Re: Repost dutch test results…
u/drwillpowers
r/DrWillPowers2026-06-23T04:58:34Z
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Summary (paraphrased)
Reply in a thread about a community gene list for gene.iobio analysis (the export also appends some unrelated Powers replies about subreddit scope and a DUTCH repost). Powers describes three PFS phenotypes with overlap driven by each patient's specific gene glitches, and two PSSD flavors: either "PFS wearing another hat" (the SSRI caused a hormone-metabolite pileup rather than a primary neurological lesion, functioning effectively like PFS) or a variant where overactive 5HT2C suppresses dopamine despite normal dopaminergic neurons — which is why temporary overrides work but the system returns to a bad rest state. For post-Accutane syndrome he theorizes ABCC transporter glitches plus accutane's deliberate epigenetic downregulation of androgen transport, binding, and downstream transcription in skin cells: a "falling tide" that cures acne in some by lowering androgen drive, but in already-compromised patients lowers unrelated struggling cells to near zero. He also thanks the community member for their data-collection effort, expresses interest in chemical-castration volunteer outcomes for PSSD, and mentions a helpful AI tool built by his sister.
Key points (paraphrased)
- Three PFS phenotypes (overlapping); two PSSD flavors (metabolite-pileup PFS-equivalent vs. 5HT2C-mediated dopamine suppression).
- PAS hypothesis: ABCC transporter glitches + epigenetic androgen-drive downregulation by isotretinoin; "falling tide" analogy.
- Community genome/lab data collection welcomed; chemical-castration PSSD volunteers anticipated.
Why it’s in the corpus
Extends Powers' model to PSSD and post-Accutane syndrome in one place — the 5HT2C/dopamine PSSD flavor and the ABCC/epigenetic PAS hypothesis are distinct mechanistic claims that broaden the corpus beyond finasteride-triggered cases.
Context — the post Powers was replying toVerbatim third-party text, shown for context only — not Powers’ statement. Usernames removed.ShowHide
Powers' comment replies to a community member:
Yeah sorry about that didn’t mean to throw you off. Just jumpy about supplements. Afraid to crash. Def a boon for the ugt2b17 deleted pssd case
(Parent context recovered from the r.genit.al mirror on 2026-10-07; Powers' comment text itself is from John's user-provided export.)
Some fields on this page come from the release’s Markdown edition, which carries text the JSON edition omits.
Related records
- Powers · Reddit commentCurated Powers pick
Re: Anhedonic Substance Blockage with PFS/PSSD/PAS
u/drwillpowers · r/DrWillPowers
Powers' current theory of anhedonic substance blockage: dopaminergic signaling breaks down because efflux pump/transporter defects let substances accumulate intra- or extracellularly, destroying concentration gradients and effectively silencing signaling…
ABCC5PRH-11912026-04-20T22:15:56ZPFSPSSDPRSDPowers Reddit history - Powers · Reddit commentCurated Powers pick
Re: CDG Theory
u/drwillpowers · r/DrWillPowers
Powers gave a deliberately simple account of calcium D-glucarate: as a beta-glucuronidase inhibitor it causes glucuronidated compounds and catechols to be dumped into the gut and lost rather than reabsorbed, leaving COMT (catechol-O-methyltransferase) with…
COMTHTR2CPRH-05602026PFSPSSDPRSDPowers Reddit history - Powers · Reddit commentCurated Powers pick
Re: How does progesterone therapy work within the new PFS model of the disease?
u/drwillpowers · r/DrWillPowers
Powers names his three most common PFS subtypes: (1) androgenic signal loss, a metabolite pileup problem; (2) "melty," a glucocorticoid-related (rarely mineralocorticoid) metabolite buildup; (3) neurosteroid disruption — the traditional theory, which he…
PRH-04512026-07-18T22:04:12ZPFSPSSDPowers Reddit history
