Exposure to stressful life events has been recognized as an important promoter of major psychiatric illness for many years (i.e., the classic diathesis-stress model). This belief stems from observations that episodes of psychiatric illness are more frequently observed shortly after major life stressors and that clinical symptoms of many psychiatric illnesses worsen during times of stress (Mazure and Druss, 1995). Indeed, the role of life stressors as determinants for the onset and severity of many major psychiatric conditions has been common parlance in psychiatric settings for decades. Stress has been reported to promote symptomology in diverse psychiatric conditions ranging from personality disorders, to affective disorders, to dissociative disorders, and to somatic disorders. With such a wide range of conditions affected by exposure to stressors, it is clearly of interest to understand the organization and function of stress responsive systems in the brain that might serve as common threads for promoting mental health. With that in mind, it is not enough to simply state that stress exacerbates major psychiatric symptomology. Marked differences are observed across individuals in how the consequences of stress become manifest. Many individuals who experience adverse life events do not develop major psychiatric illness, and not everyone who develops a major psychiatric illness appears to have a precipitating life event. These findings have spurred research toward understanding (a) how exposure to qualitatively distinct stressors might differentially affect health outcomes, and (b) how individual subject's vulnerability may predispose or protect against the development of major psychiatric and psychosomatic illness.
For instance, exposure to stressors for some individuals produces gastrointestinal (GI) dysfunction (ulcers, colitis, etc.), while others may manifest immunological disturbances (frequent infection due to stress-induced immunosuppression, increased occurrence or worsening of autoimmune diseases, etc.). Such disparities in physiological outcomes of stressor exposure has led many researchers to postulate that individuals vary in the organs or brain systems that are constitutionally weakest and thus more susceptible to adverse health outcomes during times of stress. In this regard, one could attempt to explain the recurrence of chronic colitis in relation to stressor exposure by merging Selye's general adaptation syndrome with modern evolutionary principles. The interpretation would be that the GI tract was the least competent physiological system within that individual (or group of individuals), and thus reached the stage of exhaustion more rapidly than other systems. As a result, adverse symptoms (as in the case of colitis) repeatedly occur during times of stress (indeed Charles Darwin's own chronic health problems following his return to England may have had such an etiology).
Multiple models have been proposed to explain how similar life stressors can produce such highly variable health outcomes across different individuals. All of these models propose that adverse life events act as a triggering mechanism that activates some underlying predisposition toward the development of a specific disorder. The inherent differences in disease susceptibility are frequently cast in the light of genetic differences/predispositions. However, the availability of effective coping strategies and social support are also critical moderating variables that can be used as predictors for health outcomes following stressor exposure. Thus, the ultimate health outcome depends on a complex interaction between precipitating life stressors, individual differences in effective coping strategies, and underlying biological predispositions. See Dohrenwend and Dohrenwend (1981) for a thorough discussion of various permutations of diathesis-stress models that are applicable to biological psychiatry.
Given our understanding of diathesis-stress models and advances in molecular cloning and gene sequencing, a new generation of researchers are tracking down genetic markers that may point toward specific disease susceptibility. Likewise, clinicians have made similar progress in identifying specific coping strategies that, when absent in an individual, might promote the occurrence of major psychiatric illness following adverse life events. One recent breakthrough was the finding that disease-prone individuals often exhibit a higher propensity to seek out stressful life situations, thus further increasing the likelihood that psychiatric illness might develop (Mazure, 1998). Furthermore, clinical observations suggest that stress may be critical for initiating the first episode of psychiatric illness (e.g., depression) and much less important for subsequent episodes (e.g., Perris, 1984), suggesting sensitization/learning processes can occur in the system, although this issue is still far from resolved.
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