For bryan and Foote.

[S Foote.]

"Proven processes", my foote! I've asked you REPEATEDLY to find one other biological process (just ONE) where the response to androgens "flips", because of previous exposure to contact inhibition. Despite the fact that you have undoubtedly spent many sleepless nights desperately searching for such an example to bolster your theory, you've come up completely empty. So you don't have "proven biological processes" at all, you charlatan.

I have shown you the "just one" example you have asked for before Bryan!

Here it is again:

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

There's nothing in that link having anything to do with the challenge I posed to you, and you know that as well as I do, you charlatan.

Bryan

I am really not interested in any so called "challenge" you care to post, unless it has a "genuine" scientific basis.

So far i just see you posting a lot of psuedo scientific crap, because you have got used to people on these sites just taking your word for things.

You are going to have to do a lot better than that Bryan, because i am wise to your tactics in these debates.

You have called me a charlatan twice now in this thread.

The first time it concerned the scientific principle of Ockhams razor. Anyone who is following this thread can see that i have asked you once (so far) to justify this remark. They can also now clearly see that you have not done this!

Before we go any further, i require you to back up your comments with some "real" science, instead of your "acting" in these debates :wink:

You said:

"The fact that YOU of all people would have the unmitigated gall to cite "Okham's Razor" is the funniest irony of all! You're lucky that the ghost of William of Okham doesn't come to haunt you every night!"

People here can see that i asked you to justify that statement Bryan, and that you can't!

In fact this whole thread demonstrates just how much scientific talent you have, by your constant asking of a completely irrelevant question to the issue at hand!

Here's your last chance for any "true" scientific credibility here Bryan :wink:

Tell us all exactly how Ockhams razor refutes my theory?

If you don't answer my question "SPECIFICALY" , everyone here will see for themselves what a sham you really are 8)

S Foote.

 

[S Foote.]

Stephen,
Do me a favor, my last post on this thread had this picture http://www.oprah.com/tows/slide/200509/ ... _107.jhtml. I posted another picture of her and her twin. And two other sets of female twins, one of which who also shot herself up with testosterone and aged her hair's and skin's appearance dramatically (and both grew beard hair)........

I KNOW you assert that fluid build up caused the thinning of the hairs, but how do you believe that it aged the hairs in these two women? How did the androgens age the skin so obviously in the second gals picture? Do you believe the lymphatic metabolic wastes bind with the vitamin D receptors on the follicles or the androgen receptors and have that ugly effect? Ive never gotten ANYONE to comment on those photos, and they are about a clear of an example of what happens when androgens are unleashed on skin/hair that you'll ever see.

Michael.

The effects of tissue edema are known to be generaly un-healthy to cells in general. There is a reduced nutrient supply, and reduced waste removal. On top of this, the increased immunological factors play a role.

Lo'real describe these conditions.

http://www.timesonline.co.uk/printFrien ... 10,00.html

So yes, there are going to be "aging" like effects in these conditions.

S Foote.

 

[michael barry]

Stephen,

I have a little question for you. In experiments, when dermal papilla cells are cultivated with keratinocyte, root sheath cells, etc., androgens are added and cells from areas of the head that are thinning already slow their cell division. Scientists conclude that the KC and ORS cells are responding directly to the androgens.
You propose, that as in the lung tissue youve cited, that the cells that slow division have "flipped" their response to slow growth from dermal papilla released antigens. So the "squeeze" as it were, changes the Dermal papillas response according to you.

Now that thats out of the way, would you propose that in a man who has submitted some hair cells from the front temples that are thinning and the vertex bald spot area THAT IS NOT THINNING YET might have his hair cells cultivated in a collagen matrix, have androgens added, and then see the already-thinning temple's cells react negatively to androgens.....................................but cells from the back of the head, where the classic bald spot will almost assuredly form if left untreated in 10-15 more years NOT RESPOND negatively to the androgens? Have you seen any experiments that substantiate this?

