For Stephen Foote, an RU58841 study

[michael barry]

http://www.blackwell-synergy.com/doi/ab ... 19382053.x


Stephen, I was wondering if you thought this study relevant to your hypothesis. Im interested in RU58841, but its efficacy here doesn't seem to be as strong as I'd thought it might be..............

Here's the article:


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02 Oct 2003

Home > List of Issues > Table of Contents > Article Abstract
British Journal of Dermatology
Volume 137 Issue 5 Page 699 - November 1997

To cite this article: B DE BROUWER, C TÉTELIN, T LEROY, A BONFILS, D VAN NESTE (1997)
A controlled study of the effects of RU58841, a non-steroidal antiandrogen, on human hair production by balding scalp grafts maintained on testosterone-conditioned nude mice
British Journal of Dermatology 137 (5), 699–702.
doi:10.1046/j.1365-2133.1997.19382053.x

Prev Article Next Article
Original Article
A controlled study of the effects of RU58841, a non-steroidal antiandrogen, on human hair production by balding scalp grafts maintained on testosterone-conditioned nude mice
B. DE BROUWER, C. TÉTELIN, T. LEROY, A. BONFILS & D. VAN NESTE0Skin Study Centre, Skinterface sprl 9 rue du Sondart-B 7500 Tournai, Belgium, 1Roussel Uclaf, Romainville, France
Correspondence to: D. Van Neste. Skin Study Centre, Skinterface sprl 9 rue du Sondart-B 7500 Tournai, Belgium
Abstract
Human hair growth can be monitored for several months after the transplantation of scalp samples from men with androgen-dependent alopecia on to female nude mice. Hair production from balding sites has been shown to be inhibited in testosterone-conditioned nude mice. We used this recently reported model to study the effect of a new non-steroidal antiandrogen — RU58841 — on human hair growth. Twenty productive scalp grafts from balding men were maintained for 8 months after grafting on to nude mice, and hair production was monitored monthly for 6 months. All mice were conditioned by the topical application of testosterone (testosterone propionate, 300 μg in 10 μL; 5 days/week) on the non-grafted flank. The scalp samples were divided equally according to the estimated hair production potential, which was based on the amount of hair present on the scalp samples before grafting. Each of the two equal groups of grafts was further allocated at random to be treated topically (5 days/week) with blinded solutions of either RU58841 1% in ethanol, or ethanol as a control.

Twenty-eight active follicles appeared on the 10 control grafts. Among them only two follicles (7%) initiated a second hair cycle. However, the 10 RU58841-treated grafts bore a total of 29 active follicles, and eight of them (28%) showed a second cycle. The values for the linear hair growth rates (LHGR) were significantly (P < 0.04) higher in the RU58841-treated group. Recycling and increased LHGR indicate a positive action for RU58841 on human hair growth from balding samples grafted on to testosterone-conditioned nude mice, and encourage a clinical trial to evaluate its potential in the treatment of androgen-dependent alopecia.

 

[Bryan]

LOUD SILENCE from the inimitable Mr. Foote!

 

[michael barry]

Bryan,

Im suprised the RU was not more effective personally.............Im wondering what Stephen's opinion was about RU in this instance, because we have seen it be much more effective with macaques than what it was here.

Bryan,

What product, if any, do you feel helps best with the buildup of collagen in the dermal sheath and the streamers beneath the follicle? Does prox-n do anything about this?

Also, have you heard of any of the guys that drain dutasteride into minoxidil having success with it? I know lipox sells topical dutas, but dont know if it works or not, but if it did, it would seem one could us the ppg and alcohol in minoxidil to deliver it?

 

[S Foote.]

LOUD SILENCE from the inimitable Mr. Foote!

My silence here is due to the simple fact that i have a "REAL" life outside of these forums Bryan :wink:

It being a weekend, have have not seen this post until now, because of my social interactions with people in the real world.

Now what i call a real silence on being challenged is yours in this thread:

http://www.hairlosstalk.com/discussions ... &start=140

As someone who can be seen to lurk these forums all the hours of the day looking for internet "friends", there is no way you could have missed that thread 8)

You are getting worse at fooling people here Bryan, time to look for status elsewhere i think :wink:

Michael.

It is late here now, i will respond tommorow.

S Foote.

 

[hair today gone tomorrow]

LOUD SILENCE from the inimitable Mr. Foote!

