Stress and Disease Processes

By Neil Schneiderman; Philip McCabe et al. | Go to book overview

parameter being investigated, it is difficult, if not misleading, to speak categorically about the nature and "direction" of these stress effects ( Ader & Cohen, 1984). Indeed, the wealth of published studies indicate that a given stressor can be associated with an enhancement as well as a depression of an immune response ( Okimura & Nigo, 1986) and that different stressors can have different qualitative, and perhaps even quantitative effects on a single immune parameter ( Solomon, 1969). Indeed, the magnitude and direction of a behaviorally driven deviation of immune function from "normalcy" appears to be related to the factors such as: the duration of exposure to the stressor ( Monjan & Collector, 1977; Moynihan, Ader et al., 1990); the timing of stress administration relative to the time of antigenic exposure ( Esterling & Rabin, 1987; Okimura & Nigo, 1986; Zalcman et al., 1988); the time of immunological assay after exposure to the stressor ( Schleifer et al., 1983); the immune status of the animal being stressed ( Edwards et al., 1980; Laudenslager et al., 1988; Moynihan, Ader, Grota, Schachtman, & Cohen, 1990; Solomon, 1969); the concentration of antigen used to elicit an antibody response in a stressed animal ( Moynihan et al., 1990); and perhaps the coping behavior of the organism ( Maier & Laudenslager, 1988; Mormede et al., 1988).

By choice, we have not attempted to review the large body of literature indicating the constellation of effects that diverse stress hormones (e.g., catecholamines, steroids, proopiomelanocortin-derived peptides, prolactin, growth hormone, etc.) can have on immunity (reviewed in Ader, Felten, & Cohen, 1990; see also citations in the introduction). Neither have we attempted to review in any detail the somewhat conflicting literature dealing with correlations between stress-associated changes in an immune parameter and changes in endogenous neuropeptides (e.g., endogenous opioids) or hormones (e.g., glucocorticoids). At this time, we believe that there are still too many gaps in our knowledge to allow us to present anything resembling a clear picture of cause and effect. We do anticipate, however, that with the expanding interest in the basic and clinical ramifications of psychoneuroimmunology that the next decade of stress-immune response research will clearly reveal what neuroendocrine changes are evoked by which stressor, how these changes modify components of the immune system, and how these changes in the immune response are causally related to increased morbidity and mortality.


ACKNOWLEDGMENTS

Research cited from the authors' laboratory has been supported by grant MH-45681 from the National Institutes of Mental Health.

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