S Foote.
Experienced Member
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I really care about better male pattern baldness treatments.
Contrary to your beliefs, I don't think a one off research paper from 2002 done in vivo using mice is the most important work in the field.
1. Mice regen/remodel quickly including the specialized structures in skin, humans don't.
2. Not paying thirty bucks to discuss the contents of the full paper with you.
3. Do it in vivo in human skin as it seems just about anything, short of killing it, done to a mouse grows freaking hair.
Let me elaborate here.
Yes you are right to say that mouse studies don't mean anything when it comes to human hair growth. But the important thing about this particular study is that it used transplanted human hair follicles. All the mouse tissue did was give them life support.
So the important thing is to identify why these human follicles don't behave in this tissue, as they do in normal human transplantation studies?
This is obviously because of a reason outside of the transplanted follicles, and not within them as is the usual claim.
So we need to know what is the physical difference in the surrounding tissue, compared to human tissue.
I think it is important to do this experiment again with variations. Body hair samples should be used as well, and the DHT levels in the mice should be set at the high end of those in human male pattern baldness scalp. Tissue biopsies should be taken to study the interface with the human and mouse tissue, looking for fibrosis and other relevant conditions and substances.
Again any valid explanation here has to show scientific parsimony. Remember all the human follicles enlarged. Even those that are not considered to be affected at all by androgens through whatever pathway. And the end result was that "ALL" of the human follicles reached the same size.
If it is to be claimed that these male pattern baldness follicles enlarged because of the lack of immunology itself, then parsimony dictates that this should also apply to the androgen "neutral" follicles as well. So why don't we see reports of over enlarged follicles in cases of human immune deficiency? There are no reports of kids born with no immune systems who have to live in isolation, having excess hair growth anywhere on their bodies.
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So you are convinced by a mouse study.. First let me tell you that in humans in vivo this approach doesn't work. It doesn't mind where you will take your miniaturized hair follicle and transplant it on your ***, hand, back or chest. It won't magically regrow. We ain't mice S. Foote. Anyway lets break that study up a bit;
1. If you have read that study you know that Van Neste contradicts this study (1.)
2.
3. The most important one by far; They might for instance have an excellent autophagy or macrophage system or something else that makes this possible. If we were the same as mice we would be happy inducing de-novo morphogenesis of hair follicles currently through wounding. But hey we ain't mice.
The process starts in Androgenetic Alopecia when androgens bind to the androgen receptors in the dermal papilla cells. Everything what happens "before" that process is irrelevant to the pathology of Androgenetic Alopecia, simple as that.
1.Van Neste D. The use of scalp grafts onto nude mice as a
model for human hair growth: is there something new for
hair growth drug screen programs? In: Maibach HI, editor.
Dermatologic research techniques. Boca Raton (FL): CRC
Press; 1996. p. 37-49.
Well of course it doesn't work in humans, that's the whole point! We need to find out the precise reasons why.
I would like to read the Van Neste study referenced in full if anyone can provide a link. I cannot comment on your take on it without the proper context of your claims.
In the particular strain of nude mice used, did the balding follicles also enlarge initially then miniaturise in response to increased androgens? Were non male pattern baldness follicles also used as a comparison, as in the other study?
Because if not then you are just not comparing like for like. Also any differences in the strains of mice here, could narrow down the reasons for any different hair growth responses.
Quote:
"The process starts in Androgenetic Alopecia when androgens bind to the androgen receptors in the dermal papilla cells."
So please explain why it is that it can take years before we see any effect of this on hair growth? Such a long delayed response in directly hormone targeted cells is just not recognised. So how can this happen through any recognised mechanism?