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Background Alcohol consumption is typically correlated with the alcohol use behaviors of one's peers. Previous research has suggested that this positive relationship could be due to social selection, social influence, or a combination of both processes. However, few studies have considered the role of shared genetic and environmental influences in conjunction with causal processes. Methods This study uses data from a sample of male twins ( N = 1,790) who provided retrospective reports of their own alcohol consumption and their peers' alcohol-related behaviors, from adolescence into young adulthood (ages 12 to 25). Structural equation modeling was employed to compare 3 plausible models of genetic and environmental influences on the relationship between phenotypes over time. Results Model fitting indicated that one's own alcohol consumption and the alcohol use of one's peers are related through both genetic and shared environmental factors and through unique environmental causal influences. The relative magnitude of these factors, and their contribution to covariation, changed over time, with genetic factors becoming more meaningful later in development. Conclusions Peers' alcohol use behaviors and one's own alcohol consumption are related through a complex combination of genetic and environmental factors that act via correlated factors and the complementary causal mechanisms of social selection and influence. Understanding these processes can inform risk assessment as well as improve our ability to model the development of alcohol use. [ABSTRACT FROM AUTHOR]

The extended twin kinship design allows the simultaneous testing of additive and nonadditive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission (Eaves et al., 1999). It also handles the contribution of these sources of variance to the (co)variation of multiple phenotypes. Keller et al. (2008) extended this comprehensive model for family resemblance to allow or a flexible specification of assortment and vertical transmission. As such, it provides a general framework which can easily be reduced to fit subsets of data such as twin-parent data, children-of-twins data, etc. A flexible Mx specification of this model that allows handling of these various designs is presented in detail and applied to data from the Virginia 30,000. Data on height, body mass index, smoking status, church attendance, and political affiliation were obtained from twins and their families. Results indicate that biases in the estimation of variance components depend both on the types of relative available for analysis, and on the underlying genetic and environmental architecture of the phenotype of interest. [ABSTRACT FROM AUTHOR]

Considerable evidence from twin and adoption studies indicates that both genetic and shared environmental factors play a substantial role in the liability to antisocial behavior. Although twin and adoption designs can resolve genetic and environmental influences, they do not provide information about assortative mating, parent-offspring transmission, or the contribution of these factors to trait variation. We examined the role of genetic and environmental factors for conduct disorder (CD) using a twin-parent design. This design allows the simultaneous estimation of additive genetic, shared and individual-specific environmental effects, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A retrospective measure of CD was obtained from twins and their parents or guardians in the Virginia Twin Study of Adolescent Behavior Development and its Young Adult Follow up sample. Both genetic and environmental factors play a significant role in the liability to CD. Major influences on individual differences appeared to be additive genetic (38%-40%) and unique environmental (39%-42%) effects, with smaller contributions from the shared environment (18%-23%), assortative mating (-2%), cultural transmission (approximately 2%) and resulting genotype-environment covariance. This study showed significant heritability, which is slightly increased by assortative mating, and significant effects of primarily nonparental shared environment on CD. [ABSTRACT FROM AUTHOR]

Illicit substance use is dangerous in both acute and chronic forms, frequently resulting in lethal poisoning, addiction, and other negative consequences. Similar to research in other psychiatric conditions, whose ultimate goal is to enable effective prevention and treatment, studies in substance use are focused on factors elevating the risk for the disorder. The rapid growth of the substance use problem despite the effort invested in fighting it, however, suggests the need in changing the research approach. Instead of attempting to identify risk factors, whose neutralization is often infeasible if not impossible, it may be more promising to systematically reverse the perspective to the factors enhancing the aspect of liability to disorder that shares the same dimension but is opposite to risk, that is, resistance to substance use. Resistance factors, which enable the majority of the population to remain unaffected despite the ubiquity of psychoactive substances, may be more amenable to translation. While the resistance aspect of liability is symmetric to risk, the resistance approach requires substantial changes in sampling (high-resistance rather than high-risk) and using quantitative indices of liability. This article provides an overview and a practical approach to research in resistance to substance use/addiction, currently implemented in a NIH-funded project. The project benefits from unique opportunities afforded by the data originating from two longitudinal twin studies, the Virginia Twin Study of Adolescent and Behavioral Development and the Minnesota Twin Family Study. The methodology described is also applicable to other psychiatric disorders.

