For bryan and Foote.

[michael barry]

Im in no way a hair expert, but I can read what some experts (Pickart, Proctor, Hagerty, Bryan, and a few others here and there) think.

On Tricomin and Folligen.............the same guy, Pickart, came up with both of them. Tricomin contains a few more synthesized ingredients and less copper peptides.......................folligen's ingredients were similar to Prox-N's but without the prydine-n-oxides (patent) and some of the extra SOD's. Folligen does have the highest copper peptide content though. So much it stings the scalp for a couple of weeks until you get used to it.

Folligen spray has water, aloe vera gel (an NO releaser), copper peptides from soy protein in copper chloride, glycerin, propelyne glycol, polysorbate 20, allatonin, diazolinydinly urea, mathylparaben, and propalparaben

The folligen cream has some extras like tocophenyl acetate (E), retinyl palimate, ergocalciferol, steric acid, saw palmetto oil, and squalane also.


Prox-n has allotoin, ascorbate, arginine, BHT, pryidine-N-Oxides, Copper peptides from CU/ZN sulfates EDTA, propylene glycol , superoxide dismutases and water.


As you can see some ingredients are in common with these lst two. Folligen lotion and cream are proboably a little better than the spray, but what a mess. Maybe not bad if you put em' on at night. Pickart really does believe in saw palmetto being an effective anti-androgen (I do too, and will explain in a sec).


To look at copper peptides used alone without any anti-androgen or anything else to help them, you can view Bryan's pics at the picture gallery here at HairLossTalk.com. He just used prox-n for a couple of years, and defininely regrew a little hair.

The regimine you outlined is a good one. You could perhaps save some money (quite a bit) by using generic proscar from Genhair.com instead of dutas. Is quite a bit cheaper. The spironolactone 2X a day with it, would keep androgen transcription remarkably low I'd think . That might save ya a bit. 2% minoxidil from Wal Mart is very cheap. I belive Ive read that the difference between 2 and 5% really isnt all that big in terms of effectiveness. Coupled with the fact that you have anti-androgen bases so thouroughly covered.......proboably wouldnt hurt. Folligen is the most economical peptide product. A big bottle would last you about a year if used every other night. Its about 40 bucks. I understand its good to wait about 30 minutes before using minoxidil and peptides though, a by product that is called peroxyide nitrate or some such that is a vaso-constricter might occur in the bod if used at the same time. Your covering the phuck out of the bases though....................I really think cloning will be along for you Aplunk in 4-5 more years. I dont think you will ever have to worry about subsatial hairloss in your life to be honest. If even that fell through, new indications being worked on or genetic therapies should come along in the coming decades and with the fact you started treating your hair so early,,,,,,,,,,,,,,,,,it shouldnt be going anywhere anytime soon.


By the way, there is one FDA copper peptide study. It was done with Tricomin, but the maker didnt want to finance phase 3 (the expensive one). Phase 1 and 2 results were good though. They (graftcyte) were proboably going to rely on the buzz fromt those to move product. Bryan knows tons about that stuff.....................check out any old post he has made on here or hairsite to find out about it.

 

[wookster]

That in-vivo mouse study, is probably the most important in a long time. It clearly refutes the assumptions of "ALL" the in-vitro studies, and shows the danger of making such assumptions in science.

This study of "genuine" male pattern baldness follicles in a "real" mammalian dermal system, completely destroys the current theory, "and" the old donor dominance idea. It clearly proves androgens do "NOT" directly restrict male pattern baldness follicles, in fact these follicles thrive!

Yes, it does appear to throw a rather large monkey wrench into the workings of the current androgen dependent male pattern baldness theory.

 

[michael barry]

Wookie,
First of all, Im glad to know Im not the only one who suffers from insomnia from time to time.

http://www.hairlosstalk.com/newsletter/article233.htm There is an editorial from hairlosstalk written by Bryan about gamma linolenic acid (free form) and spironolactone. It mentions cytoperone acetate also.

Have you ever heard of a hamster flank organ? Its a tail-like little growth on the back of certain hamsters that is androgenically stimulated. Its "body" hair. By direct theory, if you put an anti-androgen on it, you should slow its growth. The flank organ is split into two halves like a "V" of sorts. Its a perfect "specimen" to check and see if an anti-androgen works and whether or not it just works topically or systemically. Reading the studies Bryan cites you can see that gamma linolenic acid (like whats in Revivogen) inhibited hamster flank organ growth the most. Sebaceous gland production (also stimulated by androgens through androgen receptors) was reduced also. Topical spironolactone reduced the organ size, sebaceous gland output and hair growth without affecting the rest of the hamster..................thus proven it works locally and not systemically like fluridil does. Cyproterone acetate worked some, but its absorbed systemically and doesnt break down in the body like spironolactone does.


