Teens with higher genetic risk for schizophrenia showed stronger increases in cannabis use from age 16 to 20
A longitudinal study of 372 adolescents found that higher polygenic risk scores for schizophrenia were associated with stronger increases in cannabis use during ages 16-20, while no relationship was found for alcohol or tobacco, supporting a shared genetic basis between schizophrenia and cannabis use.
Quick Facts
What This Study Found
Researchers followed 372 adolescents from the RADAR-Y study, tracking substance use from ages 13-20 while measuring each participant's genetic vulnerability to schizophrenia using polygenic risk scores.
High schizophrenia genetic vulnerability was specifically associated with a stronger increase in cannabis use during ages 16-20. This relationship was consistent across multiple polygenic risk score thresholds.
No clear relationship was found between schizophrenia genetic risk and smoking or alcohol use, making the association specific to cannabis.
This specificity is particularly noteworthy: if the association were simply about genetic predisposition to substance use in general, it should have appeared for alcohol and tobacco as well. The cannabis-specific finding supports the hypothesis that shared genetic factors specifically link schizophrenia vulnerability and cannabis use behavior.
Key Numbers
372 adolescents followed ages 13-20. Higher schizophrenia PRS predicted stronger cannabis use increase ages 16-20 (multiple thresholds significant at p<0.001). No relationship with alcohol or smoking. Cannabis-specific association supports shared genetic architecture.
How They Did This
Longitudinal cohort (RADAR-Y study, N=372). Piecewise latent growth curve modeling analyzed cannabis, smoking, and alcohol use trajectories from ages 13-20 (split at age 16). Polygenic risk scores for schizophrenia calculated at multiple p-value thresholds. Bonferroni-corrected significance at p<0.001.
Why This Research Matters
This finding helps explain why cannabis use and schizophrenia co-occur: it may not be simply that cannabis causes psychosis, but that shared genetic factors make some individuals both more likely to use cannabis and more vulnerable to schizophrenia. This has profound implications for understanding causation in the cannabis-psychosis relationship.
The Bigger Picture
This study adds to growing evidence that the cannabis-schizophrenia association is partly driven by shared genetics rather than a simple one-way causal path. Individuals with higher genetic loading for schizophrenia may be drawn to cannabis for reasons related to their neurobiology, creating a complex interplay between genetic vulnerability, cannabis use, and psychosis risk.
What This Study Doesn't Tell Us
Moderate sample size (372) for genomic analyses. Dutch adolescent sample may not generalize to other populations. Polygenic risk scores explain only a small fraction of schizophrenia heritability. Cannabis use was self-reported. The study period (ages 13-20) may miss later-onset patterns.
Questions This Raises
- ?Do adolescents with high schizophrenia PRS self-medicate with cannabis for prodromal symptoms?
- ?Would cannabis prevention in genetically high-risk adolescents reduce psychosis onset?
- ?Are there specific genetic variants that drive both cannabis preference and schizophrenia risk?
Trust & Context
- Key Stat:
- Schizophrenia genetic risk predicted cannabis use increases specifically, not alcohol or tobacco
- Evidence Grade:
- Longitudinal cohort with genomic data and rigorous statistical correction provides moderate evidence on the genetic overlap between schizophrenia vulnerability and cannabis use patterns.
- Study Age:
- Published in 2018. Larger genome-wide studies have since expanded understanding of the genetic overlap between cannabis use and psychiatric disorders.
- Original Title:
- Genetic vulnerability to schizophrenia is associated with cannabis use patterns during adolescence.
- Published In:
- Drug and alcohol dependence, 190, 143-150 (2018)
- Authors:
- Hiemstra, Marieke, Nelemans, Stefanie A, Branje, Susan, van Eijk, Kristel R, Hottenga, Jouke-Jan, Vinkers, Christiaan H, van Lier, Pol, Meeus, Wim, Boks, Marco P
- Database ID:
- RTHC-01690
Evidence Hierarchy
Follows a group of people over time to track how outcomes develop.
What do these levels mean? →Frequently Asked Questions
Is the link between cannabis and schizophrenia genetic?
Partly. This study found that teens with higher genetic risk for schizophrenia showed stronger increases in cannabis use from 16-20, suggesting shared genetic factors drive both, rather than cannabis simply causing psychosis or psychosis simply causing cannabis use.
Did the genetic risk affect use of other substances?
No. Schizophrenia genetic risk was specifically linked to cannabis use, not alcohol or tobacco. This specificity suggests a unique genetic connection between schizophrenia vulnerability and cannabis use behavior.
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Cite This Study
https://rethinkthc.com/research/RTHC-01690APA
Hiemstra, Marieke; Nelemans, Stefanie A; Branje, Susan; van Eijk, Kristel R; Hottenga, Jouke-Jan; Vinkers, Christiaan H; van Lier, Pol; Meeus, Wim; Boks, Marco P. (2018). Genetic vulnerability to schizophrenia is associated with cannabis use patterns during adolescence.. Drug and alcohol dependence, 190, 143-150. https://doi.org/10.1016/j.drugalcdep.2018.05.024
MLA
Hiemstra, Marieke, et al. "Genetic vulnerability to schizophrenia is associated with cannabis use patterns during adolescence.." Drug and alcohol dependence, 2018. https://doi.org/10.1016/j.drugalcdep.2018.05.024
RethinkTHC
RethinkTHC Research Database. "Genetic vulnerability to schizophrenia is associated with ca..." RTHC-01690. Retrieved from https://rethinkthc.com/research/hiemstra-2018-genetic-vulnerability-to-schizophrenia
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkTHC research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.