Re: CDG Theory
u/drwillpowers
r/DrWillPowers2 months ago (circa 2026-08-07; export dated 2026-10-07)
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Summary (paraphrased)
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 fewer catechol substrates — including catechol estrogens — to process, so it turns over dopamine faster. He said this is the entire mechanism, and that only people with an underlying dopamine production or signaling issue would notice the effect. In the same thread he sketched three tentative PSSD phenotypes: people with disrupted 5-HT2C acting as a "resistor" throttling otherwise-normal dopamine signaling; people with very high or very low allopregnanolone (he leaned toward high); and people whose PSSD is essentially PFS — androgen/otherwise metabolite crowd-out that responds to chemical castration. He described the syndromes as Venn-diagram overlaps, speculated post-accutane syndrome connects through the ABCC transporter system and possibly SLCO genes, and dismissed cyproheptadine as a crude, dirty tool useful only for crudely gauging whether lower serotonin signaling helps or hurts.
Key points (paraphrased)
- CDG mechanism: beta-glucuronidase inhibition → gut loss of glucuronidated compounds/catechols → COMT less busy → faster dopamine turnover.
- Only patients with dopamine production/signaling issues would notice CDG's dopaminergic effect.
- Three tentative PSSD phenotypes: 5-HT2C-as-dopamine-resistor; high/low allopregnanolone (lean high); PFS-like metabolite crowd-out responsive to castration.
- Syndromes framed as Venn-diagram overlaps; PAS linked via ABCC transporters and possibly SLCO genes.
- Cyproheptadine dismissed as too dirty for precise mechanistic probing.
Why it’s in the corpus
Documents Powers' CDG pharmacology in full and his three-phenotype PSSD taxonomy, which bridges his dopamine/serotonin and androgen-metabolite models. The ABCC/SLCO speculation for PAS extends the post-drug-syndrome family the corpus tracks.
Context — the post Powers was replying toVerbatim third-party text, shown for context only — not Powers’ statement. Usernames removed.ShowHide
Powers' comment replies to the original post "My Suppression Trial results and experience" by [username removed]:
DO NOT DM ME I WILL INGORE YOU. I WILL ONLY LOOK AT COMMENTS
So I was the patient that did the "castration" trial. I would say suppression because it was temporary and the word castration scares people. I used Orgovyx and Leuprolide which are used to treat prostate cancer. The testosterone comes back folks!
TL;DR the trial wasn't that bad and now my testosterone is higher, I have stronger nocturnal erections and morning wood. I sleep much better. I still have blunted emotions/ anhedonia and sexual numbness/ low libido.
We did this trial because I had an elevated 3adg/ 3a-Androstanediol Glucuronide reading on my blood test. It was over 5000, above the highest range. For those who don't know, Dr Powers gives you hcg to see how you respond. It didn't help me right away but that's when we noticed this reading.
I also had an array of androgen metabolism mutations in my genome including but definitely not limited to a UGT2B17 deletion which showed 0 testosterone in my DUTCH test which means I can't glucoronidate testosterone. I REPEAT, THIS ALONE DOES NOT MAKE YOU VULNERABLE TO PFS. I had many more mutations, like ABCC, some others which are listed in an old email from the doctor now that I can't find.
Edit: this comment lists my relevant genome findings: https://www.reddit.com/r/DrWillPowers/s/sViR9IjK3g
3adg is a proxy for intracellular androgen buildup caused by finasteride which is the cornerstone of Dr Powers Theory on how PFS happens. I'm not going to repeat it to […]
(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 postCurated Powers pick
I'm starting to see trends in PSSD genomes, this is one. DBH
u/drwillpowers · r/DrWillPowers
Post body unavailable. From the title, Powers announced he was beginning to see recurring trends in the genomes of his PSSD patients, singling out DBH — dopamine beta-hydroxylase, the enzyme converting dopamine to norepinephrine — as one such trend. This is…
COMTDBHHTR2CUGT2B17PRH-07452026-06-11T23:41:29ZPFSPSSDPowers Reddit history - Powers · Reddit commentCurated Powers pick
Re: Why does calcium d glucarate cause anxiety…
u/drwillpowers · r/DrWillPowers
Answer to why calcium D-glucarate causes anxiety. Powers explains it downstream of his core model: buildup of two identified neurosteroids produces chronic GABA-A positive allosteric modulation — like constant endogenous Xanax — forcing downstream systems…
HTR1AHTR2CPRH-01342026-09-16T16:41:07ZPSSDPowers Reddit history - Powers · Reddit commentCurated Powers pick
Re: Repost dutch test results…
u/drwillpowers · r/DrWillPowers
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…
PRH-06472026-06-23T04:58:34ZPFSPSSDPRSDPowers Reddit history