Why is this stuff important? Well, hamsters arent really known for having edema of any kind inhibiting their hair growth for instance. It appears that the action on lessening the "body" hair was direct from the androgen receptors. I personally put revivogen on one wrist for two months. It DEFINITELY shortened, lightened, and thinned the body hair there vs. the other wrist. This would indicate the it worked directly on the androgen receptors on the cytoplasm of the dermal papilla as Ive no water retention there (I have low bodyfat).

The immuno deficient mice in that experiment Stephen cites may or may not of had much androgens flowing in their blood. Remember, these are sickly little creatures without much of an immune system at all. I really doubt mice have near the T a man has. Bryan brought that up to Stephen. Stephen dismissed it and pressed on.

The thing about "turning the direct receptor theory on its ears" et cetera is that Bryan conceeded that experimentally testosterone and its metabolites dont seem to have a killstroke type effect on the follicle all by their lonesome, they do inhibit head hair growth, but it seems like its the other damage around the follicle that does the hair in.


Ive looked over some of the experiments Stephen used to claim that testosterone(s) dont have a direct effect on hair. Usually hair cells from the dermal papilla, ORS, keratinocytes, etc. are cultivated in collagen and androgens are added. The androgen receptors have to be fooled with by scientist because they "get lost in translation" to an extent and dont express themselves "from the third to the ninth passage" and wont work right without a little help. The prevailing theory that all of these SCIENTISTS agree on is that when androgens are transcripted by the receptors, the dermal papilla releases growth inhibitors to the rest of the follicle. Experimentally follicle growth is slowed. Apparently the immune system sees the struggling follicle or the receptors bound up with DHT as a foreign body and attacks it. Thats the standard theory of baldness. If you read the studies Stephen and Bryan have both posted in this area, the guys and gals that ACTUALLY DID THE EXPERIMENTS all believe the standard theory of baldness.

That is, whatever it is that "makes your hair go" is in the DP cells themselves.................the DP cells "decision" to hurt cellular activity in the rest of the follicle is what sets hirsuite men apart from guys losin' it. The specific DNA instructions, the "hair cycle clock" is speculated to be in the parts of the follicle that do not devolve during all three phases. They might be in the stem cells that migrate down from the outer root sheath, DP itself, or the anterior cruciate muscle......................but they apparently get to the papilla and redirect the follicle in a bad way at some point. Thats what the researchers think.


Alpecin, which may or may not work worth a damn, has experimental data obtained from the German Universities of Jena and Bonn that cultivated 600 hair follicles with testosterone and caffeine, and testosterone alone. They claim the caffeine kept cAMP, an energy messenger, from being downgraded in activity when caffeine was added, and improved hair growth a little even with the testosterone present vs. a control that had no testosterone added. Maybe thats one of the actions "in the bulb" that slows hair cell growth and gets the body to think the hair is a foreign object? Who knows? I sure as hell wish they'da done that with DHT rather than T. They say they are going to be published in the Investigative Journal of Dermatology in a few months (email to me). An in vivo study is the only thing that will really get my attention personally. That this is noteworthy if its true is that ONE of the things happening may have been identified.

If you think about it, since we KNOW sebaceous glands are directly stimulated by androgen transcription through receptor sites, why NOT hair also. Stephen claims receptor blockers work because they work "further down" at the lymphatic pumps. Its hard to refute that, but fluridil has some happy users and is designed to degrade in water. Thats the problem with it according to many, they dont think it could cross the water layers to even get to the papilla without signifigant decomposition.


Stephen has worked very hard on his idea, and Im sure youve been able to tell, the disagreement between him, Bryan, and Dave (who is off the boards now as far as I can tell) devolved into an intellectual rivalry turned somewhat ugly.


Electron Microscopic observances by Hideo Uno of lymphocytic streamers and the Connective Tissue sheath having extra collagen hardening and inward growth squeezing the DP. The growth inhibitors sent towards the follicle like TGF beta-one and superoxides have been conclusively observed and recorded by real scientists studying this stuff. If an edema is occuring, I think somebody would have spotted it by now with all of the very delicate instruments that have been trained on balding scalps.


