I think male pattern baldness is dependent on the HPA axis

Hoppi

Senior Member
Reaction score
61
Ok, hey guys :)

Basically, I've been chatting with people a lot about this recently and it seems to me that male pattern baldness is fuelled by stress hormones from the HPA axis.

http://en.wikipedia.org/wiki/Hypothalamic–pituitary–adrenal_axis

The HPA axis seems to be how the body copes with all stress. It is a chain of hormones which basically goes:

CRH -> ACTH -> whole bunch of stress hormones (and enzymes)

One of those enzymes it seems to increase is - you guessed it - 5-alpha reductase type 2. It also seems to increase other pro-DHT enzymes around hair follicles, the prostate and so on.

Studies exist that demonstrate that calming the HPA axis causes hair growth:

http://www.diennet.com/hair_brochure.pdf

So what stimulates the HPA axis?

Probably all stress triggers. However, it also seems that many purely physical events can stimulate it. For example, poor digestive health tends to increase serum serotonin which increases CRH.

I also believe the reason this only harms scalp hair is due to the tight galea muscles and resultant poor bloodflow:

http://en.wikipedia.org/wiki/Galea_aponeurotica


So yeah erm, I think we need to calm down the HPA axis to stop hair loss.

This can be done by perhaps calming the gut (such as by healing it) or maybe taking a supplement of some kind to carefully reduce CRH. I'm still learning though.

Opinions? :)

Hoppi
 

Jacob

Senior Member
Reaction score
44
Hoppi is back? How'd I miss this? :cool:

Maybe DGL for healing. L-Glutamine. Also colostrum? See also: http://www.nutraingredients-usa.com...uence-metabolic-status-for-diabetics-RCT-data

I'm going to assume CRF is CRH: http://www.ncbi.nlm.nih.gov/pubmed/11518063

Hypericin showed the most potent binding inhibiton of all tested constituents to human CRF1 receptor with an IC50 value of 300 nM. Preliminary GTPgamma35S binding studies to CRF1 coupled G-protein indicated an antagonistic action for hypericin. The acylphloroglucinole hyperforin failed to inhibit 125I-astressin binding to hCRF, receptor up to 10 microM. Hyperforin inhibited binding to opioid and serotonin (5-hair transplant) receptors at IC50 values between 0.4 and 3 microM, while hypericin and pseudohypericin inhibited with weaker potency. The biflavonoid I3,II8-biapigenin inhibited 3H-estradiol binding to the estrogen-alpha receptor with an IC50 value of 1 microM. The inhibition of 3H-muscimol binding to the GABA(A) receptor is likely to be exclusively due to GABA present in the extract. We therefore hypothesize that additive or synergistic actions of several ditsinct compounds may be responsible for the beneficial antidepressant effect of St. John's wort.

Here's a couple of stress(etc) supplements I'm taking for awhile: http://innerpeace.herbworks.com/
http://tianchirealenergy.com/
 

Hoppi

Senior Member
Reaction score
61
Heya guys :)

And yes I'm kind of back.. I mean I'm usually knocking around here and there on hair loss sites!

I think that anything that:

1) Lowers serum serotonin or serotonin synthesis (be especially careful with this though as it could cause depression or constipation!)

2) Lowers serum histamine or histamine synthesis

3) Binds to the correct serotonin receptor (I think this is 5-HT2C in the Hypothalamus) or binds to serotonin receptors non-selectively

4) Binds to the correct histamine receptor (I'm unsure which one it is... none seem to be in the Hypothalamus or Pituitary, and yet apparently Histamine stimulates the HPA axis. Perhaps it's just correlation and it's serotonin doing it? Not sure)

5) Reduces CRH (also called CRF :) ) in the brain, optionally by reducing its synthesis

6) Binds to the correct CRH receptor on the pituitary gland (probably the same one that Astressin-B does... which is possibly CRF-2a, but the scientists seemed to struggle binding to the specific one. Perhaps we haven't discovered the one we need to target yet?)

stands a good chance of very positively impacting hair. Histamine is more debatable though.. I think it's best to focus on CRH, followed by serotonin.

Of course, after this chain it continues and something increases the enzymes that increase DHT in the scalp. I'm not sure what hormone does this though. The enzymes however are apparently 17a-HSD, 3a-HSD and 17b-HSD.

I'm still learning though.. it's all new to me but I'm pretty confident this is the correct route.


