Cannabis use disorder linked to elevated dopamine function in brain region associated with psychosis

Cannabis use disorder (CUD) was associated with elevated neuromelanin-MRI signal in a set of ventral substantia nigra/ventral tegmental area voxels (387 of 2,060 voxels, corrected P=0.03). CUD was also associated with elevated signal in a region previously linked to psychosis severity (P=0.04), with a dose-dependent relationship (more severe CUD symptoms correlated with higher signal, P=0.03). In contrast, first-episode schizophrenia alone did not reach significance in this analysis.

Longitudinal observational cohort study recruiting from an early psychosis service and surrounding communities in London, Ontario (2019-2023). 61 participants (36 without CUD, 25 with CUD; some with first-episode schizophrenia in each group). Neuromelanin-sensitive MRI used as a proxy measure of dopamine function. One-year follow-up for 37 participants.

This study provides neuroimaging evidence for a specific biological mechanism linking cannabis use to psychosis risk. The finding that cannabis use disorder affects the same dopamine pathway implicated in psychosis suggests a shared neural substrate, not just a statistical association.

The dopamine hypothesis of psychosis is one of the most established frameworks in psychiatry. Finding that cannabis use disorder converges on this same dopamine pathway provides a biological explanation for the epidemiological link between heavy cannabis use and psychosis, published in JAMA Psychiatry.

Small sample size (61 total, 25 with CUD). Neuromelanin MRI is a proxy measure of dopamine function, not a direct measurement. Cannot determine whether CUD causes dopamine changes or whether pre-existing dopamine differences predispose to both CUD and psychosis. Cross-sectional associations with limited longitudinal change data.