would that mean that DHT derived compounds would be likely to cause hairloss when used…like anadrol, winstrol, masteron enth, primo, proviron…
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.
- 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.
- 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.
- 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.