Some useful links and stuff:

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016377

Hello all - I haven't posted here for a while, but I have stumbled across something that I think deserves mention. I would like to know if anyone here is familiar with a new medication called Agomelatine. It is a drug that is chemically very similar to melatonin and has been in clinical trials for the past few years as a treatment for depression.

Recently, it was approved in Europe where it is available under the trade names Valdoxan and Melitor. You can read about it on Wikipedia. I first became aware of this drug in late 2007 when I got access to it through a clinical trial for sleep problems. The drug worked great for me with no side effect s(it has very few) The surprising thing was that I was almost certain that, after some 2 months, it was improving my hair. Unfortunately, in the 3rd month I moved to the East Coast and had to leave the trial and couldn't get the drug since it was not yet available.

A little over 2 months ago, I discovered that Agomelatine had been approved in Europe and was available (it should be available in the US next year) Having had a lot of sleep issues and some depression, I immediately ordered some and went back on it. I've now been on for 10 weeks. I take 25mg before bed daily. Just before starting on it, I went through a terrible shed for reasons unknown. Like many of you guys, I know just exactly how much hair I normally shed from years of monitoring different treatments, and my hair was suddenly falling out 4-6 hairs at a time and I was freaked. Well now in my 3rd month of Agomelatine my shed rate is back to normal and, more interestingly, my previous observation seems to be consistent - my hair is improving again - faster than with any other treatment I've ever used. The growth cycle seems to be longer and I have terminal hair growing in my crown where nothing has grown longer than about 1/2 inch for years. I have stylable hair there now and all my hair is growing longer and better. I have started taking pictures, but I can tell something is going on. I also know this is the case because I haven't colored any gray out of my hair and yet my hair is far darker because it is growing better.

Has anyone else had any experience with Agomelatine?

I did some research and discovered that A.G Henkel company has filed a patent for a hair treatment which uses it. http://www.wipo.int/pctdb/en/wo.jsp?WO=2009024361 I should mention that I take dutasteride daily and shampoo with 2% Nizoral daily for over 5 years, so this may be a synergistic effect.

Having used most of the treatments we discuss here, I have never noticed this much of a result nor this fast with anything else. (other than transplantation).

If anyone else has any information I'm very interested in hearing it.

Best to all,

Dean

(Agomelatine - as well as being a melatonin agonist (via both MT1 and MT2) - is also a 5-HT2C antagonist. I was actually literally doing a search for "agomelatine hair" on Google based on my suspicions about 5-HT2C when I discovered the thread with that post in it)

http://en.wikipedia.org/wiki/Agomelatine

This video by Danny Roddy also highlights the suspected significance of serotonin:

[video=youtube;lB7cQRDhqTg]http://www.youtube.com/watch?v=lB7cQRDhqTg[/video]


This all suggests to me that anything that stimulates the HPA axis can cause androgenetic alopecia. That is to say the trigger hormone (that increases the DHT-boosting enzymes) is probably not serotonin, probably not histamine and probably not CRH. It is probably either ACTH or one of the subsequent hormones ACTH increases mostly or entirely via the adrenal glands.

Serotonin and histamine are often increased in conditions like irritable bowel syndrome, due to serotonin being necessary for the movement of food through the gut. When the gut is struggling, more serotonin is released to move food, and more of the SERTs (Serotonin Transporters) are damaged and so do not respond. Histamine is involved with gut inflammation, and so when food that hurts the gut is consumed, histamine may increase causing itching, sneezing and so on, and apparently stimulating the HPA axis as well.

http://en.wikipedia.org/wiki/Serotonin

http://en.wikipedia.org/wiki/Histamine

- - - Updated - - -

This is interesting...

http://upload.wikimedia.org/wikipedia/commons/1/13/Steroidogenesis.svg
 

resu

Senior Member
Reaction score
1,339
No wonder all the old guys I see with full Norwood are all bums.
 

Armando Jose

Senior Member
My Regimen
Reaction score
980
pilosebaceous unit acts as a cutaneous hypothalamic pituitary adrenal (HPA) axis ...
 

