Question for Stephen Foote, with pictures for a point

[Bryan]

Have you EVIDENCE of different genetic in healthy scalp hairs?

All we have is the evidence that scalp follicles and body follicles respond differently to androgens. We don't yet know the exact biochemical reasons WHY they respond differently.

Bryan

 

[powersam]

is it not true that different follicles on the head have different amounts of androgen receptors?


wookie as you can probably see by looking at a mouse and a man, that 1% makes a huge amount of difference. the basics of a mouse and a man are very similar, some small skeletal differences and other little changes here and there add up to a whole different being.

 

[wookster]

is it not true that different follicles on the head have different amounts of androgen receptors?


wookie as you can probably see by looking at a mouse and a man, that 1% makes a huge amount of difference. the basics of a mouse and a man are very similar, some small skeletal differences and other little changes here and there add up to a whole different being.

http://www.dermatologytimes.com/dermato ... p?id=67681

http://www.ehrs.org/conferenceabstracts ... Conrad.htm

:freaked: :freaked: :freaked:

While the Foote "contact inhibition" proposal is very appealing due to its simplicity, it also appears that the genetic machinery within the hair follicle itself is very complex :hairy: :? :hairy:

 

[Bryan]

While the Foote "contact inhibition" proposal is very appealing due to its simplicity, it also appears that the genetic machinery within the hair follicle itself is very complex

It's time once again for my favorite Einstein quote: "Physics should be made as simple as possible, but not simpler." The same goes for biology! :wink:

Bryan

 

[wookster]

wookie as you can probably see by looking at a mouse and a man, that 1% makes a huge amount of difference. the basics of a mouse and a man are very similar, some small skeletal differences and other little changes here and there add up to a whole different being.

http://www.iowagreatapes.org/primates/index.php

How closely are humans related to other primates?

Humans, chimpanzees and bonobos share 98.4 percent of the same DNA sequence
Gorillas share 97.7 percent of their DNA with humans, chimpanzees and bonobos
Orangutans share 96.4 percent of their DNA with humans, chimpanzees, bonobos and gorillas

Some scientists tell us that we are 99% rat, other scientists tell us we are 98% chimp. That would mean that humans are more closely related to rats than apes... :x

Pass me the cheese

 

[S Foote.]

Do you think that they experienced less BEARD growth as a result? How does that jive with the often-reported complaints from minoxidil users of excessive BODY HAIR growth?

Those articles clearly show by proper histological examination, that even "extreme" visual edema, can exist in human dermal tissue, whilst the surface tissue (around follicles) remains uneffected :roll: :roll:

Just read the studies instead of jumping to conclusions 8)

Such a situation is extremely likely with minoxidil, as this is "known" to move fluid to deeper levels! In moving fluid to the deeper levels, minoxidil is reducing pressure around follicles increasing hair growth, simple 8)

Stephen, in my dealings with you over the years, I've often had the occasion to use the term "ad hoc" when discussing your theory. Do you even KNOW what that means? If not, do a Google search on it. You'll see why I use it so often with you! :wink:

Bryan

Dictionary definition of the term "ad hoc", quote:

"An ad hoc hypothesis is one created to explain away facts that seem to refute one’s theory. Ad hoc hypotheses are common in paranormal research and in the work of pseudoscientists."

Take a good look in the mirror Bryan :wink:

The "facts" you are trying to dispute, have been proven in the links i gave you! God, you even first posted the Minoxidil link "YOURSELF" :roll: :roll:

What are you smoking, and where can i get some? 8)

S Foote.

 

[S Foote.]

The upregulation process in follicles and other DHT producing structures, is natures way of trying to maintain DHT production.

OH REALLY?? :lol:

Please explain to us what the upregulation of ANDROGEN RECEPTORS within hair follicle cells (NOT the upregulation of DHT itself) has to do with "maintaining" DHT production!

Bryan

It's all part of the feed back regulation i thought you knew something about Bryan ?