Reason that I ask is this.............................lets say a guy has baldness genes like his dad and his mother's father, and will proboably start balding in his thirties........................and at age 28 or so, he submits a few hairs to be FUE'd out from the front, top, and back. He's not balding yet, but will..............................would you expect his hairs to react negatively to a weeks long bombardment of DHT in a collagen matirx experiment, or nothing to happen yet?

I suppose that would be a "hair cycle clock" vs. contact inhibition induced change in the cells in vivo that would have to "change" the cells first if your answer is no, correct?




An observation.............Ive thought of another way to test your theory if you can get a friend, someone online, whatever, to try it........ Have a guy who is just starting to lose his hair to try wearing a tight tobaggan or skullcap to bed at night, and use a topical diuretic that is not associated with hairloss treatments during the day. Not something as strong as alum, but an oil of some kind. Take before and after pictures of one year or so of doing this. See if he has better hair or has "held the line". What do you think? Just trying to help. I wish you could get a Doctor to help you test your theory on a willing subject. Youve put alot of hard work in it. Right or wrong, you seem like a nice man and you deserve to know.


Have a nice eve.



Bryan, I was hoping you'd comment on those posted pictures of the two sets of twins who injected testosterone and the effects if you have the time......the ageing in the twin that didnt lose her hair (but it did thin some) of her hair and skin. Its a fascinating pic. Like to hear your take on it.

 

[powersam]

there have been a couple of people who saw new growth after wearing a wig/toupee for ages. at the time i thought it would be because of the repeated shaving of the head, good for scalp skin. but it could be the pressure of the wig itself i guess

 

[S Foote.]

Stephen,

I have a little question for you. In experiments, when dermal papilla cells are cultivated with keratinocyte, root sheath cells, etc., androgens are added and cells from areas of the head that are thinning already slow their cell division. Scientists conclude that the KC and ORS cells are responding directly to the androgens.
You propose, that as in the lung tissue youve cited, that the cells that slow division have "flipped" their response to slow growth from dermal papilla released antigens. So the "squeeze" as it were, changes the Dermal papillas response according to you.

Yes thats the reasoning, simply because of the "actual" observations in the in-vitro tests.

You see Bryan is trying to claim that androgens are "directly causing" male pattern baldness. But the in-vitro tests prove otherwise. Androgens do not directly change pre-male pattern baldness follicles to become male pattern baldness follicles. How follicle cells "directly" respond to androgens "AFTER" the change, is meaningless to the question of "change"

Now that thats out of the way, would you propose that in a man who has submitted some hair cells from the front temples that are thinning and the vertex bald spot area THAT IS NOT THINNING YET might have his hair cells cultivated in a collagen matrix, have androgens added, and then see the already-thinning temple's cells react negatively to androgens.....................................but cells from the back of the head, where the classic bald spot will almost assuredly form if left untreated in 10-15 more years NOT RESPOND negatively to the androgens? Have you seen any experiments that substantiate this?

Yes.

One study that is relevant here is one that Bryan has posted a few times. Can't find a link straight away, but this took samples from the balding area of follicles that were still growing normal hair.

Again direct exposure to androgens of these samples in-vitro did "not" change them. They did not change into male pattern baldness samples when "soaked" in androgens. But we know that in the future in-vivo, they "are" going to become male pattern baldness follicles.

This is a consistent observation in-vitro. Androgens do not directly change the existing growth characteristics of follicles from "ANY" area of the body.

The only scientific conclusion has to be that the "change" is an in-direct effect of androgens in-vivo.

Reason that I ask is this.............................lets say a guy has baldness genes like his dad and his mother's father, and will proboably start balding in his thirties........................and at age 28 or so, he submits a few hairs to be FUE'd out from the front, top, and back. He's not balding yet, but will..............................would you expect his hairs to react negatively to a weeks long bombardment of DHT in a collagen matirx experiment, or nothing to happen yet?

I suppose that would be a "hair cycle clock" vs. contact inhibition induced change in the cells in vivo that would have to "change" the cells first if your answer is no, correct?

Yes, consider this.

The most consistent response to rising levels of androgens at puberty is increased body hair. There is more of a "direct" link time wise to the level of DHT and body hair developement in people. On the other hand male pattern baldness has no such consitency. male pattern baldness on average in most people starts around the late 20's. In some it can start in the teens, in others the 40's or even 50's.

