Meta-analysis of genome-wide association studies for extraversion:Findings from the Genetics of Personality Consortium

Extraversion is a relatively stable and heritable personality trait associated with numerous psychosocial, lifestyle and health outcomes. Despite its substantial heritability, no genetic variants have been detected in previous genome-wide association (GWA) studies, which may be due to relatively small sample sizes of those studies. Here, we report on a large meta-analysis of GWA studies for extraversion in 63,030 subjects in 29 cohorts. Extraversion item data from multiple personality inventories were harmonized across inventories and cohorts. No genome-wide significant associations were found at the single nucleotide polymorphism (SNP) level but there was one significant hit at the gene level for a long non-coding RNA site (LOC101928162). Genome-wide complex trait analysis in two large cohorts showed that the additive variance explained by common SNPs was not significantly different from zero, but polygenic risk scores, weighted using linkage information, significantly predicted extraversion scores in an independent cohort. These results show that extraversion is a highly polygenic personality trait, with an architecture possibly different from other complex human traits, including other personality traits. Future studies are required to further determine which genetic variants, by what modes of gene action, constitute the heritable nature of extraversion

Co-occurrence of depressive moods and delinquency in early adolescence: The role of failure expectations, manipulativeness and social contexts

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Sexual orientation and psychiatric vulnerability: A twin study of neuroticism and psychoticism

Recent evidence indicates that homosexuals and bisexuals are, on average, at greater risk for psychiatric problems than heterosexuals. It is assumed with some supporting evidence that prejudice often experienced by nonheterosexuals makes them more vulnerable to psychiatric disorder, but there has been no investigation of alternative explanations. Here we used Eysenck's Neuroticism and Psychoticism scales as markers for psychiatric vulnerability and compared heterosexuals with nonheterosexuals in a community-based sample of identical and nonidentical twins aged between 19 and 52 years (N = 4904). Firstly, we tested whether apparent sexual orientation differences in psychiatric vulnerability simply mirrored sex differences-for our traits, this would predict nonheterosexual males having elevated Neuroticism scores as females do, and nonheterosexual females having elevated Psychoticism scores as males do. Our results contradicted this idea, with nonheterosexual men and women scoring significantly higher on Neuroticism and Psychoticism than their heterosexual counterparts, suggesting an overall elevation of psychiatric risk in nonheterosexuals. Secondly, we used our genetically informative sample to assess the viability of explanations invoking a common cause of both nonheterosexuality and psychiatric vulnerability. We found significant genetic correlation between sexual orientation and both Neuroticism and Psychoticism, but no corresponding environmental correlations, suggesting that if there is a common cause of both nonheterosexuality and psychiatric vulnerability it is likely to have a genetic basis rather than an environmental basis

Stability of Genetic and Environmental Contributions to Anxiety Symptoms in Older Adulthood

Anxiety symptoms are common in later life and are associated with diverse adverse health outcomes. Little is known about how genetic and environmental influences on anxiety symptoms might vary across older adulthood. The purpose of this study was to explore change and stability of contributions to anxiety symptoms across older adulthood. We examined data from the Swedish Adoption/Twin Study of Aging (SATSA). Between the years 1984 and 2010, 2,021 participants (including 753 complete twin pairs) completed up to seven assessments containing two measures of anxiety symptoms. Longitudinal genetic simplex models were fit to examine the stability and change in genetic and environmental influences. Amplification of genetic factors at ages 75–80 suggests tentative new genetic contributions to anxiety symptoms. These findings suggest that the heritability of anxiety symptoms may increase later in life. Physiological factors associated with aging are discussed as potential factors explaining this increase