For bryan and Foote.

[CCS]

One thing that really bothers when I read Bryan and Foote's arguments is their constant personal attacks on each other. Actually Foote is the most guilty of this. He'll address Bryan directly once or twice per post, at least in the ones I read. Very distracting from the topic.

 

[powersam]

no they are most definately equally guilty of that. it may vary from thread to thread but they both get in there.

 

[S Foote.]

The current theory is based upon "SOME" in-built difference within follicles that changes their growth rate when exposed to androgens.

I for one are still waiting for any genuine scientific evidence, for androgens "DIRECTLY" changing pre-male pattern baldness follicles into male pattern baldness follicle, as the current theory tries to claim??

Actually, I don't think the "current theory" makes that claim. I don't think anybody KNOWS what causes that change in hair follicles (assuming that they really do change, in the first place). MAYBE androgens cause them to slowly shift that way over a period of years, or MAYBE it is indeed a built-in genetic "clock" of some sort. You don't have any business trying to speak for what the current theory claims, because that hasn't been elucidated yet.

Bryan

Well Bryan, the "business" of scientists is to keep to the accepted scientific standards, when proposing hypotheses or theories.

It's no good trying to just gloss over the major flaws in the current ideas with could be's and may be's!

In fact your statement above that the claims of the current theory haven't been elucidated yet is clearly false!

The current theory is very clear in it's claims of a direct androgen induced "change" in follicle growth.

You can cherry pick the 50 year studies to try to support your personal opinions Bryan, but the current theory just cannot stand up to the modern body of evidence, simple :roll:

S Foote.

 

[S Foote.]

I dont know where you get the nerve Bryan! :roll:

Apart from the info "YOU" posted on the effects of minoxidil on fluid movement, i have also posted other "real" scientific support for my argument!

The proof that edema can exist in layers of tissue whilst not effecting the outer layers, is in the reports on lipedematous scalp/alopecia.

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

http://alopecia.researchtoday.net/archive/1/2/66.htm

These are genuine histological examinations of the conditions in the tissue layers for God's sake, and still you would try to deny the implications! :roll:

Is THAT the best you can do, Stephen? Dig up some information on a rare condition that occurs mainly in black women that involves a THICK, fatty scalp and has an unknown etiology, and try to make us all believe that it somehow supports your theory on how minoxidil stimulates hairgrowth? Sorry, but you've got to do a LOT better than that! :wink:

Despite your attempts at distraction, my previous question remains unanswered. There apparently is no evidence that minoxidil causes a shift of fluid away from the scalp.

Bryan

The relevance of those studies both to my argument about how fluid levels in tissues can vary considerably, and how edema caused by whatever reason can miniaturised follicles, is very clear.

Your attempts to play this down are just not playing the scientific game Bryan :wink:

People here are not stupid, and can judge the validity of a genuine scientific argument for themselves Bryan.

S Foote.

 

[S Foote.]

One thing that really bothers when I read Bryan and Foote's arguments is their constant personal attacks on each other. Actually Foote is the most guilty of this. He'll address Bryan directly once or twice per post, at least in the ones I read. Very distracting from the topic.

I think you should re-read the posts, when have i not addressed Bryan "directly"?

It is very easy to claim scientific support for an argument with fancy words, but it is something else to back up those words with true scientific evidence!

This is where i fall out with Bryan, because his tactics are purely designed to mislead people on the true evidence!

Given the following example, you tell me what is the scientific argument?

Bryan posted an old study claiming this proved conclusively that the donor dominance claims the current theory is based on, were true.

In particular he tried to use this to put down my personal theory.

http://www.hairlosstalk.com/discussions ... hp?t=17571

Now if you go back a few posts in this thread, you can see that i asked Bryan to explain the later research that clearly refutes his claims about these older studies. You will also note that Bryan (as usual when confronted with actual science), has now refused to answer my question.

Now if people here want to just go along with fancy sounding psuedo scientific buls**t, thats fine!!

But i reserve the right to ask for "true" scientific justification of the claims some people make, and if they don't do this i call a spade a spade, sorry!


