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. 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). These results led us to test the hypothesis that genetic variants that are expressed on aggression during childhood and adolescence also are significantly associated with aggression later in the life-course.
Studies with longitudinal twin designs show that genetic factors contribute significantly to the stability of aggression during preschool age, school age, and puberty (van Bijsterveldt et al. Although individuals retain their genetic make-up throughout their lives, this does not necessarily imply that the same genetic variants play a role in aggression across the life-course. Across the lifespan, heritability estimates of aggression and antisocial behavior seem to increase somewhat from childhood through adulthood, as the importance of shared environmental effects decreases (Tuvblad and Baker 2011 Waltes et al. Twin and family studies, mostly focusing on children, indicate that genetic factors explain around 50% of the variation in aggression (Veroude et al. Several factors have been identified that help explain individual differences in continuity of aggression, such as parenting, peers, socioeconomic and cultural context, mental processes and genetic predisposition (Boomsma 2015 Farrington 1989 Labella and Masten 2018 Murray and Farrington 2010 Tolan et al. ( 2009) showed that most individuals retain their relative position in a population, regardless of their starting position. Although it is clear that the ‘life-course persistent’ individuals explain part of the stability in aggression, Huesmann et al. The rest, she argues, are the ‘adolescent limited’ type, for whom aggressive behavior is limited to adolescence. 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. There has been some debate about the continuation of individual differences in aggression from childhood to adulthood. In other words, the most aggressive child often grows up to be the most aggressive adult (Farrington 1989). rank order) in the population persist across the life-course (Pulkkinen and Pitkänen 1993 Tuvblad and Baker 2011). The relative positions in terms of aggression (i.e. Social or relational aggression emerges in the preschool years, continues through childhood and adolescence and subsequently declines in adulthood (e.g. 2008 Loeber and Stouthamer-Loeber 1998 Tremblay et al 2004 Tremblay 2010), as neurological, cognitive and social development empower children with other means to get what they want. 1989 Cairns and Cairns 1994 Karriker-Jaffe et al.
Physical aggression tends to peak at age 2–4 years and then decreases (Alink et al. 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.Īggression 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). In Australia, there was a peak in the effect of the PGS around age 40 years. In The Netherlands, the estimated effect of the PGS was relatively similar from age 12 to age 41, and decreased from age 41–70. We call this approach a ‘rolling weights’ model. 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. 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. We test whether genetic influences that explain individual differences in aggression in early life also explain individual differences across the life-course.
0 kommentar(er)
