Alcohol & Cannabis
Cannabis (weed/marijuana) contains cannabinoids such as THC that act primarily on the endocannabinoid system (ECS), especially CB1 receptors in the brain and CB2 receptors in immune/peripheral tissues. The ECS interacts with multiple systems involved in mood, stress response, sleep, appetite, motivation, and sexual function, and it also interfaces with neuroendocrine regulation (including aspects of the hypothalamic–pituitary–gonadal axis). Because of this broad reach, cannabis effects can vary widely by dose, THC/CBD ratio, route of use, frequency, and individual sensitivity.
Alcohol (ethanol) is a potent CNS-active drug that rapidly shifts neurochemistry—most notably by enhancing GABA-A signaling and reducing glutamate/NMDA signaling. It can also influence sex hormones and HPG-axis function, with acute and chronic effects depending strongly on amount and pattern of use. Many people experience relaxation or social facilitation, but alcohol can also produce rebound effects as it wears off, including worse sleep, anxiety, and agitation in susceptible individuals.
In PFS/PSSD/PAS discussions, cannabis and alcohol are often treated as high-variance exposures because they can strongly affect CNS signaling and may plausibly intersect with hormone pathways. On the androgen side, cannabis is not comparable to finasteride as a “DHT blocker,” but there are mechanistic signals—for example, an older study reported cannabinoids inhibiting DHT binding to the androgen receptor in an in-vitro rat prostate model. Human data on testosterone and fertility markers are mixed and appear dependent on dose and use pattern. On the neurochemistry side, alcohol’s strong GABA-A “push” followed by rebound excitation is frequently cited as a reason sensitized individuals sometimes feel destabilized rather than experiencing a typical “buzz,” especially if baseline GABA/neurosteroid systems are already fragile.
(1) https://pmc.ncbi.nlm.nih.gov/articles/PMC5871916/
(2) https://pubmed.ncbi.nlm.nih.gov/6249575/
(3) https://pmc.ncbi.nlm.nih.gov/articles/PMC5660879/
(4) https://pmc.ncbi.nlm.nih.gov/articles/PMC165791/
(5) https://pubmed.ncbi.nlm.nih.gov/36880700/
(6) https://www.frontiersin.org/journals/neural-circuits/articles/10.3389/fncir.2023.1218737/full
Crash Anecdotes (Community Reports):
https://www.reddit.com/r/FinasterideSyndrome/comments/1j5p422/crashed_hard_after_alcohol/
https://www.reddit.com/r/PSSD/comments/uwwiop/does_alcohol_and_weed_cause_crash/
https://www.reddit.com/r/PSSD/comments/mv9e5f/anyone_here_experience_a_crash_from_weed/
How to Interpret This Page
This page summarizes anecdotal reports and community observations, not medical evidence. “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.
Risk Signal Based on User Reports
Reports of Symptom Flares Are Not Uncommon (for PFS/PSSD/PAS):
Among individuals who already have PFS/PSSD/PAS, cannabis and alcohol are commonly mentioned in community reports as potential triggers for symptom flares. Reports vary widely: some people feel temporary relief (sleep, anxiety), while others describe worsening anxiety, sleep disruption, emotional blunting, fatigue, or sexual symptoms—sometimes described as prolonged after heavier or repeated use. Community risk cues often include frequent/heavy cannabis use, high-THC products, and alcohol binge patterns, as well as next-day rebound effects.
For individuals without these conditions, cannabis and alcohol are widely used, but both can still cause mood, motivation, sleep, sexual, and anxiety-related adverse effects in a subset of users, especially at higher doses or with frequent use. Given the variability and the uncertainty described in some anecdotes, some people with PFS/PSSD/PAS choose to treat these as personal triggers and keep intake minimal or avoid them during stabilization.
Evidence basis: Anecdotal reports (online forums, self-reports); established neuropharmacology of alcohol and cannabinoids; mixed human data on endocrine outcomes; no controlled studies examining PFS/PSSD/PAS-specific outcomes.