It is clear that DHT make grow hair,..., in body and sexual hair, but what in scalp hair??? why is different? Maybe the amount of DHT?
we have not yet all the keys.
Regarding point 2, Sebaceous gland is a part, as hair, of the hair follicle, or better pilosebacous unit, and the important DHT is the locally fabricated, in the words of Bryan
[FONT="]"How on earth can DHT levels in the blood not affect the follicles? Please explain that to me, how all this nice, fresh new DHT doesn't just make it's way up there and attach to the androgen receptors?
I'm going to single-out this one point from your post to address, because it's always interested me for years; I may reply to the rest of your post separately.
For years back on alt.baldspot, Dr. Proctor always used to tell us that the consensus among endocrinologists is that DHT only has an effect (a significant effect?) in the tissues where it's actually produced. I never really understood _why_ that would be the case, I just made a mental note of it whenever he would say that.
Nowadays I've come to fully believe that claim, and it makes perfect sense to me. It's based not only on LOGIC, but also on actual physical experiments. For example, topical 5a-reductase inhibitors have been shown to have a "local" effect where they're applied, and that's in both humans and animals. Topical gamma-linolenic acid (GLA) in that hamster study of topical fatty acids was shown to have an effect that was starting to approach what you get with castration on the flank-organ to which it was applied, but not on the opposite flank-organ. A similar effect on a human volunteer was found by the same researchers who did the hamster study: topical GLA on his forehead significantly reduced sebum production where it was applied. The point of all this is screamingly obvious: if serum DHT were much of a factor, why didn't it keep the topical GLA from having an obvious DHT-suppressing effect in the human and in the hamsters where it was applied?
If you do a little reading, it really shouldn't be that surprising that DHT only seems to have a significant effect where it's actually produced. I was reading an interesting article in a medical journal a long time ago (sorry, I didn't even bother to write it down for later citation) that said that the great majority of DHT molecules that are manufactured inside cells (by 5a-reductase, of course) go on to bind to androgen receptors in those same cells, and produce their usual androgenic effects RIGHT THERE WHERE THEY WERE PRODUCED. Only a relatively small number of the DHT molecules "leak out" of the cell and into the bloodstream (according to the article).
Furthermore, DHT in the bloodstream is eliminated rather rapidly, with a "half-life" of a couple of hours. From a study that I've quoted many times over the years ("A Model for the Turnover of Dihydrotestosterone in the Presence of the Irreversible 5a-Reductase Inhibitors GI198745 and Finasteride", Gisleskog
et al, Clin Pharmacol Ther 1998;64:636-47): (page 641) "...The elimination rate of DHT, k(OUT), was relatively high, corresponding to an elimination half-life of 2 hours."
So let's sum it all up this way:
1) Only a (small?) minority of DHT molecules make it into the bloodstream in the first place, compared to all the ones that stay inside the cells and do their dirty work right away;
2) The ones that DO make it into the bloodstream are eliminated rather rapidly, before they have a chance to do much mischief;
3) Actual physical experiments with humans and animals verify that serum DHT seems to have no significant effect as an androgenic stimulus. In other words, DHT isn't much of an
endocrine hormone, it's mainly an
autocrine hormone.How on earth can DHT levels in the blood not affect the follicles? Please explain that to me, how all this nice, fresh new DHT doesn't just make it's way up there and attach to the androgen receptors?[/FONT]
[FONT="]I'm going to single-out this one point from your post to address, because it's always interested me for years; I may reply to the rest of your post separately.
For years back on alt.baldspot, Dr. Proctor always used to tell us that the consensus among endocrinologists is that DHT only has an effect (a significant effect?) in the tissues where it's actually produced. I never really understood _why_ that would be the case, I just made a mental note of it whenever he would say that.
Nowadays I've come to fully believe that claim, and it makes perfect sense to me. It's based not only on LOGIC, but also on actual physical experiments. For example, topical 5a-reductase inhibitors have been shown to have a "local" effect where they're applied, and that's in both humans and animals. Topical gamma-linolenic acid (GLA) in that hamster study of topical fatty acids was shown to have an effect that was starting to approach what you get with castration on the flank-organ to which it was applied, but not on the opposite flank-organ. A similar effect on a human volunteer was found by the same researchers who did the hamster study: topical GLA on his forehead significantly reduced sebum production where it was applied. The point of all this is screamingly obvious: if serum DHT were much of a factor, why didn't it keep the topical GLA from having an obvious DHT-suppressing effect in the human and in the hamsters where it was applied? [/FONT][FONT="]
[/FONT][FONT="]
If you do a little reading, it really shouldn't be that surprising that DHT only seems to have a significant effect where it's actually produced. I was reading an interesting article in a medical journal a long time ago (sorry, I didn't even bother to write it down for later citation) that said that the great majority of DHT molecules that are manufactured inside cells (by 5a-reductase, of course) go on to bind to androgen receptors in those same cells, and produce their usual androgenic effects RIGHT THERE WHERE THEY WERE PRODUCED. Only a relatively small number of the DHT molecules "leak out" of the cell and into the bloodstream (according to the article).
Furthermore, DHT in the bloodstream is eliminated rather rapidly, with a "half-life" of a couple of hours. From a study that I've quoted many times over the years ("A Model for the Turnover of Dihydrotestosterone in the Presence of the Irreversible 5a-Reductase Inhibitors GI198745 and Finasteride", Gisleskog
et al, Clin Pharmacol Ther 1998;64:636-47): (page 641) "...The elimination rate of DHT, k(OUT), was relatively high, corresponding to an elimination half-life of 2 hours."
So let's sum it all up this way:
1) Only a (small?) minority of DHT molecules make it into the bloodstream in the first place, compared to all the ones that stay inside the cells and do their dirty work right away;
2) The ones that DO make it into the bloodstream are eliminated rather rapidly, before they have a chance to do much mischief;
3) Actual physical experiments with humans and animals verify that serum DHT seems to have no significant effect as an androgenic stimulus. In other words, DHT isn't much of an
endocrine hormone, it's mainly an
autocrine hormone.[/FONT]