My silence here is due to the simple fact that i have a "REAL" life outside of these forums Bryan :wink:

It being a weekend, have have not seen this post until now, because of my social interactions with people in the real world.

Now what i call a real silence on being challenged is yours in this thread:

http://www.hairlosstalk.com/discussions ... &start=140

As someone who can be seen to lurk these forums all the hours of the day looking for internet "friends", there is no way you could have missed that thread 8)

You are getting worse at fooling people here Bryan, time to look for status elsewhere i think :wink:

Michael.

It is late here now, i will respond tommorow.

S Foote.

WOW, pwn3d

 

[elguapo]

I wish my sh*t didn't stink.

 

[elguapo]

By the way, I'm only kidding.

I consider everybody on this site smarter than I... same at work. Unless proven otherwise, I suppose, but even then my philosophy is give the other a break, let them catch up.

Anyway, just bugs me when I see a bunch of smart people "cybersparring". No need for it, our goal is one in the same, yadeyade combayae.

Peace!

 

[S Foote.]

Hi Michael.

I think that this ten year old mouse study, is typical of the tradition it seems happens in hair loss research, in that it raises more questions than it answers.

Why oh why don't they go the whole hog in these studies?

To be relevant to the direct/indirect question of the androgen influence, they should have tested the same balding follicles in mice with no testosterone treatment as well to test different androgen level baselines.

They should also have transplanted androgen dependent body hair follicles as well as the balding follicles, to see if any changes were "opposite".

What they should do, as i have suggested before, is repeat that later immuno deficient mouse study we debated, and prime those mice with testosterone as in this earlier study!

We never seem to get any studies aimed at the whole androgen related hair growth/loss questions?

I also agree with you that the results are pretty dissapointing if you go along with the current theory, and i don't think that indirect effects can be ruled out anyway.

At the end of the day, where are the RU topicals for male pattern baldness ten years after this study?

The most telling data in my opinion, is from the latest reports involving the "human" male pattern baldness area. In particular your reports of the increased growth of body hair to scalp transplants, and the apparent zero effect of systematic 5ARi's on these grafts.

This both goes completely against the old donor dominance idea, "AND" the need for androgens to "directly" stumulate body hair growth as the old theory claims!

S Foote.

 

[Bryan]

Bryan,

Im suprised the RU was not more effective personally......Im wondering what Stephen's opinion was about RU in this instance, because we have seen it be much more effective with macaques than what it was here.

Michael, you've lost me on this one. What makes you think the RU wasn't very effective? All they used was a 1% solution in alcohol (not terribly impressive), and they don't even specify the quantity that was applied; what if the total amount of RU that got to the hair follicles was pretty small?

Also, the big obstacle that such follicles have to contend with in a situation like that isn't the (presumed) growth suppression by androgens from the very start, it's simply SURVIVING that initial transplant, and not being severely damaged!

I have no particular reason not to think that the RU was _quite_ effective in that experiment, taking all that into consideration.

What product, if any, do you feel helps best with the buildup of collagen in the dermal sheath and the streamers beneath the follicle? Does prox-n do anything about this?

I would imagine that yes, SODs would be helpful for that.

Also, have you heard of any of the guys that drain dutasteride into minoxidil having success with it? I know lipox sells topical dutas, but dont know if it works or not, but if it did, it would seem one could us the ppg and alcohol in minoxidil to deliver it?

Like everyone else, all I know about the success of such an approach is from what I read on these forums, and I don't recall anybody claiming success from that. Of course, there's also an important secondary issue associated with that question: even if someone DOES have a degree of success, is it a purely "local" success, or is it just caused by the systemic absorption of the dutasteride? :wink: That's always a tough issue to resolve...

Bryan

 

[Bryan]

We never seem to get any studies aimed at the whole androgen related hair growth/loss questions?

Why is it that you have never once, not EVER, replied to my references to the topical 11a-hydroxyprogesterone study, in which hair growth was improved in the ONE area of the scalp where it was applied, but not in the other area of the scalp that was untreated and left as a control? You wouldn't be trying to EVADE a study that refutes your theory, would you? :wink:

At the end of the day, where are the RU topicals for male pattern baldness ten years after this study?

It's owned by that one company ("Proskelia", or whatever). Their own in-house testing indicates that it's about as effective as Propecia, maybe even a little better. What's your point?