My theory explains this as follows.

The "nature" of DHT is to increase hair growth in general by reducing the pressure around follicles. In some people the fluid dynamics can cause the opposite effect of increasing pressure in the male pattern baldness area. But being an opposite effect, this can vary a lot in the period of developement in individuals depending on other factors.

The pressure "release" around body vellous follicles as DHT levels rise at puberty, allows these to enlarge more immediately. On the other hand, the pressure increase in the male pattern baldness area, "when it happens in the individual", will not effect follicles already fully grown. It is only after the normal hair cycle shrinks these in the resting phase, and they then try to enlarge in anagen again, that contact inibition "pressure" will stop them enlarging.

The anagen period can last up to 12 years in terminal scalp hair. Also the follicles are not syncronised, so over time you get thinning with eventual baldness. You "will" get odd follicles surviving longer in the male pattern baldness area for this reason.

You don't need any "magic" genetic clocks in follicles to explain what is seen in DHT related hair growth/loss.

An observation.............Ive thought of another way to test your theory if you can get a friend, someone online, whatever, to try it........ Have a guy who is just starting to lose his hair to try wearing a tight tobaggan or skullcap to bed at night, and use a topical diuretic that is not associated with hairloss treatments during the day. Not something as strong as alum, but an oil of some kind. Take before and after pictures of one year or so of doing this. See if he has better hair or has "held the line". What do you think? Just trying to help. I wish you could get a Doctor to help you test your theory on a willing subject. Youve put alot of hard work in it. Right or wrong, you seem like a nice man and you deserve to know.


Have a nice eve.

Tight caps or whatever are not really going to be the best way to test my theory. You would also restrict the natural drainage! Consitency would be another problem.

In the male pattern baldness area, surgicaly reducing the blood feed would be one way to test the theory, and this has already been shown to markedly improve follicles.

Ask Bryan :wink:

S Foote.

 

[Bryan]

Yes, consider this.

The most consistent response to rising levels of androgens at puberty is increased body hair. There is more of a "direct" link time wise to the level of DHT and body hair developement in people...

My theory explains this as follows.

The "nature" of DHT is to increase hair growth in general by reducing the pressure around follicles....The pressure "release" around body vellous follicles as DHT levels rise at puberty, allows these to enlarge more immediately.

No matter how hard you try to evade my questions, I'm not going to let you do it, so you might as well bite the bullet and face them. I ask you again: how does your eccentric theory explain the fact that both scalp hair AND body hair show the same responses to androgens in vitro that they do in vivo? You claim that it's actually contact inhibition that causes the damage to scalp hair (although you haven't provided any plausible explanation for why it also happens in vitro), but why would BODY HAIR (beard hair, just as an example) be stimulated in vitro by androgens, and suppressed by antiandrogens? Once beard hair gets growing after puberty and during all the decades of an adult male's life afterwards, it certainly isn't being affected by contact inhibition, nor is there any other process I can think of which could be presumed to be an "indirect" effect of androgens; and it even works the same way in vitro, too. So how do you explain that, Stephen? :wink:

Bryan

 

[S Foote.]

Yes, consider this.

The most consistent response to rising levels of androgens at puberty is increased body hair. There is more of a "direct" link time wise to the level of DHT and body hair developement in people...

My theory explains this as follows.

The "nature" of DHT is to increase hair growth in general by reducing the pressure around follicles....The pressure "release" around body vellous follicles as DHT levels rise at puberty, allows these to enlarge more immediately.

No matter how hard you try to evade my questions, I'm not going to let you do it, so you might as well bite the bullet and face them. I ask you again: how does your eccentric theory explain the fact that both scalp hair AND body hair show the same responses to androgens in vitro that they do in vivo? You claim that it's actually contact inhibition that causes the damage to scalp hair (although you haven't provided any plausible explanation for why it also happens in vitro), but why would BODY HAIR (beard hair, just as an example) be stimulated in vitro by androgens, and suppressed by antiandrogens? Once beard hair gets growing after puberty and during all the decades of an adult male's life afterwards, it certainly isn't being affected by contact inhibition, nor is there any other process I can think of which could be presumed to be an "indirect" effect of androgens; and it even works the same way in vitro, too. So how do you explain that, Stephen? :wink:

Bryan

OK Bryan whilst everyone now knows you can't justify your statement about Ockhams razor, i will still respond here.

