For bryan and Foote.

[S Foote.]

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.

It is related to general fluid dynamics, and it does get a bit complicated.

A simple analogy is a muti storey building with one drainpipe for all the baths in the building. If everyone has a bath, then pulls the plug at the same time, the drainage capacity of the pipe is high (effect of DHT).

The highest bath at the end of the system (at the top of the drain), has to drain through the same pipe, but this is being swamped by the other baths lower down. So the drainage from the top is reduced because of the restriction of increased drainage lower down.

This is the simplist analogy.

Really this comes down to reducing the production of DHT to reduce the restriction, and using topicals on the male pattern baldness area that reduce the formation of inflammation that increases edema.

This is generaly the kind of treatment conclusion that people on these boards are reaching by experience.

S Foote.

 

[S Foote.]

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?

Yes it is related to fluid dynanic effects, please see my post to zackb.

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 is a good explaination of lymphatic fluid drainage.

http://www.lymphnotes.com/article.php/id/151/

I think the increased pumping of lymph vessels is what DHT was designed to do in evolution to increase tissue performance. Body, beard hair and male pattern baldness are the side effects in my opinion.

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?

If you are increasing your heart rate, you are increasing the pressure to the scalp that feeds any inflammation or edema.

[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>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> 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.

There are many articles that demonstrate that NO increases lymph drainage.

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=15192027

http://www.annalssurgicaloncology.org/c ... suppl/275S

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?

At this point my theory is just that, a theory. I do not make specific recommendations on drug treatments.

But scalp massage is good, as is Toms exercise. Also i would say that cold water hair washing would help as would ice packs if you have the time.

S Foote.

 

[Bryan]

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.

Let's assume for just a moment that that's true. Can you suggest any explanation for why androgens would affect hair follicles that way ONLY in vitro, but not in vivo?

In any event, I think your claim is false. What about that famous "twin study" which has been cited several times on hairloss sites? That's the one where the castrated twin (who still had all his hair) was given testosterone injections, and soon went as bald as his non-castrated brother. Furthermore, I believe one of the pseudohermaphrodites was involved in an experiment in which he was given large amounts of DHT, and he started getting frontal recession. Both of those tests were in vivo, so you're obviously WRONG.

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!

I've already commented on that several times. We don't know for sure that it wasn't directly suppressed by androgens. It very easily COULD have been. There was a lack of information about a lot of the details in that study. Speculation abounds in that one.

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"

I've already told you. NOBODY KNOWS for sure. Whiting mentions that "genetic clock" possibility, but I think that's just a tentative hypothesis.

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!!!!!

Because I think it's TRUE. For god's sake, you STILL seem to be confusing the two different issues! I'm talking about the effect of androgens on hair follicles AFTER they have become androgen-sensitive, not what causes pre-pubertal hair follicles to BECOME sensitive to them during or after puberty! Do you STILL not understand that???

http://www.hairlosstalk.com/discussions/viewtopic.php?t=27525&postdays=0&postorder=asc&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!

The word is IMPLY, not INFER. And no, it implies no such thing. I was talking about post-pubertal hair follicles. It has nothing whatsoever to do with what I'm now calling the "transformation" of hair follicles.

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

No, because that's taken for granted.

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:

I'm going to assume that you're referring to "transformation". I don't dwell on that, because I'm not as obsessed with it as you are! :wink:

Bryan

 

[Bryan]

At this point my theory is just that, a theory.

It's not even a theory, it's just a hypothesis. The distinction is important.

Bryan

 

[michael barry]

Bryan,

I asked earlier in the thread, but I doubt you seen it. Have you ever asked Proctor to examine just one of his patients and look for any edema? He could diagnose it I would think, and no doubt has the tools in his office to do so.


One thing that I think works against Stephen's theory is L'Oreal's and Alpecin's observation that testosterone ages men's dermal tissues and hair faster. Men's EYEBROWS grey and age must faster than womens do. Men's chest hair gets grey quite fast as well as their arm hair long before most women even start to grey. I bet if women let their leg hair grow, we'd see that their hair is "younger" looking than men's leg hair.


If Stephen's theory was correct........................I think Emu Oil, which penetrates skin better than just about anything and has fatty acids in it, is a potent anit-inflammatory, anti-fungal, and anti-microbial, as well as a diuretic, would be about the best thing one could use. Especially on top of copper peptides that help give remodelling signals to skin. Pickart literally advises this: put on folligen about half an hour after minoxidil, then put on emu to "push" the folligen down. He also advises propecia, saw palmetto oil, flaxseed oil, and MSM. That would be a pretty darn good regimine for not too much money.



Here is the latest on Androgenic Alopecia from "DOW STOUGH, MD; KURT STENN, MD; ROBERT HABER, MD; WILLIAM M. PARSLEY, MD; JAMES E. VOGEL, MD; DAVID A. WHITING, MD; KEN WASHENIK, MD, PHD
From The Stough Hair Center, Hot Springs, Ark (D.S.); Aderans Research Institute, Inc, Philadelphia, Pa (K.S.); University Hospitals, Cleveland, Ohio (R.H.); Louisville Medical Center, Louisville, Ky (W.M.P.); Division of Plastic Surgery, Johns Hopkins School of Medicine and Hospital, Baltimore, Md (J.E.V.); Baylor Hair Research and Treatment Center, Dallas, Tex (D.A.W.); and Bosley, Beverly Hills, Calif (K.W.)."


