Self-control is the ability to control one's impulses when faced with challenges or temptations, and is robustly associated with physiological and psychological well-being. Twin studies show that self-control is heritable, but estimates range between 0% and 90%, making it difficult to draw firm conclusions. The aim of this study was to perform a meta-analysis to provide a quantitative overview of the heritability of self-control. A systematic search resulted in 31 included studies, 17 reporting on individual samples, based on a sample size of >30,000 twins, published between 1997 and 2018. Our results revealed an overall monozygotic twin correlation of 0.58, and an overall dizygotic twin correlation of 0.28, resulting in a heritability estimate of 60%. The heritability of self-control did not vary across gender or age. The heritability did differ across informants, with stronger heritability estimates based on parent report versus self-report or observations. This finding provides evidence that when aiming to understand individual differences in self-control, one should take genetic factors into account. Recommendations for future research are discussed.

This study used a theoretically-derived set of items of the Achenbach System of Empirically Based Assessment to develop the Achenbach Self-Control Scale (ASCS) for 7–16 year olds. Using a large dataset of over 20,000 children, who are enrolled in the Netherlands Twin Register, we demonstrated the psychometric properties of the ASCS for parent-, self- and teacher-report by examining internal and criterion validity, and inter-rater and test–retest reliability. We found associations between the ASCS and measures of well-being, educational achievement, and substance use. Next, we applied the classical twin design to estimate the genetic and environmental contributions to self-control. Genetic influences accounted for 64–75% of the variance in self-control based on parent- and teacher-report (age 7–12), and for 47–49% of the variance in self-control based on self-report (age 12–16), with the remaining variance accounted by non-shared environmental influences. In conclusion, we developed a validated and accessible self-control scale, and show that genetic influences explain a majority of the individual differences in self-control across youth aged 7–16 years.

Whether well-being and depressive symptoms can be considered as two sides of the same coin is widely debated. The aim of this study was to gain insight into the etiology of the association between well-being and depressive symptoms across the lifespan. In a large twin-design, including data from 43,427 twins between age 7 and 99, we estimated the association between well-being and depressive symptoms throughout the lifespan and assessed genetic and environmental contributions to the observed overlap. For both well-being (range 31–47%) and depressive symptoms (range 49–61%), genetic factors explained a substantial part of the phenotypic variance across the lifespan. Phenotypic correlations between well-being and depressive symptoms across ages ranged from −0.34 in childhood to −0.49 in adulthood. In children, genetic effects explained 49% of the phenotypic correlation while in adolescents and young adults, genetic effects explained 60–77% of the phenotypic correlations. Moderate to high genetic correlations (ranging from −0.59 to −0.66) were observed in adolescence and adulthood, while in childhood environmental correlations were substantial but genetic correlations small. Our results suggest that in childhood genetic and environmental effects are about equally important in explaining the relationship between well-being and depressive symptoms. From adolescence onwards, the role of genetic effects increases compared to environmental effects. These results provided more insights into the etiological underpinnings of well-being and depressive symptoms, possibly allowing to articulate better strategies for health promotion and resource allocation in the future.

Theoretical studies propose an association between family violence and low self-control in adolescence; however, empirical findings of this association are inconclusive. The aim of the present research was to systematically summarize available findings on the relation between family violence and self-control across adolescence. We included 28 studies with 143 effect sizes, representing more than 25,000 participants of eight countries from early to late adolescence. Applying a three-level meta-analysis, taking dependency between effect sizes into account while retaining statistical power, we examined the magnitude and direction of the overall effect size. Additionally, we investigated whether theoretical moderators (e.g., age, gender, country), and methodological moderators (e.g., time lag between family violence and self-control, informant) influenced the magnitude of the association between family violence and self-control. Our results revealed that family violence and self-control have a small to moderate significant negative association (r = −0.191). This association did not vary across gender, country, and informants. The strength of the association, however, decreased with age and in longitudinal studies. This finding provides evidence that researchers and clinicians may expect low self-control in the wake of family violence, especially in early adolescence. Recommendations for future research in the area are discussed.

Recent advances in sociogenomics offer new opportunities to integrate genetic and epigenetic measures into social science research on human lifespan development. Now, German social science cohorts have followed suit with this global trend. We anticipate that the integration of genetic measures into German social science cohorts is likely to be met with hesitation and dismay. Historically, racialized pseudo-science disguised as genetic research was used to justify the political exploitation, oppression, and genocide conducted by colonial and Nazi Germany regimes. In response, German institutions and social sciences actively avoided race-related research. However, avoiding the intersection of socially constructed race and genetics may stall the deconstruction of enduring racial discrimination and the identification of racialized social inequalities. Recent survey studies show that half of the German population still believe in the existence of biologically distinct human “races” and that racism is rampant. This article is aimed at providing a biosocial perspective on sociogenomics and racism in Germany. First, we discuss the biologistic construction of race that became prevalent in colonial and Nazi Germany. We argue that racist legacies are sources of social inequality in contemporary German society. We further review recent human genomic science that clearly demonstrates that there is no biological basis to socially constructed race. Second, we propose a biosocial perspective that integrates how genes “get out of the skin” and racism “gets under the skin”. Transactional genetic effects, which involve human behavior and interactions between people in society, are expected to depend on environmental inequalities tied to systemic racism. We summarize recent sociogenomics studies using polygenic indices and epigenetic profile scores showing that a) genes contribute to complex human traits and b) the expression of genetic variation is affected by socioeconomic and racialized inequality. Finally, we offer a roadmap toward race-critical biosocial research that breaks with the historically informed avoidance of race to reconstruct race-critical concepts, datasets, and scientific systems.