Fin blocks the conversion of T to DHT, that rarely causes lower blood serum testosterone levels and can possibly even increase them depending on what else you've got going on hormonally.
indeed, finasteride raised my T levels slightly, from 18 ng/dL to 30 ng/dL. the same enzyme that converts T to DHT (5α reductase) can also to convert progesterone to DHT via the backdoor pathway, but i reckon that would have a very small effect for most cis men (where normal progesterone levels range from 0.0-0.5 ng/mL, compared to 2.0-24.0 ng/mL in cis women during the luteal phase, and much higher during pregnancy).
a sudden hormonal change can absolutely cause changes to mood and libido, but with finasteride these seem to be rare and generally mild. i would expect them to lessen or even disappear after some time of continued treatment. i wonder how often finasteride is discontinued before the body even has a chance to adjust to the new hormone levels. the claims that the side effects persist after discontinuation are particularly dubious, and they remind me of castration anxiety.
Right, but it's not the serum levels that matter: it's the agonistic effect on various receptors. (Most) hormones don't have direct chemical effects on the body. According to Wikipedia:
> Relative to testosterone, DHT is considerably more potent as an agonist of the androgen receptor (AR).
> Right, but it's not the serum levels that matter: it's the agonistic effect on various receptors. (Most) hormones don't have direct chemical effects on the body. According to Wikipedia:
>> Relative to testosterone, DHT is considerably more potent as an agonist of the androgen receptor (AR).
Judging from this and your other comments in the thread, I'm assuming you're not an endocrinologist.
You're pulling quotes from tertiary sources that at first glance seem to support the argument you're making, but you're missing the broader context, which is that pharmacokinetics and our endocrine systems are way more complicated than you're giving them credit for. It's not as simple as "drug A makes X go down, and X does Y, so A decreases Y".
It would make a lot of people's jobs much easier if that were the case, but the clinical reality is actually much more complicated.
The endocrine system is indeed extremely complicated, but this is one of the simplest and best-understood parts of it. We know relatively little about the mechanism behind the psychological effects of sex hormones (for example, we have no idea why they seem to have different effects in different people, with some people being severely affected, and other people barely noticing), but we have a lot of data showing that there is an effect.
"Drug A makes X go down, and X does Y, so A decreases Y" is a good description of the operation of finasteride and dutasteride (if we disregard the unexplained differences between the effects of the two drugs (we'd naïvely expect one to be strictly "better" than the other, but this is not the case)) on everything except the brain. Everything else responds as you'd expect a priori from modelling hysteresis with pencil and paper. But there's a lot we don't understand about the brain.
