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

[Georgie]

Thanks i'll have a dig.

@IdealForehead could there not be a surgical procedure where by the Galea / attachment muscle is sliced in varying position to allow it to stretch out before essentially healing in its new more elongated position ?

It would be like a reverse face lift

 

[Georgie]

Temple points and retrograde stresses were addressed here:
https://www.hairlosstalk.com/intera...gens-are-secondary.113256/page-2#post-1647067

It is hard for me to know exactly how temple points work, as everyone seems to draw the anatomy differently in this area. But here is yet another diagram that would support why temple points would be potentially vulnerable, as these areas appear to be a transition point for fascia and muscle:

View attachment 86301

We all have different skull and muscular structures of our heads which would be expected to lead to slightly different tension patterns and degrees of nape/temple sensitivity.

You can see how different variations of Norwood balding were predicted by this thread with just subtle differences in tension on a simple 2D mesh, showing how much slight tension pattern variation can change the outcome:

https://www.hairlosstalk.com/intera...alopecia-von-mises-2d-analysis-models.113276/

We don't have good maps of how aromatase distributions vary from one woman to another. Women might be expected to have even greater pattern variation due to added variations in aromatase expression.

It would be reasonable to tell them you're interested in Botox for migraines. Once you get your foot in the door, during the consult you could mention that you also have hair loss, and saw this article summary linked in this post with the protocol here for hair:

https://www.hairlosstalk.com/intera...-androgens-are-secondary.113256/#post-1646795

And ask them if that's the same as what they'd do for migraine. I just looked and I can confirm the migraine protocol uses essentially the same number of total units, so they are probably very similar:

The protocol for use of Botox-A injection therapy for treating chronic migraine is based upon the clinical research studies that earned the treatment its FDA approval and subsequent guidelines provided by the FDA. Each treatment involves 31 injections (5 Botox-A units per injection, for a total of 155 units).​

In fact I would bet the hair study just used a standard migraine protocol with 150 units given that the principle behind relaxing scalp muscles for headaches and hair should be identical.

Ah I see. Thank you. Well assuming that these theories are correct, and scalp tension caused by both galea and areas of fascia at the sides and nape of the hair are predetermining patterns of hairloss, it could indeed explain a fair bit for me. In the diagram that you provided here:

We can hypothetically say that the white areas are potential areas of stress causing hairloss/recession. Besides the ear obviously, that is exactly how I have been losin hair, with very slight density variation in that small area between the back/crown and lower nape where it isn’t as bad. It’s bizarre, because I’m looking at this and see where my hair recedes in those white areas, even behind the ears, down the sides of my head, temples, forelock, nape, crown, top. I find it to be conflicting with some of the other things that I believe about hairloss however. We know that patterns are genetic, hormone and sex-related, so how does this relate to any of those things? (apart from perhaps genetics). I did read that stresser tension can upregulate scalp androgen sensitivity, but how? I can’t say that I am totally convinced about this theory, but it does seem to conveniently explain a few things for myself anyway. I couldn’t quite understand why my nape, around the ears and forelock were affected even without adequate aromatase activity. All those who acquired male pattern baldness from aromatase inhibitor treatment had preservation of the back of the head. I would love to see more studies to prove, scientifically how this works and especially how it interacts with androgen sensitivity. I think I’d like to dig more into this myself.

 

[Georgie]

It doesn't explain any of these things because it's bullshit.

InBeforeTheCure posted no shortage of research in the RepliCel hype thread that disproved this whole galea thing.

Link?

 

[Armando Jose]

Discussion of the study

Hey, have you a link to the full study?

