Why you go bald...............the two genes that do it.....

[squeegee]

Seven times more suceptible with these two genes. Thats profoundly statistically signifigant. Someone who wont accept that, wont accept anything. The variant of the A-receptor ALONE is not enough to produce baldness according to another article I read. There has to be both these genes present.

There are more than just two genes involved in baldness. It is not that simple. :hairy:

:agree:

 

[michael barry]

[edit] Male pattern baldness and genetics
Main article: Androgenic alopecia
Much research went into the genetic component of male pattern baldness, or androgenetic alopecia (Androgenetic Alopecia). Research indicates that susceptibility to premature male pattern baldness is largely X-linked. Other genes, that aren’t sex linked, are also involved.

Large studies in 2005 and 2007 stress the importance of the maternal line in the inheritance of male pattern baldness. German researchers name the androgen receptor gene as the cardinal prerequisite for balding[8]. They conclude that a certain variant of the androgen receptor is needed for Androgenetic Alopecia to develop. In the same year the results of this study were confirmed by other researchers [9]. This gene is recessive and a female would need two X chromosomes with the defect to show typical male pattern alopecia. Seeing that androgens and their interaction with the androgen receptor are the cause of Androgenetic Alopecia it seems logical that the androgen receptor gene plays an important part in its development.

Other research in 2007 suggests another gene on the X chromosome, that lies close to the androgen receptor gene, is an important gene in male pattern baldness. They found the region Xq11-q12 on the X-chromosome to be strongly associated with Androgenetic Alopecia in males. They point at the EDA2R gene as the gene that is mostly associated with Androgenetic Alopecia.

Other genes involved with hair loss have been found. One of them being a gene on chromosome 3. The gene is located at 3q26[10]. This gene is also involved in a type of baldness associated with mental retardation. This gene is recessive .

Another gene that might be involved in hair loss is the P2RY5. This gene is linked to hair structure. Certain variants can lead to baldness at birth while another variant cause “wooly hairâ€￾.

Whelp, thats four genes they have identified. If you get the first two, you are 700% more likely to be bald. Pretty goddamm strong correlation.


I for one trust the scientists who research this.






Keep in mind (STEPHEN FOOTE), those androgen-receptor-KNOCKOUT-mice have strong hairgrowth even when androgens are introduced, but their wild-type mates have their hair grow weaker with androgens. Do you contend that they TOO HAVE EDEMA ON THEIR BODIES, or do you conclude that their hairs react DIRECTLY to androgens via the androgen receptor? Here is the info:



Dihydrotestosterone inhibits mouse hair growth via the androgen receptor

CUTANEOUS BIOLOGY
Dihydrotestosterone inhibits murine hair growth via the androgen receptorA. Naito, T. Sato*, T. Matsumoto*, K. Takeyama*, T. Yoshino, S. Kato* and M. Ohdera
Biological Science Research Laboratories, Research and Development Headquarters, LION Corporation, 100 Tajima, Odawara, Kanagawa 256-0811, Japan
*Institute of Molecular and Cellular Biosciences, University of Tokyo, Bunkyo-ku, Japan
Correspondence to A. Naito.
E-mail: a-naito@lion.co.jp

Conflicts of interest
None declared.

Copyright Journal Compilation © 2008 British Association of Dermatologists
KEYWORDS
androgenetic alopecia • androgen receptor knockout mouse • hair cycle
ABSTRACT
Background Androgens cause regression of human hair follicles in the parietofrontal scalp, but the precise mechanisms by which they do so are unknown. Although many investigators have elucidated the effect of androgens on hair growth by using rodents and other animals, some of the evidence is conflicting.

Objectives To investigate the effect of androgens on mouse hair regrowth and hair cycle by using androgen receptor knockout (ARKO) mice.

Methods We examined the effects of dihydrotestosterone (DHT) on hair regrowth by using ARKO mice and wild-type (WT) littermates, compared the hair cycles in ARKO mice and WT littermates by histology and histomorphometry, and measured hair length and thickness in ARKO mice and WT littermates.