"Several lines of circumstantial evidence support the crucial role of androgens—and DHT in particular—in male pattern baldness. First, this condition is not observed in eunuchs, who lack androgens; in individuals who lack functional androgen receptors; or in pseudohermaphrodites, who lack 5α-reductase.4,25-27 The absence of baldness in those lacking the gene for 5α-reductase type 2 suggests a necessary role for DHT. Second, the progression of androgenetic alopecia in men is halted coincident with castration among postpubertal men.5 Third, balding scalp contains excessive concentrations of 5α-reductase, DHT, and the androgen receptor.4,28,29 Finally, hair loss is mitigated or inhibited by finasteride, a medication that prevents the conversion of testosterone to DHT by selectively inhibiting the activity of 5α-reductase type 2.23 Although the presence of androgens and a genetic predisposition are necessary for androgenetic alopecia in men........................"



A little more from these men is particularily illustrative
"PATHOPHYSIOLOGY


Normal hair growth occurs at the level of the hair follicle in a 3-phased cycle: (1) anagen, a 2-to 7-year active growth phase during which hair is produced continuously via the division and growth of specialized keratin-producing epidermal cells that surround a dermal papilla at the base of the hair follicle; (2) catagen, a 1-to 2-week transition and involution phase, during which the hair follicle contracts as a result of apoptosis and the hair bulb ascends toward the surface of the skin, loses its root sheaths that anchor the hair in place, and develops a club-shaped end to form a club hair (ie, a hair in the resting state); and (3) telogen, a 5-to 12-week resting phase during which the old club hair is shed. At the end of telogen, germinal cells of the hair follicle once again begin to grow to form a new hair bulb, which becomes the source of a new hair.4 On average, in the normal scalp, at least 90% of hairs are in anagen, 1% are in catagen, and 9% are in telogen.20

The basis of androgenetic alopecia in men is a progressive decrease in the density of terminal (thick and pigmented) hairs and a concurrent increase in density of vellus (short, fine, nonpigmented) hairs.20 In effect, terminal hairs are turned off and are transformed into vellus hairs. This effect is attributed to miniaturization of the hair follicle, which is associated with a substantial reduction in hair diameter. Miniaturization may occur abruptly in 1 or a few hair cycles.21 In 1 illustrative study of biopsy specimens from 106 men with male pattern baldness and 44 nonbalding control subjects, the ratio of terminal to vellus hairs was 7:1 in the nonbalding scalp compared with 2:1 in the balding scalp.22 In male pattern baldness, the anagen phase shortens, and the telogen phase lengthens or remains the same so that hair length—which depends primarily on the duration of anagen—decreases.23 Eventually, the hair does not reach the skin surface. Also, the time between the telogen stage and the anagen stage lengthens so that the number of scalp hairs decreases.4

Although the mechanisms of these changes have not been established definitively, male pattern baldness is known to depend on androgens—in particular, the androgen dihydrotestosterone (DHT).23-25 Dihydrotestosterone is synthesized from testosterone by 5α-reductase type 1 and type 2, lipophilic enzymes found on intracellular (nuclear) membranes.24 Type 2 5α-reductase, expressed in hair follicles and other androgen-dependent tissues such as the prostate gland, appears to be more important than type 1 in male pattern baldness."



Stephen and Bryan, ..............Dr. Kurt Stenn, Dr. David Whiting, Dr. Ken Washenik are among the names that signed off on what I quoted above. Ive been willing to give Stephen's theory a chance because of its 1) abilitly to explain transplantation and 2) the noted "coincidences" of things that WE KNOW are good for baldness having a fluid shifting effect in the body or even gynochomosteia as a side effect. Lavendar is even linked with gynochomostia now, and its been an "essential oil" forever. Finasteride, Dutasteride, Saw Palmetto, Flutamide all get you tits. Minoxidil, Copper Peptides, Proanthocyanidins, Emu Oil, Caffeine, Latanaprost, are ALL diurectics and minoxidil and proanthocyanidns (as I know from experience) can literally painfully swell your hands. Cyclosporin shifts fluid in rats. Its a fascinating set of coincidences there.

But the "docs'" that research hair for a living sure haven't seen it. And they are very close to being able to offer a cloning procedure now. Intercytex is PLANNING on a 2008 release date 'in-house' in England for their protocol. So Dr. Paul Kemp, the world's foremost tissue engineering scientist and the man who "cloned" the first organ from stem cells (and a bald man who wants hair for himself), has not seen edema as a factor in baldness either.


This is why I'd like for Bryan to email Proctor (he'd listen to Bryan) and just check out one of his next patients for edema and see what he says. The good Doctor, whos always seemed like a pretty nice guy the few times Ive emailed him, would be honest about what he saw in my opinion.



One more thing before I go. Stephen pointed out that hair follicles transplanted between individuals dont suffer an immune reaction (or thats how I took it). Thats not the case, this "transplantation of human follicle dermal sheath tissue between incompatible individuals of different sex can induce the formation of new hair follicles." is the case. Dermal papilla stem cells are "immuno priveledged" not existing dermal papillas . When Colin Jahoda moved those cells to Amanda Reynolds arm all those years ago, the hair that grew was black and thick, not thin and blonde like Reynolds arm hair. Jahoda doesnt have baldness either, but that wouldnt matter in a females arm anyway.......

 

[S Foote.]

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.

