Dr Will Powers’ own statements and theorizing
Powers’ claim (paraphrased)
A defective HSD17B2 (which converts testosterone to androstenedione) worsens the backup; androstenedione remains androgenic and still requires glucuronidation, sulfation, or aromatization for exit.
Some fields on this page come from the release’s Markdown edition, which carries text the JSON edition omits.
Related records
- Powers · Reddit post
I think I have figured out at least one specific phenotype of PFS, and it is different from the "allopregnanolone" theory
u/drwillpowers · r/DrWillPowers
Powers' key genetics-first post: he proposed a specific PFS phenotype whose "base, core defect" is defective UGT2B17, disabling testosterone's main glucuronidation exit pathway. Carriers show shockingly low 3α-androstanediol glucuronide and near-zero urinary…
AKR1C1AKR1C2AKR1C3AKR1C4HSD17B2+3DWP-0032026PFSCore corpus - Powers · Reddit post
Has anyone here taken finasteride or dutasteride and gotten post finasteride syndrome (PFS) from them? I have a theory as to why this seems to happen in transgender women more than cis men
u/drwillpowers · r/asktransgender
Powers proposed that PFS stems from deficient allopregnanolone, a neurosteroid produced downstream of 5-alpha-reductase via the AKR1C enzyme family. He hypothesized that only people carrying decreased-function variants in AKR1C genes develop the syndrome when…
DWP-0012020PFSCore corpus - Powers gene claim
UGT2B17 — defective (major)
Confidence: direct
A defective UGT2B17 disables the main glucuronidation exit pathway for testosterone — the "base, core defect" of this PFS phenotype. Carriers show shockingly low 3α-androstanediol glucuronide and near-zero urinary testosterone on DUTCH despite normal serum T…
UGT2B17PGL-UGT2B17circa May 2026 (archived 2026-05-08)PFSCore corpus