First you say above:

"No matter how hard you try to evade my questions, I'm not going to let you do it, so you might as well bite the bullet and face them. I ask you again: how does your eccentric theory explain the fact that both scalp hair AND body hair show the same responses to androgens in vitro that they do in vivo?

But they don't do they Bryan, you haven't been listening!

In-vivo androgens "CHANGE" the growth characteristics of hair follicles, in-vitro, they don't do this!

You tell me how you can possibly justify your belief that androgens are directly changing follicle growth, when this just doesn't happen in-vitro?

You say:

" but why would BODY HAIR (beard hair, just as an example) be stimulated in vitro by androgens, and suppressed by antiandrogens?"

In my opinion, this has to be related to the artificial seeding of the tested culture with androgen receptors.

http://www.fasebj.org/cgi/content/full/16/14/1967

Without this androgens have no direct effects "AT ALL" in-vitro. I could argue that this refutes your argument altogether Bryan, but i wont because it's not scientific. :wink:

Let me be clear on my position on the in-vitro tests Bryan.

I am of the opinion that the in-vitro methodology involved rules out any accurate reflection of what happens in the real world of "in-vivo".

In fact i think the only useful thing this testing tells us, is that androgens do not change the pre-existing growth characteristics, whatever they are.

If the culturing of the cells is in itself changing the cell characteristics, how is this then a true test?

If the genetic expression of androgen receptors changes when the cells are cultured, what other genetic expressions are also being changed??

How can the subsiquent behavior of these cells in-vitro then truly reflect the in-vivo response, it just can't. Especially when the test involves artificialy increasing androgen receptors "then" testing the response of androgens!

You say:

"Once beard hair gets growing after puberty and during all the decades of an adult male's life afterwards, it certainly isn't being affected by contact inhibition"

But of course contact inhibition effects beard follicles, as it effects all "normal" cell growth in-vivo. You really should research normal multi-cellular physiology Bryan :roll:

For example, if the beard follicle cell growth you refer to in-vitro, had been allowed to reach the edges of the test dish, it would have stopped Bryan! Why, because of normal contact inhibition.

http://users.rcn.com/jkimball.ma.ultran ... lture.html

Anything that would promote hair follicle enlargement in-vivo "OR" in-vitro, is only going to do so until contact inhibition stops this cell growth.

This is the central point, in-vivo when it comes to cell growth, contact inhibition is "overulling".

Now don't try to say i have not answered your questions Bryan :wink:

S Foote.

 

[Bryan]

In-vivo androgens "CHANGE" the growth characteristics of hair follicles, in-vitro, they don't do this!

You DENY the findings of all those in vitro studies I know you've seen, including the one you cite yourself below??

You tell me how you can possibly justify your belief that androgens are directly changing follicle growth, when this just doesn't happen in-vitro?

I hope you realize you're on unbelievably shaky ground, if all you can do is deny the results of all those scientific studies.

You say:

" but why would BODY HAIR (beard hair, just as an example) be stimulated in vitro by androgens, and suppressed by antiandrogens?"

In my opinion, this has to be related to the artificial seeding of the tested culture with androgen receptors.

http://www.fasebj.org/cgi/content/full/16/14/1967

Without this androgens have no direct effects "AT ALL" in-vitro. I could argue that this refutes your argument altogether Bryan, but i wont because it's not scientific. :wink:

But the researchers themselves clearly explained that it was due to the natural loss of androgen receptors during cultivation of those cells:

"We then assumed that in vitro cultivation of DPCs might alter the expression level of androgen receptor (AR). Semiquantitative RT-PCR showed that AR mRNA in DPCs from Androgenetic Alopecia was decreased during subcultivation from the third to ninth passage."

