Aggression can be defined as behavior directed at an object, human or animal, which causes harm or damage (Bushman and Anderson
2001; Gannon et al.
2007), and is one of the most frequent reasons for referral of children and adolescents to mental health services (Armbruster et al.
2004; Rutter et al.
2010). Aggression is assumed to be a heterogeneous construct, and a distinction is often made between two different subtypes, reactive and proactive aggression. Reactive aggression refers to an emotionally charged response to provocations or frustration and is also known as “impulsive”, “hot blooded” or “affective” aggression (Dodge and Coie
1987; Kockler et al.
2006; Stanford et al.
2003). Proactive aggression refers to a conscious and planned act, used for personal gain or egocentric motives, also known as “premeditated”, “instrumental” or “cold-blooded” aggression (Blair et al.
2006; Blair
2001; Dodge and Coie
1987; Frick and Ellis
1999).
Support for the distinction between proactive and reactive aggression is provided by several
variable-based studies (using factor analysis and correlations) in clinical and nonclinical samples of adolescents and adults (Cima et al.
2013; Dodge and Coie
1987; Raine et al.
2006). Furthermore, these subtypes of aggression have been related to distinct behavioral, neurocognitive and treatment profiles (Card and Little
2006; Polman et al.
2007). Reactive aggression is associated with attention problems, anxiety problems, peer rejection, hostile attribution bias, emotional dysregulation, deficits in problem solving, low verbal intelligence, and often appears earlier in life than proactive aggression. In contrast, proactive aggression is related to delinquent behaviour, lower levels of victimization, positive outcome expectancies, and higher self-efficacy about aggression (Blair
2013; Cima and Raine
2009; Dodge and Coie
1987; Merk et al.
2007; Vitaro et al.
2006). Moreover, different neural mechanisms have been suggested to underlie reactive and proactive aggression. Reactive aggression has been linked to hypofunction of in particular the orbitofrontal and anterior cingulate cortex, and increased responsiveness of the amygdala to distress, whereas proactive aggression has been associated with dysfunction of the ventromedial prefrontal cortex and the striatum, and decreased responsiveness of the amygdala to distress (Blair et al.
2006; Blair
2013).
An untouched aspect of this variable-based approach is whether a distinction between reactive and proactive aggression can be made at the level of the individual (
person-based approach). In other words, can we reliably distinguish individuals predominantly showing reactive aggression from those predominantly showing proactive aggression? Previous research shows that identifying distinct correlations using variable-based methods cannot necessarily be clearly translated to clinical characteristics within a person (Crapanzano et al.
2010). Therefore, results of methods using multiple regression procedures may appear not significant in one person or are misleading, due to the absence of a proactive-only group or to overlapping constructs (Crapanzano et al.
2010). Previous research has suggested that proactive and reactive aggression tend to co-occur in the same individuals, with only a small proportion of clinically referred children and adolescents presenting with proactive aggression only (Barker et al.
2006; Barker et al.
2010; Kempes et al.
2005). Furthermore, research shows that informants (teachers, parents or peers) find it hard to observe and identify the distinction between proactive or reactive aggression (Kempes et al.
2005). Therefore, it may be questioned whether the distinction holds in clinical practice.
Discussion
This study was designed to examine whether proactive and reactive aggression are meaningful distinctions at the variable- and person-based level, and to determine their associated behavioral profiles. These aims were examined in 587 adolescents (mean age 15.6; 71.6 % male) from clinical samples of four different sites. The variable-based approach (factor analyses) yielded a three factor solution that was robust across the four different recruitment sites, consisting of proactive aggression and two forms of reactive aggression: reactive aggression due to internal frustration and reactive aggression due to external provocation. Proactive aggression was significantly correlated with lower levels of internalizing problems and higher levels of conduct problems; and “reactive aggression due to internal frustration” was significantly stronger correlated with anxiety problems and ADHD problems. Also, internalizing problems rated by parents were uniquely predicted by “reactive aggression due to internal frustration” and self-reported internalizing problems predicted by both subtypes of reactive aggression. However, results showed moderate to high overlap between all three factors. Also, despite the finding that on a variable-based level three different types of aggression seem to be distinguished, the person-based approach (multi-level LCA) identified four classes that mainly differed quantitatively (no “proactive-only” class present), yet also qualitatively when age was taken into account, with reactive aggression becoming more severe with age in the highest affected class yet diminishing with age in the other classes. No proactive-only group could be determined, suggesting that proactive aggression does not exist without reactive aggression or that adolescents with proactive-only aggression are not being referred to clinical practice.
