are working on this. So Tsuji's approach may in fact circumvent the transplant density issue.

 

[Kagaho]

Yes, hair transplants are all limited in final density due to how closely incisions can be packed. There is no way to overcome this except by giving up on single hair transplantation altogether. Packing too many individual hairs into too small an area will risk compromising the blood supply to the neighboring hairs, whether it is done at once or in multiple stages.

Yes, replacing an entire head of hair with Tsuji cloned hair would require multiple procedures. But even still, it would be subject to the same limitations as all transplants. Furthermore, you'd have risks of the hairs not all lining up or displaying perfect texture or caliber of growth, as a previous poster in this thread was complaining about with his transplant.

The only way to circumvent the density problem of conventional hair transplantation would be to instead take a completely different approach and instead grow a "lawn" of say 20x30 cm of fully functioning new scalp generated from the NW7 zone to maximize its androgen resistance. This "lawn" could be cut into a shape that matches the balding pattern, and transplanted as an entire single unit to the scalp to replace the entire bald scalp in one procedure.

You would have to try to avoid scarring around the edges with trichophytic closure, and possibly use some FUE to camouflage the scar if needed. Maintaining vascular

Yes, replacing an entire head of hair with Tsuji cloned hair would require multiple procedures

Again, Tsuji is not going to implant the cloned hair. What he will be attempting to do is 'seeding' the scalp with their so called hair germs. Which are considerably smaller than a full grown hair.

Thats why he is so confident about restoring full density. There was an illustration by kyocera showing what they expect. Something close to 175 hairs per square cm i think or something like that

 

[IdealForehead]

Again, Tsuji is not going to implant the cloned hair. What he will be attempting to do is 'seeding' the scalp with their so called hair germs. Which are considerably smaller than a full grown hair.

Thats why he is so confident about restoring full density. There was an illustration by kyocera showing what they expect. Something close to 175 hairs per square cm i think or something like that

My mistake then. Thanks. It's been 6 months since I read through his research and I have muddled the nature of it. Just checked his rat article again here.

I almost never read anything about these stem cell therapies since my own goal is the chemical maintenance and support of my existing healthy natural hair.

 

[Kev123]

Finasteride, dutasteride, and RU all failed for me. So I had to be more creative. Some of my history of hair loss and treatments I've tried is here:
https://www.hairlosstalk.com/intera...than-enzalutamide.105402/page-24#post-1610020

I have had great success over the past 6 months with a custom topical mix I am making of:

- Darolutamide 0.2%
- Niacinamide 5%
- Desloratadine 1%

Usually mixed into a base of Kirkland minoxidil 5%, or since I have cut out minoxidil for the past month, in a base of 50% propanediol, 30% ethanol, 20% water.

I have found oral minoxidil helpful also but cut that out for the past month also. I have been using a bit of estriol cream (this one) at the corners and hairline for around 2 months and plan to add genistein and possibly equol to my solution next.

In what way did finasteride, dutasteride and RU fail you? Like they didn't stop or slow down your hair loss? They did stop/slow down your hair loss but gave you no regrowth? There was no response whatsoever? What was the nature of the failure?

 

[IdealForehead]

In what way did finasteride, dutasteride and RU fail you? Like they didn't stop or slow down your hair loss? They did stop/slow down your hair loss but gave you no regrowth? There was no response whatsoever? What was the nature of the failure?

I did finasteride 1.25 mg for 11 months exactly with clear progression of loss. At no point did my shedding noticeably slow down. After that I went straight to dutasteride 0.5 mg and felt calm thinking, "there's no way I can lose hair now". Yet again, at no point did my shedding noticeably slow down. By 11 months, yet again there was clear evidence of progression. I panicked and started researching. I decided to get my DHT levels checked to figure out if there was something wrong. Sure enough, there was. My DHT levels were completely normal. Dutasteride in normal men annihilates DHT levels down to almost nothing. Yet for me it did nothing.

I was getting my dutasteride from a legit local major chain pharmacy with a real prescription, so I know it was good. But I thought maybe I had a bad batch of dutasteride. So I got a new batch of brand name Avodart. Tried that again. Still, my DHT was normal. Then I thought, maybe I just need more. I read the dutasteride studies where they went up to 2.5 mg during initial testing. So I said f*** it, and started taking 5 tablets a day (2.5 mg). Still my DHT was normal.

