Yes, but in opposite to fin it converts to cortisol? Fin is an irreversible progestin in my eyes, not 0converting to cortisol. So kinda cortisol blocker.
To rebalance the lack of dht resp. to exhibit fin, estradiol rises. This is what he have seen in some fin users. They gain weight, have got a more feminine face.
Who could be targeted mostly?
ppl with high cag repeats - they are less sensitive to androgens so they have a higher androgen level. What happens when DHT goes down?
Right, their AR upregulate immensely, and this is followed by increased estradiol levels to exihibit the function of fin.
But if DHT returns massively, the upregulated AR shut down resp.partially close their function. And because AR are to be found nearly everywhere in the body (also gut), this process affects different locations and causes different issues.
Who is not that much affected: ppl with higher sensitivity to androgens.
When DHT is lowered, body needs not to upregulated extremely. So AR are not upregulated or not too upregulated.
When dht comes in again, those AR can better adapt or downregulate a bit.
Maybe there is case 3: extreme sensitive to androgens. Those ppl will have down regulated AR.
Conclusion: Upregulated AR? How to down regulate them?
Steps: DHT must be lowered again.
Question is: Testo as well or not?
I read that bringing down testo and dht with that as well, can downsentisize AR by uprising androgens (slowly?naturally?) to normal levels. So reduce to really bottom like testo levels and then slow increasing testo levels to normal plateau.
Background: cancer cells in prostate survive dht deprivation. And stopping fin is somehow not downregulating them if I remember well. That is the opposite situation with normal cells.
If I am right, we need to understand why AR in cancer cells react differently resp. downregulate. What is the mechanism? In both cases the cells resp. the AR want to survive.
Idea: We would need to study the prostate cancer patients when they stop fin.
