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Background: Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a 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 in individual differences for smoking initiation (SI) 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, while also estimating the regression of the prevalence of SI on age. A dichotomous lifetime 'ever' smoking measure was obtained from twins and relatives in the 'Virginia 30,000' sample and the 'Australian 25,000'.Results: Results demonstrate that both genetic and environmental factors play a significant role in the liability to SI. 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. Age regression of the prevalence of SI was significant. 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: (1) age × gene interaction, and (2) social homogamy. Neither of the mechanism provided a significantly better explanation of the data.Conclusions: This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on liability to SI. [ABSTRACT FROM AUTHOR]

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]

This article reports results from the first twin study of adults in the United States that focuses exclusively and comprehensively on political traits. These data allow us to test whether a common set of genetic and environmental influences act upon a broad variety of values, personality traits, and political attitudes. In short, it allows us to empirically investigate whether there are a core set of predispositions that form the basis of our political orientations and, if so, whether these predispositions are shaped by the same environmental and innate forces. The key finding from our analysis is that there are core political predispositions that are rooted in common genetic and environmental influences and that these predispositions are empirically distinct from broader personality traits. [ABSTRACT FROM AUTHOR]

Ideological preferences within the American electorate are contingent on both the environmental conditions that provide the content of the contemporary political debate and internal predispositions that motivate people to hold liberal or conservative policy preferences. In this article we apply Jost, Federico, and Napier's top-down/bottom-up theory of political attitude formation to a genetically informative population sample. In doing so, we further develop the theory by operationalizing the top-down pathway to be a function of the social environment and the bottom-up pathway as a latent set of genetic factors. By merging insights from psychology, behavioral genetics, and political science, we find strong support for the top-down/bottom-up framework that segregates the two independent pathways in the formation of political attitudes and identifies a different pattern of relationships between political attitudes at each level of analysis. [ABSTRACT FROM AUTHOR]

In this article, we explore the effect of public policy on the extent to which genes influence smoking desistance. Using a sample of adult twins (n(mz) = 363, n(dz) = 233) from a large population registry, we estimate Cox proportional hazards models that describe similarity in the timing of smoking desistance among adult twin pairs. We show that identical twin pairs are significantly more likely to quit smoking within a similar time frame compared with fraternal twin pairs. Importantly, we then show that genetic factors for smoking desistance increase in importance following restrictive legislation on smoking behaviors that occurred in the early and mid-1970s. These findings support the social push perspective and make important contributions to the social demography and genetic epidemiology of smoking as well as to the gene-environment interaction literatures. [ABSTRACT FROM AUTHOR]

We examine the hypothesis that environmental transmission is a significant factor in individual differences for Neuroticism among 45,850 members of extended twin kinships from Australia (N = 20,945) and the United States (N = 24,905). To this large data set we fitted a model estimating genetic and environmental components of variance and gene-environmental covariance to examine the causes of individual differences in Neuroticism. For the combined sample we reject models including environmental transmission, shared environment, and a special twin environment in favor of more parsimonious genetic models. The best-fitting model involved only modest assortative mating, nonshared environment, and both additive and nonadditive genetic components. We conclude, first, that there is no evidence for environmental transmission as a contribution to individual differences in Neuroticism in these replicated samples, drawn from different continents, and, second, that a simple genetic structure underlies familial resemblance for the personality trait of Neuroticism. It is interesting that, despite the opportunity provided by the elaborate design and extensive power of our study, the picture revealed for the causes of individual differences in Neuroticism is little more complex than that found from earlier, simpler designs applied to smaller samples. However, this simplicity could not have been confirmed without using a highly informative design and a very large sample. [ABSTRACT FROM AUTHOR]

There has been recent interest in the possibility of dividing bulimia nervosa into two sub- types based on the method of weight prevention utilized by the individual. In an attempt to see if such division is justified, this study, compared 54 purging bulimics with G9 nonpurging bulimics ascertained from a population-based register of Virginia female twins. A bulimic was defined as a ‘purger’ if she engaged in vomiting or laxativee abuse. These two groups were examined on a variety of demographic, weight, and personality measures after controlling for the presence of obesity. No significant differences were found between the two groups on any of the variables examined. [ABSTRACT FROM AUTHOR]

