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Anger
C H A P T E R
35 Anger R.W. Novaco University of California, Irvine, CA, USA
O U T L I N E Anger and Stress
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The Experience and Expression of Anger
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Anger Physiology
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Abstract Anger is an affective response to survival threats or otherwise stressful experiences. It is a primary emotion having adaptive functions linked to survival mechanisms that are biological, psychological, and social in nature. Threat perception is intrinsic to its activation, and symbolic structures govern such perception. Cognitive processing of anger-provoking experiences can alternatively prolong or disengage anger. Anger is primed and demarcated by neurophysiological arousal, and, as a high arousal state, anger can constitute an internal stressor, causing wear and tear on the body when it is recurrently activated. Behaviorally, anger is associated with approach motivational systems and can activate aggressive behavior. While anger expression is governed by social rules, it can be part of an antagonistic style of coping with the stressors of daily life, particularly in responding to interpersonal conflict. The role of anger as an activator of violent behavior is interpersonally and societally problematic. Anger dysregulation produces impairment in functioning across life domains and is associated with various psychiatric disorders through transdiagnostic processes, such as selective attention, threat perception, and rumination. The efficacy of psychotherapeutic interventions for anger, principally cognitive-behavioral therapy, is well-established for a wide variety of clinical populations.
ANGER AND STRESS Anger is a negatively toned emotion, subjectively experienced as an aroused state of antagonism toward someone or something perceived to be the source of an aversive event. Prototypically, it is triggered or provoked by events that are perceived to constitute deliberate harm-doing by an instigator toward oneself or toward
Stress: Concepts, Cognition, Emotion, and Behavior http://dx.doi.org/10.1016/B978-0-12-800951-2.00035-2
Anger Dyscontrol: Physical and Psychological Health Problems
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Anger Treatment
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References
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those to whom one is endeared. It can also be a product of goal-blocking or frustrations, particularly when recurrent, or be a reactive response to pain, physical or psychological. Provocations usually take the form of insults, unfair treatments, or intended thwarting. Anger is prototypically experienced as a justified response to some “wrong” that has been done. While anger is situationally triggered by acute, proximal occurrences, it is shaped and facilitated contextually by conditions affecting the cognitive, physiological, and behavioral systems that comprise anger reactions and by social rules that govern anger expression. Anger activation is centrally linked to threat perceptions and to survival responding. Although it is neither necessary nor sufficient for aggression or violence, anger impels aggressive behavior, particularly when its intensity overrides regulatory control mechanisms.1 Clinically problematic anger often has traumatic stress origins. The experience of anger can be prolonged or revivified by cognitive processes, such as rumination, imagery, and symbolic cues, in reciprocal feedback loops with neurological and somatovisceral systems. As anger impels antagonistic action, it can amplify the noxious qualities of the circumstances that have evoked the anger activation, through escalating exchanges of anger and aggressive behavior. The cognitive, physiological, and behavioral bases of anger activation correspondingly provide portals for anger regulating interventions.
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Copyright © 2016 Elsevier Inc. All rights reserved.
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Anger is a primary human emotion, observable in infancy.2 Since the landmark works of Darwin3 and Cannon,4 anger has been understood as an adaptive response to survival threat (danger or pain). Although there are sociocultural variations in the acceptability of its expression and the form that such expression takes,5 in the face of adversity, anger can mobilize psychological resources, energize behaviors for corrective action, and facilitate perseverance. Anger serves as a guardian to self-esteem, operates as a means of communicating negative sentiment, potentiates the ability to redress grievances, and boosts determination to overcome obstacles to our happiness and aspirations. Akin to aggressive behavior, anger has functional value for survival.6 Anger energizes behavior as a high arousal state, increasing the amplitude of responding; it focuses attention on situational elements having threat significance; it expresses or communicates negative sentiment to convey displeasure and to prompt conflict resolution; it defends the self by social distancing and fear suppression, and it also defends self-worth by externalizing attributions of blame for misfortune; it potentiates a sense of personal control or empowerment among social groups as well as individuals; it instigates aggressive behavior due to its survival relevance, symbolic linkages, and learned connections; it signals information about personal state and situational significance which is relevant to self-monitoring; and it dramatizes a social role enactment, in the sense of anger expression being dramaturgy played out in accord with social scripts. Despite having multiple adaptive functions, anger can have maladaptive effects on personal and social wellbeing. Generally, strong physiological arousal impairs the processing of information and lessens cognitive control of behavior. Because heightened physiological arousal is a core component of anger,7 people are not cognitively proficient when they become angry. Also, because the activation of anger is accompanied by aggressive impulses, anger can motivate harm toward other people, which in turn can produce undesirable consequences for the angered person, either from direct retaliation, loss of supportive relationships, or social censure8. An angry person is not optimally alert, thoughtful, empathic, prudent, or physically healthy. Being a turbulent emotion ubiquitous in everyday life, anger is now known to be substantially associated with a range of physical health problems, including stress-related cardiovascular disorders.9,10 Anger is also a symptom of posttraumatic stress disorder (PTSD), and it has high relevance to PTSD derivative of disasters, health traumas, violent crime victimization, and especially to combat or war zone exposure.11 Among combat veterans, anger is a salient postdeployment problem affecting social relationships, job performance, physical health, and violence risk, and it is intensified when PTSD and depression are comorbid.12,13
KEY POINTS • Anger is prototypically experienced as a justified response to some “wrong” that has been done. Its activation is centrally linked to threat perceptions and to survival responding. Although anger has multiple adaptive functions, when its intensity is high and/or prolonged, it can impair social relationships, work performance, and health, as well as propel harmful aggressive behavior. • Whether or not anger has problematic status can be gauged by its frequency, latency, intensity, duration, and mode of expression. High intensity arousal overrides inhibitory controls on aggressive behavior. Rumination about provoking events extends or revivifies anger reactions. • Aversive events or stressful circumstances activate anger through cognitive processes of attention and meaning structures. Anger arousal is marked by activation in the cardiovascular, endocrine, and central nervous systems, and by tension in the skeletal musculature. Anger has evolutionary roots in preparing the organism for attack, including signaling attack readiness so as to ward off opponents or to coerce compliance. In dealing with survival threat, anger serves to suppress fear, pain, and shame. • There are feedback loops between anger's cognitive, physiological, and behavioral systems, along with its environmental triggers. This can involve deviation-amplifying processes, such as the escalation of anger and aggression, or deviation-counteracting processes, such as self-control strategies. • Anger dysregulation appears in a wide range of psychopathologies, as a product of transdiagnostic processes, such as selective attention, threat perception, interpretive bias, rumination, and selfcontrol deficiencies. Perceived malevolence is a common anger-inducing appraisal, invoking anger by externalizing blame and entraining justification. • There is a preponderance of evidence for the efficacy of psychotherapeutic interventions for anger dyscontrol, especially cognitive-behavioral therapies.
