Question for Stephen Foote, with pictures for a point

[Bryan]

Bryan, what the hell are you talking about????

You clearly tried to claim that "because" DHT is produced in follicles, it "MUST" be having a direct effect on them!! Here it is "YET" again :roll: :roll: :roll:

"Now answer the question that I asked you: if androgens don't directly affect hair follicles, then why do they upregulate their own androgen receptors when you reduce their supply of DHT? The way that cells respond to androgens in the first place is THROUGH the presence of androgen receptors. There clearly is a feedback loop here which is trying to maintain AN ANDROGENIC EFFECT in the hair follicle cells themselves,"

Yes. And you continue to ignore that question above.

What the hell has this claim got to do with that sweating study???

Nothing, directly. But you wanted me to speculate about why even follicles that aren't sensitive to DHT apparently still produce it. Citing the evolutionary reasons for balding was my response to that.

The proposed evolutionary "reason" given by Professor Cabanac in that sweating study for the observations, was pure conjecture!

Yes. And it seems as reasonable a conjecture for the cause of male pattern baldness as any other I've seen.

Speculation for the "reason" for something in evolution, is "completely different to understanding the physical mechanisms in the evolved process for God's sake!

Of course. You asked me to speculate about the evolutionary reasons for male pattern baldness. And I think the one in the "Sweating" paper is about as reasonable as any other I've seen.

You are trying to claim the "VERY" fact that DHT is produced in follicles, "PROVES" the "MECHANISM" of action of DHT upon hair follicles!!

No, let's be very precise here: the upregualtion of androgen receptors with finasteride usage is ANOTHER POWERFUL PIECE OF EVIDENCE DISPROVING YOUR OFTEN-REPEATED CLAIM THAT ANDROGENS HAVE NO DIRECT EFFECT AT ALL ON HAIR FOLLICLES. At the very least, it shows that finasteride DOES have at least that one specific effect on them (the upregulation of androgen receptors). Other powerful evidence (like Sawaya's in vitro test of beard and scalp follicles) goes even farther, and shows that androgens affect their actual GROWTH in a differential way that's right in line with the standard theory of balding.

And what's funny is that in the latter study, you used the excuse that it was only in vitro, so we couldn't use that as proof of what happens in vivo. But now with the finasteride/androgen receptor study, that WAS in vivo, so your little excuse goes bye-bye!

But your contention is clearly thrown out by the "MECHANISTIC" fact that DHT is also produced in follicles that show absolutely "NO" growth change to the presence of DHT produced in those follicles!

And I've clearly explained to YOU a quite plausible evolutionary theory for why scalp follicles developed a different kind of RESPONSE to androgens than body hair follicles.

So tell us all the evolutionary advantage of the development of "direct" androgen induced male pattern baldness???

It's explained in the "Beards, Balding, and Sweat Secretion" paper, as I've already told you several times.

I don't think many people would agree this was an evolutionary advantage for God's sake :roll:

ROTFLMAO!! YOU are the one who has already cited that paper YOURSELF in the past in some effort to support your theory! I only found out about it from YOU!!

I have to say Bryan, if you are really sincere in your last post, you are clearly an idiot.

We have a saying in England, that trying to enlighten an idiot is a waste of both your time, and the idiots!

Further support for your idiot status, comes from your continued refusal to back up your arogant post on Einsteins principle, by comforming to it yourself 8)

Let the record show that I've hit such a nerve with this most recent evidence about androgen receptors, all you can do in reply is call me an "idiot". I think that speaks volumes. "The lady doth protest too much, methinks." Shakespeare, Hamlet

Bryan

 

[S Foote.]

Bryan, what the hell are you talking about????

You clearly tried to claim that "because" DHT is produced in follicles, it "MUST" be having a direct effect on them!! Here it is "YET" again :roll: :roll: :roll:

"Now answer the question that I asked you: if androgens don't directly affect hair follicles, then why do they upregulate their own androgen receptors when you reduce their supply of DHT? The way that cells respond to androgens in the first place is THROUGH the presence of androgen receptors. There clearly is a feedback loop here which is trying to maintain AN ANDROGENIC EFFECT in the hair follicle cells themselves,"

Yes. And you continue to ignore that question above.

[quote="S Foote.":39886]What the hell has this claim got to do with that sweating study???

Nothing, directly. But you wanted me to speculate about why even follicles that aren't sensitive to DHT apparently still produce it. Citing the evolutionary reasons for balding was my response to that.

The proposed evolutionary "reason" given by Professor Cabanac in that sweating study for the observations, was pure conjecture!

