A request for PFS and PSSD patients taking CDG to help symptoms. Can you do something for me?
u/drwillpowers
r/DrWillPowers2026-08-23T18:16:29Z
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Summary (paraphrased)
Post body unavailable. From the title, Powers issued a direct request to PFS and PSSD patients who were taking calcium D-glucarate for symptom relief, asking them to do something for him — evidently a data-collection or experimental ask tied to his CDG work (the beta-glucuronidase-inhibition mechanism detailed in PRH-0052 and PRH-0560). Given the timing (one month before export), this likely relates to gathering CDG outcome reports or requesting a specific protocol adherence/measurement from CDG users. The exact request could not be recovered.
Key points (paraphrased)
- Direct request to PFS/PSSD patients taking CDG.
- Tied to his CDG/beta-glucuronidase treatment program.
- Exact ask unavailable — re-fetch target.
Why it’s in the corpus
Documents the community-experiment phase of his CDG program — Powers actively recruiting patient-reported outcomes, the evidentiary basis for his CDG claims. Re-fetch needed for the protocol details.
Original post textVerbatim text recovered via the r.genit.al mirror; other users’ names removed.ShowHide
Original post by Powers — full self-text recovered from the r.genit.al mirror on 2026-10-07 (the export captured the title only):
I think I may have solved something recently with some various posts and comments by people on the subreddit.
The persistent forms of PFS and PSSD are the same condition, just caused via different mechanisms, and the slightly different phenotypes relate to which specific neurosteroid pile up is the case in that specific human. .
Here is what I think is happening for those with mental symptoms, anhedonia, genital numbness, etc. I suspect that each sub phenotype is related to whatever inborn error of metabolism/enzymes they have, that results in one specific neurosteroid being their primary pile up, and thereby affecting different neurons/brain regions slightly differently.
Calcium d glucarate is reducing the recycling of various 3A reduced androgen metabolites:
3a-androstanediol
Androsterone
Etiocholanolone
Possibly other 3a-hydroxysteroids
Allopregnanolone and pregnanolone
(Other phenotypes probably exist with neurosteroids like THDOC related to 11BHSD glitches)
The free 3a-hydroxysteroids can positively modulate GABA-A. Their glucuronides, (what I'm clocking on labs rather often above the measurable limit) such as 3A-ADG are much more polar and probably function mostly as transport/excretion products rather than strong central GABA-A modulators. They however reveal the truth, inside the brain, the 3A-AD and related molecules are at absurd levels. Why did they get like this? Finasteride caused the pileup via 5ari or an SSRI drove up their synthesis, creating the feedback loop. The mic gets too close to the speaker, and we get trapped in a loop.
With the GABA-A channels propped open all the time, substances like alcohol just....don't do anything. As they are like pissing into an ocean of GABA-A, but on the other side, the system adjusts to this constant GABA-A activity, and networks reconfigure around it. More semi-permanent neurological rewiring as a result.
So whats up with the CDG?
Early phase (slight neurosteroid level drop): CDG reduces pathological steroid deconjugation/recycling and lowers excessive tissue exposure. Sexual sensation, cognition, anhedonia or other PFS/PSSD symptoms briefly improve.
Later phase (significant drop): continued blockade depletes the recyclable pool enough that inhibitory 3a-neurosteroid tone suddenly becomes inadequate. GABA-A no longer is propped wide open due to the drop off in neurosteroids. People start to feel anxious, not great. Some negative symptoms they dislike.
Collapse: The GABA-A receptor population, already extremely over adapted to abnormal steroid levels propping it open almost permanently for many years prior to this, becomes functionally very under-modulated, producing panic and neuromuscular hyperexcitability. (Aka, the palpitations, anxiety, and "stiffness" of the muscles) that people are reporting in comments after taking high dose CDG for a while.
The subjective “cliff” does not require CDG pharmacokinetics to suddenly change. A slowly falling neurosteroid concentration can cross a nonlinear receptor/network threshold and then BAM, panic, anxiety, stiffness, and if bad enough, seizure.
These negative symptoms feel bad. People are not having a good time. This drug that helped them at first now feels like something that's going to cause them to literally die. They stop taking it, and call it a failure.
Many of you got these disorders from a single pill, and have spent years chasing windows. Lets change the plan a little bit here. You've spent years in a state with massive fuckery happening with GABA-A, this isn't going to be fixed instantly. I've been taking a stimulant medication for the past 26 years, if I quit tomorrow, I would take probably 3-6 months to return to some sort of "Baseline" and in some ways, I might take even longer than that to truly "normalize".
If you are taking CDG, and you start to get these symptoms, back off. The goal is to do this slowly, to allow the system time to adjust to these changes, and to gradually get back to normal functional levels of GABA-A signaling. That will not be accomplished overnight with 1 pill.
If you get into a car accident, it takes only a single second of not paying attention to wreck your car. One little mistake. But it takes much longer than that for the repair shop to fix it. There is no "accident reversal" button. Things are messed up, they will need time to be repaired. Stop chasing windows. Think about the situation as slowly changing the steroid environment such that your brain can gradually return to baseline.
(Valproate does this as well, separately from its HDAC abilities, which is something I realized could be an explanation for why people have recovered from using it, among many other things that tinker with this process).
My brain is great at pattern recognition and zooming out and seeing the big picture. Let me worry about figuring out what are the BEST treatment strategies to do this in the most efficient and safe way.
But CDG is OTC, so if you elect to take it and it "crashes" you, consider microdosing it right up to this "I feel anxious" threshold. Ideally, you will just faintly feel something, and that "faint effect" over months is what we're looking to do.
Castration was the solution for androgenic signal loss, as that system can adapt vastly faster than the brain can. Will it also help for the neurosteroid pile up? Possibly, but it may take much much longer in that state for things to normalize, and that's what I'm trying to figure out. If I can do that without having to castrate someone for months, that seems like a safer and better option. But treatment isn't going to be a one pill solution. I am certain of this.
If you want to help me figure this out, and you personally have chosen to try CDG, do me this solid.
Take it, and if you reach a point where you're getting anxiety/palpitations/muscle spasm, back off. Go back to a dose where maybe you just barely feel that a bit. But not anything severe. Do that for a while, and then when you feel settled out there, you can try pushing it harder until you reach the edge of the chasm again, then again, back off. The goal is to look over the edge without falling in. That slight pressure will cause the system to modulate around it.
This is not a normal staircase, this is a staircase with many very long landings, allowing your system time to gradually adapt and return to how it was before all this started.
As is always the case, this is not medical advice, please check with your own doctor about the safety of anything for your own medical care. But if you ARE going to take this supplement and do this anyway, let me know if this information works out the way I think it's going to.
- Dr P
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