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Purpose: To investigate the association between social isolation and loneliness, how they relate to depression, and whether these associations are explained by genetic influences.Methods: We used data from the age-18 wave of the Environmental Risk Longitudinal Twin Study, a birth cohort of 1116 same-sex twin pairs born in England and Wales in 1994 and 1995. Participants reported on their levels of social isolation, loneliness and depressive symptoms. We conducted regression analyses to test the differential associations of isolation and loneliness with depression. Using the twin study design, we estimated the proportion of variance in each construct and their covariance that was accounted for by genetic and environmental factors.Results: Social isolation and loneliness were moderately correlated (r = 0.39), reflecting the separateness of these constructs, and both were associated with depression. When entered simultaneously in a regression analysis, loneliness was more robustly associated with depression. We observed similar degrees of genetic influence on social isolation (40 %) and loneliness (38 %), and a smaller genetic influence on depressive symptoms (29 %), with the remaining variance accounted for by the non-shared environment. Genetic correlations of 0.65 between isolation and loneliness and 0.63 between loneliness and depression indicated a strong role of genetic influences in the co-occurrence of these phenotypes.Conclusions: Socially isolated young adults do not necessarily experience loneliness. However, those who are lonely are often depressed, partly because the same genes influence loneliness and depression. Interventions should not only aim at increasing social connections but also focus on subjective feelings of loneliness. [ABSTRACT FROM AUTHOR]

Background: Studies assessing sex differences in the associations of psychosocial strain with depression have shown mixed and inconsistent results. Our objective was to examine prospective associations of job strain and family strain with risk of major depressive episode (MDE) among United States workers, as well as assess potential effect modification by sex.Methods: Using data from the nationally representative and population-based Mid-life in the United States (MIDUS) study with a prospective cohort design and a 9-year follow-up period, the effects of job strain and family strain at baseline on risk of MDE within the 12 months prior to the follow-up assessment were examined in 1581 workers (805 men, 776 women) who were free from MDE within the 12 months prior to the baseline survey, by multivariate Poisson regression analysis.Results: After adjustment for relevant covariates, there was evidence for effect modification by sex for the association between job strain and MDE but not for the association between family strain and MDE. Indeed, high job strain was prospectively associated with the risk of MDE (RR and 95% CI = 2.14 [1.14, 4.03]) in men but not in women. Moreover, high family strain was prospectively associated with a higher risk of MDE (RR and 95% CI = 1.57 [1.05, 2.37]) in the whole sample.Conclusion: Family strain was associated with risk of MDE regardless of the sex of a person. In contrast, high job strain may involve an increased risk of developing MDE only in men but not in women. [ABSTRACT FROM AUTHOR]

This study tested implications of new genetic discoveries for understanding the association between parental investment and children's educational attainment. A novel design matched genetic data from 860 British mothers and their children with home-visit measures of parenting: the E-Risk Study. Three findings emerged. First, both mothers' and children's education-associated genetics, summarized in a genome-wide polygenic score, were associated with parenting-a gene-environment correlation. Second, accounting for genetic influences slightly reduced associations between parenting and children's attainment-indicating some genetic confounding. Third, mothers' genetics were associated with children's attainment over and above children's own genetics, via cognitively stimulating parenting-an environmentally mediated effect. Findings imply that, when interpreting parents' effects on children, environmentalists must consider genetic transmission, but geneticists must also consider environmental transmission. [ABSTRACT FROM AUTHOR]

Objective: Borderline personality disorder in adolescence remains a controversial construct. We addressed concerns about the prognostic significance of adolescent borderline pathology by testing whether borderline symptoms at age 12 years predict functioning during the transition to adulthood, at age 18 years, in areas critical to life-course development.Method: We studied members of the Environmental Risk (E-Risk) Longitudinal Twin Study, which tracks the development of a birth cohort of 2,232 British twin children. At age 12, study members' borderline symptoms were measured using mothers' reports. At age 18, study members' personality, psychopathology, functional outcomes, and experiences of victimization were measured using self-reports, coinformant reports, and official records.Results: At age 18, study members who had more borderline symptoms at age 12 were more likely to have difficult personalities, to struggle with poor mental health, to experience poor functional outcomes, and to have become victims of violence. Reports of poor outcomes were corroborated by coinformants and official records. Borderline symptoms in study members at 12 years old predicted poor outcomes over and above other behavioral and emotional problems during adolescence. Twin analyses showed that borderline symptoms in 12-year-olds were influenced by familial risk, particularly genetic risk, which accounted for associations with most poor outcomes at age 18.Conclusion: Borderline symptoms in 12-year-olds signal risk for pervasive poor functioning during the transition to adulthood. This association is driven by genetic influences, suggesting that borderline symptoms and poor outcomes are manifestations of shared genetic risk. [ABSTRACT FROM AUTHOR]