More to the point of the "direct" "indirect" question.

The so called androgen insensitive scalp follicles at the sides and back of the head, also have androgen receptors and produce DHT.

Your theory "MUST" include the evolution of some follicles to respond one way or the other to androgens, and some follicles to not respond at all.

So why do these evolved "non" responsive follicles have the same DHT production "machinery"???

This makes no sense at all in evolutionary terms, if your theory is to be believed. :wink:

The follicles as "factories" for the production of systematic DHT, is the only sensible conclusion.

Tell us all what the "direct" function of DHT is in the liver Bryan?????????? :wink:

S Foote.

 

[S Foote.]

Does the combination of DHT AND [aromatased]estrogen cause baldness, not just DHT alone?

No. Just androgen alone.

Bryan

Errrrrr.......?

Just like androgens did in that mouse study then Bryan :wink:

S Foote.

 

[S Foote.]

While the Foote "contact inhibition" proposal is very appealing due to its simplicity, it also appears that the genetic machinery within the hair follicle itself is very complex

It's time once again for my favorite Einstein quote: "Physics should be made as simple as possible, but not simpler." The same goes for biology! :wink:

Bryan

Bloody hell Bryan, are you actualy begining to learn something about the scientific method! :freaked: :freaked:

If so, your next lesson is this :wink:

Based upon your quotation above, tell us the simplist "possible" way to explain these characteristics in the male pattern baldness scalp?

1/ Follicle miniaturisation.

2/ increased immune sensitivity and fibrosis.

3/ increased sweating capacity.

According to the scientific method, the "ideal" explaination is a change in "one" factor that explains "ALL" the subsequent changes, through recognised biological physics.

Here's my one changing factor, that can explain "ALL" the factors in male pattern baldness., according to Einstein's rules you quote.

DHT increases the tissue fluid pressure in the balding scalp!

I would love to hear the explaination for your idea's, by the "SAME" rules Bryan? :wink:

S Foote.

 

[S Foote.]

:hairy: :x :hairy:

Estrogen and ...water retention? scalp tissue edema?

http://www.ultrapms.com/pms/estrogen.htm

Estrogen also increases the level of the adrenal hormone aldosterone, which prevents the normal excretion of salt from the kidneys, adding to fluid retention. This creates edema-like symptoms of bloating, abdominal swelling, and swollen breasts

I wonder if the hydraulic theory makes any new testable predictions? :wink:

Thank's for posting the links.

I think many hormones have "Hydraulic" effects in-vivo, and this is at least partly why there can be contrary in-vitro results.

This is why in-vivo confermation of in-vitro results is necessary to support the test tube claims.

That mouse study proved this important point.

S Foote.

 

[Bryan]

[quote="S Foote.":788e1]The upregulation process in follicles and other DHT producing structures, is natures way of trying to maintain DHT production.

OH REALLY?? :lol:

Please explain to us what the upregulation of ANDROGEN RECEPTORS within hair follicle cells (NOT the upregulation of DHT itself) has to do with "maintaining" DHT production!

Bryan

It's all part of the feed back regulation i thought you knew something about Bryan ?[/quote:788e1]

NOT SO FAST, Junior! You haven't answered my question. Don't try to slip-slide around a piece of evidence that can't be explained by your theory! :wink:

You're trying to claim that hair follicles don't respond directly to androgens, and that the only reason for them to produce DHT is for it to go into the general circulation and then into the lymphatic system to stimulate drainage (although you've never explained exactly how DHT performs that function).

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, not a production of DHT to go into the general circulation. DHT production is one thing, and androgen receptors are another. So how do you explain that, Stephen? You might as well acknowledge this problem for your theory, because I'm not going to let you evade it! :wink:

More to the point of the "direct" "indirect" question.

The so called androgen insensitive scalp follicles at the sides and back of the head, also have androgen receptors and produce DHT.

