What's Happening to Androgen Metabolism in PFS? Dr. Will Powers #finasteride #podcast

• 0:00–0:18Thesis: "To summarize how we think PFS works... when I looked at the genomes of people with PFS, specifically the androgen metabolism systems of them, they are broken at baseline in their genome before they ever took finasteride."
• 0:21–0:35Exit pathways: A testosterone molecule "gets options" like Google Maps destinations: sulfation, hydroxylation, DHT 3-alpha metabolites, glucuronidated. "Most of these people lack glucuronidation in some capacity."
• 0:38–0:53Highway analogy: 15-lane highway for testosterone disposal; finasteride removes 5 lanes — "no big deal" with 10 remaining, "no side effects, no issues at all."
• 0:53–1:06Selection bias: With only 6–7 lanes at baseline from genetic deficiency, glucuronidation-deficient people run masculine/high-DHT (seen in women too).
• 1:10–1:33The trap: High DHT → hair-loss complaint → doctor prescribes finasteride → "then you find out, 'Oh god, I had no redundancy pathways.'"

Timestamps come from auto-captions and can be off by about five seconds.

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