Question for Stephen Foote, with pictures for a point

[Bryan]

I gave you every chance to add such "subtleties" in your claim about the in-vitro tests! Yet you continued to claim androgens directly suppress male pattern baldness follicle growth, with no added "extra's"!

Oh, for f***'s sake. Do you really think I'm going to write a TOME every time I respond to you, in some hopeless effort to educate you??

As you pointed out "yourself" in the mouse study thread, you can lower androgen levels in humans below the level in those mice, and you still won't get the male pattern baldness follicle re-enlargement seen in those mice!

No sh*t, Sherlock. I've been explaining that to people on hairloss sites (starting with alt.baldspot) since prior to the turn of this century. Where were YOU when I was citing Hamilton's 1960 paper on the lack of hair regrowth in castrated men??

Then in a later thread, you go back to how you think the in-vitro tests prove the mechanism of in-vivo male pattern baldness for God's sake!

Correct. So what's your point? :wink:

Yet you knew full well that there was no possible influence of immunology in the in-vitro tests you "raved" about as "proof" :roll: Plus, you are even stupid enough to repeat this claim above :freaked:

You're talking about the immunodeficient mouse study, I presume? Yes, that provides some fairly compelling evidence for the IMMUNE component of human balding. So I ask again: what's your point? :wink:

So then tell us all about the role of the immune component in Sawaya's study, you "neglected" in your original claim?

There wasn't any. All she did was demonstrate the effects of androgens and antiandrogens on beard hair follicles and scalp hair follicles. That was the only point of her study. It wasn't DESIGNED to do any more than that.

Your continued attempts to distract from your proven hypocrisy in this thread now, only serves to further prove my point about how dishonest you are in these debates. :wink:

Yeah, right. You're the only intellectually dishonest person here.

Bryan

 

[S Foote.]

I gave you every chance to add such "subtleties" in your claim about the in-vitro tests! Yet you continued to claim androgens directly suppress male pattern baldness follicle growth, with no added "extra's"!

Oh, for f***'s sake. Do you really think I'm going to write a TOME every time I respond to you, in some hopeless effort to educate you??

[quote="S Foote.":8860e]As you pointed out "yourself" in the mouse study thread, you can lower androgen levels in humans below the level in those mice, and you still won't get the male pattern baldness follicle re-enlargement seen in those mice!

No $#iT, Sherlock. I've been explaining that to people on hairloss sites (starting with alt.baldspot) since prior to the turn of this century. Where were YOU when I was citing Hamilton's 1960 paper on the lack of hair regrowth in castrated men??

Then in a later thread, you go back to how you think the in-vitro tests prove the mechanism of in-vivo male pattern baldness for God's sake!

Correct. So what's your point? :wink:

Yet you knew full well that there was no possible influence of immunology in the in-vitro tests you "raved" about as "proof" :roll: Plus, you are even stupid enough to repeat this claim above :freaked:

You're talking about the immunodeficient mouse study, I presume? Yes, that provides some fairly compelling evidence for the IMMUNE component of human balding. So I ask again: what's your point? :wink:

So then tell us all about the role of the immune component in Sawaya's study, you "neglected" in your original claim?

There wasn't any. All she did was demonstrate the effects of androgens and antiandrogens on beard hair follicles and scalp hair follicles. That was the only point of her study. It wasn't DESIGNED to do any more than that.

Your continued attempts to distract from your proven hypocrisy in this thread now, only serves to further prove my point about how dishonest you are in these debates. :wink:

Yeah, right. You're the only intellectually dishonest person here.

Bryan[/quote:8860e]

To anyone here who may still think Bryan has any credibility in matters of "real" science, consider this?

According to Bryans "expert" opinion, he claimed that the in-vitro tests proved the mechanism of in-vivo male pattern baldness. That is that androgens were "directly" causing male pattern baldness follicle miniaturisation and "directly" keeping them in this condition.

These in-vitro responses of male pattern baldness follicles to androgens, happened in the total absense of "ANY" kind of immune reaction!

So according to Bryan's "proof", the exact same reactions should have happened in that mouse study because here also there was a complete lack of any immunology.