Your theory "MUST" include the evolution of some follicles to respond one way or the other to androgens, and some follicles to not respond at all.

So why do these evolved "non" responsive follicles have the same DHT production "machinery"???

This makes no sense at all in evolutionary terms, if your theory is to be believed. :wink:

As I've already told you in the past, I tend to think that the theory presented in that "Beards, Baldness, and Sweat Secretion" study (or whatever the exact title is) is a fairly reasonable one: maybe a genetic sensitivity to androgens slowly evolved in scalp hair follicles to help provide extra cooling to the brain. I think it's about as good a theory as any other I've seen...

Bryan

 

[S Foote.]

[quote="S Foote.":03b10]The upregulation process in follicles and other DHT producing structures, is natures way of trying to maintain DHT production.

OH REALLY?? :lol:

Please explain to us what the upregulation of ANDROGEN RECEPTORS within hair follicle cells (NOT the upregulation of DHT itself) has to do with "maintaining" DHT production!

Bryan

It's all part of the feed back regulation i thought you knew something about Bryan ?

NOT SO FAST, Junior! You haven't answered my question. Don't try to slip-slide around a piece of evidence that can't be explained by your theory! :wink:

You're trying to claim that hair follicles don't respond directly to androgens, and that the only reason for them to produce DHT is for it to go into the general circulation and then into the lymphatic system to stimulate drainage (although you've never explained exactly how DHT performs that function).

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, not a production of DHT to go into the general circulation. DHT production is one thing, and androgen receptors are another. So how do you explain that, Stephen? You might as well acknowledge this problem for your theory, because I'm not going to let you evade it! :wink:

More to the point of the "direct" "indirect" question.

The so called androgen insensitive scalp follicles at the sides and back of the head, also have androgen receptors and produce DHT.

Your theory "MUST" include the evolution of some follicles to respond one way or the other to androgens, and some follicles to not respond at all.

So why do these evolved "non" responsive follicles have the same DHT production "machinery"???

This makes no sense at all in evolutionary terms, if your theory is to be believed. :wink:

As I've already told you in the past, I tend to think that the theory presented in that "Beards, Baldness, and Sweat Secretion" study (or whatever the exact title is) is a fairly reasonable one: maybe a genetic sensitivity to androgens slowly evolved in scalp hair follicles to help provide extra cooling to the brain. I think it's about as good a theory as any other I've seen...

Bryan[/quote:03b10]

Your talking absolute crap now Bryan!!

What the hell has your ramblings above, got to do with the principles of Einstein's principles you originaly posted???????

Just for once, you answer "MY" questions Bryan!

You have the arogance to post a quote from an eminent scientist, as if it provides "YOU" with some kind of personal credibilty!

Then when i ask you to put your own arguments in the context of these same scientific rules, you just chicken out!! :roll: :roll:

The complex feed back loops involved in changes in systematic hormone levels, have nothing "AT ALL" to do with the claims "YOU" are trying to make here!!

The whole basis of your claims is that the conversion of testosterone to DHT takes place in hair follicles, so DHT "must" be having a direct action on hair follicles.

So explain the DHT "resistent" follicles that DHT is produced in???

If you are not prepared to explain the three male pattern baldness observations i posted, in accordence with the scientific principle you posted, and "claim" to agree with, just Butt out!

Put up or shut up Bryan :roll:

S Foote.

 

[Bryan]

Your talking absolute crap now Bryan!!

OH MY...did I hit a little nerve with this last question of mine about androgen receptors?? Don't worry, it's only going to get WORSE for you, Stephen! :wink:

The complex feed back loops involved in changes in systematic hormone levels, have nothing "AT ALL" to do with the claims "YOU" are trying to make here!!

OH REALLY?? Why don't you explain in detail why not, my friend?

The whole basis of your claims is that the conversion of testosterone to DHT takes place in hair follicles, so DHT "must" be having a direct action on hair follicles.

