Genetic and Environmental Contributions to Associations between Infant Fussy Temperament and Antisocial Behavior in Childhood and Adolescence

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 two years of life and ASB in childhood and late adolescence. Analyses were conducted on data from a prospective cohort (9,237 at 4-9 years and 7,034 at 14-17years) who are the offspring of a nationally representative sample of U.S. 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.

Genetic and environmental sources of covariation between early drinking and adult functioning.

“…Further, the presence of common genetic influences on the covariation between adolescent drinking and adult adjustment is consistent with the concern that genetic risk could confound the relationship (see, e.g., Bornovalova, Huibregtse, Hicks, Keyes, McGue, & Iacono, 2013; Goodnight et al, 2016, for additional discussions of this interpretation). These findings underscore that researchers interested in the causal impact of alcohol consumption in adolescence should utilize methodology (e.g., propensity score-matching, co-twin control design) to address possible confounding.…”

Explaining the relationship between temperament and symptoms of psychiatric disorders from preschool to middle childhood: hybrid fixed and random effects models of Norwegian and Spanish children

“…In both countries, time‐invariant causes of symptoms of psychiatric disorders were not correlated with temperament; thus, they could not explain the prospective associations between symptoms and temperament. This is seemingly at odds with twin studies showing that at least part of the associations between early temperament and later psychopathology is due to shared genetics (Gjone & Stevenson, ; Goodnight et al., ; Silberg et al., ). Furthermore, the heterotypic stability of symptoms was moderate at 2‐year intervals but was merely modest over longer time intervals (except for ADHD).…”

“…Although the continuity hypothesis is widely supported by studies showing correlational patterns between specific temperamental/personality traits and specific psychopathology (De Bolle et al, 2012;De Pauw & Mervielde, 2010;Nigg, 2006), the common cause explanation has seldom been addressed directly. However, genetically informed studies report that some concurrent (Tackett et al, 2013) and prospective (Gjone & Stevenson, 1997;Goodnight et al, 2016) correlations between temperament and psychopathology are fully or partly explained by common genetics. More scattered and/or less consistent support has been obtained for the complication hypothesis (De Bolle et al, 2012;Shiner, Masten, & Tellegen, 2002).…”

An Examination of Within- and Between-Family Influences on the Intergenerational Transmission of Violence and Maltreatment

“…Second, a series of sibling comparison models were estimated. These models follow the same underlying logic as other genetically informed modeling approaches (i.e., MZ difference score approach) and are popular within behavioral genetics (D’Onofrio et al, 2016; Ellingson, Goodnight, Van Hulle, Waldman, & D’Onofrio, 2014; Goodnight et al, 2016). Because similarities between siblings from the same household are the result of a combination of (shared) environmental and genetic influences, controlling for such similarities would effectively remove any variance in the examined source of influence (i.e., maltreatment) that may be the result of environmental and genetic influences that cluster within families.…”