Powers gene claimCore corpus

ABCC (family) — unspecified

Confidence: interview2026-04-29

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 His mechanistic and genetic claims are unpublished hypotheses — read them as “Powers theorizes…”, not as established fact.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)

ABCC intracellular transporter genes are among the key gene classes in his experimentally verifiable mechanism, alongside UGTs and the epigenetic genes above.

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

Powers · Reddit commentCurated Powers pick
Re: Can you stop Hairloss effectively without risking PFS?
u/drwillpowers · r/DrWillPowers
Powers offered a thought experiment: if a PFS-susceptible man were chemically castrated, given dutasteride for two months, withdrawn, then "uncastrated," he would never develop PFS if the theory is correct — because it is about metabolite load, not just the…
CYP2D6 CYP3A4 LRP2
PRH-03302026-07-30T04:02:01ZPFS PSSDPowers Reddit history
Powers · Reddit post
Has anyone here taken finasteride or dutasteride and gotten post finasteride syndrome (PFS) from them? I have a theory as to why this seems to happen in transgender women more than cis men
u/drwillpowers · r/asktransgender
Powers proposed that PFS stems from deficient allopregnanolone, a neurosteroid produced downstream of 5-alpha-reductase via the AKR1C enzyme family. He hypothesized that only people carrying decreased-function variants in AKR1C genes develop the syndrome when…
DWP-0012020PFSCore corpus
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

Related records

Powers · Reddit commentCurated Powers pick

Re: Can you stop Hairloss effectively without risking PFS?

u/drwillpowers · r/DrWillPowers

Powers offered a thought experiment: if a PFS-susceptible man were chemically castrated, given dutasteride for two months, withdrawn, then "uncastrated," he would never develop PFS if the theory is correct — because it is about metabolite load, not just the…

CYP2D6 CYP3A4 LRP2

PRH-03302026-07-30T04:02:01ZPFS PSSDPowers Reddit history

Powers · Reddit post

Has anyone here taken finasteride or dutasteride and gotten post finasteride syndrome (PFS) from them? I have a theory as to why this seems to happen in transgender women more than cis men

u/drwillpowers · r/asktransgender

Powers proposed that PFS stems from deficient allopregnanolone, a neurosteroid produced downstream of 5-alpha-reductase via the AKR1C enzyme family. He hypothesized that only people carrying decreased-function variants in AKR1C genes develop the syndrome when…

DWP-0012020PFSCore corpus

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