Almost everyone answers this by asking whether they take finasteride. That is the wrong question. Finasteride blocks one enzyme, and most compounds do not use that enzyme. This works out what fraction of your androgenic load is actually reachable by what you are taking, and what fraction is walking straight past it.
This is the single most informative input. Androgenic alopecia that has already begun behaves very differently under an androgenic load to a hairline that has never moved.
Once you know your risk, build the protocol around it with the Hair Loss Protocol Engine.
Only against testosterone. Finasteride blocks the conversion of testosterone to DHT, so it works where that conversion is the problem. Compounds that are already 5-alpha reduced, such as masteron, winstrol, anavar and proviron, arrive at the follicle with nothing left to block. Trenbolone and primobolan are not substrates for the enzyme at all.
It works against you. Testosterone and nandrolone are both 5-alpha reductase substrates, but the reaction runs in opposite directions. Testosterone converts to the more androgenic DHT, so blocking it protects you. Nandrolone converts to dihydronandrolone, which is considerably weaker, so blocking the enzyme leaves more of the stronger parent compound acting on your follicles.
Trenbolone and halotestin sit at the top, followed by masteron, winstrol and superdrol. What they share is that no oral hair medication reaches them, either because they are already reduced or because they bypass the enzyme entirely.
It has a reputation for being mild that does not extend to hair. Anavar is a DHT derivative, which puts it entirely outside finasteride's reach regardless of dose.
Only things that act downstream of the enzyme. Minoxidil works regardless of which compound you run because it acts on the follicle rather than the androgen. Topical antiandrogens act at the receptor, though they are unapproved research chemicals with no human safety data, which is a real trade.