We can hypothetically say that the white areas are potential areas of stress

It is not to try to rule out these possible problems in hair loss, ...., try to explain the loss of hair in the temporary area seems very interesting, but personally I would add that it is the area where hair naturally grazes, is To say that they suffers much more from the oxidative processes derived from the continous contraction of the muscles, for example, when we eat.
What this theory does not explain to me is the dynamics of the common hair loss process, because it usually begins in the frontal line and in the crown area, ..., according to this theory of muscular stress it should be that the hair loss began at the same time in all the hairs, and will affect everyone as a whole.causing hairloss/recession

I can’t say that I am totally convinced about this theory, but it does seem to conveniently explain a few things for myself anyway.

clap, clap, me too.

 

[bboy]

For every complex problem there's an answer that is clear, simple and wrong.

 

[IdealForehead]

For every complex problem there's an answer that is clear, simple and wrong.

I don't think this is a simple answer at all. It involves complex mechanical cell receptor, protein and androgen signalling, and epigenetic interplay all the way through early development and later life.

Are you aware of any other developmental explanation for how the Norwood pattern of androgen sensitivity is created?

You can't just say "because genetics". Genetics do not just manifest different tissues from thin air without signal pathways for different influences to be applied to different cells. Eg. Influences like the ones I described.

 

[Georgie]

Hey, have you a link to the full study?


It is not to try to rule out these possible problems in hair loss, ...., try to explain the loss of hair in the temporary area seems very interesting, but personally I would add that it is the area where hair naturally grazes, is To say that they suffers much more from the oxidative processes derived from the continous contraction of the muscles, for example, when we eat.
What this theory does not explain to me is the dynamics of the common hair loss process, because it usually begins in the frontal line and in the crown area, ..., according to this theory of muscular stress it should be that the hair loss began at the same time in all the hairs, and will affect everyone as a whole.causing hairloss/recession




clap, clap, me too.

What it does not explain for me is facial and body hair loss.

 

[IdealForehead]

What it does not explain for me is facial and body hair loss.

Your facial and body hair loss are features i always come back to with you because i think they clearly indicate the problem is not primarily androgenic.

Androgenic alopecia does not cause facial or body hair loss. In women its often associated with facial and body hair growth. Ie. The opposite problem.

The only things i know that can cause total hair body loss in a woman are:

- estrogen imbalances. Eg. Menopause
- nutritional or thyroid abnormalities
- alopecia universalis which is freakishly rare and should show up on biopsy
- drug toxicities.

You might be following the ludwig pattern just because those hairs are the weakest to begin with due to the factors described in this thread. But if you're still losing your whole body hair it suggests something else as the biggest problem.

 

[hanginginthewire]

@IdealForehead is eyebrow hair loss in men because of androgenetic alopecia/DHT?

 

[Georgie]

Your facial and body hair loss are features i always come back to with you because i think they clearly indicate the problem is not primarily androgenic.

Androgenic alopecia does not cause facial or body hair loss. In women its often associated with facial and body hair growth. Ie. The opposite problem.

The only things i know that can cause total hair body loss in a woman are:

- estrogen imbalances. Eg. Menopause
- nutritional or thyroid abnormalities
- alopecia universalis which is freakishly rare and should show up on biopsy
- drug toxicities.

You might be following the ludwig pattern just because those hairs are the weakest to begin with due to the factors described in this thread. But if you're still losing your whole body hair it suggests something else as the biggest problem.

I do have the haillmarks of female Androgenetic Alopecia: Miniturisation, diffuse loss with an emphasis on the crown/top, temporal recession. Yes, I’m a freak in other ways ie the bod hair thinning and global hairline recession. I think the estrogen theory is the best we have to explain these things, and I have read studies which detail the importance of estrogen in body hair growth. I do also believe that my unique condition ties in with cortisol and irregular hair loss and growth cycling. It’s been shown that the hair and skin have a unique hpa-like negative feedback response which can regulate various responses. The hair follicle in itself contains levels of serum cortisol and estrogen which give us an indication of our inner hormonal workings. For example, men and women were exposed to a painful experience and thereafter hair was dissected and examined for cortisol levels (both before and after). It showed the immediate change in cortisol levels in response to the stressful encounter. They did the same thing with women during their 4 week cycle, showing how estrogens inside the follicle fluctuated. What I mean to say is that I’ve many factors here which align with disruption of healthy, normal hair cycling. I also have the miniturisation and patterns to show that it’s Androgenetic Alopecia. How I go about correcting all this stuff at once is all trial and error.