At that point I was really freaking out. My doctor and pharmacist had no explanation for why this was. I contacted one of the doctors involved in the big Avodart trials where they measured DHT on thousands of men on the drug to ask if he had seen anything like this. He said he hadn't and didn't know why I wasn't responding. I thought I was completely fucked at this point.

Then I found RU and had hope again. I used that for a year at 5% with minoxidil 5% and had good maintenance at least. I then foolishly cut out the minoxidil and dropped the RU to 3.75% for a year. I lost more hair. That brings me to around 7 months ago when I: Tried high dose 7.5% RU 2 mL twice a day (with a bit of fatigue), then tried 200 mg spironolactone per day (truly exhausting), then tried 100 mg cyproterone per day (neutering and depressive), and over top of spironolactone & cypro tried ~5 mg minoxidil orally per day (awful for the skin).

Lastly, I found daro, switched to that topically around 6 months ago, and I've been exceedingly happy with the result. After 2-3 months of major shedding, my hair simply stopped falling out. Like at all. Like I've never lost this little hair daily in my entire life that I can remember. I'm pretty sure if I let my hair grow as long as it wanted now it would grow down to damn near my ankles, because the follicles all seem to be in continuous anagen now. Any rare hair that does come out is thick and healthy - no more corkscrew hairs or fine damaged hairs. Density and hairline have improved and I am continuing to grow new hair.

I consider my hair loss functionally cured at this stage on my current regimen.

 

[Kev123]

I did finasteride 1.25 mg for 11 months exactly with clear progression of loss. At no point did my shedding noticeably slow down. After that I went straight to dutasteride 0.5 mg and felt calm thinking, "there's no way I can lose hair now". Yet again, at no point did my shedding noticeably slow down. By 11 months, yet again there was clear evidence of progression. I panicked and started researching. I decided to get my DHT levels checked to figure out if there was something wrong. Sure enough, there was. My DHT levels were completely normal. Dutasteride in normal men annihilates DHT levels down to almost nothing. Yet for me it did nothing.

I was getting my dutasteride from a legit local major chain pharmacy with a real prescription, so I know it was good. But I thought maybe I had a bad batch of dutasteride. So I got a new batch of brand name Avodart. Tried that again. Still, my DHT was normal. Then I thought, maybe I just need more. I read the dutasteride studies where they went up to 2.5 mg during initial testing. So I said f*** it, and started taking 5 tablets a day (2.5 mg). Still my DHT was normal.

At that point I was really freaking out. My doctor and pharmacist had no explanation for why this was. I contacted one of the doctors involved in the big Avodart trials where they measured DHT on thousands of men on the drug to ask if he had seen anything like this. He said he hadn't and didn't know why I wasn't responding. I thought I was completely fucked at this point.

Then I found RU and had hope again. I used that for a year at 5% with minoxidil 5% and had good maintenance at least. I then foolishly cut out the minoxidil and dropped the RU to 3.75% for a year. I lost more hair. That brings me to around 7 months ago when I: Tried high dose 7.5% RU 2 mL twice a day (with a bit of fatigue), then tried 200 mg spironolactone per day (truly exhausting), then tried 100 mg cyproterone per day (neutering and depressive), and over top of spironolactone & cypro tried ~5 mg minoxidil orally per day (awful for the skin).

Lastly, I found daro, switched to that topically around 6 months ago, and I've been exceedingly happy with the result. After 2-3 months of major shedding, my hair simply stopped falling out. Like at all. Like I've never lost this little hair daily in my entire life that I can remember. I'm pretty sure if I let my hair grow as long as it wanted now it would grow down to damn near my ankles, because the follicles all seem to be in continuous anagen now. Any rare hair that does come out is thick and healthy - no more corkscrew hairs or fine damaged hairs. Density and hairline have improved and I am continuing to grow new hair.

I consider my hair loss functionally cured at this stage on my current regimen.

Interesting. Thanks for explaining.

Where do you get the things you buy? And how exactly do you mix them?