But in actual fact, exactly the opposite happened! In-vivo, human male pattern baldness follicles enlarged in the "same" absense of immunology, whilst completely ignoring the presense of more than enough androgens to keep them miniaturised according to "one" of Bryans opinions!

This is the actual science that proves Bryan wrong in the in-vitro debate.

Your continued "spin" to try deny your past posts, dosen't fool anyone here Bryan. :wink:

You haven't got a clue about the proper evaluation of scientific evidence, and the more you try to deny your past posts, the more ridiculous you make yourself look. :roll:

If you had any sense, you would just shut the hell up :wink:

S Foote.

 

[Bryan]

According to Bryans "expert" opinion, he claimed that the in-vitro tests proved the mechanism of in-vivo male pattern baldness. That is that androgens were "directly" causing male pattern baldness follicle miniaturisation and "directly" keeping them in this condition.

These in-vitro responses of male pattern baldness follicles to androgens, happened in the total absense of "ANY" kind of immune reaction!

So according to Bryan's "proof", the exact same reactions should have happened in that mouse study because here also there was a complete lack of any immunology.

But in actual fact, exactly the opposite happened! In-vivo, human male pattern baldness follicles enlarged in the "same" absense of immunology, whilst completely ignoring the presense of more than enough androgens to keep them miniaturised according to "one" of Bryans opinions!

This is the actual science that proves Bryan wrong in the in-vitro debate.

Are you RETARDED? How many times do I have to tell you that we don't know the level of androgens in those mutated mice? Furthermore, the follicles didn't "enlarge" all that much. Their growth is stunted when transplanted onto mice. Explain THAT, Junior.

Bryan

 

[wookster]

The question seems to be, how is the :x immune response :x triggered by DHT?

 

[S Foote.]

According to Bryans "expert" opinion, he claimed that the in-vitro tests proved the mechanism of in-vivo male pattern baldness. That is that androgens were "directly" causing male pattern baldness follicle miniaturisation and "directly" keeping them in this condition.

These in-vitro responses of male pattern baldness follicles to androgens, happened in the total absense of "ANY" kind of immune reaction!

So according to Bryan's "proof", the exact same reactions should have happened in that mouse study because here also there was a complete lack of any immunology.

But in actual fact, exactly the opposite happened! In-vivo, human male pattern baldness follicles enlarged in the "same" absense of immunology, whilst completely ignoring the presense of more than enough androgens to keep them miniaturised according to "one" of Bryans opinions!

This is the actual science that proves Bryan wrong in the in-vitro debate.

Are you RETARDED? How many times do I have to tell you that we don't know the level of androgens in those mutated mice? Furthermore, the follicles didn't "enlarge" all that much. Their growth is stunted when transplanted onto mice. Explain THAT, Junior.

Bryan

This last response of yours just proves my point about your U turns, and hypocrisy Bryan, and "YOU" call "ME" retarded!

You were pretty sure that the level of androgens in those mice, was more than enough to effect male pattern baldness follicles when you posted the study!

You said as much to daytona when "HE" raised that point you are "NOW" trying to push yourself. People can see what you said above Bryan, so there's nowhere for you to hide on this blatent contradiction you are patheticaly still trying to squirm out of!

The author of the mouse study was sure enough about normal gender levels of male hormones in those mice, or why bother comparing male and female mouse reaction?

There was certainly enough androgens produced in those male mice to produce normal sexual developement! They were "NOT" psuedohermaphrodites were they! You would have realised the importance of that fact yourself Bryan, if you had any scientific talent. :roll:

So there was more than enough androgens to "directly" supress male pattern baldness follicle growth, as you claim happens in-vivo.

Your opinion is that it is not the level of androgens that create male pattern baldness, but the "genetic sensitivity" of the follicle DP cells? In male pattern baldness the DP is miniaturised, so less DP cells require less androgens to maintain any "direct" growth supression in the first place.

So even if normal mouse levels of androgens "were" reduced in those mice, and the evidence is they were normal (see above), there would still be more than enough to "directly" supress male pattern baldness follicle growth (according to "YOUR" claims Bryan!!!)