The main findings of the variable-based approach showed that proactive and reactive aggression can be distinguished. However, in line with a recent review of Blair (
2013) and study of Fite et al. (
2006), our factor model favored a
three factor solution instead of the expected two factor solution, with “a proactive factor”, a factor “reactive aggression due to internal frustration” and a factor “reactive aggression due to external provocation”. These three factors thus reflected distinguishable but moderate correlated aspects of aggression. Also, the factor “reactive aggression due to external provocation” only revealed three unique items, however this detracts not from the finding that the 3-factor solution described presents the best and justified factor solution. Moreover, a similar three factor model of Blair (
2013) was based on neurobiological data to differentiate between “proactive aggression” and “frustration-based reactive aggression”, putatively linked to decreased striatal and ventromedial prefrontal cortex responsiveness, and “threat-based reactive aggression”, associated with increased amygdala responsiveness (Blair
2013). “Frustration-based aggression” is supposed to partly arise as a consequence of inflexibility to changes in the environment, impairments in decision making and is linked to psychopathy and callous-unemotional traits (CU-traits), which seems to correspond with our factor “reactive aggression due to internal frustration”. Furthermore, our “reactive aggression due to external provocation” seems to correspond with the “threat-based aggression” (linked to anxiety and social provocation) since several factor items focus on aggression due to threats or provocation by other people. Our data thus support the hypothesis that reactive aggression may be meaningfully distinguished into frustration-based and threat-based aggression.
Further, we hypothesized differential associations between the aggression factors and YSR and CBCL subscales (Table
5). To be more specific, we expected proactive aggression to be associated with increased levels of conduct disorder symptoms. This hypothesis was confirmed. Overall, very similar associations between all the three factors and ODD/CD scores were reported (all
r > 0.50). However, proactive aggression was significantly stronger correlated with YSR and CBCL conduct disorder problems (CD) than the two reactive forms of aggression. Furthermore, associations between reactive and proactive aggression and anxiety, affective, somatic and total internalizing symptoms were very similar. However, the YSR (but not CBCL) anxiety scale was significantly stronger correlated with “reactive aggression due to internal frustration” compared to the proactive and the “reactive aggression due to external provocation”. This is in line with our hypothesis that reactive aggression is associated with anxiety, but in contrast with the model of Blair (
2013) where “threat-based reactive aggression” was associated with anxiety problems. This could be explained by the fact that the items of the YSR and CBCL anxiety scale mainly focus on fear of animals, going to school, being worried and nervous, and do not focus on being anxious because of threats or provocation, causing a low level of anxiety in the present study. Also, similar associations between ADHD and the three different factors were found, but with significant stronger correlations between the YSR ADHD scale (not the CBCL scale) and the “frustration-based” reactive aggression factor, compared to the “proactive factor”. This is in line with previous research showing inhibition and inattention problems within reactive aggression. Furthermore, the model of Blair shows impaired levels of decision making in the “frustration-based” reactive factor, which is also associated with ADHD problems (Luman et al.
2010). Internalizing problems were significantly stronger associated with the two forms of reactive aggression compared to the proactive form of aggression, which is in line with results of a meta-analysis of Card and Little (
2006) regarding proactive and reactive aggression in children and adolescents. Multiple regression analyses showed that internalizing problems were uniquely predicted by “reactive aggression due to internal frustration” rated by parents and predicted by both subtypes of reactive aggression on self-report. Externalizing behavior problems were predicted by all three factors on self-report, and by proactive and reactive aggression due to external provocation on parent-report. However, high interrelatedness of the three factors was shown.
The main results of person-based approach (multi-level LCA) revealed four classes that were characterized by different levels of severity, but with some qualitatively differences when age was taken into account. We were unable to find support for our hypothesis that we would identify individuals with predominantly proactive aggression without reactive aggression. No crossing lines (showing high proactive aggression with low reactive aggression or vice versa) were shown; only gradient, parallel lines of severity. Also, results showed that proactive aggression was not present without reactive aggression in the most severe classes. This shows that moderately severe reactive aggression was present without clinically relevant levels of proactive aggression, but also more severe reactive aggression is generally accompanied by proactive aggression. This is in line with previous research of children between 9 and 14 years old (Crapanzano et al.
2010), showing severity-based subgroups of aggressive individuals, and no proactive-only group. The joint presence of proactive and reactive aggression in the same individuals could be explained in part through how aggression was measured. The correlation between reactive and proactive aggression has found to be lower in observation and computer tasks, as compared to studies using (self-report) questionnaires (Polman et al.
2007). Moreover, it is possible that a proactive-only group does exist in population samples, but not in clinical samples, as this subtype may be less overt (Kempes et al.
2005) and hence does not automatically lead to clinical referral or contacts with police or justice. However, proactive and reactive aggression may be more distinguishable in a population sample. In clinical samples with increasing overall severity of aggression the clinical relevance of these subtypes may be less clear
.
Furthermore, no moderating effect of gender was found, which is in line with a meta-analysis of 51 studies regarding proactive and reactive aggression (Polman et al.
