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The assumption in the personality and politics literature is that a person's personality motivates them to develop certain political attitudes later in life. This assumption is founded on the simple correlation between the two constructs and the observation that personality traits are genetically influenced and develop in infancy, whereas political preferences develop later in life. Work in psychology, behavioral genetics, and recently political science, however, has demonstrated that political preferences also develop in childhood and are equally influenced by genetic factors. These findings cast doubt on the assumed causal relationship between personality and politics. Here we test the causal relationship between personality traits and political attitudes using a direction of causation structural model on a genetically informative sample. The results suggest that personality traits do not cause people to develop political attitudes; rather, the correlation between the two is a function of an innate common underlying genetic factor. [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]

The assumption that the transmission of social behaviors and political preferences is purely cultural has been challenged repeatedly over the last 40 years by the combined evidence of large studies of adult twins and their relatives, adoption studies, and twins reared apart. Variance components and path modeling analyses using data from extended families quantified the overall genetic influence on political attitudes, but few studies have attempted to localize the parts of the genome which accounted for the heritability estimates found for political preferences. Here, we present the first genome-wide analysis of Conservative-Liberal attitudes from a sample of 13,000 respondents whose DNA was collected in conjunction with a 50-item sociopolitical attitude questionnaire. Several significant linkage peaks were identified and potential candidate genes discussed. [ABSTRACT FROM PUBLISHER]

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]

The classical twin design uses data on the variation of and covariation between monozygotic and dizygotic twins to infer underlying genetic and environmental causes of phenotypic variation in the population. By using data from additional relative classes, such as parents, extended twin family designs more comprehensively describe the causes of phenotypic variation. This article introduces an extension of previous extended twin family models, the Cascade model, which uses information on twins as well as their siblings, spouses, parents, and children to differentiate two genetic and six environmental sources of phenotypic variation. The Cascade also relaxes assumptions regarding mating and cultural transmission that existed in previous extended twin family designs. The estimation of additional parameters and relaxation of assumptions is potentially important, not only because it allows more fine-grained descriptions of the causes of phenotypic variation, but more importantly, because it can reduce the biases in parameter estimates that exist in earlier designs. [ABSTRACT FROM AUTHOR]

The authors seek to determine whether the clinical characteristics of generalized anxiety disorder (GAD) differ in individuals with a high vs. low familial vulnerability to illness. We identified 486 personally interviewed female twins front a population-based register who had both an interviewed co-twin and a lifetime history of GAD using modified DSM-III-R criteria which required a one-month minimum duration of illness. We attempted to predict risk for GAD in the co-twin from the clinical features of the GAD in the prohand twin using the Cox proportional hazard model, controlling for year of birth and zygosity. Only two variables uniquely predicted an increased risk for GAD in the co-twin: number of GAD symptoms endorsed and comorbidity with bulimia. Variables that did not uniquely predict risk of illness in the co-twin included age at onset, duration of the longest episode and number of episodes. The familial vulnerability to GAD can be meaningfully indexed by clinical features of the syndrome. These results suggest that if the syndrome of GAD is to be narrowed, it would, from a familial perspective, be more valid to increase the minimum number of required symptoms rather than to increase the minimum duration of illness. [ABSTRACT FROM AUTHOR]