Sensation seeking and impulsive traits as personality endophenotypes for antisocial behavior: Evidence from two independent samples

Abstract

Sensation seeking and impulsivity are personality traits that are correlated with risk for antisocial behavior (ASB). This paper uses two independent samples of twins to (a) test the extent to which sensation seeking and impulsivity statistically mediate genetic influence on ASB, and (b) compare this to genetic influences accounted for by other personality traits. In Sample 1, delinquent behavior, as well as impulsivity, sensation seeking and Big Five personality traits, were measured in adolescent twins from the Texas Twin Project. In Sample 2, adult twins from the Australian Twin Registry responded to questionnaires that assessed individual differences in Eysenck's and Cloninger's personality dimensions, and a structured telephone interview that asked participants to retrospectively report DSM-defined symptoms of conduct disorder. Bivariate quantitative genetic models were used to identify genetic overlap between personality traits and ASB. Across both samples, novelty/sensation seeking and impulsive traits accounted for larger portions of genetic variance in ASB than other personality traits. We discuss whether sensation seeking and impulsive personality are causal endophenotypes for ASB, or merely index genetic liability for ASB.

Keywords: Antisocial behavior; Endophenotype; Impulsivity; Novelty seeking; Sensation seeking.

Fig. 1

A secondary phenotype (e.g. ASB) is regressed on the latent genetic and environmental components of a primary phenotype (e.g. personality trait). Path diagram is shown for one twin only.

Fig. 2

Latent genetic and environmental overlap between personality & antisocial behavior. Notes. Portions of variance calculated from parameter estimates reported in Table 2. In the Texas sample results control for the linear and quadratic effects of age, sex, age × sex interaction and race. In the Australia sample, results are reported separately for females and males controlling for the sex-specific linear and quadratic effects of age. Asterisks (*) mark estimates of additive genetic overlap that are significantly different from zero at p < 0.01. Addition signs (+) mark estimates of additive genetic overlap that are marginally significant from zero at p < 0.10.