The authors sought to decompose the covariance between seven dimensions of religiosity and two internalizing psychiatric disorders (major depression and phobia) and two externalizing substance use disorders (alcohol dependence and nicotine dependence). Significant negative correlations, accounted for by shared additive genetic effects, were found between alcohol dependence and six of the seven religiosity factors. Additive genetic effects accounted for significant negative correlations between nicotine dependence and one religiosity factor, social religiosity, and between phobia and unvengefulness. Common environmental effects accounted for a significant positive correlation between phobia and the factor God as judge. No statistically significant covariance due to genetic or environmental effects was found for major depression and any of the seven religiosity factors. Overall, although several statistically significant bivariate relationships were found, the estimates of covariance due to additive genetic effects were modest.

In recent years there has been a renewed scientific interest in the study of religiosity, including research on genetic and environmental contributions to religiosity. In this article, we investigate genetic and environmental effects on 7 religiosity factors and explore how genetic and environmental effects covary across these factors. Seven religiosity factors estimated from 78 items were examined in a sample of adult male and female twins. The 7 religiosity factors were largely influenced by additive genetic and unique environmental effects, with relatively little influence from common environmental effects. Multivariate genetic analyses found the 7 religiosity factors were influenced by 1 common additive genetic factor, 3 common unique environmental factors, and unique environmental effects specific to each religiosity factor. The results suggest that for the population studied, additive genetic and unique environmental effects largely account for the variance across the religiosity construct.

Background: Longitudinal, genetically informed, prospective data collected on a large population of male twins (n=1037) were used to examine developmental differences in the etiology of antisocial behavior., Method: Analyses were carried out on both mother- and child-reported symptoms of conduct disorder (CD) in 10- to 17-year-old twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and self-reported antisocial behavior by the twins as young adults from the Young Adult Follow-Up (YAFU) study., Results: The following trends were identified: (1) a single genetic factor influencing antisocial behavior beginning at age 10 through young adulthood ('life-course persistent'); (2) a shared-environmental effect beginning in adolescence ('adolescent-onset'); (3) a transient genetic effect at puberty; and (4) a genetic influence specific to adult antisocial behavior., Conclusions: Overall, these etiological findings are consistent with predictions from Moffitt's developmental theory of antisocial behavior. The genetic effect at puberty at ages 12-15 is also consistent with a genetically mediated influence on the timing of puberty affecting the expression of genetic differences in antisocial outcomes.

Background: Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a significant role in the initiation of smoking behavior. Although twin and adoption designs are powerful to detect genetic and environmental influences, they do not provide information on the processes of assortative mating and parent-offspring transmission and their contribution to the variability explained by genetic and/or environmental factors., Methods: We examined the role of genetic and environmental factors for smoking initiation using an extended kinship design. This design allows the simultaneous testing of additive and non-additive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A dichotomous lifetime smoking measure was obtained from twins and relatives in the Virginia 30,000 sample., Results: Results demonstrate that both genetic and environmental factors play a significant role in the liability to smoking initiation. Major influences on individual differences appeared to be additive genetic and unique environmental effects, with smaller contributions from assortative mating, shared sibling environment, twin environment, cultural transmission and resulting genotype-environment covariance. The finding of negative cultural transmission without dominance led us to investigate more closely two possible mechanisms for the lower parent-offspring correlations compared to the sibling and DZ twin correlations in subsets of the data: (i) age x gene interaction, and (ii) social homogamy. Neither mechanism provided a significantly better explanation of the data, although age regression was significant., Conclusions: This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on smoking initiation.

Background: Very little is known about how different sets of risk factors interact to influence risk for psychiatric disorder., Objective: To replicate a recent report of a genotype-environment interaction that predicts risk for antisocial behavior in boys., Design: Characterizing risk for conduct disorder in boys in association with monoamine oxidase A genotype and exposure to familial adversity, defined by interparental violence, parental neglect, and inconsistent discipline., Setting: A community-based sample of twin boys., Participants: Five hundred fourteen male twins aged 8 to 17 years., Main Outcome Measure: Conduct disorder., Results: There was a main effect of adversity but not of monoamine oxidase A on risk for conduct disorder. Low monoamine oxidase A activity increased risk for conduct disorder only in the presence of an adverse childhood environment. Neither a passive nor an evocative genotype-environment correlation accounted for the interaction., Conclusion: This study replicates a recent report of a genotype-environment interaction that predicts individual variation in risk for antisocial behavior in boys.