SRD5A1 — epigenetic silencing (acquired, not germline)
Confidence: directcirca May 2026
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Powers’ claim (paraphrased)
SRD5A1 (like AKR1C enzymes) can be epigenetically silenced, and valproic acid (an HDAC inhibitor) appears able to reverse this in his patients, with slow normalization over months.
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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 gene claim
AKR1C1; AKR1C2; AKR1C3; AKR1C4 — defects (unspecified)
Confidence: direct
Defects in AKR1C enzymes can contribute, but their products are mostly cleared via glucuronidation — so a bad glucuronidation enzyme (UGT2B1X) is the more fundamental defect. AKR1C enzymes and SRD5A1 are also epigenetically silenceable, and valproic acid may…
AKR1C1AKR1C2AKR1C3AKR1C4SRD5A1PGL-AKR1C1-AKR1C2-AKR1C3-AKR1C4circa May 2026PFSCore corpus - Peer-reviewed paper
Epigenetic regulation of 5α reductase-1 underlies adaptive plasticity of reproductive function and pubertal timing
Ben Bar-Sadeh; Or E. Amichai; Lilach Pnueli; Khurshida Begum; Gregory Leeman; Richard D. Emes; Reinhard Stöger; Gillian R. Bentley · BMC Biology
Women who experienced high energetic demands in childhood show altered adult ovarian function and shorter reproductive lifespan, suggesting early-life programming of reproduction. Combining a mouse model with methylation analysis of proxy-tissue DNA from a…
ARSRD5A1LIT-0582022Literature sweep · Oct 2026