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Anger and Disease RiskLess investigated than depression and anxiety, anger traits and hostility also appears to predispose to diseases. By meta-analysis, conducted in 1996 of 45 studies, hostility as measured by the Cook-Medley Hostility Scale has been shown to be an independent and significant risk factor for all-cause mortality (weighted correlation coefficient r = 0.16) and CHD (weighted r = 0.08) (). They also found that inclusion of high-risk studies produced an increase in null findings. A significant relationship has been shown between expressed anger and incident stroke (). A population based longitudinal study of risk factors included 2,074 men (mean age 53.0 ± 5.2 years. Average follow-up time was 8.3 ± 0.9 years. Men with a history of ischemic heart disease who had the highest level of expressed anger (anger-out) had a risk ratio of 6.87; 95% CI, 1.50-31.4) after risk factor adjustment. Men who reported the highest level of expressed anger had a relative risk for stroke of 2.03; 95% CI 1.05-3.94) vs. those who had the lowest level of expressed anger. Suppressed anger (anger-in) and controlled anger were not consistently related to stroke risk. The known risk factors that were controlled make quite a list: age, resting blood pressure, smoking, alcohol consumption, body mass index, low-density lipoprotein cholesterol, fibrinogen, socioeconomic status, and diabetes. In a different study of 537 initially normotensive men followed for 4 years, high levels of expressed (anger-out) and high levels of suppressed anger (anger-in) both resulted in higher levels of hypertension (). Using Spielberger’s Anger-out Anger-in scales showed that for every 1 point increase in anger-out there was a 12% increase in risk of hypertension (p<0.002). This also corresponds to an increased risk of 2 (95% CI 1.20 to 3.38) of men in the highest tertile vs. the lowest tertile for anger-out. Each point in the anger-in scale also saw an increased risk of 12% of hypertension (p<0.01). Little impact was seen on these risks by considerations of body mass index, smoking, alcohol consumption, physical activity, positive parental history of hypertension, and baseline diastolic blood pressure. Extensive literature suggests that possible psychosocial risk factors for coronary artery disease (CAD) are acute and chronic stress, depression, hostility, social support, and socioeconomic status (). Another way of looking at the risk factors is the following psychosocial constructs: 1) hostility/over commitment, 2) depression, vital exhaustion, 3) social support and a stressful psychosocial work environment, 4) in terms of the demand–control model, 5) in terms of the effort-reward imbalance model (). Loss of control over one’s environment is perhaps a common link (). A review published in 2002 in Cardiovascular Research has propounded a PNI model of the acute coronary syndrome (ACS) (). They believe that starting with an existing mild atherosclerotic plaque, and a dysfunctional endothelium, the ACS will pass through 3 stages. First is plaque instability. Second are extra-plaque factors promoting rupture. Third is superimposed thrombosis at a ruptured site. They postulate that this chain of events may persist if there is a deficiency of neuroendocrine-to-immune negative feedback resulting from cortisol resistance. In stage one, proinflammatory cytokines (IL-1, IL-6, and TNF- á) and chemoattractants (MCP-1, IL-8) lure white blood cells to the site. Along with these, the costimulation system (CD40L-CD40) attracts monocytes/macrophages that produce matrix metalloproteinases that disintegrate the extra-cellular plaque matrix. The result is coronary instability. The PNI connection to this stage is the increase in proinflammatory cytokines associated with negative emotions: depression, anxiety, and anger. In stage two, neuroendocrine factors (norepinephrine) and cytokines stimulate vasoconstriction and increased blood pressure, which causes a susceptible plaque to rupture. Acute stress, anger and hostility via stimulation of catecholamines may result in vasoconstriction and elevated blood pressure. In stage three, inflammation induces coagulation factors to increase and anticoagulation factors (notably protein C) to decrease. This enhances platelet aggregation a key step in thrombosis, which can lead to severe coronary occlusion. Depression, hostility and vital exhaustion have been shown to be positively correlated to platelet aggregation. Anger can provoke potentially life-threatening physiological responses in people with CAD. Emotional stress and anger can increase severity and frequency of angina pectoris, and modify treatment. It is thought that this increased angina is due to increased oxygen demand rather than progression of CAD, and as such is tractable to beta-blockers (). On the other hand, a meta-analysis of prospective studies through 1998 on CHD and hostility or Type A personality (TAP) showed slightly different conclusions (). The correlation coefficient r was used to derive the population effect size R and variance. The weighted average of all correlation coefficients (r) for TAP and CHD is r = 0.003 (n =74,326, p = 0.213), a nonsignificant association. For hostility and CHD, r = 0.022 (n = 15,038, P = 0.003) a significant association. However, the effect size is so low that they do not see as yet any practicality for prediction or prevention. The number of medically certified work absences in men but not women has been shown to be predicted by hostility in one 4-year prospective study (9638087). Men with high hostility had greater than twice the risk of all-cause and CHD mortality than men with lower hostility over a 9-year span (). |
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