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Let's focus on the FUNDAMENTALS, not the little details (Topicals)

posted by benji, 09.04.2008, 22:27

Bryan,

Men WITHOUT MPB have body hair that responds well to androgens.

Studying the difference between body hair and head hair is an empty procedure in my opinon. Body hair does not grow in big follicular units of groups of 3-6 hairs like head hair does in donor-areas of the scalp. Body hair grows in 1 and 2 hair units (mostly ones), is usually thinner, and does not grow as long as head hair, even when transplanted to the scalp (usually about doubles its length at best).We are never going to be able to "change" head hair so fundamentally that it will actuall "like" androgens. Beard hair has the longest growth cycle on the body, but beard hairs are huge in thickness and only grow one hair at a time. I see no way to convert beard hairs into head hairs or vice versa. Im interested in the difference between MPB-hairs and donor-area hairs...............and what we can do to get these two similar hair types to behave the same, i.e. be relatively unaffected by androgens most of one's life.

What goes on when scalp skin in the first trimester of a woman's pregnancy "makes" hair at the top of the head so much more sensitive to androgens vs. donor-area hair? That is something perhaps we can effect. I dont think we will ever be able to fiddle with DNA enough to make head hair not only like androgens, but look like head hair is supposed to look (big folliclar units, not kiky and ugly, etc.)


DKK-1 and its causation of keratinocyte cell death in or near the infidulum seems to be the best clue as to why the first inflammation in AGA happens at the infidulum first and its centered around that area for the duration (upper third of the follicle). I'd love to see if this is *the* reason for the immunological response. I keep cyclosporin's prowess in regrowing hair in mind here....................what if we could make the immunse system no longer interested in the follicle with a DKK-1 inhibitor Bryan? Then things like Prox-n might have a chance of regrowing long-miniaturized hairs -perhaps- with a relatively mild anti-androgen like finasteride. Thats my hope anyway.

Harold, over at HLT, has pointed out before that balding follicles seem to lose CD200 molecules around the follicle itself and that this substance tells the immune system "not to attack". Ive wondered if that has anything to do with it also.



Other than DKK-1, we are back to DNA within the follicle (which might take years to figure out), and finding better and better skin-remodellers and anti-androgens (AJSC-9 maybe). In other words, kinda stuck.













By the way......................here is that article about sebaceous gland androgen receptors uptaking more androgen in experiments that receptors from occipital scalp:

Increased androgen binding capacity in sebaceous glands in scalp of male-pattern baldness.Sawaya ME, Honig LS, Hsia SL.
Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Florida 33101.

Sebaceous glands were isolated by manual dissection under a microscope from surgical specimens of scalp skin with male pattern baldness and skin specimens of hairy and bald scalp obtained at autopsy. The 800 X g pellet (nuclear fraction) and the 164,000 X g supernatant fraction (cytosol) of homogenates of the sebaceous glands were used for measurements of androgen binding characteristics, using dextran-coated charcoal and sucrose gradient methods. Scatchard plots showed high affinity binding for [3H]dihydrotestosterone (DHT) and [3H]methyltrienolone (R1881). Nuclei prepared from bald scalp contained greater total androgen binding capacity than nuclei of hairy scalp, although Kd values of type I binding were similar (0.68 vs 0.56 nM, respectively). On sucrose gradient, the binding protein from cytosol was found in the 7 to 8S density range. Androgen binding by cytosol of sebaceous glands of hairy scalp had Kd of 1.89 +/- .79 and 2.05 +/- .56 nM for DHT and R1881, respectively, and Bmax of 18.7 +/- 4.4 and 20.0 +/- 4.6 fmol/mg protein for DHT and R1881, respectively. Cytosol from sebaceous glands of bald scalp had Kd values approximately half those of hairy scalp, and Bmax values 50%-100% higher. The bound 3H labeled DHT and R1881 could be partially displaced by testosterone (40-50%), moxestrol (28-32%), promegestone (19-26%), and delta 4-androstenedione (6-12%), but not by dehydroepiandrosterone. These data demonstrate the presence of specific androgen binding protein in sebaceous glands, and that sebaceous glands of bald scalp have greater binding affinity and capacity for androgens than those in hairy scalp. This difference may explain the greater androgenic response in androgenic alopecia.

PMID: 2909628 [PubMed - indexed for MEDLINE]


 

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