So explain the DHT "resistent" follicles that DHT is produced in???

Can you even READ?? I've already explained to you (more than once) that I find the theory in "Beards, Baldness, and Sweat Secretion" to be a fairly credible one to explain the evolution of male pattern baldness.

If you are not prepared to explain the three male pattern baldness observations i posted, in accordence with the scientific principle you posted, and "claim" to agree with, just Butt out!

Which "3 male pattern baldness observations" are you referring to?

ANSWER THE QUESTIONS THAT I POSED TO YOU. This issue about the androgen receptors isn't going away, Stephen, no matter how uncomfortable it makes you! It's time to face the music! :wink:

Bryan

 

[michael barry]

Stephen,

I think Bryan's question about why a dermal papilla presents more androgen receptors in response to propecia is a valid one myself........


Youre response of why some hairs on the back and sides of the heads of balding men make DHT and have receptors is an interesting response, but it does not indicate a direct response to Byran's query. I think it would be fair for Bryan to answer your question only after you present an answer to his......



Stephen, one way I could concieve of the hydraulic dermal model to be true AND hairs to have a direct reaction negatively to androgens is this: ..................fluid levels in the level of the scalp rise, at a certain point the dermal papilla's "flip" their response to androgens and begin to make smaller hairs in consequent phases and stay in the rest phases in longer in response to decrease the pressure in that level of the scalp. Have you ever noticed Stephen that younger bald men have that "shiny" scalp that looks like its a balloon surface, just pressed "full" from below? Ever notice older bald men whove been bald for years dont? Its as if there is a "break" in the pressure from below, and they lymph nodes perhaps "slam" open, releasing all the metabolic wastes, stagnant protiens, etc. to the tissues below. But the damage is done by then and the scalp takes on that old, aged appearance we see in older bald men (white scars, differences in pigmentation, liver spots, age spots). Its interesting to speculate.

One other thing................................since as Wookiewannabe posted that rats and men have 99% DNA similarities, our baldness is perhaps alike (with respect to androgenic rodents and men with male pattern baldness)? I mean if peptides, minoxidil, proanthocyandins, finasteride works on rodents, they should be doing so pretty much in the same way they do people. Then the rodents would have a mild lymphedema at the follicle papilla level also?


Cyclosporin restores hair in bald rats http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Bryan, any thoughts on cyclosporin and rat hair?

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract . Thats info on rats and proanthocyanidins.

You two are conducting this debate in a very postive fashion. Not nasty like some of the others have been by the way. If you'd like to see a nasty one, Im in it on the surgical alternatives forum. Arguing with salesman posing over there. Trying to talk youngsters into cutting up their scalps. Cant stand those guys.

 

[S Foote.]

Your talking absolute crap now Bryan!!

OH MY...did I hit a little nerve with this last question of mine about androgen receptors?? Don't worry, it's only going to get WORSE for you, Stephen! :wink:

In your wildest dreams Bryan.

The complex feed back loops involved in changes in systematic hormone levels, have nothing "AT ALL" to do with the claims "YOU" are trying to make here!!

OH REALLY?? Why don't you explain in detail why not, my friend?

Yes really! We are talking about this Sawaya study are we not?

http://www.hairlosshelp.com/qna/Detail. ... ExpertID=8

And you claim this right, quote:

"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, not a production of DHT to go into the general circulation. DHT production is one thing, and androgen receptors are another. So how do you explain that, Stephen? You might as well acknowledge this problem for your theory, because I'm not going to let you evade it!"

I did answer your question previously Bryan, but as usual it seems to have gone over your head, and you some how thought this was about that sweating study :roll:

The whole basis of your claims is that the conversion of testosterone to DHT takes place in hair follicles, so DHT "must" be having a direct action on hair follicles.

So explain the DHT "resistent" follicles that DHT is produced in???