S Foote.

 

[Guest]

Ok guys.

Foote I find the study in which vellous and terminal hairs were transplanted on mice very interesting.The vellous hairs grew very quickly if I am correct eventhough (assuming, why wouldn't they?)the mice had normal androgen levels, which would prove that androgens don't have direct effect on balding.

Really I got a headache after reading all those pages!

A few short questions:

1)Propecia in many men stops shedding and gives them some regrowth. In your theory Foote, DHT decreases edema which would be beneficial for hair. When a person uses finasteride DHT is lowered, but many still have positive effects for their hair. How is this explained?

2)What is the reason for the increased fluid in the scalp? I know you believe it is poor lymph drainage. What is the reason for the poor lymph drainage? Has it to do with vasodilation?

A theory I just thought about:

When you compare animals and humans. Animals have sex when it is mating season and/or when the females are ready to mate. Human
beings have sex for pleasure. A lot of teens at very early age start to
masturbate and have sex. This leads to continous high production of androgens/androgens receptors.

Could it be that the hair follicles which would normally have no problems with androgens, become sensitized after being continously exposed to increased androgen and androgen receptors resulting in the follicles starting to perceive the androgens as foreign invaders?

If there could be any truth in my theory. When the hair follicles have been sensitized by continous exposure to relatively high amounts of androgens, they react to androgens(because they are now perceived as foreign invaders) causing the inflammation and swelling. Auto-immunity?

So that would mean the fluid pressure is the result of the hair follicles becoming sensitive to androgens and perceiving them as foreign invaders initiating a immune response?

Just some thoughts.

 

[Bryan]

It's no good trying to just gloss over the major flaws in the current ideas with could be's and may be's!

In fact your statement above that the claims of the current theory haven't been elucidated yet is clearly false!

The current theory is very clear in it's claims of a direct androgen induced "change" in follicle growth.

Really? Then give me a citation or two to the medical literature where that claim appears.

Bryan

 

[S Foote.]

It's no good trying to just gloss over the major flaws in the current ideas with could be's and may be's!

In fact your statement above that the claims of the current theory haven't been elucidated yet is clearly false!

The current theory is very clear in it's claims of a direct androgen induced "change" in follicle growth.

Really? Then give me a citation or two to the medical literature where that claim appears.

Bryan

Huh?

You very clearly made this claim yourself!!

http://www.hairlosstalk.com/discussions ... hp?t=17571

Quote:

"Nowadays we have overwhelming evidence for what causes male pattern balding: the direct, suppressive influence of androgens on human scalp follicles is a prime factor in this condition"

You are also on the record as claiming in the in-vitro debates, that direct exposure to androgens eventualy "changes" the follicles growth response!

So are you now accepting that your wrong Bryan? :freaked:

S Foote.

 

[Bryan]

http://www.hairlosstalk.com/discussions ... hp?t=17571[/url]

Quote:

"Nowadays we have overwhelming evidence for what causes male pattern balding: the direct, suppressive influence of androgens on human scalp follicles is a prime factor in this condition"[/quote:f793d]

Oh, BULLSHIT, Stephen! Either you're deliberately trying to twist things around in an effort to obscure the point being made, or you really ARE totally confused about what we're talking about here! :roll:

This is the original statement you made with which I took issue: "I for one are still waiting for any genuine scientific evidence, for androgens 'DIRECTLY' changing pre-male pattern baldness follicles into male pattern baldness follicle, as the current theory tries to claim??"

Dumbbell, you were referring to what we've already discussed at great length in the past, and that's what causes hair follicles to be transformed from NON-androgen senstive (prior to puberty) to ANDROGEN-SENSITIVE (after puberty), for chrissake. I was questioning your claim that the "current theory" assumes that it's the exposure to androgens that causes that transformation.

