Inhibiting cytochrome CYP450 3A4 actually increases a higher bioavailability of certain drugs, thus...inducing the very same enzyme means it's not benefiting E. (St. John's wort is a good example inducing CYP-3A4). What we (aria and i) found out (3-4 years ago) is that statins inhibit T and benefits E.
Keep in mind, PM needs liver activation to synthesize dexoy & miroestriol, there's a high significance that an interconversion between E2(estradiol) & E1(estriol) are working under the hood..or...like a very active ping-pong game, needless to say PM acts more like estriol (less powerful) than E2, which as we know E2 is the highest feminizing hormone, but " free E2 " is technically the mother of all feminzing because it's bioactive to E receptors.
Keep in mind, PM needs liver activation to synthesize dexoy & miroestriol, there's a high significance that an interconversion between E2(estradiol) & E1(estriol) are working under the hood..or...like a very active ping-pong game, needless to say PM acts more like estriol (less powerful) than E2, which as we know E2 is the highest feminizing hormone, but " free E2 " is technically the mother of all feminzing because it's bioactive to E receptors.