Dr Will Powers’ own statements and theorizing
Powers’ claim (paraphrased)
Defects in these secondary glucuronidation enzymes can compound the UGT2B17 defect, further reducing testosterone exit capacity.
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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 · 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 - 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…
ARUGT2B15UGT2B17DISC-0032015 (epub 2014)PFSPSSD Discord picks