So then you came along and posted the following crap: "In fact your statement above that the claims of the current theory haven't been elucidated yet is clearly false! The current theory is very clear in it's claims of a direct androgen induced "change" in follicle growth." Again, I'm not talking about whether or not the "current theory" assumes that growth is inhibited by androgens during full adulthood (it probably does assume that), I'm talking about the claim you made about what it assumes causes the TRANSFORMATION of hair follicles from androgen INSENSITIVE to androgen SENSITIVE.

Now that you (hopefully) understand what the hell it is that we're talking about, stop twisting things around and answer my original question!

Bryan

 

[S Foote.]

http://www.hairlosstalk.com/discussions ... hp?t=17571[/url]

Quote:

"Nowadays we have overwhelming evidence for what causes male pattern balding: the direct, suppressive influence of androgens on human scalp follicles is a prime factor in this condition"

Oh, BULLSHIT, Stephen! Either you're deliberately trying to twist things around in an effort to obscure the point being made, or you really ARE totally confused about what we're talking about here! :roll:

This is the original statement you made with which I took issue: "I for one are still waiting for any genuine scientific evidence, for androgens 'DIRECTLY' changing pre-male pattern baldness follicles into male pattern baldness follicle, as the current theory tries to claim??"[/quote:2dce2]

Yes thats right, the in-vitro tests we talked about don't show androgens "directly" changing the growth rate of follicles.

The current direct theory by its very nature requires androgens to directly change the growth rate of follicles, because of the claim of different "genetics" in follicles! This is what everyone here understands the current theory to claim for God's sake!

So again Bryan, show us some evidence for this direct conversion????

Dumbbell, you were referring to what we've already discussed at great length in the past, and that's what causes hair follicles to be transformed from NON-androgen senstive (prior to puberty) to ANDROGEN-SENSITIVE (after puberty), for chrissake. I was questioning your claim that the "current theory" assumes that it's the exposure to androgens that causes that transformation.

So then you came along and posted the following crap: "In fact your statement above that the claims of the current theory haven't been elucidated yet is clearly false! The current theory is very clear in it's claims of a direct androgen induced "change" in follicle growth." Again, I'm not talking about whether or not the "current theory" assumes that growth is inhibited by androgens during full adulthood (it probably does assume that), I'm talking about the claim you made about what it assumes causes the TRANSFORMATION of hair follicles from androgen INSENSITIVE to androgen SENSITIVE.

Now that you (hopefully) understand what the hell it is that we're talking about, stop twisting things around and answer my original question!

Bryan

You have clearly lost the plot altogether now Bryan :roll:

You know damm well that the current theory if it is valid "HAS" to have a mechanism of directly changing follicle growth. Thats the whole central claim it makes!

Anyone who can be bothered to search the in-vitro debates can clearly see you vigorously tried to make that claim "YOURSELF" when it suited your argument of the day Bryan :roll:

Then you were trying to support the current theory by claiming it took a while of "soaking" in androgens to directly change follicle growth!!

Just what exactly are you trying to claim now then?

Are you now saying the direct theory accepts that something other than a direct interaction with androgens and pre-programed follicle cells is changing follicle growth?

Just what the hell "are" you ranting at here Bryan?

S Foote.

 

[S Foote.]

Ok guys.

Foote I find the study in which vellous and terminal hairs were transplanted on mice very interesting.The vellous hairs grew very quickly if I am correct eventhough (assuming, why wouldn't they?)the mice had normal androgen levels, which would prove that androgens don't have direct effect on balding.

I think that study is very important, and should be followed up.

A few short questions:

1)Propecia in many men stops shedding and gives them some regrowth. In your theory Foote, DHT decreases edema which would be beneficial for hair. When a person uses finasteride DHT is lowered, but many still have positive effects for their hair. How is this explained?

2)What is the reason for the increased fluid in the scalp? I know you believe it is poor lymph drainage. What is the reason for the poor lymph drainage? Has it to do with vasodilation?

You have to remember that the consitant effect of DHT is to "grow" hair over the larger area of the body. I suggest this is because DHT increases the contraction rate of lymphatic vessels, and this combined with the one way valves in the vessels pumps more fluid. This action reduces tissue fluid pressure allowing follicles to enlarge more increasing hair growth.

http://www.healthy.net/scr/article.asp?ID=993

The problem with the male pattern baldness area is this lies at the end of the lymphatic pipework, and a lot of DHT is being produced lower down in the large follicles of the scalp and the beard area.