However, Ive asked and proposed many ways for Stephen to test his theory over time. He never thought any of em' would really work. A strong diuretic like a coal tar or petroleum jelly could be used by a balding guy on his head for about a year.....................he should have less fluid tension by then and better hair growth if the hydraulic dermal model was correct. Ive asked Stephen to get with lymphoedema specialists and try to asses some balding men for measurable edema. He stated that the edema wouldnt be obvious, but the increases in fluid pressure would be slight. Ive asked Stephen to get/pay a balding man to have 2-3 hairs in the receeding area moved to the front of the scalp's hairline to see if his theory of a tissue scaffold saving transplants was valid. He didnt think a transplant Doctor would go for it (I think if the money was right, those w****s would fellate bin Laden, but thats my own personal opinoin). I asked Stephen to get somebody to try cold presses on their head for a period of time to get better contraction and to lower fluid pressure, and compression bandages. He didnt make these things happen. Ive pointed out to him that "its YOUR theory, and if you just had one successful experiment (with a photo or two of success) of course, somebody who is in the postition to REALLY test it and publish the results might look into it. Nothing. Stephen's strategy for getting it noticed seems to be to win arguments in internet forums. But few docs proboably even venture into forums (unless its to hawk a product, or sell surgery). He may be trying to get his idea tested with a physician as we speak, and I hope he can at some point.

In the meantime Wookie, if youre intrigued by it..............spironolactone is a diureteic topically, minoxidil is diuretic, SuperoxideDismutases improve lymphatic drainage, propecia would slow the action of the lymphatic pumps if they work like Stephen's theory contends, rinsing your hair in cold water for about one minute after a shampoo will contract the skin there and force water down as well as be an effective anti-inflammatory. So you see, some of the things you can do for the regular accepted theory would also help if Stephen was right. Until he can prove/disprove it for us (because its really his idea to prove) Im not going to get bent out of order over it. However, if youre really motivated by it............I hope you look into it, go to a edema specialist, and let him take a look at your head and see what he diagnoses. Or if you plan on a little surgery, if you can talk the Doctor into it.............move a couple of hairs from where youve experienced recession to the very front of your widows peak and see if they continue to grow or miniaturize. Stephen would be happy to know the outcome Im sure if he ever posts here again. To be honest, I think he's left the forums until he can test his idea to a definite conclusion, but I might be wrong about that.

 

[wookster]

In the meantime Wookie, if youre intrigued by it..............spironolactone is a diureteic topically, minoxidil is diuretic, SuperoxideDismutases improve lymphatic drainage, propecia would slow the action of the lymphatic pumps if they work like Stephen's theory contends, rinsing your hair in cold water for about one minute after a shampoo will contract the skin there and force water down as well as be an effective anti-inflammatory. So you see, some of the things you can do for the regular accepted theory would also help if Stephen was right. Until he can prove/disprove it for us (because its really his idea to prove) Im not going to get bent out of order over it. However, if youre really motivated by it............I hope you look into it, go to a edema specialist, and let him take a look at your head and see what he diagnoses. Or if you plan on a little surgery, if you can talk the Doctor into it.............move a couple of hairs from where youve experienced recession to the very front of your widows peak and see if they continue to grow or miniaturize. Stephen would be happy to know the outcome Im sure if he ever posts here again. To be honest, I think he's left the forums until he can test his idea to a definite conclusion, but I might be wrong about that.

:freaked: :hairy: :freaked:

I do recall reading of an association between pattern baldness and insulin resistance, which would definitely tie in with the edema and folliclular miniaturization via contact inhibition, i.e. the "squeezing" of the follicular tissues as a consequence of heretofore undiscovered swelling issues.

The mechanics of the Foote hypothesis would appear to describe a hydraulic shift after puberty where the lymphatic pumping system creates the equivalent of a siphon effect. This effect then effectively maximizes drainage efficiency in the face/beard area and minimizes lymphatic efficiency on the top of the scalp. Of course each pump infrastructure would be different for different individuals, being an inherited trait, so genetics still has its role in the male pattern baldness equation. Some people would naturally have better drainage than others. That would also be a way to test the Foote hypothesis and refute the androgen receptor theory. Do some type of medical scan on many different individuals and then compare the results. Bald male pattern baldness scalps would most likely have poor lymphatic vascularity with respect to highly vascular - hairy non-male pattern baldness scalps.

