Trait displaced aggression and psychopathy differentially moderate the effects of acute alcohol intoxication and rumination on triggered displaced aggression
Introduction
The causes of many acts of aggression are difficult to comprehend. For example, the excessive aggression commonly observed in cases of intimate partner violence and road rage are often instigated by fairly trivial triggering events. Research and theory within the triggered displaced aggression (TDA) paradigm can explain such perplexing instances of aggression that exceed normative tit-for-tat responding (Axelrod, 1984). The classic displaced aggression effect occurs when a person is provoked, is unwilling or unable to retaliate against the original provocateur and subsequently aggresses against a seemingly innocent target (Dollard et al., 1939, Hovland and Sears, 1940, Marcus-Newhall et al., 2000). In contrast to classic displaced aggression, TDA occurs when the subsequent target is the source of a second, subjectively annoying provocation, (referred to as the trigger), and the aggressor responds with a disproportionate level of aggression (Pedersen et al., 2000, Vasquez et al., 2005). To illustrate, a man who is scolded by his superior (e.g., “you really messed up that presentation”) and does not retaliate, but then encounters a co-worker who is less than sympathetic (e.g., “well, maybe you should have tried harder”) and subsequently shouts insults at the co-worker, has engaged in TDA.
A number of factors increase the severity of TDA. These include alcohol intoxication, rumination, and the stable dispositional tendency to displace aggression (Aviles et al., 2005, Bushman et al., 2005, Denson, Aviles, et al., 2008, Denson et al., 2006). These effects can be understood within the context of the General Aggression Model (GAM; Anderson & Bushman, 2002). The GAM proposes that personal characteristics interact with situational features such as provocation and alcohol intoxication to activate aggressive cognition, angry affect, and/or physiological arousal. When sufficiently activated, these internal states bias appraisal and decision-making processes, which subsequently increase the likelihood and severity of aggressive behavior.
Recent research suggests that rumination increases all three of the internal antecedents to aggression specified in the GAM: angry affect, aggressive cognition, and physiological arousal (Kross et al., 2005, Ray et al., 2008, Rusting and Nolen-Hoeksema, 1998, Wimalaweera and Moulds, 2008). Miller and colleagues (Miller, Pedersen, Earleywine, & Pollock, 2003) theorized that prolonged rumination facilitates TDA because it maintains these routes to aggression over time, which in turn, increase hostile reactions to subsequent triggering events. The findings of recent TDA experiments are consistent with this theorizing.
Specifically, relative to distraction, rumination increases displaced aggression, but only when individuals are provoked and rumination is followed by a triggering event (Bushman et al., 2005, Denson et al., 2006, Denson et al., 2008).
Only one previous experiment has simultaneously examined the effects of rumination and alcohol in eliciting aggression. Denson, Spanovic, et al. (2008) found that alcohol and self-focused rumination independently augmented TDA. Self-focused rumination is defined as thoughts and feelings about one’s thoughts, behavior, and negative emotions (Rusting & Nolen-Hoeksema, 1998). This is distinct from provocation-focused rumination, wherein the individual’s thoughts and feelings are primarily externally focused on reliving the provoking incident and planning revenge (Denson et al., 2006). The current study is the first to simultaneously examine the effects of alcohol and provocation-focused rumination on aggression.
Researchers have proposed a number of psychological mechanisms to explain the aggression-augmenting effects of alcohol. One such mechanism, the attention–allocation model (also known as alcohol myopia), posits that alcohol consumption interferes with cognitive functioning by narrowing one’s attention toward the most salient cues in the environment and steering attention away from less salient cues (Giancola and Corman, 2007, Steele and Josephs, 1990). This model is consistent with a recent TDA experiment which found that intoxicated participants were only able to pay attention to highly salient triggering events, whereas sober participants were able to allocate their attention to triggers that were both high and low in salience (Denson, Aviles, et al., 2008).
A second compatible mechanism is that of diminished inhibitory control. Giancola, 2000, Giancola, 2004 suggests that intoxicated aggression occurs as the result of temporary impairment of executive functioning, primarily via a reduction in the ability to control aggressive thoughts and actions. Such theorizing is consistent with neuroimaging research demonstrating that acute alcohol intoxication disrupts activity predominantly in the prefrontal cortex (Volkow, Wang, & Doria, 1995). Similarly, a recent study also reported alcohol dose-related increases in impulsive responses on a measure of inhibitory control (Dougherty, Marsh-Richard, Hatzis, Nouvion, & Mathias, 2008).
Section snippets
Trait displaced aggression and psychopathy
Although the consistency of the alcohol–aggression relationship is robust, it is well established that alcohol does not facilitate aggression in everyone. Meta-analyses have shown that the magnitude of the alcohol–aggression link is moderate, supporting the notion that additional situational and dispositional variables are necessary to fully explain for whom and under what conditions alcohol increases aggression (Bushman and Cooper, 1990, Ito et al., 1996). Theorists have speculated that
The present research
The primary aim of the current research was to simultaneously examine the effects of trait displaced aggression and psychopathy on alcohol- and rumination-induced TDA. We expected that alcohol intoxication and rumination would independently and additively augment TDA, and that the effects of the alcohol and rumination manipulations would be moderated by trait displaced aggression and psychopathy. A secondary aim was to test the hypothesis that alcohol would temporarily reduce inhibitory control
Participants and design
A total of 110 participants volunteered from either the UNSW first year psychology pool (n = 38), or through a campus advertisement (n = 72), and were at least 18 years old (i.e., of legal drinking age in Australia). To avoid obtaining a biased sample, no mention of alcohol appeared in the advertisement. The research was advertised as a study on ‘taste preferences, personality, and cognitive ability’. Three participants were excluded due to failure to believe that the feedback or fictitious partner
BAL assessments
A 2 (rumination, distraction) × 4 (BAL at times 2–5) mixed ANOVA for those in the alcohol condition revealed a main effect for time only, F(3, 144) = 5.76, p = .001, η2 = .11. Thus, among intoxicated participants, the rumination and distraction conditions did not differ in their BALs prior to aggressing against the bogus participant, nor at any point throughout the experiment (see Table 1).
Subjective alcohol assessments
Prior to beverage administration, there were no differences between the alcohol and placebo conditions for the
Discussion
This was the first experiment to examine the moderating effects of trait displaced aggression and psychopathy on alcohol- and rumination-induced TDA. Both experimental manipulations reliably augmented TDA. In addition to replicating prior research showing that provocation-focused rumination and alcohol augment TDA (Aviles et al., 2005, Bushman et al., 2005), the current research is also consistent with a previous study demonstrating the TDA-augmenting effects of alcohol and self-focused
Conclusions
Despite these limitations, our findings confirm the importance of both situational and personality factors as predictors of TDA. It is hoped that by identifying the moderating variables and understanding the cognitive processes involved, we may eventually reduce the harm associated with common, yet seemingly inexplicable displays of TDA, such as many acts of intimate partner violence.
Acknowledgments
This research was supported under the Australian Research Council’s Discovery Projects funding scheme (DP0985182).
We thank Sang Cheung for help with data collection.
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