THE EXPERIENCE AND EXPRESSION OF ANGER There is a duality of psychosocial images associated with anger experience and anger expression. The
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THE EXPERIENCE AND EXPRESSION OF ANGER
emotional state is depicted as eruptive, destructive, unbridled, savage, venomous, burning, and consuming, but also as energizing, empowering, justifying, signifying, rectifying, and relieving. The metaphors, on the one hand, connote something pressing for expression and utilization, and, alternatively, they imply something requiring containment and control. This duality in psychosocial imagery reflects conflicting intuitions about anger, its expression, and its consequences that abound in ordinary language and are reflected in both scholarly literature and artistic works from the classical period to contemporary times. This Janus-faced character of anger foils attempts to understand it and to therapeutically intervene with recurrently angry individuals. The facial and skeletal musculature is strongly affected by anger, mobilized by a mixture of adrenaline and noradrenaline hormonal secretions. The face becomes flushed, and the brow (corrugator) muscles move inward and downward, fixing a hard stare on the target. The eyes narrow, nostrils flare, and the jaw tends toward clenching. This is an innate pattern of facial expression that can be observed in toddlers,2,14 and angry faces are rapidly detected even when there are distractors.15 Tension in the skeletal musculature, including raising of the arms and adopting a squared-off stance, as well as squaring the jaw, are preparatory actions for attack and defense. The muscle tension provides a sense of strength and selfassurance. An impulse to strike out accompanies this subjective feeling of potency. From an evolutionary perspective, our perceptual system has been shaped to detect angry faces and angry postures rapidly, especially those of angry males. Correspondingly, arousal of anger engages an approach motivational system16 that has survival value for defense or for corrective action. When people report anger experiences, they most typically give accounts of things that have “happened to them.” For the most part, they describe events physically and temporally proximate to their anger arousal. As a rule, they provide accounts of provocations ascribed to events in the immediate situation of the anger experience. This fosters the illusion that anger has a discrete external cause. The provocation sources are ordinarily identified as the aversive and deliberate behavior of others; thus, anger is portrayed in the telling as being something about which anger is quite fitting. People are very much inclined to attribute the causes of their anger to the personal, stable, and controllable aspects of another person's behavior—akin to what is called the “fundamental attribution error” in social psychology. However, the response to the question, “What has made you angry?” hinges on self-observational proficiencies and is often based on intuitions. Precisely because getting angry involves a loss in self-monitoring capacity, people are often neither good nor objective observers when they are angry. Inspecting any particular
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episode, the immediate activators (“causes”) of the anger are readily identifiable. People far less commonly disaggregate their anger experiences into multicausal origins, some of which may be prior, remote events and ambient circumstances, rather than acute, proximal events. Anger experiences are embedded or nested within an environmental-temporal context. Disturbances that may not have involved anger at the outset leave residues that are not readily recognized but which operate as a lingering backdrop for focal provocations. Anger, as an approach motivation system affect, is inherently a disposition to respond aggressively, but aggressive behavior is not an automatic consequence of anger, as it is regulated by inhibitory control mechanisms, engaged by internal and external cues.1,17 In this regard, physical constraints, expectations of punishment or retaliation, empathy, consideration of consequences, and prosocial values operate as regulatory controls on aggression. While the experience of anger creates a readiness to respond with aggression, that disposition may be otherwise directed, suppressed, or reconstituted. Thus, the expression of anger is differentiated from its experience. One aspect of anger that influences the probability of aggression is its degree of intensity. The higher the level of arousal, the stronger the motivation for aggression, and the greater the likelihood that inhibitory controls will be overridden.18 Strong arousal not only impels action, it impairs cognitive processing of aggression-mitigating information. A person in a state of high anger arousal is perceptually biased toward the confirmation of threat, is less able to attend to threat-discounting elements of the situation, and is not so capable of reappraising provocation cues as benign. Because anger and aggression occur in a dynamic interactional context, the occurrence of aggression will, in turn, influence the level of anger. Thus, anger reactivity can be seen as a mode of responding characterized by automaticity, high intensity, and short latency. An important aspect of the dynamic interrelation of anger and aggression is the escalation of provocation. Escalation involves increases away from equilibrium, whereby succeeding events intensify their own precursors. In the case of anger and aggression, escalation refers to incremental change in their respective probabilities, occurring as reciprocally heightened antagonism in an interpersonal exchange. The consumption of alcohol can further amplify this process. Anger-elicited aggression may evoke intensified anger in response, thus progressively generating justification for retaliation. A model of the neural organization of the escalation of both anger and aggression has been formulated by Potegal.19 When physical aggression is deployed by an angry person against the anger instigator, and there is no
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retaliation, anger arousal and subsequent aggression are then diminished in that situation. Konecni20 called this the “cathartic effect,” and its conditions should not be confused (as they often are) with those involving aggression by nonangry people, vicarious or observed aggression, or aggression not received by the anger-instigator. Such nonqualifying conditions are often prevalent in social psychology laboratory studies of catharsis as “venting,”21 which moreover do not ecologically map onto the clinical contexts in which anger catharsis might be encouraged (i.e., in clinical implementation, catharsis is a substitute and preventive for harm-doing and the client returns for subsequent therapy visits). However, the arousal-reducing cathartic effect of aggression carried out by angry people against those who have made them angry does reinforce aggressive behavior. This means that when anger is reinstated by a new provocation, the likelihood of aggressive behavior is increased. The cathartic expression of anger, whether through destructive aggression or through verbal communication intended to be constructive, can be understood as an organismic action to restore equilibrium. Alternative to the deliberate expression of anger is suppression, which is largely a product of inhibitory controls, and which is often discussed in the larger context of “emotion regulation.” While suppression, as a habitual coping strategy has adverse consequences,22 anger suppression can be quite functional in promoting interpersonal or social conciliation, and diminishing the likelihood of triggering a physical assault. Whether in a domestic, occupational, or street context, anger is adaptively muffled when physical retaliation can be expected or when a cool head is needed to solve a problem. Depending on the context, suppressing even the verbalization of anger may not only be beneficial interpersonally, it may also serve to regulate physiological reactivity levels. However, recurrent deployment of anger suppression as a stress-coping style will likely have deleterious effects on cardiovascular health.9 The suppression of anger, as a customary mode, is associated with rumination, which can lead to prolonged anger, cognitive perseveration, aggressive behavior, and heightened sympathetic nervous system activation.21,23 Because anger and aggression are thought to be differentially socialized for males and females, the question of gender differences in the experience and expression of anger arises. It has generally been found that the anger of women is comparable to that of men from the standpoint of experienced intensity.5,24 An exception is that women in prison/correctional settings report higher anger than do men.25 Style of anger expression does vary by gender, especially according to the context of anger activation and its anticipated consequences. Males are more likely to be angered in a public place or by impersonal triggers, whereas females are more likely to be
angered at home or by being let down by someone close to them. Females are more likely to become angered by verbal aggression and insensitive/condescending behavior, and males more likely to be angered by behavior causing physical harm. Men, when angered, are more inclined to use physical aggression than women, who in turn are more likely to fear aggressive retaliation. On the other hand, a number of studies have found that, compared to women, anger suppression among men, especially those at risk for hypertension, is associated with higher blood pressure reactivity.26 At a more aggregate social level, anger has a pivotal role in the general strain theory of Agnew27 to account for criminal conduct and delinquency, especially aggressive behavior. This sociological theory is convergent with psychological conceptions.1 Strain occurs when people are prevented from achieving goals, lose valued possessions, and are exposed to noxious stimuli. Strain results in negative affect, which creates pressure for corrective action, but anger has superordinate value. Anger is considered the crucial emotion, as it is produced by strain when others are blamed for personal adversity, it increases the sense of being injured or wronged, and it creates a motivation for retaliation or revenge, energizes action, and lowers inhibitory control. Many large sample studies have supported Agnew's theory with multifaceted life stress measures and finding a mediation effect of anger on aggression.28
ANGER PHYSIOLOGY A defining condition of anger is physiological arousal, the activation of which has evolutionary roots, as anger serves to mobilize us to response energetically and to sustain effort. The “flight-or-fight” response4 refers to this hard-wired physiological mechanism that is triggered instantaneously to engage survival behavior, to focus attention on the survival threat, and to enable the organism to not succumb to fear, pain, or shame. Anger is the emotional complement of the organismic preparation for attack, which also entails the orchestration of signals of attack readiness so as to ward off opponents or to coerce compliance. The latter has been conceptualized in an evolutionary perspective in terms of a formidability posture to induce an opponent to recalibrate the “welfare tradeoff ratio.”29 The arousal of anger is marked by activation in the cardiovascular, endocrine, and limbic systems, as well as other autonomic and central nervous system areas, and by tension in the skeletal musculature. The autonomic signature of anger corresponds to a mixture of adrenaline and noradrenaline. Autonomic system arousal, especially cardiovascular, has been commonly observed in conjunction with anger by scholars from
