I think the chief cause of AGA/MPB/FPB is corticotropin-releasing hormone

As in, CRH seems to be the hormone that increases the enzymes like 5ar2 that elevate DHT and lead to hair loss, prostate enlargement and so on. Not sure how many of you have thought of this.

I do not think it is ACTH or β-endorphin (the two hormones stimulated by CRH) or any hormone they themselves increase. What I'm saying is that hair loss and prostate enlargement and stuff isn't so much caused by the HPA axis in its entirety but instead SPECIFICALLY by CRH ITSELF acting upon the hair and prostate by stimulating one or more of its receptors.

Obviously evidence of this can be seen in places like the Astressin-b experiments/studies:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016377

"Slominski et al. [8] , [9] have also shown that CRF, urocortin 1 and CRF receptor subtypes 1 and 2 (CRF1 and CRF2) are expressed in the normal skin and cycling hair follicles of humans and mice."

I suppose this means that urocortin could also be an issue, but surely that's also less likely. I'll research that

Here is another interesting bit of text:

http://www.fasebj.org/content/15/10/1678.long

"The extracranial tissues in which CRH receptors have been identified include the adrenal glands, testes, ovaries, prostate, kidney, liver, gut, spleen, circulating immune cells, synovium, heart, skeletal muscle, uterine myometrium, vascular endothelium, arterial smooth muscle, endometrium, placenta, lungs, and skin."

Also, interesting that DS Labs put the non-selective CRH receptor blocker Astressin-B in their Spectral F7 topical solution. Suggests it has a positive effect even topically, which goes some way to backing up it is the hormone that directly affects the follicles.

http://www.dslaboratories.com/spectralf7

The only real other possibility as far as I can see is another hormone acting on a CRH receptor like I think just urocortin. I'll research that. However, I think at this point CRH is looking like the one.

Additionally, seeing as a selective CRF1 OR a selective CRF2 blocker didn't work (there are 4 CRH receptors known at present):

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

"There are four subtypes of this receptor known at present, defined as CRF-1, CRF-2a, CRF-2b and CRF-2g."

This means that either you have to hit CRF 1 and 2 at the same time for it to work, OR (as I suspect) there is ANOTHER CRH receptor like say CRF-1b or CRF-2c that we haven't discovered yet.


Either way, I think the chance of the trigger hormone being CRH via a CRH receptor is incredibly high.

Hope this helps,

Hoppi


EDIT -- Apparently Urocortin has been shown to interact with CRF-1 and I think that's all to date. I think it's unlikely to be Urocortin though.

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

its seems to me, that every few weeks u discover some part of human biology, and then state that thats the cause. why not invest some time and do a degree or something, then use that knowledge to form a hypothesis. instead of subliminal messaging urself into believing watever ur currently reading about is the cause.

rofl wrote:its seems to me, that every few weeks u discover some part of human biology, and then state that thats the cause. why not invest some time and do a degree or something, then use that knowledge to form a hypothesis. instead of subliminal messaging urself into believing watever ur currently reading about is the cause.

People always make out my theory is changing but it hasn't changed too considerably for about 2-3 years now, it's just got more specific.

Now my theory for myself goes:

Dysbiosis/Candida leads to an increase of a hormone like serotonin or histamine -> this stimulates CRH release -> CRH increases 5ar2 and other similar enzymes in my scalp follicles and other places, but the scalp follicles struggle more due to the Galea muscles -> scalp DHT and sebum increases -> this gets infected (dandruff, in my case) -> histamine regulates the inflammatory response to the infection -> hair is lost

It's really not THAT complex and other than learning of the HPA axis' role recently (from which I determined it likely to be CRH), all I'm adding is specificity, can you not see that? o.O

>> Dysbiosis/Candida leads to an increase of a hormone like serotonin or histamine -> this stimulates CRH release -> CRH increases 5ar2 and other similar enzymes in my scalp follicles and other places, but the scalp follicles struggle more due to the Galea muscles -> scalp DHT and sebum increases -> this gets infected (dandruff, in my case) -> histamine regulates the inflammatory response to the infection -> hair is lost

And what leads to dysbiosis and candida in the first place? And don't say diet cause half of Americans would be completely bald by age 30.

Candida also wouldn't explain low SHBG levels found in balding men. LOW SHBG is caused EXCLUSIVELY by low thyroid. Go to PCOS forums - half of them have hypothyroid, and half are probably undiagnosed. This can't be a coincidence. Also, I'm sure thyroid does some CRH regulation itself.