Is the best you can do to try to refute the OVERWHELMING evidence against your theory is try to take advantage of one little peculiarity having to do with cultured cells, and trumpet that up all out of proportion? Weak, Stephen...VERY weak...

Let me be clear on my position on the in-vitro tests Bryan.

I am of the opinion that the in-vitro methodology involved rules out any accurate reflection of what happens in the real world of "in-vivo".

In fact i think the only useful thing this testing tells us, is that androgens do not change the pre-existing growth characteristics, whatever they are.

If the culturing of the cells is in itself changing the cell characteristics, how is this then a true test?

Yeah, that's all you can do: try to take advantage of an insignificant little loophole by pointing out that androgen receptors tend to decline during culture. Very very weak. Shows your desperation.

If the genetic expression of androgen receptors changes when the cells are cultured, what other genetic expressions are also being changed??

We also know that the expression of 5a-reductase type 2 declines during culture, too. There was a Japanese study a while back about that. So you can add that to your little bag of tricks and holler: "SEE! SEE! The in vitro studies don't count because a couple of factors get altered, so my theory is safe from refutation!"

It's amusing to me to wonder what your reaction would be if it were the opposite case: suppose that androgen receptors and 5a-reductase INCREASE during culture, instead of DECREASE. You'd holler and scream, "See, THAT is why androgens affect hair follicles in culture!" You'd be whistling a different tune, in that case! :wink:

How can the subsiquent behavior of these cells in-vitro then truly reflect the in-vivo response, it just can't. Especially when the test involves artificialy increasing androgen receptors "then" testing the response of androgens!

You're pathetic, Stephen. And desperate. If androgen receptors disappear during culture, then OBVIOUSLY androgens can't have an effect on those cells. So they merely take the step of putting them back in, the way they were before. Big whoopee. If that's all you can say in defense of your theory, it's very very sad...

You say:

"Once beard hair gets growing after puberty and during all the decades of an adult male's life afterwards, it certainly isn't being affected by contact inhibition"

But of course contact inhibition effects beard follicles, as it effects all "normal" cell growth in-vivo. You really should research normal multi-cellular physiology Bryan :roll:

For example, if the beard follicle cell growth you refer to in-vitro, had been allowed to reach the edges of the test dish, it would have stopped Bryan! Why, because of normal contact inhibition.

I think you know what I meant. I'm not going to draw you a picture.

Now don't try to say i have not answered your questions Bryan :wink:

You haven't. I think it's only served to demonstrate your desperation more clearly to everyone here.

Bryan

 

[S Foote.]

Bryan.

You have clearly lost the plot here, as you always finally do in these debates.

Your desperation to try to put me down personaly, at the expense of any true science, should now be blatantly obvious to all.

The facts of the matter are not going to be changed by your desperation to cling on to some fantasy you have about your scientific expertise.

I have better things to do than try to contantly argue real science with a desperate internet attention seeker. I have a life :roll:

Good luck everone, i'm outa here.

S Foote.

 

[Bryan]

BTW, I'm going to post an excerpt from yet another very interesting study (and by Sawaya, too!) that clearly demonstrates a DIRECT effect of androgens and antiandrogens on human hair follicles grown in culture; what's interesting about this one is that they didn't even find it necessary to transfect extra androgen receptors into the hair follicles, thus completely negating and making moot Stephen Foote's silly objection to that other study he cited! :wink: This would be: "RU58841, a new therapeutic agent affecting androgen receptor molecular interactions in human hair follicles", M.E. Sawaya, from the book "Hair Research for the Next Millenium", 1996. I'm going to skip some of the less important stuff at the beginning, and get right to the meat of this issue:


---------------------------------------------------------------------------
[...]

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.
-----------------------------------------------------------------------------

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! :wink:

Bryan

 

[michael barry]

Interesting stuff,


Im still putting revivogen on my right wrist. Its hair growth in notiecably thinner and less pigmented than my left. I aim to start a similar little experiment with spironolactone soon.


I think the pictures of the twins prove that testosterone, however it does it, ages the skin and hair tremendously in people. It may be wonderful for one's musculature, but its miserable on one's dermal tissues.

