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Introduction: Previous studies in adolescents were not adequately powered to accurately disentangle genetic and environmental influences on smoking initiation (SI) across adolescence.Methods: Mega-analysis of pooled genetically informative data on SI was performed, with structural equation modeling, to test equality of prevalence and correlations across cultural backgrounds, and to estimate the significance and effect size of genetic and environmental effects according to the classical twin study, in adolescent male and female twins from same-sex and opposite-sex twin pairs (N = 19 313 pairs) between ages 10 and 19, with 76 358 longitudinal assessments between 1983 and 2007, from 11 population-based twin samples from the United States, Europe, and Australia.Results: Although prevalences differed between samples, twin correlations did not, suggesting similar etiology of SI across developed countries. The estimate of additive genetic contributions to liability of SI increased from approximately 15% to 45% from ages 13 to 19. Correspondingly, shared environmental factors accounted for a substantial proportion of variance in liability to SI at age 13 (70%) and gradually less by age 19 (40%).Conclusions: Both additive genetic and shared environmental factors significantly contribute to variance in SI throughout adolescence. The present study, the largest genetic epidemiological study on SI to date, found consistent results across 11 studies for the etiology of SI. Environmental factors, especially those shared by siblings in a family, primarily influence SI variance in early adolescence, while an increasing role of genetic factors is seen at later ages, which has important implications for prevention strategies.Implications: This is the first study to find evidence of genetic factors in liability to SI at ages as young as 12. It also shows the strongest evidence to date for decay of effects of the shared environment from early adolescence to young adulthood. We found remarkable consistency of twin correlations across studies reflecting similar etiology of liability to initiate smoking across different cultures and time periods. Thus familial factors strongly contribute to individual differences in who starts to smoke with a gradual increase in the impact of genetic factors and a corresponding decrease in that of the shared environment. [ABSTRACT FROM AUTHOR]

Symptoms of anxiety and depression are relatively stable over time. Can this stability be explained by genetic influences, or is it caused by the long-lasting effects of accumulating environmental experiences? To address this question, we analyzed longitudinally assessed symptoms of anxiety and depression in eight samples of monozygotic twins of widely varying ages. These samples were drawn from American and European population-based registries. Using hierarchical linear modeling, we examined individual differences and individual changes in the level of symptoms over time. This method enabled us to decompose the variance into the predictable variance shared by both members of each pair of twins, the differences between individuals within pairs, and the residual variance. We then modeled how these components of individual variation changed over time. Within pairs, the twins' predicted levels of symptoms increasingly diverged from childhood until late adulthood, at which point the divergence ceased. By middle adulthood, environmental experiences contributed substantially to stable and predictable interindividual differences in levels of anxiety and depression.