“Drake, Lynn, et al. “The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia.” Journal of the American Academy of Dermatology 41.4 (1999): 550-554.”.
Can’t post a link because it’s behind a paywall my university has a subscription for. That study is published in a well respected journal and sees to be cited many times
“Scalp skin DHT levels declined significantly by 13.0% with placebo and by 14.9%, 61.6%, 56.5%, 64.1%, and 69.4% with 0.01, 0.05, 0.2, 1, and 5 mg doses of finasteride, respectively. Serum DHT levels declinied significantly (P<.001) by 49.5%, 68.6%, 71.4%, and 72.2% in the 0.05, 0.2, 1 and 5 mg finasteride treatment groups, respectively.”
The values are without error margins but I’m willing to bet that they might not even differ significantly.
I’m not sure why you claim that my post contains mis-information and then proceed to say the exact same thing.
It’s a competitive inhibitor, sure. But that just means that the affinity for finasteride to the enzyme is much larger than the affinity of testosterone to the enzyme. If it was reversible you wouldn’t see such a flat response and it also wouldn’t take 2 weeks for DHT to go back to baseline.
Finasteride does irreversibly inhibit any 5alpha-reductase it comes into contact with (see e.g. the Merck patent which is even called “Irreversible inhibition of human 5?-reductase ” https://www.google.com/patents/US5962442 ” In practice, the halflife of the enzyme-inhibitor complex is so long that the inhibition is for all intents irreversible, and release of the inhibitor probably occurs by death of the enzyme rather than turnover to regenerate catalytically competent enzyme.”) .
That’s as good as destroying the enzyme because it forms a strong bond with it that has a longer half-life than the enzyme itself. In other words, the enzyme will die long before it’s able to release finasteride.
The body replenishes 5AR constantly and that’s exactly why it takes >2 weeks for the DHT to go back to baseline.
Nice citations; however, the effectiveness of finasteride may be due to other factors such as the sensitivity of the receptors and the rate at which the enzyme is turned over in response to the blockade, etc.. Enzymes are always consumed in a chemical reaction and the human body just produces more of it. Skin levels may not be reflective of the type of response seen clinically. This is the practical side, because we see patient who do not respond to the drug regardless of the dose and then we see great responders. I can’t address your mechanistic point very well and correlate the DHT levels, enzyme levels and clinical responses. You have clearly spent more time on this than I have; however, what I focus upon is clinical responses and side effects to the drug. With my focus, the pharmacology you reference does not produce a one-to-one clinical response with the values of DHT in the skin as you are referencing.
I like it when the consumer does research on what is happening to them and the treatment options. Sometimes what is read needs to be filtered by an expert so that is my role here in this reader’s posting which I am publishing at his request.