High Testosterone as well as DHT can cause apoptosis in hair

[michael barry]

1: Skin Pharmacol Physiol. 2006;19(6):311-21. Epub 2006 Aug 23.Links
Effect of 5alpha-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells.Winiarska A, Mandt N, Kamp H, Hossini A, Seltmann H, Zouboulis CC, Blume-Peytavi U.
Department of Dermatology and Allergy, Charité-Universitatsmedizin Berlin, Berlin, Germany.

Pathogenetic mechanisms in androgenetic alopecia are not yet fully understood; however, it is commonly accepted that androgens like testosterone (T) and 5alpha-dihydrotestosterone (5alpha-DHT) inhibit hair follicle activity with early induction of the catagen. Thus, [b]we investigated the influence of T and 5alpha-DHT on proliferation, cell death and bcl-2/bax expression in cultured dermal papilla cells (DPC) from nonbalding scalp regions of healthy volunteers[/b]. T and 5alpha-DHT induced apoptosis in DPC in a dose-dependent and time-related manner; in addition a necrotic effect due to T at 10(-5) M was found. Interestingly, bcl-2 protein expression was decreased in T- and 5alpha-DHT-treated cells, leading to an increase in the bax/bcl-2 ratio. In addition, T and 5alpha-DHT induced proteolytic cleavage of caspase 8 and inhibited proliferation of DPC at 10(-5) M. High concentrations of T and 5alpha-DHT were needed to induce apoptotic effects in DPC. These data suggest that DPC from nonbalding scalp regions do have the capacity to undergo apoptosis, but need a high androgen stimulus. The present study provides an interesting new pathogenetic approach in androgenetic alopecia.

PMID: 16931898 [PubMed - indexed for MEDLINE]





This is a repost of a study from 2006. I think its instructive

 

[joemadrid]

Can Testostetone be reduced with a topical cream or something?

 

[IBM]

Can Testostetone be reduced with a topical cream or something?

Maybe with spironolactone cream?

 

[michael barry]

Im going out on a limb here, but based on a sebum secretion study on the human forehead in a patent by Liang and Lao in which a man had his sebum reduced to damn near nothing.............................Id say use topical green tea extract put in purified water, shaken up to near saturation levels of solubility..............then add about 30% alcohol as a carrier. I'd bet that would outdo spironolactone. Green tea's EGCG outdid spironolactone on hamster flank organs. I'd make sure I bought the good green tea extract from a well-known very reputable supplier like Natures Choice or Vitamin World or GNC however. Get the good stuff.

 

[blaze]

Excessive sebum production is a problem for alot of ppl. Why havent they brought out a topical green tea for this problem if it works so well?

 

[harold]

A lot of reasons potentially. Firstly and foremostly as a powerful antioxidant EGCG tends to...oxidise. The same problem as with spironolactone solutions only worse. In that patent that michael posted they mention at the end how quickly most of these polyphenols tended to "go bad" (keeping the ph low is supposed to be greatly beneficial as mentioned by Liao et al. Also keeping it in a sealed container and refrigerated is going to help a lot also. Possibly the addition of another antioxidant to help spare it.). Curcumin incidentally has an insane degradatiuon time with something like 90% being degraded in solution within about 30 minutes IIRC. And thats if you can get it in solution - its pretty much only soluble in oil. So yeah there are practical problems with a lot of this stuff that would more or less rule them out as a prepackaged mass produced topical.

 

[harold]

Yeah DHT is a lot more androgenic than testosterone but its not that much more androgenic. Which is probably why some people can still function sexually with almost no DHT and some continue to bald whilst on several mg of avodart. Interestingly you could kill hair follicles with estrogen in a test tube if the concentration was high enough - it binds the androgen receptor also - only with much lesss affinity than testosterone or DHT. But if the concentrations were high enough and you could remove the estrogen receptor mediated effects it should be possible to do just that.
hh

 

[philly]

...

 

[JayB]

getting real sick of "spironolactone" still mentioned on here. Noone has gotten benefits from, face it.

 

[abcdefg]

Yeah spironolactone is mentioned all the time but its not approved for male pattern baldness and as far as I know has no major studies to prove it even works. We know androgens like testosterone also effect hair. We know enough as of today to come up with a much better treatment but no one seems to do it. It certainly seems possible that a treatment could bind to receptor sites and lower androgens to near 0 and it would prevent male pattern baldness if you caught it in time. Propecia while good is now like 15 years dated and we have learned a lot since then.

 

[harold]

What would be awesome/the most desirable treatment IMO would be a hair thickening agent or majorly effective hypertrichotic. Kind of like a scary versiopn of minoxidil. Like dont spill this on your hands or you will be shaving your palms for the next 6 months. I think we are getting near to the stage where we could develop such a thing and quit messing about with androgens altogether. The manipulation of substances like wnt/BMP/EDAR/p63 that directly effect hair development and hair thickness is the goal and luckily for us there is a lot more research going on in this area than there is in creating "another finasteride". In fact half the reason another finasteride or RU hasnt come along is because people are pouring more into understanding hair growth at the molecular level and anyone who was working on a new RU would have to be concerned that someone else would make their product and their investment redundant with their super hair growing formula.
Of course though we are close to being able to do such a thing in the lab it might be years before we see it ourselves - depending on how succesful Follica is.
hh

 

[michael barry]

Harold,

Its my understanding after the androgen receptor brings DHT to the nucleus, then it gets "read" and the negative anti-gens get released to the rest of the follicle. Docj077 used to think that if we could keep TGF-beta from getting released, none of the other bad stuff would happen. I had noted that DKK-1 might be another important antigen to block also. The best thing (of course) would be to find what gene is directing the process and somehow counteract it or induce it to tell the DP cells to release mitogens to the rest of the follicle instead.------------------------but how do we do this without risking runaway cell growth. I know that TGF-beta is cancer-protective over the long term. Its been speculated that the hair cycles themselves are "there" to shut off mitogen activity in each hair for a while during shedding and rest phases perhaps as a chemopreventive event in mammals and evolved that way just for that. Thoughts?