I can’t remember exactly when, but I discovered that the serious side effects from Propecia came from excessive amounts of estradiol. Finasteride isn’t supposed to do anything else than lower the DHT level by around 70%, and increase the total testosterone- and estradiol level by around 10%. However, DHT is a potent estradiol antagonist, and in some cases, the estradiol level gets out of control. This causes a chain reaction, and people end up with a wrecked endocrine system. I believe that estrogen dominance as a consequence of androgen deprivation, is the root cause. Not everyone develops secondary hypogonadism, but I believe that everyone here suffers from estrogen dominance, and that everything else - like problems with adrenal and thyroid hormones - are just a natural consequence. The way I, and two other people responded to low doses of Proviron, and the results from all the other experiments that I have conducted on myself since then, suggest that I’m right. I know more people have tried Proviron, but I suspect that they used too much. The ratio between androgens and estrogens is critical.
I currently don’t have access to Proviron, but I am treating myself with an alternative, and by the same principle. The transition isn’t that easy when you have been on TRT for years, because exogenous testosterone causes the testicles to atrophy. I’ve attempted to restart the system several times this year, but I’ve been forced to abort. Last time, I ended up in some sort of wave pattern, where my testicles grew and shrunk, while symptoms improved and got worse. It was like the body was tying to increase the production of testosterone, but couldn’t because something is off balance. I suspect that it’s because of DHT and 3a-DIOL deficiency. The reason I’m doing this, is because natural testosterone production with its rhythm, feels better than exogenous testosterone.
Btw, I have also found independent studies which shows that finasteride decreases the free testosterone level, and messes around with neurohormones - especially allopregnanolone, in everyone who’s using the drug! There is no doubt that the drug hasn’t been studied properly before it got approved by the FDA. I see the reduction in free testosterone as a natural consequence of the reduction in the DHT level, as DHT has stronger affinity for SHBG, and testosterone is next in line. I’m not sure why it interferes with neurohormones, because it’s a 5AR Type 2 inhibitor only - and those neurohormones are created by 5AR Type 1 only - but I have two hypotheses. 1) The levels decreases as a natural consequence to the reduction in the DHT level. Androgens, and especially DHT stimulates the brain significantly. 2) Testosterone binds to 5AR Type 1 as well, which creates DHT. Blocking the 5AR Type 2 enzymes will put more pressure on the 5AR Type 1 enzymes. We have a lot more testosterone than other hormones like progesterone, which is a precursor to allopregnanolone - and the affinity for the 5AR Type 1 enzymes may be stronger. In other words, precursors to neurohormones may get down prioritized.