Results DHT inhibited the hair regrowth of WT mice but not that of their ARKO littermates. The anagen phase in the second hair cycle was longer in ARKO mice than in their WT littermates. The hair of ARKO mice was longer and thicker than that of their WT littermates.

Conclusions Androgens inhibit hair growth in mice, and this inhibition might be caused by androgen–androgen receptor signals.

 

[wookster]

http://www.copewithcytokines.de/cope.cgi/cope.cgi?key=Cystatin-11

Cystatin-11

This protein is a member of the cystatin superfamily of the papain family of cysteine proteases (Brown and Dziegielewska, 1997) and has been identified by Hamil et al (2002) in Macaca mulatta epididymis. The human gene on chromosome 20p11.2 is expressed predominantly in the male reproductive tract and gives rise to an alternatively spliced transcript lacking one exon. Expression of the gene is regulated by androgens. The protein also has antimicrobial activity.

http://en.wikipedia.org/wiki/CST11

Cystatin 11, also known as CST11, is a human gene.[1]

The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and the kininogens. The type 2 cystatin proteins are a class of cysteine proteinase inhibitors found in a variety of human fluids and secretions. The cystatin locus on chromosome 20 contains the majority of the type 2 cystatin genes and pseudogenes. This gene is located in the cystatin locus and encodes an epididymal-specific protein whose specific function has not been determined. Alternative splicing yields two variants encoding distinct isoforms.[1]

The interwoven factors associated with the baldness genes look to be very complex :badmood:

 

[S Foote.]

[editKeep in mind (STEPHEN FOOTE), those androgen-receptor-KNOCKOUT-mice have strong hairgrowth even when androgens are introduced, but their wild-type mates have their hair grow weaker with androgens. Do you contend that they TOO HAVE EDEMA ON THEIR BODIES, or do you conclude that their hairs react DIRECTLY to androgens via the androgen receptor?

How does this demonstrate that the androgen effect is a "direct" effect within follicles, or an indirect effect mediated by androgen receptors in other tissues (the lymphatic system for example)?

You are not addressing my question Michael!

The direct theory you support demands that there has to be pre-existing differences in the internal genetic function of "future" male pattern baldness follicles compared to other scalp follicles. This has to be so if androgens are going to effect hair growth in different ways "directly" as you claim.

Are you saying that any of these complex genetic studies you keep referencing demonstrates that?

Yes or no Michael?

S Foote.

 

[Bryan]

How does this demonstrate that the androgen effect is a "direct" effect within follicles, or an indirect effect mediated by androgen receptors in other tissues (the lymphatic system for example)?

I'll say just two words to you: DONOR DOMINANCE.

 

[S Foote.]

How does this demonstrate that the androgen effect is a "direct" effect within follicles, or an indirect effect mediated by androgen receptors in other tissues (the lymphatic system for example)?

I'll say just two words to you: DONOR DOMINANCE.

I suppose that once again, this is your distorted opinion of the transplantation study you always throw at people Bryan?

Strange how you always conveniently "forget" what the author himself said about his results! Something you yourself highlighted once as significant, but as usual your opinion changes from thread to thread in your quest for "glory" in internet debates :whistle:

This is your original post about the study that you claimed "PROVED" your opinions Bryan:

viewtopic.php?t=17571

The authors conclusion, and the part "YOU" highlighted, quote:

"This shows that the cause of male pattern baldness lies in the follicle itself or in its very close surrounding"

Both my theory and the other "pressure" theories involve the conditions in the follicles "very close surrounding", and in that respect are in line with that authors conclusions.

Are you "NOW" trying to claim the scientist that actually did this study was wrong in his conclusions Bryan :nono:

Getting back on topic, can you quote any studies that demonstrate a pre-existing genetic "difference" in scalp hair follicles prior to male pattern baldness?

S Foote.