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the classical age (such as Seneca, Aristotle, and Plutarch) to the early behavioral scientists of the nineteenth and twentieth centuries (especially Charles Darwin, William James, G. Stanley Hall, and Walter B. Cannon). Laboratory research has reliably found anger arousal to entail increases in both systolic and diastolic blood pressure, in respiration, heart rate, and skin conductance responses. It is differentiated from fear by a stronger increase in diastolic pressure, in muscle tension (electromyogram recordings), in total peripheral resistance, and in facial temperature, the latter associated with facial flushing, often reported by people reflecting on their anger experience. The sensation of anger is highly correlated with anger's physiological profile.7 In terms of psychosocial imagery, there is no better metaphor for anger than hot fluid in a container. Autonomic arousal is primarily engaged through adrenomedullary and adrenocortical hormonal activity. In anger, the catecholamine activation is more strongly noradrenaline than adrenaline (the reverse being the case for fear). The adrenocortical effects, which have longer duration than the adrenomedullary ones, are mediated by secretions of the pituitary gland, which also influences testosterone levels. The pituitary-adrenocortical and pituitary-gonadal systems are thought to affect readiness or potentiation for anger responding. Testosterone provides vigor and reduces fear. A number of central nervous system structures have been identified in anger activation, most prominently the amygdala, the almond-shaped, limbic system component located deep in the temporal lobe that is well-established for its activation in threat-detection, its association with trauma, and anger-activated aggressive behavior.30,31 Activation in the amygdala has been found to be associated with anger and attack priming. Interconnections with the ventromedial and orbital frontal cortex, which are recruited during anger states, serve to regulate behavior and mediate how anger affects aggressive responding.32 The amygdala is the key site for aversive motivational system, and it has been thought that anger is derived from that system, as it is a negatively valenced emotion that is evoked by aversive experiences. Similarly, anger is conjectured to be a product of a defensive, “rage system.”33 However, anger has also been linked with asymmetric left-prefrontal cortical activity, which has typically been associated with positive affect and approach motivation.16,34 Although the complexities of the neuropsychological and psychophysiological processing of anger seem to be far from straightforward, particularly how it might bear on psychopathology,35 Potegal and Stemmler32 have put forward a neuroanatomical conjecture about the dynamics of anger involving the amygdala, temporal lobe, and the ventromedial and orbital frontal cortex.
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The central nervous system neurotransmitter serotonin, which is also present in blood platelets, affects anger potentiation, as low levels of this hormone are associated with irritable mood, as are functional polymorphisms in serotonin receptor genes.36 Serotonin imbalances are related to deficits in the modulation of emotion. While serotonin and other neurotransmitters (noradrenaline and dopamine) are involved in anger activation, the neural structures and circuitry in anger dysregulation and aggressive behavior remain to be disentangled. These various physiological mechanisms pertain not only to the intensity of anger arousal but also its duration. Arousal activation eventually decays to baseline levels, but recovery time may be prolonged by exposure to new arousal sources or by rumination. The potency of a provocation may be heightened by the carryover of undissipated excitation from a prior arousal source, which may not have been anger-specific (i.e., an otherwise stressful circumstance, such as exposure to bad news, work pressure, or traffic congestion). This “excitation transfer” of arousal residues facilitates anger, augments its intensity, amplifies blood pressure, and raises the probability of aggression.18 Residual arousal from unresolved anger events can transfer to future conflicts and further intensify anger reactivity to instigating events. In turn, unexpressed anger is associated with exaggerated and more prolonged cardiovascular responses to a variety of stressful stimuli. In this regard, a stress framework is highly useful. Both acute and prolonged exposure to common stressors (e.g., noise, crowding, difficult tasks, and high-pressure job environments filled with time demands, or exposure to abrasive interactions) may induce physiological activation that decays slowly. When someone experiences an event that pulls for the cognitive label “anger,” and this event occurs concurrently with already elevated arousal, the anger system is then more easily engaged.
ANGER DYSCONTROL: PHYSICAL AND PSYCHOLOGICAL HEALTH PROBLEMS Anger is a highly functional human emotion and is to be appreciated as a rich part of cultural life, but the survival value of the aggression-enabling function of anger is an archaic remnant with rare contemporary necessity. Outside of warfare, the survival challenges presented by civilized society are predominantly psychological, rather than physical. Effective coping with the demands of modern life requires understanding complex information, problem-solving, and prudent action, not energized rapid responding. Even in emergency situations, anger requires regulation. Contrary to intuitions, anger can be detrimental to survival in a physical threat crisis. It is counterproductive for energy conservation in a prolonged fight, for monitoring additional threat elements
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and hazards, and for effective strategy selection in circumstances where survival threat lingers and/or remains obscure. The regulation of the intensity and duration of anger arousal is pivotal to its merit or utility. To get angry about something, one must pay attention to it. Anger is often the result of selective attention to cues having high provocation value. A principal function of cognitive systems is to guide behavior, and attention itself is guided by integrated cognitive structures, known as schemas, which incorporate rules about environmentbehavior relationships. What receives attention is a product of the cognitive network that assigns meaning to events and the complex stimuli that configure them. The appraisal process is in the seeing and the hearing, not something tandem to the perception, and it is an ongoing process. Expectations guide attentional search for cues relevant to particular needs or goals. Once a repertoire of anger schemas has been developed, events (e.g., being asked a question by someone) and their characteristics (e.g., the way the question was asked, when it was asked, or who asked it) are encoded or interpreted as having meaning in accord with the preexisting schema. Rumination about provoking events extends or revivifies anger reactions. Because of their survival function, the threat-sensing aspect of anger schemas carries urgent priority and can preempt other information processing. Perceived malevolence is one of the most common forms of anger-inducing appraisal. It pulls for anger by involving the externalization of blame and the theme of justification. That, in turn, engages social norms of retaliation and retribution. Averill's view of anger is that it is a socially constituted syndrome or a transitory social role governed by social rules.5 While anger and physical aggression may be viewed as applying a legitimate punitive response for transgression or as ways of correcting injustice, justifications can be embellished to serve the exoneration of blame for destructive outcomes of expressed anger. Physiological components of anger, such as increased blood flow, may be adaptive for survival in a short-term danger episode, but the byproducts of recurrent engagement of anger are hazardous in the long term. Unregulated anger is associated with physical and psychological health impairments, including detrimental effects on the cardiovascular system bearing on mortality.9 Persons who are reactively angry are at considerable risk for coronary heart disease. An angry, hostile, and distrusting outlook necessitates high vigilance for thwarting and malevolence, resulting in prolonged neurohormonal activation conducive to atherosclerosis. In addition to these pathogenic effects for a personality style that is overly expressive of anger, the coronary system is also impaired by recurrently suppressed anger, long identified as a causal variable in the etiology of essential hypertension. People having difficulties expressing anger tend to be at risk for chronically
elevated blood pressure, as mediated by high plasma renin activity and norepinephrine. The suppression of anger has been robustly correlated to elevated blood pressure and greater cardiovascular reactivity to provocation in laboratory studies and to sustained hypertension in field studies. Anger suppression also amplifies pain sensitivity.37 With regard to psychological well-being, anger occurs in conjunction with a wide range of psychiatrically classified disorders, emerging in conjunction with the emotional instability attributes of personality disorders, irritability and “attacks” in mood disorders, delusions and command hallucinations in psychotic disorders (especially paranoid schizophrenia), impulse control disorders, intellectual disabilities, dementia, substance abuse disorders, and exotic cultural-bound syndromes.38,39 As anger often results from trauma, it can be salient in PTSD, affecting the severity and course of PTSD symptoms, and it is associated with major adjustment problems for military veterans.12,13 The central quality of anger in the broad context of clinical disorders is dysregulation—its activation, expression, and experience occur without appropriate controls. Transdiagnostic processes of threat perception, selective attention, interpretative bias, confirmation bias, rumination, and self-control deficits are involved. Among hospitalized psychiatric patients in long-term care in both civil commitment and forensic institutions, anger is a pervasive problem, as identified by both clinical staff and by the patients themselves. Studies with multiple control variables show anger to be related to the violent behavior of psychiatric patients before, during, and after hospitalization and to physical aggression within institutions by incarcerated adults.40 Anger is not only an important clinical need among many psychiatric and custodial populations, it also bears on the therapeutic milieu and on the wellbeing of clinical and custodial staff. Anger dysregulated people often have traumatic life histories, replete with experiences of abandonment and rejection, as well as economic and psychological impoverishment. For them, anger becomes entrenched as a mode of reactance to stressful or aversive experiences. Chronically angry people are reluctant to surrender the anger-aggression system that they have found useful to engage, because they discount the costs of its engagement.
