events such as the death of a loved one. Although daily stress has been linked to exacerbation of RA, major life events have actually been associated with decreases in disease activity (Potter & Zautra, 1997). This finding is supported by differences in immunological responses in RA patients to minor and major stressors. Some have suggested that acute, minor stressors are generally associated with increases in immune system activity, whereas major stressors are generally associated with decreases in the same immune parameters (Huyser & Parker, 1998; Zautra et al., 1989). As already mentioned, T-cells, especially CD4 cells, and autoantibodies from B-cells are responsible for the joint inflammation and destruction seen in RA. Therefore, increases in the activity of these cells in response to minor stress should be associated with increases in disease activity. Likewise, the decreases in immune system activity following major stressors should be associated with less disease activity (Huyser & Parker, 1998; Potter & Zautra, 1997).
These differential effects appear to be mediated by the release of catecholamines and cortisol (Huyser & Parker, 1998). Rheumatoid arthritis is typically characterized by decreases in HPA axis activity (i.e., cortisol) and increases in SNS activity (i.e., epinephrine and norepinephrine). Each of these systems have opposing effects on RA management and symptoms. Cortisol has important anti- inflammatory actions that decrease RA activity by reducing the chemical activators of the inflammation process and by suppressing the immune system (Guyton, 1991). Consequently, corticosteroids are often prescribed to RA patients to help manage their symptoms. In contrast, SNS activation has been associated with changes in immune activity and RA symptoms (Huyser & Parker, 1998). Additionally, RA patients have heightened SNS reactivity to minor stressors (Zautra et al., 1998). Although both cate- cholamine and cortisol levels increase in response to stress, it has been proposed that the heightened SNS reactivity to minor stressors counteracts any anti-inflammatory effects of HPA axis activation and cortisol release and results in exacerbations of RA activity and symptoms (Huyser Bt Parker, 1998). In contrast, RA patients who report major life events may experience dramatic increases in HPA axis activation and cortisol release, which in turn may result in decreases in disease activity (Huyser & Parker, 1998; McFarlane & Brooks, 1990).
Although stress can have a profound impact on the etiology and course of RA, there is a subset of RA patients who appear to be immune to its effects. In these patients genetic and etiological influences appear to be more influential in determining RA symptoms (Rimon & Laakso, 1985). Two subgroups of RA patients have been identified based on whether or not RA patients are seropositive for the autoantibody rheumatoid factor. In patients who are seronegative, the occurrence of negative life events are associated not only with increases in disease activity but also with the onset of the disease. In contrast, in people who are seropositive, no such relations exist (Stewart, Knight, Palmer, & Highton, 1994), suggesting that vulnerability to stress is linked to the physiology of the disease process.
Stress is a critical crosscutting process that is basic to research, theory, and application in health psychology. It repesents modifiable variance in the etiology of disease, affects nearly every behavior that contributes to good or bad health outcomes, and has direct effects on all or most bodily systems and can thereby contribute to developing health problems as well. Stress is basic to the commerce between organisms and their environments, motivating them to take action against stressors or to insulate themselves from stress effects. It also produces nonspecific catabolic arousal, driven primarily by neural-endocrine regulatory loops that supports adaptive capabilities such as fight or flight. More specific aspect of stress responding, tied more closely to the stressful situation and its interaction with the organism's resources and abilities, are reflected in emotional responding and coping as well as in cognitive appraisal processes and memory.
Most people are able to adapt to stressful situations and even in the most extreme cases, it would be expected that most people would be able to cope effectively and move on to new challenges. The multiple changes that occur during stress facilitate adaptation. However, there are negative effects of stress that have been observed, including aspects of the pathophysiology of cardiovascular disorders, infectious illnesses (including HIV disease and hepatitis), cancer, diabetes, and autoimmune diseases like rheumatoid arthritis. These effects appear most often when stress responses are extremely intense or abnormally prolonged. They can also become manifest when resources and coping are not able to immediately overcome or displace stressful conditions. Uncontrollable stress appears to be more difficult to resist than controllable and predictable periods of threat or demand.
Quantification of contributions of stress to disease etiology and personal susceptibility to major health problems has been a slow project, but has been increasingly successful in measuring harmful and beneficial effects of stress. Similarly, the ability to intervene and modify lifestyle, coping, social resources, and appraisals of major chronic illnesses, stressors, and associated conditions has continued to improve. Research during the next 10 years should continue framing the extent and limits of stress effects on health and disease and designing ways to minimize unnecessary risk.
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