IDW2BB

Established Member
Reaction score
19
pilosebaceous unit acts as a cutaneous hypothalamic pituitary adrenal (HPA) axis ...
Would like your opinion on this study Armandohttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684595/
Although many reports have indicated the involvement of sebaceous glands in hair canal development, most, if not all, of the experiments were conducted in sheep and rodents [35], [36]. In agreement with these reports, hair shaft emergence was readily observed in grafted dissociated neonatal murine-only ESS. Considering that their pilosebaceous units were not developed until after birth, results should be interpreted cautiously. In human fetal development, complete pilosebaceous units formed around 20–21 weeks of gestational age [37]. Early establishment of human hair canals was observed intra-epidermally prior to initial eruption of vellus hairs [37][39]. Although results from this study suggested that incomplete hair canal formation in ESS may be due to the lack of sebaceous glands, we could not rule out the unusual cornification, which occurred after complete epidermal stratification. The sequence of hair and skin keratinization may also play a key role in human hair canal development. While future studies may need to emphasize developing ESS under submerged, instead of air-exposed, conditions to promote the proper order of hair and skin keratinization, this study provides a practical model for mechanistic studies of hair development in human epidermis of engineered skin.
 

Hoppi

Senior Member
Reaction score
61
pilosebaceous unit acts as a cutaneous hypothalamic pituitary adrenal (HPA) axis ...

I do agree with sebum's role in Androgenetic Alopecia, but I just think it's the result of increasing DHT (via the hormonal pathway) in a low bloodflow environment (the galea).

I don't know why the galea seems to be tighter in balding people, but maybe that's just because we can see it more easily when the hair is gone? Perhaps it's always tight?

Or perhaps the stress hormones tighten it, I don't know. But I think the hormones that increase DHT surrounding the follicles and elsewhere are a bigger problem.

However, I believe that either relaxing the galea muscles or correcting the hormonal pathway (or both) will easily fix Androgenetic Alopecia. They're just tricky to do is all...
 

Armando Jose

Senior Member
My Regimen
Reaction score
980
To iDW288, off topic
when I worked in the tanning industry, I learned that the only skin where hair forming holes through the skin was the pigskin, the human and the apes. In all other animals, goats, sheep, cows, rats etc. hair fails to penetrate the skin. In language there are only holes in the split of the pig skins

I have also understood that the sebum and sebaceous gland therefore, it is necessary to "break" the ORS and allow hair shaft output

BTW Interesting study
"this study suggested that incomplete hair canal formation in ESS may be due to the lack of sebaceous glands"
 

squeegee

Banned
Reaction score
132
To iDW288, off topic
when I worked in the tanning industry, I learned that the only skin where hair forming holes through the skin was the pigskin, the human and the apes. In all other animals, goats, sheep, cows, rats etc. hair fails to penetrate the skin. In language there are only holes in the split of the pig skins

I have also understood that the sebum and sebaceous gland therefore, it is necessary to "break" the ORS and allow hair shaft output

BTW Interesting study
"this study suggested that incomplete hair canal formation in ESS may be due to the lack of sebaceous glands"

Kids have heads full of hair, no sebum involved!

- - - Updated - - -

I do agree with sebum's role in Androgenetic Alopecia, but I just think it's the result of increasing DHT (via the hormonal pathway) in a low bloodflow environment (the galea).

I don't know why the galea seems to be tighter in balding people, but maybe that's just because we can see it more easily when the hair is gone? Perhaps it's always tight?

Or perhaps the stress hormones tighten it, I don't know. But I think the hormones that increase DHT surrounding the follicles and elsewhere are a bigger problem.

However, I believe that either relaxing the galea muscles or correcting the hormonal pathway (or both) will easily fix Androgenetic Alopecia. They're just tricky to do is all...

PGD2 induces constriction my friend.. **** the galea theory!
 

Armando Jose

Senior Member
My Regimen
Reaction score
980
Kids have heads full of hair, no sebum involved!

- - - Updated - - -



PGD2 induces constriction my friend.. **** the galea theory!


Kids have sebum in scalp hair, regarding sebum scalp is not skin or face...
Sebum is vital to form ORS disgregation around bulge zone

healthy hair needs sebum, if not hair must be dry, brittle, and bad condition, the reality is different
 

Hoppi

Senior Member
Reaction score
61
I was under the impression that the galea led to accumulation of oil and DHT, which subsequently gets infected and then the body's immune response causes inflammation.

Anyway, it's hormonal at its core surely, so all of this is secondary to the true cause o_O
 

squeegee

Banned
Reaction score
132
I was under the impression that the galea led to accumulation of oil and DHT, which subsequently gets infected and then the body's immune response causes inflammation.

Anyway, it's hormonal at its core surely, so all of this is secondary to the true cause o_O

If the galea theory exist.. tell me why hair transplant works in the same environment?
 

