A genetic differentiation hypothesis common to both phenotypes was supported by common genetic factors associated with the developmental heterogeneity of proactive and reactive aggression in childhood. A genetic maturation hypothesis common to both phenotypes, albeit stronger for proactive aggression, was supported by common genetic factors associated with proactive and reactive aggression slopes. A shared environment set point hypothesis for proactive aggression was supported by shared environmental factors associated with proactive aggression baseline and slope. Although there are many common features to proactive and reactive aggression, the current research underscores the advantages of differentiating them when studying aggression.

Common genetic factors accounted for 64% of the total variation of proactive and reactive aggression’s intercepts. Two other sets of uncorrelated genetic factors accounted for reactive aggression’s intercept (17%) on the one hand, and for proactive (43%) and reactive (13%) aggression’s slopes on the other. Common shared environmental factors were associated with proactive aggression’s intercept (21%) and slope (26%) and uncorrelated shared environmental factors were also associated with reactive aggression’s slope (14%). Common nonshared environmental factors explained most of the remaining variability of proactive and reactive aggression slopes.

Few studies are grounded in a developmental framework to study proactive and reactive aggression. Furthermore, although distinctive correlates, predictors and outcomes have been highlighted, proactive and reactive aggression are substantially correlated. To our knowledge, no empirical study has examined the communality of genetic and environmental underpinning of the development of both subtypes of aggression. The current study investigated the communality and specificity of genetic-environmental factors related to heterogeneity in proactive and reactive aggression’s development throughout childhood.

Data Availability: Covariance matrices by sex and zygosity are included in supplementary material S1 Table . They can be used as inputs in structural equation modeling software such as Mplus and R to test alternative models. Raw data are proprietary but may be obtained by filling a request for access to data available from the Research Unit on Children’s Psychosocial Maladjustment Website ( http://www.gripinfo.ca/grip/public/www/etudes/en/dadprocedures.asp ).

Background

Aggression is a broadly defined construct that covers many normative and pathological behaviors that can differ throughout development. Heterogeneity in forms (e.g., physical, relational) and functions (i.e., proactive, reactive) are noted in many previous studies [1, 2]. The consideration of both forms and functions of aggression have inspired researchers to propose a dimensional conceptualization of aggression [3, 4]. With respect to functions, the distinction between proactive aggression (aggression that is directed toward others with an intent to harm, PA) and reactive aggression (aggression that is a defensive behavior against provocations or threats, RA) was inspired by studies of offensive and defensive aggression in animals [3]. The proactive and reactive concepts were later proposed by Dodge & Coie [2] who developed two scales based on factor analysis of twelve items chosen to capture Bandura [5] and Berkowitz [6] respective notion of aggression. Bandura [5] stated that aggression could be understood as a learned instrumental behavior intended to obtain a reward or reach an objective. He showed that aggression could be initiated by imitation [7] and learned through operant conditioning. According to this theory, the positive expected outcome could be the main driving force of aggressive behavior. In contrast, Berkowitz’s frustration-aggression model stated that aggression was an angry reaction to frustration [8, 9]. In the frustration-aggression model, threat, goal blocking and anger are all potential triggers to aggressive behavior. These theories refer to multiple functions or motivations behind individual’s aggressive behaviors [9–11]. Essentially, Bandura’s social learning approach is cited to explain proactive, instrumental aggression whereas the frustration-aggression model is used to describe reactive aggressive behaviors that are generally more impulsive or anger-driven and triggered by perception of contextual cues, such as an apparent threat.

Studies of the development of aggression suggest that physical aggression against others is the first form to be expressed in early life. Developmental studies have shown that physical aggression peaks between 2 and 4 years of age [12] and gradually decreases until adulthood [13, 14]. Researchers have suggested that the development of cognitions and language skills with more frequent interactions with peers during early childhood led to the onset and increase of other more subtle forms of aggression, such as relational aggression [15]. It has also been hypothesized that aggression starts to serve different functions during childhood as cognitive skills develop. Researchers have shown evidence that instrumental aggression is observable by 6 months of age [16, 17]. Childhood is thus a suitable developmental period to study the development of the functions of aggression because sufficient development is needed to enable planning of an aggressive act such as PA or voluntary control over RA. Surprisingly, individual development of PA and RA has rarely been investigated. The few existing studies are consistent with research on general aggression and show a small declining tendency for both functions of aggression through childhood [18, 19] and into adolescence [20].