 

[michael barry]

Stephen wrote:

The direct theory you support demands that there has to be pre-existing differences in the internal genetic function of "future" male pattern baldness follicles compared to other scalp follicles. This has to be so if androgens are going to effect hair growth in different ways "directly" as you claim.

Stephen,

Studies have attested that there are more androgen RECEPTORS present in frontal scalp of men and apes. There apparently is no difference in the alpha five reductase genes between balding men and hirsute men if the South Korean researchers are correct. They looked at the seven genes associated with alpha five reductase and tested to see if balding men had specific ones more oft than hirsute men, but found that they did not. Over time, more androgen receptors gets more androgen to affected hairs. Ken Washenik once talked about how the skin grows over your scalp in fetal development in your mother's first trimester. Its now known that a gene called ectodysplasin, located close to the androgen receptor gene, goes along with the new skin in this process and encodes how strong androgen receptor expression will be in various parts of the scalp. Guess what? It encodes the highest expression in places that go bald..............on the top. Occipital hairs (and occipital hair thins with age Stephen, look at Dick Cheney) have less androgen receptors than hairs on the top and front of the scalp.


You bald and grey where there are more androgen receptors present. Men's hair typically ages faster than women's hair, even when they keep it. Men's hair usually gets thinner than women's hair pre-menopause, even when they keep it. Androgens are simply not good for head hair, but hair on the sides and back due to less androgen receptors just dont get enough to thin ALL THAT MUCH.



There are now 6 genes identified that are associated with male pattern baldness (google it). Every one researching it believes in the direct theory of baldness. I dont think they are wrong.



BTW---I read one study that showed hair moved to various parts of the head even GREYED at the same rate as the other hairs back where it came from, so strong is donor dominance (or better to say...........androgen receptor dominance).





Back to the mice..........................the androgen receptor knock out mice have hair unaffected by DHT. But DHT made hairs on their wild-type LITTERMATES grow slower and enter catagen faster. OF course its happening directly through the androgen receptor, unless you want to claim that there is edema on these mice squeezing those hairs.

 

[abcdefg]

Just to throw in a common sense statement, lets all remember there are more then 2 genes at work in male pattern baldness.We need to find more of the genes and how these genes interact with each other. Really science needs better ways of just testing for certain genes since guessing will not ever piece together this puzzle.

 

[Bryan]

Both my theory and the other "pressure" theories involve the conditions in the follicles "very close surrounding", and in that respect are in line with that authors conclusions.

And yet there are the in vitro studies showing that both balding and non-balding hair follicles show the EXACT same response to androgens that one would expect, given the standard theory of balding: a stimulation of body hair follicles, and a suppression of scalp hair follicles. Since they aren't even on the scalp (or body) anymore, that shows a DIRECT effect on them by the androgens.

And your hilarious response to that fact is that it's apparently just a huge COINCIDENCE, and not what really causes balding! My only regret is that I can't look you in the eye when you say that, to see if you're able to say it with a straight face! :mrgreen:

Getting back on topic, can you quote any studies that demonstrate a pre-existing genetic "difference" in scalp hair follicles prior to male pattern baldness?

Let me answer that by asking YOU a question first: if I were to cite you a new stumptailed macaque study which involved transplanting non-balding occipital hair follicles to the frontal area (and vice versa) while the monkeys were still pre-pubertal (and non-yet balding), and after puberty when they _were_ balding it was found that donor dominance was STILL maintained (even with those follicles that were transplanted prior to puberty), would you finally accept that as proof that there IS a pre-existing genetic "difference" in hair follicles?

 

[Bryan]

Just to throw in a common sense statement, lets all remember there are more then 2 genes at work in male pattern baldness.We need to find more of the genes and how these genes interact with each other. Really science needs better ways of just testing for certain genes since guessing will not ever piece together this puzzle

I continue to be a little bothered by that kind of talk. I think there's any number of genes which could have an effect on male pattern baldness, but by far the most important one we really need to unravel is the gene (or genes) responsible for the basic design of the hair follicle, the design that makes them sensitive to androgens. Until we can understand that, I believe we're mainly just wasting our time by looking at all these ancillary issues having to do with numbers and types of androgen receptors, numbers and types of 5a-reductase enzymes, levels of androgens in general, etc.

