Abstract
We test whether genetic influences that explain individual differences in aggression in early life also explain individual differences across the life-course. In two cohorts from The Netherlands (N = 13,471) and Australia (N = 5628), polygenic scores (PGSs) were computed based on a genome-wide meta-analysis of childhood/adolescence aggression. In a novel analytic approach, we ran a mixed effects model for each age (Netherlands: 12–70 years, Australia: 16–73 years), with observations at the focus age weighted as 1, and decaying weights for ages further away. We call this approach a ‘rolling weights’ model. In The Netherlands, the estimated effect of the PGS was relatively similar from age 12 to age 41, and decreased from age 41–70. In Australia, there was a peak in the effect of the PGS around age 40 years. These results are a first indication from a molecular genetics perspective that genetic influences on aggressive behavior that are expressed in childhood continue to play a role later in life.
Highlights
Aggression is broadly defined as common human behavior that intends to cause harm, by verbal, psychological, and physical means, to others (Baron and Richardson 1994; Anderson and Bushman 2002)
Moffitt (1993) argued that this statistical continuation is driven by a small number of highly aggressive individuals in a population who remain aggressive throughout their lives, the ‘life-course persistent’ individuals
The Ip et al (2021) aggression GWAMA is the largest childhood aggression GWAS to date, but no single genome-wide significant hits were observed. Despite this lack of single significant hits, Ip et al (2021) demonstrated that polygenic scores (PGSs), which sum the effects of a range of genetic markers, with markers included based on whether their p-value from the GWAS clears any of 16 thresholds between P = 1 and P < 1.0E-5, explained between 0.036 and 0.44% of the phenotypic variance in aggression in a hold-out sample of 7 year-old Dutch children (N = 4491)
Summary
Aggression is broadly defined as common human behavior that intends to cause harm, by verbal, psychological, and physical means, to others (Baron and Richardson 1994; Anderson and Bushman 2002). Odintsova and colleagues (2019) published an extensive overview of the current state of genomics aggression research, concluding that clear genome wide significant effects have not yet been found in genetic association studies (GWAS) This is partly attributable to the fact that aggression, like many other complex human behaviors, is influenced by a multitude of individual genetic variants, each of which likely has a small effect. The Ip et al (2021) aggression GWAMA is the largest childhood aggression GWAS to date, but no single genome-wide significant hits were observed Despite this lack of single significant hits, Ip et al (2021) demonstrated that polygenic scores (PGSs), which sum the effects of a range of genetic markers, with markers included based on whether their p-value from the GWAS clears any of 16 thresholds between P = 1 and P < 1.0E-5, explained between 0.036 and 0.44% of the phenotypic variance in aggression in a hold-out sample of 7 year-old Dutch children (N = 4491). Collection of aggression data in adolescent and adult twins, their sibs, spouses and parents (1991–2014) and in young twins and their siblings (2005–2014)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
