michael barry said:
Stephen,
My interpretations of the sweat study were this:
Pre pubescent male (no hair on forehead, or chin)
Chin sweat=(lets say 1.0)
Forehead sweat=(lets say 1.0)
Shaven post pubescent male (forehead, shaven chin)
Chin sweat=(.6) -----due to the 40% decrease in sweating exp. result
Forehead sweat=(1.0)
The shaven post pubescent chin sweated less. THe post pubescent chin contains big thick (biggest in the body) follilces. They are there even if they are shaven. You dont think the big-thick dermal papillas, larger arrector pilli muscles, dermal sheaths, adult sized sebaceous glands wouldnt "shield" the water under them at least "some"?
That was my point about the scalp skin. Even if shaven, there are still big philosebacous units on the non-balding scalp, and vellus-sized philosebaceous units on the bald scalp. Perhaps I oversimplify be "reading this" into that study, but it would seem the same shading of the follicles could apply there?
Do you have a different take on it? Bryan or Dave have a take on it?
Hi Michael.
The sweat glands are independent structures, not shielded or directly influenced by other dermal structures.
I would add that the subjects were required to ride exercise bikes to start the sweating through "internal" heat generation. The external temperature and so any shielding from this, was not rellevant.
The methodology in this study was very precise, even the physiology of the sweat glands themselves was examined. This showed that androgens were not "directly" effecting the glands. There was no changes in the size of the glands, like there are changes in the size of hair follicles.
Really the only explaination for this major change in the capacity of sweating in these areas, is DHT induced changes in the local tissue fluid pressures. Sweat is after all tissue fluid!
Michael said:
Further note on L'Oreal.......I dont take everything as gospel that "a huge and clever marketing company"--Dr. Loren Pickart on L'Oreal on his chat forum in a response to me----comes up with, but I could'nt help thinking about your ideas when I seen that part of the study. Stephen, have you ever considered its the hormones that shrink the follicle initially, and the contact inhibition (be it from collagen thickening, hardening of the skin, fluid pressue) that restricts it from re-enlarging even after one is using anti-androgens, etc. I mean If DHT causes pressure to rise one way or another......then if youre castrated, all your hair should re-enlarge theoretically, but that doesnt happen. Do you have a take on that?
I think the only logical train of events is a DHT induced change in the local fluid pressure, via increasing lymphatic pumping. This one action combined with the layout of the lymphatics and the human vascular system, explains "all" subsequent events in DHT related hair growth/loss.
The changes in the local fluid pressure explains the increased body and beard growth by reducing the pressure around these follicles. The "opposite" effect of increasing fluid pressure in the male pattern baldness area, because of the local fluid dynamics, shrinks the follicles through early contact inhibition.
These same fluid pressure changes explain the sweating changes in these same areas. The increased fluid levels in the male pattern baldness scalp over time, also explain the immune infiltrate, cell damage noted in the L'Oreal article, and the fibrosis that developes in male pattern baldness tissue. As i have referenced before, all these tissue effects noted in male pattern baldness are already recognised in lymphedema.
In my opinion just removing the hormone trigger does not reverse male pattern baldness because of the secondary formation of fibrose tissue around the "already" miniaturised follicles in male pattern baldness. This is why the longer an individual has been balding, the harder it is to reverse as you state above.
This is the only logical sequense of events given the observations in my opinion.
Any other explaination for the sequense of events, needs to use more "mechanisms", and is not therefore "Ockham's razor friendly"
For example, If DHT is directly effecting follicle growth, how is it also effecting sweating production? Unlike the follicles, cell multiplication is not changed in sweat glands, so straight away another mechanism has to be added. Likewise in answering the immunology question the "direct" theory needs another mechanism.
An initial "Hydraulic" change caused by DHT, explains it all through one basic "mechanism"
The "Hydraulics" also make sense in terms of the evolution of hair as an insulator, and the performance effects of androgens.
Michael said:
Further note: I hope the antimosity between Stephen, Bryan, and Dave dont get them to stop posting on threads with/against one another. That would be a shame.......everybody has the same goal (I hope) which is the most successful treatment of male pattern baldness currently possible....
I hope that my record speaks for itself here, in that i respond in kind to people. I have no problem with any critism of my personal ideas, as long as they are presented with basic common courtesy as your points are.
Points scoring word "games" and pure attention seeking on these forums dosen't move us forward, and i will point it out when i think i see it .
Going away for a couple of days now, good luck to all.
S Foote.