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 and 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 and 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 and 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 and 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 and 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 and 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 and 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).