ANGER TREATMENT The first step in the provision of therapeutic intervention for anger is facilitating client “readiness” for anger treatment, which can be very challenging due to client background adversities, multifaceted clinical comorbidities, and resource limitations in facilities where treatment might be implemented.41 Nevertheless, there is
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REFERENCES
substantial evidence for the efficacy of anger treatment. Nine meta-analyses on the effectiveness of psychotherapy for anger have been published, involving a wide range of clinical populations, which overall have found medium to strong effect sizes, indicating that approximately 75% of those receiving anger treatment improved compared to controls. Cognitive behavioral therapy (CBT) approaches have greatest efficacy in reducing anger, and now with encouraging evidence for reducing physically assaultive behavior in hospital.42 CBT approaches incorporate training in self-monitoring, relaxation, and social skills, but centrally seek to modify cognitive structures and the way a person processes information about social situations. They strongly emphasize self-regulation, cognitive flexibility in appraising situations, arousal control, and learning prosocial values and scripts. Making extensive use of therapist modeling and client rehearsal, anger proneness is modified by first motivating client engagement and then restructuring cognitive schemas, increasing capacity to regulate arousal and facilitating the use of constructive coping behaviors. Priority is given to self-regulatory controls of anger activation. The parameters or state markers for anger activation that receive attention in CBT anger treatment are: reactivity (frequency on onset and how easily anger is triggered); latency (how rapidly activated); intensity (how strongly engaged), and duration (persistence of arousal). Treatment aims to minimize anger reactivity, intensity, and duration and to moderate anger expression to reduce the costs of anger dyscontrol. To facilitate anger regulation, anger treatment procedures strive to disconnect anger from the threat system. This is done first through the provision of safety, patience, and psychological space for reflection, exploration, and choice. The client's view of anger is normalized, to obviate worries about being a “bad” or unworthy person. The therapist will acknowledge the legitimacy of the client's feelings, affirming his or her self-worth. Building trust in the therapeutic relationship is pivotal. As self-regulation hinges on knowledge, education about anger and discovery of the client's personal anger patterns or “anger signature” is facilitated. Much is done to augment selfmonitoring and to encourage the moderation of anger intensity. The therapist models and reinforces nonanger alternative responding so as to build replacements for the automatized angry reactions that had been the client's default coping style. One CBT approach to anger treatment that has received significant support for its efficacy is called “stress inoculation” (SI). In this treatment approach, anger provocation is simulated by therapeutically paced progressive exposure to anger incidents created in imaginal visualization and in role play, based on a hierarchy of anger incidents produced by the collaborative work of client and therapist. This graduated, hierarchical exposure is the
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basis for the “inoculation” metaphor. The SI involves the following key components: (1) client education about anger, stress, and aggression; (2) self-monitoring of anger frequency, intensity, and situational triggers; (3) construction of a personal anger provocation hierarchy, created from the self-monitoring data; (4) arousal reduction techniques of progressive muscle relaxation, breathingfocused relaxation, and guided imagery training; (5) cognitive restructuring by altering attentional focus, modifying appraisals, and using self-instruction; (6) training behavioral coping in communication and respectful assertiveness as modeled and rehearsed with the therapist; and (7) practicing the cognitive, arousal regulatory, and behavioral coping skills while visualizing and role playing progressively more intense anger-arousing scenes from the personal hierarchies. While therapeutic mechanisms underlying anger treatment gains are not clear, nor are their sustainability or generalizability, the field is fortified by the evidence base and continues to seek advances in providing remedies for anger dyscontrol.
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15. Pinkham AE, Griffin M, Baron R, Sasson NJ, Gur RC. The face in the crowd effect: anger superiority when using real faces and multiple identities. Emotion. 2010;10:141–146. 16. Carver CS, Harmon-Jones E. Anger is an approach-related affect: evidence and implications. Psychol Bull. 2009;135:183–204. 17. Bandura A. Psychological mechanisms in aggression. In: Geen R, Donnerstein E, eds. Aggression: Theoretical and Empirical Reviews. New York, NY: Academic Press; 1983:1–40. 18. Zillmann D. Cognition-excitation interdependencies in aggressive behavior. Aggress Behav. 1988;14:51–64. 19. Potegal M. Temporal and frontal lobe initiation and regulation of the top-down escalation of anger and aggression. Behav Brain Res. 2012;231:386–395. 20. Konecni VJ. Annoyance, type, and duration of postannoyance activity, and aggression: “The cathartic effect” J Exp Psychol Gen. 1975;104:76–102. 21. Bushman B. Does venting anger feed or extinguish the flame? Catharsis, rumination, distraction, anger, and aggressive responding. Pers Soc Psychol Bull. 2002;28:724–731. 22. Gross JJ, John OP. Individual differences in two emotion regulation processed: implications for affect, relationships, and well-being. J Pers Soc Psychol. 2003;85:348–362. 23. Ray RD, Wilhelm FH, Gross JJ. All in the mind's eye? Anger rumination and reappraisal. J Pers Soc Psychol. 2008;94:133–145. 24. Archer J. Sex differences in aggression in real-world settings: a metaanalytic review. Rev Gen Psychol. 2004;8:291–322. 25. Suter JM, Byrne MK, Byrne S, Howells K, Day A. Anger in prisoners: women are different from men. Pers Individ Dif. 2002;32:1087–1100. 26. Vogele C, Jarvis A, Cheeseman K. Anger suppression, reactivity, and hypertension risk: gender makes a difference. Ann Behav Med. 1997;19:61–69. 27. Agnew R. Foundation for a general strain theory of crime and delinquency. Criminology. 1992;30:47–86. 28. Aseltine RH, Gore S, Gordon J. Life stress, anger and anxiety, and delinquency: an empirical test of general strain theory. J Health Soc Behav. 2000;41:256–275.