 

[Guest]

This thread is great.

BTW, What happen to Nesta?

 

[vegeguy]

If foote's theory is correct then..

Assuming that hair loss is caused by swelling, hydraulic, etc ... or some damge to the tissue as it has been stated on these threads, then
hair transplant should not work....actually, nothing should work unless you fixed the tissue...right?

however, transplant has worked ...

 

[michael barry]

Wookie,
Thats actually a pretty good idea................to get medical scans of balding scalps vs. non-balding ones and compare lymphaitc traits. I wonder if Steve ever got up to getting some Doctor to do that. BTW, Stephen did have kudos for the scalp excercises also draining the scalp of excess fluid build up by stretching the top layer of the scalp skin, pressing the fluids back down. You can learn those on hairloss-reversible.com.


Phatky007,
If you read through the threads Stephen's explanation for the survival of transplants were the extracellular healing growth around the plugs when they were cut into the skin. The healing, or scarring process around the plugs involves extra fast skin growth (the SCAR tissue) around the follicle which would conserve space for the plug to enlarge in and for the dermal papilla to "get wide" enough in so the keratinocytes could make a fat hair follicle.

I do think its interesting to note that hair grows supposedly about the same speed up front where one is thinning and in the back where one is not, its the thickness of the shafts that leads to the obvious difference in hair mass. The reason the thinner hair in the front cant easily get as long is that its growth phases end much sooner by the time they are "intermediate" hairs.

 

[wookster]

Wookie,
Thats actually a pretty good idea................to get medical scans of balding scalps vs. non-balding ones and compare lymphaitc traits. I wonder if Steve ever got up to getting some Doctor to do that. BTW, Stephen did have kudos for the scalp excercises also draining the scalp of excess fluid build up by stretching the top layer of the scalp skin, pressing the fluids back down. You can learn those on hairloss-reversible.com.

I have been doing the scalp exercise for almost 9 months now. Can't say that I've had any really cosmetically significant regrowth yet but there are new hairs sprouting in the temple and front areas where the galea and frontalis meet. I am starting rogaine to see if it helps :hairy:

Baldness is very bad for us wookies.

 

[Bryan]

That in-vivo mouse study, is probably the most important in a long time. It clearly refutes the assumptions of "ALL" the in-vitro studies, and shows the danger of making such assumptions in science.

This study of "genuine" male pattern baldness follicles in a "real" mammalian dermal system, completely destroys the current theory, "and" the old donor dominance idea. It clearly proves androgens do "NOT" directly restrict male pattern baldness follicles, in fact these follicles thrive!

Yes, it does appear to throw a rather large monkey wrench into the workings of the current androgen dependent male pattern baldness theory.

The immuno deficient mice in that experiment Stephen cites may or may not of had much androgens flowing in their blood. Remember, these are sickly little creatures without much of an immune system at all. I really doubt mice have near the T a man has. Bryan brought that up to Stephen. Stephen dismissed it and pressed on.

There's a certain important issue with that immunodeficient mouse study which I've mentioned in the threads here and on HLH, but it's something that tends to get overlooked, so I'm going to drive the point home once and for all: unlike what Stephen claimed in his quote above, human hair follicles didn't "thrive" when transplanted onto those mice. To the contrary, their growth was actually STUNTED to a significant degree! :wink: Without digging out that study and re-reading it again, I believe they were limited to about half or so of their normal growth. So the point of it isn't that ALL transplanted hair follicles (both balding and non-balding) grew to full size and "thrived" on those mice, it's that all hair follicles regrew COMPARABLY WELL on the mice, even though they were BOTH limited in their growth to about half of normal.

The obvious question is, WHY were they limited in their growth when transplanted onto those mice? The researchers themselves don't really know, and neither do I; however, I suggest to you that the answer (or at least part of the answer) may possibly have something to do with the remaining level of androgens in those mice. So it makes no sense at all for either Stephen or "wookiewannabe" to go off the deep end and claim that the mouse study "throws a large monkey wrench" into the standard androgen theory of balding. While the mouse study is an interesting one to read and speculate about, by no means can you draw any firm conclusions about it. As I've already said several times, it's rather SUGGESTIVE that an immune component exists in human balding. But not by any stretch of the imagination does it "clearly prove" that androgens don't directly restrict male pattern baldness follicles.

BTW, that mouse study hasn't been duplicated anywhere else, as far as I know.

