خشونت خانگی، خصومت و مجرمان مرد از خشونت: بررسی فراتحلیلی

There has been significant interest in, and controversy about, whether anger and hostility problems are meaningfully related to male-to-female intimate partner violence (IPV). In this meta-analytic review, we empirically evaluated whether the constructs of anger and hostility discriminated between IPV perpetrators and nonviolent comparison males. Thirty-three studies reporting data from 28 independent samples were included for analysis. IPV perpetrators consistently reported moderately higher levels of anger and hostility than nonviolent men across assessment methods (i.e., self-report, observational, and spouse-specific). In prior reviews, relationship distress has been proposed as a moderating variable between relationship distress and IPV. In this review, IPV perpetrators also consistently reported moderately higher levels of anger and hostility than relationship-discordant nonviolent men. Additionally, comparisons of subtypes of IPV perpetrators found that men in moderate-high severity IPV subtypes reported higher levels of anger and hostility than low-moderate IPV subtypes. While the pattern of results in this review suggests that elevated anger and hostility are distinguishing characteristics of IPV perpetrators, empirically based conclusions regarding the functional and contextual relationship between anger, hostility, and IPV remain elusive. The implications and limitations suggested by this review are discussed in the context of emerging models of anger and IPV and treatment programs for abusive men.

Attempts to understand the correlates and causes of intimate partner violence (IPV) have increasingly focused on the role of individual factors specific to the abusive male. Several reviews of this research have consistently concluded that in addition to childhood precursors, societal influences, and interpersonal contexts, male IPV perpetrators are characterized by problems related to psychopathology (Holtzworth-Munroe & Stuart, 1994 and Kessler et al., 2001), cognitive distortions and deficiencies (Eckhardt & Dye, 2000), and social skills deficiencies (Anglin & Holtzworth-Munroe, 1997). While few, if any, researchers in this area would endorse a purely intrapersonal model of IPV, more careful consideration of the characteristics internal to the abuser may assist in the elucidation of etiological models of IPV and in the development of more targeted intervention programs for IPV than currently exist. The present review is focused on a particular internal characteristic of abusive males that would seem to have much potential as an aid to understanding IPV etiology, treatment, and prevention: anger arousal. In this paper, we focus on why anger might be relevant to IPV, discuss relevant etiological models that may explain how problematic anger may relate to IPV, and provide a quantitative review of the evidence regarding whether male IPV perpetrators can be distinguished from nonviolent men in terms of anger and hostility. 1.1. Setting the stage: why should disturbed anger relate to IPV? On the surface, disturbed anger and hostility would appear to be obvious risk factors for partner violence; does it not follow that aggressive people also tend to be angry people? The scenario wherein an enraged husband explodes with verbal and physical aggression directed toward his spouse appears to have ample face validity and frequent representation in media reports of IPV incidents (Purdy & Nickle, 1981, Sonkin et al., 1985 and Walker, 1979). Clinically focused authors have long advocated the usage of anger deescalating treatments for men who abuse their partners (e.g., Deschner et al., 1986 and Hamberger, 1997). Likewise, the accumulated data suggest that problems relating to anger arousal are at least moderately consistent in discriminating domestically violent from nonviolent males (Eckhardt et al., 1997 and Schumacher et al., 2001). There are several problems, however, that seriously limit enthusiasm among both researchers and practitioners concerning the status of anger as a risk factor for IPV. First, despite being a central feature of the human emotional experience, we know little about the anger construct relative to the accumulated knowledge concerning other negative emotions such as depression or anxiety. Anger is underresearched and infrequently defined in the general clinical research literature and in IPV research in particular (DiGiuseppe et al., 1994, Eckhardt et al., 1997 and Eckhardt & Deffenbacher, 1995). Researchers in this area infrequently define their constructs, especially in terms of addressing conceptual distinctions between anger and hostility, resulting in a hodgepodge of loosely connected results that defy integration. Indeed, Berkowitz (1994) suggested that, “[a]ny really close and thorough examination of the psychological research into the origins of anger and emotional aggression must leave the thoughtful reader somewhat dissatisfied. The literature presents us with occasional inconsistencies and unexpected findings that most of the investigators seem not to have noticed…” (p. 35). In a review of two dozen studies examining anger and the perpetration of marital violence, Eckhardt et al. (1997) reported that there was substantial inconsistency in findings related to anger, hostility, and IPV due in part to researchers' inconsistent attention to the basic theoretical and conceptual nuances of the anger and hostility constructs. In a later section of this paper, we will more specifically address these issues. A second related factor concerns a diffuse confusion