Daniel Benjamin, Meike Bartels, Philipp Koellinger and colleagues report a genome-wide association meta-analysis of subjective well-being, depressive symptoms and neuroticism. The study leverages a large sample size together with genetic correlations between the phenotypes to identify, with high confidence, loci associated with each phenotype. Very few genetic variants have been associated with depression and neuroticism, likely because of limitations on sample size in previous studies. Subjective well-being, a phenotype that is genetically correlated with both of these traits, has not yet been studied with genome-wide data. We conducted genome-wide association studies of three phenotypes: subjective well-being (n = 298,420), depressive symptoms (n = 161,460), and neuroticism (n = 170,911). We identify 3 variants associated with subjective well-being, 2 variants associated with depressive symptoms, and 11 variants associated with neuroticism, including 2 inversion polymorphisms. The two loci associated with depressive symptoms replicate in an independent depression sample. Joint analyses that exploit the high genetic correlations between the phenotypes (|ρ^| ≈ 0.8) strengthen the overall credibility of the findings and allow us to identify additional variants. Across our phenotypes, loci regulating expression in central nervous system and adrenal or pancreas tissues are strongly enriched for association.

The relative importance of nature and nurture for various forms of expertise has been intensely debated. Music proficiency is viewed as a general model for expertise, and associations between deliberate practice and music proficiency have been interpreted as supporting the prevailing idea that long-term deliberate practice inevitably results in increased music ability. Here, we examined the associations ( rs = .18–.36) between music practice and music ability (rhythm, melody, and pitch discrimination) in 10,500 Swedish twins. We found that music practice was substantially heritable (40%−70%). Associations between music practice and music ability were predominantly genetic, and, contrary to the causal hypothesis, nonshared environmental influences did not contribute. There was no difference in ability within monozygotic twin pairs differing in their amount of practice, so that when genetic predisposition was controlled for, more practice was no longer associated with better music skills. These findings suggest that music practice may not causally influence music ability and that genetic variation among individuals affects both ability and inclination to practice.

Scientific interest in expertise-superior performance within a specific domain-has a long history in psychology. Although there is a broad consensus that a long period of practice is essential for expertise, a long-standing controversy in the field concerns the importance of other variables such as cognitive abilities and genetic factors. According to the influential deliberate practice theory, expert performance is essentially limited by a single variable: the amount of deliberate practice an individual has accumulated. Here, we provide a review of the literature on deliberate practice, expert performance, and its neural correlates. A particular emphasis is on recent studies indicating that expertise is related to numerous traits other than practice as well as genetic factors. We argue that deliberate practice theory is unable to account for major recent findings relating to expertise and expert performance, and propose an alternative multifactorial gene-environment interaction model of expertise, which provides an adequate explanation for the available empirical data and may serve as a useful framework for future empirical and theoretical work on expert performance.

Humans are social animals that experience intense suffering when they perceive a lack of social connection. Modern societies are experiencing an epidemic of loneliness. Although the experience of loneliness is universally human, some people report experiencing greater loneliness than others. Loneliness is more strongly associated with mortality than obesity, emphasizing the need to understand the nature of the relationship between loneliness and health. Although it is intuitive that circumstantial factors such as marital status and age influence loneliness, there is also compelling evidence of a genetic predisposition toward loneliness. To better understand the genetic architecture of loneliness and its relationship with associated outcomes, we extended the genome-wide association study meta-analysis of loneliness to 511 280 subjects, and detect 19 significant genetic variants from 16 loci, including four novel loci, as well as 58 significantly associated genes. We investigated the genetic overlap with a wide range of physical and mental health traits by computing genetic correlations and by building loneliness polygenic scores in an independent sample of 18 498 individuals with EHR data to conduct a PheWAS with. A genetic predisposition toward loneliness was associated with cardiovascular, psychiatric, and metabolic disorders and triglycerides and high-density lipoproteins. Mendelian randomization analyses showed evidence of a causal, increasing, the effect of both BMI and body fat on loneliness. Our results provide a framework for future studies of the genetic basis of loneliness and its relationship to mental and physical health.

Background: Major depression (MD) and anxiety disorders such as panic disorder (PD), agoraphobia (AG), and social phobia (SP) are heritable and highly co‐morbid. However, the relative importance of genetic and environmental etiology of the covariation between these disorders, particularly the relationship between PD and AG, is less clear. Methods: This study measured MD, PD, and AG in a population sample of 5,440 twin pairs and 1,245 single twins, about 45% of whom were also scored for SP. Prevalences, within individual co‐morbidity and twin odds ratios for co‐morbidity, are reported. A behavioral genetic analysis of the four disorders using the classical twin design was conducted. Results: Odds ratios for MD, PD, AG, and SP in twins of individuals diagnosed with one of the four disorders were increased. Heritability estimates under a threshold‐liability model for MD, PD, AG, and SP respectively were .33 (CI: 0.30–0.42), .38 (CI: 0.24–0.55), .48 (CI: 0.37–0.65), and .39 (CI: 0.16–0.65), with no evidence for any variance explained by the common environment shared by twins. We find that a common genetic factor explains a moderate proportion of variance in these four disorders. The genetic correlation between PD and AG was .83. Conclusion: MD, PD, AG, and SP strongly co‐aggregate within families and common genetic factors explain a moderate proportion of variance in these four disorders. The high genetic correlation between PD and AG and the increased odds ratio for PD and AG in siblings of those with AG without PD suggests a common genetic etiology for PD and AG. Depression and Anxiety 26:1004–1011, 2009. Published 2009 Wiley‐Liss, Inc.