Have scientists studied the following...

[gutted]

But to imply, as he did, that androgens aren't responsible is downright nonsense. It's been known for centuries that eunuchs (castrated men) don't go bald. The reason is because androgens are the first step in what's turning out to be an increasingly complicated chain of events. We're not entirely sure what the other steps are, but if you stop the androgens the chain is never started in the first place.

castration does not lead to a total, 0 redcution of tesosterone, it only minimizes the levels,(to levels that do not cause any damage), this implies hair growth is still being maintained by androgens. I wonder if castration leads to a loss of hair in body hair grwoth too?

No it's not. For a couple of big reasons.

First, it doesn't take 30 years to break down regular hair. If you take Propecia for 20 years, your hair will be protected from DHT, but if you then stop taking it, you experience 'catch-up balding' where you quickly return to the point your hair loss would have been at had you never taken Propecia at all.

So even though your hair has been protected for 20 years, it will go through 20 years of balding in about six months. This shows that it's nothing to do with cumulative effects of DHT. There is something else going on - and that something is related to AGE, but not TIME exposed to DHT.

this is another common myth sparked by HT surgeons and merck and spread by these forums, there is no such thing as catchup balding. People who get off of propecia, induce a very very big spike in androgen levels once they are off it, hence this percieved "catchup balding happens"
they will continue to "minituarise" at a normal rate...you will not instantyl lose all the hairs that were being maintained by propecia...mintarising will take its course.

Not necessarily. As I said above, it could be that PDG2 is an active part of the process, but that it's not an ISOLATED part. In other words, it has to be activated by the chain of events that starts with DHT and ends with miniaturisation.

Think of it this way. What if DHT binds to a receptor, which does something, which releases PDG2, which does something, which results in the hair miniaturising. Then you would lots of PDG2 in bald scalp because it's getting lots of activation by DHT. But it doesn't stand that any transplanted hair should fall victim eventually, because the transplanted hair won't get attacked by DHT in the first place, so it won't produce any PGD2.

[/QUOTE]

this is flawed and needs to be re-researched.

pgd2 is upregulated anywhere where there is inflamation present, it can also be found upregulated in wounds, scars...

this can easily state the obvious, that the body is attacking something and itself, which it is, the traditional theory may state its dht, which it probably is not and i believe it not to be.
there probably is an infection going on in follicular cells.

transplanted follciles/sebcaceous glands are genetically immune in the sense they dont have a high sensitivity to androgens and so dont take androgens up as much as balding susceptible follciles/glands... when hair from donor regions is trasplanted its sebcaceous gland is also taken with the follicle.

[Aston]

pgd2 is upregulated anywhere where there is inflamation present, it can also be found upregulated in wounds, scars...

this can easily state the obvious, that the body is attacking something and itself, which it is, the traditional theory may state its dht, which it probably is not and i believe it not to be.
there probably is an infection going on in follicular cells.

transplanted follciles/sebcaceous glands are genetically immune in the sense they dont have a high sensitivity to androgens and so dont take androgens up as much as balding susceptible follciles/glands... when hair from donor regions is trasplanted its sebcaceous gland is also taken with the follicle.

Mice treated with PGD2 lost their fur in the treated area. There is little doubt PGD2 is part of an active chain of events following the androgen receptor. Nothing's flawed about the research. Prostaglandins are simply molecules which act as "local" signals and don't necessarily produce inflamation. In fact, they have a multitude of roles which have nothing to do with inflamation at all.

Research: http://stm.sciencemag.org/content/4/...6ra34.abstract
Prostaglandin info: http://en.wikipedia.org/wiki/Prostaglandin

[gutted]

Mice treated with PGD2 lost their fur in the treated area. There is little doubt PGD2 is part of an active chain of events following the androgen receptor. Nothing's flawed about the research. Prostaglandins are simply molecules which act as "local" signals and don't necessarily produce inflamation. In fact, they have a multitude of roles which have nothing to do with inflamation at all.

Research: http://stm.sciencemag.org/content/4/...6ra34.abstract
Prostaglandin info: http://en.wikipedia.org/wiki/Prostaglandin

i said they are upregulated in inflamed areas.

your link to wikipedia -
"prostaglandin levels are increased by COX-2 in scenarios of inflammation."

prostglandins are involved with inflamation.

pgd2 and its role in inflammation.
http://www.caymanchem.com/app/templa...326280AABDD091

[gutted]

Mice treated with PGD2 lost their fur in the treated area. There is little doubt PGD2 is part of an active chain of events following the androgen receptor. Nothing's flawed about the research. Prostaglandins are simply molecules which act as "local" signals and don't necessarily produce inflamation. In fact, they have a multitude of roles which have nothing to do with inflamation at all.

Research: http://stm.sciencemag.org/content/4/...6ra34.abstract
Prostaglandin info: http://en.wikipedia.org/wiki/Prostaglandin

i said the theory that dht targeting the androgen receptor on the hair follicle causing minituarisation is flawed.