 

[Old Baldy]

BTW, I'm going to post an excerpt from yet another very interesting study (and by Sawaya, too!) that clearly demonstrates a DIRECT effect of androgens and antiandrogens on human hair follicles grown in culture; what's interesting about this one is that they didn't even find it necessary to transfect extra androgen receptors into the hair follicles, thus completely negating and making moot Stephen Foote's silly objection to that other study he cited! :wink: This would be: "RU58841, a new therapeutic agent affecting androgen receptor molecular interactions in human hair follicles", M.E. Sawaya, from the book "Hair Research for the Next Millenium", 1996. I'm going to skip some of the less important stuff at the beginning, and get right to the meat of this issue:


---------------------------------------------------------------------------
[...]

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.
-----------------------------------------------------------------------------

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! :wink:

Bryan

Stephen: When I read that study a while back, it became apparent to me that androgens trigger the onset of male pattern baldness. (Well it "drove it home" if you know what I mean.)

Now what gene(s) cause the follicle to respond that way to androgens? I have found very little info. on that question. I found theories but no concrete studies, etc.

Research is going in that direction from what I've read but the genetic "mapping" ain't done yet. It may be eccentric for me to say that's where we're going to finally find the "cure" but - well - that's what I think. :?

Have you read anything showing there's a gene(s) that is/are responsible for your contact inhibition theory?

I guess what you're saying, in part, is contact inhibition causes the genetic expression that results in male pattern baldness? Without contact inhibition the genetic expression never occurs?

Well I agree to a point, but I believe the genetic expression occurs when follicles are exposed to androgens. I also agree that blood vessel health is extremely important, just not as important as androgen sensitivity.

One very, very knowledgable doctor says anti-androgens aren't all that effective, but attacking the blood vessel and "skin health" area of male pattern baldness is VERY important. (And his stuff works for me.)

So I'm kind of "torn" on this argument between you and Bryan. I agree with Bryan on the effect of androgens but agree with you on the skin health aspect. Although, I don't think Bryan is even discussing that aspect. He's just discussing what starts the male pattern baldness process. And from all I've read, Bryan seems to be correct.

 

[Bryan]

Stephen: When I read that study a while back, it became apparent to me that androgens trigger the onset of male pattern baldness. (Well it "drove it home" if you know what I mean.)

Hmmm.....you know, I thought maybe I had already posted information about that Sawaya study some time ago, but I really couldn't remember for sure!

Now what gene(s) cause the follicle to respond that way to androgens?

Perhaps a bit better way to ask that question is this: which are the specific androgen-sensitive genes in human hair follicles, and why does there seem to be a different pattern of them in body hair versus scalp hair, or at least a different way that they are expressed in those different kinds of follicles?

One very, very knowledgable doctor says anti-androgens aren't all that effective, but attacking the blood vessel and "skin health" area of male pattern baldness is VERY important. (And his stuff works for me.)

It's not so much that antiandrogens aren't effective, it's that REGROWTH of lost hair is fairly minimal from antiandrogens alone. A truly effective antiandrogen should completely halt further balding, however. So in that one limited sense, they ought to be quite effective. I'm sure that's what Dr. Proctor meant, too.

So I'm kind of "torn" on this argument between you and Bryan. I agree with Bryan on the effect of androgens but agree with you on the skin health aspect. Although, I don't think Bryan is even discussing that aspect. He's just discussing what starts the male pattern baldness process. And from all I've read, Bryan seems to be correct.

To be quite precise, all I've been discussing lately is one very specific issue: whether or not hair follicles respond DIRECTLY to androgens and antiandrogens. Stephen's ludicrous idea that hair follicles aren't affected at all by sex hormones is patently and palpably false. I guess he bailed-out of the discussion at just the right time, since Sawaya's study is absolutely AIR-TIGHT on that one specific issue! :wink:

Bryan

 

[Bryan]

Have you read anything showing there's a gene(s) that is/are responsible for your contact inhibition theory?