Apart from exposing your hypocrisy Bryan, that mouse study also represents the perfect in-vivo test of your claim that the in-vitro tests "truly" reflect what happens in-vivo! Now remember you are on the record as saying this.

There was no immunology in the in-vitro tests, and no immunology in the mouse in-vivo test. So if your claim about the in-vitro tests was true, the exact same result should have been seen in those mice?

You were obviously completely "WRONG" about the relevance of the in-vitro tests, as i said at the time. :wink:

Furthermore, the follicles didn't "enlarge" all that much. Their growth is stunted when transplanted onto mice. Explain THAT, Junior.

So you don't consider an enlargement of 400% to be "much" then Bryan? That's strange, because when you posted that study you "raved" about the "exeptional" ability of these male pattern baldness follicles to regenerate!!!

You said quote:

"The abstract gives the salient points: they found that fine vellus hairs from balding human scalps had an EXCEPTIONAL ability to regenerate, when transplanted onto test mice that had severe immune deficiency (they use those for transplant experiments so that the mice don't suffer rejection of the foreign tissue). In fact, after about 5 to 6 months, transplanted follicles with vellus hairs regrew to the same size as the transplanted terminal hairs in one set of mice, and actually grew LARGER than the terminal hairs in another set of mice (for which phenomenon they don't yet have any explanation)! Here's an extended excerpt from the Discussion section at the end in which they speculate about the various implications of their findings:"

If people reading this thread didn't believe your contradictions before, they do now Bryan. 8)

S Foote.

 

[S Foote.]

The question seems to be, how is the :x immune response :x triggered by DHT?

There is no evidence that there is any "direct" immune attack on male pattern baldness follicles. Certainly there is immunology going on around male pattern baldness follicles, and this does have effects on follicle growth later on. But Uno's work clearly showed androgen related male pattern baldness, can happen in the absense of significant immunology.

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

I don't think the fact these mice had no immunology, was the reason for male pattern baldness follicle re-growth. I also think the fact that the male pattern baldness follicles enlarged, whilst already enlarged follicles didn't and actualy shrank, can be explained.

But first i want to see Bryans explaination for that according to "his" theory?

S Foote.

 

[michael barry]

Stephen


The macaque baldness happens without any inflammation or fibrosis.
1) Would you agree that if the above statement is true, then that reflects
androgens having a *direct* effect upon them?


2) I had asked you earlier in the thread, but you proboably missed the
question, about accupunture to poke holes in the galea, thereby
making better drainage possible. Accupunture is used in edema, think
this might help? Ive heard of some Aryuvedic docs using accupunture
for baldness, but didnt think that even worth lookin' into. Have you
ever researched this. The accupunture is widely accepted to combat
edema, and if it punctured the galea, which you suggested helps back
up fluids at the top dermal layers..............it stands to reason that this
would be helpful if your theory was right.


3) Bryan posted an experiment by Sawaya that showed entire follicles
that were cultured for 14 days, having a direct effect to androgens
(slowed keratinocytes 23%, DNA and RNA by 12%). Alpecin's studies
at the University of Jena and Bonn cultivated 600 hairs for 6 to 10 days
from men with Androgenetic Alopecia with testoserone (not DHT though). They found that
hairs cultivated with testosterone slowed keratinocyte activity as
opposed to hairs cultivated with no testosterone. Again, these were
whole hairs. The difference was not so great (like Sawaya's) that you
would expect Testosterone alone to shut a follicle down however (I cant
recall the exact figures----this is to be presented at the EHRS conf-
erence next month). Why do you think these experiments with WHOLE
HAIR follicles are "flawed"? Do you not accept that androgens have a
direct effect in vivo? Do you believe that human hair follicles only
develop a direct effect to androgens after an edema has pressured
them for a while?