about how anger should be assessed and whether existing anger assessment methods are psychometrically adequate (Biaggio et al., 1981, Eckhardt et al., 1997 and Eckhardt et al., 2004). Thus, the issue of whether high levels of anger and hostility are unique risk factors for IPV may be dependent upon, and attenuated by, the methods of assessment used. Given the degree of conceptual confusion about the very nature of anger and hostility as well as the functional issue of how they may relate to aggressive behavior, it would seem likely that methods of assessing these constructs are similarly unclear. Given the close relationship existing between the quality of assessment of a particular construct and the development of etiological models of that construct (e.g., Loevinger, 1957), the conceptual status of the anger–IPV relationship will continue to be limited by the inadequacies surrounding anger assessment. Finally, and perhaps most importantly, there is a persistent bias against the mere notion of anger as a correlate of IPV among many professionals in the domestic violence field. Gondolf and Russell (1986) made “a case against anger control treatment programs,” noting that such programs not only may be ineffective treatments but may actually put victims at risk for being the recipient of future violence. The argument raised by these and other authors (Pence & Paymar, 1993 and Tolman & Saunders, 1988) is that by attributing the cause of battering to anger disturbances rather than the societal supports for domestic violence and men's choice to engage in that behavior, anger management interventions may overlook other significant causes of violence. In approximately one-half of states, guidelines for batterer programs explicitly prohibit anger management programs as recognized interventions for IPV perpetrators (Healey, Smith, & O'Sullivan, 1998), with adherence to these guidelines a requirement for programs to receive state and county funding. The net result of this stance has not only been a resistance toward anger-based interventions, but a steadfast dismissal of anger as a potential risk factor for violent behavior. Ultimately, however, all of these concerns must be answered empirically rather than ideologically. That is, before making decisions in favor of, or against, anger-focused treatments, it would first be prudent to investigate whether problems relating to anger arousal indeed relate to increased risk of male-to-female IPV perpetration. Thus, regardless of one's theoretical perspective concerning the etiological role of factors internal to the perpetrator, it is hoped that the available evidence will provide the most persuasive answer to these questions. We commence this review by first outlining several theoretical models addressing the potential linkage between anger arousal and IPV perpetration. 1.2. Etiological models of anger and aggression Does being angry make one aggressive? As noted by Tavris (1989), the anger-leads-to-aggression hypothesis exists primarily as a social myth and is not well supported by existing data, as most studies utilizing community samples of adults do not support a simple linear relation between the two. For example, Averill (1982) reported that in a sample of community adults, aggressive behaviors occurred in conjunction with anger arousal in only about 10% of angry episodes. Verbally aggressive responses to anger arousal were significantly more common, occurring 49% of the time. Other investigators have suggested that the likelihood of aggressive behavior following episodes of anger covary with the individual's enduring disposition to experience anger arousal cross-situationally (Deffenbacher et al., 1996 and Tafrate & Kassinove, 2002). Thus, individuals scoring high on measures of trait anger typically report more aggressive behaviors in the context of their anger episodes than those scoring low on such measures. But at this point, we should emphasize the sizable gap in the literature, both generally and within the IPV area in particular, concerning anger arousal as a causal factor in episodes of violence. Studies that have examined anger as an important etiological factor in IPV are scarce, and there are surprisingly few causal models of IPV that directly incorporate anger-related factors as etiological components. Disturbances in anger arousal are therefore likely to be related to aggressive behavior only in the context of other factors of theoretical and practical relevance. Thus, intimate partner violence is a complex set of behaviors that is multidetermined and resistant to univariate predictions such as the anger-leads-to-aggression hypothesis. In order to understand the range of the factors theoretically related to aggressive outcomes, we turn to a variety of recent data-driven theoretical models from the general aggression literature that may provide useful heuristics for understanding whether, and how, anger arousal may be related to intimate partner violence. More traditional social learning theory models (e.g., Bandura, 1973) have suggested that aggressive behavior can be learned in the same manner as other complex behaviors, either via direct conditioning or observational learning. Indeed, one of the more accepted causal explanations of the origins of domestic violence is based on the social learning theory-based notion that witnessing parental aggression as a child may set the stage for partner violence perpetration as an adult (Clarke, Stein, Sobota, Marisi, & Lucy, 1999). While this more general model provides the topography for the contextual, individual, and historical factors that may