The most telling data in my opinion, is from the latest reports involving the "human" male pattern baldness area. In particular your reports of the increased growth of body hair to scalp transplants, and the apparent zero effect of systematic 5ARi's on these grafts.

This both goes completely against the old donor dominance idea, "AND" the need for androgens to "directly" stumulate body hair growth as the old theory claims!

I'll try to help you break through your simple-minded assumptions: just because a given hair follicle's response to androgens clearly demonstrates donor dominance, that doesn't mean that ALL growth characteristics of a hair follicle demonstrate donor dominance. If those BHT experiments are indeed accurate, then it simply shows that _some_ characteristics of a follicle are dependent (to some extent) on its location.

And it's well-known that some body hair seems to take-on a life of its own, once it gets going good. Sometimes body hair growth is suppressed to only a relatively limited degree when you reduce the androgenic stimulus.

Bryan

 

[michael barry]

Stephen and Bryan.......

I have alot to answer, and I think some pretty interesting info.....



Stephen,

I can post the article if you would like, but French researchers looking closely at baldness under microscopes wrote a great article (Tom Hagerty LOVED it) that describes the dermal sheath getting 2 to 2.5 times thicker with crosslinked, bulky collagen deposits as well as the well-knonw collagenous streamers underneath the follicle. I read an Indian dermatology article that opined that in categen and early anagen, when the dermal papilla is moving either up or down in the dermal sheath, is when the big damage in AA is done and when the papilla is vunerable. All the factors for "contact inhibition" are there, but they are collagen blocking the follicle from widening on all sides and migrationg downward. The only place to go is UP, to the infidilum (sp.?) or the opening in the dermis where the follicle emerges.

The thing is Stephen, the opening where the follicle emerges is the first place that gets inflammed according to the french researchers. The dermal papilla is literally being boxed in and forced upwards where the inflammation is the worst. Have you considered that your contact inhibition theory may be right on alot of counts, but its collagen and not water restricting the dermal papilla from widening?

I say this because of a couple of phenomena Ive noticed when looking at extremely bald BLACK men. Their skin, the bald skin, is lighter than the forehead skin or facial skin or the rest of the scalp. I considered youre idea when I first really looked at this, thinking it was water under the scalp.......................but if its collagen, it would fit perfect. The vellus follicles are right near the top of the dermis, the sheath is much thicker with crosslink curdled collagen, the collagenous streamers are underneath, the sebaceous glands are now cauliflowered..............so the scalp is somewhat altered by all of that. Stephen I work with a bald guy (late thirties) whose scalp literally GLEAMS. You can damn near comb your hair in the reflection off his scalp......................its something to ponder.

I can link those articles for you if you'd like...




Bryan,

Thanks for the prox-n info. I got nosy and emailed Proctor (I try not to bother him, but hell, he has looked at hair under microscopes probably more than any other human being and therefore knows alot about something Im interested in.......He said the same thing you did, that SODs have been shown to.... " Specifically, the SODs, known to cause reversion of myofibroblasts", just like you did.


ON the RU............................I just expected more than 28% of the follicles to enter a second phase. To be truthful, its kind of depressing. Perhaps you are right about the trauma to miniaturized follicles being tranpslanted though and they just cant take it.


I appreciate the topical dutasteride info...............I'll guess I'll eventually be looking for ways to make topical spironolactone at home that does not stink like all hell like others have (add spearmint oil or something?) as finas/spironolactone combos seem to be the best anti-androgenice duo.


One more thing Bryan.....................Ive been washing one wrist in nizoral for about a month now, and am not seeing any real reduction in hair there yet. I'll be able to come to a conclusion on it in two more months, but I did have one bright idea about testing topical anti-androgens and its obvious.....

Remember when you were a teenager and all we had for acne back in the day was Stridex pads? It hit my like a ton of bricks about testing topical anti-androgens in a way that would not take 3-4 months to wait for hair to reduce in a certain area. Just "wash" half of the forehead in Nizoral, Pine oil, Revivogen, or whatever (or leave in for a few minutes) and gently wash off. At the end of the day, take two stridex pads and wipe one half of the forehead in one, and the other half of the forehead with the other....perhaps two strokes, one up and one down. If one pad has alot less oil after 16 hours or so than the other...............if would seem that at least at the sebaceous gland level some substance would be anti-androgenic.