Let's assume for just a moment that that's true. Can you suggest any explanation for why androgens would affect hair follicles that way ONLY in vitro, but not in vivo?

Yes i can Bryan.

As you know, i have previously argued that trying to equate the behaviour of in-vitro "artificial" cultures of DP cells with the in-vivo reality, is misleading.

I quote the mouse study because it is "the" real test of your conclusions about what you think androgens do in-vivo, based on in-vitro tests.

Your in-vitro conclusions failed the in-vivo "reality" test Bryan!

Now we have an up to date study from the EHRS abstracts posted earlier, that clearly shows major differences in how DP cells behave in-vivo and in-vitro.

http://content.karger.com/ProdukteDB/pr ... =92842.pdf

________________________________

Initial Characterisation of a New Model of
Dermal Papilla Cell Culture
C. Higgins1, G. Richardson1, G. Westgate2, M. Green3,
D.J. Tobin4, C. Jahoda1
1Department of Biological Sciences, Durham University,
2Westgate Consultancy, Stevington, Bedfordshire, 3Unilever
R&D Colworth, Sharnbrook, Bedford, 4School of Life
Sciences, University of Bradford, UK


Human dermal papilla (DP) cells grown in culture have been studied
extensively. However, some key differences between DP cell
behaviour in vivo and in culture have been identified. Smooth muscle
 actin (SMA) is a sheath-cell specific marker in vivo, but once in
culture both papilla and sheath cells express SMA. Cells derived
from anagen DP’s are highly proliferative whilst the same cells in vivo
do not proliferate..................................

___________________________________________

In any event, I think your claim is false. What about that famous "twin study" which has been cited several times on hairloss sites? That's the one where the castrated twin (who still had all his hair) was given testosterone injections, and soon went as bald as his non-castrated brother. Furthermore, I believe one of the pseudohermaphrodites was involved in an experiment in which he was given large amounts of DHT, and he started getting frontal recession. Both of those tests were in vivo, so you're obviously WRONG.

Stop trying to misrepresent my theory Bryan :roll:

My theory as you well know involves an indirect effect of androgens upon hair growth, based on systematic levels.

Androgen injections increase systematic level, so how do your quoted studies prove i'am wrong?

Do you "actually" understand my theory???

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!

I've already commented on that several times. We don't know for sure that it wasn't directly suppressed by androgens. It very easily COULD have been. There was a lack of information about a lot of the details in that study. Speculation abounds in that one.

Huh?

I just refer to your own comments on that study at the time you posted it Bryan!

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

These now regular U turns in your opinions, are not helping your credibility Bryan :roll:

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"

I've already told you. NOBODY KNOWS for sure. Whiting mentions that "genetic clock" possibility, but I think that's just a tentative hypothesis.

[quote="S Foote.":5f957]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!!!!!

Because I think it's TRUE. For god's sake, you STILL seem to be confusing the two different issues! I'm talking about the effect of androgens on hair follicles AFTER they have become androgen-sensitive, not what causes pre-pubertal hair follicles to BECOME sensitive to them during or after puberty! Do you STILL not understand that???

http://www.hairlosstalk.com/discussions/viewtopic.php?t=27525&postdays=0&postorder=asc&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!

The word is IMPLY, not INFER. And no, it implies no such thing. I was talking about post-pubertal hair follicles. It has nothing whatsoever to do with what I'm now calling the "transformation" of hair follicles.

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

No, because that's taken for granted.

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:

I'm going to assume that you're referring to "transformation". I don't dwell on that, because I'm not as obsessed with it as you are! :wink:

Bryan[/quote:5f957]

The "WHOLE" scientific quest in male pattern baldness, and the very basic question people here want an answer to, is "HOW" are our normal scalp follicles "transformed" into male pattern baldness follicles!!

The mechanism of transformation "IS" what we need to know before we have any chance of dealing with male pattern baldness!

This is very basic science Bryan! Just because you know the current theory can't answer the important "change" issue, you try to play it down!

True theories "HAVE" to explain the mechanisms of change, simple!

My theory explains the mechanisms of change by recognised physical factors.

Sorry Bryan but healthy hair "abracadabra" male pattern baldness, just isn't good enough :wink:

S Foote.

 

[S Foote.]

At this point my theory is just that, a theory.

It's not even a theory, it's just a hypothesis. The distinction is important.

Bryan

Damm right the distinction is important Bryan :roll:

Sometimes i start to think you really have no grasp of science at all?


For the benefit of the people here Bryan why don't you explain to us all in a proper scientific way, "exactly" how the current theory you support explains what we actually see!

We all know that androgens are involved in changing our nice terminal hair follicles into miniaturised male pattern baldness follicles.

So simply tell us Bryan the "mechanisms" of this change according to the current theory?

Remember if you can't support "each" step involved in these changes with genuine scientific evidence, you haven't got a theory! If you can provide "some" precedent for the mechanisms you propose, you may just have a hypothesis?

But as i am sure you know now, there is an ever growing body of evidence that continues to blow gaping holes in the "old" idea's!

If you can't justify the idea's you continue to support in "true" scientific terms, you should really stop telling some vunerable people on these sites that androgens are "directly causing" male pattern baldness!

Many people then waste their time and money with many topical treatments that do very little, as is constantly reported by those previously duped by so called "scientific" advice.

So if you can't justify the current theory with real science, just say so! thats OK. What is not OK is unsupported claims.

S Foote.

