Dr Will Powers’ own statements and theorizing
Powers’ claim (paraphrased)
Weakening mutations in SULT2A1 impair the sulfation exit route for testosterone, amplifying the glucuronidation defect.
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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 postCurated Powers pick
Had another random PSSD/PFS thought about the glucuronidation theory. Do any of you with PFS have elevated sul...
u/drwillpowers · r/DrWillPowers
Post body unavailable. From the title (truncated in the export at "elevated sul…"), Powers shared a new thought extending his glucuronidation theory and asked PFS patients whether they have elevated sulf- markers — in context, most plausibly…
SULT2A1PRH-14052026-03-30T19:44:12ZPFSPSSDPowers Reddit history - Peer-reviewed paper
SULT2A1 Gene Copy Number Variation is Associated with Urinary Excretion Rate of Steroid Sulfates
Jenny Jakobsson Schulze; Maria Johansson; John-Olof Thörngren; Mats Garle; Anders Rane; Lena Ekström · Frontiers in Endocrinology
In healthy volunteers given exogenous testosterone, the authors tested whether copy-number variation in sulfotransferase genes predicted urinary excretion of steroid sulfates. SULT2A1 copy number was significantly associated with excretion rates of sulfate…
SULT2A1MECH-0192013Systems review · Oct 2026