29. Sell A, Tooby J, Cosmides L. Formidability and logic of human anger. Proc Natl Acad Sci U S A. 2009;106:15073–15078. 30. Davidson RJ. Dysfunction in the neural circuitry of emotion regulation—a possible prelude to violence. Science. 2000;289:591–594. 31. Blair RJR. Considering anger from a cognitive neuroscience perspective. Wiley Interdiscip Rev Cogn Sci. 2012;3:65–74. 32. Potegal M, Stemmler G. Constructing a neurology of anger. In: Potegal M, Stemmler G, Spielberger C, eds. International Handbook of Anger. New York, NY: Springer; 2010:39–59. 33. Panksepp J, Zellner MR. Towards a neurobiologically based unified theory of aggression. Rev Int Psychol Soc. 2004;17:37–61. 34. Harmon-Jones E, Gable PA, Peterson CK. The role of asymmetric frontal cortical activity in emotion-related phenomena: a review and update. Biol Psychiatry. 2010;84:451–461. 35. Dougherty DD, Shin LM, Alpert NM, et al. Anger in healthy men: a PET study using script-driven imagery. Biol Psychiatry. 1999;46:466–472. 36. Conner TS, Jensen KP, Tennen H, Furneaux HM, Kranzler HR, Covault J. Functional polymorphisms in the serotonin 1B receptor gene [HTR1B] predict self-reported anger and hostility among young men. Am J Med Genet B. 2010;153B:67–78. 37. Quartana PJ, Burns JW. Painful consequences of anger suppression. Emotion. 2007;7:400–414. 38. Novaco RW. Anger and psychopathology. In: Potegal M, Stemmler G, Spielberger C, eds. International Handbook of Anger. New York, NY: Springer; 2010:465–497. 39. DiGuiseppe R, Tafrate RC. Understanding Anger Disorders. New York, NY: Oxford University Press; 2007. 40. Novaco RW. Anger dysregulation: driver of violent offending. J Forensic Psychiatry Psychol. 2011;22:650–668. 41. Howells K, Day A. Readiness for anger management: clinical and theoretical issues. Clin Psychol Rev. 2003;23:319–337. 42. Novaco RW, Taylor JL. Reduction of assaultive behavior following anger treatment of forensic hospital patients with intellectual disabilities. Behav Res Ther. 2015;65:52–59.
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35 Anger R.W. Novaco University of California, Irvine, CA, USA
O U T L I N E Anger and Stress
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The Experience and Expression of Anger
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Anger Physiology
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Abstract Anger is an affective response to survival threats or otherwise stressful experiences. It is a primary emotion having adaptive functions linked to survival mechanisms that are biological, psychological, and social in nature. Threat perception is intrinsic to its activation, and symbolic structures govern such perception. Cognitive processing of anger-provoking experiences can alternatively prolong or disengage anger. Anger is primed and demarcated by neurophysiological arousal, and, as a high arousal state, anger can constitute an internal stressor, causing wear and tear on the body when it is recurrently activated. Behaviorally, anger is associated with approach motivational systems and can activate aggressive behavior. While anger expression is governed by social rules, it can be part of an antagonistic style of coping with the stressors of daily life, particularly in responding to interpersonal conflict. The role of anger as an activator of violent behavior is interpersonally and societally problematic. Anger dysregulation produces impairment in functioning across life domains and is associated with various psychiatric disorders through transdiagnostic processes, such as selective attention, threat perception, and rumination. The efficacy of psychotherapeutic interventions for anger, principally cognitive-behavioral therapy, is well-established for a wide variety of clinical populations.
ANGER AND STRESS Anger is a negatively toned emotion, subjectively experienced as an aroused state of antagonism toward someone or something perceived to be the source of an aversive event. Prototypically, it is triggered or provoked by events that are perceived to constitute deliberate harm-doing by an instigator toward oneself or toward
Stress: Concepts, Cognition, Emotion, and Behavior http://dx.doi.org/10.1016/B978-0-12-800951-2.00035-2
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Anger Treatment
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those to whom one is endeared. It can also be a product of goal-blocking or frustrations, particularly when recurrent, or be a reactive response to pain, physical or psychological. Provocations usually take the form of insults, unfair treatments, or intended thwarting. Anger is prototypically experienced as a justified response to some “wrong” that has been done. While anger is situationally triggered by acute, proximal occurrences, it is shaped and facilitated contextually by conditions affecting the cognitive, physiological, and behavioral systems that comprise anger reactions and by social rules that govern anger expression. Anger activation is centrally linked to threat perceptions and to survival responding. Although it is neither necessary nor sufficient for aggression or violence, anger impels aggressive behavior, particularly when its intensity overrides regulatory control mechanisms.1 Clinically problematic anger often has traumatic stress origins. The experience of anger can be prolonged or revivified by cognitive processes, such as rumination, imagery, and symbolic cues, in reciprocal feedback loops with neurological and somatovisceral systems. As anger impels antagonistic action, it can amplify the noxious qualities of the circumstances that have evoked the anger activation, through escalating exchanges of anger and aggressive behavior. The cognitive, physiological, and behavioral bases of anger activation correspondingly provide portals for anger regulating interventions.
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Anger is a primary human emotion, observable in infancy.2 Since the landmark works of Darwin3 and Cannon,4 anger has been understood as an adaptive response to survival threat (danger or pain). Although there are sociocultural variations in the acceptability of its expression and the form that such expression takes,5 in the face of adversity, anger can mobilize psychological resources, energize behaviors for corrective action, and facilitate perseverance. Anger serves as a guardian to self-esteem, operates as a means of communicating negative sentiment, potentiates the ability to redress grievances, and boosts determination to overcome obstacles to our happiness and aspirations. Akin to aggressive behavior, anger has functional value for survival.6 Anger energizes behavior as a high arousal state, increasing the amplitude of responding; it focuses attention on situational elements having threat significance; it expresses or communicates negative sentiment to convey displeasure and to prompt conflict resolution; it defends the self by social distancing and fear suppression, and it also defends self-worth by externalizing attributions of blame for misfortune; it potentiates a sense of personal control or empowerment among social groups as well as individuals; it instigates aggressive behavior due to its survival relevance, symbolic linkages, and learned connections; it signals information about personal state and situational significance which is relevant to self-monitoring; and it dramatizes a social role enactment, in the sense of anger expression being dramaturgy played out in accord with social scripts. Despite having multiple adaptive functions, anger can have maladaptive effects on personal and social wellbeing. Generally, strong physiological arousal impairs the processing of information and lessens cognitive control of behavior. Because heightened physiological arousal is a core component of anger,7 people are not cognitively proficient when they become angry. Also, because the activation of anger is accompanied by aggressive impulses, anger can motivate harm toward other people, which in turn can produce undesirable consequences for the angered person, either from direct retaliation, loss of supportive relationships, or social censure8. An angry person is not optimally alert, thoughtful, empathic, prudent, or physically healthy. Being a turbulent emotion ubiquitous in everyday life, anger is now known to be substantially associated with a range of physical health problems, including stress-related cardiovascular disorders.9,10 Anger is also a symptom of posttraumatic stress disorder (PTSD), and it has high relevance to PTSD derivative of disasters, health traumas, violent crime victimization, and especially to combat or war zone exposure.11 Among combat veterans, anger is a salient postdeployment problem affecting social relationships, job performance, physical health, and violence risk, and it is intensified when PTSD and depression are comorbid.12,13
KEY POINTS • Anger is prototypically experienced as a justified response to some “wrong” that has been done. Its activation is centrally linked to threat perceptions and to survival responding. Although anger has multiple adaptive functions, when its intensity is high and/or prolonged, it can impair social relationships, work performance, and health, as well as propel harmful aggressive behavior. • Whether or not anger has problematic status can be gauged by its frequency, latency, intensity, duration, and mode of expression. High intensity arousal overrides inhibitory controls on aggressive behavior. Rumination about provoking events extends or revivifies anger reactions. • Aversive events or stressful circumstances activate anger through cognitive processes of attention and meaning structures. Anger arousal is marked by activation in the cardiovascular, endocrine, and central nervous systems, and by tension in the skeletal musculature. Anger has evolutionary roots in preparing the organism for attack, including signaling attack readiness so as to ward off opponents or to coerce compliance. In dealing with survival threat, anger serves to suppress fear, pain, and shame. • There are feedback loops between anger's cognitive, physiological, and behavioral systems, along with its environmental triggers. This can involve deviation-amplifying processes, such as the escalation of anger and aggression, or deviation-counteracting processes, such as self-control strategies. • Anger dysregulation appears in a wide range of psychopathologies, as a product of transdiagnostic processes, such as selective attention, threat perception, interpretive bias, rumination, and selfcontrol deficiencies. Perceived malevolence is a common anger-inducing appraisal, invoking anger by externalizing blame and entraining justification. • There is a preponderance of evidence for the efficacy of psychotherapeutic interventions for anger dyscontrol, especially cognitive-behavioral therapies.
