Evidence-Based Reviews

Does marijuana contribute to psychotic illness?

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References

Recent evidence. Better-designed studies have shown that marijuana use increases the risk of psychosis later in life.

Adolescents who used marijuana by age 15 were more likely to develop a schizophreniform disorder by age 26 than nonusers, according to data from 759 New Zealanders who took part in a prospective, longitudinal, general population study. Marijuana use by age 15 was associated with a higher risk than later use (by age 18).9

A 3-year, longitudinal, population-based study from the Netherlands found marijuana use associated with increased risk of psychosis in 4,045 previously psychosis-free individuals. More than 50% of psychosis diagnoses could be attributed to marijuana use.10

Data from the 21-year longitudinal Christchurch Health and Development Study in New Zealand showed elevated rates of psychotic symptoms in young people with cannabis dependence at ages 18 and 21. The associations remained even after adjustments were made for previous psychotic symptoms and other confounding factors.11

Follow-up analysis of data from the Swedish military conscripts study8 showed that the use of other psychoactive drugs or prodromal cases in the cohort did not explain the association between self-reported marijuana use and hospital admissions for schizophrenia and other psychoses.12

Box 2

Risk factors for psychotic illness onset in marijuana users
  • Starting marijuana use in adolescence
  • Using cannabis often (weekly or daily) or for long periods
  • Unusual, psychotic-like experiences (such as fleeting persecutory ideas or ideas of reference) or displaying high “psychoticism” on the self-report Symptom Checklist-90-R
  • Family history of psychosis
  • Prior cannabis-induced psychotic episode


Box 3

Cannabis and psychosis: 4 clinical pearls
  • Cannabis use increases the risk of developing psychosis and is estimated to double the risk for later schizophrenia (5 to 10 new cases per 10,000 person-years)
  • The association is not an artifact of confounding factors such as prodromal symptoms or concurrent use of other substances (including amphetamines)
  • The risk increases with the frequency and length of use (a dose-effect relationship)
  • Self-medication is not the connection between cannabis use and schizophrenia, according to empiric evidence

Source: References 9-14

Researchers in Israel cross-linked a cohort of 9,724 youths aged 16 to 17 screened by the Israeli Draft Board with a national registry of psychiatric hospital admissions for schizophrenia in the following 4 to 15 years. Self-reported drug abuse (mostly marijuana) was higher in adolescents who were later hospitalized for schizophrenia (12.4%) than in those not hospitalized (5.9%).13

Box 4

Cannabis-induced psychotic episode vs schizophrenia

Is the diagnosis worthwhile? Acute-phase cannabis-induced psychosis and schizophrenia have similar presentations, making differential diagnosis difficult. If their treatment also is similar, is it clinically meaningful to distinguish whether marijuana use or schizophrenia triggered psychotic symptoms? The answer is yes, because:

  • schizophrenia has a worse course and prognosis
  • many patients with cannabis-induced psychosis do not develop schizophrenia.

Diagnostic clues. Some clinicians believe cannabis-induced psychosis is more likely than schizophrenia to feature:

  • expansive mood
  • derealization or depersonalization experiences
  • visual hallucinations
  • less overall severity.

Consider the course. The only way to differentiate the two disorders is to consider the illness course. Cannabis-induced psychotic episodes occur during periods of intoxication or withdrawal, tend to be short-lived, and usually respond well to treatment if the person abstains.

Up to one-half of patients with a cannabis-induced psychosis develop a schizophrenia-spectrum disorder. Monitoring them (such as at 6-month intervals) is important, therefore, because schizophrenia onset often occurs >12 months after the cannabis-induced psychosis.

Summary. A review of these 5 studies concluded that evidence supports the hypothesis that marijuana use acts as a risk factor in schizophrenia onset.14 Although marijuana use is not a “necessary” causal factor in psychotic illness—most users do not develop the disorder, and many persons with schizophrenia do not use marijuana—strong evidence indicates that it is one of many factors that can cause a psychotic illness (Box 2).9-14

Who is at risk?

Can marijuana cause psychosis in any person or specifically in those at increased risk of psychosis? If the latter, then marijuana—rather than causing new, unanticipated cases—might bring forward schizophrenia onset in individuals who would have developed it later. This explanation is consistent with data showing that persons born in more-recent cohorts seem to have an earlier age of schizophrenia onset.15

Vulnerability for psychosis. Evidence strongly suggests that marijuana-induced psychotic symptoms are more prevalent among vulnerable or psychosis-prone individuals.

  • When given 2.5 mg of delta-9-THC, 80% of 13 patients with well-controlled schizophrenia experienced high Positive and Negative Syndrome Scale scores, compared with 35% of 22 healthy controls.2
  • Unusual perceptions or thought influence were more common following marijuana use in all participants in a naturalistic experiment, but much more so in “at risk” individuals who had previously described isolated psychotic symptoms.16
  • Adolescents and young adults ages 14 to 24 who used marijuana and displayed high “psychoticism” scores at baseline had more than twice the risk of a psychosis outcome 4 years later than did those without high scores.17

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