Nathan A Gillespie1, Steven H Aggen1, Michael C Neale1,2, Gun Peggy Knudsen3, Robert F Krueger4, Susan C South5, Nikolai Czajkowski3,6, Ragnar Nesvåg3,7, Eivind Ystrom3,8,9, Kenneth S Kendler1,2, Ted Reichborn-Kjennerud3,10. 1. Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA. 2. Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA, USA. 3. Department of Mental Disorders, Norwegian Institute of Public Health, Norway. 4. Department of Psychology, University of Minnesota, Minneapolis, MN, USA. 5. Department of Psychological Sciences, Purdue University, West Lafayette, IN, USA. 6. Department of Psychology, University of Oslo, Oslo, Norway. 7. Department of Psychiatric Research, Diakonhjemmet Hospital, Oslo, Norway. 8. Section of Health, Developmental and Personality Psychology, Department of Psychology, University of Oslo, Norway. 9. PharmacoEpidemiology and Drug Safety Research Group, School of Pharmacy, University of Oslo, Norway. 10. Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Abstract
BACKGROUND AND AIMS: Individual differences in DSM-IV personality disorders (PDs) are associated with increased prevalence of substance use disorders. Our aims were to determine which combination of PDs trait scores best predict cannabis use (CU) and cannabis use disorder (CUD), and to estimate the size and significance of genetic and environmental risks in PD traits shared with CU and CUD. DESIGN: Linear mixed-effects models were used to identify PD traits for inclusion in twin analyses to explore the genetic and environmental associations between the traits and cannabis use. SETTING: Cross-sectional data were obtained from Norwegian adult twins in a face-to-face interview in 1999-2004 as part of a population-based study of mental health. PARTICIPANTS: Subjects were 1419 twins (μage = 28.2 years, range = 19-36) from the Norwegian Institute of Public Health Twin Panel with complete PD and cannabis data. MEASUREMENTS: PD traits were assessed using DSM-IV criteria. Life-time CU and CUD were based on DSM-IV abuse and dependence criteria, including withdrawal and craving. FINDINGS: After adjusting for age and sex, antisocial [β = 0.23, 95% confidence interval (CI) = 0.19-0.28] and borderline PDs (β = 0.20, 95% CI = 0.14-0.26) were associated strongly with CU. Antisocial (β = 0.26, 95% CI = 0.21-0.31) and borderline PDs (β = 0.12, 95% CI = 0.06-0.18) were also linked strongly to CUD. Genetic risks in antisocial and borderline PD traits explained 32-60% of the total variance in CU and CUD. Dependent and avoidant PDs explained 11 and 16% of the total variance in CU and CUD, respectively. CONCLUSIONS: Individual differences in the liability to cannabis use and cannabis use disorder appear to be linked to genetic risks correlated with antisocial and borderline personality disorder traits.
BACKGROUND AND AIMS: Individual differences in DSM-IV personality disorders (PDs) are associated with increased prevalence of substance use disorders. Our aims were to determine which combination of PDs trait scores best predict cannabis use (CU) and cannabis use disorder (CUD), and to estimate the size and significance of genetic and environmental risks in PD traits shared with CU and CUD. DESIGN: Linear mixed-effects models were used to identify PD traits for inclusion in twin analyses to explore the genetic and environmental associations between the traits and cannabis use. SETTING: Cross-sectional data were obtained from Norwegian adult twins in a face-to-face interview in 1999-2004 as part of a population-based study of mental health. PARTICIPANTS: Subjects were 1419 twins (μage = 28.2 years, range = 19-36) from the Norwegian Institute of Public Health Twin Panel with complete PD and cannabis data. MEASUREMENTS: PD traits were assessed using DSM-IV criteria. Life-time CU and CUD were based on DSM-IV abuse and dependence criteria, including withdrawal and craving. FINDINGS: After adjusting for age and sex, antisocial [β = 0.23, 95% confidence interval (CI) = 0.19-0.28] and borderline PDs (β = 0.20, 95% CI = 0.14-0.26) were associated strongly with CU. Antisocial (β = 0.26, 95% CI = 0.21-0.31) and borderline PDs (β = 0.12, 95% CI = 0.06-0.18) were also linked strongly to CUD. Genetic risks in antisocial and borderline PD traits explained 32-60% of the total variance in CU and CUD. Dependent and avoidant PDs explained 11 and 16% of the total variance in CU and CUD, respectively. CONCLUSIONS: Individual differences in the liability to cannabis use and cannabis use disorder appear to be linked to genetic risks correlated with antisocial and borderline personality disorder traits.
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