Re: Dutasteride still a decent option…
u/drwillpowers
r/DrWillPowers2026-07-16T14:12:07Z
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Summary (paraphrased)
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 own genome: no defects across UGTs, ABCCs, or LRP2. The quantitative threshold — how many mutations, what percent enzyme reduction, what testosterone level, what additional factors — remains unknown; what he claims to know is that people who develop PFS have baseline defects. He adds that brute-force AI analysis of genomic data failed, and that the solution required understanding molecular biochemistry first and reverse-engineering from there.
Key points (paraphrased)
- Heterozygous UGT2B17 deletion alone is insufficient for PFS.
- N-of-1 control: his own genome is clean across UGT/ABCC/LRP2; long-term 5ARI use without PFS.
- The quantitative threshold (mutation count, enzyme-reduction %, T level) is still unknown.
- Method claim: biochemistry-first reverse-engineering succeeded where brute-force AI genomic analysis failed.
- Specificity/nocebo objection addressed via the multi-hit requirement.
Why it’s in the corpus
The dosage/threshold nuance and the N-of-1 control genome — his strongest answer to "these variants are common, so the theory overpredicts." It also documents his methodological stance against naive genomic data-mining.
Context — the post Powers was replying toVerbatim third-party text, shown for context only — not Powers’ statement. Usernames removed.ShowHide
Powers' comment replies to [username removed], who asked about specificity: whether asymptomatic finasteride users show the same genetic patterns, and whether pursuing genome testing would merely set up nocebo given how common some of these variants are. (The OP, since deleted, had asked whether dutasteride remains a decent option.)
(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.
Related records
- Powers · Reddit commentCurated Powers pick
Re: Had another random pssdpfs thought about the…
u/drwillpowers · r/DrWillPowers
Reply to a community member's glucuronidation-theory thought about sulfation labs. Powers notes the discussed factor interacts with androgen production and ABCC-family transporters (he believes ABCB1 specifically, with the caveat that he read it long ago)…
ABCB1LRP2UGT2B15UGT2B17UGT2B7PRH-13982026-04-01T15:22:34ZPFSPSSDPowers Reddit history - Powers · Reddit commentCurated Powers pick
Multi-hit model: a glucuronidation defect alone is necessary but not sufficient
u/drwillpowers · r/DrWillPowers
Replying to [username removed]'s question about why East Asian populations — with roughly 60–70% homozygous UGT2B17 deletion prevalence — don't show higher PFS rates, Powers states that glucuronidation failure alone is insufficient: it was merely the first…
LRP2UGT2B17PRH-15002026-04-14T13:22:58ZPFSPowers Reddit history - Powers · Reddit commentCurated Powers pick
Re: You know pssd and pfs may actually be the same…
u/drwillpowers · r/DrWillPowers
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…
UGT2B17PRH-15072026-03-25T23:31:59ZPFSPSSDPowers Reddit history
