Abstract
Aims: To investigate the association between cognitive ability in late adolescence and subsequent substance misuse-related events in men, and to study the underlying genetic and environmental correlations.
Design: A population-based longitudinal study with three different family-based designs. Cox proportional hazards models were conducted to investigate the association at the individual level. Bivariate quantitative genetic modeling in (1) full brothers and maternal half-brothers, (2) full brothers reared together and apart, and (3) monozygotic and dizygotic twin brothers was used to estimate genetic and environmental correlations. Setting. Register-based study in Sweden.
Participants: The full sample included 1,402,333 Swedish men born 1958-1991 and conscripted at mean age 18.2 (SD=0.5) years. 1,361,066 men who had no substance misuse events before cognitive assessment at mandatory military conscription were included in the Cox regression models with a follow-up time of up to 35.6 years.
Measures: Cognitive ability was assessed at conscription with the Swedish Enlistment Battery. Substance misuse events included alcohol and drug related court convictions, medical treatments, and deaths, available from governmental registries.
Findings: Lower cognitive ability in late adolescence predicted an increased risk for substance misuse events (hazard ratio [HR] for a 1-stanine unit decrease in cognitive ability: 1.29, 95% CI: 1.29-1.30). The association was somewhat attenuated within clusters of full brothers (HR=1.21, 95% CI: 1.20-1.23). Quantitative genetic analyses indicated that the association was primarily due to genetic influences; the genetic correlations ranged between -.39 (95% CI: -.45, -.34) and -.52 (-.55, -.48) in the three different designs.
Conclusions: Our findings from different family designs indicate that shared genetic influences underlie the association between low cognitive ability and subsequent risk for substance misuse events.