Now what causes low thyroid? Heavy metal toxicity(which also causes Candida). What makes one susceptible to heavy metals? Vaccines and antibiotics. There was some rat study where they found that antibiotics mess up your mercury excretion mechanism in your gut so that's that.

The root of MPB is heavy metals or whatever else that's suppresses thyroid. hoppipolla, have you ever checked yourself for heavy metals? Have you measured your basal temperature?

It doesn't have to be IBS... many things stimulate CRH release.

>> It doesn't have to be IBS... many things stimulate CRH release.

I didn't say anything about IBS

Also, many things cause IBS, including food poisoning and overuse of antibiotics (both I think lead to dysbiosis, SIBO or Candida which are all IBS causes).

Ok moby look erm, here's the thing.

I do agree that you can go closer to the source of why androgenetic alopecia happened. I agree with you that it is rooted in health, and that by fixing health the whole thing can be solved at the root.

However, I focus on things like CRH with a significant portion of my time while researching this because I think the more we understand about the immediate cause of AGA, the better a chance we have of quickly fixing the problem before the person has lost too much hair. I think it would be great to have a quick and easy supplement of Astressin-B or something similar that can just stop the person's hair loss and therefore give them time to fix the rest of their body without feeling like their hair is being lost day by day.

Additionally, being able to calm the HPA axis via reducing or blocking CRH is potentially an incredible tool I believe for promoting overall health and longevity, because the stress response is responsible for a lot of damage and aging in the body if it is excessively stimulated.

I figured if we could strip AGA/MPB/FPB down to something like:

Physical or mental stress -> CRH -> CRF-2b (for example) -> 5ar2 -> DHT

and so on, it means we can better target quick-fix treatments and help people regain control of the situation faster, giving them more confidence and ensuring they don't end up a fast NW4 or something!

Additionally, I really don't believe there is sufficient evidence to pin the blame solely on heavy metals or even hypothyroidism. Surely the fact that food poisoning or long-term antibiotic use can cause "IBS" is enough to prove that other things can tip the balance? Gut flora is incredibly complex and I think incredibly fragile. Decreased digestive enzymes, stomach acid or bile can also I believe cause dysbiosis, SIBO etc, and this can be the result of many things including gallstones or fatty liver. Or consumption of foods containing parasites that might infect and upset the gut.

Hell, I even met someone once who noticed AGA after heavy consumption of green tea, and once I advised him to stop drinking it as much, his hair stopped falling out (which as far as I know is one of the few examples of the CRH path being omitted, due to a directly androgenic supplement).

Logic states that anything that increases CRH and possibly urocortin could cause AGA.

I am interested in your POV though, and I do agree that heavy metals and hypothyroidism can be big players in declining health and infections and make you more susceptible and vulnerable to pretty much everything. But I'm just not convinced that it's the only potential cause.


Oh, and additionally just for the record, SHBG tends to RISE in aging men, not fall:

http://www.ncbi.nlm.nih.gov/pubmed/15807883

http://www.ncbi.nlm.nih.gov/pubmed/17895324

http://www.ncbi.nlm.nih.gov/pubmed/16329620

i think your idea has merit hoppi

that would explain a lot to me as well in regard to my history

because i was adopted i was only formula fed which probably altered my gut flora thereby setting me up for psoriasis starting in my early childhood. then as i got in my midteens started getting AGA

found those intesting pages on the connection between SIBO and psoriasis, so its pretty much a definite that i got SIBO myself

http://www.healgrowthrivemedicine.com/health_information/psoriasis/index2.html

http://books.google.com.au/books?id=xVRoseYyvVYC&printsec=frontcover&hl=de&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false

Small intestine microflora at psoriasis.
Its possible role in pathogenesis.