 

[wookster]

if I were to cite you a new stumptailed macaque study which involved transplanting non-balding occipital hair follicles to the frontal area (and vice versa) while the monkeys were still pre-pubertal (and non-yet balding), and after puberty when they _were_ balding it was found that donor dominance was STILL maintained (even with those follicles that were transplanted prior to puberty), would you finally accept that as proof that there IS a pre-existing genetic "difference" in hair follicles?

Yes, I would like to see that study

 

[S Foote.]

Stephen wrote:

The direct theory you support demands that there has to be pre-existing differences in the internal genetic function of "future" male pattern baldness follicles compared to other scalp follicles. This has to be so if androgens are going to effect hair growth in different ways "directly" as you claim.

Stephen,

Studies have attested that there are more androgen RECEPTORS present in frontal scalp of men and apes. There apparently is no difference in the alpha five reductase genes between balding men and hirsute men if the South Korean researchers are correct. They looked at the seven genes associated with alpha five reductase and tested to see if balding men had specific ones more oft than hirsute men, but found that they did not. Over time, more androgen receptors gets more androgen to affected hairs. Ken Washenik once talked about how the skin grows over your scalp in fetal development in your mother's first trimester. Its now known that a gene called ectodysplasin, located close to the androgen receptor gene, goes along with the new skin in this process and encodes how strong androgen receptor expression will be in various parts of the scalp. Guess what? It encodes the highest expression in places that go bald..............on the top. Occipital hairs (and occipital hair thins with age Stephen, look at Dick Cheney) have less androgen receptors than hairs on the top and front of the scalp.


You bald and grey where there are more androgen receptors present. Men's hair typically ages faster than women's hair, even when they keep it. Men's hair usually gets thinner than women's hair pre-menopause, even when they keep it. Androgens are simply not good for head hair, but hair on the sides and back due to less androgen receptors just dont get enough to thin ALL THAT MUCH.



There are now 6 genes identified that are associated with male pattern baldness (google it). Every one researching it believes in the direct theory of baldness. I dont think they are wrong.



BTW---I read one study that showed hair moved to various parts of the head even GREYED at the same rate as the other hairs back where it came from, so strong is donor dominance (or better to say...........androgen receptor dominance).





Back to the mice..........................the androgen receptor knock out mice have hair unaffected by DHT. But DHT made hairs on their wild-type LITTERMATES grow slower and enter catagen faster. OF course its happening directly through the androgen receptor, unless you want to claim that there is edema on these mice squeezing those hairs.

Michael.

You say quote:

"Studies have attested that there are more androgen RECEPTORS present in frontal scalp of men and apes."

You dont say there is any difference in this factor between pre-balding men, and men who wont get male pattern baldness? Some pre-existing difference is what you need to prove.

Again in the mice study you quote, you cannot just assume that because hair growth is effected this is a direct effect of DHT. Thats just not scientific Michael!.

The other point about this kind of mouse study is it doesn't say anything about the mechanisms of opposite effects of DHT on hair growth, we get in humans.

S Foote.

 

[S Foote.]

Both my theory and the other "pressure" theories involve the conditions in the follicles "very close surrounding", and in that respect are in line with that authors conclusions.

And yet there are the in vitro studies showing that both balding and non-balding hair follicles show the EXACT same response to androgens that one would expect, given the standard theory of balding: a stimulation of body hair follicles, and a suppression of scalp hair follicles. Since they aren't even on the scalp (or body) anymore, that shows a DIRECT effect on them by the androgens.

And your hilarious response to that fact is that it's apparently just a huge COINCIDENCE, and not what really causes balding! My only regret is that I can't look you in the eye when you say that, to see if you're able to say it with a straight face! :mrgreen:

As you well know Bryan, the in-vitro studies clearly show that there is "NO" pre-existing genetic make up in future male pattern baldness follicles, that turns them into male pattern baldness follicles when exposed to androgens. These follicles show no "change" in their pre-existing growth rates.