Look at this diagram:

http://137.222.110.150/calnet/DeepNeck/ ... m#section6

What i suggest is happening in male pattern baldness is the increased pumping of the lymph vessels lower down, is increasingly closing the one way valves against the flow through these vessels from the male pattern baldness area. This is causing an opposite effect of DHT of reducing fluid drainage from the vunerable male pattern baldness area.

This would not by itself necessarily cause edema enough to cause male pattern baldness. What makes the difference in my opinion is the individuals blood pressure within the scalp.

If this is high enough, the reduced lymphatic drainage will then not be able to cope, and edema will develop.

This in my opinion is the reason for the link with male pattern baldness, and heart problems.

http://www.news.harvard.edu/gazette/200 ... /bald.html

Finasteride reduces DHT levels, so reducing the back pressure in the male pattern baldness area, increasing hair growth.

A theory I just thought about:

When you compare animals and humans. Animals have sex when it is mating season and/or when the females are ready to mate. Human
beings have sex for pleasure. A lot of teens at very early age start to
masturbate and have sex. This leads to continous high production of androgens/androgens receptors.

Could it be that the hair follicles which would normally have no problems with androgens, become sensitized after being continously exposed to increased androgen and androgen receptors resulting in the follicles starting to perceive the androgens as foreign invaders?

If there could be any truth in my theory. When the hair follicles have been sensitized by continous exposure to relatively high amounts of androgens, they react to androgens(because they are now perceived as foreign invaders) causing the inflammation and swelling. Auto-immunity?

So that would mean the fluid pressure is the result of the hair follicles becoming sensitive to androgens and perceiving them as foreign invaders initiating a immune response?

Just some thoughts.

The problem with the "auto immune" idea, is follicle miniaturisation induced by androgens doesn't need any immune reaction. The Macaque studies have shown this.

http://www.hairsite4.com/dc/dcboard.php ... ting_type=

Also there are studies that show hair follicles are immune "priviledged", in that even transplantation to another person does not cause them to be rejected.

http://www.newhair.com/info/news-transgender.asp

The inflammation in human male pattern baldness, can most easily be explained by increasing levels of edema.

Edema is known to encourage inflammation.

http://www.lymphoedema.org.au/index.htm

Click "what is lymphedema"

I think the immune reactions around the follicles do not directly effect them. But over time, the fibrosis also known in lymphedema, can "wrap" the follicles preventing re-enlargement. So the inflammation does need to be treated to get the best effects from other treatments.

S Foote.

 

[Bryan]

Yes thats right, the in-vitro tests we talked about don't show androgens "directly" changing the growth rate of follicles.

No, not overnight in a petri dish. If it _does_ happen that way, it undoubtedly takes a long time (years?).

The current direct theory by its very nature requires androgens to directly change the growth rate of follicles, because of the claim of different "genetics" in follicles! This is what everyone here understands the current theory to claim for God's sake!

So again Bryan, show us some evidence for this direct conversion????

Again, you seem confused. What do you mean by "direct conversion"? Do you mean the idea that the direct exposure of androgens causes pre-pubertal hair follicles to eventually become sensitive to androgens? How many times do I have to tell you that I don't have any evidence for it? It's just a hypothesis.

You know damm well that the current theory if it is valid "HAS" to have a mechanism of directly changing follicle growth. Thats the whole central claim it makes!

???

What the hell are you talking about?? Are you talking about TRANSFORMATION, or are you talking about the simple growth inhibition of scalp hair follicles by androgens? WILL YOU PLEASE SPECIFY WHAT YOU MEAN FROM NOW ON, so I don't have to waste my time guessing about what you mean?

Anyone who can be bothered to search the in-vitro debates can clearly see you vigorously tried to make that claim "YOURSELF" when it suited your argument of the day Bryan :roll:

Which claim are you talking about? I can't read your mind...

