Delta(9)-Tetrahydrocannabinol (THC), the main psychoactive component of cannabis, can cause psychomotor effects, psychotic reactions, and cognitive impairment similar to schizophrenia. These effects can be reduced by two other cannabinoids: cannabidiol (CBD) and SR141716. CBD, the second most abundant cannabis constituent, weakly antagonizes the CB(1) receptor, inhibits anandamide reuptake and hydrolysis, and has neuroprotective antioxidant activity. SR141716 is a potent and selective CB(1) receptor antagonist. Both can reverse many effects of CB(1) receptor agonists, suggesting antipsychotic properties. Experimental studies in animals, healthy volunteers, and schizophrenic patients support this, with a pharmacological profile similar to atypical antipsychotic drugs. This review presents preclinical and clinical studies on the potential antipsychotic effects of CBD and SR141716.
Alcohol use disorders are a major contributor to the global disease burden. After the acute withdrawal phase, the main goal of post-acute treatment is long-term abstinence, though reducing consumption is also recognized as an intermediate aim. In Switzerland, four medications—acamprosate, naltrexone, nalmefene, and disulfiram—are approved for this phase and have well-established efficacy in reducing relapse risk, drinking days, and overall alcohol consumption. Off-label use of baclofen, topiramate, and gabapentin lacks sufficient evidence of effectiveness. Emerging treatments such as cannabidiol, psilocybin, and glucagon-like peptide-1 receptor agonists show promising potential that requires further clinical confirmation. Pharmacological interventions can improve patient outcomes, reduce inpatient treatment needs, and lower healthcare costs.