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Suppressed Anger and Coronary Heart Disease

As early as 1939, Franz Alexander suggested that the repression of anger is associated with chronic elevations in blood pressure and ultimately with essential hypertension (Alexander, 1939). However, because of inconsistent findings in efforts to support this hypothesis, interest in repressed and suppressed anger as a risk factor for coronary heart disease (CHD) declined for many decades (Diamond, 1982). It was not until Rosenman and Friedman’s work on Type A Behavior Pattern (TABP) that anger reentered the spotlight as potentially being involved in the development of CHD. Rosenman and Friedman clearly included expressed anger as part of the TABP construct (Rosenman, 1978). Yet anger once again became largely ignored as coronary-prone behavior researchers shifted their attention to another dimension of TABP, the “potential for hostility.” However, when the criteria for “potential for hostility was later carefully examined, it was found that these judgments of the “potential for hostility” involve both anger and hostile attitudes (Siegman, 1994). In fact, leaders in the field of hostility-CHD research such as Theodore Dembroski, later renamed what they were measuring from “potential for hostility” to “anger-hostility.” Only very recently has the hypothesis that anger is a significant risk factor for CHD been a question that coronary-prone behavior researchers have focused on.

What is anger and how is it assessed?

Psychologists distinguish between anger, hostility, and aggression, with the first referring to affect, the second to attitudes, and the last to destructive behavior. Anger is often described as the emotion evoked when a person is blocked in the attainment of a goal or in the fulfillment of a need. Hostility, on the other hand, is a general attitude of ill will and negative evaluation of people and events (Mendes de Leon and Meesters, 1991).

As previously mentioned, coronary-prone behavior researchers have concentrated on measuring hostility, not anger, and as a result popular techniques have not done well at separating the two. Assessment of anger and hostility can be divided into two general types: self-report and interview based. Each general type has its own strengths and weaknesses, and create a need for multiple types of self-report and interview-based methods. Self-report measures include the Cook-Medley Ho scale, Factor L, and the Buss-Durkee Hostility Inventory. Interview-based assessments have been developed from the Structured Interview (SI) method developed originally to assess TABP, consisting of a set of questions concerning competitiveness, time urgency, and anger expression.

Assessing Modes of Anger Coping: Expression, Suppression, and Repression of Anger

Another interest of coronary-prone behavior researchers has been to determine which modes of coping with angry feelings are most detrimental to cardiovascular health. Anger-in and anger-out constructs have been created to help assess anger coping styles. Those that tend to hold anger inside and not display it outwardly are “anger-in,” while those that vent their anger readily are termed “anger-out.” (Spielberger et al., 1985) Assessing unexpressed anger (anger-in) has proved difficult without first having valid methods to determine whether anger is being experienced but not expressed, or whether anger is not being experienced. Assessments of whether anger is being experienced have been developed by Siegman and colleagues using factor analyses of the Buss-Durkee Hostility Inventory subscales (Siegman et al., 1987). Two factors were identified. The first was defined by subscales that measure the frequency with which feelings of anger and hostility are experienced, and the second factor was defined by subscales that measure the expression of anger that occurs in response to provocation (Siegman, 1994). If anger is being experienced, failure to express anger through overt aggression (anger-out) could reflect autonomic or voluntary inhibition of aggressive urges (i.e., repression or suppression of anger), or it could reflect alternative methods of coping through other social responses, such as assertiveness (Smith, 1994).

Cardiovascular Consequences of Repressing or Suppressing Anger vs. Expressing Anger

It has long been known that anger is associated with heightened levels of cardiovascular arousal, which has been identified as the mechanism that translates behavior into coronary heart disease. Anger is also associated with increased rates of testosterone production and platelet formation, which are also involved in the pathogenesis of CHD (Siegman, 1994). Other biological mechanisms by which anger may increase the risk of CHD include discharge of circulating catecholamines, increased myocardial oxygen demand, and vasospasm (Kawachi et al., 1996). Whatever the biological mechanisms are, if anger is indeed a crucial risk factor for CHD, it is important to understand which forms of coping with anger are most related to the development of CHD.