Then you were trying to support the current theory by claiming it took a while of "soaking" in androgens to directly change follicle growth!!

Do you mean transformation? That's just a hypothesis.

Are you now saying the direct theory accepts that something other than a direct interaction with androgens and pre-programed follicle cells is changing follicle growth?

I'm tired of trying to figure out what you mean by "changing follicle growth". Either state your question to me PRECISELY so that I know if you're talking about either 1) transformation, or 2) just the normal and accepted growth inhibition by androgens, or don't waste my time at all.

Bryan

 

[S Foote.]

Let's just cut the crap, and get down to the facts Bryan.

You said quote:

"This is the original statement you made with which I took issue: "I for one are still waiting for any genuine scientific evidence, for androgens 'DIRECTLY' changing pre-male pattern baldness follicles into male pattern baldness follicle, as the current theory tries to claim??"

You are now saying that the current theory does "not" claim that androgens are directly changing follicle growth, this is the "issue" you said you had with my statement above right?


The current theory is very clear in its claims that androgens are directly causing a change in hair growth based upon the built in genetics of the follicles. There is no room in this for any "external" factor influencing this change!

The whole donor dominance notion you often use to defend the current theory "CLAIMS" that the reaction to androgens is purely internal within follicle cells!

This is what everyone here understands the current theory to claim, as i said above, but you now take "issue" with???

If there is anyone else who takes issue with this interpretation of the current theory, lets hear about it?

This latest babble of yours is clearly completely against your on the record personal claims, and those of the theory you support Bryan.

So how can we take you seriously, when you are not even consistent in your claims from thread to thread? :roll:

I am now off for the weekend, as i have a life outside of these forums :wink:

S Foote.

 

[zackb]

C'mon guys. I know that you have differing views on male pattern baldness, androgens, Stephen's theories, but can we get back to discussing the theories and not arguing?

 

[Guest]

Thank you very much for answering S. Foote. I understand your theory much more now.

What i suggest is happening in male pattern baldness is the increased pumping of the lymph vessels lower down, is increasingly closing the one way valves against the flow through these vessels from the male pattern baldness area. This is causing an opposite effect of DHT of reducing fluid drainage from the vunerable male pattern baldness area.

So your are saying that the increased pumping of the lymph vessels lower down is bad for hair follicles because this inhibits the pumping/reducing fluid in the male pattern baldness area because this somehow creates a barriere(valve) for good fluid drainage in the male pattern baldness area?

Do you Foote have a diagram which makes this more easy to understand. I understand the lymphe system is fluids going around the body like blood circulation, but I dont understand the valve thing.

Why is there an increased pumping of the lymph vessels lower down in male pattern baldness?

This may sound stupid Foote, during sex I always feel an increasing pressure in my head and then the itching starts. Could this have anything to do with your theory?

Found this:

[Effects of nitric oxide on peritoneal lymphatic stomata and lymph drainage via NO-cGMP-Ca(2+) pathway.]

[Article in Chinese]

Li YY, Li JC.

Department of Lymphology, Institute of Cell Biology, Zhejiang University, Hangzhou 310031, China; E-mail: lijichen@zju.edu.cn.