Meaningful differences The conceptual distinction of PA and RA have often been addressed because the two behaviors are highly correlated when measured concurrently (between .68 - .71) [21–23]. Nevertheless, the distinction is supported by research showing that PA and RA are associated with specific cognitive, temperamental and socialization predictors and outcomes. For example, during the cognitive process of response in social interactions, PA children selected instrumental goals and were more confident in the use of aggression compared to reactive children [24]. Callous-unemotional traits have also been associated with PA [25] along other psychopathic traits [26]. Socialization factors are also differently related to PA and RA. Some specifically associated with PA are parents’ endorsement of aggressive behavior as an adequate goal-directed behavior [27], lack of parental discipline and monitoring [28–32], affiliation with deviant peers [33, 34] and popularity status [35]. In comparison, RA has been associated with hostile attributions toward potential sources of threats or pain [36, 37], low effortful control [38, 39], and generally to deficits in executive functioning [40, 41]. RA has also been associated with traits such as negative emotionality [42], anxiety [26] and anger [43]. Researchers also suggested that the endocrine system would likely be involved in the regulation of RA through its effect on the modulation of impulsivity [44]. Socialization factors that might increase or decrease RA include lack of parental warmth and care [36], physical or emotional abuse and neglecting parents [30, 33, 45], and peer victimization [46, 47]. Behavioral genetic studies have shown that aggressive behavior is moderately to strongly related to genetic factors (A). Environmental factors that are shared by twins (C) and environmental factors unique to each twin (E) seem to play a lesser role [48–51]. However, few genetically informed studies have specifically examined the genetic and environmental architecture of PA and RA. In children aged 9–10 years, Baker, Raine [52] found that genetic factors accounted for 45% of the variance of teacher-rated PA, but only 20% of the variance of RA. They also found significant shared environmental factors, explaining respectively 14% and 43%, of the variance of teacher-rated PA and RA. Another cross-sectional study of 6 years-old children from Brendgen et al. found that genetic factors accounted for 41% of PA and 39% of RA’s variance [53] while the remaining phenotypic variance was associated with nonshared environmental factors that also include measurement errors.

Explanation for the overlap Some factors seem less clearly associated with a specific function. Actually, some of the factors identified in the literature as specific to one function are based on residualized correlations (associated with the residual of a function or conditional on the other function). Scholars have suggested interpreting these residualized associations with caution [54] because residuals correspond to different things based on the statistical model that is executed. Besides, the validity of these residualized constructs is not demonstrated once the common variance with the other form of aggression is partialed out. For example, while psychopathy is generally only associated with PA when using residualized scores, the use of raw scores show that most components of psychopathy are associated with both PA and RA [26, 55]. Also, researchers have recently proposed that neurotransmitters from the aminergic system could be involved in the regulation of both PA and RA [44] through their role in response to stress and rewards. Finally, an influential study from Little, Henrich (4) suggests the overlap between PA and RA is likely due to the form of aggression captured by these measures, namely the overt form of aggression. Yet, none of the above studies considered the possibility of common genetic influences. Furthermore, a previously cited study found the correlation between PA and RA’s genetic factors was about .87 and this correlation was entirely accounted for by their joint overlap with physical aggression, a measure of the form of aggression [53]. This study suggests that PA and RA in children 6 years of age have substantial common genetic factors, yet this cross-sectional study can’t inform on genetic factors associated with interindividual variance of intraindividual development of PA and RA. Longitudinal studies of aggression shows that the stability of aggression through childhood has a relatively high level of heritability; around 60% to 80% [51]. Few behavioral genetic studies examined specifically PA and RA at two or more time points and provided information regarding the relative influence of genetic and environmental factors during childhood and the beginning of adolescence. One study used parent-rated aggression scores at two time points (ages 9–10 and 11–14 years) allowing the estimation of common genetic and environmental factors associated with the stability of PA and RA [56]. The study show that common genetic factors explained 63% of the stability of PA and 80% of the stability of RA. Common nonshared environmental factors explained the remaining 37% and 20% of the stability of PA and RA. In line with the Brendgen’s study, their results suggest genetic factors are substantially associated with interindividual stability between 9–10 and 11–14 years of age, however, it does not inform on the variations in the baseline level of aggression and on its change over time. Finally, in another study, Paquin, Lacourse (57) investigated PA and RA through childhood (from age 6 to age 12 years) using a time-specific general latent factor model. Their model allowed to simultaneously investigate the genetic and environmental factors associated with latent aggression factors (measured by PA and RA) as well as the genetic and environmental underpinnings of their residual variances at each time point. They showed that the latent aggression factors at each age were influenced by common genetic factors but with a decreasing magnitude through time. Innovative genetic factors at 7, 9 and 10 years were associated with latent aggression factors for shorter time spans. Thus, Paquin et al. study showed evidence that some genetic factors are common to PA and RA and have persistent associations with aggression states through childhood. Together, the results from the Tuvblad et al. and the Paquin et al. studies suggest common genetic factors have a persistent effect on PA and RA states through childhood [57] and at the beginning of adolescence [56]. These studies also suggest that nonshared environmental factors have influences of shorter duration. To conclude, few studies have described and explained the intraindividual developmental process of PA and RA, and none have examined their joint development. Furthermore, while the literature has established significant overlap between PA and RA, few have examined the possibility of common genetic factors, and none have looked at the genetic and environmental factors associated with interindividual differences in development [58].