 

[Bryan]

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

These now regular U turns in your opinions, are not helping your credibility Bryan :roll: [/quote:c07f4]

I've already explained to you why that's not a "U turn". I'm not going to keep repeating myself.

The "WHOLE" scientific quest in male pattern baldness, and the very basic question people here want an answer to, is "HOW" are our normal scalp follicles "transformed" into male pattern baldness follicles!!

The mechanism of transformation "IS" what we need to know before we have any chance of dealing with male pattern baldness!

This is very basic science Bryan! Just because you know the current theory can't answer the important "change" issue, you try to play it down!

True theories "HAVE" to explain the mechanisms of change, simple!

My theory explains the mechanisms of change by recognised physical factors.

LOL!!! I've asked you repeatedly to explain how contact inhibition would alter cells to become sensitive to androgens, or even just to provide ONE known example of such a thing happening in the field of biology, but you stand mute before the court, unable to provide any such evidence. You're a HYPOCRITE, Stephen!

Bryan

 

[Administrator]

Just wanted to say hi to Bryan and S. Foote - hope you guys are doing well. Glad to see you're still around here. Wow .... Page 57 already of this thread ... I wonder who will win the debate in the end?

Guys can I move this to the General forum please? Would that be okay? Just think this is one of the few truly intelligent discussions going on on this forum, and I'd like others to read along and learn a bit.

Admin

 

[S Foote.]

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

These now regular U turns in your opinions, are not helping your credibility Bryan :roll:

I've already explained to you why that's not a "U turn". I'm not going to keep repeating myself.[/quote:ca468]

No you have not Bryan, and your obvious U turns are clear from your different opinions in different threads.

Your constant denials now only serve to further prove your unscientific atitudes

The "WHOLE" scientific quest in male pattern baldness, and the very basic question people here want an answer to, is "HOW" are our normal scalp follicles "transformed" into male pattern baldness follicles!!

The mechanism of transformation "IS" what we need to know before we have any chance of dealing with male pattern baldness!

This is very basic science Bryan! Just because you know the current theory can't answer the important "change" issue, you try to play it down!

True theories "HAVE" to explain the mechanisms of change, simple!

My theory explains the mechanisms of change by recognised physical factors.

LOL!!! I've asked you repeatedly to explain how contact inhibition would alter cells to become sensitive to androgens, or even just to provide ONE known example of such a thing happening in the field of biology, but you stand mute before the court, unable to provide any such evidence. You're a HYPOCRITE, Stephen!

Bryan

Those people that are reading this debate, and have also followed our previous debates, now know what a liar you are Bryan. :wink:

They know that i have responded to this same old question of yours many times before!

Once again, the mechanism of the "direct" action of androgens on male pattern baldness follicle cells in-vitro, is via the TGF beta-1 pathway.

Prior contaqct inhibition in-vivo, is known to alter the gene expression involved in the TGF beta-1 pathway.

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

The key words in this abstract are "common mechanisms"! I wonder how many future posts it will take, for you to once again try to claim i have not answered this question. 8)

Everyone reading my debates with Bryan, should by now have noticed something?

This is Bryans constant demands that "prove" every word of what i say :?

Yet it is very clear that every time i ask Bryan to "prove" his arguments, or even justify his statements scientificaly, i get no response! :roll:

Nuff said 8)

S Foote.

 

[S Foote.]

Just wanted to say hi to Bryan and S. Foote - hope you guys are doing well. Glad to see you're still around here. Wow .... Page 57 already of this thread ... I wonder who will win the debate in the end?

Guys can I move this to the General forum please? Would that be okay? Just think this is one of the few truly intelligent discussions going on on this forum, and I'd like others to read along and learn a bit.

Admin

Hi admin.

I don't have a problem with that.

I just want to say that it should not be about "winning" debates. It should be about getting to the scientific truth of the causes of male pattern baldness.

It is the people who are more concerned with a percieved "winning" of an internet debate, that are just distracting from this goal in my opinion.

My advice is for people to learn for themselves what is "true" science and what is not! There is plenty of info about "true" science out there on the net.

Learn about science for yourself, then no one can dupe you :wink:

S Foote.

 

[michael barry]

One aspect of the mouse study that the two of you have both missed (unless I didn't see your response on it) is the fact that IT SHOULD NOT MATTER WHETHER THOSE MICE HAD ANY ANDROGENS AT ALL.


Men who get castrated dont see their vellus follicles "regenerate" as well as terminal sized follicles do on their heads. But vellus hairs from male pattern baldness-men transplanted on those mouse backs DID regenerate as well as the terminal follicles transplanted from the backs and sides of the heads from the same men to those mice. That alone, regardless of the androgen levels in the mice, is signifigant. Norman Orentriech http://www.orentreich.org/report04.htm and his foundation, OFAS, is looking into this apparently "Balding Hairs Grow Long and Thick on Immunodeficient Mice
Because immunodeficient mice do not reject foreign tissues, they will accept transplants of human hairs that can then be studied. We transplanted both miniaturized and normal hair follicles from scalp affected by common balding. Our study found that miniaturized hair follicles can quickly regenerate once removed from the human scalp; in fact they grew as well as or better than the transplanted normal, non-balding hair follicles as assessed by their diameter and length achieved at 22 weeks.
Krajcik RA, Vogelman JH, Malloy VL, Orentreich N.
Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice. Journal of the American Academy of Dermatology 48(5):752-59, 2003"

That really is fascinating. Whether the immune sytem supresses male pattern baldness hairs or it is in fact an unrecognized edema of the scalp where drainaige is bad ought to be somewhat encouraging for young men just starting to resist male pattern baldness.