Yes. And it seems as reasonable a conjecture for the cause of male pattern baldness as any other I've seen.

Speculation for the "reason" for something in evolution, is "completely different to understanding the physical mechanisms in the evolved process for God's sake!

Of course. You asked me to speculate about the evolutionary reasons for male pattern baldness. And I think the one in the "Sweating" paper is about as reasonable as any other I've seen.

You are trying to claim the "VERY" fact that DHT is produced in follicles, "PROVES" the "MECHANISM" of action of DHT upon hair follicles!!

No, let's be very precise here: the upregualtion of androgen receptors with finasteride usage is ANOTHER POWERFUL PIECE OF EVIDENCE DISPROVING YOUR OFTEN-REPEATED CLAIM THAT ANDROGENS HAVE NO DIRECT EFFECT AT ALL ON HAIR FOLLICLES. At the very least, it shows that finasteride DOES have at least that one specific effect on them (the upregulation of androgen receptors). Other powerful evidence (like Sawaya's in vitro test of beard and scalp follicles) goes even farther, and shows that androgens affect their actual GROWTH in a differential way that's right in line with the standard theory of balding.

And what's funny is that in the latter study, you used the excuse that it was only in vitro, so we couldn't use that as proof of what happens in vivo. But now with the finasteride/androgen receptor study, that WAS in vivo, so your little excuse goes bye-bye! [/quote:39886]

Now you are trying to skirt around your original claim Bryan, but i'am afraid this is a matter of record :wink:

You claimed that because a process of androgen activity happens in follicle cells, that this proves a "designed" intent for a direct effect on follicle growth.

I showed that this is just plain wrong, simply because of the same androgen activity in follicles that don't respond to them!

Now you are trying to place "add on" factors to your original arguments, but it wont wash Bryan :wink:

Let's be very clear.

Your claim above that i deny direct effects of androgens is not true, just read my posts. What i am saying is the "direct" effects seen on "already" growth changed follicles in-vitro, is misleading and not relevant to the in-vivo mechanism of male pattern baldness.

Now you can make all the claims in the world about your so called evidence for the current theory, but if this was true you would have seen the same results in that mouse study!

That was a major upset for the current theory, as the authors made clear, and "YOU" accepted at the time :roll:

But your contention is clearly thrown out by the "MECHANISTIC" fact that DHT is also produced in follicles that show absolutely "NO" growth change to the presence of DHT produced in those follicles!

And I've clearly explained to YOU a quite plausible evolutionary theory for why scalp follicles developed a different kind of RESPONSE to androgens than body hair follicles.

[quote="S Foote.":39886]So tell us all the evolutionary advantage of the development of "direct" androgen induced male pattern baldness???

It's explained in the "Beards, Balding, and Sweat Secretion" paper, as I've already told you several times.

I don't think many people would agree this was an evolutionary advantage for God's sake :roll:

ROTFLMAO!! YOU are the one who has already cited that paper YOURSELF in the past in some effort to support your theory! I only found out about it from YOU!! [/quote:39886]

You miss the scientific point as usual Bryan!

I have the full paper on that sweating study, professor Cabanac wrote to me about it after my first paper was published.

It does show links with the body's thermoregulatory systems, and hair growth, as you would expect considering hair evolved in this capacity.

But for you to then try to claim that this proves a "direct" effect of androgens on "differently" programed follicles, just shows your ignorence Bryan!

That study reports proven facts, but does "NOT" make any claims at all for the mechanisms involved! The facts reported, cannot in any way be made to support the mechanism of action you claim Bryan, in any true scientific way!

It does support the mechanism of action i propose through scientific principles, as i have made clear before.

The other big problem the current theory has, is that it claims androgens are directly changing the growth of follicles from one state to another. For example, normal terminal scalp follicles into male pattern baldness follicles.

But "EVERY" in-vitro study you quote in support of the current theory, clearly shows direct contact with androgens does "NOT" do this!!

Again Bryan, you can make all the claims in the world, but this one basic fact screws the current theory, just as that mouse study screws the donor dominance aspect.

I note you are still dodging my request for your explaination for those three male pattern baldness observations.

You have mine, and my explaination conforms to the principle you claim to support! So let's hear yours Bryan 8)

S Foote.

PS,

Over the weekend i will post my explaination for the results of that important mouse study. It's clear by now that you don't have any explainations :wink:

 

[Bryan]

Now you are trying to skirt around your original claim Bryan, but i'am afraid this is a matter of record :wink:

You claimed that because a process of androgen activity happens in follicle cells, that this proves a "designed" intent for a direct effect on follicle growth.