THE EXPERIENCE AND EXPRESSION OF ANGER There is a duality of psychosocial images associated with anger experience and anger expression. The
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emotional state is depicted as eruptive, destructive, unbridled, savage, venomous, burning, and consuming, but also as energizing, empowering, justifying, signifying, rectifying, and relieving. The metaphors, on the one hand, connote something pressing for expression and utilization, and, alternatively, they imply something requiring containment and control. This duality in psychosocial imagery reflects conflicting intuitions about anger, its expression, and its consequences that abound in ordinary language and are reflected in both scholarly literature and artistic works from the classical period to contemporary times. This Janus-faced character of anger foils attempts to understand it and to therapeutically intervene with recurrently angry individuals. The facial and skeletal musculature is strongly affected by anger, mobilized by a mixture of adrenaline and noradrenaline hormonal secretions. The face becomes flushed, and the brow (corrugator) muscles move inward and downward, fixing a hard stare on the target. The eyes narrow, nostrils flare, and the jaw tends toward clenching. This is an innate pattern of facial expression that can be observed in toddlers,2,14 and angry faces are rapidly detected even when there are distractors.15 Tension in the skeletal musculature, including raising of the arms and adopting a squared-off stance, as well as squaring the jaw, are preparatory actions for attack and defense. The muscle tension provides a sense of strength and selfassurance. An impulse to strike out accompanies this subjective feeling of potency. From an evolutionary perspective, our perceptual system has been shaped to detect angry faces and angry postures rapidly, especially those of angry males. Correspondingly, arousal of anger engages an approach motivational system16 that has survival value for defense or for corrective action. When people report anger experiences, they most typically give accounts of things that have “happened to them.” For the most part, they describe events physically and temporally proximate to their anger arousal. As a rule, they provide accounts of provocations ascribed to events in the immediate situation of the anger experience. This fosters the illusion that anger has a discrete external cause. The provocation sources are ordinarily identified as the aversive and deliberate behavior of others; thus, anger is portrayed in the telling as being something about which anger is quite fitting. People are very much inclined to attribute the causes of their anger to the personal, stable, and controllable aspects of another person's behavior—akin to what is called the “fundamental attribution error” in social psychology. However, the response to the question, “What has made you angry?” hinges on self-observational proficiencies and is often based on intuitions. Precisely because getting angry involves a loss in self-monitoring capacity, people are often neither good nor objective observers when they are angry. Inspecting any particular
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episode, the immediate activators (“causes”) of the anger are readily identifiable. People far less commonly disaggregate their anger experiences into multicausal origins, some of which may be prior, remote events and ambient circumstances, rather than acute, proximal events. Anger experiences are embedded or nested within an environmental-temporal context. Disturbances that may not have involved anger at the outset leave residues that are not readily recognized but which operate as a lingering backdrop for focal provocations. Anger, as an approach motivation system affect, is inherently a disposition to respond aggressively, but aggressive behavior is not an automatic consequence of anger, as it is regulated by inhibitory control mechanisms, engaged by internal and external cues.1,17 In this regard, physical constraints, expectations of punishment or retaliation, empathy, consideration of consequences, and prosocial values operate as regulatory controls on aggression. While the experience of anger creates a readiness to respond with aggression, that disposition may be otherwise directed, suppressed, or reconstituted. Thus, the expression of anger is differentiated from its experience. One aspect of anger that influences the probability of aggression is its degree of intensity. The higher the level of arousal, the stronger the motivation for aggression, and the greater the likelihood that inhibitory controls will be overridden.18 Strong arousal not only impels action, it impairs cognitive processing of aggression-mitigating information. A person in a state of high anger arousal is perceptually biased toward the confirmation of threat, is less able to attend to threat-discounting elements of the situation, and is not so capable of reappraising provocation cues as benign. Because anger and aggression occur in a dynamic interactional context, the occurrence of aggression will, in turn, influence the level of anger. Thus, anger reactivity can be seen as a mode of responding characterized by automaticity, high intensity, and short latency. An important aspect of the dynamic interrelation of anger and aggression is the escalation of provocation. Escalation involves increases away from equilibrium, whereby succeeding events intensify their own precursors. In the case of anger and aggression, escalation refers to incremental change in their respective probabilities, occurring as reciprocally heightened antagonism in an interpersonal exchange. The consumption of alcohol can further amplify this process. Anger-elicited aggression may evoke intensified anger in response, thus progressively generating justification for retaliation. A model of the neural organization of the escalation of both anger and aggression has been formulated by Potegal.19 When physical aggression is deployed by an angry person against the anger instigator, and there is no
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retaliation, anger arousal and subsequent aggression are then diminished in that situation. Konecni20 called this the “cathartic effect,” and its conditions should not be confused (as they often are) with those involving aggression by nonangry people, vicarious or observed aggression, or aggression not received by the anger-instigator. Such nonqualifying conditions are often prevalent in social psychology laboratory studies of catharsis as “venting,”21 which moreover do not ecologically map onto the clinical contexts in which anger catharsis might be encouraged (i.e., in clinical implementation, catharsis is a substitute and preventive for harm-doing and the client returns for subsequent therapy visits). However, the arousal-reducing cathartic effect of aggression carried out by angry people against those who have made them angry does reinforce aggressive behavior. This means that when anger is reinstated by a new provocation, the likelihood of aggressive behavior is increased. The cathartic expression of anger, whether through destructive aggression or through verbal communication intended to be constructive, can be understood as an organismic action to restore equilibrium. Alternative to the deliberate expression of anger is suppression, which is largely a product of inhibitory controls, and which is often discussed in the larger context of “emotion regulation.” While suppression, as a habitual coping strategy has adverse consequences,22 anger suppression can be quite functional in promoting interpersonal or social conciliation, and diminishing the likelihood of triggering a physical assault. Whether in a domestic, occupational, or street context, anger is adaptively muffled when physical retaliation can be expected or when a cool head is needed to solve a problem. Depending on the context, suppressing even the verbalization of anger may not only be beneficial interpersonally, it may also serve to regulate physiological reactivity levels. However, recurrent deployment of anger suppression as a stress-coping style will likely have deleterious effects on cardiovascular health.9 The suppression of anger, as a customary mode, is associated with rumination, which can lead to prolonged anger, cognitive perseveration, aggressive behavior, and heightened sympathetic nervous system activation.21,23 Because anger and aggression are thought to be differentially socialized for males and females, the question of gender differences in the experience and expression of anger arises. It has generally been found that the anger of women is comparable to that of men from the standpoint of experienced intensity.5,24 An exception is that women in prison/correctional settings report higher anger than do men.25 Style of anger expression does vary by gender, especially according to the context of anger activation and its anticipated consequences. Males are more likely to be angered in a public place or by impersonal triggers, whereas females are more likely to be