Can you even READ?? I've already explained to you (more than once) that I find the theory in "Beards, Baldness, and Sweat Secretion" to be a fairly credible one to explain the evolution of male pattern baldness.

That sweating study has nothing to do with my point above Bryan??

You are trying to claim that DHT has evolved to be produced in follicles, because it is designed to "directly" effect some growth change on them.

So i want you to explain why DHT is produced in exactly the same way within other follicles, that even you accept DHT has "NO" effect on?

Did Sawaya bother to check if androgen receptors were upregulated in those other scalp follicles that DHT doesn't effect at all!!


Have you got the full study Bryan?

If you are not prepared to explain the three male pattern baldness observations i posted, in accordence with the scientific principle you posted, and "claim" to agree with, just Butt out!

Which "3 male pattern baldness observations" are you referring to?

I'am sure everyone else who read my post understood it Bryan, so why is it so hard for you 8) Here is my challenge you are avoiding again :roll:

Bryan said:

"It's time once again for my favorite Einstein quote: "Physics should be made as simple as possible, but not simpler." The same goes for biology!

Bryan"

Based upon your quotation above, tell us the simplist "possible" way to explain these characteristics in the male pattern baldness scalp?

1/ Follicle miniaturisation.

2/ increased immune sensitivity and fibrosis.

3/ increased sweating capacity.

According to the scientific method, the "ideal" explaination is a change in "one" factor that explains "ALL" the subsequent changes, through recognised biological physics.

Here's my one changing factor, that can explain "ALL" the factors in male pattern baldness., according to Einstein's rules you quote.

DHT increases the tissue fluid pressure in the balding scalp!

Let's hear how your theory explains these three male pattern baldness observations, according to your "favorite" Einstein quote Bryan?

S Foote.

 

[S Foote.]

Stephen,

I think Bryan's question about why a dermal papilla presents more androgen receptors in response to propecia is a valid one myself........


Youre response of why some hairs on the back and sides of the heads of balding men make DHT and have receptors is an interesting response, but it does not indicate a direct response to Byran's query. I think it would be fair for Bryan to answer your question only after you present an answer to his......

I have answered his question Michael, and depending on the full Sawaya study i will have more to say on this.

Stephen, one way I could concieve of the hydraulic dermal model to be true AND hairs to have a direct reaction negatively to androgens is this: ..................fluid levels in the level of the scalp rise, at a certain point the dermal papilla's "flip" their response to androgens and begin to make smaller hairs in consequent phases and stay in the rest phases in longer in response to decrease the pressure in that level of the scalp. Have you ever noticed Stephen that younger bald men have that "shiny" scalp that looks like its a balloon surface, just pressed "full" from below? Ever notice older bald men whove been bald for years dont? Its as if there is a "break" in the pressure from below, and they lymph nodes perhaps "slam" open, releasing all the metabolic wastes, stagnant protiens, etc. to the tissues below. But the damage is done by then and the scalp takes on that old, aged appearance we see in older bald men (white scars, differences in pigmentation, liver spots, age spots). Its interesting to speculate.

Thats a good analogy Michael.

I would say that the effects of prior contact inhibition, are what changes the TGF beta-1 gene expression potential, and that this then "allows" androgens to directly effect follicles in the in-vitro tests.

This study shows that contact inhibition and the TGF beta-1 pathway are linked.

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

But i think the important thing among all these things, is that mouse study clearly blows the current theory out of the water. That was the acid test of donor dominance as it is claimed by the current theory, and it failed!

There is only one sensible explaination for why the male pattern baldness follicles enlarged in the mouse study, and the large follicles shrank!

You will note i have asked for Bryans explaination for this more than once, and he has said nothing :wink:

Let me ask people this?

If they repeated that mouse study, only this time they injected the mice with androgens to ensure they had more than enough to mimic the highest human levels.

If the growth results of human male pattern baldness follicles stayed the same as the first study, would people here then accept that the current theory is screwed, and new ideas are needed?

S Foote.

