Stress and Disease Processes

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

associated immune system changes cannot be definitively compared. The nature of chronic stress is sufficiently complex to defy simple categorization. In this chapter, we have broken it down on a crude index of duration, comparing intermediate and long-term stressors and finding similar effects of both. However, we have not considered the many different sources of chronic stress. Are traumatic stress syndromes, wherein distress far outlasts the physical presence of an acute but powerful event, different from situations such as caregiving or occupational stress where stressors persist continuously for long periods of time? Studies of bereavement, divorce, caregiving, and the TMI situation suggest that they can have similar effects, but these different situations have not been studied systematically. If we are to arrive at a thorough and applicable understanding of stress and immune function, these and other questions must be addressed.

Similarly, the timing and selection of immune measures and neuroendocrine mediator indices must be considered more systematically. In studies of acute stress, such measures are typically collected during or shortly after challenge. Thus, these measures can be thought of as "reactivity" measures. Proliferation assessments in the Weisse and colleagues ( 1990) or Zakowski et al. ( 1990) studies involved measurement of cells challenged in vitro after they had been challenged in vivo. Studies of chronic stress are different in that they usually measure people at resting levels who have been challenged in the past. Thus, finding that people living near TMI exhibit elevated blood pressure and latent viral antibody titers 5 or 6 years after the accident cannot easily be compared with finding increased blood pressure or suppressed lymphocyte proliferation during or after acute laboratory stress. Whether these effects are comparable, whether different subsets of immune cells or factors are involved, and whether different mediators are involved are all questions that need to be answered.

Whether differences in acute or chronic stress-related changes in immune function are of clinical interest, provide insights into the basic mechanisms underlying appraisal or coping, or ultimately tell us about the stress response, they are useful objects of study. The lack of systematic consideration of these issues in favor of demonstration that such phenomena exist should no longer characterize research in this challenging area of research.


ACKNOWLEDGMENT

This chapter was supported in part by USUHS grants, CO7216 and R07265. The opinions and assertions contained herein are those of the authors and do not necessarily reflect those of the Department of Defense or the Uniformed Services University of the Health Sciences.

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