Also,,,,,,,,,,,,,,,,,,beer and green tea on a pinky finger hair seems to do the exact opposite of what I expected. Its actually stimulated the hair there instead of lessened it. Folligen on an index finger seems to be slightly anti-androgenic as it now has less hair than the other finger. Not nearly as strong as pine oil was however, which really did lessen hair. Revivogen still had the best results Ive seen as a topical anti-androgen at reducing hair. Im now trying lavendar/tea tree oil on my big toe (Im a hairy guy) to see if it will reduce it. I'll know in about two more months for certain. I want to try spearmint tea or oil at some point. That will be about it as far as my experimenting will go.

 

[Matgallis]

Also,,,,,,,,,,,,,,,,,,beer and green tea on a pinky finger hair seems to do the exact opposite of what I expected. Its actually stimulated the hair there instead of lessened it. Folligen on an index finger seems to be slightly anti-androgenic as it now has less hair than the other finger. Not nearly as strong as pine oil was however, which really did lessen hair. Revivogen still had the best results Ive seen as a topical anti-androgen at reducing hair. Im now trying lavendar/tea tree oil on my big toe (Im a hairy guy) to see if it will reduce it. I'll know in about two more months for certain. I want to try spearmint tea or oil at some point. That will be about it as far as my experimenting will go.

You have to consider the cycles of hair before ruling out effects of tropicals... Glad to see revivogen being most effective

 

[S Foote.]

We never seem to get any studies aimed at the whole androgen related hair growth/loss questions?

Why is it that you have never once, not EVER, replied to my references to the topical 11a-hydroxyprogesterone study, in which hair growth was improved in the ONE area of the scalp where it was applied, but not in the other area of the scalp that was untreated and left as a control? You wouldn't be trying to EVADE a study that refutes your theory, would you? :wink:

I have always responded to such questions Bryan, but if i missed a post just post it again here.

At the end of the day, where are the RU topicals for male pattern baldness ten years after this study?

It's owned by that one company ("Proskelia", or whatever). Their own in-house testing indicates that it's about as effective as Propecia, maybe even a little better. What's your point?

The point Bryan is that the dismal performance of topical anti-androgens compared to systematic anti-androgens, clearly does not support the "its all in the follicle" claims.

The most telling data in my opinion, is from the latest reports involving the "human" male pattern baldness area. In particular your reports of the increased growth of body hair to scalp transplants, and the apparent zero effect of systematic 5ARi's on these grafts.

This both goes completely against the old donor dominance idea, "AND" the need for androgens to "directly" stumulate body hair growth as the old theory claims!

I'll try to help you break through your simple-minded assumptions: just because a given hair follicle's response to androgens clearly demonstrates donor dominance, that doesn't mean that ALL growth characteristics of a hair follicle demonstrate donor dominance. If those BHT experiments are indeed accurate, then it simply shows that _some_ characteristics of a follicle are dependent (to some extent) on its location.

And it's well-known that some body hair seems to take-on a life of its own, once it gets going good. Sometimes body hair growth is suppressed to only a relatively limited degree when you reduce the androgenic stimulus.

Bryan

Rubbish Bryan.

There is no way the body hair transplant "real world" results can be explained by the donor dominance idea you support. Trying to change the rules of evidence when results dont suit you, isn't going to get you any scientific credibility here.

Your opinions on donor dominance are very clear in this thread.

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

Funny how you "NOW" try to add "other" factors into the equasion, when the evidence doesnt suit your very clear original claims! :wink:

S Foote.

 

[Bryan]

ON the RU.....I just expected more than 28% of the follicles to enter a second phase. To be truthful, its kind of depressing. Perhaps you are right about the trauma to miniaturized follicles being tranpslanted though and they just cant take it.

Balding human hair follicles are transplanted onto mice and treated with only a weak solution of RU58841, and you're "depressed" that only FOUR TIMES as many of the grafts went to a second cycle as the vehicle-treated grafts?

But seriously, considering the fact that we don't even know for sure what the expected successful graft rate is even for nornal NON-balding follicles under those conditions, I don't know that that's a bad result at all.

One more thing Bryan.....................Ive been washing one wrist in nizoral for about a month now, and am not seeing any real reduction in hair there yet. I'll be able to come to a conclusion on it in two more months...