 

[Georgie]

@IdealForehead is eyebrow hair loss in men because of androgenetic alopecia/DHT?

If they thin from the outer corners it could be thyroid. I find mine began to thin from the inner part and slowly the hair throughout grew thinner. For me I believe it’s tied up with estrogen deficiency, or an imbalance in cortisol /hPa axis.

 

[Georgie]

@IdealForehead just to show you the top...
that area just behind my hairline is the worst, but overall the top is getting worse fast. The last one is from January.

 

[IdealForehead]

@IdealForehead just to show you the top...
that area just behind my hairline is the worst, but overall the top is getting worse fast.

Oh definitely I would agree it's a Ludwig pattern matching what you have described. And although you're not in too bad shape, I would agree it has definitely progressed matching what you've said about the amount you shed. Fortunately, usually rapid loss is also rapidly recovered once the problem is fixed, so I am still optimistic this will not be permanent.

Part of why I think this theory is so important to conceptualize hair loss is the fact that despite knowing that women can be "converted" from Ludwig to Norwood loss simply by blocking aromatase (and thus it seems aromatase is the key difference and they are thus still similar processes), male galeal distribution hair loss seems far more androgen dependent than female.

The gender difference in androgen dependence is discussed by this article on female pattern hair loss:

Despite the name androgenetic alopecia, the exact role of hormones is uncertain. It is well known that androgens affect the growth of the scalp and body hair and even Hippocrates observed 2,400 years ago that eunuchs did not experience baldness (Yip et al., 2011). However, hyperandrogenism cannot be the only pathophysiologic mechanism for FPHL because the majority of women with FPHL neither have abnormal androgen levels nor do they demonstrate signs or symptoms of androgen excess (Atanaskova Mesinkovska and Bergfeld, 2013, Schmidt and Shinkai, 2015, Yip et al., 2011). Furthermore, cases have been reported in which FPHL developed in patients with complete androgen insensitivity syndrome or hypopituitarism with no detectable androgen levels (Cousen and Messenger, 2010, Orme et al., 1999).

Male pattern hair loss has been established as androgen-dependent because it is associated with changes in the androgen receptor and responds to antiandrogen therapy (Ellis et al., 2002). With FPHL, genes that encode aromatase, which converts testosterone to estradiol, are also implicated (Yazdabadi et al., 2008, Yip et al., 2009).
​

This therefore clearly implies that androgens are not the only potential mediator of galeal pattern hair loss, and are likely not the underlying issue. They can be more likely considered as perhaps the primary "messenger" of hair loss. But likely they are not the only messenger. And all those messengers can likely bring follicular destruction.

But where do the messages come from?

The fact that Galeal stress patterns mirror Norwood patterning suggests this is a plausible underlying root of the issue. Androgens may play a bigger role in messaging for that follicular destruction in men because we have more androgens to begin with. While in women, other pathways that are activated may play a bigger role. We know many, many pathways can affect hair growth or loss (eg. JAK inhibitors, estrogens, growth factors). There is likely a complex interplay between many of these pathways that is weighted differently between the genders and also between individuals.

Studies suggest about 88% of women with FPHL respond to anti-androgens, either maintaining stability or regrowing hair by a year with spironolactone or cypro (ref). If you're in the 12% that doesn't, then the goal should be to disrupt or correct the balding through different pathways.

That leaves numerous other options most of which you are already exploring:

- Maintain a good healthy estrogen balance without too much ER-alpha activity (avoid estrone & ethinyl estradiol).
- Try growth stimulators (like AGF39 or if affordable PRP as discussed).
- Increase dose of topical anti-androgen to see if greater scalp castration helps silence the androgenic pathways better.
- Use downstream anti-inflammatory agents like topical anti-histamines (eg. desloratadine 1%).
- Block another damaging pathway like the JAK pathway with topical JAK inhibitors.
- Try Botox to relieve underlying scalp tension and mechanical stress.

