Re: My doctor, William Powers, is looking for data from PSSD patients

Powers reported having seen recoveries following alteration of gut flora, and cited a PMC article (PMC6962501) for the mechanism: changing the gut microbiome changes beta-glucuronidase production, which changes how much glucuronidated hormone is de-conjugated and reabsorbed — i.e., the body's ability to eliminate the backed-up metabolites. He presented this as fitting the quirks of these disorders, while openly noting the theory is probably wrong but less wrong than anything prior, and said he was actively stress-testing it against counterexamples. He explained that for someone with glucuronidation failure and intracellular metabolite buildup, a microbiome shift could accelerate metabolite elimination and produce a "window" of improvement. He emphasized there are on the order of a hundred ways to create the backup, visible as anomalies on DUTCH tests and obscure androgen metabolite testing while standard testosterone/DHT labs look normal. He gave the signature pattern: unmeasurably high 3α-androstanediol glucuronide with normal serum testosterone but zero urinary androgens — nonsensical until the genome reveals ABCC-type enzyme failures or a homozygous UGT2B17 deletion, with an SSRI interacting with the same transporters/glucuronidation machinery or finasteride fully disabling 5AR removing the last exit pathway. Replying to a PSSD patient's DUTCH results in the same thread, he said the patient showed the exact pattern all his PFS patients show — most commonly a UGT2B17 deletion — with SSRIs interacting with the same mechanisms, and exclaimed that a great deal of PSSD may simply be "PFS wearing a new hat": the identical failure pattern induced by a different drug.