Re: You know pssd and pfs may actually be the same…
u/drwillpowers
r/DrWillPowers2026-03-25T23:31:59Z
Dr Will Powers’ own statements and theorizing
Summary (paraphrased)
Reading a commenter's labs in the PFS/PSSD-sameness data thread, Powers identifies a likely heterozygous UGT2B17 defect: DHT high but the 3α metabolite at the very bottom — the conversion step incompletely performed, less than half of what the androgen load would predict. He stresses the values are not out of reference range, but are wrong relative to the androgen load: the step is clearly not being fully completed. He also notes a functional biotin deficiency in the same read.
Key points (paraphrased)
- Worked lab-reading example: high DHT with bottomed-out 3α metabolite suggests heterozygous glucuronidation defect.
- In-range values can still be pathological relative to androgen load — ratios over ranges.
- Mild-case pattern: partial defect, still sufficient given a drug trigger.
- Functional biotin deficiency noted as a co-finding.
Why it’s in the corpus
A worked example of his lab-reading method — the "wrong relative to load" principle — and the mild/heterozygous case pattern, important for not restricting the model to extreme lab presentations.
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 now-deleted comment by u/Drwillpowers himself in the "PSSD and PFS may actually be the same thing" data-request thread; the parent comment's text is unrecoverable.
(Parent context recovered from the r.genit.al mirror on 2026-10-09; 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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Answering specificity concerns — UGT2B17 deletion is common, so would testing just produce nocebo? — Powers states that a heterozygous UGT2B17 deletion alone is insufficient for PFS, citing his own long-term finasteride/dutasteride use without issue and his…
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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
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
