Citation

Goodnight JA, Donahue KL, Waldman ID, Van Hulle CA, Rathouz PJ, Lahey BB, D'Onofrio BM. Behav. Genet. 2016; 46(5): 680-692.

Affiliation

Indiana University, Bloomington, IN, USA.

Copyright

(Copyright © 2016, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s10519-016-9794-2

PMID

27105627

Abstract

Previous research suggests that fussy temperament in infancy predicts risk for later antisocial behavior (ASB) in childhood and adolescence. It remains unclear, however, to what extent infant fussiness is related to later ASB through causal processes or if they both reflect the same family risk factors for ASB. The current study used two approaches, the comparison of siblings and bivariate biometric modeling, to reduce familial confounding and examine genetic and environmental influences on associations between fussiness in the first 2 years of life and ASB in childhood and late adolescence. Analyses were conducted on data from a prospective cohort (9237 at 4-9 years and 7034 at 14-17 years) who are the offspring of a nationally representative sample of US women. In the full sample, fussiness predicted both child and adolescent ASB to small but significant extents, controlling for a wide range of measured child and family-level covariates. When siblings who differed in their fussiness were compared, fussiness predicted ASB in childhood, but not ASB during adolescence. Furthermore, results from a bivariate Cholesky model suggested that even the association of fussiness with childhood ASB found when comparing siblings is attributable to familial factors. That is, although families with infants who are higher in fussiness also tend to have children and adolescents who engage in greater ASB, the hypothesis that infant fussiness has an environmentally mediated impact on the development of future ASB was not strongly supported.

Language: en