Admin mentioned that the level of discussion on the site is diminishing. I think this is true of various hair related sites in general in the past two or three years unfortunately. Rude people with dogmatic opinions, no matter how lane-brained try to dominate the forums. One can link studies science backing an opinion only to see it casually dismissed by various idiots who are certain that baldness is just stress, shampoo usage, masturbation, drinking milk, big pillows or whatever other idiocy.

 

[Bryan]

Excuse me, but you haven't answered my question. Let's try it again: Can you suggest any explanation for why androgens would affect hair follicles that way ONLY in vitro, but not in vivo?

Err?

Didn't you understand the references i posted to the basic differences in genetic expression of various factors in DP cells in-vitro, compared to in-vivo?

Is that the best you can do? I challenge you by asking a SPECIFIC question about hair follicles and androgens which you're unable to answer, so you try to disguise that fact by citing something completely different about other in vivo and in vitro effects, hoping that people will think you answered my question? :wink:

Weak, Stephen. Really really weak.

LOL!!! I've asked you repeatedly to explain how contact inhibition would alter cells to become sensitive to androgens, or even just to provide ONE known example of such a thing happening in the field of biology, but you stand mute before the court, unable to provide any such evidence. You're a HYPOCRITE, Stephen!

Those people that are reading this debate, and have also followed our previous debates, now know what a liar you are Bryan. :wink:

They know that i have responded to this same old question of yours many times before!

Once again, the mechanism of the "direct" action of androgens on male pattern baldness follicle cells in-vitro, is via the TGF beta-1 pathway.

Prior contaqct inhibition in-vivo, is known to alter the gene expression involved in the TGF beta-1 pathway.

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

The key words in this abstract are "common mechanisms"! I wonder how many future posts it will take, for you to once again try to claim i have not answered this question. 8)

LOL!! I don't care about common mechanisms, Stephen! ANSWER THE QUESTION THAT I ASKED YOU! Explain to me how contact inhibition would cause cells to become sensitive to androgens, and give me an example in biology where that has actually happened! You can't do it, and you know it! :wink:

Just because contact inhibition may in fact cause the expression of TGF-b1 and androgens also cause the expression of TGF-b1, that says absolutely NOTHING about whether or not contact inhibition causes cells to become androgen-sensitive. That's one of the STUPIDEST things you've ever said in this debate. You should be embarrassed. That's like saying that since the flu causes a fever, and typhoid fever causes a fever, then getting the flu makes you get typhoid fever.

Bryan

 

[michael barry]

Potential inhibitory regulation by TGF-beta 1 is discussed here:http://www.ncbi.nlm.nih.gov/entrez/..._uids=12473061&query_hl=7&itool=pubmed_docsum


"Procyanidin B-3, isolated from barley and identified as a hair-growth stimulant, has the potential to counteract inhibitory regulation by TGF-beta1.

Kamimura A, Takahashi T.

Tsukuba Research Laboratories, Kyowa Hakko Kogyo Co, Tsukuba, Ibaraki, Japan. ayako.kamimura@kyowa.co.jp

With the aim of identifying natural products, which possess hair-growing activity, we examined more than 1000 plant extracts with respect to their growth-promoting effects on hair epithelial cells. We discovered intensive growth-promoting activity, about 140% relative to controls, in barley extract. Our strategy for identifying active compounds in barley extract involved subjecting it to column chromatography using HP-20 resin columns, an LH-20 resin column, and preparative high-performance liquid chromatography (HPLC) using an ODS column. The 60% (v/v) aqueous methanol eluted fraction from the HP-20 column and the 75% (v/v) aqueous methanol eluted fraction from the subsequent LH-20 column showed high hair-growing activity in vivo. We isolated two major substances from the LH-20 active fraction using preparative HPLC. By means of mass spectrometry, 1H-NMR, and 13C-NMR analyses, one substance was revealed to be procyanidin B-3 and the other substance was identified as (+)-catechin. Purified procyanidin B-3 showed high hair-growing activity in the form of in vitro hair epithelial cell growth-promoting activity and in vivo anagen-inducing activity; however (+)-catechin showed no hair-growing activity. For the purpose of examining the hair-growing mechanisms of procyanidin B-3, we examined its relationship to the TGF-beta signal pathway, which is known to be a regulator of catagen induction. Addition of TGF-beta1 to hair epithelial cell cultures dose-dependently decreased the cell growth, and addition of procyanidin B-3 to the culture neutralized the growth-inhibiting effect of TGF-beta1. From these results, it is concluded that procyanidin B-3 can directly promote hair epithelial cell growth in vitro, has the potential to counteract the growth-inhibiting effect caused by TGF-beta1 in vitro, and has potential to stimulate anagen induction in vivo.

PMID: 12473061 [PubMed - indexed for MEDLINE] "


Thats what pubmed has on that subject, now I may be comparing apples and organges here, as contact inhibition isn't mentioned, but TGF-beta 1 (as the proanthocyandins that Stephen thinks would be good for both edema and baldness) is also mentioned. These are extracted from barley. A little beer and eggs shampoo anyone.