Theses:

For the first time researches of transient microflora of proximal small intestine at 121 psoriatics (PASI >=20) are conducted. Сontrol group consists from 43 healthy persons.
Level SIBO more than 105 CFU/ml (TBC > 5) was found at 95 (78,5%) psoriatics.
TBC (total bacterial count) for psoriatics has made average 3х106 CFU/ml that is much more than in the control group - 1,1х103 CFU/ml.
The correlation between SIBO level and PASI (correlation coefficient R=0,46), between SIBO level and duration of psoriasis disease (R=0,43) has been found.
At 93% of psoriatics Bifidobacterium spp. was found - on average 2х105 CFU/ml (in the control group at 40%, on average 250 CFU/ml).
At 84% of psoriatics Lactobacillus spp. was found, on average 4,6х104 CFU/ml; (in the control group at 19%, on average 350 CFU/ml).
At 79 from 121 (65%) of psoriatics Enterococcus spp. was found - on average 2х105 CFU/ml.
In the control group Enterococcus spp. not found at all.
At part of psoriatics Str.pyogenes (9%) and Str.viridans (30%) were found (in the control group not found).

hoppipolla, but Astressin-B has already been tested for hair loss purposes with minimal to no results. Also, blocking CRH is probably more dangerous than blocking DHT so why not just do that while you figure your things out?

Antibiotics can make someone more prone to IBS, but it's not the cause. Most importantly, antibiotics makes a person more prone to heavy metals by reducing their excretion rate. That's more harful to your health than IBS.

Low SHBG, high LP(a), high insulin, high homocysteine, higher chances for heart disease, cholesterol, metabollic syndrome - all associated with AGA and further all associated with under performing thyroid.

Gut may very well be the root cause by making someone prone to heavy metals and future thyroid problems.

moby wrote:

The root of MPB is heavy metals or whatever else that's suppresses thyroid.

Then whoy don't we go slick bald outside the galea area? Why do botox injections and scalp looseners reverse hairloss on their own?

>> Then whoy don't we go slick bald outside the galea area? Why do botox injections and scalp looseners reverse hairloss on their own?

Because those follicles are less prone to MPB due to lower number of 5AR receptors? What is the root cause of galea problems then? Is it just a coincidence how many people here have hypothyroidism or sub-clinical hypothyroidism?

SlowMoe wrote:

moby wrote:

The root of MPB is heavy metals or whatever else that's suppresses thyroid.

Then whoy don't we go slick bald outside the galea area? Why do botox injections and scalp looseners reverse hairloss on their own?

Oh yeah 100% agreed

I think it's a combination of hormonal (CRH/DHT) and Galea muscle tension.

I do agree with moby that it's ALSO health issues like low thyroid, but that's more distant from the basic biology of what's causing AGA.

Astressin-B definitely works in mice, I haven't seen human studies? It's entirely possible that we have more CRH receptors than mice

moby wrote:>> Then whoy don't we go slick bald outside the galea area? Why do botox injections and scalp looseners reverse hairloss on their own?

Because those follicles are less prone to MPB due to lower number of 5AR receptors? What is the root cause of galea problems then? Is it just a coincidence how many people here have hypothyroidism or sub-clinical hypothyroidism?

I think it's a combination of many things. I also believe the tight scalp is the major contributor since loosening stops loss in everyone and regrows in most.

SlowMoe wrote:

moby wrote:>> Then whoy don't we go slick bald outside the galea area? Why do botox injections and scalp looseners reverse hairloss on their own?

Because those follicles are less prone to MPB due to lower number of 5AR receptors? What is the root cause of galea problems then? Is it just a coincidence how many people here have hypothyroidism or sub-clinical hypothyroidism?

I think it's a combination of many things. I also believe the tight scalp is the major contributor since loosening stops loss in everyone and regrows in most.

Once again, agreed. I just think loosening the Galea muscles seems difficult and maybe even unnatural? Unless of course CRH or another stress hormone tightens them o.O

Also, I got an uncomfortably large amount of body hair and also mild BPH at the same time roughly as my MPB, so I'd love to stop/reverse those too!!

Alphadelta,

Very cool information you posted. Do you happen to have the link to the study? I'd be very interested to see that if you still have it.

This is something I've wondered... If we consider loss of head hair to be a disease, is an overgrowth of body hair also a disease or an imbalance?
Another thing, the receptors that are 'genetically sensitive' to androgens, is there an explanation why it's the pattern it is?
It's like facial hair, is there an explanation as to why we grow facial hair in the areas we do?

I agree with Slowmoe on this one. Having a tight Galea is the main culprit and everything else is without a doubt a secondary factor (including nutrition). Thyroid problems can be the main culprit for some as well, too. The people that don't exprience regrowth from scalp loosening definitely need a violet ray to get those follicles to start waking up. I can't believe people still debate about these things anymore...

IMO the best way to restore a full head of hair is to take the bull by the horns and attack this problem from every angle without forgetting that a LOOSE SCALP is essential. Unless you have a thyroid issue and loose scalp, you will regain little to no hair at all if you focus mainly on nutrition and not on loosening the Galea.