I showed that this is just plain wrong, simply because of the same androgen activity in follicles that don't respond to them!

Go back and re-read my post above, until you can understand what I'm saying.

Sawaya's in vivo finasteride/androgen receptor study proves that androgens have SOME direct effect on hair follicles. Sawaya's in vitro beard/scalp study shows not only that androgens have a direct effect on hair follicles, but also that the effect on scalp follicles is a negative one. The two studies together provide powerful refutation of your claim that androgens have no direct effect whatsoever.

Let's be very clear.

Your claim above that i deny direct effects of androgens is not true, just read my posts. What i am saying is the "direct" effects seen on "already" growth changed follicles in-vitro, is misleading and not relevant to the in-vivo mechanism of male pattern baldness.

So you finally admit that androgens DO have a direct effect on hair follicles, but you doubt that it has anything to do with balding. Ok, you're making a little progress, at least! :wink:

You miss the scientific point as usual Bryan!

I have the full paper on that sweating study, professor Cabanac wrote to me about it after my first paper was published.

It does show links with the body's thermoregulatory systems, and hair growth, as you would expect considering hair evolved in this capacity.

But for you to then try to claim that this proves a "direct" effect of androgens on "differently" programed follicles, just shows your ignorence Bryan!

But I DON'T make any such claim! Stephen, listen to me: I'm getting tired of repeating the same things to you OVER AND OVER AND OVER AND OVER!! You don't listen to what I'm saying, Stephen! How many times in the last couple of posts have I REPEATEDLY told you that I cited the "Sweating" paper to provide a plausible explanation for the evolution of balding in human beings?? I never EVER hinted or suggested that the "Balding" paper proved anything at all about the specific role of androgens. Why do I have to keep repeating myself to you like I have to do with a child??

The other big problem the current theory has, is that it claims androgens are directly changing the growth of follicles from one state to another. For example, normal terminal scalp follicles into male pattern baldness follicles.

But "EVERY" in-vitro study you quote in support of the current theory, clearly shows direct contact with androgens does "NOT" do this!!

OH REALLY? Then explain to all of us how Sawaya's beard/scalp study "clearly shows" what you just said! :wink: I think what Old Baldy said recently about that study is shared by almost everybody reading this thread: it's a "slam dunk" for the standard theory of balding.

Bryan

 

[S Foote.]

Now you are trying to skirt around your original claim Bryan, but i'am afraid this is a matter of record :wink:

You claimed that because a process of androgen activity happens in follicle cells, that this proves a "designed" intent for a direct effect on follicle growth.

I showed that this is just plain wrong, simply because of the same androgen activity in follicles that don't respond to them!

Go back and re-read my post above, until you can understand what I'm saying.

I know what you are saying Bryan, and it makes no scientific sense.

You miss the scientific point as usual Bryan!

I have the full paper on that sweating study, professor Cabanac wrote to me about it after my first paper was published.

It does show links with the body's thermoregulatory systems, and hair growth, as you would expect considering hair evolved in this capacity.

But for you to then try to claim that this proves a "direct" effect of androgens on "differently" programed follicles, just shows your ignorence Bryan!

But I DON'T make any such claim! Stephen, listen to me: I'm getting tired of repeating the same things to you OVER AND OVER AND OVER AND OVER!! You don't listen to what I'm saying, Stephen! How many times in the last couple of posts have I REPEATEDLY told you that I cited the "Sweating" paper to provide a plausible explanation for the evolution of balding in human beings?? I never EVER hinted or suggested that the "Balding" paper proved anything at all about the specific role of androgens. Why do I have to keep repeating myself to you like I have to do with a child??

Then just explain the results of that sweating study, as i keep asking you to do, as you "think" it supports "your" claims of the "mechanisms"!!!

The current theory cannot explain the changes seen in that sweating study, in the proper way required by a valid theory.

But you already know this, and thats why you wont answer my questions :wink:

The other big problem the current theory has, is that it claims androgens are directly changing the growth of follicles from one state to another. For example, normal terminal scalp follicles into male pattern baldness follicles.

But "EVERY" in-vitro study you quote in support of the current theory, clearly shows direct contact with androgens does "NOT" do this!!

OH REALLY? Then explain to all of us how Sawaya's beard/scalp study "clearly shows" what you just said! :wink: I think what Old Baldy said recently about that study is shared by almost everybody reading this thread: it's a "slam dunk" for the standard theory of balding.

Bryan

Oh yeah!