I think those are all the things that can reasonably be tried. I know I say this over and over but it's because I believe it - I think your problem will get considerably better in 3-5 months since it's only been a few weeks since you changed your estrogens. In the mean time, you could continue to work through as many things on that list as possible.

Old damage and catagen signalling won't turn around overnight even if you fix the underlying issue. But hitting the hairs with more positive changes at once could help turn the tide a bit faster. From that article on FPHL:

It is important to ensure that patients understand that progress is slow, and months or years can be required to see a significant improvement (Boersma et al., 2014, Yeon et al., 2011). In our practice, we wait at least 6 months to assess treatment efficacy.​

 

[hanginginthewire]

If they thin from the outer corners it could be thyroid. I find mine began to thin from the inner part and slowly the hair throughout grew thinner. For me I believe it’s tied up with estrogen deficiency, or an imbalance in cortisol /hPa axis.

Mine are totally from the outer corners in, yup. Thank you!

 

[Sam1]

@Georgie your hair does not look too bad ..early stages.. does FPB run in your family?

 

[Georgie]

Oh definitely I would agree it's a Ludwig pattern matching what you have described. And although you're not in too bad shape, I would agree it has definitely progressed matching what you've said about the amount you shed. Fortunately, usually rapid loss is also rapidly recovered once the problem is fixed, so I am still optimistic this will not be permanent.

Part of why I think this theory is so important to conceptualize hair loss is the fact that despite knowing that women can be "converted" from Ludwig to Norwood loss simply by blocking aromatase (and thus it seems aromatase is the key difference and they are thus still similar processes), male galeal distribution hair loss seems far more androgen dependent than female.

The gender difference in androgen dependence is discussed by this article on female pattern hair loss:

Despite the name androgenetic alopecia, the exact role of hormones is uncertain. It is well known that androgens affect the growth of the scalp and body hair and even Hippocrates observed 2,400 years ago that eunuchs did not experience baldness (Yip et al., 2011). However, hyperandrogenism cannot be the only pathophysiologic mechanism for FPHL because the majority of women with FPHL neither have abnormal androgen levels nor do they demonstrate signs or symptoms of androgen excess (Atanaskova Mesinkovska and Bergfeld, 2013, Schmidt and Shinkai, 2015, Yip et al., 2011). Furthermore, cases have been reported in which FPHL developed in patients with complete androgen insensitivity syndrome or hypopituitarism with no detectable androgen levels (Cousen and Messenger, 2010, Orme et al., 1999).

Male pattern hair loss has been established as androgen-dependent because it is associated with changes in the androgen receptor and responds to antiandrogen therapy (Ellis et al., 2002). With FPHL, genes that encode aromatase, which converts testosterone to estradiol, are also implicated (Yazdabadi et al., 2008, Yip et al., 2009).
​

This therefore clearly implies that androgens are not the only potential mediator of galeal pattern hair loss, and are likely not the underlying issue. They can be more likely considered as perhaps the primary "messenger" of hair loss. But likely they are not the only messenger. And all those messengers can likely bring follicular destruction.

But where do the messages come from?

The fact that Galeal stress patterns mirror Norwood patterning suggests this is a plausible underlying root of the issue. Androgens may play a bigger role in messaging for that follicular destruction in men because we have more androgens to begin with. While in women, other pathways that are activated may play a bigger role. We know many, many pathways can affect hair growth or loss (eg. JAK inhibitors, estrogens, growth factors). There is likely a complex interplay between many of these pathways that is weighted differently between the genders and also between individuals.

Studies suggest about 88% of women with FPHL respond to anti-androgens, either maintaining stability or regrowing hair by a year with spironolactone or cypro (ref). If you're in the 12% that doesn't, then the goal should be to disrupt or correct the balding through different pathways.