I guess whay you're saying, in part, is contact inhibition causes the genetic expression that results in male pattern baldness? Without contact inhibition the genetic expression never occurs?

Well I agree to a point, but I believe the genetic expression occurs when follicles are exposed to androgens.

OB, there is simply no evidence that contact inhibition plays a role in balding at all. None at all. It's just a pet theory of one individual.

Bryan

 

[S Foote.]

Have you read anything showing there's a gene(s) that is/are responsible for your contact inhibition theory?

I guess whay you're saying, in part, is contact inhibition causes the genetic expression that results in male pattern baldness? Without contact inhibition the genetic expression never occurs?

Well I agree to a point, but I believe the genetic expression occurs when follicles are exposed to androgens.

OB, there is simply no evidence that contact inhibition plays a role in balding at all. None at all. It's just a pet theory of one individual.

Bryan

Now your talking about a different issue Bryan. So people should be aware of a "real" hair loss researchers opinion on the matter :wink:

Quote:

"Dear Stephen:
Your note is very interesting. I have been following your work on the hydraulics of tissue (regarding mostly on scalp physiology).
I find your work is brilliant and it must be continued since it may open one of the gates we need for solving the problem.
Our research deals with some of the proposed ideas. We find contact inhibition is a true factor in the dermal model. In respect to HM, and particularly my own method that is called SIT (scalp impregnation therapy) the life expectancy and normal cycling of the follicular complex is of utmost importance. We expect an anagen telogen catagen cycle to be repetitive and self adjusting to the environment while conserving donor dominance. We have so much to do. Keep it up.
Best of luck (and hard work),

Dr. Carl
http://www.itzan.com
(Mexico)"

S Foote.

 

[Bryan]

Never mind what "Dr. Carl" said, address yourself to what Dr. Sawaya said! :wink:

Bryan

 

[S Foote.]

Never mind what "Dr. Carl" said, address yourself to what Dr. Sawaya said! :wink:

Bryan

But iv'e already shown you what Dr Sawaya said about my theory Bryan, here it is again.


"Alot of good points are brought up regarding the hair follicle growth and the fact that anagen is a bit predetermined by the previous hair cycle and the "clock" that is set or how long the matrix cells can grow and divide, making a big, anagen follicle, or a smaller and smaller follicle with each hair cycle. The idea of pressure changes from localized factors is interesting as the problem with male pattern hair loss is the fibrosis/scarring that takes place so that the follicles and surrounding tissues are damaged and cannot regenerate.
Male pattern hair loss is not supposed to be a scarring, cicatricial process, but it is a mixed inflammatory process in that many people do have inflammatory changes but usually in the middle follicle, and not as much in the lower follicle, as in alopecia areata.

Overall, these are interesting arguments to stimulate anagen follicles, keeping in mind that there are many substages of anagen, each similar to the cell cycle in carrying out a specific function for a certain period of time.
Many researchers are working on similar concepts with use of growth factors to see if there is any certain one or mix of them that can effect the process.

It is a very complex process, but your thoughts are very organized and on the right path, similar to what others have been proposing, and in some ways yours are more straightforward. I think you've done a good job in thinking this through......
Hope this helps...
regards
Marty Sawaya"

As far as this (once "again" pointless to the issue) in-vitro study of Sawaya's goes, where does it say that existing follicle growth characteristics are directly "converted" by androgens?

I'll put this in the most simple way possible just one last time.

OK, lets go along with androgens directly effecting the various growth rates of follicles in-vitro, in a way that mirrors the in-vivo effect.

But the "same" studies also clearly show that androgens are not directly changing the growth rates in-vitro, as we know happens "somehow" in-vivo.

So what is "enabling" this change Bryan?

You have claimed that androgens themselves are directly changing the follicle response, so describe the mechanism of this with some "genuine" evidence for it?

S Foote.

 

[Bryan]

As far as this (once "again" pointless to the issue) in-vitro study of Sawaya's goes, where does it say that existing follicle growth characteristics are directly "converted" by androgens?

You'll have to be a bit more specific. What do you mean by the word "converted" here? What _I_ am talking about is the fact that androgens STIMULATE the growth of beard hair follicles, but SUPPRESS the growth of scalp hair follicles. What's your reply to those clear and unambiguous experimental findings from Sawaya?