angered at home or by being let down by someone close to them. Females are more likely to become angered by verbal aggression and insensitive/condescending behavior, and males more likely to be angered by behavior causing physical harm. Men, when angered, are more inclined to use physical aggression than women, who in turn are more likely to fear aggressive retaliation. On the other hand, a number of studies have found that, compared to women, anger suppression among men, especially those at risk for hypertension, is associated with higher blood pressure reactivity.26 At a more aggregate social level, anger has a pivotal role in the general strain theory of Agnew27 to account for criminal conduct and delinquency, especially aggressive behavior. This sociological theory is convergent with psychological conceptions.1 Strain occurs when people are prevented from achieving goals, lose valued possessions, and are exposed to noxious stimuli. Strain results in negative affect, which creates pressure for corrective action, but anger has superordinate value. Anger is considered the crucial emotion, as it is produced by strain when others are blamed for personal adversity, it increases the sense of being injured or wronged, and it creates a motivation for retaliation or revenge, energizes action, and lowers inhibitory control. Many large sample studies have supported Agnew's theory with multifaceted life stress measures and finding a mediation effect of anger on aggression.28
ANGER PHYSIOLOGY A defining condition of anger is physiological arousal, the activation of which has evolutionary roots, as anger serves to mobilize us to response energetically and to sustain effort. The “flight-or-fight” response4 refers to this hard-wired physiological mechanism that is triggered instantaneously to engage survival behavior, to focus attention on the survival threat, and to enable the organism to not succumb to fear, pain, or shame. Anger is the emotional complement of the organismic preparation for attack, which also entails the orchestration of signals of attack readiness so as to ward off opponents or to coerce compliance. The latter has been conceptualized in an evolutionary perspective in terms of a formidability posture to induce an opponent to recalibrate the “welfare tradeoff ratio.”29 The arousal of anger is marked by activation in the cardiovascular, endocrine, and limbic systems, as well as other autonomic and central nervous system areas, and by tension in the skeletal musculature. The autonomic signature of anger corresponds to a mixture of adrenaline and noradrenaline. Autonomic system arousal, especially cardiovascular, has been commonly observed in conjunction with anger by scholars from
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the classical age (such as Seneca, Aristotle, and Plutarch) to the early behavioral scientists of the nineteenth and twentieth centuries (especially Charles Darwin, William James, G. Stanley Hall, and Walter B. Cannon). Laboratory research has reliably found anger arousal to entail increases in both systolic and diastolic blood pressure, in respiration, heart rate, and skin conductance responses. It is differentiated from fear by a stronger increase in diastolic pressure, in muscle tension (electromyogram recordings), in total peripheral resistance, and in facial temperature, the latter associated with facial flushing, often reported by people reflecting on their anger experience. The sensation of anger is highly correlated with anger's physiological profile.7 In terms of psychosocial imagery, there is no better metaphor for anger than hot fluid in a container. Autonomic arousal is primarily engaged through adrenomedullary and adrenocortical hormonal activity. In anger, the catecholamine activation is more strongly noradrenaline than adrenaline (the reverse being the case for fear). The adrenocortical effects, which have longer duration than the adrenomedullary ones, are mediated by secretions of the pituitary gland, which also influences testosterone levels. The pituitary-adrenocortical and pituitary-gonadal systems are thought to affect readiness or potentiation for anger responding. Testosterone provides vigor and reduces fear. A number of central nervous system structures have been identified in anger activation, most prominently the amygdala, the almond-shaped, limbic system component located deep in the temporal lobe that is well-established for its activation in threat-detection, its association with trauma, and anger-activated aggressive behavior.30,31 Activation in the amygdala has been found to be associated with anger and attack priming. Interconnections with the ventromedial and orbital frontal cortex, which are recruited during anger states, serve to regulate behavior and mediate how anger affects aggressive responding.32 The amygdala is the key site for aversive motivational system, and it has been thought that anger is derived from that system, as it is a negatively valenced emotion that is evoked by aversive experiences. Similarly, anger is conjectured to be a product of a defensive, “rage system.”33 However, anger has also been linked with asymmetric left-prefrontal cortical activity, which has typically been associated with positive affect and approach motivation.16,34 Although the complexities of the neuropsychological and psychophysiological processing of anger seem to be far from straightforward, particularly how it might bear on psychopathology,35 Potegal and Stemmler32 have put forward a neuroanatomical conjecture about the dynamics of anger involving the amygdala, temporal lobe, and the ventromedial and orbital frontal cortex.
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The central nervous system neurotransmitter serotonin, which is also present in blood platelets, affects anger potentiation, as low levels of this hormone are associated with irritable mood, as are functional polymorphisms in serotonin receptor genes.36 Serotonin imbalances are related to deficits in the modulation of emotion. While serotonin and other neurotransmitters (noradrenaline and dopamine) are involved in anger activation, the neural structures and circuitry in anger dysregulation and aggressive behavior remain to be disentangled. These various physiological mechanisms pertain not only to the intensity of anger arousal but also its duration. Arousal activation eventually decays to baseline levels, but recovery time may be prolonged by exposure to new arousal sources or by rumination. The potency of a provocation may be heightened by the carryover of undissipated excitation from a prior arousal source, which may not have been anger-specific (i.e., an otherwise stressful circumstance, such as exposure to bad news, work pressure, or traffic congestion). This “excitation transfer” of arousal residues facilitates anger, augments its intensity, amplifies blood pressure, and raises the probability of aggression.18 Residual arousal from unresolved anger events can transfer to future conflicts and further intensify anger reactivity to instigating events. In turn, unexpressed anger is associated with exaggerated and more prolonged cardiovascular responses to a variety of stressful stimuli. In this regard, a stress framework is highly useful. Both acute and prolonged exposure to common stressors (e.g., noise, crowding, difficult tasks, and high-pressure job environments filled with time demands, or exposure to abrasive interactions) may induce physiological activation that decays slowly. When someone experiences an event that pulls for the cognitive label “anger,” and this event occurs concurrently with already elevated arousal, the anger system is then more easily engaged.
