Development and Psychopathology

Regular Articles

Resting heart rate and the development of antisocial behavior from age 9 to 14: Genetic and environmental influences

Laura A. Bakera1 c1, Catherine Tuvblada1, Chandra Reynoldsa2, Mo Zhenga1, Dora Isabel Lozanoa3 and Adrian Rainea4

a1 University of Southern California

a2 University of California, Riverside

a3 Universidad Autónoma de Ciudad Juárez, Mexico

a4 University of Pennsylvania


The genetic and environmental basis of a well-replicated association between antisocial behavior (ASB) and resting heart rate was investigated in a longitudinal twin study, based on two measurements between the ages of 9 and 14 years. ASB was defined as a broad continuum of externalizing behavior problems, assessed at each occasion through a composite measure based on parent ratings of trait aggression, delinquent behaviors, and psychopathic traits in their children. Parent ratings of ASB significantly decreased across age from childhood to early adolescence, although latent growth models indicated significant variation and twin similarity in the growth patterns, which were explained almost entirely by genetic influences. Resting heart rate at age 9–10 years old was inversely related to levels of ASB but not change patterns of ASB across age or occasions. Biometrical analyses indicated significant genetic influences on heart rate during childhood, as well as ASB throughout development from age 9 to 14. Both level and slope variation were significantly influenced by genetic factors. Of importance, the low resting heart rate and ASB association was significantly and entirely explained by their genetic covariation, although the heritable component of heart rate explained only a small portion (1–4%) of the substantial genetic variance in ASB. Although the effect size is small, children with low resting heart rate appear to be genetically predisposed toward externalizing behavior problems as early as age 9 years old.


c1 Address correspondence and reprint requests to: Laura A. Baker, Department of Psychology (SGM 501), University of Southern California, 3620 South McClintock Avenue, Los Angeles, CA 90089-1061; E-mail:


This study was funded by the NIMH (R01 MH58354). Catherine Tuvblad was supported by postdoctoral stipends from the Swedish Council for Working Life and Social Research (Project 2006-1501) and the Sweden–America Foundation. Adrian Raine was supported by the NIMH (Independent Scientist Award K02 MH01114-08). We thank the Southern California Twin Project staff for their assistance in collecting data, and the twins and their families for their participation. We are also indebted to Jack McArdle for his guidance in the conceptual and practical aspects in the analyses involving latent growth models.