Michael, I've seen your previous posts about those experiments you've done, but what bothers me a little about them is your specific choice of body hair. I don't know for absolutely certain-sure, but I suspect that wrist/arm/hand hair isn't as sensitive to androgens (or the lack of androgens) as hair in certain other body locations. I'm not saying that it's IMPOSSIBLE that you could detect a slight difference in growth in such a test after only a month or so, but I bet the difference could be awfully subtle. Why don't you do those experiments on BEARD hair, which I would imagine might be more sensitive to androgens (or their lack)?

...but I did have one bright idea about testing topical anti-androgens and its obvious.....

Remember when you were a teenager and all we had for acne back in the day was Stridex pads? It hit my like a ton of bricks about testing topical anti-androgens in a way that would not take 3-4 months to wait for hair to reduce in a certain area. Just "wash" half of the forehead in Nizoral, Pine oil, Revivogen, or whatever (or leave in for a few minutes) and gently wash off. At the end of the day, take two stridex pads and wipe one half of the forehead in one, and the other half of the forehead with the other....perhaps two strokes, one up and one down. If one pad has alot less oil after 16 hours or so than the other...............if would seem that at least at the sebaceous gland level some substance would be anti-androgenic.

Oh man....NOW you're really hitting me close to home!! :thumbs_up:

For a few years now I've posted off and on about the possibility of testing topical antiandrogens and 5a-reductase inhibitors by measuring their effect on sebum production. The method you suggest should work, in principle, but I suggest a much easier and more scientific tool for that purpose: Sebutape test-stripes. Those can you give you a more precise estimate of sebum production than attempting to compare Stridex pads. I've used Sebutape strips myself on numerous occasions, and I even used them in an experiment which I posted on an acne site a year or two ago to demonstrate that washing your skin doesn't stimulate sebum production (see the last line of my sig file)!

BTW, Kligman writes in his 1958 study on sebum production that the most sensitive test of all for sebum production that can be done with simple materials is just to press a glass slide against your skin for a few seconds. When you then hold the slide up to a light, the resulting visible grease spot is a VERY SENSITIVE indication of sebum. He humorously points out that when you walk along storefront windows, you can easily see the grease spots on the windows where people stopped to stare at the merchandise inside, and pressed their foreheads against the glass! :wink:

If you do decide to go ahead and try a test like that, be aware that it still takes at least a month or so for sebum production to be altered enough to be noticeable in tests. That's about the minimum length of time that even serious scientific studies using REAL antiandrogens take for a test like that.

Also,,,,,,,,,,,,,,,,,,beer and green tea on a pinky finger hair seems to do the exact opposite of what I expected. Its actually stimulated the hair there instead of lessened it. Folligen on an index finger seems to be slightly anti-androgenic as it now has less hair than the other finger. Not nearly as strong as pine oil was however, which really did lessen hair. Revivogen still had the best results Ive seen as a topical anti-androgen at reducing hair. Im now trying lavendar/tea tree oil on my big toe (Im a hairy guy) to see if it will reduce it. I'll know in about two more months for certain. I want to try spearmint tea or oil at some point.

You know, that's a problem I've been wanting to post about for quite a while: we can't really ASSUME that an effect on body hair like that is really due to some antiandrogenic property. What if there are some weird chemicals in something like lavender or tea tree oil that would have some kind of mild TOXIC effect on hair follicles (ALL hair follicles, not just body hair follicles), and that's what causes the mild growth suppression in your experiments? While your experiments are certainly interesting, I think they need to be interpreted with caution.

Bryan

 

[S Foote.]

Stephen,

I can post the article if you would like, but French researchers looking closely at baldness under microscopes wrote a great article (Tom Hagerty LOVED it) that describes the dermal sheath getting 2 to 2.5 times thicker with crosslinked, bulky collagen deposits as well as the well-knonw collagenous streamers underneath the follicle. I read an Indian dermatology article that opined that in categen and early anagen, when the dermal papilla is moving either up or down in the dermal sheath, is when the big damage in AA is done and when the papilla is vunerable. All the factors for "contact inhibition" are there, but they are collagen blocking the follicle from widening on all sides and migrationg downward. The only place to go is UP, to the infidilum (sp.?) or the opening in the dermis where the follicle emerges.

The thing is Stephen, the opening where the follicle emerges is the first place that gets inflammed according to the french researchers. The dermal papilla is literally being boxed in and forced upwards where the inflammation is the worst. Have you considered that your contact inhibition theory may be right on alot of counts, but its collagen and not water restricting the dermal papilla from widening?

