Abstract
Extant research has highlighted meaningful distinctions in the development, personality structures, and etiologies of physically aggressive (AGG) and nonaggressive rule-breaking (RB) antisocial behavior (as reviewed by Clinical Psychology Review, 2012). AGG appears to be a highly heritable behavioral dimension that emerges in early childhood and exhibits specific ties to negative emotionality. Although the frequency of aggressive behaviors decreases after early childhood, those who are most aggressive early in life typically continue to aggress at relatively high rates across the lifespan. By contrast, RB demonstrates specific associations with impulsivity, is most frequent during adolescence, and evidences more moderate levels of stability and stronger environmental influences as compared to AGG. The results of new empirical analyses assessing etiological distinctions across development are also presented. The review concludes that future research on antisocial behavior should distinguish between AGG and RB.
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Notes
- 1.
The current review centers on physical aggression and nonaggressive rule-breaking but does not explore social aggression or callous-unemotional traits. Although some efforts have already been made to explore similarities and differences among physical aggression, rule-breaking, social aggression, and callous-unemotional traits (Burt, 2012; Burt, Donnellan, & Tackett, 2012), far more work is needed before any firm conclusions can be drawn.
- 2.
Data were examined and are included here with permission from study PIs: Matt McGue and William G. Iacono.
- 3.
The moderation analyses were restricted to the AGO and ANTI scales, in part because I hoped to evaluate whether prior findings extended to attitudes, but also for psychometric reasons. In particular, the AGG and RB symptom count variables remained very skewed even after transformation (skews after transformation were 3.3 and 2.5, respectively) and thus are not well suited to moderation analyses (see Purcell, 2002). The AGG scale fashioned out of 5 items on the DBI was also quite skewed (skew following transformation was 1.7) and moreover, was not particularly reliable (α = 0.69). ANTI and AGO are thus far better suited to moderation analyses.
- 4.
One issue that could conceivably influence these results is a lack of measurement invariance across age. I thus examined the data for evidence of factorial invariance, a core aspect of measurement invariance in which the relationships between the indicators (i.e., the items) and the trait are the same across groups (in this case, age groups). I specifically calculated standardized item loadings for the ANTI and AGO factors separately in younger (ages 11–14) and older (ages 15–18) participants. I then evaluated their persistence across the two age groups. The mean age group difference in item factor loadings was 0.020 for ANTI and 0.044 for AGO. Moreover, the correlation across item loadings in the two age groups was 0.97 for ANTI and 0.90 for AGO. In short, there is little evidence to suggest that the above findings of etiological change with age for ANTI are a consequence of measurement variance.
- 5.
Another issue worth considering is the genetic similarity between AGO and ANTI. The genetic correlation between AGO and ANTI was estimated at 0.64 (while rC and rE were estimated at 0.98 and 0.38, respectively). In short, the genetic factors influencing AGO overlap only moderately (41 %) with those influencing ANTI, suggesting that while they do share some genetic effects, others are specific to each phenotype.
- 6.
To ensure that these results were also unaffected by issues of measurement variance, I calculated standardized item loadings for the ANTI and AGO factors, respectively, at ages 11, 14, and 17. The mean age group differences in item factor loadings across both assessments were 0.084 for ANTI and 0.042 for AGO. Moreover, the correlations across item loadings at ages 11 and 14 were 0.83 for ANTI and 0.89 for AGO. The correlations across item loadings at ages 14 and 17 were 0.93 for ANTI and 0.97 for AGO. In short, there is again little evidence that the above findings of etiological change with age are a consequence of measurement variance.
- 7.
The genetic correlation between ANTI and AGO at ages 11, 14, and 17, respectively, was estimated at 1.0, 0.53, and 0.65 at ages 11, 14, and 17 (all p < 0.05). rC was estimated at −1.0, 0.94, and 0.60 at ages 11, 14, and 17 (although none of the rC estimates were significant at p < 0.05). rE was estimated at 0.40, 0.52, and 0.38 at ages 11, 14, and 17, respectively (all p < 0.05). Such results suggest that while there is no evidence of genetic differentiation between AGO and ANTI at age 11, they have differentiated by age 14 (genetic overlap was 28.1 % at age 14) and remain partially distinct through age 17 (at which age genetic overlap was estimated at 42.3 %).
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Burt, S.A. (2014). Additional Evidence for Meaningful Etiological Distinctions Within the Broader Construct of Antisocial Behavior. In: Rhee, S., Ronald, A. (eds) Behavior Genetics of Psychopathology. Advances in Behavior Genetics, vol 2. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9509-3_4
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