Community accountAbout Powers’ workSelf-report · N=1Core corpus

PFS/PSSD: I'm going to try something interesting…

u/various (r/DrWillPowers members)

r/DrWillPowersnot verified (mirror crawled ~161 days before 2026-10-07)

Presents Dr Will Powers’ theory

Made by others to describe his unpublished model. Attribute its claims to Powers — not to the presenter, and not to established science.

Patient / community self-report

An uncontrolled personal account (N=1). The author’s own caveats are preserved; it is not evidence that any intervention is safe or effective.

Summary (paraphrased)

A patient with ~3 years of PSSD followed by PFS described Powers' theory back to the community (metabolite backlog → epigenetic androgen-receptor changes → persistent "crash") and proposed a 30-day fast as an experiment: fasting blunts the HPG axis, induces the HDAC inhibitor beta-hydroxybutyrate, and pauses androgenic input so the body can clear weak metabolites. Shows how Powers' Reddit theorizing was being interpreted and operationalized by patients, including the HDAC/epigenetic angle.

Why it’s in the corpus

Evidence of the theory's dissemination and the specific mechanistic claims patients took from Powers (metabolite backlog, epigenetic AR changes). Useful corpus context on how his hypotheses circulate; also flags the fasting/HDAC-inhibitor sub-hypothesis.

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

Video
Dr. Will Powers Interview [PFS / PAS / PSSD Summit 2026]
Dr. Will Powers · SIDEfxHUB - PFS & PSSD Patient Organisation · 21:27 (1287s)
PFS, PAS, PSSD mechanism theory; Powers' unifying model; vulnerability screening
AR ARID1A CHD8 HDAC10
YT-iWFDBRTgT3g2026-04-29PFS PSSD PRSDCore corpus
Powers gene claim
AR — upregulated expression (~1.7x, citing Khera); theorized epigenetic silencing in his phenotype
Confidence: interview/direct
Citing Khera's published finding of ~1.7x AR upregulation in PFS cells, Powers theorizes intracellular weak-metabolite crowding blocks potent androgens from binding, and that in extreme cases the body epigenetically silences AR expression — producing…
AR
PGL-AR2026-04-29; circa May 2026PFSCore corpus
Powers gene claim
ARID1A; CHD8; HDAC10 — recurring "glitches" (unspecified)
Confidence: interview
In whole-genome sequencing of ~100 PFS patients, glitches in epigenetic monitoring genes — ARID1A, CHD8, HDAC10 — appear "more than they should" statistically. Epigenetic flags (e.g., for AR upregulation) may fail to be removed after drug discontinuation.
AR ARID1A CHD8 HDAC10
PGL-ARID1A-CHD8-HDAC102026-04-29PFSCore corpus

Summary (paraphrased)

Related records

Video

Dr. Will Powers Interview [PFS / PAS / PSSD Summit 2026]

Dr. Will Powers · SIDEfxHUB - PFS & PSSD Patient Organisation · 21:27 (1287s)

PFS, PAS, PSSD mechanism theory; Powers' unifying model; vulnerability screening

AR ARID1A CHD8 HDAC10

YT-iWFDBRTgT3g2026-04-29PFS PSSD PRSDCore corpus

Powers gene claim

AR — upregulated expression (~1.7x, citing Khera); theorized epigenetic silencing in his phenotype

Confidence: interview/direct

Citing Khera's published finding of ~1.7x AR upregulation in PFS cells, Powers theorizes intracellular weak-metabolite crowding blocks potent androgens from binding, and that in extreme cases the body epigenetically silences AR expression — producing…

PGL-AR2026-04-29; circa May 2026PFSCore corpus

Powers gene claim

ARID1A; CHD8; HDAC10 — recurring "glitches" (unspecified)

Confidence: interview

In whole-genome sequencing of ~100 PFS patients, glitches in epigenetic monitoring genes — ARID1A, CHD8, HDAC10 — appear "more than they should" statistically. Epigenetic flags (e.g., for AR upregulation) may fail to be removed after drug discontinuation.

AR ARID1A CHD8 HDAC10

PGL-ARID1A-CHD8-HDAC102026-04-29PFSCore corpus