I think the important thing to remember Michael is the macaque model. Here there is androgen related scalp balding, with non of the immunology collagen build up etc. So i think the balding process itself is not "caused" by the factors you mention, but these are associated effects in humans.

I think the evidence is that the immunology etc in humans is just because of a higher tissue fluid level build up compared to macaques. Of course the fibrosis caused "then" also presents a problem.

Edema as the "cause" of the immunology makes perfect sense as this relationship is well known in phsiology. This is a simple article that explains this well.

http://www.lymphnotes.com/article.php/id/43/

Note this quote:

"The amount of swelling is not an indicator as to the risk for developing fibrosis. Fibrosis can occur in tissues that are only moderately swollen."

So it is not required that edema be "obvious" for the conditions known in the male pattern baldness area to develope.

S Foote.

 

[Bryan]

Why is it that you have never once, not EVER, replied to my references to the topical 11a-hydroxyprogesterone study, in which hair growth was improved in the ONE area of the scalp where it was applied, but not in the other area of the scalp that was untreated and left as a control? You wouldn't be trying to EVADE a study that refutes your theory, would you? :wink:

I have always responded to such questions Bryan, but if i missed a post just post it again here.

Yeah, right.

I'll have to dig that study up again. I'll post the relevant parts of it again later for you to dodge.... er, I mean RESPOND to! :wink:

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

Funny how you "NOW" try to add "other" factors into the equasion, when the evidence doesnt suit your very clear original claims! :wink:

I've already explained all that to you until I was blue in the face. I go by REAL WORLD results, not goofy hypothetical theories like yours. If serious scientific experiments show that body hair transplants do in fact show somewhat different growth characteristics that depend on the exact location of the transplant, then I bow to that scientific evidence and accept it. That's a far cry, however, from the conclusive evidence presented by the Nordstom study (and others) that androgen-sensitivity IS INDEED DONOR-DOMINANT. Against THAT, you have no defense, except to waste everybody's time by whining about body hair transplants. If you would bother to read Norman Orentreich's original study from the late 1950's about his experiments with human hair follicle transplantation which I've referenced on numerous occasions, you would understand that he did NOT find "donor-dominance" to be apparent for EVERY type of hair dysfunction that he tested. Certain other problems like alopecia areata DIDN'T demonstrate pure donor-dominance, but alopecia androgenetica DID demonstrate pure donor-dominance. Your problem, Stephen, is that you are so desperate to support your goofy theory that you talk about things like this that you don't really know anything about.

BTW, how come you didn't say much about that study Michael posted? I would have thought you would have said something about the following line: "Human hair growth can be monitored for several months after the transplantation of scalp samples from men with androgen-dependent alopecia on to female nude mice. Hair production from balding sites has been shown to be inhibited in testosterone-conditioned nude mice." Apparently, androgen levels in the mice themselves (although they were female) wasn't sufficient to inhibit the balding follicles; they had to be testosterone-conditioned for that to happen! Why didn't you acknowledge that? :wink: The obvious point I'm making here (you have to have so many things spelled-out for you, so I'm going to explain it to you) is that you can't ASSUME that all mice (even male mice) have androgen levels that are sufficient to inhibit the growth of human hair follicles. You may have to add ADDITIONAL androgen to them for that to happen (even the male ones). If you haven't caught-on yet, I'm referring to that other study about human hair follicles transplanted onto immuno-deficient mice that you like to harp about so much! :wink:

Bryan

 

[S Foote.]

I am not going to get into yet another long debate involving your usual unscientific distractions, side stepping of the issues and sarcastic distractions Bryan. Everyone here can search the old posts and see your tactics for themselves if they dont believe me on this. I'll be as brief as possible here.

Why is it that you have never once, not EVER, replied to my references to the topical 11a-hydroxyprogesterone study, in which hair growth was improved in the ONE area of the scalp where it was applied, but not in the other area of the scalp that was untreated and left as a control? You wouldn't be trying to EVADE a study that refutes your theory, would you? :wink:

I have always responded to such questions Bryan, but if i missed a post just post it again here.

Yeah, right.

I'll have to dig that study up again. I'll post the relevant parts of it again later for you to dodge.... er, I mean RESPOND to! :wink:

Just post it Bryan! If your sarcastic remarks are designed to try to convince people i have deliberately avoided this before, reference the threads?