So where "exactly" does it say in Sawayas study, that androgens are "CHANGING" the pre-existing follicle growth???

And it is pretty clear to anyone with any sense, that your "standard" theory of balding, got blown away completely by that mouse study.

You should get your head out of the sand Bryan :roll:

S Foote.

 

[S Foote.]

In the mouse study we have talked about, human miniaturised male pattern baldness follicles significantly enlarge when transplanted to immune deficient mice. Full size scalp follicles reduced their size when transplanted to the same mice.

http://www.hairlosshelp.com/forums/mess ... &forumid=1

This is my explaination for these observations.

According to my theory, hair follicle size is controled in-vivo by the natural resistence of the surrounding tissue. Hair follicles are "hollow" pockets, and surrounding dermal cells will naturaly tend to resist the developement of such pockets.

The fluid pressure in the dermis "backs up" the dermal cell resistence, and the higher the fluid pressure, the higher the resistence to follicle enlargement.

As the follicle enlarges the natural resistence increases as a function of the increasing area of the follicle, until the point is reached where the cell to cell resistence stops follicle growth through normal contact inhibition.

So according to my theory, follicle size can only be as large as the resistence of the dermal tissue allows.

I suggest this principle is the only realistic explaination for "BOTH" the enlargement of male pattern baldness follicles, and the shrinkage of the already enlarged follicles transplanted in those mice.

The large follicles are already "too" large for the pressure/area resistence equasion in the mouse dermal tissue. The miniaturised male pattern baldness follicle area still allows enlargement in the same "pressure" conditions.

Put simply, the follicles are self adjusting to the natural dermal resistence, as nature intended.

In conventional transplantation, the healing process forms a fibrose structure around nearby follicles. It is "ONLY" follicles transplanted to the male pattern baldness area, that are very close to the healed edge of the graft, that survive long term.


I suggest the fibrose structure that forms around these follicles, acts like a "mould", and preserves this space for future anagen enlargements. This fibrose "shell" holds back the dermal cells, and acts as an extra cellular matrix for the re-growth of anagen follicles.

The difference in immune deficient mice, is the formation of fibrose tissue is effected by their lack of immunology.

http://www.pnas.org/cgi/content/full/94/20/10663

So there is little or no fibrose shell formed around the transplanted follicles, and these follicle are then free to adjust their size in accordence with the natural dermal resistence.




S Foote.

 

[michael barry]

Bryan and Stephen,

I, nosy as I am, will be conducting a little photographical experiment with various topicals on myself for the next few months.

My plan is to photograph various areas of my body hair and apply topicals to them to see if the anti-androgens depress body hair growth and the stimulants stimulate body hair growth. I did this with revivogen on my right wrists for about 2 and half months a little while back, and was pleased to report that it DEFINITELY reduced hair on that wrist vs. the other one (that I tried Crinagen on to no effect).

Here's the plan: spironolactone left pinky finger twice a day.

Alpecin left wrist

Fluridil right wrist

polygro proanthocyanidins left knee

copper peptides (when folligen arrives) right knee

avocado oil (beta sis) left forearm

blueberry juice right forearm


Since Im going to do all of this, I figured I might as well try an ice pack for a reasonable period of time while online on my right leg (I literally read more political blogs than I watch TV) to see if the Ice has any effect on hair growth...............right thigh. If Stephen has any strong contractory/diuretic substance that he'd like to see tried to attempt to stimulate body hair growth by this means.............I'd be willing to substitute it. But I wouldnt want anything that already has known hair growing properties.

Ive cut out a shape for most of the areas so the application size will be the same. Im going to try and measure out about an equal amount of the various solutions so Im being fair to them. Youve proboably noticed Ive put the stimulants on my legs (If one worked really well, I would not want a very hairy patch on my forearm).

Hopefully, if something works very well, I'll see if hairsite will post the before and after pics. Its not much, but Im a human being and not a lab rat, so perhaps we'll get an idea on how something works in a HUMAN dermal system in this fashion.

 

[Bryan]

Then just explain the results of that sweating study, as i keep asking you to do, as you "think" it supports "your" claims of the "mechanisms"!!!

???

How many more times do I have to tell you that I do NOT think that it supports the "mechanisms"?? Another dozen times? Two dozen times? Three dozen times?

So where "exactly" does it say in Sawayas study, that androgens are "CHANGING" the pre-existing follicle growth???

Right here:

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

 

[michael barry]

Bryan,

Stephen is going to claim that the follicles that Sawaya studied were extracted from men who were already suffering from male pattern baldness. The hairs were extracted from frontal follicles that were already weakened to an extent by androgens, whilst the follicles in the middle of the donor area were not used.