If you think about it, since we KNOW sebaceous glands are directly stimulated by androgen transcription through receptor sites, why NOT hair also. Stephen claims receptor blockers work because they work "further down" at the lymphatic pumps.

Uhhh....we don't need to scratch our heads and wonder if hair follicles respond directly to androgens. We already KNOW that they do. Remember, Sawaya's nifty little study with whole follicles in vitro clearly showed that both beard follicles and scalp follicles had the expected changes in growth characteristics from androgens and antiandrogens. The only question here is whether or not that direct effect from androgens is the ONLY way that they are affected, or if there are other additional indirect ways, such as the one that Stephen hypothesizes. But all he has is talk and theory. He has no evidence. In fact, the available evidence (like donor dominance) is all against him. And so powerful is the Sawaya study, even Stephen himself now apparently admits that androgens have _some_ direct effect, although he still denies that that's what's responsible for balding. It only took me two or three years to drag him kicking and screaming to that admission! :wink:

Bryan

 

[wookster]

I did find this bit of interesting information with regards to chronic inflammation:

http://goliath.ecnext.com/comsite5/bin/ ... 99-4504316

OBJECTIVE--INSULIN RESISTANCE AND C-REACTIVE PROTEIN (CRP) LEVELS ARE STRONGLY CORRELATED IN ADULTS.

http://www.immunesupport.com/library/sh ... T/CFIDS_FM

Vitamin C can reduce levels of C-reactive protein, a marker of inflammation and chronic disease

 

[michael barry]

Bryan,

Thats pretty much what I was leaning towards. Good info.

I think what "causes" baldness is the different response the DP cells have in affected hairs in men. Men with full heads of hair have androgen receptors. The variant of the androgen receptor gene that German scientists found in 98.6% of bald men was present in over 76% of non bald men. Its not the "pattern" DHT binds to receptors in.

It seems logical to me that since the DP releases growth inhibitors to the rest of the follicle in balding men, that the immune-component happens because cirulating immune cells detect the struggling mini-organ is a foreign body and begins to attack it. The difference initially, before inflammation is a problem between bald and not bald men should be going on inside the papilla's DNA.

 

[wookster]

Bryan,

It seems logical to me that since the DP releases growth inhibitors to the rest of the follicle in balding men, that the immune-component happens because cirulating immune cells detect the struggling mini-organ is a foreign body and begins to attack it.

:freaked: :freaked: :freaked:

This appears to be a non-sequitur. A Follicle's miniaturization in itself wouldn't cause the immune system to attack it. There appears to be a glaring gap in the logic.

:? :freaked2: :?

 

[Old Baldy]

Wookie: I'm a little slow. Can you re-read Bryan's posted study again (posted below) and explain to me how you still think androgens don't have a direct influence on hair growth and follicle health?

Dr. Sawaya study:

The study of beard and scalp hair follicles of 6 male donors in longer term culture (up to 14 days) appears to be an interesting model. The whole follicles were mounted in a collagen matrix. The study revealed significant differences (p<0.005) when the follicles were cultured in DHT (10 nM and 100 nM) in the presence or absence of 1 uM RU58841 added, i.e.:

a) in the presence of RU58841 hair follicle growth rates were found to be increased by 23% for scalp follicles but a 16% decrease was noted in beard follicles.

b) protein, DNA and RNA polymerase II activity revealed increases in scalp (25%, 12% and 12% respectively) and respectively equivalent relative decreases in beard hair follicles.

c) thioredoxin reductase activity, a sulfhydryl-reducing enzyme important for keratin protein synthesis, increased by 16% in scalp follicles after 14 days in culture but decreased by 10% in beard hair follicles.
-----------------------------------------------------------------------------

Bryan commented:

I think the relevance of the above findings in Sawaya's study for the DIRECT effects of androgens on hair follicles is screamingly obvious, and Stephen Foote doesn't even have the luxury of screaming "FOUL!" because of any added androgen receptors; that's because there WEREN'T any.

To me, that study says it all. Androgens have a direct effect on the growth of hair and the health of follicles. Why are you fighting the facts?

 

[Old Baldy]

Bryan,

It seems logical to me that since the DP releases growth inhibitors to the rest of the follicle in balding men, that the immune-component happens because cirulating immune cells detect the struggling mini-organ is a foreign body and begins to attack it.

:freaked: :freaked: :freaked:

This appears to be a non-sequitur. A Follicle's miniaturization in itself wouldn't cause the immune system to attack it. There appears to be a glaring gap in the logic.

