In my opinion based on studying of endocrinology, getting sides depends on various factors, not just on suppressed level of DHT. Major sides are not result of low level of DHT, but increased level of estrogen, estradiol, prolactin, and loss of hormonal balance. I am aware, that DHT inhibitors block conversion of T to DHT and in that way boost E and E2, because free T can be converted either to DHT (by I and II-5ard) or E (by aromatic enzyme).
Maybe high doses of finasteride cause some kind of shock and rebound effect- body notice lack of DHT by its receptors and start to produce more free T and even more 5ard enzymes (endless loop - this makes no logic to me, but its possible). And if you go with small doses then body gradually adjust to new condition - some hair loss veterans here suggest the same - to start with small doses and then gradually increase. Same with quiting finasteride, not cold turkey but taper off.
Except shock and rebound effect, pharmacokinetics and dynamics of drug play huge role. 1 mg dose or more neutralizes certain percent of 5ard,but I suppose it doesn't achieve its full potential because ofhalf-life time, after which finasteride become degraded. That's common effect in all medical drugs. It takes a while for active drug ingredients and molecules to spread within whole body (intra and extra cellular tissue). So, 0.25 mg works the same way but in a slower rate.
But important part is that finasteride "attacks“ other substrates and enzymes (not just II 5-alpha-reductase). And for finasteride to be effective it is important to inhibit specific enzyme 5ard-II but it would be perfect for drug to inhibit only 5ard, not other molecules and substances. Maybe finasteride molecules bind / adhere to other enzymes, substrates or so, is there any study to confirm that ?