Conclusion: A TIGHT SCALP IS THE MAIN CULPRIT STOP FIGHTING IT. I wouldn't doubt all of these new studies that endorse certain pharmaceutical pills and topicals were federally funded.

Edited for spelling errors.

>> Also, I got an uncomfortably large amount of body hair and also mild BPH at the same time roughly as my MPB, so I'd love to stop/reverse those too!!

Exactly. How would the tight galea cause excessive hair growth everywhere else and other problems? Obviously tight galea is probably the result of some fault rather than the other way around.

Hey Xenon how is your prostate?

moby wrote:>> Also, I got an uncomfortably large amount of body hair and also mild BPH at the same time roughly as my MPB, so I'd love to stop/reverse those too!!

Exactly. How would the tight galea cause excessive hair growth everywhere else and other problems? Obviously tight galea is probably the result of some fault rather than the other way around.

Well, I currently have the view that the Galea is just naturally tight. I don't think my Galea got tighter as I aged or anytime recently, I think that the hormonal shift towards elevated CRH (due to something like elevated serotonin or histamine from my gut issues) and elevated DHT affects different parts of the body in different ways:

- The scalp loses hair due to the tightness of the Galea

- The arms, legs, chest and so on grow more hair due to the hair-promoting properties of DHT

- The prostate gets larger... although I'm not quite sure why! But it's well known I believe that BPH is associated with elevated local, tissue DHT (ie serum DHT may fall but DHT in the skin, hair, prostate and so on goes up).

When I learned that CRH receptors are not only found in the scalp and skin but also in the prostate, and that the only things CRH increases in the blood are ACTH and b-endorphin (neither of which appear to affect hair loss)... it all sort of fit together tremendously well for me!

Also, sorry I didn't comment on your post alphadelta, I think I missed it somehow! And yeah it seems that way too many things are capable of messing up gut flora to blame just one specific thing. But I'm open to being convinced of almost anything if the evidence is there!!

I do think that if we can determine that it is in fact CRH or even just a CRH receptor that is increasing the 5ar2 and/or other DHT-promoting enzymes then that is a massive step in the right direction. Over stimulation of CRH isn't a good thing because it goes on to stimulate the rest of the HPA axis, increasing cortisol and other hormones that you really don't want knocking around in excess. I think the quicker it can be calmed down, the better. And the more we understand about this process, the better

AS54 wrote:Alphadelta,

Very cool information you posted. Do you happen to have the link to the study? I'd be very interested to see that if you still have it.

sry cant seem to find the studies, heaps of references all over that document though, but some studies are russian as well so hard to find things
http://books.google.com.au/books?id=xVRoseYyvVYC&printsec=frontcover&hl=de&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=true

under Subprocess 2 SP2 and appendix 6 especially Table 3 there is all the interesting information to dysbiosis and SIBO

moby wrote:>> Also, I got an uncomfortably large amount of body hair and also mild BPH at the same time roughly as my MPB, so I'd love to stop/reverse those too!!

Exactly. How would the tight galea cause excessive hair growth everywhere else and other problems? Obviously tight galea is probably the result of some fault rather than the other way around.

Androgens play a role too. They hurt your hair UNDER LOW OXYGEN CONDITIONS; apparently the hair cells can't process excess androgens when in a sickly low oxygen stare, and it over works them. Androgens are good for healthy hair cells.

So excess androgens should result in increased hair, unless there were a low oxygen environment.

hoppipolla wrote:

moby wrote:>> Also, I got an uncomfortably large amount of body hair and also mild BPH at the same time roughly as my MPB, so I'd love to stop/reverse those too!!

Exactly. How would the tight galea cause excessive hair growth everywhere else and other problems? Obviously tight galea is probably the result of some fault rather than the other way around.

(ie serum DHT may fall but DHT in the skin, hair, prostate and so on goes up).

DHT goes up locally in a low bloodflow area because it's testosterone compeditor, estradiol, needs a lot of oxygen; if it doesn't have it more DHT gets produced due to having less competition.

Sloemoe, every time you hit back with the blood flow thing, I find it hard to disagree. To the layman like myself, it seems to trump a lot of other theories.Have you an answer to this - Science tells us there's a genetic 'switch' that causes mpb. you see men bald in the same pattern and it begin around the same time as their elders did.