Recently a guy had a great post on another site about lavendar oil-skin products and gynochomostia in pre-adolescent boys. It turns out that lavendar oil has alot of estrogen-mimicking compounds. Potential anti-androgen treatment from an old essential oil here? I think thats interesting in that using a compound that mimicks estrogen may not see an uptick in androgen-receptor production.........neat stuff.

 

[S Foote.]

One aspect of the mouse study that the two of you have both missed (unless I didn't see your response on it) is the fact that IT SHOULD NOT MATTER WHETHER THOSE MICE HAD ANY ANDROGENS AT ALL.


Men who get castrated dont see their vellus follicles "regenerate" as well as terminal sized follicles do on their heads. But vellus hairs from male pattern baldness-men transplanted on those mouse backs DID regenerate as well as the terminal follicles transplanted from the backs and sides of the heads from the same men to those mice. That alone, regardless of the androgen levels in the mice, is signifigant. Norman Orentriech http://www.orentreich.org/report04.htm and his foundation, OFAS, is looking into this apparently "Balding Hairs Grow Long and Thick on Immunodeficient Mice
Because immunodeficient mice do not reject foreign tissues, they will accept transplants of human hairs that can then be studied. We transplanted both miniaturized and normal hair follicles from scalp affected by common balding. Our study found that miniaturized hair follicles can quickly regenerate once removed from the human scalp; in fact they grew as well as or better than the transplanted normal, non-balding hair follicles as assessed by their diameter and length achieved at 22 weeks.
Krajcik RA, Vogelman JH, Malloy VL, Orentreich N.
Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice. Journal of the American Academy of Dermatology 48(5):752-59, 2003"

That really is fascinating. Whether the immune sytem supresses male pattern baldness hairs or it is in fact an unrecognized edema of the scalp where drainaige is bad ought to be somewhat encouraging for young men just starting to resist male pattern baldness.

There is no doubt Michael that this particular mouse study is a landmark study, and needs to be repeated with more detail.

As i have said before, i think the results are due to the fibrotic tissue differences in the healing in immune deficient mice. This is something that could easily be determined by specific histology tests.

I just cannot see any real hard evidence for a directly mediated immune action "causing" male pattern baldness follicles.

S Foote.

 

[S Foote.]

Excuse me, but you haven't answered my question. Let's try it again: Can you suggest any explanation for why androgens would affect hair follicles that way ONLY in vitro, but not in vivo?

Err?

Didn't you understand the references i posted to the basic differences in genetic expression of various factors in DP cells in-vitro, compared to in-vivo?

Is that the best you can do? I challenge you by asking a SPECIFIC question about hair follicles and androgens which you're unable to answer, so you try to disguise that fact by citing something completely different about other in vivo and in vitro effects, hoping that people will think you answered my question? :wink:

Weak, Stephen. Really really weak.

I have answered your "specific" question Bryan, just by quoting the only "actual" in-vivo testing that is rellevant to your claim! :roll:

You are trying to claim that there is no evidence that the same in-vitro mechanism of androgen growth restriction of follicles that are "already" male pattern baldness follicles, is not "also" what happens in-vivo.

That mouse study proves you wrong, simple! You can complain all you like about this but you cannot reasonably argue with the science! :wink:

There is of course one other recognised fact that disproves your disillusioned claim that androgen inducible TGF beta-1 (the in-vitro effect), is what also happens in-vivo!

The in-vitro suppresion of pre-existing male pattern baldness follicle cells by androgens, is through androgen induced expression in those cells of TGF beta-1. This is a very simple "internal" action within these cells, that "NOTHING" that did not effect internal androgen levels, or the expression or blocking of TGF beta-1 could possibly effect!

So if your claim that this is what is stopping male pattern baldness follicle enlargement in-vivo is correct, how the hell can Minoxidil increase male pattern baldness hair growth?????

Minoxidil has no effect at all on the mechanisms you claim cause male pattern baldness, so how could it possibly change the situation Bryan? :freaked:

The truth is that we all know minoxidil increases hair growth in male pattern baldness, in fact you yourself have often quoted studies that show minoxidil has more effect that anti-androgen treatments in male pattern baldness!! 8)

LOL!!! I've asked you repeatedly to explain how contact inhibition would alter cells to become sensitive to androgens, or even just to provide ONE known example of such a thing happening in the field of biology, but you stand mute before the court, unable to provide any such evidence. You're a HYPOCRITE, Stephen!

Those people that are reading this debate, and have also followed our previous debates, now know what a liar you are Bryan. :wink:

They know that i have responded to this same old question of yours many times before!

Once again, the mechanism of the "direct" action of androgens on male pattern baldness follicle cells in-vitro, is via the TGF beta-1 pathway.

Prior contaqct inhibition in-vivo, is known to alter the gene expression involved in the TGF beta-1 pathway.

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

The key words in this abstract are "common mechanisms"! I wonder how many future posts it will take, for you to once again try to claim i have not answered this question. 8)

LOL!! I don't care about common mechanisms, Stephen! ANSWER THE QUESTION THAT I ASKED YOU! Explain to me how contact inhibition would cause cells to become sensitive to androgens, and give me an example in biology where that has actually happened! You can't do it, and you know it! :wink:

Just because contact inhibition may in fact cause the expression of TGF-b1 and androgens also cause the expression of TGF-b1, that says absolutely NOTHING about whether or not contact inhibition causes cells to become androgen-sensitive. That's one of the STUPIDEST things you've ever said in this debate. You should be embarrassed. That's like saying that since the flu causes a fever, and typhoid fever causes a fever, then getting the flu makes you get typhoid fever.

