Contributions of Genes and Environment to Developmental Change in Alcohol Use.

The precise nature of how genetic and environmental risk factors influence changes in alcohol use (AU) over time has not yet been investigated. Therefore, the aim of the present study is to examine the nature of longitudinal changes in these risk factors to AU from mid-adolescence through young adulthood. Using a large sample of male twins, we compared five developmental models that each makes different predictions regarding the longitudinal changes in genetic and environmental risks for AU. The best-fitting model indicated that genetic influences were consistent with a gradual growth in the liability to AU, whereas unique environmental risk factors were consistent with an accumulation of risks across time. These results imply that two distinct processes influence adolescent AU between the ages of 15-25. Genetic effects influence baseline levels of AU and rates of change across time, while unique environmental effects are more cumulative.

The heritability of alcohol use disorders: a meta-analysis of twin and adoption studies.

BACKGROUND: To clarify the role of genetic and environmental risk factors in alcohol use disorders (AUDs), we performed a meta-analysis of twin and adoption studies and explored the impact of sex, assessment method (interview v. hospital/population records), and study design (twin v. adoption study) on heritability estimates. METHOD: The literature was searched for all unique twin and adoption studies of AUD and identified 12 twin and five adoption studies. The data were then reconstructed and analyzed using ordinal data full information maximum likelihood in the OpenMx program. Heterogeneity was tested with likelihood ratio tests by equating the parameters across studies. RESULTS: There was no evidence for heterogeneity by study design, sex or assessment method. The best-fit estimate of the heritability of AUD was 0.49 [95% confidence interval (CI) 0.43-0.53], and the proportion of shared environmental variance was 0.10 (95% CI 0.03-0.16). Estimates of unique environmental proportions of variance differed significantly across studies. CONCLUSIONS: AUD is approximately 50% heritable. The multiple genetically informative studies of this syndrome have produced consistent results that support the validity of this heritability estimate, especially given the different potential methodological weaknesses of twin and adoption designs, and of assessments of AUD based on personal interviews v. official records. We also found evidence for modest shared environmental effects suggesting that environmental factors also contribute to the familial aggregation of AUDs.

Disruptive behavior disorders and indicators of disinhibition in adolescents: The BRIEF-SR, anti-saccade task, and D-KEFS color-word interference test.

Disinhibition contributes to the development of disruptive behavior disorders (DBD) in adolescents. Self-reports and behavioral tasks are commonly used to assess disinhibition, each with their unique strengths and limitations. Accordingly, it is important to identify which measure, or combination thereof, is the most effective in predicting DBD symptoms. This study assessed the relationship between DBD (symptoms of ADHD/ODD/CD) and two behavioral disinhibition tasks: the anti-saccade task and the D-KEFS color-word interference test, as well as a self-report measure (the BRIEF-SR). The results indicated that the BRIEF-Inhibit scale accounted for the majority of the variance in the DBD sum score. The anti-saccade task and color-word interference test were also significantly associated with an increase in the number of DBD symptoms endorsed. These behavioral tasks accounted for 9% additional variance than the self-report alone. Therefore, combining self-report measures with behavioral disinhibition tasks may provide the most thorough assessment of adolescent DBD.