If proviron, adex/ldex, clomid and femara among others are anti aromotase anti-Es that downregulate or fully block estrogen from ever being produced, why would we still use anti-Es such as nolva or exemastane?
Wouldn't we all like to stop estrogen at the source instead of "fixing" it while it has already been produced?
One argument that I could possibly see is to stack nolva with an anti-aromotaze anti-E because of nolva's positive effects on your lipid profile and cholesterol, but other than that, I see none.
Wouldn't we all like to stop estrogen at the source instead of "fixing" it while it has already been produced?
One argument that I could possibly see is to stack nolva with an anti-aromotaze anti-E because of nolva's positive effects on your lipid profile and cholesterol, but other than that, I see none.