:? :freaked2: :?

I don't follow this statement either. Michael appears to be correct from what I've read.

Dr. Kligman and Dr. Proctor both have concluded that male pattern baldness is an inflammatory disorder. This would indicate a negative immune system response is taking place.

I realize the term "inflammatory disorder" is a broad description but it does point to the immune system playing a major role doesn't it?

Where androgens have a negative impact, the immune system reaction comes into play and "finishes" the job so to speak.

Why aren't you accepting this scenario?

I know there isn't a cure for male pattern baldness (yet), however, there are many diseases exacerbated by negative immune system reactions that have no cure yet.

Just because there is no cure for an ailment doesn't mean the cause is unknown or interpreted incorrectly IMHO.

 

[wookster]

Androgens have a direct effect on the growth of hair and the health of follicles. Why are you fighting the facts?

ensativo:

Those facts support the "donor dominance" idea. Big bucks are behind it. They might be true but then again the complexities of baldness might not be so complex.

:freaked: :hairy: :freaked:

What is the mechanism causing the immune attack, if, while in the presence of androgens, follicles send out growth inhibitors. Follicle miniaturization wouldn't in itself cause an immune attack of the follicle would it? :x

 

[Old Baldy]

All I can tell you is what Dr. Proctor says:

Balding begins when male sex hormones do "something " to the scalp hair follicle which causes it to be read as a "foreign body". Your immune system then mounts an attack on the hair folllicle. The main damage in pattern hair loss is probably immunologically-mediated. Damage to lining of blood vessels, which produces hair growth factors, makes the balding process worse

.

Note where he says "damage to lining of blood vessels, which produces growth factors, makes the balding process worse".

The why is apparently unknown at this point in time but note again that there are some growth factors delivered by our blood vessels.

This is why I'm always harping on keeping our scalps and blood vessels healthy.

 

[wookster]

lNote where he says "damage to lining of blood vessels, which produces growth factors, makes the balding process worse".

The why is apparently unknown at this point in time but note again that there are some growth factors delivered by our blood vessels.

This is why I'm always harping on keeping our scalps and blood vessels healthy.

Vitamin C is a requirement for healthy blood vessels. Glad it is in my regimen

 

[Old Baldy]

Wookie, blood vessel health is so important to overall human health that I just can't over emphasize it.

I knew that before reading up on male pattern baldness but I never realized those of us with male pattern baldness had a probable blood vessel system problem. :-x

 

[wookster]

http://www.naturalproductsinsider.com/h ... 16452.html

Researchers found CRP levels decreased 24 percent in subjects receiving vitamin C supplements compared to subjects receiving placebo. CRP levels decreased 4.7 percent in subjects receiving the antioxidant mixture compared to the placebo group--an insignificant change, according to researchers. Those taking placebo experienced an increase of 4.3 percent in CRP levels.

“C-reactive protein is a marker of inflammation and there is a growing body of evidence that chronic inflammation is linked to an increased risk of heart disease, diabetes and even Alzheimer’s disease,â€￾ said Gladys Block, Ph.D., lead author of the study and professor of epidemiology and public health nutrition at UC Berkeley. “If our finding of vitamin C’s ability to lower CRP is confirmed through other trials, vitamin C could become an important public health intervention.â€￾

:freaked: :hairy: :freaked:

Is this :x "C-reactive protein" :x more prevalent in balding scalps also? :

 

[Bryan]

Androgens have a direct effect on the growth of hair and the health of follicles. Why are you fighting the facts?

ensativo:

Those facts support the "donor dominance" idea. Big bucks are behind it. They might be true but then again the complexities of baldness might not be so complex.

That's a rather enigmatic answer. Are you hinting that Sawaya was BRIBED by the hair transplant industry to fake a study showing a direct effect of androgens on hair follicles? :wink:

So stop hemming and hawing: do you or do you not believe this and all the other studies showing a direct effect of androgens and antiandrogens on hair growth?

What is the mechanism causing the immune attack, if, while in the presence of androgens, follicles send out growth inhibitors. Follicle miniaturization wouldn't in itself cause an immune attack of the follicle would it? :x

I think the bottom-line is that nobody KNOWS exactly what causes balding hair follicles to eventually draw the attention of the immune system. But whatever it is (I'm assuming here that it really does happen), it's obviously some downstream effect of androgens.

Bryan