Interesting random study I found while puttering around pubmed... it's significant because there is no real specific knowledge about how the mechanism works in hair loss, just DHT's action at the hair follicle.
Dihydrotestosterone inhibits murine hair growth via the androgen receptor.
Naito A, Sato T, Matsumoto T, Takeyama K, Yoshino T, Kato S, Ohdera M. Biological Science Research Laboratories, Research and Development Headquarters, LION Corporation, 100 Tajima, Odawara, Kanagawa 256-0811, Japan. firstname.lastname@example.org BACKGROUND: Androgens cause regression of human hair follicles in the parietofrontal scalp, but the precise mechanisms by which they do so are unknown. Although many investigators have elucidated the effect of androgens on hair growth by using rodents and other animals, some of the evidence is conflicting. OBJECTIVES: To investigate the effect of androgens on mouse hair regrowth and hair cycle by using androgen receptor knockout (ARKO) mice. Methods We examined the effects of dihydrotestosterone (DHT) on hair regrowth by using ARKO mice and wild-type (WT) littermates, compared the hair cycles in ARKO mice and WT littermates by histology and histomorphometry, and measured hair length and thickness in ARKO mice and WT littermates. RESULTS: DHT inhibited the hair regrowth of WT mice but not that of their ARKO littermates. The anagen phase in the second hair cycle was longer in ARKO mice than in their WT littermates. The hair of ARKO mice was longer and thicker than that of their WT littermates. CONCLUSIONS: Androgens inhibit hair growth in mice, and this inhibition might be caused by androgen-androgen receptor signals.
It depends on the individual compound. I'd certainly concur on mast, from personal experience. But simply having a DHT base doesn't mean you're going to lose handfuls of hair. Additionally, there are many AAS that are metabolized after the fact... i.e. in the body by 5AR, leading to strong DHT derivatives, hence the reason some peeps use 5AR-inhibitors.
True. It would seem most likely that DHT derived compounds retain the higher affinity for the AR that the parent molecule has, but this cannot be directly tested via assays due to legal status and a lack of demand in the research field. Also there are other questions at hand--for instance some class 1 steroids (AR binding) seem not as bad in terms of hair loss as others, despite maybe having a higher binding affinity for the AR than their competitors. Further, although the AR may be very important it is surely not the only pathway involved in determining hair loss.
However, I felt it was an interesting study because for the most part the biochemical mechanisms/pathways to hair loss are incompletely understood, and BBer's can run into trouble with all the exogenous hormones they might decide to use.
More importantly, though, this means you have another avenue for protecting your hair if you are prone to hair loss and decide to use AAS.
1) inhibit the production of DHT in the scalp--finasteride and dutasteride do this. However, unless you are using a topical formulation of the drugs (and I am not aware of whether their bioavailability or effectiveness through topical formulations is any good), you will be taking the drugs orally, suppressing DHT production system wide.
This is usually what is done by BBers, although this can lead to a separate set of problems (albeit not very likely).
Also this does NOT do anything to stop the metabolites of of non-testosterone derived steroids from doing their thing on the AR, and it does not stop the action of DHT once it is produced.
2) You can block the binding of compounds (not just DHT) to the AR in the scalp itself. This can be done by using a competitive inhibitor, an anti-androgen, in a topical formula. I would [u]NEVER[/u] use an oral formula unless you were being treated for cancer under personal doctor supervision. You don't want the AR inhibited system wide. Spironolactone is the most widely available anti-androgen. I am sure somewhere somebody has made a topical preparation.
Bicalutamide and flutamide may also be available, but they carry in general more incidence of side effects when used orally, and flutamide is recommended against. I have no knowledge of bicalutamide, but it is supposed to have less incidence of sides. In addition bicalutamide is supposed to accelerate the actual degradation of the AR itself besides inhibiting binding of compounds to the receptor.
3) You can increase blood flow to the scalp. Minodixil (that's Rogaine) does this and a few other compounds do this. There are probably other effects, as minoxidil's mechanism is not known but is believed to maybe act directly on the hair follicle itself. It is, however, known that the compound is a vasodilator. It has a topical availability of approximately 1.5% according to some sources I've seen, so any topical formulation must contain a large excess of the drug in order to ensure saturation.
Oh, and I meant to post this up a while ago with the first abstract, but it didn't go through and I forgot about it....
Melatonin and the hair follicle.
Fischer TW, Slominski A, Tobin DJ, Paus R. Department of Dermatology, University Hospital Schleswig-Holstein, University of LÃ¼beck, LÃ¼beck, Germany. Melatonin, the chief secretory product of the pineal gland, has long been known to modulate hair growth, pigmentation and/or molting in many species, presumably as a key neuroendocrine regulator that couples coat phenotype and function to photoperiod-dependent environmental and reproductive changes. However, the detailed effects and mechanisms of this surprisingly pleiotropic indole on the hair follicle (HF) regarding growth control and pigmentation have not yet been completely understood. While unspecific melatonin binding sites have long been identified (e.g., in goat and mouse HFs), specific melatonin membrane MT2 receptor transcripts and both protein and mRNA expression for a specific nuclear melatonin binding site [retinoid-related orphan receptor alpha (RORalpha)] have only recently been identified in murine HFs. MT1, known to be expressed in human skin cells, is not transcribed in mouse skin. After initial enzymologic data from hamster skin related to potential intracutaneous melatonin synthesis, it has recently been demonstrated that murine and human skin, namely human scalp HFs in anagen, are important sites of extrapineal melatonin synthesis. Moreover, HF melatonin production is enhanced by catecholamines (as it classically occurs in the pineal gland). Melatonin may also functionally play a role in hair-cycle control, as it down-regulates both apoptosis and estrogen receptor-alpha expression, and modulates MT2 and RORalpha expression in murine skin in a hair-cycle-dependent manner. Because of melatonin's additional potency as a free radical scavenger and DNA repair inducer, the metabolically and proliferatively highly active anagen hair bulb may also exploit melatonin synthesis in loco as a self-cytoprotective strategy.
BR showed me quite how much extra Test'rone is freed up by adding Proviron; WRT SHBG, and it is considerably too small to notice jack. Ever.
Trust me, i used to be a big proponent of Mesterolone too.. so for anyone to say this it should mean the most from me.
However adding it DOES have some benefits (although they are benefits you can also get from other AAS which also provide more positives that proviron does NOT have). That is not to say it doesn't have uses though. It does IMO.
Yes it is Androgenic - of course it is, it is derived from DHT. It is prescribed as an Androgen too.
Surely you have come across all that if you have read quite a bit on the drug?
I never said it had no effect on the hair. It does aggravate MPB in those who have the gene, although i am confident other androgenic substances are worse in that area, but seeing as Provion has no real anabolic effect, it is a non-issue.
You should know that it is not necessary to know the exact actions of androgens and all the other endocrine functions affected by AAS use - in order to use them.
Some members here are fascinated with the subject and as such study a great deal in their spare time, for personal or professional reasons - others are students or hold related degrees and others are employed or used to be employed in a related field.
However this is not a pre-requisite of using AAS. You DON'T need to know the molecular structure of Test or the weight of esters to use the shit. A decent basic knowledge (such as in the 'stickies') will more than suffice.
Just making sure that you aren't under the impression you NEED to learn tons of stuff to use the drugs safely - ie. Androgens role in Libido.