Bryan

So yet again you expect me to prove every last detail of my arguments, whilst you just expect everyone to take your word Bryan! :roll:

You say you don't care about common mechanisms, but "real" scientists "DO" Bryan :wink:

You asked me to explain how prior contact inhibition that changes the very basic growth response of all normal cells, could result in a different response to androgen induced TGF beta-1 in-vitro?

I have answered your question by referencing studies relevant to the question. This is the way scientific theories are defended, by reference to hard evidence Bryan, try to learn something about the scientific process Bryan! :roll:

Now do me the courtesy of supporting "your" opinions within the same rules Bryan? :wink:

You launched a personal attack on my theory by quoting a 50 odd year old transplantation study.

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

This rant of yours has been shot to pieces by more modern research, and i asked you to justify your opinion in the light of this latest study that i posted in this thread.

http://content.karger.com/ProdukteDB/pr ... =92842.pdf

Everyone can see how you refused to respond to me, instead choosing to respond to Michael about this with some irrelevant babble 8)

Quote: (again!)


________________________________________________


Evaluation of Hair Transplantation into
Various Recipient Sites: Lower Leg, Nape
of the Neck, Palm, Hand Dorsum, Lower
Back and Wrist
S.T. Hwang
Dr. Hwang’s Hair Clinic, Seoul, Korea


In 1998, scalp hairs were transplanted to the lower leg. Three years
later, some of the scalp hairs previously transplanted on the lower leg
were re-transplanted to the nape of the neck near the occipital scalp.
Hair transplantation to the palm, hand dorsum, lower back was done
in 2001. We reported different hair growth characteristics according
to the recipient site. The purpose of this study is to evaluate whether
the transplanted hairs show different growth characteristics during
long-term follow-up. The survival rate, growth rate and hair diameter
were measured at the 8 years post surgery. The results showed:
(1) The survival rate and growth rate of the transplanted hairs is influenced
by the recipient site.
(2) The cycles of the transplanted hairs may change according to the
recipient area. rather than being fixed by the internal clock of hair
follicles.
(3) The hair growth rate may change immediately after transplantation
according to the recipient site and is maintained afterwards.
(4) The volume of transplanted hair follicles may not change regardless
of the recipient site.
(5) Skin thickness and/or blood vascularity play a role in hair growth and survival.


_______________________________________________________



Now i know "if" you respond, it will be with a lot of if's but's and may be's. but that won't fool anyone Bryan, and if you were man enough you would just admit you are out of touch with modern research. :wink:

S Foote.

 

[michael barry]

Stephen, I get stuck on number 4 in that study's conclusions.

Ive studied body hair transplants pretty thoroughly. The one pertinent thing that Ive noticed about them is that although the guys body hair starts growing long on their heads, the wavyness of the hair still remains somewhat. MOST IMPORTANT however is the diameter of the hair (the volume as the researchers seem to indicate) does not seem to change to me.

I'll post a good picture of one here for you and Bryan to look at:
http://www.bodyhairtransplant.blogspot.com/ About halfway down that guys page he has pictures of his body hair transplant to his head. This guy is in grad school in cancer research, so he is VERY smart. He had a failed scalp reduction in the past. The circumference and texture of the body hair hasnt changed all that much, but as you can see he is definitely getting length. What you see on him cost over 30 thousand dollars in the pictures. Everything you see on this guys head in the second set of pictures is his body hair http://www.myhairtransformation.com/


I'd love to get a look at those in person. Both these guys do minoxidil on their heads. Ive mentioned peptides and proanthocyanidins as growth stimulants with no anti-androgenic properties. Ive wondered if one of those three main stimulants (and caffeine) might have a "thickening" effect on body hair moved to the head. Those are the two most extensive BHT's I know of, however there are more men getting those things every day, so in a couple of years we should know for sure (I can guarantee you men will be using growth stimulants on the body hair) if the body hair can, with chemical help, "widen". My interpretation of that study is that the body hair wont get "fatter" without some external stimulant.

 

[Bryan]

LOL!! I don't care about common mechanisms, Stephen! ANSWER THE QUESTION THAT I ASKED YOU! Explain to me how contact inhibition would cause cells to become sensitive to androgens, and give me an example in biology where that has actually happened! You can't do it, and you know it! :wink:

Just because contact inhibition may in fact cause the expression of TGF-b1 and androgens also cause the expression of TGF-b1, that says absolutely NOTHING about whether or not contact inhibition causes cells to become androgen-sensitive. That's one of the STUPIDEST things you've ever said in this debate. You should be embarrassed. That's like saying that since the flu causes a fever, and typhoid fever causes a fever, then getting the flu makes you get typhoid fever.

So yet again you expect me to prove every last detail of my arguments, whilst you just expect everyone to take your word Bryan! :roll:

No, Stephen, I want you to prove JUST THIS ONE LITTLE THING that you've been claiming for a long time! :wink:

You asked me to explain how prior contact inhibition that changes the very basic growth response of all normal cells, could result in a different response to androgen induced TGF beta-1 in-vitro?

No, I asked you to explain how contact inhibition could result in a different response to androgens. Note the subtle but important difference between those two statements.

I have answered your question by referencing studies relevant to the question.

No you haven't. Not the least little bit. That study you referenced never even USED the word "androgen" in its abstract, so it obviously doesn't say anything about contact inhibition causing a change in the way that cells respond to androgens!!