Baldie101

Established Member
Reaction score
7
I semi-agree. I didn't read much of the article or the wiki. The HG234 actually made me laugh. Their site got a video that's hilarious. If you scroll down you see where the company is from, google their product to check where it can be bought you are brought you Ali Baba. The place is quite famous but the warning here should be that it's in China. ;)

Now to the stress part, I agree. I can't speak for others or with research (in this specific case) except for myself. When I was 22 I started to lose hair, and I noticed that my head was shiny when I came out from the bath. I had dried my head but it was still wet. It was much later I found out by myself that it's sebum production. That sebum/ooze would dry and become big dandruff flakes which would fall with my hair stuck in it. I also noticed that I got acne/pimples on my scalp where I lost most hair. Mainly temples and crown leaving nice dark round hard skin. :kaputt:
Anyway fastforward 5 years with the **** still happening and no doctors being able to help me.

One day I suddenly saw a mysterious pattern in my hair loss.
When I get extremely tired or just mentally tired, I piss some white/transparent liquid with my urine. I don't know what it is but it can easily be sperm thrown out by the system so new can be produced in the testes. I don't think so though because it only happens when I get very tired. The next day my head shines and I lose hair....and the next day I will get dandruff since the shine(the sebum/oozing liquid) will dry and stick to my scalp.

It's still happening now that I'm a Norwood 5/6 and I still don't know what I can do to stop it. I'm sure that it's one of the main reasons for my hair loss.

Still if the deal with stress is the reason for sebum on my head, it kinda makes sense: More stress -> more DHT -> more sebum -> more hair loss.

Anyone got ideas on what I could do to lower my stress other than Vitamin B and bodytraining?
If it works I would be more than happy to throw out the drugs if I got my hair back :love:
 

IDW2BB

Established Member
Reaction score
19
I semi-agree. I didn't read much of the article or the wiki. The HG234 actually made me laugh. Their site got a video that's hilarious. If you scroll down you see where the company is from, google their product to check where it can be bought you are brought you Ali Baba. The place is quite famous but the warning here should be that it's in China. ;)

Now to the stress part, I agree. I can't speak for others or with research (in this specific case) except for myself. When I was 22 I started to lose hair, and I noticed that my head was shiny when I came out from the bath. I had dried my head but it was still wet. It was much later I found out by myself that it's sebum production. That sebum/ooze would dry and become big dandruff flakes which would fall with my hair stuck in it. I also noticed that I got acne/pimples on my scalp where I lost most hair. Mainly temples and crown leaving nice dark round hard skin. :kaputt:
Anyway fastforward 5 years with the **** still happening and no doctors being able to help me.

One day I suddenly saw a mysterious pattern in my hair loss.
When I get extremely tired or just mentally tired, I piss some white/transparent liquid with my urine. I don't know what it is but it can easily be sperm thrown out by the system so new can be produced in the testes. I don't think so though because it only happens when I get very tired. The next day my head shines and I lose hair....and the next day I will get dandruff since the shine(the sebum/oozing liquid) will dry and stick to my scalp.

It's still happening now that I'm a Norwood 5/6 and I still don't know what I can do to stop it. I'm sure that it's one of the main reasons for my hair loss.

Still if the deal with stress is the reason for sebum on my head, it kinda makes sense: More stress -> more DHT -> more sebum -> more hair loss.

Anyone got ideas on what I could do to lower my stress other than Vitamin B and bodytraining?
If it works I would be more than happy to throw out the drugs if I got my hair back :love:
As a NW5/6 I would suggest you seek medications to reduce scarring. Regrowth is all the harder with scar tissue build-up.
 

Baldie101

Established Member
Reaction score
7
As a NW5/6 I would suggest you seek medications to reduce scarring. Regrowth is all the harder with scar tissue build-up.

Interesting, I would love some names of that great stuff, you are talking about.

You see, those acne/pimples I get on my scalp and temples, leaves dark marks/scars and hard tissue/skin. Those don't look pretty at all. Furthermore the next time I get acne/pimples there's a high chance of them appearing on the same place. This results in darker mark/scar.

I did ask my dermadocs about them and medication to make the hard tissue go away together with the darkness but they went: "They will do it by themselves, it will just take time...a lot of time." That didn't help a lot...cuz they keep appearing and not giving the old one the chance to disappear, sigh.

So I would be damn happy to know of this reduce scarring medicaition which will help removed the hard scar tissue build-up on my head. :wow:
 

Sparky4444

Senior Member
Reaction score
44
This just doesn't wash with me...My front has receded, but there are a few hairs that refuse to die...they still are black and when I pluck them, they grow back...they are surrounded by bald scalp...
 
Top