 

[Bryan]

And you claim this right, quote:

"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, not a production of DHT to go into the general circulation. DHT production is one thing, and androgen receptors are another. So how do you explain that, Stephen? You might as well acknowledge this problem for your theory, because I'm not going to let you evade it!"

I did answer your question previously Bryan, but as usual it seems to have gone over your head, and you some how thought this was about that sweating study :roll:

Let the record show that you're continuing to dodge the question I asked above. I can't say that I'm at all surprised, since you simply HAVE no response to it. It's something for which you can't think-up any excuse to explain, not even your typical ad hoc ones.

Can you even READ?? I've already explained to you (more than once) that I find the theory in "Beards, Baldness, and Sweat Secretion" to be a fairly credible one to explain the evolution of male pattern baldness.

That sweating study has nothing to do with my point above Bryan??

You are trying to claim that DHT has evolved to be produced in follicles, because it is designed to "directly" effect some growth change on them.

Uh, no. Re-read what I wrote above! I said in plain English that the "Beards, Baldness, and Sweat Secretion" study describes how male pattern baldness presumably evolved, not the fact that hair follicles are stimulated by androgens in the first place. That was evidently already in place, prior to the evolution of male pattern baldness.

So i want you to explain why DHT is produced in exactly the same way within other follicles, that even you accept DHT has "NO" effect on?

Presumably, ALL human hair follicles were originally susceptible to the effects of androgens very early in our evolution (their growth was stimulated by them). But then further evolutionary pressures slowly caused a change in hair follicles at or near the tops of our scalps as the eons went by: they went from being stimulated by androgens to being suppressed by them, for the reason described in "Beards, Baldness, and Sweat Secretion". Obviously, there are going to be hair follicles in the transitional regions that are sort of "balanced" between stimulation and suppression. Those are the ones for which androgens have a neutral effect.

Did Sawaya bother to check if androgen receptors were upregulated in those other scalp follicles that DHT doesn't effect at all!!

Not to my knowledge. All any of us knows is what's in that abstract.

Have you got the full study Bryan?

No. As far as I know, her paper was never actually published in a medical journal, or anywhere else.

Bryan

 

[S Foote.]

And you claim this right, quote:

"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, not a production of DHT to go into the general circulation. DHT production is one thing, and androgen receptors are another. So how do you explain that, Stephen? You might as well acknowledge this problem for your theory, because I'm not going to let you evade it!"

I did answer your question previously Bryan, but as usual it seems to have gone over your head, and you some how thought this was about that sweating study :roll:

Let the record show that you're continuing to dodge the question I asked above. I can't say that I'm at all surprised, since you simply HAVE no response to it. It's something for which you can't think-up any excuse to explain, not even your typical ad hoc ones.

[quote="S Foote.":144ff]

Can you even READ?? I've already explained to you (more than once) that I find the theory in "Beards, Baldness, and Sweat Secretion" to be a fairly credible one to explain the evolution of male pattern baldness.

That sweating study has nothing to do with my point above Bryan??

You are trying to claim that DHT has evolved to be produced in follicles, because it is designed to "directly" effect some growth change on them.

Uh, no. Re-read what I wrote above! I said in plain English that the "Beards, Baldness, and Sweat Secretion" study describes how male pattern baldness presumably evolved, not the fact that hair follicles are stimulated by androgens in the first place. That was evidently already in place, prior to the evolution of male pattern baldness.

So i want you to explain why DHT is produced in exactly the same way within other follicles, that even you accept DHT has "NO" effect on?

Presumably, ALL human hair follicles were originally susceptible to the effects of androgens very early in our evolution (their growth was stimulated by them). But then evolutionary pressures slowly caused a change in hair follicles at or near the tops of our scalps as the eons went by: they went from being stimulated by androgens to being suppressed by them, for the reason described in "Beards, Baldness, and Sweat Secretion". Obviously, there are going to be hair follicles in the transitional regions that are sort of "balanced" between stimulation and suppression. Those are the ones for which androgens have a neutral effect.

