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.
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.
Arrowood, M., Uhrich, K., Gomillion, C., Popio, K., & Raft, D.(1982). New markers of coronary-prone behavior in a rural population. Psychosomatic Medicine, 119, 44-119.
Burns, J., Hutt, J., & Weidner, G.(1993). Effects of Demand and Decisions Latitude on Cardiovascular Reactivity Among Coronary-Prone Women and Men. Behavioral Medicine, 19(3), 122-128.
Cooper, T., Detre, T., & Weiss, S.M.(1981). Coronary-prone behavior and coronary heart disease: A critical review. Circulation, 63, 1199-1215.
Dembroski, T.M., & Czajkowski, S.M.(1989). Historical and current developments in coronary-prone behavior. In A.W. Siegman & T.M. Dembroski (Eds.), In search of coronary-prone behavior: Beyond Type A (pp.21-39). Hillsdale, NJ: Lawrence Erlbaum Associates.
Dembroski, T.M., & MacDougall, J.M.(1983). Behavioral and psycho-physiological perspectives on coronary-prone behavior. In T.M. Dembroski, T.H. Schmidt, & G. Blumchen(Eds.), Biobehavioral bases of coronary heart disease (pp. 106-129). New York: Karger.
Dembroski, T.M., & MacDougall, J.M.(1985). Beyond global Type A: Relationships of paralinguistic attributes, hostility, and anger-in coronary heart disease. In T. Field, P. McCabe, & N. Schneiderman (Eds.), Stress and Coping. Hillsdale, NJ: Lawrence Erlbaum Associates.
Dembroski, T.M., MacDougall, T.M., Costa, P.T., & Grandits, G.A.(1989). Components of hostility as predictors of sudden death and myocardial infarction in the Multiple Risk Factor Intervention Trial. Psychosomatic Medicine, 47, 514-522.
Dembroski, T.M., & Williams, R.B.(1989) In N. Schneiderman, P. Kaufman, & S.M. Weiss (Eds.), Handbook of research methods in cardiovascular behavioral medicine. New York: Plenum.
Helmers, K.F., Posluszny, D.M., & Kranz, D.S.(1994) In A.W. Siegman, & T.W. Smith (Eds.), Anger, Hostility, and the Heart (pp. 67-96). Hillsdale, NJ: Lawrence Erlbaum Associates.
Helmig, L., Houston, B.K., Vavak, C.R., & Mullin, J.(March 1991). Hostility related variables, self-schemata and CHD. Paper presented at the meetings of the Society for Behavioral Medicine, Washington, DC.
Matthews, K.A.(1988). Coronary heart disease and Type A behavior: Update on and alternative to the Booth-Kewley and Friedman(1987) quantitative review. Psychological Bulletin, 104, 373-380.
McCranie, E.W., Watkins, L., Brandsma, J., & Sisson, B.(1986). Hostility, coronary heart disease(CHD) incidence, and total mortality: Lack of association in a 25-year follow-up study of 478 physicians. Journal of Behavioral Medicine, 9, 119-125.
Mendes de Leon, C.F.(1992). Anger and impatience/irritability in patients of low socioeconomic status with acute coronary heart disease. Journal of Behavioral Medicine, 15, 273-284.
Mendes de Lwon, C.F., & Meesters, M.G.(1991). In A. Appels, J. Groen, J. Koolhaas, J. van Dixhoorn, L. van Doornen, C. Mendes de Leon, & C. Meesters (Eds.), Behavioral Observations in Cardiovascular Research (pp. 107-128). Amsterdam: Swets & Zeitlinger B.V.
Miller, T.Q., Smith, T.W, Turner, C.W., Guijarro, M.L., & Hallet, A.J. (1996). A meta-analytic review of research on hostility and physical health. Psychological Bulletin, 119(2), 322-348.
Scherwitz, L., McKelvain, R., Laman, C., Patterson, J., Dutton, L., Yusim, S., Lester, J., Kraft, I., Rochelle, D., & Leachman, R.(1983). Type A behavior, self-involvement, and coronary atherosclerosis. Psychosomatic Medicine, 45, 47-57.
Schnall, P.L., Landsbergis, P., & Baker, D.(1994). Job Strain and Cardiovascular Disease. Annu. Rev. Public Health, 15, 381-411.
Schnall, P.L., Pieper, C., Schwartz, J.E., Karasek, R.A., Schlussel, Y, et al.(1990) The relationship between “job strain,” workplace diastolic blood pressure, and left ventricular mass index: Results of a case-control study. J. Am. Med. Assoc, 267, 1209.
Shekelle, R.B., Hulley, S., Neaton, J., Billings, J., Borhani, N., Gerace, T., Jacobs, D., Lasser, N., Mittlemark, M., & Stamler, J. (1985). MRFIT Research Group: The MRFIT behavior pattern study. II. Type A behavior pattern and incidence of coronary heart disease. American Journal of Epidemiology, 122, 559-570.
Siegman, A.W.(1994) In A.W. Siegman, & T.W. Smith (Eds.), Anger, Hostility, and the Heart (pp. 1-22, 173-198). Hillsdale, NJ: Lawrence Erlbaum Associates.
Siegman, A.W., Feldstein, S., Tommaso, C., Ringel, N., & Lating, J.(1987). Expressive vocal behavior and the severity of coronary artery disease. Psycholosomatic Medicine, 49, 545-561.
Van Egeren, L.F.(1992). The relationship between job strain and blood pressure at work, at home, and during sleep. Psychosomatic Medicine, 54, 337-343.