That leaves numerous other options most of which you are already exploring:

- Maintain a good healthy estrogen balance without too much ER-alpha activity (avoid estrone & ethinyl estradiol).
- Try growth stimulators (like AGF39 or if affordable PRP as discussed).
- Increase dose of topical anti-androgen to see if greater scalp castration helps silence the androgenic pathways better.
- Use downstream anti-inflammatory agents like topical anti-histamines (eg. desloratadine 1%).
- Block another damaging pathway like the JAK pathway with topical JAK inhibitors.
- Try Botox to relieve underlying scalp tension and mechanical stress.

I think those are all the things that can reasonably be tried. I know I say this over and over but it's because I believe it - I think your problem will get considerably better in 3-5 months since it's only been a few weeks since you changed your estrogens. In the mean time, you could continue to work through as many things on that list as possible.

Old damage and catagen signalling won't turn around overnight even if you fix the underlying issue. But hitting the hairs with more positive changes at once could help turn the tide a bit faster. From that article on FPHL:

It is important to ensure that patients understand that progress is slow, and months or years can be required to see a significant improvement (Boersma et al., 2014, Yeon et al., 2011). In our practice, we wait at least 6 months to assess treatment efficacy.​

What’s bizarre is that I find that I do grow a lot of new hair, it’s just that a substantial portion of it is miniturised or miniturising. At my part line there are tons of little new hairs but I would guess they are 80% not fully terminal or on their way out. I was standing under my bathroom lights this morning looking at these hairs thinking, of only I could reverse that miniturisation, I would have so much hair. It’s so frustrating literally having tried everything to do this without any success.

 

[Georgie]

@Georgie your hair does not look too bad ..early stages.. does FPB run in your family?

I’ve been losing my hair for almost 4 years. I have thrown quite a few aggressive treatments at it which may have slowed things down a bit, but I had a ridiculous amount of hair to begin with. You would have had to dig to find any scalp.

My mother has thinned hair after menopause but it’s not Androgenetic Alopecia. My dad however has diffuse male pattern baldness and thinned eyebrows and eyelashes.

 

[IdealForehead]

What’s bizarre is that I find that I do grow a lot of new hair, it’s just that a substantial portion of it is miniturised or miniturising. At my part line there are tons of little new hairs but I would guess they are 80% not fully terminal or on their way out. I was standing under my bathroom lights this morning looking at these hairs thinking, of only I could reverse that miniturisation, I would have so much hair. It’s so frustrating literally having tried everything to do this without any success.

That's also a good sign. It is very easy and rapid for miniaturizing hairs to reverse and thicken up in my experience - much faster than growing from nothing. My deep thinning reversed in the span of 2-3 months once I got on a good treatment despite continuing to shed from Telogen Effluvium at the exact same time, because those areas were just miniaturized and not truly "bald".

You're working hard, but you still have lots of things you can do. I would keep your head down and keep working. Life is not fair and we don't get equally easy problems to face or fix, but if you keep working at it, I'm sure one or a combination of those approaches I listed should reverse the problem. As I said, you may have already just fixed the biggest problem, but it will still take time to see the outcome. So just keep working on the rest in the mean time so you can be sure you've covered everything and don't stop.

 

[Sam1]

Something is bound to work for you...going on birth control helps to regulate hormones sometimes....but I’m sure you’ve Been down that road. It is very frustrating so frinkin hard to believe they haven’t come up with decent treatment yet. it’s 2018 it’s time people..companies out there if you’re reading launch some new products already.

 

[Georgie]

Something is bound to work for you...going on birth control helps to regulate hormones sometimes....but I’m sure you’ve Been down that road. It is very frustrating so frinkin hard to believe they haven’t come up with decent treatment yet. it’s 2018 it’s time people..companies out there if you’re reading launch some new products already.

I recently just came off diane35 since it seemed to do little for me. I’m hoping that growth factors are magic