The association between saving disposition and financial distress: A genetically informed approach.

Saving disposition, the tendency to save rather than consume, has been found to be associated with economic outcomes. People lacking the disposition to save are more likely to experience financial distress. This association could be driven by other economic factors, behavioral traits, or even genetic effects. Using a sample of 3,920 American twins, we develop scales to measure saving disposition and financial distress. We find genetic influences on both traits, but also a large effect of the rearing family environment on saving disposition. We estimate that 44% of the covariance between the two traits is due to genetic effects. Saving disposition remains strongly associated with lower financial distress, even after controlling for family income, cognitive ability, and personality traits. The association persists within families and monozygotic twin pairs; the twin who saves more tends to be the twin who experiences less financial distress. This result suggest that there is a direct association between saving disposition and financial distress, although the direction of causation remains unclear.

A Century of Behavioral Genetics at the University of Minnesota.

The University of Minnesota has played an important role in the resurgence and eventual mainstreaming of human behavioral genetics in psychology and psychiatry. We describe this history in the context of three major movements in behavioral genetics: (1) radical eugenics in the early 20th century, (2) resurgence of human behavioral genetics in the 1960s, largely using twin and adoption designs to obtain more precise estimates of genetic and environmental influences on individual differences in behavior; and (3) use of measured genotypes to understand behavior. University of Minnesota scientists made significant contributions especially in (2) and (3) in the domains of cognitive ability, drug abuse and mental health, and endophenotypes. These contributions are illustrated through a historical perspective of major figures and events in behavioral genetics.

Parent Contributions to the Development of Political Attitudes in Adoptive and Biological Families.

Where do our political attitudes originate? Although early research attributed the formation of such beliefs to parent and peer socialization, genetically sensitive designs later clarified the substantial role of genes in the development of sociopolitical attitudes. However, it has remained unclear whether parental influence on offspring attitudes persists beyond adolescence. In a unique sample of 394 adoptive and biological families with offspring more than 30 years old, biometric modeling revealed significant evidence for genetic and nongenetic transmission from both parents for the majority of seven political-attitude phenotypes. We found the largest genetic effects for religiousness and social liberalism, whereas the largest influence of parental environment was seen for political orientation and egalitarianism. Together, these findings indicate that genes, environment, and the gene-environment correlation all contribute significantly to sociopolitical attitudes held in adulthood, and the etiology and development of those attitudes may be more important than ever in today's rapidly changing sociopolitical landscape.

Genetic and neural bases of the neuroticism general factor.

We applied structural equation modeling to conduct a genome-wide association study (GWAS) of the general factor measured by a neuroticism questionnaire administered to ∼380,000 participants in the UK Biobank. We categorized significant genetic variants as acting either through the neuroticism general factor, through other factors measured by the questionnaire, or through paths independent of any factor. Regardless of this categorization, however, significant variants tended to show concordant associations with all items. Bioinformatic analysis showed that the variants associated with the neuroticism general factor disproportionately lie near or within genes expressed in the brain. Enriched gene sets pointed to an underlying biological basis associated with brain development, synaptic function, and behaviors in mice indicative of fear and anxiety. Psychologists have long asked whether psychometric common factors are merely a convenient summary of correlated variables or reflect coherent causal entities with a partial biological basis, and our results provide some support for the latter interpretation. Further research is needed to determine the extent to which causes resembling common factors operate alongside other mechanisms to generate the correlational structure of personality.

Educational attainment, health outcomes and mortality: a within-sibship Mendelian randomization study.

BACKGROUND: Previous Mendelian randomization (MR) studies using population samples (population MR) have provided evidence for beneficial effects of educational attainment on health outcomes in adulthood. However, estimates from these studies may have been susceptible to bias from population stratification, assortative mating and indirect genetic effects due to unadjusted parental genotypes. MR using genetic association estimates derived from within-sibship models (within-sibship MR) can avoid these potential biases because genetic differences between siblings are due to random segregation at meiosis. METHODS: Applying both population and within-sibship MR, we estimated the effects of genetic liability to educational attainment on body mass index (BMI), cigarette smoking, systolic blood pressure (SBP) and all-cause mortality. MR analyses used individual-level data on 72 932 siblings from UK Biobank and the Norwegian HUNT study, and summary-level data from a within-sibship Genome-wide Association Study including >140 000 individuals. RESULTS: Both population and within-sibship MR estimates provided evidence that educational attainment decreased BMI, cigarette smoking and SBP. Genetic variant-outcome associations attenuated in the within-sibship model, but genetic variant-educational attainment associations also attenuated to a similar extent. Thus, within-sibship and population MR estimates were largely consistent. The within-sibship MR estimate of education on mortality was imprecise but consistent with a putative effect. CONCLUSIONS: These results provide evidence of beneficial individual-level effects of education (or liability to education) on adulthood health, independently of potential demographic and family-level confounders.

Within-sibship genome-wide association analyses decrease bias in estimates of direct genetic effects.

Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes. Within-sibship GWAS estimates were smaller than population estimates for height, educational attainment, age at first birth, number of children, cognitive ability, depressive symptoms and smoking. Some differences were observed in downstream SNP heritability, genetic correlations and Mendelian randomization analyses. For example, the within-sibship genetic correlation between educational attainment and body mass index attenuated towards zero. In contrast, analyses of most molecular phenotypes (for example, low-density lipoprotein-cholesterol) were generally consistent. We also found within-sibship evidence of polygenic adaptation on taller height. Here, we illustrate the importance of family-based GWAS data for phenotypes influenced by demographic and indirect genetic effects.

Examining the association between family status and depression in the UK Biobank.

BACKGROUND: We examined associations between family status (living with a spouse or partner and number of children) and lifetime depression. METHODS: We used data from the UK Biobank, a large prospective study of middle-aged and older adults. Lifetime depression was assessed as part of a follow-up mental health questionnaire. Logistic regression was used to estimate associations between family status and depression. We included extensive adjustment for social, demographic and other potential confounders, including depression polygenic risk scores. RESULTS: 52,078 participants (mean age = 63.6, SD = 7.6; 52% female) were included in our analyses. Living with a spouse or partner was associated with substantially lower odds of lifetime depression (OR = 0.67, 95% CI 0.62-0.74). Compared to individuals without children, we found higher odds of lifetime depression for parents of one child (OR = 1.17, 95% CI 1.07-1.27) and parents of three (OR = 1.11, 95% CI 1.03-1.20) or four or more children (OR = 1.27, 95% CI 1.14-1.42). Amongst those not cohabiting, having any number of children was associated with higher odds of lifetime depression. Our results were consistent across age groups, the sexes, neighbourhood deprivation and genetic risk for depression. Exploratory Mendelian randomisation analyses suggested a causal effect of number of children on lifetime depression. LIMITATIONS: Our data did not allow distinguishing between non-marital and marital cohabitation. Results may not generalise to all ages or populations. CONCLUSIONS: Living with a spouse or partner was strongly associated with reduced odds of depression. Having one or three or more children was associated with increased odds of depression, especially in individuals not living with a spouse or partner.