To study the cell signal transduction mechanism of nitric oxide (NO) on the peritoneal lymphatic stomata and lymph drainage in the rat, cGMP content were measured by a commercially available radioimmunoassay kit, and the [Ca(2+)](i) were observed by a confocal laser scanning microscope in the cultured peritoneal mesothelial cell. Animal experiment was practiced to study the effect of NO-cGMP-Ca(2+) pathway on the lymphatic stomata and lymph absorption. The results showed that: (1) Sper/NO increased cGMP of the rat peritoneal mesothelial cell (RPMC) in a dose-dependent manner (P<0.01) compared to the control group. This effect was blocked by 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) (P<0.05), a specific inhibitor of soluble guanylyl cyclase (sGC). The level of [Ca(2+)](i) in single RPMC decreased by adding Sper/NO (P<0.05). Pretreatment with ODQ for 10 min blocked the Sper/NO-induced decrease in [Ca(2+)](i). L-typed calcium channel blocker nifedipine induced an immediate and marked decrease in [Ca(2+)](i) (P<0.05).. After [Ca(2+)](i) reached a balance again, adding Sper/NO could not change [Ca(2+)](i) (P>0.05). (2) Sper/NO increased the area of the stomata (P<0.01) and the quantity of the tracer in a dose-dependent manner (P<0.05) compared to the control group. Pretreatment with ODQ significantly inhibited Sper/NO-induced change of lymphatic stomata and lymph drainage (P<0.01). Nifedipine increased the opening area of the lymphatic stomata (P< 0.01) and the concentration of absorbed trypan blue of the diaphragm (P<0.05). Sper/NO could not make a further change in the samples pretreated by nifedipine (P> 0.05). The results indicate that NO can decrease [Ca(2+)](i) in the RPMC through the NO-cGMP pathway. This procession is related with the L- type voltage-gated Ca(2+) channel. NO enlarges the opening area of the lymphatic stomata and enhances the lymph drainage of tracer by NO-cGMP-[Ca(2+)](i) pathway.

Ultrastructural study of pleural lymphatic drainage unit and effect of nitric oxide on the drainage capacity of pleural lymphatic stomata in the rat.

Li YY, Li JC.

Department of Lymphology, Zhejiang University School of Medicine, 310031 Hangzhou, China.

The objective of this study was twofold: first to investigate the ultrastructure of the lymphatic drainage unit on the costal pleura of rats by electron microscopy, and secondly to examine the effect of nitric oxide on the pleural lymphatic stomata and fluid absorption from the pleural cavity. The lymphatic drainage unit of the rat costal pleura is composed of three special components: the lymphatic stomata between the mesothelial cells, the initial part of the lymphatic vessels and the underlying connective tissue containing many foramina. The unit is the main passage to drainage fluid, particles and cells in the pleural space. To investigate the regulator of the lymph drainage, nitric oxide synthase inhibitor and nitric oxide donor were injected into the peritoneal cavity of the rats, respectively. Trypan blue was used as tracer. The ultrastructural changes of pleural lymphatic stomata were observed under scanning electron microscope and analyzed by a computer image processing system. It turned out that the area and density of the pleural lymphatic stomata were positively correlated with the nitric oxide quantity (p < 0.05). After the tracer was injected into the pleural cavity, the nitric oxide donor group exhibited a higher trypan blue concentration than the control group (p < 0.05). The ability of the pleura to absorb trypan blue was enhanced because of the larger opening of the lymphatic stomata (p < 0.05). It is suggested that nitric oxide can increase lymphatic absorption of the pleura by opening pleural lymphatic stomata.

My English really is not that good, but do these studies say that NO increases lymph drainage?

This would not by itself necessarily cause edema enough to cause male pattern baldness. What makes the difference in my opinion is the individuals blood pressure within the scalp.

I know arginine is very good for my hair because it increases NO/vasodilation.More NO/better circulation will lower the blood pressure in general including the blood pressure within the scalp and therefore promotes hair growth.

I have this week started doing scalp exercises. I massage the scalp for 5 minutes untill I feel it reall gettin warm. When my scalp gets warm I can see a big vein popping out just under my right and left temples

What would you Foote advise for better lymph drainage in the scalp besides finasteride and other androgen influencing medicine?

 

[Bryan]

You said quote:

"This is the original statement you made with which I took issue: "I for one are still waiting for any genuine scientific evidence, for androgens 'DIRECTLY' changing pre-male pattern baldness follicles into male pattern baldness follicle, as the current theory tries to claim??"

You are now saying that the current theory does "not" claim that androgens are directly changing follicle growth, this is the "issue" you said you had with my statement above right?