Did Sawaya bother to check if androgen receptors were upregulated in those other scalp follicles that DHT doesn't effect at all!!

Not to my knowledge. All any of us knows is what's in that abstract.

Have you got the full study Bryan?

No. As far as I know, her paper was never actually published in a medical journal, or anywhere else.

Bryan[/quote:144ff]

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,"



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

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

What is "NOT" guesswork is the relationship proven. So we have to explain the "MECHANISM" of this relationship :roll:

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

I am begining to think you really have no idea what your talking about Bryan?

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

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!

Your wild speculation about how follicles have evolved to respond in different ways to androgens, has to be supported by some kind of "real world" biological mechanism! Apart from that very basic requirement, you also have to explain the evolutionary advantage of the changes you propose!

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

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

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)

S Foote.

 

[michael barry]

Stephen wrote: "If they repeated that mouse study, only this time they injected the mice with androgens to ensure they had more than enough to mimic the highest human levels.

If the growth results of human male pattern baldness follicles stayed the same as the first study, would people here then accept that the current theory is screwed, and new ideas are needed? "


If that experiment was performed in that fashion, and the mice with weak immunology had human hair from frontal balding scalps attatched to their backs along with hair from the donor area also..................and growth was the same, I would imagine researchers would be asking questions. However, Stephen has speculated before that hair's "flip" their response to androgens through contact inhibition over time. Even if the hydraulic theory were true, wouldn't you (Stephen) expect the hairs from the balding areas to be sensitive to the androgens to some degree (even if the mice had no immune system to attack the hairs with)?

I was assuming this was where the TGF-beta pathway responded differently to tissue thats been squeezed?


This is a fruitful discussion by the way. I hope it can be congenial. Both of you are very smart men with a divergence of opinion on male pattern baldness, nobody who can follow a thread like this is an idiot.

 

[S Foote.]

Stephen wrote: "If they repeated that mouse study, only this time they injected the mice with androgens to ensure they had more than enough to mimic the highest human levels.

If the growth results of human male pattern baldness follicles stayed the same as the first study, would people here then accept that the current theory is screwed, and new ideas are needed? "


If that experiment was performed in that fashion, and the mice with weak immunology had human hair from frontal balding scalps attatched to their backs along with hair from the donor area also..................and growth was the same, I would imagine researchers would be asking questions. However, Stephen has speculated before that hair's "flip" their response to androgens through contact inhibition over time. Even if the hydraulic theory were true, wouldn't you (Stephen) expect the hairs from the balding areas to be sensitive to the androgens to some degree (even if the mice had no immune system to attack the hairs with)?

I was assuming this was where the TGF-beta pathway responded differently to tissue thats been squeezed?

I think the whole body of evidence shows that the TGF beta-1 pathway, is a distraction in male pattern baldness studies. In my opinion, this pathway only comes into play in the "artificial" environment in in-vitro studies.

I only mentioned the recognised link with prior contact inhibition and TGF beta-1, as a plausible explaination for the in-vitro results. But i dont think this has any rellevance to what is going on "in-vivo" where it matters!

Quite simply, if the in-vitro results were important, they would have matched the in-vivo results in that mouse study. They didn't (just the opposite in reality).

This is a fruitful discussion by the way. I hope it can be congenial. Both of you are very smart men with a divergence of opinion on male pattern baldness, nobody who can follow a thread like this is an idiot.

It should be obvious to anyone by now, that Bryan is more concerned with word games than genuine science. His priority is obviously to try to convince people on internet sites, that he is some kind of science "expert".

Personaly, i could not care less about what Bryan thinks. I "know" that he is a classic psuedoscientist.

But this kind of distortion of true scientific principles, just adds insult to injury for many vunerable people, who just want accurate information from these forums.

That annoys me!!

S Foote.