I have a PhD in Pharmacology and Toxicology, with a BS in Neurobiology, Physiology, and Behavior and a minor in Biochemistry.
I have been published.
I have been a biomedical researcher for 17 years.
I know more about the detailed workings of the human body than any MD you have seen or will ever see.
There are probably less than 50 researchers in this country who have attained the level of knowledge that I have regarding novel drug development and treatment, such as the treatment of severe acne with high dose B5..
Or running a SERM on cycle to prevent suppression, because SERMs are ER-alpha inverse agonists and ER-beta agonists, and circulating androgens inhibit LH secretion at the pituitary level (J Steroid Biochem Mol Biol. 1996 Nov;59(3-4):315-22) while inhibiting GNRH secretion at the hypothalamic level (J Clin Endocrinol Metab. 1992 Jun;74(6):1227-35.), both sites SERMs act upon. So, since E2 is a much more potent stimulus for negative feedback, blocking ER-alpha thus more than cancels out the inhibitory effects of elevated androgen levels. It's analogous to taking two steps forward (SERM inverse agonism at ER-alpha) and one step back (androgen-induced negative feedback on hypothalamic and pituitary AR).
"The inhibitory effect on gonadotropin secretion is mediated mainly by estradiol from endogenous conversion of testosterone rather than direct androgen action, at least in the pituitary gland (J Androl (1994) 15(1):15–21 ) Indeed, other studies suggested that in situ aromatization of testosterone is required both at the hypothalamic and pituitary levels to insure a complete feedback mechanism of gonadotropins (J Clin Endocrinol Metab (2001) 86(6):2600–610.1210, [and] ( J Clin Invest (1987) 80(3):631–810.1172)"
You. Stop. Talking.