Genetic similarity between relatives provides evidence on the presence and history of assortative mating.

Assortative mating - the non-random mating of individuals with similar traits - is known to increase trait-specific genetic variance and genetic similarity between relatives. However, empirical evidence is limited for many traits, and the implications hinge on whether assortative mating has started recently or many generations ago. Here we show theoretically and empirically that genetic similarity between relatives can provide evidence on the presence and history of assortative mating. First, we employed path analysis to understand how assortative mating affects genetic similarity between family members across generations, finding that similarity between distant relatives is more affected than close relatives. Next, we correlated polygenic indices of 47,135 co-parents from the Norwegian Mother, Father, and Child Cohort Study (MoBa) and found genetic evidence of assortative mating in nine out of sixteen examined traits. The same traits showed elevated similarity between relatives, especially distant relatives. Six of the nine traits, including educational attainment, showed greater genetic variance among offspring, which is inconsistent with stable assortative mating over many generations. These results suggest an ongoing increase in familial similarity for these traits. The implications of this research extend to genetic methodology and the understanding of social and economic disparities.

Intergenerational transmission of ADHD behaviors: genetic and environmental pathways.

BACKGROUND: We investigate if covariation between parental and child attention-deficit hyperactivity disorder (ADHD) behaviors can be explained by environmental and/or genetic transmission. METHODS: We employed a large children-of-twins-and-siblings sample (N = 22 276 parents and 11 566 8-year-old children) of the Norwegian Mother, Father and Child Cohort Study. This enabled us to disentangle intergenerational influences via parental genes and parental behaviors (i.e. genetic and environmental transmission, respectively). Fathers reported on their own symptoms and mothers on their own and their child's symptoms. RESULTS: Child ADHD behaviors correlated with their mother's (0.24) and father's (0.10) ADHD behaviors. These correlations were largely due to additive genetic transmission. Variation in children's ADHD behaviors was explained by genetic factors active in both generations (11%) and genetic factors specific to the children (46%), giving a total heritability of 57%. There were small effects of parental ADHD behaviors (2% environmental transmission) and gene-environment correlation (3%). The remaining variability in ADHD behaviors was due to individual-specific environmental factors. CONCLUSIONS: The intergenerational resemblance of ADHD behaviors is primarily due to genetic transmission, with little evidence for parental ADHD behaviors causing children's ADHD behaviors. This contradicts theories proposing environmental explanations of intergenerational transmission of ADHD, such as parenting theories or psychological life-history theory.

The ADHD deficit in school performance across sex and parental education: A prospective sibling-comparison register study of 344,152 Norwegian adolescents.

Background: Attention-Deficit Hyperactivity Disorder (ADHD) is associated with impaired school performance, but the impact of ADHD may vary across sex, family background, and school subjects. By using prospective population-wide register data, we describe impairment in academic performance related to ADHD across different school subjects and investigate how this impairment differ across sex and parental education. Methods: We examined grades and Grade Point Averages (GPA) at age ∼16 among 344,152 Norwegian children born between 1997 and 2002. We linked grades with diagnoses from publicly funded general practitioners and with demographic information. Associations between ADHD diagnosed between age 10 and 16 and school performance were estimated with linear models, including sibling-models which control for unobserved variables shared within families. Results: Children with ADHD (4.0%) had -1.11 standard deviations lower GPAs compared to children without ADHD. This difference remained substantial after adjusting for demographic factors (-0.87), comorbid mental disorders (-0.82), early school performance (-0.54), and when comparing full siblings (-0.60). The relative ADHD deficit was 22% larger for girls than for boys and 39% larger for children with highly educated parents than for children of parents without completed high school, but the absolute deficit was smaller. Conclusion: The ADHD deficit in school performance was large and not easily attributable to other factors. Because the ADHD deficit was large in all school subjects, interventions should ideally address factors that affect school performance broadly, although targeting theoretical subjects specifically may be most effective given limited resources.