Genetics of Aggressive Behavior

In many respects, aggression serves as the raw material that drives conduct problems across the life course. Whether assessing difficult temperament in infancy and toddlerhood, self-regulation deficits in childhood, delinquency in adolescence, or criminal violence in adulthood, aggression—defined as a behavior directed toward another person with the intention of doing harm (Anderson & Bushman, 2002)—is the fundamental, elemental construct [Page 188]that is involved. Aggression is an umbrella term that captures diverse forms of harm-causing conduct, such as proactive aggression (instrumental planning to harm), reactive aggression (impulsive, affective reaction to real or perceived threat), direct aggression (overt physical infliction of harm), and indirect aggression (relational aggression involving gossip and social exclusion). This entry focuses on genetics as a factor in aggressive behavior, including heritability and genetic variants.

The first step toward understanding the genetics of aggressive behavior is to assess the heritability of aggression using twin studies. Behavioral genetics research has used twin data to statistically estimate and disaggregate variance in antisocial conditions into three components: genes, shared environmental factors, and nonshared environmental factors. The extent that antisocial conditions are caused by genetic factors is known as heritability and indicated as h2. The extent that antisocial conditions are caused by environmental factors that are common to twins, such as family conditions, is known as shared environment and indicated as c2. The extent that antisocial conditions are caused by environmental factors that are unique to twins such as their peer associations is known as nonshared environment and indicated as e2.

Based on data from diverse samples selected across nations, psychologists have shown that aggression is substantially heritable. In a U.S. sample, Laura A. Baker and colleagues (2007) studied multiple symptom measures of antisocial behavior, including diagnostic counts for conduct disorder and ratings of aggression, delinquency, and psychopathic traits obtained through self-reports, teacher ratings, and caregiver ratings. The broadest composite measure of antisocial behavior spanning all raters was profoundly heritable (h2 = .96). A related study with the same data found that proactive or cold-blooded aggression is also moderately heritable (h2 = .50) compared with reactive or hot-blooded aggression (h2 = .38) (Baker, Raine, Liu, & Jacobson, 2008).

Based on data from the Netherlands Twin Register, Edwin J. C. G. van den Oord, Frank C. Verhulst, and Dooret I. Boomsma (1996) examined the underpinnings of problem behaviors and found heritability estimates were moderate to high across twin pairs. These included total problems (h2 = .38), externalizing problems (h2 = .60), oppositional behavior (h2 = .66), aggressiveness (h2 = .69), and over/hyperactivity (h2 = .65). Based on twin data from the Quebec (Canada) Newborn Twin Study, van Lier and colleagues (2007) reported a similar heritability estimate for aggression (h2 = .66). A 2011 summary review of research and metaanalyses indicated that aggression is 50% heritable (Tuvblad & Baker, 2011).

The moderate-to-high heritability of aggression leads to the next step: finding genetic variants that are associated with it and related antisocial conditions. One of the most studied susceptibility genes for aggressive antisocial behavior generally and temper specifically is the monoamine oxidase A (MAOA) gene. MAOA is a catabolic enzyme that is involved with regulating serotonin, norepinephrine, and dopamine in the synapses. Localized to chromosome Xp11.23, the variable number of tandem repeats polymorphism (MAOA-uVNTR) produces alleles with low activity and high activity. The low-activity allele is the risk allele and reflects MAOA deficiency.

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