I'll put this in the most simple way possible just one last time.

OK, lets go along with androgens directly effecting the various growth rates of follicles in-vitro, in a way that mirrors the in-vivo effect.

But the "same" studies also clearly show that androgens are not directly changing the growth rates in-vitro, as we know happens "somehow" in-vivo.

So what is "enabling" this change Bryan?

You mean, why did the pre-pubertal hair follicles in that one stumptailed macaque study appear to be insensitive to androgens? I really don't know for sure. Future research will probably eventually explain that. At least, I hope it will.

You have claimed that androgens themselves are directly changing the follicle response, so describe the mechanism of this with some "genuine" evidence for it?

Like I've said several times before, I don't for sure what causes that change (assuming that the same thing even happens at all in humans). I've just speculated about it.

Ok, so getting back to the subject at hand: how do you reply to Sawaya's air-tight evidence showing a DIRECT effect of androgens (and antiandrogens) on both body hair and scalp hair?? :wink:

Bryan

 

[S Foote.]

As far as this (once "again" pointless to the issue) in-vitro study of Sawaya's goes, where does it say that existing follicle growth characteristics are directly "converted" by androgens?

You'll have to be a bit more specific. What do you mean by the word "converted" here? What _I_ am talking about is the fact that androgens STIMULATE the growth of beard hair follicles, but SUPPRESS the growth of scalp hair follicles. What's your reply to those clear and unambiguous experimental findings from Sawaya?

[quote="S Foote.":ef85c]I'll put this in the most simple way possible just one last time.

OK, lets go along with androgens directly effecting the various growth rates of follicles in-vitro, in a way that mirrors the in-vivo effect.

But the "same" studies also clearly show that androgens are not directly changing the growth rates in-vitro, as we know happens "somehow" in-vivo.

So what is "enabling" this change Bryan?

You mean, why did the pre-pubertal hair follicles in that one stumptailed macaque study appear to be insensitive to androgens? I really don't know for sure. Future research will probably eventually explain that. At least, I hope it will.[/quote:ef85c]

But the "non conversion" of one type of follicle growth, to another "directly" by androgens, is not limited to that "one" macaque study as you know.

You have quoted another even more relevant to "human" male pattern baldness study yourself!

This is the one where in thinning male pattern baldness areas, those follicles that are going to bald but are still in full anagen, are not directly "changed" into male pattern baldness mode by in-vitro saturation with androgens.

If you are still tring to claim "any" of the in-vitro studies show that androgens "flip" the growth of any kind of follicle sample, then post these??

Otherwise you are just "assuming" this Bryan!

You have claimed that androgens themselves are directly changing the follicle response, so describe the mechanism of this with some "genuine" evidence for it?

Like I've said several times before, I don't for sure what causes that change (assuming that the same thing even happens at all in humans). I've just speculated about it.

But your whole theory relies upon androgens "directly" changing the way follicles respond "to" androgens Bryan!

Ok, so getting back to the subject at hand: how do you reply to Sawaya's air-tight evidence showing a DIRECT effect of androgens (and antiandrogens) on both body hair and scalp hair?? :wink:

Bryan

So if say tomato sauce also had the same growth effect on follicles in Sawaya's in-vitro experiment, you would say that tomato sauce "caused" male pattern baldness right Bryan?

I will answer your question, after you first qualify it as valid to the point Bryan :wink:

To do this, you must provide me with "hard" evidence that androgens are directly changing follicle growth rates in-vitro.

Any example will do, vellous body hair to pubic/armpit hair. Or terminal scalp to vellous male pattern baldness.

Just anything to put your question in a true scientific context.

S Foote.

 

[Old Baldy]

Stephen wrote:

But your whole theory relies upon androgens "directly" changing the way follicles respond "to" androgens Bryan

I can't speak for Bryan but he appears to be saying that androgens change the way follicles carry on their life cycle.

I've read studies at Pubmed that seem to indicate growth factors change when follicles are exposed to androgens.