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 Endocrinology2013
Summary (paraphrased)
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 metabolites: carriers of fewer gene copies excreted less of the sulfated androgens, and testosterone-sulfate and DHEA-sulfate levels tracked genotype even at the low concentrations seen after exogenous testosterone dosing. The study provides in-vivo evidence that SULT2A1 gene dosage controls androgen clearance through the sulfation route.
Why it’s in the systems review
Powers' glucuronidation discussion tends to center on UGT enzymes, but sulfation (SULT2A1) is the parallel clearance route for androgens — and it too varies by gene copy number. This human in-vivo study is the exact counterpart of the UGT2B17-deletion logic in the corpus: clearance genotype predicts how fast steroid metabolites leave the body. It belongs here because a complete causal-pathway map must include both conjugation systems, and it surfaces another genetically variable clearance node.
Related records
- 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 - 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 gene claim
SULT2A1 — weakening mutations
Confidence: direct
Weakening mutations in SULT2A1 impair the sulfation exit route for testosterone, amplifying the glucuronidation defect.
SULT2A1PGL-SULT2A1circa May 2026PFSCore corpus