4) Ive never looked into it throroughly, but is contact inhibition the reason
that lymphoedema is speculated to cause body hair to be lost? You
can save me a little web work with that answer. : )


5). If you speculate that edema of the scalp could be relieved (and hair follicles saved) by a surgery to cut blood flow to the scalp, do you think a severe edema of a womans leg could be relieved by a ligature also? If so, is it tried anywhere that youve seen? It would be interesting on garnering a doctors opinon on that who specializes in it.

 

[S Foote.]

Stephen


The macaque baldness happens without any inflammation or fibrosis.
1) Would you agree that if the above statement is true, then that reflects
androgens having a *direct* effect upon them?

No Michael, i dont think the body of evidence supports that at all.

There are far more logical "indirect" ways androgens can effect follicles, based on already accepted medical principles.

The later generation of immune problems in human male pattern baldness, is perfectly in line with the proven tissue effects of edema. The only difference between macaque and human male pattern baldness in terms of edema, is the scale of this. In macaques, the edema miniaturises the follicles, but doesn't increase much beyond the level required to do this. In humans the edema continues to build up, so increasing the immune sensitivity.

2) I had asked you earlier in the thread, but you proboably missed the
question, about accupunture to poke holes in the galea, thereby
making better drainage possible. Accupunture is used in edema, think
this might help? Ive heard of some Aryuvedic docs using accupunture
for baldness, but didnt think that even worth lookin' into. Have you
ever researched this. The accupunture is widely accepted to combat
edema, and if it punctured the galea, which you suggested helps back
up fluids at the top dermal layers..............it stands to reason that this
would be helpful if your theory was right.

By itself i don't think such "perferation" of the galea would amount to much. There is a procedure to remove the galea that is claimed to help in male pattern baldness, but this is only one part of the problem in my opinion.

3) Bryan posted an experiment by Sawaya that showed entire follicles
that were cultured for 14 days, having a direct effect to androgens
(slowed keratinocytes 23%, DNA and RNA by 12%). Alpecin's studies
at the University of Jena and Bonn cultivated 600 hairs for 6 to 10 days
from men with Androgenetic Alopecia with testoserone (not DHT though). They found that
hairs cultivated with testosterone slowed keratinocyte activity as
opposed to hairs cultivated with no testosterone. Again, these were
whole hairs. The difference was not so great (like Sawaya's) that you
would expect Testosterone alone to shut a follicle down however (I cant
recall the exact figures----this is to be presented at the EHRS conf-
erence next month). Why do you think these experiments with WHOLE
HAIR follicles are "flawed"? Do you not accept that androgens have a
direct effect in vivo? Do you believe that human hair follicles only
develop a direct effect to androgens after an edema has pressured
them for a while?

My opinion is that "any" in-vitro testing of growth potential of organs including hair follicles, has to be suspect? Both the culturing itself and the potential growth in the test tube, cannot possibly reflect the more complex in-vivo situation.

This is why that mouse study is so important. It studies "genuine" human male pattern baldness follicles within the mammalian dermal system. Look what happened compared to the in-vitro speculations!

4) Ive never looked into it throroughly, but is contact inhibition the reason
that lymphoedema is speculated to cause body hair to be lost? You
can save me a little web work with that answer. : )

That is what i propose Michael, but there is a lack of research into the amount of tissue fluid pressure, and follicle size. I wish there was more!

If you search the web on this question, you will find that anything that causes edema, can also be shown to cause hair loss.

5). If you speculate that edema of the scalp could be relieved (and hair follicles saved) by a surgery to cut blood flow to the scalp, do you think a severe edema of a womans leg could be relieved by a ligature also? If so, is it tried anywhere that youve seen? It would be interesting on garnering a doctors opinon on that who specializes in it.

I think that reducing the blood feed to an edemous leg, could be dangerous because it would reduce the circulation that helps to move "some" of this edema via the normal circulation.

In the case of an edemous leg, gravity plays a major role in the venous drainage, and veins in this area also have one way valves.

It is a completely different situation to the circulation in the scalp. But i do think the human circulation as a whole is sadly lacking in this kind of original research.

S Foote.

 

[michael barry]

Stephen wrote: "There is a procedure to remove the galea that is claimed to help in male pattern baldness, but this is only one part of the problem in my opinion."