Therefore contact inhibition had "changed" these follicles response to androgenic stimuli. Stephen believes that there is no "hair cycle clock", but that contact inhibiton, proboably through the tgf beta pathway, gets the dermal papilla cells to change their response to androgens.



BRYAN,
My whole purpose in starting this thread was to get Stephen to look at THESE photos http://www.hairsite4.com/dc/dcboard.php ... &mode=full of a mans donor area after six months of finasteride. Even the hairs in the wreath appear "fatter" to me. Its obvious that they are. Every hair on a man's head, who has male pattern baldness, must have #some# response to androgens, they just dont weaken enough to fall all the way out. This picture of Robert Duvall, the great actor, http://images.google.com/imgres?imgurl= ... n%26sa%3DN show that practically all male hair is due to minaturize in time. I seen Duvall on Letterman about a week back, hair buzzed for a movie roll, he has less hair than he does in that pic. Its extremely thin even on the sides.

To me this illustrates a weakness in Steves theory to an extent........eyebrow hair thins (due to tissue fluid pressure?), body hair in old men thins, especially on their arms (due to fluid pressure?). Perhaps the body hair is getting LESS androgenic stimulation as a man gets very old, but eyebrow hair isn't supposedly androgenically stimulated. Its just ageing of the hair follicle, which is pretty much exactly what Dr. Bernard Bertrand and Dr. Olivier LaCharrie, heads of L'Oreal's labs claim. They state fairly straightforwardly that baldness is just a very fast ageing scalp, no doubt sped up by androgens. See the discoloration on Duvall's scalp? Those age spots? He no doubt used to have that "shiny", "pressed" appearance up there where it looks like its under lots of pressure, but its "broken" somehow now and the scalp is thinned out and aged.


Even if Stephen was 100% right by the way and rising pressure on follicles got them to "change" their expression towards androgens at a point in which the sqeeze on them got too much, chances of scientists being able to extract them at just the right point in time before/after that happened for a 2 week culture test with a synthetic male hormone would be practically impossible wouldn't it?


The only easy way to test Stephen Foote's theory would be to extract a small hair on top of a man's head who is pretty much bald, but has peach fuzz left.......................and move it up front and see if it regrew. It would be better to take 5 or 6 of them because weakening hairs in this state is proboably pretty easy.

 

[S Foote.]

Then just explain the results of that sweating study, as i keep asking you to do, as you "think" it supports "your" claims of the "mechanisms"!!!

???

How many more times do I have to tell you that I do NOT think that it supports the "mechanisms"?? Another dozen times? Two dozen times? Three dozen times?

So you finally admit the current theory cannot explain the mechanisms effecting DHT related hair growth/ loss in humans!

Thanks for making that clear Bryan :wink:

So where "exactly" does it say in Sawayas study, that androgens are "CHANGING" the pre-existing follicle growth???

Right here:

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

So the scalp follicles refered to, were healthy terminal follicles then?

Androgens directly converted them to male pattern baldness follicles in-vitro, and then RU converted them back?

Is that the claim you make Bryan???

S Foote.

 

[S Foote.]

Bryan,

Stephen is going to claim that the follicles that Sawaya studied were extracted from men who were already suffering from male pattern baldness. The hairs were extracted from frontal follicles that were already weakened to an extent by androgens, whilst the follicles in the middle of the donor area were not used.

Therefore contact inhibition had "changed" these follicles response to androgenic stimuli. Stephen believes that there is no "hair cycle clock", but that contact inhibiton, proboably through the tgf beta pathway, gets the dermal papilla cells to change their response to androgens.

This is basicaly my opinion, but i think the TGF beta-1 pathway is only a mechanism relevant to the in-vitro tests. Prior contact inhibition of the samples in-vivo, has "primed" the cells to then allow androgens to act via TGF beta-1 in-vitro.

But if this was "truly" relevant in-vivo, the human male pattern baldness follicles transplanted in those mice would have remained miniaturised wouldn't they?

The TGF beta-1 pathway still exists in those follicles, and there were more than enough androgens in those mice to act on this pathway if it "mattered" in-vivo!

The only easy way to test Stephen Foote's theory would be to extract a small hair on top of a man's head who is pretty much bald, but has peach fuzz left.......................and move it up front and see if it regrew. It would be better to take 5 or 6 of them because weakening hairs in this state is proboably pretty easy.

No to test my theory by transplantation, you have to extract follicles that are still terminal from the thinning male pattern baldness area, then plant them back in the same area. They should then not miniaturise as they would have originaly.