give rise to a complex behavior such as aggression, more detailed causal models are needed to explain why particular contexts give rise to aggression. The models reviewed in the next section, therefore, advance the role of cognitive factors in the onset and maintenance of aggressive behavior. Beck (1999) has recently suggested that aggression can be understood through a cognitive vulnerability model that focuses on particular style of cognitive processing termed “primal thinking.” According to this perspective, adverse childhood experiences produce a tendency to experience situations egocentrically. Thus, individuals with this frame may overinterpret situations in terms of their own self-interest, especially in regard to a preoccupation with perceived present and past injustices, and perceived threats to the self. This tendency of the aggressive individual to overperceive others' behaviors as unjust and deliberate attempts to block his/her goals in a personally threatening manner sets the stage for the individual to take corrective actions, such as punishing acts of aggressive behavior. This process is reinforced by a characteristic set of tacit, automatic cognitive biases, such as overgeneralization (establishing inflexible rules and conclusions that apply to all situations), dichotomous thinking (viewing events or people in all-or-nothing abstractions), personalization (inferring the self to be critically affected by otherwise impersonal events), causal thinking (establishing inferences and conclusions in the absence of supporting evidence), and demandingness (absolutistic and inflexible demands that others act and events occur in accordance with the individual's desires). Together, this model presumes that following some environmental event, which need not be aversive, the aggressive individual is prone to perceive the event as indicative of loss and a threat to the self, which then leads to the experience of distress and the conclusion that the event is an unjustified violation of a strongly held personal rule. This awareness of a rule violation activates memories of prior violations in similar contexts, which may further intensify affective arousal. The quality and degree of anger eventually experienced is generated by the final meaning placed on the event by the perceiver, which then sets the stage for the relative acceptability of aggressive responding. However, while this model establishes the cognitive contexts surrounding intense anger in aggressive individuals, it is less clear in its delineation of how contexts come to be associated with particular cognitive processing styles, and is similarly unclear about the intervening steps between angry experiences and aggressive behavior. A more comprehensive account of human aggression was provided by Berkowitz, 1989, Berkowitz, 1993 and Berkowitz, 2001, who noted that a variety of aversive external (loud noises, unpleasant smells, object classes) stimuli have the ability to produce an unpleasant and undifferentiated negative affective state in the perceiver. This negative affect, in turn, gives rise to automatically associated memories, images, cognitive processes, physiological processes, and behavioral intentions and produces either a tendency toward a “fight” or “flight” response. If a fight response is activated rudimentary feelings of anger are experienced, which become more fully differentiated based upon the specific contextual cues present in the environment, as well as the specific nature of the automatic context-activated thoughts, memories, and images. In keeping with a spreading activation model of memory and mood (Bargh, 1994, Blaney, 1986, Bower, 1981 and Collins & Loftus, 1975), contexts automatically give rise to semantically related concepts stored in memory networks, with the activation spreading to other parts of the network with conceptually related meanings. As one part of the system is activated (e.g., a man perceiving a critical statement by one's wife), it automatically activates contiguous elements of the system (memories of similar statements from parents; inferences about being disrespected; feelings of anger), further solidifying the associative connections existing between the various interlinkages within the system. Thus, depending upon the individual's learning history and range of associative experiences, a variety of cues can serve to initiate the anger arousal process. Higher-level cognitions, such as cognitive biases (demands that others treat him fairly) or causal attributions (concluding that his wife says these things because she is a disrespectful nag), may be experienced in the midst of this ongoing anger reaction to further refine the quality and intensity of the angry affect, and other social problem solving cognitions (the man believing it is his role to keep her “in line”) may then guide possible aggressive response options. These general models of aggression, as well as more recent integrative models combining these approaches (e.g., Anderson & Bushman, 2002), suggest that anger may play a significant role in determining aggressive behavior, although this role may not necessarily be causal. Based upon the evidence generated by these theoretical models to date, Anderson and Bushman (2002) concluded that anger may influence aggression in three ways. First, anger may reduce prohibitions against aggression, either by justifying the aggressive response (for a review of the literature on attributions and IPV, see Eckhardt & Dye, 2000) or by disrupting normal cognitive processes that would otherwise suppress aggressive retaliations. For example, maritally