ANGER DYSCONTROL: PHYSICAL AND PSYCHOLOGICAL HEALTH PROBLEMS Anger is a highly functional human emotion and is to be appreciated as a rich part of cultural life, but the survival value of the aggression-enabling function of anger is an archaic remnant with rare contemporary necessity. Outside of warfare, the survival challenges presented by civilized society are predominantly psychological, rather than physical. Effective coping with the demands of modern life requires understanding complex information, problem-solving, and prudent action, not energized rapid responding. Even in emergency situations, anger requires regulation. Contrary to intuitions, anger can be detrimental to survival in a physical threat crisis. It is counterproductive for energy conservation in a prolonged fight, for monitoring additional threat elements
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and hazards, and for effective strategy selection in circumstances where survival threat lingers and/or remains obscure. The regulation of the intensity and duration of anger arousal is pivotal to its merit or utility. To get angry about something, one must pay attention to it. Anger is often the result of selective attention to cues having high provocation value. A principal function of cognitive systems is to guide behavior, and attention itself is guided by integrated cognitive structures, known as schemas, which incorporate rules about environmentbehavior relationships. What receives attention is a product of the cognitive network that assigns meaning to events and the complex stimuli that configure them. The appraisal process is in the seeing and the hearing, not something tandem to the perception, and it is an ongoing process. Expectations guide attentional search for cues relevant to particular needs or goals. Once a repertoire of anger schemas has been developed, events (e.g., being asked a question by someone) and their characteristics (e.g., the way the question was asked, when it was asked, or who asked it) are encoded or interpreted as having meaning in accord with the preexisting schema. Rumination about provoking events extends or revivifies anger reactions. Because of their survival function, the threat-sensing aspect of anger schemas carries urgent priority and can preempt other information processing. Perceived malevolence is one of the most common forms of anger-inducing appraisal. It pulls for anger by involving the externalization of blame and the theme of justification. That, in turn, engages social norms of retaliation and retribution. Averill's view of anger is that it is a socially constituted syndrome or a transitory social role governed by social rules.5 While anger and physical aggression may be viewed as applying a legitimate punitive response for transgression or as ways of correcting injustice, justifications can be embellished to serve the exoneration of blame for destructive outcomes of expressed anger. Physiological components of anger, such as increased blood flow, may be adaptive for survival in a short-term danger episode, but the byproducts of recurrent engagement of anger are hazardous in the long term. Unregulated anger is associated with physical and psychological health impairments, including detrimental effects on the cardiovascular system bearing on mortality.9 Persons who are reactively angry are at considerable risk for coronary heart disease. An angry, hostile, and distrusting outlook necessitates high vigilance for thwarting and malevolence, resulting in prolonged neurohormonal activation conducive to atherosclerosis. In addition to these pathogenic effects for a personality style that is overly expressive of anger, the coronary system is also impaired by recurrently suppressed anger, long identified as a causal variable in the etiology of essential hypertension. People having difficulties expressing anger tend to be at risk for chronically
elevated blood pressure, as mediated by high plasma renin activity and norepinephrine. The suppression of anger has been robustly correlated to elevated blood pressure and greater cardiovascular reactivity to provocation in laboratory studies and to sustained hypertension in field studies. Anger suppression also amplifies pain sensitivity.37 With regard to psychological well-being, anger occurs in conjunction with a wide range of psychiatrically classified disorders, emerging in conjunction with the emotional instability attributes of personality disorders, irritability and “attacks” in mood disorders, delusions and command hallucinations in psychotic disorders (especially paranoid schizophrenia), impulse control disorders, intellectual disabilities, dementia, substance abuse disorders, and exotic cultural-bound syndromes.38,39 As anger often results from trauma, it can be salient in PTSD, affecting the severity and course of PTSD symptoms, and it is associated with major adjustment problems for military veterans.12,13 The central quality of anger in the broad context of clinical disorders is dysregulation—its activation, expression, and experience occur without appropriate controls. Transdiagnostic processes of threat perception, selective attention, interpretative bias, confirmation bias, rumination, and self-control deficits are involved. Among hospitalized psychiatric patients in long-term care in both civil commitment and forensic institutions, anger is a pervasive problem, as identified by both clinical staff and by the patients themselves. Studies with multiple control variables show anger to be related to the violent behavior of psychiatric patients before, during, and after hospitalization and to physical aggression within institutions by incarcerated adults.40 Anger is not only an important clinical need among many psychiatric and custodial populations, it also bears on the therapeutic milieu and on the wellbeing of clinical and custodial staff. Anger dysregulated people often have traumatic life histories, replete with experiences of abandonment and rejection, as well as economic and psychological impoverishment. For them, anger becomes entrenched as a mode of reactance to stressful or aversive experiences. Chronically angry people are reluctant to surrender the anger-aggression system that they have found useful to engage, because they discount the costs of its engagement.
ANGER TREATMENT The first step in the provision of therapeutic intervention for anger is facilitating client “readiness” for anger treatment, which can be very challenging due to client background adversities, multifaceted clinical comorbidities, and resource limitations in facilities where treatment might be implemented.41 Nevertheless, there is
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REFERENCES
substantial evidence for the efficacy of anger treatment. Nine meta-analyses on the effectiveness of psychotherapy for anger have been published, involving a wide range of clinical populations, which overall have found medium to strong effect sizes, indicating that approximately 75% of those receiving anger treatment improved compared to controls. Cognitive behavioral therapy (CBT) approaches have greatest efficacy in reducing anger, and now with encouraging evidence for reducing physically assaultive behavior in hospital.42 CBT approaches incorporate training in self-monitoring, relaxation, and social skills, but centrally seek to modify cognitive structures and the way a person processes information about social situations. They strongly emphasize self-regulation, cognitive flexibility in appraising situations, arousal control, and learning prosocial values and scripts. Making extensive use of therapist modeling and client rehearsal, anger proneness is modified by first motivating client engagement and then restructuring cognitive schemas, increasing capacity to regulate arousal and facilitating the use of constructive coping behaviors. Priority is given to self-regulatory controls of anger activation. The parameters or state markers for anger activation that receive attention in CBT anger treatment are: reactivity (frequency on onset and how easily anger is triggered); latency (how rapidly activated); intensity (how strongly engaged), and duration (persistence of arousal). Treatment aims to minimize anger reactivity, intensity, and duration and to moderate anger expression to reduce the costs of anger dyscontrol. To facilitate anger regulation, anger treatment procedures strive to disconnect anger from the threat system. This is done first through the provision of safety, patience, and psychological space for reflection, exploration, and choice. The client's view of anger is normalized, to obviate worries about being a “bad” or unworthy person. The therapist will acknowledge the legitimacy of the client's feelings, affirming his or her self-worth. Building trust in the therapeutic relationship is pivotal. As self-regulation hinges on knowledge, education about anger and discovery of the client's personal anger patterns or “anger signature” is facilitated. Much is done to augment selfmonitoring and to encourage the moderation of anger intensity. The therapist models and reinforces nonanger alternative responding so as to build replacements for the automatized angry reactions that had been the client's default coping style. One CBT approach to anger treatment that has received significant support for its efficacy is called “stress inoculation” (SI). In this treatment approach, anger provocation is simulated by therapeutically paced progressive exposure to anger incidents created in imaginal visualization and in role play, based on a hierarchy of anger incidents produced by the collaborative work of client and therapist. This graduated, hierarchical exposure is the
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basis for the “inoculation” metaphor. The SI involves the following key components: (1) client education about anger, stress, and aggression; (2) self-monitoring of anger frequency, intensity, and situational triggers; (3) construction of a personal anger provocation hierarchy, created from the self-monitoring data; (4) arousal reduction techniques of progressive muscle relaxation, breathingfocused relaxation, and guided imagery training; (5) cognitive restructuring by altering attentional focus, modifying appraisals, and using self-instruction; (6) training behavioral coping in communication and respectful assertiveness as modeled and rehearsed with the therapist; and (7) practicing the cognitive, arousal regulatory, and behavioral coping skills while visualizing and role playing progressively more intense anger-arousing scenes from the personal hierarchies. While therapeutic mechanisms underlying anger treatment gains are not clear, nor are their sustainability or generalizability, the field is fortified by the evidence base and continues to seek advances in providing remedies for anger dyscontrol.
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