If you can't then people will see your inuendo's here are just plain lies won't they! 8)

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

Funny how you "NOW" try to add "other" factors into the equasion, when the evidence doesnt suit your very clear original claims! :wink:

I've already explained all that to you until I was blue in the face. I go by REAL WORLD results, not goofy hypothetical theories like yours. If serious scientific experiments show that body hair transplants do in fact show somewhat different growth characteristics that depend on the exact location of the transplant, then I bow to that scientific evidence and accept it.

Well apart from all the hard data Michael has posted on body hair to scalp transplantation, there is this study concerning the assumptions of the old donor dominance notions.


http://www.dhi.gr/images/pdf/bht.pdf

You better start bowing Bryan! :wink:

That's a far cry, however, from the conclusive evidence presented by the Nordstom study (and others) that androgen-sensitivity IS INDEED DONOR-DOMINANT. Against THAT, you have no defense, except to waste everybody's time by whining about body hair transplants. If you would bother to read Norman Orentreich's original study from the late 1950's about his experiments with human hair follicle transplantation which I've referenced on numerous occasions, you would understand that he did NOT find "donor-dominance" to be apparent for EVERY type of hair dysfunction that he tested. Certain other problems like alopecia areata DIDN'T demonstrate pure donor-dominance, but alopecia androgenetica DID demonstrate pure donor-dominance. Your problem, Stephen, is that you are so desperate to support your goofy theory that you talk about things like this that you don't really know anything about.

Just plain lie's is it now Bryan? :roll:

You know damm well that those early "androgen" related transplant studies we debated before, and i have linked in this thread, just fall down with modern knowledge!

People can read those old threads and see your lies here for themselves Bryan!

When i pointed out back then that there is now recognised long term hairloss in the "same" grafts as used in those old "male pattern baldness" studies, you just tried to ignore it! You could not grasp the concept of what the hairloss pattern called "doughnutting" in those grafts means in terms of the whole body of evidence. You even tried to claim this doesn't exist, as it has not been refered to in a "peer reviewed" medical journal. This is despite the fact that a whole industry now exists to offer repair services for hair loss in these larger old grafts!

All people have to do to see this for themselves is google "hair transplant doughnutting". :wink:

There was "NO" reference whatsoever to such a now recognised hairloss patern in Nordstroms old study or any other for that matter, and the conclusions of these old studies cannot explain this by the old donor dominance notion.

Oh i know you will try to use the same old excuses that the transplantation industry uses to try to avoid compensation claims. But the science is very clear on this issue given "ALL" the evidence. Hypoxia can very definately be ruled out as the cause of this continuation of male pattern baldness in these grafts. :wink:

BTW, how come you didn't say much about that study Michael posted? I would have thought you would have said something about the following line: "Human hair growth can be monitored for several months after the transplantation of scalp samples from men with androgen-dependent alopecia on to female nude mice. Hair production from balding sites has been shown to be inhibited in testosterone-conditioned nude mice." Apparently, androgen levels in the mice themselves (although they were female) wasn't sufficient to inhibit the balding follicles; they had to be testosterone-conditioned for that to happen! Why didn't you acknowledge that? :wink: The obvious point I'm making here (you have to have so many things spelled-out for you, so I'm going to explain it to you) is that you can't ASSUME that all mice (even male mice) have androgen levels that are sufficient to inhibit the growth of human hair follicles. You may have to add ADDITIONAL androgen to them for that to happen (even the male ones). If you haven't caught-on yet, I'm referring to that other study about human hair follicles transplanted onto immuno-deficient mice that you like to harp about so much! :wink:

Bryan

If you had even bothered to read my response to Michael properly, you would have seen like everyone else that i "DID" address that point!

I clearly said they should have tested before androgen treatment to test the androgen baselines! People only need to refer to my posts in this thread to confirm your distraction from the point tactics!

From your statement above quote:

"Human hair growth can be monitored for several months after the transplantation of scalp samples from men with androgen-dependent alopecia on to female nude mice. Hair production from balding sites has been shown to be inhibited in testosterone-conditioned nude mice." Apparently, androgen levels in the mice themselves (although they were female) wasn't sufficient to inhibit the balding follicles; they had to be testosterone-conditioned for that to happen! Why didn't you acknowledge that?

"Apparently" Bryan? :freaked:

You cannot possibly "assume" that the testosterone primed female mice "HAVE" responded any differently in this test than pure female mice would have! That is just not in the data, and is the reason why i said in this thread that they "SHOULD" have tested "BOTH" situations!

