Healthcare of the Transgender Patient (Powers Method)

• 46:28–46:40Blocker philosophy: Historical blockers "stuff like finasteride and spironolactone which I despise"; his method uses bioidentical hormones and rarely bicalutamide (androgen receptor inhibitor).
• 50:35–50:54Allopregnanolone–finasteride link: Brexanolone (IV allopregnanolone, 48-hour infusion) treats severe postpartum depression; allopregnanolone is "heavily depleted" in those patients — "do you know what else depletes [allo]pregnanolone? 5-alpha reductase inhibitors. It blocks the synthesis of it. I wonder why there's such severe depression associated with the usage of finasteride but yet we hand it out like candy."
• 51:04–51:21Prescribing stance: Finasteride depletes a neurosteroid "super important to their general functioning"; he almost never prescribes oral 5ARIs — only topical compounded finasteride/dutasteride with minoxidil.
• 51:24–51:53Pointless blockade: 5ARIs don't lower testosterone, only block conversion to DHT ("three times stronger"); in patients with already-low T (0–15), prescribing finasteride means "you just expose them to the side effects for no reason."
• 55:19–58:54Rectal progesterone protocol (background for later PFS work): Oral progesterone ~95% destroyed by liver first-pass; rectal administration (distal third → systemic circulation) gives sustained 24h absorption; absorbed progesterone is a GABA agonist ("best sleep they've had"); at sufficient levels acts as a GnRH agonist — continuous (non-pulsatile) stimulation suppresses LH/FSH to zero, shutting down testicular testosterone to ~10–20 (adrenal levels), eliminating need for other blockers. (Mechanistic background relevant to his later PFS progesterone observations and "castration trial" concept.)

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