I think your topical experiments are a good idea, do you have much beard growth Michael?

S Foote.

 

[S Foote.]

By the way Michael.

I think that the "island's" of hair growth known as eyebrows, significantly support my theory!

With hindsight, it would have been more descriptive to call my theory the "tissue resistence" theory, and quote the "Hydraulic" effect that alters natural resistence.

If you feel the tissue beneath your eyebrows if feels softer than the surrounding tissue. Boxers easily get cuts on the eyebrows because of this.

This "strip" of soft weak tissue, has a lower resistence to anagen follicle enlargement, and this allows the local growth we call eyebrows.

S Foote.

 

[michael barry]

Stephen wrote : " But if this was "truly" relevant in-vivo, the human male pattern baldness follicles transplanted in those mice would have remained miniaturised wouldn't they? "

He wrote that in response to my suggestion that pressure causes follicles to "change" their response to androgens through the tgf beta 1 pathway and become sensitive to them, instead of a "hair cycle clock".

I say that if those mice DID in fact have human levels of androgens, this would appear to be a problem for the current theory, but we cant assertively state this without really their blood measurements of testosterone can we? Thats the big question. Even if they did, they DIDNT enlarge as much as human hair normally does on human skin, neither did the hairs from the non-male pattern baldness areas. That alone suggests the human skin on the mouse's back did have something to do with restricting growth up to a point.


Stephen asked if my beard growth was good. It is, but I just dont want a patch of very hairy beard or little hair growth on my face. My little experimnet with revivogen would have looked funny on my face unless I shaved every single day. Thats why Ive picked a little body hair thats normally covered with clothing. I just want to find out what works, and let the other lads here at HairLossTalk.com know that I had success with it. I hate seeing the young fellas waste their money. Crinagen, for instance, to me is a poor economic investment when Revivogen is available and works much better.

 

[Bryan]

Even if Stephen was 100% right by the way and rising pressure on follicles got them to "change" their expression towards androgens at a point in which the sqeeze on them got too much, chances of scientists being able to extract them at just the right point in time before/after that happened for a 2 week culture test with a synthetic male hormone would be practically impossible wouldn't it?

Michael, I'm not sure I understand your question. What is this "just the right point in time" that you're referring to here? I don't understand what kind of test it is that you're proposing. If you're suggesting some way of directly testing whether or not "pressure" causes hair follicles to become sensitive to androgens, then yeah, I have no idea how you'd really go about proving that in a short period of time in a laboratory.

The only easy way to test Stephen Foote's theory would be to extract a small hair on top of a man's head who is pretty much bald, but has peach fuzz left.......................and move it up front and see if it regrew.

But that's basically just like a test of "donor dominance", which has already been done, most notably by Nordstrom. We know that such hairs continue to go bald.

Bryan

 

[Bryan]

Right here:

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

So the scalp follicles refered to, were healthy terminal follicles then?

I don't know. Why do you ask?

Androgens directly converted them to male pattern baldness follicles in-vitro, and then RU converted them back?

Is that the claim you make Bryan???

Androgens didn't "convert" them into male pattern baldness follicles in the laboratory, I'm sure they were already male pattern baldness follicles. However, I have no idea where they were in the process of balding at the time they were extracted. Were they severely balding, moderately balding, just in the beginning stages of balding, or not even yet showing any signs of balding? I have no idea. Sawaya didn't provide any information about that.

Bryan

 

[Bryan]

The TGF beta-1 pathway still exists in those follicles, and there were more than enough androgens in those mice to act on this pathway if it "mattered" in-vivo!

Uh-huh. I guess you're psychic, Stephen! You KNOW what the level of androgens was in those mice, even though the researchers didn't! :wink:

No to test my theory by transplantation, you have to extract follicles that are still terminal from the thinning male pattern baldness area, then plant them back in the same area. They should then not miniaturise as they would have originaly.

ROTFLMAO!! I'm gonna say just three words to you:

The Nordstrom study.

Bryan

 

[michael barry]

Bryan,

I think I can clarify what I meant with this example:

You take a man who is 25 just starting to lose hair at the temples, but has no back bald spot. Let's say he will start thinning on the crown at 30, and have the classic back bald spot at 35-40 if he lets things proceed natrually.

Now, we test hairs extracted from the crown at 25, before he starts losing hair there. We add androgens to them in experiments. If Stephen is correct, the experimental androgens will not effect the hairs, no matter how much you add to them.