Heightened levels of systolic and diastolic blood pressure (BP) reactivity have been identified as a risk factor for future development of hypertension, CAD, and CHD (Manuck et al., 1992; Williams, 1989; Fredrickson & Matthews, 1990; Light et al., 1992). Experiments have been done to test the hypothesis that the expression of anger is associated with heightened levels of cardiovascular reactivity (CVR)(Siegman et al., 1990; Siegman & Boyle, 1992). The findings by Siegman and colleagues indicated that only the expression of anger, not its mere experience, was associated with appreciable increases in BP reactivity.

Correlational studies examining the relationship between the experience of anger, the expression of anger, and cardiovascular reactivity (CVR) have also been done. The distinction between the experience of anger versus the expression of anger is based upon the results of several factor analytic studies of the Buss-Durkee Hostility Inventory (BDHI). In three studies, significant positive correlation has been obtained only between BDHI-derived expression of anger and BP reactivity during an anger-arousing task (Siegman et al., 1988; Siegman et al., 1992; Suarez & Williams, 1990). However, findings showing insignificant correlation between BDHI-derived experience of anger and BP reactivity does not mean that suppression and repression of anger do not have any association with heightened BP reactivity or higher resting BP levels. As previously mentioned, people cope with anger in a variety of different ways, and therefore any attempts to correlate the experience of anger to BP reactivity says little about the effects of specific modes of coping with anger on BP reactivity. In fact, there is evidence suggesting that people who have a tendency to suppress their anger also have a tendency to have high blood pressure (Harburg et al., 1973; Harburg et al., 1979; Gentry et al., 1982). The suppression of anger has been considered an important component of the “hypertensive personality” by many investigators (Pernini et al., 1988; Schneider et al., 1986). Several of the previous prospective studies in this area have found suppressed anger to be predictive of increases in blood pressure (Kahn et al., 1972; Rose et al., 1978; McCelland, 1979; Pernini et al., 1991), and a number of cross-sectional studies have found increased anger suppression in hypertensive individuals (Schneider et al., 1986; Pernini et al., 1990; Goldstein et al., 1988). It should be mentioned that one of the most recent prospective studies (Markovitz et al., 1993) found no relationship between mode of anger expression and later hypertension, but a large number of studies still support the view that suppression of anger is an important risk factor for hypertension.

Numerous studies have also been completed analyzing the relationship between the expression of anger, the experience of anger, and CAD or CHD (Siegman et al., 1987; Helmig et al., 1991; Mendes de Leon, 1992; Dembroski et al., 1989). Results have been consistent with those where BP reactivity was the endpoint, with only the expression of anger, not its mere experience, being related to the development of CAD and CHD.

Evidence in regard to the possible relationship between the suppression or repression of anger, and CAD or CHD is fairly sparse. Positive findings include Haynes et al.’s 1980 study that found that suppression of anger in both men and women was related to future development of CAD. Additionally, two 1985 studies (Demroski et al., 1985; MacDougall et al., 1985) evaluated both anger suppression and hostility and demonstrated that those who were hostile and suppressed their anger had the most severe CAD.

Validity of these studies on anger suppression and CHD are still quite questionable, because satisfactory measures of suppression and repression have not yet been developed (Siegman, 1994). Many studies have used the “anger-in” construct to assess suppression and repression of anger, however none of the assessments of anger-in (Haynes et al., 1978; Spielberger et al., 1985; Dembroski et al., 1983, 1989) distinguish between suppressing anger and repressing anger. Also, there has been some confusion concerning the assessments of anger-in. Some anger-in measures appear to assess other characteristics such as shyness and unassertiveness, or cognitive factors such as brooding and resentment (Miller et al., 1996). Results from studies examining the relationship between anger-in and CVR mostly report null findings, as reviewed by Mills et al., 1989. One of the most recent, major prospective studies found that neither anger-in nor anger-out was associated with a higher incidence of CHD (Russek et al., 1990). Other than the problem of distinguishing what each anger-in measure really assesses, these negative findings may be partly due to the fact that in these studies some of the participants may not have been angered sufficiently, and therefore have little or no anger to suppress or repress (Siegman, 1994).

