Links Between Callous-Unemotional Behaviors and Prosociality in Early Childhood

In middle childhood through adolescence, callous-unemotional traits (CU) and prosociality are negatively correlated (e.g., Roose et al., 2010). Despite the conceptualization of CU as a disruption of the moral behaviors... [ view full abstract ]

In middle childhood through adolescence, callous-unemotional traits (CU) and prosociality are negatively correlated (e.g., Roose et al., 2010). Despite the conceptualization of CU as a disruption of the moral behaviors necessary for prosocial development, many correlations tend to be moderate, highlighting that prosociality and CU are not simply opposites. Nothing is known, however, about how the two are related in early childhood, or the shared genetic and environmental etiology at any point in development. The present study explored the underlying genetic and environmental overlap between CU and prosociality in 309 twin pairs (123 MZ, 186 DZ) at ages 3 and 4 years, when these moral behaviors are emerging. CU was assessed using the Child Behavior Checklist 1.5-5 (Achenbach & Rescorla, 2000), and prosociality using the Strengths and Difficulties Questionnaire (Goodman, 1997). CU (r=.46) and prosociality (r=.53) were stable across age; and correlated within age (age 3: r=-.26; age 4: r=-.35) and across age (CU3→prosociality4: r=-.31; prosociality3→CU4: r=-.16). A biometric cross-lagged model revealed a cross-lagged effect from CU to prosocial only. This demonstrates that whereas high CU at age 3 results in lower prosociality at age 4, low prosociality is not putting the child at risk for high CU 1 year later. At both ages there were significant genetic, shared, and nonshared environmental influences on CU, and genetic and nonshared environmental influences on prosociality. At age 3, the phenotypic relation between CU and prosociality was explained by overlap in genetic effects (r_g3=-.56). At age 4, there were novel genetic and nonshared environmental effects on CU and prosociality. The covariance at age 4 was due to shared genetic effects from age 3, and novel nonshared environmental influences at age 4 (r_e4=-.32). Although genetic factors contributed to stability and reciprocal effects, they also demonstrated developmental change in both phenotypes.