This is yet another clear example of your unscientific cherry picking of studies, to try to support your arguments of the day! :roll:

This thread was just about Michael asking my opinion of a study. But you had to jump in with your arrogant sarcasm, and your desperate amatuer attempts to play down my personal theory.

I really dont care what you think Bryan, i have posted before on what "real" experts have said about my theory.

You don't agree with my theory, fine. We all know that Bryan, so why dont you just keep your sarcastic remarks out of threads like this? Everyone gets fed up of the distraction from the issues at hand, including me! :roll: :roll:

S Foote.

 

[powersam]

"The market for prevention is likely to be worth more than treatment. So why has it been shelved? Obviously because it "cannot" prevent male pattern baldness topicaly! "

plain and simple, people will always pay more for a cure than a preventative.

 

[Bryan]

It is well known that "everything" works better in macaques than humans Bryan, probably because of the immune component in humans as stated by Uno.

WHOA there, pardner!! You're trying to "spin" this by very subtly suggesting that RU only works well in macaques. Stop trying to bullshit everybody, and listen carefully to what I'm about to say: Uno and his colleagues said that OF ALL THE AGENTS THEY HAD TESTED IN MACAQUES, RU WAS THE MOST EFFECTIVE OF ALL THOSE AGENTS. More effective than minoxidil, finasteride, 4-MA, and diazoxide. Since minoxidil and finasteride have been solidly proven to work in humans, that strongly suggests that RU58841 ought to work at least as well in humans as those other agents.

But according to the old ideas you cling to, topical RU "should" at "least" be able to "prevent" male pattern baldness in humans! The market for prevention is likely to be worth more than treatment. So why has it been shelved? Obviously because it "cannot" prevent male pattern baldness topicaly!

Can't you understand PLAIN ENGLISH??? The company itself said that RU works about as well as Propecia, if not actually better. There could be any number of reasons why they haven't put it on the market yet. The most likely is that they don't have the money to get FDA approval.

Incidently, the old ideas you are so fond of, never made any mention of the "now" known immunology in male pattern baldness. It is only recently that you and some others are now desperately trying to reconcile your "direct" action of androgens with this, and failing completely.

I have no idea what you're talking about.

Just plain lie's is it now Bryan? :roll:

You know damm well that those early "androgen" related transplant studies we debated before, and i have linked in this thread, just fall down with modern knowledge!

People can read those old threads and see your lies here for themselves Bryan!

When i pointed out back then that there is now recognised long term hairloss in the "same" grafts as used in those old "male pattern baldness" studies, you just tried to ignore it!

You have NEVER EVER documented for me from genuine medical sources that there is "long term hairloss" in hair transplants.

You could not grasp the concept of what the hairloss pattern called "doughnutting" in those grafts means in terms of the whole body of evidence. You even tried to claim this doesn't exist, as it has not been refered to in a "peer reviewed" medical journal. This is despite the fact that a whole industry now exists to offer repair services for hair loss in these larger old grafts!

I don't doubt the existence of "doughnutting". The only difference between you and me on this issue is what CAUSES it.

There was "NO" reference whatsoever to such a now recognised hairloss patern in Nordstroms old study or any other for that matter, and the conclusions of these old studies cannot explain this by the old donor dominance notion.

ROTFLMAO!!! So you're accusing Nordstrom and Orentreich of LYING or DECEPTION in their studies??

Oh i know you will try to use the same old excuses that the transplantation industry uses to try to avoid compensation claims. But the science is very clear on this issue given "ALL" the evidence. Hypoxia can very definately be ruled out as the cause of this continuation of male pattern baldness in these grafts. :wink:

You have never EVER presented so much as one whit of credible evidence that suggests that "doughnutting" is caused by anything other than what the transplant industry says it's caused by.

Bryan

 

[S Foote.]

"The market for prevention is likely to be worth more than treatment. So why has it been shelved? Obviously because it "cannot" prevent male pattern baldness topicaly! "

plain and simple, people will always pay more for a cure than a preventative.

Hmmm?

Think about the marketing and the people who "think" they have the first signs of male pattern baldness thinning? The basic fear is clear on these sites!

"Does male pattern baldness run in your family? Avoid the inevitable, prevention is better than cure and our simple daily treatment can stop male pattern baldness before it starts. Just send etc, etc"

Just consider the potential of something that could be "proven" to stop this before it starts? (if only).

S Foote.