It runs in the family: A genetically informative study of individual differences in aggression

The goal of the research described in this dissertation was to investigate the importance of family factors in explaining individual differences in levels of aggression, in explaining whether individuals conform or desist from the overall downward trend we see in aggression over time and across the life-course, and in explaining the continuity of relative aggression levels across the life-course and across generations. Most of the work described in this dissertation is based on data that was collected by the Netherlands Twin Registry (NTR) from 1991 onwards. In total, 360,801 aggression observations of 83,027 individuals from 33,653 families were used in the analyses. Observations came from multiple raters, i.e. teachers, parents and self-reports, and multiple instruments, the majority of which ASEBA questionnaires. Aggression runs in the family. This implies that risk factors for aggression reside in families. From 1991 to 2015, aggression levels slightly declined in our sample. However, not all individuals follow this overall observed trend. In a novel mixed effects approach, we showed that not only the propensity for aggression, but also changes over time cluster within families. Aggression not only decreases over time, but also across the life-course. However, there is some relative stability: the most aggressive children are likely to become the most aggressive adults. In a novel 'rolling weights' approach, we show that genetic influences in childhood, measured with a polygenic score, continue to affect aggression until around age 40. These results were found in the Dutch NTR sample, but did not replicate in an Australian sample. The results in the Dutch cohort are the first indication from a molecular genetic perspective that genes drive part of the stability in aggression across the life-course. The fact that parents and offspring are similar in their propensity for aggression can have two causes: genetic transmission or cultural transmission. Genetic transmission occurs through the inheritance of genes from parents, while cultural transmission occurs through the process of passing on knowledge, norms, and values. We showed with a twin study that the shared environment, which leads to similarities in outcomes in families, only explains a negligible amount of variance in rule-breaking behaviour. Genetic effects explained 60 percent of the variance in rule-breaking behaviour. Because cultural transmission is part of the shared environment, we concluded that the main drivers of intergenerational continuity of aggression are genetic influences. These findings were supported by a following study of direct and indirect polygenic effects on aggression. Direct polygenic effects reflect a direct effect of a genotype on aggression. If there are genotype-environment correlation mechanisms, however, genetic influences may in part reflect environmental influences. Such indirect genetic effects may arise, for example, by environmental manifestations of parental and sibling genotypes. We found no evidence for contributions of such indirect genetic effects on aggression. Polygenic scores of early-life aggression, educational attainment, and ADHD, solely had direct genetic effects, both in a within-/ between-family design and in a transmitted/non-transmitted PGSs design. The studies bundled in this dissertation show that familial clustering of aggression is mainly driven by genetic factors. Additionally, we show that family factors, most notably genetic factors, drive changes in aggression over time and across the life-course. These results do not mean that the environment is not important. The environment does not contribute significantly to similarities within families, but it does contribute significantly to observed differences.