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Objective: Using Swedish nationwide registry data, we investigated the contribution of genetic and environmental risk factors to the etiology of alcohol use disorder (AUD) by extended twin pedigree modeling. Method: AUD was defined using public inpatient, outpatient, prescription, and criminal records. Three-generational pedigrees were selected for index individuals born between 1980 and 1990, obtained from the national twin and genealogical registers, whose parents were twins. Relatives of the twins included in the pedigrees were their parents, siblings, spouses, and children. Genetic structural equation modeling was applied to the population-based data on AUD, using OpenMx, with age used as a covariate. Results: Analyses including up to 162,469 individuals in 18,971 pedigrees estimated AUD prevalence at 5%-12% in men and 2%-5% in women. Results indicated substantial heritability (about 50%-60%), of which a portion upwards of 5% was attributable to the consequences of assortative mating. Contributions of shared environmental factors to AUD, which represent a mix of within- and cross-generational effects, appeared to be moderate (about 10%-20%). Unique environment accounted for the remaining variance (about 20%-30%). Sex differences in the magnitude of the variance components suggested higher heritability in men and correspondingly higher shared environmental contributions in women. Conclusions: Using objective registry data, we found that AUD is highly heritable. Furthermore, shared environmental factors contributed significantly to the liability of AUD in both men and women. [ABSTRACT FROM AUTHOR]

Objective: Social relationships, such as committed partnerships, limit risky behaviors like heavy drinking, in part, because of increased social control. The current analyses examine whether involvement in committed relationships or social support extend beyond a main effect to limit genetic liability in heavy drinking (gene-environment interaction) during young adulthood.Method: Using data from the young adult wave of the Finnish Twin Study, FinnTwin12 (n = 3,269), we tested whether involvement in romantic partnerships or social support moderated genetic influences on heavy drinking using biometric twin modeling for gene-environment interaction.Results: Involvement in a romantic partnership was associated with a decline in genetic variance in both males and females, although the overall magnitude of genetic influence was greater in males. Sex differences emerged for social support: increased social support was associated with increased genetic influence for females and reduced genetic influence for males.Conclusions: These findings demonstrate that social relationships are important moderators of genetic influences on young adult alcohol use. Mechanisms of social control that are important in limiting genetic liability during adolescence extend into young adulthood. In addition, although some relationships limit genetic liability equally, others, such as extensive social networks, may operate differently across sex. [ABSTRACT FROM AUTHOR]

Objective: Twin studies have shown that genetic factors in part explain the established relation between alcohol use (i.e., problematic use or abuse/dependence) and eating disorder symptoms in adolescent and adult females. However, studies have yet to elucidate if there are similar shared genetic factors between other aspects of substance involvement, such as illicit drug use and repeated cigarette smoking. Method: For those sex-specific phenotypic correlations above our threshold of .20, we used a behavioral genetic design to examine potential shared genetic overlap between self-reported lifetime illicit drug use and repeated cigarette smoking and the eating disorder symptoms of drive for thinness (DT), bulimia (BU), and body dissatisfaction (BD), as assessed with the Eating Disorder Inventory-II, in 16- to 17-year-old female and male twin pairs. Results: Only phenotypic correlations with illicit drug use met our threshold for twin modeling. Small to moderate genetic correlations were observed between illicit drug use and BU in both girls and boys and between illicit drug use and DT in girls. Conclusions: Similar etiological factors are at play in the overlap between illicit drug use and certain eating disorder symptoms in girls and boys during adolescence, such that genetic factors are important for covariance. Specifically, illicit drug use was associated with bulimia nervosa symptoms in girls and boys, which parallels previous substance use research finding a genetic overlap between alcohol use and bulimia nervosa symptoms. Future research should prospectively examine developmental trajectories to further understand the etiological overlap between substance involvement and eating disorder symptoms. [ABSTRACT FROM AUTHOR]