violent men induced to feel angry in the laboratory articulated fewer anger reducing thoughts than similarly angered nonviolent comparison husbands, suggesting that such disruption is especially likely at higher levels of anger arousal (Eckhardt, Barbour, & Davison, 1998). Second, each episode of anger keeps individuals focused on aggressive motivations over time by serving as an information cue and as a prime for aggressive “scripts.” To the extent that certain thoughts, images, and memories are closely linked to anger experience, each new episode of anger arousal will serve to activate those same processes and enhance the motivational set that promotes aggressive responding. Thus, as an individual experiences intense anger, this reaction automatically activates a set of anger relevant scripts (Abelson, 1981 and Huesmann, 1988) that serve to give meaning to the situation and guide the behaviors necessary to successfully manage that situation. Aggressive individuals enact aggressive behaviors in part because they have effortlessly and tacitly accessed a highly routinized script that dictates how that individual should think (“I've been disrespected”), feel (“I'm furious!”), and respond (“No one gets away with that; I'm gonna make them pay!”) to that situation. This hypothesis has been supported in a number of studies investigating the social information processing of martially violent men (Eckhardt et al., 1998 and Holtzworth-Munroe & Hutchinson, 1993). Third, anger energizes behavior by increasing arousal levels. Excitation-transfer models (Zillman, 1979) have shown that individuals experiencing increased physiological arousal from one source will transfer that arousal to a temporally related second source and misattribute the cause of the arousal to the second source. If the present context is conflict- or anger-related, the already-energized individual will exhibit higher levels of anger arousal than if there was no prior excitation. Thus, the data clearly support social stress and marital conflict as reliable risk factors for IPV perpetration (e.g., Kessler et al., 2001 and O'Leary et al., 1989). To the extent that individuals bring a high level of physiological arousal stemming from these stressors into new conflict situations, that arousal may be misattributed to the partner and in turn motivate aggressive responding. While there are no laboratory studies that provide direct evidence of this causal sequence, clinically focused authors have long discussed the idea that IPV may be exacerbated by ongoing social, financial, and lifestyle stressors (e.g., see Cano & Vivian, 2001). In summary, available theoretical models imply a relationship between anger arousal disturbances and aggressive behavior in close relationships. Indeed, several authors in the IPV area have also constructed theoretical models that suggest anger may at least be indirectly related to IPV (Dutton, 1995, Holtzworth-Munroe & Stuart, 1994 and O'Leary, 1993). However, anger does not cause aggression, and all aggressive individuals are not angry, but for some individuals in certain situations with a characteristic style of processing social information, anger hyperarousal may be a variable of critical importance to understanding aggressive responding. In the next section, we consider what previously published reviews of this literature have concluded as a prelude to the meta-analytic focus of the present paper. 1.3. Prior literature reviews Numerous reviews examining the characteristics of IPV perpetrators have appeared in the past 20 years (Edleson et al., 1985, Holtzworth-Munroe et al., 1997, Holtzworth-Munroe et al., 1997, Hotaling & Sugarman, 1986, Rosenbaum & O'Leary, 1981 and Tolman & Bennett, 1990). Most had little to say about the role of anger and hostility until the 1990s, and few differentiated between these two constructs. Qualitative reviews of the literature by Tolman and Bennett (1990) and Holtzworth-Munroe et al. (1997) suggested that high levels of anger were related to partner violence perpetration although this relationships was somewhat inconsistent, with Tolman and Bennett concluding that “men who batter are more hostile and angrier than nonviolent controls. However, they do not seem to differ from generally violent men” (p. 93). Eckhardt et al.'s (1997) qualitative review reported similar conclusions, and suggested that measurement problems and inconsistencies surrounding the definitions of hypothetical constructs were the foundation for these inconsistencies (rather than the anger–IPV relationship at the construct level), subjects we will return to in a subsequent section. In the only meta-analytic review examining anger as a discriminating characteristic of IPV perpetrators, Schumacher et al. (2001) reviewed five studies and concluded that “anger and hostility are consistent predictors of [IPV], but the effects range from relatively small (r=0.18) to large (r=0.52) depending on the study and the measures used” (p. 327). However, these authors suggested that these specific relationships may be mediated by marital distress, noting that three of the five studies did not use a relationship-distressed nonviolent sample of IPV perpetrators, and a fourth study indeed found a hostility–marital distress–IPV mediational relationship. Only one study reviewed by Schumacher et al. (2001) suggested that anger/hostility was higher in IPV perpetrators relative to a distressed nonviolent sample of males ( Barbour, Eckhardt, Davison, & Kassinove, 1998). While the Schumacher et al. (2001) meta-analysis was a timely and critically important quantitative review