Polygenic scores now explain approximately 10% of the variation in educational attainment. However, they capture not only genetic propensity but also information about the family environment. This is because of passive gene–environment correlation, whereby the correlation between offspring and parent genotypes results in an association between offspring genotypes and the rearing environment. We measured passive gene–environment correlation using information on 6,311 adoptees in the UK Biobank. Adoptees’ genotypes were less correlated with their rearing environments because they did not share genes with their adoptive parents. We found that polygenic scores were twice as predictive of years of education in nonadopted individuals compared with adoptees ( R2s = .074 vs. .037, p = 8.23 × 10−24). Individuals in the lowest decile of polygenic scores for education attained significantly more education if they were adopted, possibly because of educationally supportive adoptive environments. Overall, these results suggest that genetic influences on education are mediated via the home environment.
Background: Anxiety in parents is associated with anxiety in offspring, although little is known about the mechanisms underpinning these intergenerational associations. We conducted the first genetically sensitive study to simultaneously examine the effects of mother, father and child anxiety symptoms on each other over time. Method: Adoptive parent and child symptoms were measured at child ages 6, 7 and 8 years from 305 families involved in the Early Growth and Development Study, using a prospective adoption design. Children were adopted at birth to non-relatives and composite data on internalising problems within birth families were used as a proxy measure of offspring inherited risk for anxiety. Structural equation models were fitted to the data to examine prospective associations between adoptive mother, father and child symptoms, whilst accounting for individuals’ symptom stability over time. Results: Child anxiety symptoms at age 7 predicted adoptive mothers’ anxiety symptoms at age 8. No mother-to-child or child-to-father effects were observed. These results were consistent in sensitivity analyses using only paternal offspring reports and using a second measure of child anxiety symptoms. Fathers’ anxiety symptoms at child age 6 prospectively predicted child symptoms, but only when paternal offspring reports were included in the model. Composite data on birth family internalising problems were not associated with child anxiety symptoms. Conclusions: Results show environmentally mediated associations between parent and child anxiety symptoms. Results support developmental theories suggesting that child anxiety symptoms can exert influence on caregivers, and mothers and fathers may play unique roles during the development of child symptoms. Further research is needed on the role of genetic transmission associated with anxiety symptoms in biologically related families. In the meantime, researchers and clinicians should strive to include fathers in assessments and consider the effects of child symptoms on caregivers.
Background Many studies detect associations between parent behaviour and child symptoms of anxiety and depression. Despite knowledge that anxiety and depression are influenced by a complex interplay of genetic and environmental risk factors, most studies do not account for shared familial genetic risk. Quantitative genetic designs provide a means of controlling for shared genetics, but rely on observed putative exposure variables, and require data from highly specific family structures. Methods The intergenerational genomic method, Relatedness Disequilibrium Regression (RDR), indexes environmental effects of parents on child traits using measured genotypes. RDR estimates how much the parent genome influences the child indirectly via the environment, over and above effects of genetic factors acting directly in the child. This ‘genetic nurture’ effect is agnostic to parent phenotype and captures unmeasured heritable parent behaviours. We applied RDR in a sample of 11,598 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) to estimate parental genetic nurture separately from direct child genetic effects on anxiety and depression symptoms at age 8. We tested for mediation of genetic nurture via maternal anxiety and depression symptoms. Results were compared to a complementary non-genomic pedigree model. Results Parental genetic nurture explained 14% of the variance in depression symptoms at age 8. Subsequent analyses suggested that maternal anxiety and depression partially mediated this effect. The genetic nurture effect was mirrored by the finding of family environmental influence in our pedigree model. In contrast, variance in anxiety symptoms was not significantly influenced by common genetic variation in children or parents, despite a moderate pedigree heritability. Conclusions Genomic methods like RDR represent new opportunities for genetically sensitive family research on complex human traits, which until now has been largely confined to adoption, twin and other pedigree designs. Our results are relevant to debates about the role of parents in the development of anxiety and depression in children, and possibly where to intervene to reduce problems.
Individual-level polygenic scores can now explain ~10% of the variation in number of years of completed education. However, associations between polygenic scores and education capture not only genetic propensity but information about the environment that individuals are exposed to. This is because individuals passively inherit effects of parental genotypes, since their parents typically also provide the rearing environment. In other words, the strong correlation between offspring and parent genotypes results in an association between the offspring genotypes and the rearing environment. This is termed passive geneenvironment correlation. We present an approach to test for the extent of passive geneenvironment correlation for education without requiring intergenerational data. Specifically, we use information from 6311 individuals in the UK Biobank who were adopted in childhood to compare genetic influence on education between adoptees and non-adopted individuals.Adoptees' rearing environments are less correlated with their genotypes, because they do not share genes with their adoptive parents. We find that polygenic scores are twice as predictive of years of education in non-adopted individuals compared to adoptees (R 2 = 0.074 vs 0.037, difference test p= 8.23 x 10 -24 ). We provide another kind of evidence for the influence of parental behaviour on offspring education: individuals in the lowest decile of education polygenic score attain significantly more education if they are adopted, possibly due to educationally supportive adoptive environments. Overall, these results suggest that genetic influences on education are mediated via the home environment. As such, polygenic prediction of educational attainment represents gene-environment correlations just as much as it represents direct genetic effects.Cheesman et al.
Background: Many studies detect associations between parent behaviour and child symptoms of anxiety and depression. However, most do not account for shared genetic risk. Quantitative genetic designs provide a means of controlling for shared genes, but rely on observed putative exposure variables, and require data from highly specific family structures. Methods: The intergenerational genomic method, Relatedness Disequilibrium Regression (RDR), indexes environmental effects of parents on child traits using measured genotypes. RDR estimates how much the parent genome influences the child indirectly via the environment, over and above effects of genes acting directly in the child. This "genetic nurture" effect is agnostic to parent phenotype and captures unmeasured heritable parent behaviours. We applied RDR in a sample of 11,598 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) to estimate parental genetic nurture separately from direct child genetic effects on anxiety and depression symptoms at age 8. We also tested for mediation of genetic nurture via maternal emotional symptoms. Results were compared to a complementary non-genomic pedigree model. Results: Parental genetic nurture significantly influenced depression symptoms at age 8, explaining 14% of the phenotypic variance. Subsequent analyses suggested that maternal anxiety and depression partially mediated the parental genetic nurture effect. The genetic nurture effect was mirrored by the finding of shared family environmental influence in our complementary pedigree model. In contrast, variance in anxiety symptoms was not significantly influenced by common genetic variation in children or parents, despite a moderate pedigree heritability. Conclusions: Genomic methods like RDR represent new opportunities for genetically sensitive family research in humans, which until now has been largely confined to adoption, twin and other pedigree designs. Our results are relevant to debates about the role of parents in the development of emotional problems in children, and possibly where to intervene to reduce problems.
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