Work environments and anger-hostility

It is becoming increasingly clear that environmental factors have a large impact on how psychosocial factors, such as anger, effect CHD development. Research primarily by Burns and colleagues suggests that psychosocial traits of anger expression and hostility may be differentially related to CVR depending on the qualities of the situation and gender (Burns et al., 1993). Also according to Burns, one group of men at risk for CHD may be those who are chronically angry, who prefer to suppress their anger, and who are also faced with constant and excessive interpersonal harassment, demands, or criticism on the job or at home (Burns et al., 1995).

“Job strain” has been defined by Karasek (1979) as work in jobs with high psychological demands and low control. In a half-dozen epidemiological studies over the last decade, occupational stress researchers have implicated “job strain” as a risk factor for heart disease (Schnall et al., 1994). Although the mechanism by which the stress of “job strain” influences development of CHD is unknown, previous findings suggest that “job strain” may be related to elevations of blood pressure at work (Schnall et al., 1990; Van Egeren, 1992). In the Cornell prospective study of job strain and hypertension, anger was associated with lower job control (decision latitude) and lower workplace social support among men. Lower SES and non-White adults experience lower levels of control at work and in other aspects of their lives. Another recent study by Burns (Burns, Hutt, & Wiedner, 1993) examined whether anger-hostility could moderate the effects of demand and decision latitude on CVR. The results suggest that anger-hostility may operate in concert with dimensions of job stress to affect CVR, and presumably CHD. It remains to be seen how anger suppression and anger expression operate in relation to dimensions of job stress, and hopefully this weakness in the literature will soon be remedied.

Suppressed anger and its determinants

There has been remarkably little research on the determinants on suppressed anger, particularly social class and job stress. Such factors might shape personality development in childhood. For example, certain parental behavior patterns (i.e., overly strict, critical and demanding of conformity) are more common in low SES households, and may be viewed as a reflection of the parents’ occupational and other life experiences, which are characterized by low control and insecurity. Similarly, an adult’s experience, which might include stressful, low control jobs, may shape their personality development (Kohn and Schooler, 1982). Psychosocial work environments which enforce a non-complaining attitude and prevent development of active emotional coping with anger may result in suppressed anger that could have an adverse effect on long-term cardiovascular health of the employees (Theorell, 1990; Cottington et al., 1986). Thus, research on the social determinants of personality measures believed to be associated with illness outcomes needs to be a major priority in future research.

Conclusions

There is an abundance of conflicting results in the literature regarding the cardiovascular consequences of different anger coping styles. Despite the controversy over which anger coping style is most detrimental to the heart, there is a mass of evidence suggesting that anger coping styles, not the mere experience of anger, are related to CVR and possible development of CHD. However, recent research (Burns et al., 1995) suggests that CVR depends not only on how anger is dealt with, but also on how much anger must be managed, at least among anger suppressors. To gain further insight into whether anger suppression versus anger expression is more important in the etiology of CHD, more valid measures of anger suppression must first be created. Additionally, environmental factors must be better accounted for, such that attempts to establish associations between anger suppression or anger expression and CHD are elicited during relevant stressful situations. Although job stress has already been identified as a risk factor for CHD, more research is needed to determine how specific anger coping styles and “job strain” are related to CHD, and whether they are independent relationships or mutually reinforcing. Lastly, more research is needed to better elucidate the determinants of depression, particularly social class and job stress.


References

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Hostility and Coronary Heart Disease

Just as Type A Behavior Pattern (TABP) was being accepted by the biomedical community in the early 1980s as the first significant independent psychosocial risk factor for Coronary Heart Disease (CHD)(Cooper et al., 1981), negative findings concerning the presumed relationship between TABP and CHD began to emerge (Shekelle et al., 1985; Arrowood et al., 1982; Dembroski et al., 1985; Scherwitz et al., 1983; Siegman et al., 1987). In order to explain the negative findings that challenged the validity of TABP as a risk factor for CHD, the Type A construct was broken down into its constituent components (Dembroski & MacDougall, 1983). Based on the work of many researchers, Theodore M. Dembroski was credited with proposing that the “potential for hostility” was the most likely candidate to be the “toxic” component of Type A. Numerous studies found that hostility was a more reliable predictor of CHD than TABP, and today this still holds true (Helmers et al., 1994; Miller, Smith et al. 1996).

