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This study provided a test of the minority status stress model by examining whether perceived discrimination would directly affect health outcomes even when perceived stress was taken into account among 215 Mexican-origin adults. Perceived discrimination predicted depression and poorer general health, and marginally predicted health symptoms, when perceived stress was taken into account. Perceived stress predicted depression and poorer general health while controlling for the effects of perceived discrimination. The influence of perceived discrimination on general health was greater for men than women, and the effect of perceived stress on depression was greater for women than men. Results provide evidence that discrimination is a source of chronic stress above and beyond perceived stress, and the accumulation of these two sources of stress is detrimental to mental and physical health. Findings suggest that mental health and health practitioners need to assess for the effects of discrimination as a stressor along with perceived stress. (Contains 3 tables and 2 figures.)

Relations between repressive coping and a variety of health-related variables, including insulin, lipids, catecholamines, and cellular immune components, were investigated in a laboratory study of acute stress among a sample of healthy male college students (N = 83). Compared to nonrepressors, at baseline, repressors had fewer numbers of circulating CD4 (T-helper) cells, greater numbers of natural killer (NK) cells, lower high-density lipoprotein (HDL), a higher total/HDL cholesterol ratio, and higher fasting insulin levels, in response to an acute laboratory stressor (Stroop Color Word Conflict Test), repressors demonstrated an attenuated increase in the number of circulating NK cells compared to nonrepressors. Confounds such as physical activity, age, and smoking were unrelated to the dependent measures.

Psychological stress is known to affect immune function and to predict infectious disease susceptibility. However, not all individuals who are stressed develop disease. In the present article, we report on a series of studies from our laboratory describing interindividual variability of immune responses to psychological stress. In our initial series of experimental investigations, we demonstrated that acute laboratory stress alters both quantitative and functional components of cellular immunity. An examination of response variability revealed that individuals differ substantially in the magnitude of these immune responses. These differences were found to parallel (and be predicted by) interindividual variability in stress-induced sympathetic nervous system activation. Further investigation revealed that individuals vary consistently in the magnitude of their immune responses to stress, making it conceivable that individual differences in immune reactivity provide a vulnerability factor mediating relationships between stress and disease. In support of this possibility, we have recently reported initial evidence that individual differences in the magnitude of stress-induced reduction of immune function may be of clinical significance, being related to an immune response relevant for protection against infection, antibody response to hepatitis B vaccination. [Copyright &y& Elsevier]