I'm going to give you a personal word of advice here, Stephen: I suggest that you go ahead and admit defeat on this specific issue, because I'm not going to let you slip away from this. Everybody knows now that you can't back-up that claim. _I_ know it, YOU know it, and everybody reading this thread up to this point knows it. It's not going away, Stephen, because I'm not letting it go away. Admit your mistake, take your lumps like a man, and then we'll move on to other matters...

Bryan

 

[S Foote.]

Stephen, I get stuck on number 4 in that study's conclusions.

Ive studied body hair transplants pretty thoroughly. The one pertinent thing that Ive noticed about them is that although the guys body hair starts growing long on their heads, the wavyness of the hair still remains somewhat. MOST IMPORTANT however is the diameter of the hair (the volume as the researchers seem to indicate) does not seem to change to me.

I'll post a good picture of one here for you and Bryan to look at:
http://www.bodyhairtransplant.blogspot.com/ About halfway down that guys page he has pictures of his body hair transplant to his head. This guy is in grad school in cancer research, so he is VERY smart. He had a failed scalp reduction in the past. The circumference and texture of the body hair hasnt changed all that much, but as you can see he is definitely getting length. What you see on him cost over 30 thousand dollars in the pictures. Everything you see on this guys head in the second set of pictures is his body hair http://www.myhairtransformation.com/


I'd love to get a look at those in person. Both these guys do minoxidil on their heads. Ive mentioned peptides and proanthocyanidins as growth stimulants with no anti-androgenic properties. Ive wondered if one of those three main stimulants (and caffeine) might have a "thickening" effect on body hair moved to the head. Those are the two most extensive BHT's I know of, however there are more men getting those things every day, so in a couple of years we should know for sure (I can guarantee you men will be using growth stimulants on the body hair) if the body hair can, with chemical help, "widen". My interpretation of that study is that the body hair wont get "fatter" without some external stimulant.

I will take a look at the links and get back to you Michael, thanks.

S Foote.

 

[S Foote.]

LOL!! I don't care about common mechanisms, Stephen! ANSWER THE QUESTION THAT I ASKED YOU! Explain to me how contact inhibition would cause cells to become sensitive to androgens, and give me an example in biology where that has actually happened! You can't do it, and you know it! :wink:

Just because contact inhibition may in fact cause the expression of TGF-b1 and androgens also cause the expression of TGF-b1, that says absolutely NOTHING about whether or not contact inhibition causes cells to become androgen-sensitive. That's one of the STUPIDEST things you've ever said in this debate. You should be embarrassed. That's like saying that since the flu causes a fever, and typhoid fever causes a fever, then getting the flu makes you get typhoid fever.

So yet again you expect me to prove every last detail of my arguments, whilst you just expect everyone to take your word Bryan! :roll:

No, Stephen, I want you to prove JUST THIS ONE LITTLE THING that you've been claiming for a long time! :wink:

You clearly asked me in our initial debate to provide some evidence that contact inhibition in-vivo, "could" be altering the androgen response in-vitro that involves TGF beta-1.

Everyone here can see i have provided a precedent for such a possibility.

But no, you now demand absolute "PROOF" of my arguments :roll:

You asked me to explain how prior contact inhibition that changes the very basic growth response of all normal cells, could result in a different response to androgen induced TGF beta-1 in-vitro?

No, I asked you to explain how contact inhibition could result in a different response to androgens. Note the subtle but important difference between those two statements.

[quote="S Foote.":c2580]I have answered your question by referencing studies relevant to the question.

No you haven't. Not the least little bit. That study you referenced never even USED the word "androgen" in its abstract, so it obviously doesn't say anything about contact inhibition causing a change in the way that cells respond to androgens!!

I'm going to give you a personal word of advice here, Stephen: I suggest that you go ahead and admit defeat on this specific issue, because I'm not going to let you slip away from this. Everybody knows now that you can't back-up that claim. _I_ know it, YOU know it, and everybody reading this thread up to this point knows it. It's not going away, Stephen, because I'm not letting it go away. Admit your mistake, take your lumps like a man, and then we'll move on to other matters...

Bryan[/quote:c2580]

So you are saying that just because i cannot offer absolute proof of a mechanism, i should admit defeat ?

Does that mean that you are now going to admit defeat in your support of the current theory Bryan?

Because you cannot ever even test the "genetic clock" idea in follicles that is necessary for that theory to work, let alone prove it! 8)

Or as usual is it just me that has to "prove" everything, whilst the mighty Bryan Sheltons opinion should be good enough for everyone?

Your varying standards of proof and validity in science are just laughable Bryan. :roll:

Why don't you just concentrate on the real point most people are interested in here, instead of trying to divert from this by demanding absolute proof of my theory?

The current theory of male pattern baldness that people are sold treatments for, is falling apart at the seams!

Modern transplantation studies and the "doughnutting" issue, clearly go against the old donor dominance claims.

That one mouse study clearly refutes the direct action of androgens as a valid claim for the in-vitro mechanism.

Uno's studies clearly show the immunology is not responsible for androgen mediated follicle miniaturisation.

There is a host of experimental data now, that seriously refutes claims made by the old theory you continue to support Bryan!

So "YOU" prove your theory Bryan :wink:

The experimental evidence doesn't even provide you with circumstantial evidence, as you well know or you would have answered "MY" questions about these studies 8)

S Foote.