What is hostility and how is it assessed?

Hostility is often confused with anger, and although closely related, they are not identical concepts. Hostility is often defined as a personality characteristic of having a rather stable attitude of ill will and negative evaluation of people and events. Anger, on the other hand, is often described as an emotion evoked when a person is blocked in the attainment of a goal or in the fulfillment of a need (Mendes de Leon & Meesters, 1991). Hostility is a multifaceted phenomenon that includes cognitive, affective, and behavioral manifestations. Cognitive aspects include negative beliefs about others. Affective components include anger, as well as disgust and contempt. Behavioral manifestations can take many forms, such as overt aggression or more commonly more subtle and socially acceptable ways of expressing hostility (Siegman, 1994).

There is no standard assessment of hostility. This presents problems in the measurement of hostility in that different studies have targeted different aspects of hostility, and have led to variable results in the study of the link of hostility to CHD (Siegman, 1994). The two general approachs used are interview-based and self-report-based measures. Self-report measures include the Cook-Medley Ho scale, Factor L, and the Buss-Durkee Hostility Inventory. Interview-based assessments have been developed from the Structured Interview (SI) method developed originally to assess TABP. The first system for assessing hostility was developed by Dembroski et al. (1989) in which the potential for hostility was measured by breaking hostility down into three facets: Content, Intensity, and Style. Most SI measures of hostility seem to assess “anger-out”, the expression of anger (Miller, Smith et al., 1996).

Does hostility play a direct role in developing CHD?

There is a significant amount of evidence favoring the theory that hostility is a risk factor for CHD (Dembroski & Czajkowski, 1989; Dembroski & Williams, 1989; Matthews, 1988; Miller, Smith et al., 1996). A recent literature review of 45 studies found that the correlation between structured interview (SI) indicators of hostility and CHD was r=.18. After controlling for other risk factors for CHD, the widely used Cook-Medley Hostility Scale and other cognitive-experiential measures were most predictive of all-cause mortality (r=.16) and CHD (r=.08) (Miller, Smith et al., 1996). However, there also have been some negative findings (McCranie et al., 1986). One explanation is the increasing use of high-risk populations which may increase null findings (Miller, Smith et al., 1996).

Another explanation likely lies in the fact that hostility may be a multidimensional construct, and that only some of its dimensions may be coronary prone (Siegman et al., 1987). For example, results from studies headed by Siegman (1987) showed that only the expression of anger-hostility, not its mere experience, is positively related to the severity of Coronary Artery Disease (CAD). Further studies (Helmig et al., 1991; Mendes de Leon, 1992; Dembroski etal., 1989) confirmed that only the expression of hostility is positively correlated to CAD and CHD. This returns us to the problems with measuring hostility, since the various systems previously mentioned measure expression of anger-hostility and the experience of hostility in different degrees. Furthermore, some of the methods used to measure hostility have questioned validity (Siegman, 1994).

Although research analyzing the interplay between hostility and job stress is a recent pursuit and therefore the amount of studies conducted has been few, a recent study by Miller, Dolgoy et al., 1996) has found that male undergraduates who were categorized into high and low expressive hostility groups showed significantly different cardiovascular responses in response to interpersonal stress through anger-provoking statements. It has already been reported that there is a link between expressive hostility and CAD (Siegman et al., 1987). Also, it has already been proposed that cardiovascular response is dependent on the interaction of stable traits and affective states (Manuck et al., 1985). However, the 1996 paper by Miller, Dolgoy et al. has now shown that only in the high expressive hostility group exposed to interpersonal stress was there a significantly elevated cardiovascular response. These results suggest that cardiovascular response to stress is dependent on being in a hostile state.

