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Schizophr Bull. 2017 May 1;43(3):644-653. doi: 10.1093/schbul/sbw101.

Genetic and Environmental Contributions to the Association Between Cannabis Use and Psychotic-Like Experiences in Young Adult Twins.

Author information

1
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway.
2
Department of Psychiatric Research, Diakonhjemmet Hospital, Oslo, Norway.
3
Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
4
Virginia Institute for Psychiatric and Behavioral Genetics and Departments of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA.
5
The Norwegian Centre for Addiction Research, University of Oslo, Oslo, Norway.
6
Department of Psychology, University of Oslo, Oslo, Norway.
7
School of Pharmacy, University of Oslo, Oslo, Norway.

Abstract

To investigate contributions of genetic and environmental risk factors and possible direction of causation for the relationship between symptoms of cannabis use disorders (CUD) and psychotic-like experiences (PLEs), a population-based sample of 2793 young adult twins (63.5% female, mean [range] age 28.2 [19-36] y) were assessed for symptoms of CUD and PLEs using the Composite International Diagnostic Interview. Latent risk of having symptoms of CUD or PLEs was modeled using Item Response Theory. Co-twin control analysis was performed to investigate effect of familiar confounding for the association between symptoms of CUD and PLEs. Biometric twin models were fitted to estimate the heritability, genetic and environmental correlations, and direction for the association. Lifetime use of cannabis was reported by 10.4 % of the twins, and prevalence of PLEs ranged from 0.1% to 2.2%. The incidence rate ratio of PLEs due to symptoms of CUD was 6.3 (95% CI, 3.9, 10.2) in the total sample and 3.5 (95% CI, 1.5, 8.2) within twin pairs. Heritability estimates for symptoms of CUD were 88% in men and women, and for PLEs 77% in men and 43% in women. The genetic and environmental correlations between symptoms of CUD and PLEs were 0.55 and 0.52, respectively. The model allowing symptoms of CUD to cause PLEs had a better fit than models specifying opposite or reciprocal directions of causation. The association between symptoms of CUD and PLEs is explained by shared genetic and environmental factors and direct effects from CUD to risk for PLEs.

KEYWORDS:

THC; direction of causation; item response theory; psychosis

PMID:
27431873
PMCID:
PMC5464089
DOI:
10.1093/schbul/sbw101
[Indexed for MEDLINE]
Free PMC Article

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