Powers gene claimCore corpus

UGT2B17 — defective (major)

Confidence: directcirca May 2026 (archived 2026-05-08)

Dr Will Powers’ own statements and theorizing

Paraphrased from his public posts and talks. His mechanistic and genetic claims are unpublished hypotheses — read them as “Powers theorizes…”, not as established fact.

Powers’ claim (paraphrased)

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. Finasteride then closes the remaining DHT exit, causing intracellular androgen overcrowding, receptor downregulation, and eventual epigenetic silencing of androgen signaling.

Some fields on this page come from the release’s Markdown edition, which carries text the JSON edition omits.

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…
AKR1C1 AKR1C2 AKR1C3 AKR1C4 HSD17B2+3
DWP-0032026PFSCore corpus
Powers gene claim
UGT2B15; UGT2B7 — defective (minor)
Confidence: direct
Defects in these secondary glucuronidation enzymes can compound the UGT2B17 defect, further reducing testosterone exit capacity.
UGT2B15 UGT2B17 UGT2B7
PGL-UGT2B15-UGT2B7circa May 2026PFSCore corpus
Peer-reviewed paperPSSD Discord pick
Multiple roles for UDP-glucuronosyltransferase (UGT)2B15 and UGT2B17 enzymes in androgen metabolism and prostate cancer evolution
Gauthier-Landry L, Bélanger A, Barbier O · Journal of Steroid Biochemistry and Molecular Biology
Review of two glucuronidation enzymes, UGT2B15 and UGT2B17, that convert DHT metabolites (3α-diol and androsterone) into inactive, easily excreted glucuronide conjugates. It describes how these enzymes control local androgen availability and androgen-receptor…
AR UGT2B15 UGT2B17
DISC-0032015 (epub 2014)PFSPSSD Discord picks

Powers’ claim (paraphrased)

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…

AKR1C1 AKR1C2 AKR1C3 AKR1C4 HSD17B2+3

DWP-0032026PFSCore corpus

Powers gene claim

UGT2B15; UGT2B7 — defective (minor)

Confidence: direct

Defects in these secondary glucuronidation enzymes can compound the UGT2B17 defect, further reducing testosterone exit capacity.

UGT2B15 UGT2B17 UGT2B7

PGL-UGT2B15-UGT2B7circa May 2026PFSCore corpus

Peer-reviewed paperPSSD Discord pick

Multiple roles for UDP-glucuronosyltransferase (UGT)2B15 and UGT2B17 enzymes in androgen metabolism and prostate cancer evolution

Gauthier-Landry L, Bélanger A, Barbier O · Journal of Steroid Biochemistry and Molecular Biology

Review of two glucuronidation enzymes, UGT2B15 and UGT2B17, that convert DHT metabolites (3α-diol and androsterone) into inactive, easily excreted glucuronide conjugates. It describes how these enzymes control local androgen availability and androgen-receptor…

AR UGT2B15 UGT2B17

DISC-0032015 (epub 2014)PFSPSSD Discord picks