Had another random PSSD/PFS thought about the glucuronidation theory. Do any of you with PFS have elevated sul...

Original post by Powers — full self-text recovered from the r.genit.al mirror on 2026-10-07 (the export captured the title only):

Having looked at a bunch of these genomes, it is glaringly obvious to me that there are 1000 roads to rome when it comes to PFS. Yeah, the UGT2B17 defect is the most common and slam dunk one, but I'm finding varied mutations all over the body's glucuronidation pathways, and thus it seems different drug combos can produce different outcomes with different metabolite build up outcomes.

Sure, the textbook labs right now are a dutch test with some absurd result (high or low), a 3a-Androstanediol Glucuronide blood test (super high or low).

But I noticed the bilirubin glitch running labs the other day (looks like gilberts on testing, you can see a slightly off panel on a fractionated bilirubin test or just a plain elevated bilirubin (like 1.4 or something) on a CMP. Shows overall strain on the "glucuronidation" systemic process, but its slight.

But I haven't been considering the idea that if glucuronidation is down, perhaps sulfation will be utilized by the body as an alternative highway to crank up to compensate(like how people with these glucuronidation defects seek out finasteride because they had a high DHT at baseline BECAUSE of their inborn glitch in glucuronidation genes makes DHT high at baseline).

Anybody out there have some weird lab result in say Estrone or Estradiol Sulfate? Or Dhea vs DHEA sulfate? I would imagine very high sulfation labs in someone with a glucuronidation defect bad enough to force the shunt down that pathway.

I also can plausibly imagine really odd SHBG values, either quite high or quite low, again.

Basically the theme here is "this lab makes no sense in ratio to this other one".

For example, the first ones I noticed:

Dude has totally normal T value in the dead middle of the band. His T is say 650ng/dl

But then, dude has a urinary T of 2. Like barely detectable.

That makes no sense, so it begs the question, why? Then we identify what gene is down that does that (UGT2B17) and then you have your answer.

I'm trying to think of any other "Screening" labs that would be weird in PFS and possibly PSSD patients if my theory is truly correct, so let me know if you already have any oddball results in these. This is not a call to go get them done, I have no idea if they are relevant or not, its just a an early theory.

E1S, E2S, DHEA : DHEAS

• Dr P