Stephen is postulating that these hairs get squeezed for a while and become male pattern baldness-hairs after they change their expression towards androgens through the tgf beta one pathway. He doesnt believe in a hair cycle clock in the follicle being activated on its own, but a hair cycle clock that is activated by external pressure.


You noted the nordstrom study..................Perhaps Stephen hasn't considered that there is a way for Nordstrom to be right and him to be right. Bald to bald didnt regrow hair...................of course it didnt, according to Uno the follicles' structure are scarred and they are damaged.

The intermediate hairs were proboably becoming sensitive to androgens when extracted. Once hairs become sensitive to the androgens directly, even if you put them on your feet..........they will still host androgens. My suggestion is that if Steve is correct, you'd have to move the hairs before they were really shrinking, because that would be too late.


Its a shame that Nordstrom is all we have in this area, because lets face it, big plug grafts donut anyway. Three big grafts in the seventies-era is pretty lousy surgical work by todays standards. It would be nice to extract a few single follicles, let the fibrose scaffolds form around them in scalp slightly forward of the donor site, and see what happens. That, could conclusively end the discussion on the hydraulic theory in my estimation. Or.....................if you could get a guy with male pattern baldness genetics just starting to thin to wear one of those blue ice helments for a couple of hours a day that they give chemo patients and see if he progressed in a couple of years. Perhaps a very strong topical diuretic/contractory substance that could be topically applied to someone at the first signs of male pattern baldness to be used for a couple of years and see if they "held the line".

These are about the only ways to really test his theory other than getting a primate pre-adolescent and doing the scalp surgery that he suggests to restricts blood flow to the scalp.

Other than such aforementioned tests, or getting a mouse study performed that shoots up the mice with some androgens, I can only see you two going round' and round' on the skim available data trying to disprove Stephen's theory (and thats what one does to a theory to test it, constantly try to disprove it with new info if they cant really test it). It may be frustrating to Stephen, but cloning may be available before he ever gets to test his beliefs anyway (John the Revelator has evidently talked to someone in the know over at hairsite, and is saying that HM is coming, and will suprise us...................he wouldn't betray the confidence though. Ive never known him, a lawyer by profession, to blow smoke up anyone's skirt over there----something really may be up.).

 

[Bryan]

Bryan,

I think I can clarify what I meant with this example:

You take a man who is 25 just starting to lose hair at the temples, but has no back bald spot. Let's say he will start thinning on the crown at 30, and have the classic back bald spot at 35-40 if he lets things proceed natrually.

Now, we test hairs extracted from the crown at 25, before he starts losing hair there. We add androgens to them in experiments. If Stephen is correct, the experimental androgens will not effect the hairs, no matter how much you add to them.

Stephen is postulating that these hairs get squeezed for a while and become male pattern baldness-hairs after they change their expression towards androgens through the tgf beta one pathway. He doesnt believe in a hair cycle clock in the follicle being activated on its own, but a hair cycle clock that is activated by external pressure.

Yes, but suppose we do that test and we find that sure enough, the follicles aren't (yet) affected by androgens. So what do we conclude from that? Answer: there's nothing we CAN conclude, because it proves neither Stephen's peculiar theory, nor the "standard" theory of male pattern baldness (the hair cycle clock, in other words). So what's the point of doing that test in the first place?

BTW, I'll add here that I've been on Stephen's case for a long time to find even ONE example in biology where something external (ANYTHING) was able to alter the cellular response to androgens. He hasn't come up with anything, and I'm sure it's not from lack of effort! :wink: In other words, his idea that the in vitro response of male pattern baldness hair follicles to androgens is a result of "contact inhibition" is just sheer and utter speculation. There is no biological precedent for such an explanation.

You noted the nordstrom study..................Perhaps Stephen hasn't considered that there is a way for Nordstrom to be right and him to be right. Bald to bald didnt regrow hair...................of course it didnt, according to Uno the follicles' structure are scarred and they are damaged.

The intermediate hairs were proboably becoming sensitive to androgens when extracted. Once hairs become sensitive to the androgens directly, even if you put them on your feet..........they will still host androgens. My suggestion is that if Steve is correct, you'd have to move the hairs before they were really shrinking, because that would be too late.

Yes, but Stephen goes MUCH farther than that: he has claimed recently that the in vitro response to androgens is just an artifact of those experiments, and doesn't really have anything to do with the in vivo phenomenon of balding. So he can't use the continued presence of androgens as an EXCUSE to explain the results of the Nordstrom study!

Furthermore, it's not just that the balding follicles in the Nordstrom study failed to REGROW, it's that they continued to WORSEN, right on schedule! :wink: There's just no way for him to "spin" the results of that study. It clearly and unequivocally refutes his theory.

