Re: Im back from the pfs congress i know everyone…
u/drwillpowers
r/DrWillPowers2026-05-13T16:42:59Z
Dr Will Powers’ own statements and theorizing
Summary (paraphrased)
Reply in his post-PFS-congress update thread addressing heritability. Powers distinguishes susceptibility from the syndrome itself: the androgen-metabolism glitches (e.g., a homozygous UGT2B17 deletion) can be passed on, but PFS itself cannot be inherited — offspring inherit only susceptibility, mixed with the other parent's genes. He illustrates with a hypothetical cross: if one parent had a fully deleted UGT2B17 (no functional enzyme) and the other had two normal copies, essentially all children would be heterozygous carriers (barring rare de novo mutation).
Key points (paraphrased)
- Susceptibility is heritable; PFS itself is not.
- Illustrated inheritance pattern for a homozygous UGT2B17 deletion × normal genotype → heterozygous offspring.
- Offspring risk is a blend of both parents' variant load.
Why it’s in the corpus
Powers' clearest statement on PFS heritability — relevant for the corpus's genetics section and for framing patient-family counseling questions that arise in community discussion.
Context — the post Powers was replying toVerbatim third-party text, shown for context only — not Powers’ statement. Usernames removed.ShowHide
Powers' comment replies to a community member:
Thank you very much Dr! It's relieving to know that altough there's 1000's of genes over/under expressed & DNA methylation, all because of Fin, this disease would not be directly transferred to the child. It would be an extremely tough pill to swallow for me.
You've explained that PFS patients already have androgen metabolism broken at baseline, before taking Finasteride. (Hope I got that right) I assume you were somewhat referring to this with homo-& heterozygous reference. I understand that these specific features can be inherited, as they've been a part of me for years before getting this disease.
(Parent context recovered from the r.genit.al mirror on 2026-10-07; Powers' comment text itself is from John's user-provided export.)
Some fields on this page come from the release’s Markdown edition, which carries text the JSON edition omits.
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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…
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