Stephen, Im STRONGLY of the opinion that if the galeaotomies that the Sweedish doctors were performing decades ago worked worth a damn, we'd have seen many before-and-after pictures of them plastered all over various websites, and they would be more popular than hair transplantation. I really dont think those things worked, but they were sold. Ive yet to even read a testomonial on any hairloss discussion board detailing how happy any recipient was.


Dr. Uno didn not detect any immunology or edema in the macaques. You could write him and ask him his opinion of this?



By the way, nosy as I am, I bought some proanthocyanidins (PolyGro). I can see why they would be very useful in edema cases. Its sort of like when youre a kid and spill apple juice on yourself. Stuff gets sticky and contracts when it dries. Your head feels like a piece of leather that has gotten wet, being squeezed.

The proanthocyanidins that PolyGro sells aslo has Bryan Shelton's favorite ingredient, Tocopherol in them. Its contents are: deionized water, proprietary apple proacyanidins 4%, denatured alchohol, aloe leaf extract (thats for nitric oxide release almost surely), ascorbyl palmitaete, tocopherol, retinyl palmitate, propylene glycol, fragrance (smells vaguely of apple juice). Stuff is made from GREEN apples, not red. I think Waseda's recipie for this stuff is proboably just as good. Think I'll make my own from here on out.

 

[michael barry]

More on Galeotomies:

Scalp Transplanted to the Skin of the Arm in Male Pattern Baldness", Rolf E. A. Nordstrom, Acta Derm Venereol 1979; 59: 266-268), which include the first three paragraphs:

"During the past few decades, several hypotheses concerning the etiology of male pattern baldness (male pattern baldness) have been presented. In 1933, Wadel reported findings of decreased motility of the scalp. He was convinced that this decrease was due to the fact that in male pattern baldness patients the scalp is both frontally and sagittally too short, and thus it has to be stretched like a too-small cap to cover the relatively too-big skull. For hair nutrition and rooting this persisting tension creates unbearable conditions, leading to gradual loss of hair. In 1935 he wrote that male pattern baldness is the end result of the tension atrophy of the scalp covering the galea aponeurotica. This atrophy is caused by a disproportion between the skull bone and the galea aponeurotica, due to an isolated growth of the skull bone to which the tendon-like structure of the galea is not able to adapt. He reported excellent results in the treatment of male pattern baldness with 'loosening' massage to the scalp.

"In 1941, Kessler started experimental work with frontal galeotomies in order to reduce the supposed increased tension of the galea aponeurotica. In 1961 he reported a success rate of 87% with this treatment of male pattern baldness. At that time this operation was popular in Europe. In 1963, Ponten reported that after frontal galeotomy he could not find any objective improvement in his 56 patients and he still holds this view concerning this operation (personal communication, 1976).

"The present author has seen several patients who have undergone frontal galeotomy and later developed an advanced degree of male pattern baldness. The popularity of this operation has waned."

And here is what he says in the Discussion section at the end:

"In the receding hairline and in the graft taken from it the loss of hairs remains synchronous even though the latter is transplanted to a remote skin area. In male pattern baldness the 'balding clock' in the follicle or in its very close surrounding keeps time even when the follicle is transplanted to the skin of the forearm. The presence or absence of the galea aponeurotica does not influence the balding process in male pattern baldness. Nor does the supposed increased tension of the scalp or its muscles or a diminished vascular supply to the scalp have an effect on balding. Neither do any other factors localized to the head cause balding. The cause seems to lie in the follicle itself or its very close surrounding. The graft taken from the denuded area did not grow new hairs, and so the male pattern baldness process of the hair follicle is not reversed by a change in its location on the human body


Thats cut out of a very old post from Bryan, which I know you'll hate, but the citations are in order. The verdict on galeotomies is that only one clinic in the world I could find online, Wellnessklinic in Amsterdam/Belgium still performs it. Despite the fact they have pictures of the results of every other cosmetic procedure that they perform, and they do everything from tummy-tucks, boob jobs, cellulite, hair transplants, face-lifts, etc. They DONT HAVE ONE SINGLE BEFORE AND AFTER of the galeotomy. Even a pic of years afterwards to prove that it stops loss. I cant buy this would work. If it did, docs would much rather perform it (because it just takes 45 minutes) than to perform an extensive transplant. If it were a cure, they'd push it on really young men as a way to stop further loss and it really would be a "Cure" as every 18 year old who was afraid he might bald would get one and be through with worrying about baldness.

