While adolescent cannabis use was associated with higher adult psychoticism scores, co-twin control analyses found no evidence of a causal effect, suggesting shared family factors explain the link.
Psychiatrists, geneticists, cannabis-psychosis researchers
No evidence of causal effect when comparing twins who used different amounts of cannabis
What the researchers found
In 1,544 twins, both cumulative adolescent cannabis use and cannabis use disorder were associated with higher adult Psychoticism scores, but comparing twins within pairs (where one used more cannabis) showed no within-pair difference, pointing to familial confounds rather than causal effects.
Why it matters
This twin design is one of the strongest methods for separating causal effects from confounding. Finding no within-twin-pair effect challenges the assumption that cannabis directly causes psychotic traits and suggests shared genetic or environmental factors drive both.
The numbers in context
1,544 twins for cannabis use analysis; 1,458 for CUD analysis; no significant within-pair effect in co-twin models; no interaction between polygenic risk for schizophrenia and cannabis use on psychoticism.
How the study worked
Longitudinal co-twin control analysis using two cohorts of twins with prospective measures of adolescent cannabis use (N=1,544) and cannabis use disorder symptoms (N=1,458) linked to adult Psychoticism (PID-5), with polygenic risk scores for schizophrenia.
What this study cannot tell us
Psychoticism scale measures a broad dimension, not clinical psychosis diagnosis; predominantly White sample from Minnesota; may not generalize to populations with different genetic backgrounds; cannabis potency not measured.
How to read the evidence
Strong genetically informative design using prospective twin cohort data, limited by dimensional rather than clinical outcome measure.
When this study was published
Longitudinal data with adolescent cannabis measures and adult psychoticism assessment.
The bigger picture
If the cannabis-psychosis link is largely explained by shared genetic liability rather than direct causation, it would shift the focus of prevention from cannabis avoidance toward identifying and supporting individuals with underlying genetic vulnerability.
Questions still open
- Would similar co-twin designs find the same result using clinical psychosis outcomes rather than dimensional psychoticism? Does cannabis potency matter more than frequency in this relationship?
Common questions
Does this study prove cannabis doesn't cause psychosis?
What is a co-twin control design?
Read the original research
Adolescent cannabis use and adult psychoticism: A longitudinal co-twin control analysis using data from two cohorts.
Journal of abnormal psychology, 130(7), 691-701
Citation
Schaefer, Jonathan D; Jang, Seon-Kyeong; Vrieze, Scott; Iacono, William G; McGue, Matt; Wilson, Sylia. (2021). Adolescent cannabis use and adult psychoticism: A longitudinal co-twin control analysis using data from two cohorts.. Journal of abnormal psychology, 130(7), 691-701. https://doi.org/10.1037/abn0000701
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