Background:   A critical issue in devising effective interventions for the treatment of children's behavioral and emotional problems identifying genuine family environmental factors that place children at risk. In most twin and family studies, environmental factors are confounded with both direct genetic risk from parents and the indirect effect of genes influencing parents' ability to provide an optimal rearing environment. The present study was undertaken to determine whether parental psychopathology, specifically parental antisocial behavior (ASP), is a genuine environmental risk factor for juvenile conduct disturbance, depression and hyperactivity, or whether the association between parental ASP and children's behavioral and emotional problems can be explained as a secondary consequence of the intergenerational transmission of genetic factors., Methods:   An extended children of twins design comprised of data collected on 2,674 adult female and male twins, their spouses, and 2,454 of their children was used to test whether genetic and/or family environmental factors best accounted for the association between parental antisocial behavior and children's behavioral problems. An age-matched sample of 2,826 juvenile twin pairs from the Virginia Twin Study of Adolescent Behavioral Development was also included to examine developmental differences in gene expression by partitioning child-specific transmissible effects from those effects that persist into adulthood. The fit of alternative models was evaluated using the statistical program Mx., Results:   We found distinct patterns of transmission between parental antisocial behavior and juvenile conduct, depression and hyperactivity. Genetic and family environmental factors accounted for the resemblance between parents' ASP and children's conduct disturbance. Family environmental factors alone explained the association between child depression and parental ASP, and the impact of parental ASP on hyperactivity was entirely genetic., Conclusions:   These findings underscore differences in the contribution of genetic and environmental factors on the patterns of association between parental antisocial behavior and juvenile psychopathology, having important clinical implications for the prevention and amelioration of child behavioral and emotional problems., (© 2011 The Authors. Journal of Child Psychology and Psychiatry © 2011 Association for Child and Adolescent Mental Health.)

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.

Using twins assessed during adolescence (Virginia Twin Study of Adolescent Behavioral Development: 8-17 years) and followed up in early adulthood (Young Adult Follow-Up, 18-27 years), we tested 13 genetically informative models of co-occurrence, adapted for the inclusion of covariates. Models were fit, in Mx, to data at both assessments allowing for a comparison of the mechanisms that underlie the lifetime co-occurrence of cannabis and tobacco use in adolescence and early adulthood. Both cannabis and tobacco use were influenced by additive genetic (38-81%) and non-shared environmental factors with the possible role of non-shared environment in the adolescent assessment only. Causation models, where liability to use cannabis exerted a causal influence on the liability to use tobacco fit the adolescent data best, while the reverse causation model (tobacco causes cannabis) fit the early adult data best. Both causation models (cannabis to tobacco and tobacco to cannabis) and the correlated liabilities model fit data from the adolescent and young adult assessments well. Genetic correlations (0.59-0.74) were moderate. Therefore, the relationship between cannabis and tobacco use is fairly similar during adolescence and early adulthood with reciprocal influences across the two psychoactive substances. However, our study could not exclude the possibility that 'gateways' and 'reverse gateways', particularly within a genetic context, exist, such that predisposition to using one substance (cannabis or tobacco) modifies predisposition to using the other. Given the high addictive potential of nicotine and the ubiquitous nature of cannabis use, this is a public health concern worthy of considerable attention., (Copyright 2009 Elsevier Ireland Ltd. All rights reserved.)

Objective: Millions of adults in the United States travel abruptly across time zones each year. Nevertheless, the impact of traveling over relatively short distances (across 3 or fewer time zones) on diurnal patterning of typical physiological response patterns has yet to be studied in a large, epidemiological sample., Design: The current research focuses on 764 middle-aged men comparing variations in diurnal cortisol regulation based on number of time zones traveled eastward or westward the day before., Main Outcome Measure: Participants provided samples of salivary cortisol at waking, 30-min postwaking, 10 a.m., 3 p.m., and bedtime., Results: Eastward travel was associated with a steeper salivary cortisol awakening response (p < .01) and lower peak (PEAK) levels of salivary cortisol the next morning (p < .05). Westward travel was associated with lower peak levels of cortisol the next morning (p < .05). Effect sizes for these differences ranged from Cohen's d = .29 to .47. Differences were not present for 2 days in their home environment., Conclusions: The results provide evidence that traveling across time zones is associated with diurnal cortisol regulation and should be studied further to understand the subsequent impacts on health and well-being in large national samples., (Copyright 2010 APA, all rights reserved.)

Lummaa et al. (2007) presented historical data collected from twins born in Finland between 1734 and 1888 which suggested that females (N = 31) born as part of an opposite sex (OS) twin pair were 25% less likely to reproduce than female twins (N = 35) born as part of a same sex (SS) pair. They hypothesized that this reduction in fitness was due to masculinization of the female fetus via prenatal effects of the hormones of a male fetus. Because such masculinization would presumably take place in modern populations as well, it would seem important to establish to what degree it does so, and if so, whether reproduction is affected. We therefore address the question of reproduction differences in individual female twins from same-sex (N = 1979) and opposite-sex (N = 913) dizygotic pairs in studies carried out in Australia, the Netherlands, and the United States. In all three samples, there were no differences in the number of children or age of first pregnancies in women from same sex pairs compared to those from opposite sex pairs. Similarly, there were no differences in psychological femininity between women from pairs of the same or opposite sex.