2007) In addition, age moderating effects were found, with the more severe class showing highest severity of reactive aggression in older subjects, whereas the two least affected classes showed lowest levels of reactive aggression in older subjects. No effect of age was found in proactive aggression. This could implicate that the severity level of reactive aggression –but not proactive aggression- may changed over time (but note, our data were cross sectional in nature, longitudinal data are needed to confirm this). A previous study is in line with our findings showing that in 5 to 18 year old psychiatric referred children reactive aggression –but not proactive aggression- was lowest in older subjects. In contrast, a longitudinal study of Barker et al. (
2006) showed that reactive aggression and proactive aggression tend to develop similar trajectories in 13–18 year old high-risk boys. This could be explained by the fact that probably younger adolescents with higher levels of proactive aggression were not included in this study and that reactive aggression often appears earlier in life than proactive aggression (Merk et al.
2007). This might indicate that low to moderate levels of reactive aggression in younger adolescents seems to be more “normal” at younger age when coping strategies are still lacking. However, when not diminishing with age this may become more persistent and severe at older age. This suggests that treatment is needed to prevent aggravating levels of aggression in reactive aggression (and co-occurring proactive aggression). Reactive aggression due to internal frustration seems to be even more aggravating over age than reactive aggression due to external provocation. Furthermore, reactive aggression will give more insight in development of aggression over time than proactive aggression, since both types of aggression co-occur at all levels of severity and no age effect of proactive aggression was found. Overall, clinicians should take age and the development of aggression levels into account, since younger adolescents with higher levels of reactive aggression are at risk to develop more severe levels of reactive aggression (in combination with proactive aggression) at older age. However, future research should be done including longitudinal data to replicate this age by class effect.
We hypothesized differential associations on the person-based approach between aggression classes and internalizing and externalizing scores of the YSR and CBCL (Table
6). Classes with more severe proactive (and reactive) aggression showed higher scores on the ADHD, ODD, CD, and externalizing scales of YSR and CBCL, but this appeared to be driven by overall severity of aggression. Furthermore, no clinically relevant anxiety was found in any of the latent classes.
This study had some limitations. First of all, the RPQ is a self-report questionnaire and therefore answers could be biased or social desirable. However, observation methods, teacher questionnaires or computer task can be biased as well (Polman et al.
2007), therefore a combination of both should be used. Future research should include results of multiple informants and assessments to prevent this bias. Furthermore, we did not use a population sample, which could lead to selection bias and an incomplete sample where possible subgroups (proactive-only) have been left out. Moreover, more boys were included than girls and the YSR and CBCL data were not complete for every group that was included in this study. Also, this study only included “function” of aggression (proactive vs reactive), but not “form” of aggression (i.e., physical or relational aggression) which has been distinguished in previous research (Marsee et al.
2014). Future research should include both forms and functions of aggression and more girls in studies regarding aggression problems or conduct disorder problems. In addition, this study used cross-sectional data and no longitudinal data. Finally, our data-base did not include contextual information, which is information about whether and which environmental triggers and cues elicited aggression in our participants.
Overall, the variable-based analyses demonstrate that proactive and reactive aggression can be distinguished. In fact, three distinguishable but strongly correlated factors of aggression were identified. The original proactive factor and reactive aggression was divided into two different forms; “reactive aggression due to internal frustration” and “reactive aggression due to provocation”. These three forms of aggression show, besides similar and overlapping behavioral associations, also some specific associations; namely lower associations with internalizing problems and higher associations with CD in proactive aggression; higher associations of anxiety, ADHD and internalizing problems were found in the “reactive aggression due to internal frustration”.
However, despite the fact that proactive and reactive aggression can be distinguished at the variable-based level, the clinical relevance of these findings is challenged by the person-based analysis showing proactive and reactive aggression are mainly driven by aggression severity. If proactive aggression is present (in combination with reactive aggression), clinical levels of conduct disorder and externalizing behavior problems are reported. This suggests the presence of proactive aggression can be seen as a severity marker that need extra awareness of clinicians. Also, age effects are important to take into account in clinical practice. Findings suggest that reactive aggression is a more “normal” phenomenon at younger age and when not diminishing with age it may be a marker for the most severe aggression in older adolescents. Although it seems reasonable that subjects showing high levels of proactive and reactive aggression, and younger adolescents who are at risk of developing more severe reactive aggression warrant more intensive respectively preventative treatment than those showing reactive aggression only, future research should address the question of differential responsivity to treatment (Vitaro et al.
2006). Future research should focus on the differentiating and/or overlapping neurocognitive (i.e., impaired decision making), neural, biologic, behavioral (CU-traits, trauma) and genetic profiles of the three different aggression factors (proactive, frustration-induced and threat-induced). This would enable to explore whether a distinction of aggression based on these profiles would produce a stronger differentiation than a distinction based on observable behaviors.