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Modern high-potency cannabis may be changing the landscape of psychotic disorders.

Cannabis psychosis may be more than a temporary drug-induced condition.

Continued cannabis (THC) use may triple relapse risk despite taking antipsychotics.

Daily use and high-potency THC increase psychosis risk in a dose-dependent manner. (More is worse.)

If you carry a genetic or neurobiological vulnerability to psychosis, using cannabis may increase the likelihood that psychosis will emerge, particularly during adolescence and young adulthood. Cannabis-induced psychosis is not always temporary. Numerous studies have shown that many affected individuals develop schizophrenia-spectrum disorders.

Few investigators have done more to shape contemporary thinking about cannabis and psychosis than Deepak D’Souza, M.D., the Vikram Sodhi ’92 Professor of Psychiatry at Yale University School of Medicine. His work demonstrated that delta-9-tetrahydrocannabinol (THC), the principal psychoactive component of cannabis, can induce transient psychotic symptoms in healthy volunteers and worsen existing symptoms in patients with schizophrenia. For more than two decades, D’Souza’s research, scientific publications, and public statements have challenged assumptions about the psychiatric safety of cannabis.

D’Souza’s trailblazing research helped move the field beyond the simple observation that cannabis use and psychosis are associated. The more important question became whether cannabis could cause psychotic disorders. His studies also found that abstinence reduces relapse risk, whereas continued cannabis use is associated with poorer clinical outcomes and a diminished treatment response.

Today, D’Souza is asking a different question. Amid concerns about increasingly potent commercial cannabis and unprecedented levels of THC exposure, he’s raised the possibility that cannabis may trigger a lifelong psychosis in some individuals. Recently, D’Souza and colleagues published a study comparing patients hospitalized with first-episode psychosis who had documented cannabis exposure with similar patients who had no evidence of cannabis exposure.

The study examined 119 men hospitalized with first-episode psychosis, including 66 with toxicology-confirmed cannabis exposure and 53 without cannabis exposure. Patients in the cannabis-associated group exhibited fewer negative symptoms, such as affective flattening and loss of motivation, while showing comparable levels of hallucinations and delusions. They also displayed more depressive and manic features, denoting a clinical presentation differing from classic deficit-form schizophrenia.

While both groups entered the hospital with similar levels of cognitive impairment, only the cannabis-associated group demonstrated significant cognitive improvement after four weeks of treatment and cannabis abstinence. The investigators also detected distinct EEG patterns that may reflect differences in cortical excitation and inhibition. Together, these findings suggest cannabis-associated psychosis may differ from non-cannabis-associated psychosis in ways that extend beyond clinical symptoms alone.

D’Souza summarized the evolution of his thinking in a recent conversation with me:

"Schizophrenia (SCZ) or, as Bleuler in 1911 appropriately coined, the 'group of schizophrenias', is heterogeneous on a number of levels, including its phenomenology and clinical manifestation, environmental risk factors, micro-scale molecular genetics, transcriptomics, proteomics, and macro-scale alterations in brain structure, function, and connectivity. Several attempts have been made to identify and tease apart SCZ subtypes based on clinical manifestations, genetics, and biomarkers. It is a bit too early to make any definitive conclusions, but our findings raise the fascinating........

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