November 25, 2024
2 min read
Key takeaways:
- Links between teen cannabis use and psychosis symptoms may reflect self-medication and shared vulnerability.
- Researchers say results should not be interpreted as evidence against cannabis use contributing to psychosis.
Young adolescents who used cannabis more frequently reported psychosis spectrum symptoms and greater distress from such symptoms, according to results of a cohort study published in JAMA Psychiatry.
However, psychosis spectrum symptoms increased leading up to the time study participants starting using rather than after, supporting the theory that youth use cannabis to self-medicate the symptoms.
Psychosis, cannabis links still debated
Healio previously reported that youth who used cannabis were 11 times more likely to develop psychotic disorders, but the debate on the exact nature of this link continues, K. Juston Osborne, PhD, a postdoc research scholar at Washington University in St. Louis, and colleagues explained in JAMA Psychiatry.
“For example, it has been theorized that adolescent cannabis use may causally contribute to the emergence of psychosis via the disruption of normative neurodevelopmental processes,” they wrote. “Alternative models suggest that the association between cannabis use and psychosis may reflect a shared vulnerability for both cannabis use and psychosis or individuals’ attempts to self-medicate in response to distress from psychosis spectrum symptomology.”
The researchers also pointed to a self-medication hypothesis, which “suggests that individuals may initiate cannabis use in an attempt to alleviate psychosis spectrum and secondary symptoms, such as anxiety and dysphoria, reflecting an effort to self-medicate by affected individuals.
Osborne and colleagues assessed these hypotheses by using data from five waves across 4 years of follow-up from the large-scale Adolescent Brain Cognitive Development study.
The final analysis included 11,868 adolescents aged 9 to 10 years at baseline.
All three hypotheses may play a role
Osborne and colleagues found that, consistent with the shared vulnerability hypothesis, adolescents who used cannabis at any time during the study period reported a greater number of psychosis spectrum symptoms (B = 0.86; 95% CI, 0.68-1.04) and more distress from psychosis spectrum symptoms (B = 1.17; 95% CI, 0.96-1.39) vs. those who never used cannabis.
The number of psychosis spectrum symptoms (B = 0.16; 95% CI, 0.12-0.2) and distress from psychosis spectrum symptoms (B = 0.23; 95% CI, 0.21-0.26) increased in the time leading up to cannabis initiation, whereas symptoms typically did not increase after initiation.
“However, mixed evidence for the contributing risk hypothesis was observed in sensitivity analyses,” the researchers wrote.
They added that distress from psychosis spectrum symptoms actually decreased after initiation but explained that this particular finding does not suggest cannabis is an effective treatment option for reducing symptoms.
“This point is particularly important given adolescents’ already low perceptions of the risks of cannabis use,” they wrote.
The researchers said that the results should not be interpreted as evidence against adolescent cannabis use having a contributing role on psychosis risk.
“Several lines of evidence implicate a dose-dependent association between cannabis use and psychosis risk, with risk increasing with greater frequency and quantity of use and higher cannabis potency,” they wrote.
Altogether, “an integrated theory of these three hypotheses may best capture the dynamic associations between cannabis use and psychosis risk throughout development,” Osborne and colleagues added. “Specifically, shared risk vulnerabilities and attempts to self-medicate symptom-related distress may lead to initial cannabis initiation in adolescence, whereas subsequent increases in the frequency and quantity of cannabis use throughout adolescent development may then contribute to psychosis onset in young adulthood.”
They added that further research assessing youth over a longer follow-up period is needed “to provide a diagnostic test of the contributing risk hypothesis.”
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