Abstract
Cannabis consumption has radically changed over the last several decades. Tetrahydrcannbidiol concentrations are rising, cannabidiol concentrations falling and cannabis is becoming legalized in several regions of the globe. Concerns have been raised as to the impact of increased cannabis exposure within the general population on public health. One of the more serious concerns is the potential relationship between cannabis consumption and psychosis. Research has shown a relationship between increasing cannabis use and increasing psychosis risk. This risk is moderated by other factors such as stress and a family history of psychosis. Within this context, it is important to determine potential markers for future psychosis risk. Genetic and epigenetic research in cannabis and psychosis is in its early stages. One common denominator between cannabis use disorder and psychosis is dopamine dysfunction. Research has begun to link heightened dopamine reactivity with the psychotomimetic effects of cannabis. Studies in COMT and DRD2 polymorphisms have failed to show greater associations with transition to psychosis. Studies of AKT1 have shown slightly more promising results. Genome-wide association studies have recently been published some indicating novel polymorphisms. These may pave the way to alternate hypotheses to explain the missing links between cannabis use and increased risk of psychosis. Such knowledge may eventually lead to new pharmacotherapies in addition to the means of screening patients for psychosis risk.
Keywords: Cannabis use disorder, psychosis, COMT, CNR1, GWAS.
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