Dopamine changes from cannabis are linked to psychosis

Six years after cannabis legalization in Canada, scientists are still mapping its long-term health effects. While social and medical benefits remain under review, emerging neuroscience now highlights a key concern – psychosis linked to dopamine changes in the brain.

A new study led by Canadian researchers has found biological evidence linking frequent cannabis use to changes in brain chemistry that resemble those seen in early psychosis.

Using a cutting-edge brain scan called neuromelanin-sensitive magnetic resonance imaging (MRI), the experts observed elevated dopamine activity in people with cannabis use disorder (CUD).

This increase occurred in the same brain areas previously tied to hallucinations, delusions, and other symptoms of psychotic disorders. The findings appeared in JAMA Psychiatry, in a study titled “Convergence of Cannabis and Psychosis on the Dopamine System.”

The study, spanning five years and several institutions, marks a turning point in how clinicians and researchers understand cannabis’ psychiatric risks. The analysis bridges the gap between clinical symptoms and underlying brain activity – something long sought but rarely demonstrated so clearly.

Cannabis builds dopamine in key brain areas

Dopamine helps the brain regulate mood, motivation, learning, and motor control. It also plays a central role in psychosis. High dopamine activity, especially in the striatum and midbrain, has been linked to schizophrenia and related disorders. What remained uncertain was how cannabis fit into that picture.

The researchers used neuromelanin-MRI – a non-invasive method that visualizes dopamine activity indirectly by tracking neuromelanin, a vital compound in the brain.

Neuromelanin is a dark pigment that accumulates as dopamine breaks down over time. The more dopamine activity, the more neuromelanin remains behind. In brain scans, this pigment shows up as darkened regions, especially in two key midbrain areas: the substantia nigra and the ventral tegmental area.

“In people partaking in excess cannabis use, those spots are blacker than what they should be for their age compared to healthy individuals,” said Lena Palaniyappan, professor at McGill University and senior author of the study.

“This indicates they have high levels of dopamine, and in some cases are showing pigments someone 10 years older would have.”

Cannabis use elevates dopamine signals

The study was focused on 61 individuals aged 18 to 35 from London, Ontario. Participants included people with CUD, those with early psychosis, some with both conditions, and healthy controls. The researchers tracked changes in neuromelanin-MRI signals across the groups.

They found that those with CUD – regardless of schizophrenia diagnosis – had elevated neuromelanin signals in a subregion of the midbrain tied to psychosis. This was not a temporary spike. Even after one year, the signal remained high, suggesting that cannabis-related dopamine changes may have a lasting effect.

This finding was dose-dependent. Individuals with more severe CUD symptoms showed stronger signal intensity, confirming that frequency and severity of cannabis use matter.

“We now have evidence that shows a straight line linking cannabis with dopamine and psychosis that has never been shown before, and it’s crucial that clinicians, patients, and families work together to break this line,” said Palaniyappan.

Cannabis increases the risk of psychosis

Cannabis’ effects on dopamine have long been disputed. Previous PET scans often showed mixed results – some indicating lowered dopamine synthesis, others showing a spike only after THC administration.

Neuromelanin-MRI offers a longer-term view, revealing cumulative dopamine activity, not just momentary shifts.

Participants with CUD had consistently higher neuromelanin signal across multiple scans, even when researchers accounted for nicotine use and other variables.

Interestingly, participants with first-episode schizophrenia (FES) did not show significant changes unless they also had CUD, which suggests cannabis itself may play a more central role than previously thought.

“This could help explain why cannabis use increases the risk of hallucinations and delusions, key symptoms of schizophrenia and other psychotic disorders,” said Jessica Ahrens, a PhD student at McGill University and lead author of the study.

Cannabis-induced psychosis is rising

Canadian emergency departments have reported more cases of cannabis-induced psychosis since legalization. Psychiatrists working with young adults are observing troubling patterns. Brief episodes are turning into more severe psychotic breaks over time.

“In the last several years since legalization, we’re seeing adolescents who have two or three brief cannabis-induced episodes of psychosis and then have a much more major episode,” said Dr. Julie Richard, psychiatrist and physician lead at PEPP, a specialized early psychosis program.

“So, we’re trying to counsel adolescents within that first episode that they’re pushing their brain towards a major episode and show them the areas in the brain that are impacted.”

The new imaging data now offers a visual tool that can support those conversations. Showing young people their own brain scans could help clinicians explain the risks more clearly.

Dopamine changes persist after one year

Importantly, the experts found no evidence that continued cannabis use beyond a certain point further increased dopamine activity. This suggests that dopamine-related changes may plateau after repeated exposure.

Yet, this stability does not mean the brain returns to normal. Elevated neuromelanin signals remained even a year later, indicating lasting effects.

“Increased dopamine functioning in the SN/VTA may be associated with the risk of psychosis in people with cannabis use disorder,” the authors wrote. This midbrain region – the source of dopamine projections to other brain areas – appears central to how cannabis affects mental health.

The absence of a “recovery effect” raises new questions: Can these changes be reversed with abstinence? Do they set the stage for future psychiatric illness? Larger, long-term studies will be needed to explore these questions further.

Guiding public health and prevention

The authors emphasized that cannabis alone does not cause psychosis in every user. But it raises the risk, especially in those with family histories or early symptoms. By linking cannabis use to measurable brain changes, this study helps move the discussion from speculation to science.

“The lack of clear biological evidence linking cannabis to psychosis has made it harder to persuade young people with psychotic symptoms to reduce their use,” said Palaniyappan.

“Our findings could help doctors and mental health professionals better educate patients about the potential risks of frequent cannabis use.”

“I hope these findings lead patients and health-care providers to better understand the implications and for the health-care providers to give patients resources for options other than cannabis to help them cope,” Jessica Ahrens added.

Cannabis and dopamine help explain psychosis

This study does not aim to demonize cannabis but to understand its effects better. With its use becoming more socially accepted and legally accessible, especially among youth, understanding its neurological footprint is urgent.

Cannabis use disorder is now more than a behavioral diagnosis. It is increasingly linked to real, visible changes in the brain’s dopamine system that may shape vulnerability to psychosis.

For clinicians, families, and users themselves, this information could lead to more informed decisions and safer outcomes.

The study is published in the journal JAMA Psychiatry.

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