Hostility and Health

Historically, hostility is among the most widely and thoroughly investigated psychosocial risk factors for health. From the investigation of Type A behavior pattern (TABP), hostility has emerged as a multidimensional construct involving affect, behavior, and cognition. In general, anger refers to negative affect ranging from feelings of irritation and annoyance to rage and may be conceptualized as an acute emotional state or an enduring trait. Aggression refers to overt attacking or destructive behavior. Hostility refers to a set of negative attitudes, beliefs, and appraisals of the worth, intent, and motives of others. These related though distinct facets are often collectively referred to with the umbrella term hostility.

Hostility is assessed with self-report and structured interviews. Perhaps because of its origins in basic personality research, the Cook-Medley Hostility (Ho) Scale is the most widely used self-report measure of hostility. This 50-item scale was derived from the larger Minnesota Multiphasic Personality inventory. Higher scores are associated with greater interpersonal difficulties, lower social support, more difficulties at work, and more conflict within marriages. In addition, Cook-Medley hostility is associated with a variety of health outcomes and serves as the cornerstone in hostility-cardiovascular disease research. The Aggression Questionnaire (AQ) is a more recent self-report measure, which measures the hostility spectrum of cognitions (hostility), affect (anger), and behavior (physical, verbal aggression). The AQ is demonstrated to have reliable construct validity and is associated with cardiovascular reactivity (CVR) during social stress in the laboratory. The most widely researched interview is the Interpersonal Hostility Assessment Technique (IHAT). With the IHAT interview, emphasis is on how the person responds rather than the content of his or her response. The IHAT yields four subscales, which contribute to the total score, referred to as the Hostile Behavior Index (HBI). Higher HBI scores are associated with disease severity in coronary artery disease (CAD) patients and predict the magnitude of change in blood pressure during experiences of anger.

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Substantial evidence links hostility and trait anger to increased risk of cardiac disease morbidity and mortality. These conclusions are based on increasingly well designed prospective studies, which show a predictive relationship between hostility and later acute cardiac events such as myocardial infarction (MI; heart attack), sudden cardiac death, and stroke. For example, Kawachi and colleagues (1996) found that trait anger predicted incidence of MI over a 7-year follow-up. In addition, hostility and anger are also predictive of progression or worsening of atherosclerosis, the build-up of fatty plaques in the arteries that underlies coronary heart disease. Finally, hostility may play a role in triggering acute cardiac events, through the experience of anger. Episodes of anger are more common in the 2 hr prior to a coronary event (e.g., MI) than during control periods, suggesting that the arousal of anger can trigger acute myocardial infarction. In the laboratory, arousal of anger evokes ischemia in patients with coronary artery disease, which may confer increased risk of acute MI. Hence, the literature supports hostility as a significant risk factor for the development and progression of cardiac disease as well as acute cardiac events that may be triggered by hostility through the tendency to experience episodes of anger.

Cardiovascular reactivity is one proposed pathway linking psychosocial risk factors such as hostility to cardiovascular disease (CVD). The “reactivity hypothesis” suggests that larger, more frequent, and more prolonged cardiovascular responses (e.g., heart rate, blood pressure, and associated physiological changes) initiate and promote the development of CAD. Studies have shown these physiological responses are associated with atherosclerosis and myocardial ischemia in the laboratory and during daily life.

Laboratory and ambulatory studies demonstrate a reliable relationship between hostility and larger and more frequent cardiovascular responses. In particular, research suggests that individuals higher in hostility experience greater cardiovascular reactivity during experiences of anger than do less hostile individuals. For example, several laboratory investigations have demonstrated that more-hostile individuals display larger changes in blood pressure, heart rate, and other markers of cardiovascular and neuroendocrine functioning during harassment in the laboratory. Hence, CVR may mediate the relationship between hostility and experiences of psychological distress and increased disease risk.

In addition to individual risk, researchers are increasingly aware of the interactive effects between hostility and the social context. For example, in several studies hostile persons report larger changes in anger and demonstrate greater physiological reactivity to stressful interpersonal situations than less hostile persons. In addition, hostile persons appraise the actions of others as intentionally aggressive and less friendly, process negative information about others more readily, behave in less friendly ways during interactions with family members, and experience discord and conflict in personal relationships. The resulting interplay suggests that hostile individuals not only may respond to their environment in maladaptive ways, but also transactionally create increased frequency, intensity, and duration of interpersonal stress. Not surprisingly, evidence suggests that more-hostile individuals have lower levels of social support and experience more frequent episodes of interpersonal stress at home and at work. Moreover, recent evidence suggests that when faced with a stressful situation, more-hostile individuals show less psychological and physiological benefit from their social support than do less hostile individuals. These findings suggest that hostility may confer greater risk for cardiovascular disease through increased psychosocial vulnerability.

In summary, hostility is increasingly recognized as a robust psychosocial risk factor for cardiovascular disease. Future research will likely continue to focus on examining both the psychosocial and psychophysiological mechanisms involved in the relationship between hostility and health. In addition, experts in complementary areas of behavioral medicine have begun to search for suspected interpersonal and genetic determinants of hostility. Finally, although interventions tailored at managing anger are well proven, more work is needed to demonstrate that such interventions can influence health outcomes such as future MI and early cardiovascular mortality.


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