You have to make up excuses for this that have no basis at all in recognised hormone regulated tissues. Non of the in-vitro studies show that androgens "DIRECTLY CHANGE" the pre-existing growth rates of any kind of follicle.

This thread is about Michael's claim that pre-existing genetic differences in follicles, lead to different growth responses in follicles by a direct action of androgens.

The in-vitro studies prove no such thing! In fact they are very misleading as to what happens in the "real" world of in-vivo.

In theory, the most valid in-vitro studies should be those that use whole follicle cultures. This would account better for any cell to cell signaling between follicle cell types, conversion of T to DHT etc, and so better re-produce the in-vivo situation.

Here is one such in-vitro study.

http://www.springerlink.com/content/r5kvp97365370t36/


Quote:
"Testosterone and oestrogen inhibited hair growth in vitro to a similar extent"

We all know that doesn't happen in real life!

It is not what happens in the in-vitro studies that is important to the "direct" theory, it is what "doesn't" happen that scews it! That is the faliure of androgens to "DIRECTLY" cause male pattern baldness in known male pattern baldness suceptable follicles.

Getting back on topic, can you quote any studies that demonstrate a pre-existing genetic "difference" in scalp hair follicles prior to male pattern baldness?

Let me answer that by asking YOU a question first: if I were to cite you a new stumptailed macaque study which involved transplanting non-balding occipital hair follicles to the frontal area (and vice versa) while the monkeys were still pre-pubertal (and non-yet balding), and after puberty when they _were_ balding it was found that donor dominance was STILL maintained (even with those follicles that were transplanted prior to puberty), would you finally accept that as proof that there IS a pre-existing genetic "difference" in hair follicles?

Bring it on.

S Foote.

 

[michael barry]

Again in the mice study you quote, you cannot just assume that because hair growth is effected this is a direct effect of DHT. Thats just not scientific Michael!.

Lemme see

2 groups of mice. One has no androgen receptors.

The other has androgen receptors.



Mice are given DHT.


Mice with no androgen receptors dont see any difference in their fur.


Mice with androgen receptors have fur that grows smaller, slower, and weaker.




CONCLUSIONS: DHT, acting through the androgen receptors, slows growth of the fur. That is, unless, you want to claim that DHT is giving these little creatures excessive lymphatic fluid ALL OVER THEIR BACKS (edema). Go back and look at those three fluridil photos Stephen. Regrowth, one fairly impressive, with a substance that many think shouldn't even be able to get down to the dermal papilla before it starts to degrade (since its designed to degrade in water). A fluridil hirsutism study on women showed that it reduced facial hair. There is one fairly impressive picture of one woman's moustache pretty much dissapearing---------------wait a minute, I forgot, DHT can indeed act on androgen receptors directly in body hair according to you, but just not head hair. Head hairs are immune to DHT.

You dont say there is any difference in this factor between pre-balding men, and men who wont get male pattern baldness? Some pre-existing difference is what you need to prove.

--------the "pre-existing" differences in hairs are there, but pre-pubescent boys and apes dont yet have enough androgens to kick them off. Its just like the beard hairs we all have. The genetics are there to have a beard, but you aren't going to have one before puberty as you dont have enough male hormone to kick off the process. Its like acne. If you have the genes, you will have acne.........................but not as a child.

 

[CCS]

MB, are you saying there are multiple studies showing Fluridil works? I thought they just had the one study that was not placebo controlled.

 

[Bryan]

As you well know Bryan, the in-vitro studies clearly show that there is "NO" pre-existing genetic make up in future male pattern baldness follicles, that turns them into male pattern baldness follicles when exposed to androgens. These follicles show no "change" in their pre-existing growth rates.

