@DrMariano 745 wrote:

Dihydrotestosterone is the active androgen in the brain. Testosterone is the precursor to DHT.

In regard to central nervous system activity, DHT has the same functions as testosterone, except that it cannot become estrogen. It only acts as an androgen.

DHT is a very calming signal, as well as the signal than supports libido. It helps males more stoically approach stressful situations.

Perhaps excessive DHT could lead to an overly relaxed male with impaired motivation for activities other than sex. Jokingly, this would be someone like Al Bundy, in the television show, Married with Children, sitting in his couch, watching television, with his right hand under the belt, touching his crotch area.

Estrogen provides competitiveness, aggressiveness, drive, and supports libido (sexual territoriality or sexual aggression/desire). Since DHT cannot be converted to Estrogen – like Testosterone can – than DHT cannot provide these behaviors.

I thought DHT was a stressful signal, and so it proves to be the complete opposite. Interesting and most especially educating.

Clearly, too much relaxation can lead to inaction. While it’s good to approach life calmly, too much of this can prevent someone from taking appropriate action, and this can be bad under some circumstances, where one’s ability to make quick thinking is called for.

Since DHT is allegedly 30 times more powerful than Testosterone, does this mean that when present in excess as opposed to other hormonal signals, that it makes these other signals much weaker ? If so, then lowering DHT would allow other signals to perform better.

In an individual with off-the-chart serum DHT, would Finasteride be the only viable treatment modality ? Anecdotally, some men seem to experience nasty long term side effects from Finasteride, even long after they’ve discontinued taking the drug.

I’m thinking progesterone is an effective 5AR inhibitor (I do not know whether it inhibits both types of 5-AR enzymes though). I’m also thinking of green tea, which seems to inhibit DHT to some extent. Saw Palmetto or beta-sitosterols, which appear to be more potent than saw palmetto.

In one with elevated serum DHT (taking account DHT is much more powerful than T), would DHT overpower testosterone’s effect in the CNS ? Assuming some Testosterone is needed in the CNS for libido to take place. I know that there needs to be some DA present in the mesolimbic region for libido to take place, but I do not know whether some testosterone needs to be present for DA to reach the needed level, although I know that Testosterone can increase DA.

Given E2’s role in male libido (acting as an MAOI), I also assume some of the Testosterone present in the CNS (if I’m not mistaken that some is indeed needed) is aromatized to E2 to produce libido. Am I making sense ? However, if elevated DHT overpowers CNS testosterone, then E2 cannot be made then since DHT cannot aromatise to E2. On the other hand, I may be off here since DHT is stronly correlated to male libido. So there must be a link between DHT and DA in the CNS. I recall that DA can have both excitatory/inhibitory effects depending on the receptor subset that’s hit.

It seems that what’s responsible for elevated serum DHT is increased activity of the enzyme 5-Alpha Reductase, but is there anything that can cause increased activity of this enzyme to begin with ? Worded differently, what are the known causes of elevated DHT ?

Does elevated DHT have any role of play in below par erections ? I even seem to recall quite the opposite, that DHT is linked to the release of NO, but I do not know it all, so I may be missing important info here.

Is it possible for one to have both off-the-chart DHT and elevated E2 ?

Many thanks

Thanks, that discussion was quite helpful in clearing up a few points I’d been wondering about. I can now rest in peace, in a manner of speaking of course.