Re: Question to Dr Powers: What is the significance of 17-hydroxyprogesterone to progesterone ratio for PFS patients?
u/drwillpowers
r/DrWillPowers2026-08-05T17:07:58Z
Dr Will Powers’ own statements and theorizing
Mentions treatments or doses — not guidance
Summary (paraphrased)
Powers said 17α-hydroxylase deficiency is one of the mutations he has seen several times in PFS genomes, with no 3β-HSD signal observed (though 3α is a different story). He reasoned such a defect would produce higher baseline progesterone in affected males with lower 17-hydroxyprogesterone, and could increase the risk of what he calls "neurosteroid excess PFS/PSSD." He stressed this remains theoretical — mechanistically plausible but unproven. He added a deliberately withheld aside: there is a way to prove it that nobody would like, which might explain why drug reintroduction has produced cures in a few rare cases, but he declined to elaborate to avoid prompting reckless self-experimentation.
Key points (paraphrased)
- 17α-hydroxylase deficiency seen repeatedly in PFS genomes; no 3β-HSD signal.
- Predicted biochemical signature: high baseline progesterone, low 17-OHP in males.
- Hypothesized as a route into the "neurosteroid excess" phenotype — theoretical, unproven.
- Withheld a risky line of reasoning about drug reintroduction cures to prevent copycat harm.
Why it’s in the corpus
Adds a specific steroidogenic-enzyme gene (17α-hydroxylase/CYP17A1) to the corpus's gene list and connects it to the neurosteroid-excess phenotype. The withheld reintroduction remark documents his awareness of a paradoxical cure phenomenon he considers too dangerous to detail — relevant to the corpus's treatment-safety thread.
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 "Question to Dr Powers: What is the significance of 17-hydroxyprogesterone to progesterone ratio for PFS patients?" by [username removed]:
25M mild to moderate PFS for 6 years now. This is my bloodwork from a few months ago. Planning to repeat this with the DUTCH test next week. Genome results to come in 2 months. Symptoms (all started during PFS): ED, reduced genital sensitivity, slight genital shrinkage, dry mouth and joints, poor sleep, fatigue, overall poor gut health, migraines
Test Name Results Units Bio. Ref. Interval
STEROID PANEL 3,13 STEROIDS (LC-MS/MS)
Aldosterone 14.00 ng/L <25 – 229 (Seated) / 29 – 145 (Supine)
Androstenedione 1460.00 ng/L 500 – 2500 (Adult Male)
Cortisol 202.00 μg/L 50 – 250 (8 AM) / 30 – 160 (4 PM)
Cortisone 18.00 μg/L 6.00 – 27.00
Corticosterone 9.03 μg/L 1.00 – 20.00
11-Deoxycortisol 0.85 μg/L 0.50 – 3.00
21-Deoxycortisol <0.027 μg/L 0.02 – 0.15
DHEA 6.30 μg/L 1.8 – 12.5 (Adult Male)
DHEAS 1770.00 μg/L 99.00 – 6154.00
11-Deoxycorticosterone 0.13 μg/L 0.02 – 0.15
17-α-Hydroxyprogesterone 2.02 μg/L 0.20 – 2.20
Progesterone 0.24 μg/L 0.19 – 1.40
Testosterone, Total Ultrasensitive 10.50 μg/L 2.50 – 10.00
I read in Dr Powers' personal observations document that high 17-ohp may reflect slower downstream disposal or reduced metabolite appearance. What does this mean for PFS?
I have always had high T after quitting finasteride and a normal e2 and DHT but the ratio of them to test is very low. Also I read that DHEA-DHEAS ratio needs to be 1:1000 although I have no idea how important this is for PFS. I have always had high bilirubin and prolactin which Dr Powers […]
(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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