No, you're wrong. The in vitro studies don't demonstrate anything either way: they don't show that there IS a pre-existing make up, and they don't show that there ISN'T a pre-existing make up. That's because hair follicles can only be grown in culture for a short period of time. Not long enough to determine the exact mechanism of how they eventually become sensitive to androgens.

You have to make up excuses for this that have no basis at all in recognised hormone regulated tissues. Non of the in-vitro studies show that androgens "DIRECTLY CHANGE" the pre-existing growth rates of any kind of follicle.

No, not over a period of just a few days, which is all that hair follicles can be grown in culture.

This thread is about Michael's claim that pre-existing genetic differences in follicles, lead to different growth responses in follicles by a direct action of androgens.

The in-vitro studies prove no such thing! In fact they are very misleading as to what happens in the "real" world of in-vivo.

No, not over a period of just a few days. Nobody knows the exact biochemical reason(s) for why scalp hair follicles eventually become sensitive to androgens after puberty.

In theory, the most valid in-vitro studies should be those that use whole follicle cultures. This would account better for any cell to cell signaling between follicle cell types, conversion of T to DHT etc, and so better re-produce the in-vivo situation.

Here is one such in-vitro study.

http://www.springerlink.com/content/r5kvp97365370t36/

Quote:
"Testosterone and oestrogen inhibited hair growth in vitro to a similar extent"

We all know that doesn't happen in real life!

WHAT doesn't happen in real life? I'm not clear what point it is that you're trying to make here.

It is not what happens in the in-vitro studies that is important to the "direct" theory, it is what "doesn't" happen that scews it! That is the faliure of androgens to "DIRECTLY" cause male pattern baldness in known male pattern baldness suceptable follicles.

Yeah, so you must think that androgen's suppressive effect on hair follicles in vitro is just a huge COINCIDENCE! :mrgreen:

Let me answer that by asking YOU a question first: if I were to cite you a new stumptailed macaque study which involved transplanting non-balding occipital hair follicles to the frontal area (and vice versa) while the monkeys were still pre-pubertal (and non-yet balding), and after puberty when they _were_ balding it was found that donor dominance was STILL maintained (even with those follicles that were transplanted prior to puberty), would you finally accept that as proof that there IS a pre-existing genetic "difference" in hair follicles?

Bring it on.

Answer the question that I asked you.

 

[squeegee]

This thread is totally kicking ***.. I went to bed at 1:00 last night just reading on that Chromosome 20. Please guys keep this thread alive!!!!!! unk: I want more, I want more!!

 

[S Foote.]

Again in the mice study you quote, you cannot just assume that because hair growth is effected this is a direct effect of DHT. Thats just not scientific Michael!.

Lemme see

2 groups of mice. One has no androgen receptors.

The other has androgen receptors.



Mice are given DHT.


Mice with no androgen receptors dont see any difference in their fur.


Mice with androgen receptors have fur that grows smaller, slower, and weaker.




CONCLUSIONS: DHT, acting through the androgen receptors, slows growth of the fur.

Well yes Michael, but your "assuming" that the androgen receptors involved are in the hair follicles!

Prove it!

That is, unless, you want to claim that DHT is giving these little creatures excessive lymphatic fluid ALL OVER THEIR BACKS (edema).

Go back and look at those three fluridil photos Stephen. Regrowth, one fairly impressive, with a substance that many think shouldn't even be able to get down to the dermal papilla before it starts to degrade (since its designed to degrade in water). A fluridil hirsutism study on women showed that it reduced facial hair. There is one fairly impressive picture of one woman's moustache pretty much dissapearing---------------wait a minute, I forgot, DHT can indeed act on androgen receptors directly in body hair according to you, but just not head hair. Head hairs are immune to DHT.

Don't misquote me Michael.

Where have i ever said that DHT is acting directly on body hair? Again the effect i propose is an androgen action "around" the follicles. Any anti-androgen that will penetrate enough will have an effect.