 

[wookster]

I have a scar on the right temple area of scalp that has hair growing around the periphery of the scar. Hairs that if they are genetically programmed male pattern baldness hairs then they should have miniaturized, but they have not. The other temple is bare though. :freaked: Something is not quite right, with the current "donor dominance" idea.

 

[wookster]

:hairy:

http://www.ncbi.nlm.nih.gov/entrez/quer ... uery_hl=31

Nitric oxide in the human hair follicle: constitutive and dihydrotestosterone-induced nitric oxide synthase expression and NO production in dermal papilla cells.

Wolf R, Schonfelder G, Paul M, Blume-Peytavi U.

Department of Dermatology, University Medical Center Benjamin Franklin, Free University of Berlin, Berlin, Germany.

The free radical nitric oxide, generated by different types of epidermal and dermal cells, has been identified as an important mediator in various physiological and pathophysiological processes of the skin, such as regulation of blood flow, melanogenesis, wound healing, and hyperproliferative skin diseases. However, little is known about the role of NO in the human hair follicle and in hair cycling processes. Here we demonstrate for the first time that dermal papilla cells derived from human hair follicles spontaneously produce NO by measuring nitrate and nitrite levels in culture supernatants. This biomolecule is apparently formed by the endothelial isoform of nitric oxide synthase, which was detected at the mRNA and protein levels. Remarkably, basal NO level was enhanced threefold by stimulating dermal papilla cells with 5alpha-dihydrotestosterone (DHT) but not with testosterone. Addition of N-[3-(aminomethyl)benzyl]acetamidine (1400W), a highly selective inhibitor of inducible nitric oxide synthase, restrained the elevation in NO level induced by DHT. Analyses of DHT-stimulated cells at the mRNA and protein levels confirmed the expression of inducible nitric oxide synthase. These findings suggest NO as a signaling molecule in human dermal papilla cells and implicate basal and androgen-mediated NO production to be involved in the regulation of hair follicle activity.

 

[S Foote.]

Hi Michael.

Yes, i agree the galea "theory" doesn't in itself hold water (pun intended).

But as i said, i think the galea does have some influence upon defining the edge of the male pattern baldness area.

It would be interesting to see if those who had the galea removed and still suffered male pattern baldness, had more of a thinning area at the edges?

S Foote.

 

[S Foote.]

I have a scar on the right temple area of scalp that has hair growing around the periphery of the scar. Hairs that if they are genetically programmed male pattern baldness hairs then they should have miniaturized, but they have not. The other temple is bare though. :freaked: Something is not quite right, with the current "donor dominance" idea.

That's very interesting.

I think it is the formation of scar tissue close to follicles transplanted to the male pattern baldness area, that allows these to survive long term.

I think the fibrose scar tissue forms around transplanted follicles, acting as a scaffold to preserve the space for future anagen enlargements.

I would love to see an experiment where follicles still in full anagen in the balding male pattern baldness area, were just "punched" externaly with a 1mm hollow punch.

They should then not be effected by male pattern baldness according to my theory?

S Foote.

 

[michael barry]

Stephen,

If you could obtain a pre-pubescent stumptailed macaque and perform the surgery you suggest on it.................you could test your theory. If cutting blood flow to the little critters scalp saw it NOT go bald, I guess that means youre right.

The "punch" idea you have is doable if you can find someone to try it on who doesnt mind a scar. Have you approached an edema specialist with this? A transplant Doctor wouldnt do it.

Are you having any luck with your efforts to get your idea systematically tested on a subject or two with any doctors in the position to do so? One macaque could proboably prove or disprove your work...

 

[S Foote.]

