Re: Castration trial on Post anastrazole syndrome
u/drwillpowers
r/DrWillPowers2 months ago
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Summary (paraphrased)
A multi-part comment (the export concatenates several of Powers' replies, including remarks on a post-anastrozole castration-trial image post and the "melty" phenotype). The core diagnostic content: the castration trial's purpose is to test whether the blood 3α-ADG backup reflects a backup of non-glucuronidated 3α-androstanediol in blood or CSF. He says he cannot otherwise explain astronomically high 3A-ADG readings in patients with DHT under 20 — DHT that low cannot produce such values, so the source must be elsewhere, and he suspects inside the brain. He then sketches a two-phase reversal model: the initial crash is neurosteroid loss (paranoia, anxiety, hallucinations), then the body overcompensates while finasteride wrecks androgen metabolism and exit pathways fill up; SSRIs can likewise induce neurosteroid synthesis, and once neurosteroid levels cross a threshold a self-preserving feedback loop locks in a chronic GABA-A-adjusted state of anhedonia and sexual dysfunction — the opposite of what everyone assumed, with neurosteroids sharing the androgens' exit pathway and producing the astronomical blood values. He reflects that in the first castration patient, 3α-ADG persisted long after testosterone and DHT were obliterated — but he had measured the glucuronidated form, and the free (non-glucuronidated) 3α-androstanediol may never have been wiped, a mistake he now recognizes. On diagnostics he flags the CSF problem: with no reference values, interpretation requires a non-PFS volunteer lumbar puncture, and he volunteers himself. He also defines the "melty" phenotype as corticosteroid-molecule buildup in skin (localized cushions, not fat loss), attributing facial changes mainly to muscle atrophy.
Key points (paraphrased)
- Castration trial as a diagnostic probe: is blood 3α-ADG backup really a free-3α-androstanediol backup in blood/CSF?
- Unexplained astronomical 3A-ADG with DHT <20 points to a non-DHT, possibly CNS source.
- Two-phase model: neurosteroid-loss crash → compensatory overproduction → self-preserving GABA-A-adjusted loop (anhedonia/sexual dysfunction).
- SSRIs as independent inducers of neurosteroid synthesis feeding the same loop.
- Lesson from first castration patient: glucuronidated vs. free 3α-androstanediol must be distinguished.
- CSF diagnostics need a healthy-volunteer reference; he volunteers.
- Melty phenotype defined as dermal corticosteroid buildup, not fat loss.
Why it’s in the corpus
The richest single diagnostic/methods entry: it lays out the castration trial as a biomarker experiment, the unexplained 3A-ADG anomaly driving his CNS-source hypothesis, and the CSF reference-data problem — all central to the corpus's diagnostics and mechanism-validation threads.
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 "Castration trial on Post anastrazole syndrome" by [username removed]:
Disclaimer: this is not medical advice, I got my doctor to try the castration method with me. 6 weeks of relugolix with 2weeks of hydrocortisone (same time starting after 2weeks of relugolix). I used AI to write the summary about me below but I entered all the data myself. I will update you guys every two weeks. Now I got only sexual symptoms like PFS but first 6 month was so many symptoms I don’t have the patience to write them out. —————- Summary starts: Patient: 26-year-old male Crash: 5 years ago — anastrozole + exogenous testosterone (anabolic steroids), alongside ketoconazole shampoo and minoxidil. Not finasteride-triggered. Supraphysiological T converted to DHT via fully intact 5-alpha reductase; anastrozole blocked the aromatase escape valve; genetically impaired clearance system overwhelmed by the substrate load. Result: zero libido for 5 years, diffuse frontal hairline thinning (crown/mid-scalp/sides preserved, non-Norwood pattern, follicles present but miniaturized), watery/reduced semen quality, standard hormone panels reported as normal. Genetics (consumer SNP array): SLCO1B1 — homozygous *5 (rs4149056 TT) — most severe finding, clinically validated UGT2B17 — likely heterozygous deletion (rs4440295 no-call) UGT2B15 — multiple indels UGT2B7 — deletion indels ABCC2 — rs717620 CC, reduced expression (Powers flags this as a top-tier PFS gene independently) SLCO1B3 — heterozygous, partial backup capacity COMT — homozygous Met/Met (rs4680 AA) — slow, clinically […]
(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.
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