As i have explained many times before, i refer to "edema" as it is easier for most people to understand. I suggest only slight changes in tissue fluid pressures around follicles are needed to cause changes in follicle size. This is not what would be classed as "clinical" edema.

I thought you had grasped that Michael.

the "pre-existing" differences in hairs are there, but pre-pubescent boys and apes dont yet have enough androgens to kick them off. Its just like the beard hairs we all have. The genetics are there to have a beard, but you aren't going to have one before puberty as you dont have enough male hormone to kick off the process. Its like acne. If you have the genes, you will have acne.........................but not as a child.

OK, show us all a genetic study that shows these pre-existing differences in the "FOLLICLES" of men that go bald, and those that don't? There has to be some difference (according to the direct theory), for rising androgen levels to "kick off" different effects? You just assume this exists!

To prove your argument you need a study of the internal genetic function of scalp follicles, that shows a difference between male pattern baldness follicles and other scalp follicles "BEFORE" androgens come into play!

You just miss the scientifics points completely Michael, sorry.

S Foote.

 

[S Foote.]

As you well know Bryan, the in-vitro studies clearly show that there is "NO" pre-existing genetic make up in future male pattern baldness follicles, that turns them into male pattern baldness follicles when exposed to androgens. These follicles show no "change" in their pre-existing growth rates.

No, you're wrong. The in vitro studies don't demonstrate anything either way: they don't show that there IS a pre-existing make up, and they don't show that there ISN'T a pre-existing make up. That's because hair follicles can only be grown in culture for a short period of time. Not long enough to determine the exact mechanism of how they eventually become sensitive to androgens.

http://www.springerlink.com/content/r5kvp97365370t36/[/url]

Quote:
"Testosterone and oestrogen inhibited hair growth in vitro to a similar extent"

We all know that doesn't happen in real life!

WHAT doesn't happen in real life? I'm not clear what point it is that you're trying to make here.

Well you are on the record as claiming estrogen is "good" for hair growth, or at least not as bad as t or the DHT that would be produced in those whole follicle cultures. So you can't see a problem with those results then Bryan? :whistle:

Let me answer that by asking YOU a question first: if I were to cite you a new stumptailed macaque study which involved transplanting non-balding occipital hair follicles to the frontal area (and vice versa) while the monkeys were still pre-pubertal (and non-yet balding), and after puberty when they _were_ balding it was found that donor dominance was STILL maintained (even with those follicles that were transplanted prior to puberty), would you finally accept that as proof that there IS a pre-existing genetic "difference" in hair follicles?

Bring it on.

Answer the question that I asked you.

Huh??

You claim you know a study that proves me wrong Bryan. So post it!

What's up Mcfly chicken??

S Foote.

 

[Bryan]

No, not over a period of just a few days. Nobody knows the exact biochemical reason(s) for why scalp hair follicles eventually become sensitive to androgens after puberty.

But you are trying to claim that "YOU DO" know the biochemical reason why Bryan!

No, Stephen, I am most definitely NOT claiming that I know why that happens. I've suggested a couple of hypotheses (look up the word "hypothesis" in a dictionary to find out what that means) for that phenomenon, but I've never claimed that either of them is by any means conclusive.

WHAT doesn't happen in real life? I'm not clear what point it is that you're trying to make here.

Well you are on the record as claiming estrogen is "good" for hair growth, or at least not as bad as t or the DHT that would be produced in those whole follicle cultures. So you can't see a problem with those results then Bryan? :whistle:

LOL! That was your only point of posting that? Just that contrary result with the estrogen? Okay, Stephen, whatever...

Answer the question that I asked you.

Huh??

You claim you know a study that proves me wrong Bryan. So post it!

What's up Mcfly chicken??

ANSWER THE QUESTION THAT I ASKED YOU. I want to see if I can get you to commit yourself to an honest response BEFORE you see the results of any scientific experiment. You have a long history of trying to twist and distort the results of scientific experiments that disprove your bizarre theory about balding, so I'm making you agree to the ground rules BEFORE you hear the results of any new ones! :nono: