Researchers in this area have identified candidate biological markers or mechanisms that may be related to psychosocial, behavioral, and environmental factors and may also be associated with risk for disease. These mechanisms include physiological reactivity, allostatic load, psychoneuroimmunology, metabolic syndrome, and neurovisceral integration.


Physiological reactivity is defined as the magnitude of changes in some physiological system in response to acute psychological or behavioral stress. The changes most often studied, typically under laboratory conditions, involve cardiovascular reactivity (e.g., heart rate, blood pressure). The hypothesis is that frequently activated and exaggerated cardiovascular responses to stress raise resting blood pressure levels over time and damage coronary arteries (Matthews et al., 1986; Turner et al., 1992). The strongest evidence for this hypothesis comes from animal experiments that demonstrate an etiological role for stress-induced reactivity in both coronary heart disease (Manuck et al., 1990, 1995) and hypertension (Hallback, 1975; Lovallo and Wilson, 1992; Manuck et al., 1990). Among humans there is evidence that individuals at risk for hypertension—due to a family history or older age, being black or having borderline hypertension—may also exhibit cardiovascular hyperreactivity to stress (Turner et al., 1992). There is also emerging evidence in humans that cardiovascular reactivity among healthy individuals may be prospectively related to later hypertension (Carroll et al., 2001; Falkner et al., 1981; Light et al., 1992; Menkes et al., 1989). Finally, research is emerging on a possible negative correlation between socioeconomic status and reactivity (Gump et al., 1999).

In a new line of research on reactivity, acute psychological stress has been shown to elicit myocardial ischemia, an imbalance between the blood supply to the heart and the demands placed on it to supply the body with oxygenated blood. Myocardial ischemia may result in angina pain, but it is frequently silent, occurring without pain. Psychological stress has been shown to produce silent ischemia in the laboratory; such responses are predictive of ischemia in real life, as measured by ambulatory cardiac recording (Blumenthal et al., 1995). In patients with a history of heart disease, ischemia induced by psychological stress is prospectively related to subsequent cardiac events (Jiang et al., 1996).

A number of studies have explored differences between blacks and whites in stress-induced reactivity as a possible reason for group differences in hypertension. These studies generally find a tendency among black adults and children toward greater peripheral vascular responses to stress in comparison with whites (Anderson, 1989). Blacks show greater cardiovascular responses in laboratory research to stimuli associated with racism (e.g.,

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