Work environments and the development of hostility

Hostility was previously defined as a personality characteristic of having a rather stable attitude of ill will and negative evaluation of people and events (Mendes de Leon & Meesters, 1991). This implies that hostility as a risk factor for CHD is an all-or-none quantity depending on whether one possesses the “trait for hostility.” However, it is important to note that certain high stress environments might elicit hostile states in most people who find themselves in these high stress environments. Clearly, if hostility is indeed an important risk factor for CHD, this would have broad public health implications in terms of high stress work environments. Then, not only should people with “the trait of hostility” ideally be led towards work environments that avoid inciting manifestations of their hostility, but high stress work environments that could induce unhealthy levels of hostility in large numbers of employees should be transformed into more healthy working environments.

“Job strain” has been defined by Karasek (1979) as work in jobs with high psychological demands and low decision latitude. In a half-dozen epidemiologic studies over the last decade, occupational stress researchers have implicated “job strain” as a risk factor for heart disease (Schnall et al., 1994). Although the mechanism by which the stress of “job strain” influences development of CHD is unknown, previous findings suggest that “job strain” may be related to elevations of blood pressure at work (Schnall et al., 1990; Van Egeren, 1992). High blood pressure has long been known to be a marker for individuals at high risk for developing CHD, and therefore is one possible mechanism by which “job strain” might exert its deleterious influences on the heart.

As previously mentioned, the results by Miller, Dolgoy et al., 1996 suggest that cardiovascular response to stress in dependent on being in a hostile state. It still remains to be seen whether elevated cardiovascular responses to “job strain” are dependent on being in a hostile state. Nevertheless, if interpersonal stress and hostility combine to have dramatic effects on cardiovascular response, this suggests that some dimensions of “job strain” and some dimensions of hostility might also combine to have dramatic effects on cardiovascular response and CHD development. Recent work by Burns further supports this hypothesis. Burns et al., 1993 examined whether hostility could moderate the effects of demand and decision latitude on cardiovascular reactivity. According to Burns, the results suggest that hostility may operate in concert with dimensions of job stress to affect cardiovascular reactivity, and presumably CHD.

Various theories have been proposed to explain the development of hostility, including parental behavior that is overly strict, critical and demanding of conformity. A few studies have shown hostility to be associated with low socioeconomic status (SES) and non-White race. However, most developmental research on hostility has focused on mechanisms by which hostility may lead to CHD, such as through promoting unhealthy habits (e.g. ,smoking), heightened sympathetic reactivity, or through lower levels of social support, higher levels of distress and more stressful life events, which are presumably caused by the hostile individual (Miller, Smith et al., 1996). Thus, there has been remarkably little research on the determinants of hostility, either childhood experience, or adult experience, which might include stressful, low control jobs. This is a major weakness in the literature on hostility and health.

In the Cornell prospective study of job strain and hypertension, anger was associated with lower job control (decision latitude) and lower workplace social support among men. Lower SES and non-White adults experience lower levels of control at work and in other aspects of their lives. In addition, to work stress as a possible contributor to the development or promotion of hostility, we also hypothesize that childhood experiences may contribute to this personality characteristic. The parental behavior pattern described above (i.e., overly strict, critical and demanding of conformity) is more common in low SES households, and may be viewed as a reflection of the parents’ occupational and other life experiences, which are characterized again by low control and insecurity.

Conclusions

At least some of the dimensions of hostility appear to be related to the development of CHD, however, there is an obvious need for increasing the validity pertaining to hostility assessment. There is a need to better distinguish between anger, hostility, aggressive behavior, and cynical mistrust. More valid and reliable measures of these constructs must first be created. Then and only then will it be possible to determine if, and to what extent, these constructs are related to CHD, and whether they are independent relationships or mutually reinforcing (Siegman, 1994). Furthermore, with numerous epidemiologic studies implicating “job strain” as a risk factor for heart disease, it would be of great public health interest to gain insight into whether high stress (especially low control) work environments are a major cause of eliciting hostility in large numbers of people, and whether this hostility impacts on the people’s behavior towards their children. Analogous to uncovering the relationship between each of the dimensions of hostility and CHD, it would be of tremendous public health importance to determine how hostility and “job strain” are related to CHD, and whether they are independent relationships or mutually reinforcing.


References

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