Premium
The genetic and environmental architecture of substance use development from early adolescence into young adulthood: a longitudinal twin study of comorbidity of alcohol, tobacco and illicit drug use
Author(s) -
Waaktaar Trine,
Kan KeesJan,
Torgersen Svenn
Publication year - 2018
Publication title -
addiction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.424
H-Index - 193
eISSN - 1360-0443
pISSN - 0965-2140
DOI - 10.1111/add.14076
Subject(s) - twin study , medicine , zygosity , confidence interval , population , young adult , demography , illicit drug , drug , heritability , psychiatry , environmental health , genetics , biology , sociology
Aims To investigate how use of alcohol, illicit drugs and tobacco come from substance‐specific pathways and from pathways general to all three substances through adolescent development. Design Analysis of population‐based survey. Adolescent twins reported alcohol use (AU), tobacco use (TU) and illicit drug use (IDU) in three waves (2006, 2008, 2010). Restructuring data by age allowed for variance decomposition into age‐ and substance‐specific and common genetic and environmental variance components. Setting Norway. Participants Seven national twin birth cohorts from 1988 to 1994, totalling 1483 pairs (558 monozygotic; 925 dizygotic, same and opposite sex). Measurements Six‐point Likert scores of AU, TU and IDU on items from the Monitoring the Future Study. Findings Substance use was found to be highly heritable; a 2 = 0.73 [95% confidence interval (CI) = 0.61–0.94] for AU, a 2 = 0.36 (CI = 0.18–0.52); d 2 = 0.49 (95% CI = 0.29–0.62) for IDU and a 2 = 0.46 (95% CI = 0.23–0.54); d 2 = 0.05 (95% CI = 0.00–0.07) for TU during the whole adolescence period. General substance use (GSU) was also highly heritable at each age and averaged a 2 = 0.57 (95% CI = 0.48–0.66). There was a high genetic carry‐over from earlier age to later age. Genetic effects on GSU at ages 12–14 years were still detectable 4 years later. New substance (general and specific)‐genetic effects also appeared. IDU demonstrated significant non‐additive genetic effects (ages 12–14 years). Shared environment had a small impact on AU only. There was almost no non‐shared environmental carry‐over from age to age, the effect probably due partly to reliability deficiency. Common genetic effects among substance and substance‐specific genetic effects were observed at each age‐period. Conclusions Among Norwegian adolescents, there appear to be strong genetic effects on both substance‐specific and comorbid use of alcohol, illicit drugs and tobacco; individual differences in alcohol use can be explained partially by family background.