This page summarizes anecdotal reports and community observations, not medical evidence. Reports may be incomplete, biased or inaccurate and are not medical advice or recommendations. “Risk” here refers to how frequently severe or prolonged symptom worsening is reported, not to proven causation or population-wide probability. Individual responses vary widely, and absence of issues in some users does not rule out significant reactions in others.

PFS PSSD PAS Community Context & Proposed Mechanism: This suppression approach is the most direct clinical application of Dr. Powers’ intracellular androgen accumulation model described earlier on this page. The reasoning is as follows. If persistent androgen-receptor overexpression is causing androgens to accumulate inside cells, then reducing circulating androgens to castrate levels should allow that accumulated load to clear—measured indirectly by driving 3α-diol glucuronide (3adg), the proposed proxy for intracellular androgen buildup, down toward zero. Once cleared, the medications are stopped and the body is allowed to restart its own hormone production on its own, in the hope that the receptor system resets in a normalized state when hormones return.

A GnRH agonist or antagonist (leuprolide or relugolix) shuts down testicular testosterone. However, the testes are not the only source of androgens—the adrenal glands produce them as well. In practice this means 3adg can hit a floor from adrenal contribution even after the testes are fully suppressed (a floor of roughly 300 in the referenced case). This is the point at which the additional medicine, hydrocortisone, is introduced: it suppresses adrenal androgen output so that 3adg can be pushed lower (under 100 in that case). The hydrocortisone is then tapered off, and no testosterone or hCG is used to kickstart recovery so that the body’s own axis can restart naturally.

Encouraging Results to Date: The first patient under Dr. Powers in July of 2026 is only a month out of the castration, and has reported a recovery of several symptoms. This will continue to be monitored throughout 2026.

Physician-supervised and prescription-only by nature. . Leuprolide, relugolix, and hydrocortisone are all prescription medications, and the protocol depends on frequent hormone lab work to track testosterone and 3adg and to time the medication changes. In the documented case it was carried out under the close supervision of a physician with weekly blood tests. It should not be attempted outside of a monitored medical setting.

Psychological and adrenal risk—the most serious concern. In the referenced account, hydrocortisone was described as the hardest part of the protocol: it worsened the patient’s depression and produced darker thoughts while he was taking it. Given the population most likely to read this, that risk deserves emphasis. Glucocorticoids can meaningfully affect mood, and abruptly stopping hydrocortisone after adrenal suppression can precipitate an adrenal crisis, which is a medical emergency. This is a central reason the protocol requires physician oversight and a careful taper rather than self-management.

Suppression-related effects. During the castrate-level phase, reported effects included strong fatigue in the first days, genital contraction, weaker erections, and a somewhat more apathetic, lower-energy state with mildly worse sleep. In the referenced case these largely reversed after the protocol—with the patient reporting stronger nocturnal erections, deeper sleep, and higher testosterone afterward—but reversibility is not guaranteed for any individual.

Uncertainty and cost. The supporting evidence is a very small number of physician-supervised individual reports rather than controlled trials, and even the favorable account notes that the improvement could still be temporary and that overlapping PSSD-type symptoms (emotional flatness, libido) can remain afterward. The weekly blood tests are cited as the most expensive part of the protocol, ahead of the medications themselves.

Evidence Basis: Established pharmacology of GnRH agonists/antagonists and glucocorticoids; Dr. Powers’ intracellular androgen accumulation model; a small number of physician-supervised anecdotal reports. No controlled studies demonstrate the safety or efficacy of this protocol for PFS/PSSD/PAS.

Improvement:

Anecdote Link 1