of the prior two and a half decades of research on all risk factors for IPV, the two-paragraph section on anger and hostility falls short in several important respects. First, the authors reviewed only a small portion of the published research on anger, hostility, and male IPV perpetrators. In the present review, for example, we include 33 separate studies that investigated these factors. Second, the authors did not separate effect sizes according to the construct assessed or the method of assessment used. Eckhardt et al. (1997) noted that the terms anger and hostility have been used interchangeably in the IPV literature, with little attention paid to important construct-level differences between these two traits. To the extent that researchers provide conceptually clear definitions of anger and hostility, resulting models will more accurately describe and predict the phenomenon of interest. Similarly, definitional murkiness will directly impact the quality of assessment in this area as researchers utilize measures that assess the “wrong” construct or that possess weak psychometric properties for a particular assessment goal (for a more general review of anger assessment, see Eckhardt et al., 2004). These problems, in turn, will only serve to attenuate or otherwise produce spurious relationships between anger-related variables and partner violence, and will continue to thwart more general models of IPV. Thus, these issues point to the need for an additional and more comprehensive quantitative analysis of the empirical literature on anger, hostility, and male-to-female IPV perpetration. 1.4. Definitions In the previous section, we indicated the importance of distinguishing between the constructs of anger and hostility. Historically, hostility has been regarded as an attitudinal construct involving the dislike and negative evaluation of others ( Berkowitz, 1993 and Buss, 1961), or as a cognitive trait that indicates “a devaluation of the worth and motives of others, an expectation that others are likely sources of wrongdoing, a relational view of being in opposition toward others, and a desire to inflict harm or see others harmed” ( Smith, 1994, p. 26). While other researchers view hostility as being a more multifaceted construct involving affect and expressive behavior in addition to negative attitudes (e.g., Barefoot, 1992 and Barefoot & Lipkus, 1994), the hostility construct primarily involves the cognitive variables of cynicism (believing that others are selfishly motivated), mistrust (an overgeneralization that others will be hurtful and intentionally provoking), and denigration (evaluating others as dishonest, ugly, and mean) ( Miller, Smith, Turner, Guijarro, & Hallet, 1996). Most researchers assume that the negative cognitive set that is hostility in turn predisposes a tendency to produce frequent episodes of anger and to motivate aggressive and often vindictive behavior ( Spielberger, 1988). Attempts to define anger have focused on narrow indices such as physiological arousal ( Ax, 1953), subjective phenomenology ( Spielberger, Jacobs, Russell, & Crane, 1983), or social constructivism ( Averill, 1982). However, these definitions do not sufficiently address the constellation of events that occur during the experience of anger. Thus, a given angry episode involves a myriad of physiological alarm responses, escape and attack behaviors, subjective labels of internal feeling states, and transgression-related cognitions that are experienced simultaneously as an episode of anger. Not surprisingly, therefore, more current definitions regard anger as a multidimensional construct consisting of physiological (general sympathetic arousal, hormone/neurotransmitter function), cognitive (irrational beliefs, automatic thoughts, inflammatory imagery), phenomenological (subjective awareness and labeling of angry feelings), and behavioral (facial expressions, verbal/behavioral anger expression strategies) variables ( Berkowitz, 1993, Deffenbacher, 1994, Eckhardt & Deffenbacher, 1995 and Kassinove & Sukhodolsky, 1995). While it is important to conceptually distinguish between anger and hostility, most researchers would support a more functional relationship between the two constructs. For example, Suarez and Williams (1989) reported that individuals high and low in trait hostility did not differ on various physiological measurements at rest. When confronted with an anger-arousing laboratory task, however, significant differences between the two groups were noted with individuals high in hostility showing significant excesses in blood pressure and heart rate. Similarly, Fredrickson et al. (2000) found that individuals high in interview-assessed hostility had larger and longer-lasting blood pressure reactivity following laboratory anger induction. Thus, a continued theoretical and measurement-based separation of the constructs of anger and hostility may actually assist researchers in advancing our understanding of how these constructs interact conceptually and practically. In light of equivocal research findings from previous qualitative reviews, and limitations of a previous quantitative review, the purpose of the present study was to quantitatively examine the existing research literature on anger, hostility, and IPV using a more comprehensive search of the literature and a more careful consideration of potential moderating factors. It was hoped that this review would clarify the equivocal results obtained this far and provide much-needed insight concerning the ability of and hostility to differentiate IPV perpetrators from their nonviolent counterparts.