For the love of Christ, THERE ARE TWO DIFFERENT ISSUES HERE:

1) Whether or not androgens directly inhibit the growth of adult balding scalp hair follicles. (This has been conclusively proven, and the answer is YES)

2) What causes pre-pubertal hair follicles to eventually become sensitive to androgens in the first place. (Nobody knows the answer to that question. Your claim that the "current theory" assumes it to be the direct exposure to androgens is FALSE. The "current theory" makes no such assumption, to the best of my knowledge)

NOW do you understand what I've been trying to tell you? I don't know any other ways to explain it to you. I've explained it in plain English.

Bryan

 

[zackb]

Stephen,

I just really don't understand how increased drainage down below in the body would cause a buildup of fluid in the scalp? I was thinking of trying a diuretic to increase flow all over, and that made sense to me.

 

[michael barry]

Bryan,

Have you ever run Stephen's idea past Dr. Peter Proctor. Proctor has the opportunity to look at men's (his patients who come for office visits) heads under electron microscopes. Wouldn't you think that he'd have a chance to diagnose, as a M.D., an edema if he saw one?


That could end the debate over this hypothesis once and for all could it not? I think Proctor would be honest if he seen a little water retention wouldn't you?

 

[wookster]

This would not by itself necessarily cause edema enough to cause male pattern baldness. What makes the difference in my opinion is the individuals blood pressure within the scalp.

If this is high enough, the reduced lymphatic drainage will then not be able to cope, and edema will develop.

This in my opinion is the reason for the link with male pattern baldness, and heart problems.

http://www.news.harvard.edu/gazette/200 ... /bald.html

My last blood pressure reading was 105/70 which seems kind of low to me for my age, 45 :freaked:

I hope that the lower blood pressure is not a side effect of systemic absorption of minoxidil :freaked:

 

[S Foote.]

You said quote:

"This is the original statement you made with which I took issue: "I for one are still waiting for any genuine scientific evidence, for androgens 'DIRECTLY' changing pre-male pattern baldness follicles into male pattern baldness follicle, as the current theory tries to claim??"

You are now saying that the current theory does "not" claim that androgens are directly changing follicle growth, this is the "issue" you said you had with my statement above right?

For the love of Christ, THERE ARE TWO DIFFERENT ISSUES HERE:

1) Whether or not androgens directly inhibit the growth of adult balding scalp hair follicles. (This has been conclusively proven, and the answer is YES)

No Bryan, thats a distortion and you know it!

Androgens have only been shown to "directly" suppress "PRE-EXISTING" balding follicles in-vitro.

The only genuine in-vivo testing of such a direct action of androgens was that mouse study. In that study, male pattern baldness follicle growth was clearly not "directly" suppressed by androgens, as you clearly accepted when you posted the study!

2) What causes pre-pubertal hair follicles to eventually become sensitive to androgens in the first place. (Nobody knows the answer to that question. Your claim that the "current theory" assumes it to be the direct exposure to androgens is FALSE. The "current theory" makes no such assumption, to the best of my knowledge)

Thats clear enough now Bryan.

1) If the current theory does "NOT" claim that androgens are directly inducing growth suppression in previously healthy scalp follicles, just what "does" it claim is causing the growth change? Any valid theory is required to explain the "change"

2) If you are sincere about your statement above quote:

"Your claim that the "current theory" assumes it to be the direct exposure to androgens is FALSE. The "current theory" makes no such assumption, to the best of my knowledge"

Why are you clearly still trying to tell people in other threads that androgens are "directly causing" male pattern baldness!!!!!


http://www.hairlosstalk.com/discussions ... c&start=30

Quote:

"No. All human scalp hair follicles contain androgen receptors. The reason follicles on the side don't go bald is that they have a different RESPONSE to androgens. "

To any reasonable person, that statement clearly infers that "YOU" claim androgens are directly changing pre-male pattern baldness follicles into male pattern baldness follicles!

Something that the in-vitro studies disprove!

You didn't say for example that "androgens cause male pattern baldness after another factor has made the follicles androgen sensitive"!

If you are "NOW" going to insist the current theory doesnt have an explaination for how follicles are changed by androgens, just make sure you make that clear in future threads Bryan :wink:

S Foote.