Cannabis use and psychosis — structured clinical viva

"Did cannabis cause this?" Answer with calibrated causality: strong, consistent associations with dose–response and high-potency patterns; adolescent onset elevates risk; not every user develops psychosis; genetics and other factors co-travel. Name Moore/Marconi/Di Forti/EU-GEI level teaching without claiming 100% single-cause certainty. ^[1]

"If he stops, will it all go away?" Maybe for pure intoxication/some SIP — but conversion to schizophrenia or bipolar after substance-induced psychosis is clinically important in register data, so plan follow-up either way. Continued use after onset raises relapse risk. ^[2][4]

"Why tablets if just drugs?" Because frank psychosis is impairing and dangerous; antipsychotics target the dopamine final common pathway of positive symptoms; do not withhold medication for UDS positivity. Parallel CUD psychosocial care (MI/CBT/CM) treats the addiction axis. Dual formulation, not either/or. ^[4]

"Is CBD better?" McGuire RCT supports adjunctive CBD signal in schizophrenia research settings — not first-line monotherapy, not retail oil equivalence, not a CUD cure. ^[3]

Assessment spine for the examiner. Risk, collateral, potency/frequency/age of onset, CUD criteria, organic exclusion, baselines before antipsychotic, stages of change, capacity/legal principles under local law. ^[1]