 

[H]

Sorry H, it appears my memory was foggy as it has been 6 months since I read Tsuji's research, and as Kagaho has pointed out, I have mixed up how they are working on this. So Tsuji's approach may in fact circumvent the transplant density issue.

Hey he may be wrong though so humanity still needs you to make new galeas. Member when you were a kid and you said you wanted to change the world?... of balding men?

 

[IdealForehead]

Hey he may be wrong though so humanity still needs you to make new galeas. Member when you were a kid and you said you wanted to change the world?... of balding men?

Actually when I was a teenager I partly did want to become a stem cell researcher. I thought the potential of stem cells were incredible. I thought even one major breakthrough could change the course of human history/medicine. I thought it was therefore possibly the most noble pursuit a person could chase.

My dad went bald aggressively in his teens/twenties, and being born with a horribly big forehead myself, I have had hair anxiety since I was 10. So I even did think specifically about becoming a hair researcher. I wondered how I would feel telling people I am researching a cure to hairloss as I balded aggressively like my dad before me. And I wondered if I would feel like my entire life would have been dedicated to vanity.

In the end I decided not to, because research as a job market has poor job stability. You are always chasing after one source of funding or another, or needing to publish something to stay "relevant". But there was legit a time when as you say I was a kid and wanted to change the world of balding men.

 

[H]

In the end I decided not to, because research as a job market has poor job stability. You are always chasing after one source of funding or another, or needing to publish something to stay "relevant". But there was legit a time when as you say I was a kid and wanted to change the world of balding men.

I was there for the speech. Remember all those movies though where the guy/girl give up their dream for something easier and more practical but end up hating themselves in the end for it quite possibly telling their kin to right their wrongs and yada...

 

[IdealForehead]

I was there for the speech. Remember all those movies though where the guy/girl give up their dream for something easier and more practical but end up hating themselves in the end for it quite possibly telling their kin to right their wrongs and yada...

Haha. Yeah man but I f*****g have zero regrets with that. My life is pretty good in most ways. I love my job, I get paid well, etc. I'm glad I'm not in a lab 24/7 trying to make some breakthrough in stem cell signalling, which can involve years of toil for no useful outcomes, even for the best researchers, given how many pathways are dead ends, and how you have no way of knowing until you systematically try solutions as many ways as possible (or get lucky).

Research is a b**ch of a lifestyle to commit to. This is getting completely off topic, but I think if you're someone who generally has a passion for a broad range of subjects, you can love almost anything you do and there isn't any "one single right path" for life to take.

 

[Iah11]

Thanks for taking the time to actually reply @IdealForehead

Now you've said hair on the scalp is a different organ type to body hair. Ok. So why do you actually need this galea theory at all to explain the norwood pattern? If you're willing to concede that hair characteristics differ across the body why cant you accept that the reasons for balding are due to androgens and something intrinsic to the follicle itself?

Note that Androgenetic Alopecia is one of many hair loss types. DUPA, telogen effluvium, non androgenic alopecia. None of these fit into the galea theory.

Even look at androgenetic alopecia patients who bald in a diffuse manner! They dont start at the points of higher mechanical stress, all ths follicles on top fall out evenly, sometimes their hairlines are actually preserved. So even though their follices are in the galea, androgens affect them differently. How do you explain this?

 

[lemoncloak]

Everybody keeps saying muscular tension above the Galea raises androgens and is therefore the cause of balding. How do you know it's not the other way around?
We know androgens accelerate the metabolization of fat, while estrogen does the opposite. An area of the scalp high in androgens could have a reduced fat layer which could lead to extra tension. And all this tension talk might as well be an irrelevant side effect, as even dermal papillas from balding areas will shrink and die when exposed to dht in vitro.

 

[Armando Jose]

the hair on our head all appears essentially identical in terms of texture, growth, length, density, and pattern of growth. If you pluck a hair from a healthy head anywhere on the head and compare it to another hair somewhere else on the head, they will be likely indiscriminable under a microscope. You could not tell the difference. Because they are developmentally almost identical to one another.

I am with you. even more, I think that there is no huge diference between women or men hair scalp. Note that the important androgens are made inside the pilosebaceous unit.