Stephen,

If you could obtain a pre-pubescent stumptailed macaque and perform the surgery you suggest on it.................you could test your theory. If cutting blood flow to the little critters scalp saw it NOT go bald, I guess that means youre right.

The "punch" idea you have is doable if you can find someone to try it on who doesnt mind a scar. Have you approached an edema specialist with this? A transplant Doctor wouldnt do it.

Are you having any luck with your efforts to get your idea systematically tested on a subject or two with any doctors in the position to do so? One macaque could proboably prove or disprove your work...

Believe me Michael, i am trying my best to get testing relating to my theory done by those in a position to do it. But this isn't easy, as i am an engineer not a medical man.

There is an inbred resistence in medicine to "rocking" the establishment boat! Particularly when the questions are coming from "outside".

There is no way the transplantation industry would help here. Could you imagine the fallout if it is proven they have been selling procedures based on a false premise?? :freaked:

I did email the Orentreich Foundation, and asked if i could contact Prof Orentreich to discuss that mouse study.

http://www.orentreich.org/report04.htm

This was weeks ago, and i have yet to get any response.

S Foote.

 

[michael barry]

Stephen,

A balding edema doctor, or a balding dermatolgist, or a balding surgeon of some kind might be a better bet. I really doubt Orentriech would want to test something if it disproved donor dominance, which he came up with.

Stephen,

Man, Ive been telling myself for YEARS, based on an article that I read about the time that minoxidil came out that prophesized that the cure for baldness was only a matter of time, that a balding scientist, pissed off at losing his hair, was going to cure baldness for us.

Dr. Paul Kemp of Intercytex, proboably the foremost tissue engineering expert in the world, might be that man in a sense that he could come up with a protocol, cloning stem cells to be injected in the scalp, therefore giving you new hair, to come up with a "defacto" cure. RU58841 sure as hell looked like a cure as far as stopping hairloss in its tracks, but no company has picked up the ball. Getting lost hair in the front to regrow seems more or less undoable past just getting perhaps a percentage of it back even with dutasteride/proxiphen.......just dont see it. The fibriotic damage is just too much, and even if you dont have fibrosis, the follicles that are long miniaturized have just seen too much apoptosis to regenerate. Gene cures are decades away according even to the researchers. It will be a long year or so before ICX announces the results of its Phase 2. I think Anderans is obsessed with direction issues and is lagging way behind. I dont look for anything from them for a couple of more years on the testing front or new news.

I think it will be a dead time in hairloss for a while man. I dont see anyone coming up with much anything new to "turn back on" genetic instructions in dermal papillas to "regrow" hair again, no matter fluid pressure, fibrosis, etc. anyway. The Proctor and Gamble fling with Curis is particularily humiliating to me as they reason because they can shave a phucking mouse's back and make the hair grow back fast, that they have discovered something useful which we both know in terms of androgenic human alopecia means very little. I imagine the hair transplant business will be really advertising hard over the next year or so of "dead time".

Ive looked into everything man. Body hair, facial hair, some outfit in Arabia that claims that by taking one hair follicle from a 3-hair follicular unit in the back of your head sees it regenerate a 3 hair follicular unit in the front and the old, back-of-the-head-follicular unit that just has two hairs compensate by growing a brand new third hair. (Im strongly inclined to think thats bullshit). Ive looked into Gho's HST (can only move 500 hairs a day at an very high price reportedly, even though some 80-90% donor regeneration is possible). Nada. Until cloning, I dont think much anything will give us our old hairlines and frontal sides back unless you risk a transplant and hope you can keep any more hair from falling (a fool's bet to me, especially as one moves through the decades).

 

[wookster]

:hairy:

http://www.hairsite4.com/dc/dcboard.php ... &mode=full

"DHT can actually be used to treat benign
prostate hypertrophy (BPH)!"
As I started to explain before, DHT is a strong androgen that will signal the pituitary to decrease the production of gonadotropins. The decrease in gonadotropins will then cause less testosterone to be produced which will in turn cause the estrogen levels to drop. The resulting change in the hormonal milieu (high DHT, low estrogen) then apparently results in a regression of BPH. The clinical application of this theory is discussed in US patent 5,648,350 Dihydrotestosterone for use in androgenotherapy.

http://www.reformmag.com/Reform5/PDFs/Features/DHT.pdf

In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50% .

Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09. + .16.31 grams before treatment and from 26.34. + -. 12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P= 0.01).

[...]


Conclusion

Unfortunately, people seem to have a natural tendency to classify things as either good or bad, black or white with absolutely no gray areas. DHT (like estrogen) has recently been on everyone's bad list, and is often considered to be a hormone that serves no function in the body except to cause harm. Now that you have all the necessary facts you can ultimately see, this view is far from the truth.

In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that don't really need it should be highly reconsidered. After reading this I hope you'll agree with me or at least keep an open mind on this sensitive subject. In other words, why don't you just give DHT a break.

:hairy: :hairy:

 

[Bryan]

You were pretty sure that the level of androgens in those mice, was more than enough to effect male pattern baldness follicles when you posted the study!

HUH?? I'm not sure about any such thing.

You said as much to daytona when "HE" raised that point you are "NOW" trying to push yourself. People can see what you said above Bryan, so there's nowhere for you to hide on this blatent contradiction you are patheticaly still trying to squirm out of!

I've addressed this point a few times already, if only you had the wit to understand. There are two extremest positions on the subject of androgens: kooks like like you and Armando who apparently don't believe that they have any direct effect at all on hair follicles (you seem to have done an about-face on that again, after having made some recent progress), and people like my pal "maneless" who think they are EVERYTHING when it comes to hairloss, that all you have to do to get back your hair is lower androgens sufficiently (if your hair hasn't COMPLETELY regrown, then you haven't lowered androgens enough! ).

For that reason, I find myself having to walk a reasonable middle-ground between the extremests on one side (you) and the extremests on the other side (maneless et al). Human balding has components of both androgen-sensitivity AND immune issues. I often find myself emphasizing the proven androgenic issues to flakes like YOU who refuse to believe them, and the things having to do with immunity to other people (like "daytona" in this case) who may be trying to suggest that it's androgens ALONE that are at play. As someone who walks that reasonable middle-ground, I have to take pot-shots from both sides! It's the cross I have to bear! :wink:

So if you consider it to be a "contradiction" just because I sometimes talk a lot about androgens on some occasions and immune issues on others, then go right ahead and feel that way. I couldn't care less.

So there was more than enough androgens to "directly" supress male pattern baldness follicle growth, as you claim happens in-vivo.

Nope. Sorry. That's sheer speculation on your part. BTW, you still haven't addressed why the growth of ALL follicles was stunted when they were transplanted onto those mice.

Your opinion is that it is not the level of androgens that create male pattern baldness, but the "genetic sensitivity" of the follicle DP cells? In male pattern baldness the DP is miniaturised, so less DP cells require less androgens to maintain any "direct" growth supression in the first place.

God, what an idiotic thing to say! Did you REALLY just say that, or am I dreaming? :wink:

Furthermore, the follicles didn't "enlarge" all that much. Their growth is stunted when transplanted onto mice. Explain THAT, Junior.

So you don't consider an enlargement of 400% to be "much" then Bryan? That's strange, because when you posted that study you "raved" about the "exeptional" ability of these male pattern baldness follicles to regenerate!!!

Maybe a 400% enlargement is impressive when it's due to a lack of any immune-system involvement. Maybe it would be GREATER STILL (like full regrowth all the way back to normal) if there were a complete lack of androgens in those mice. Who knows for sure? As I've said before, all of this is quite speculative. This Frankenstein-like experiment of transplanting human hair follicles onto genetically-mutated mice is quite interesting, but it also raises questions for which we have no solid answers! :wink:

Bryan

 

[Bryan]

I don't think the fact these mice had no immunology, was the reason for male pattern baldness follicle re-growth. I also think the fact that the male pattern baldness follicles enlarged, whilst already enlarged follicles didn't and actualy shrank, can be explained.

And that explanation is...?

Bryan