Bryan

 

[Old Baldy]

Right here:

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

So the scalp follicles refered to, were healthy terminal follicles then?

I don't know. Why do you ask?

Androgens directly converted them to male pattern baldness follicles in-vitro, and then RU converted them back?

Is that the claim you make Bryan???

Androgens didn't "convert" them into male pattern baldness follicles in the laboratory, I'm sure they were already male pattern baldness follicles. However, I have no idea where they were in the process of balding at the time they were extracted. Were they severely balding, moderately balding, just in the beginning stages of balding, or not even yet showing any signs of balding? I have no idea. Sawaya didn't provide any information about that.

Bryan

Stephen: Dr. Sawaya was studying the effects of RU58841.

As a professional, she thought the best way to do the testing was to take a scalp follicle and a beard follicle and observe how they reacted to RU58841. (Why in the world would Sawaya take a occipital (sp?) follicle and use that instead of a follicle in the horseshoe area?)

The scalp follicles benefitted while the beard follicles responded badly.

This proves, in my mind, that androgens directly affect the way scalp and beard follicles grow and "survive". Why are you fighting this fact?

It doesn't diminish your scalp health theory as it relates to male pattern baldness.

My idol, Doctor Proctor, says the inflammation part of male pattern baldness may be the most detrimental part of our ailment. From all I've read, and trying his chemicals, he appears to be correct. (You know, inflammation and fibrosis "do the follicle in".)

However, the bottom line from reading the Sawaya study is androgens affect the growth of follicles. Just accept that fact.
The scalp health component ISN'T diminished by accepting that fact. It just shows that there is an androgen component to balding. A direct component btw.

I don't want to be too harsh and say you lose credibility when you nit pick the Sawaya study to somehow show that it doesn't prove anything. But I don't know how else to say it Stephen.

The Sawaya study, in my layman's mind, conclusively shows that androgens directly effect the growth of follicles (i.e., without regard to their condition).

 

[S Foote.]

Right here:

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

So the scalp follicles refered to, were healthy terminal follicles then?

I don't know. Why do you ask?

Androgens directly converted them to male pattern baldness follicles in-vitro, and then RU converted them back?

Is that the claim you make Bryan???

Androgens didn't "convert" them into male pattern baldness follicles in the laboratory, I'm sure they were already male pattern baldness follicles. However, I have no idea where they were in the process of balding at the time they were extracted. Were they severely balding, moderately balding, just in the beginning stages of balding, or not even yet showing any signs of balding? I have no idea. Sawaya didn't provide any information about that.

Bryan

You are well aware of the point i am making Bryan. :wink:

I will go through this again in response to Old Baldy, just to be clear.

The heart of the current theory is that androgens are directly acting upon hair follicles to "change" their growth characteristics. We have all heard people claim that hair follicles are "geneticaly predisposed" to change their growth in different ways when exposed to androgens right?

What i am saying is that the in-vitro tests show this to be just plain wrong!

Direct "soaking" in androgens in-vitro is not changing follicle growth from one state to another, as the current theory tries to claim!

The all important factor we need to know about in the "CAUSE" of male pattern baldness, is how androgens "CHANGE" healthy scalp follicles into male pattern baldness follicles?

Once the follicle growth has been "changed" by some androgen related process in the body, any number of substances could then "support" this growth characteristic in the test tube! This includes androgens!

Without knowing the mechanism of "change", it is a big leap of faith to "assume" that what is seen in-vitro, is what happens in-vivo!

But let's go along with the in-vitro results "truly" reflecting what happens in the real world of in-vivo?

That posted mouse study was the ultimate test of this assumption.

There was no immunology in the test tube, or in those mice to confuse the issue. Despite what Bryan is "now" trying to claim, there was also more than enough androgens to "directly" effect the transplanted human male pattern baldness follicles.

The "real" world confirmation of the claims made by some about the meaning of the in-vitro results, just didn't happen! In fact the results showed just the opposite!!

The lesson is that any claim based on in-vitro results, has to be realised by in-vivo confirmation. In this case the in-vitro test results became meaningless!

S Foote.

 

[Bryan]

The all important factor we need to know about in the "CAUSE" of male pattern baldness, is how androgens "CHANGE" healthy scalp follicles into male pattern baldness follicles?

Yada yada yada.

If all you can do or say in response is to continue your obsession with one specific issue which hasn't yet been scientifically explained, then you can do it all by yourself. Nobody else seems impressed by it.

Bryan