Autoimmune Diseases: Psychosocial Aspects

Autoimmune diseases result when the immune system becomes dysregulated and directs its attack not toward foreign invaders, but toward one or more aspects of the body's own healthy organ systems. The consequences of this dysregulation range from relatively mild manifestations, such as hay fever, to lifethreatening illnesses. More than 80 serious chronic autoimmune illnesses have been identified, including diseases that involve the skin and connective tissues (e.g., rheumatoid arthritis [RA]), and the endocrine (Grave's disease), nervous (e.g., multiple sclerosis), and gastrointestinal (e.g., inflammatory bowel disease) systems. The underlying causes of autoimmune diseases are still under investigation, but several prevalence patterns provide clues about factors that may contribute to their development. Because autoimmune diseases cluster in families, for example, these illnesses are thought to have a genetic component. In addition, autoimmune diseases are about 3 times as likely to occur among women compared to men, and are particularly prevalent during childbearing years, suggesting that reproductive hormones may play a role. It is important to keep in mind as well that different biological mechanisms underlie each autoimmune condition.

Although immune system activity is a key factor in progression of autoimmune disease, adaptation involves a complex interplay of biological, psychological, and social factors. Not only do the symptoms and physiological underpinnings of autoimmune disease have consequences for psychological and social functioning, but also psychological and social factors influence immune activation and suppression, to affect how individuals respond to their disease in mind and body.

Among the most widely studied psychosocial factors is social stress, which has been associated with dysregulation of immune factors known to influence the course of autoimmune disease. Although stressful events were initially studied for their role in suppression of immune function, more recent studies have found evidence that stress may also activate aspects of the immune system, especially proinflammatory processes. For example, Zautra, Smith, and Yocum (2002) have found greater T-cell activation as well as increased pain among RA patients following a stressful week, with proinflammatory cytokines such as interleukin-6 implicated. Mohr et al. (2000) found evidence of new brain lesions in multiple sclerosis patients following conflict and disruption in routine. Stress-related changes in the hypothalamic-pituitaryadrenal (HPA) system have well-established effects on immune functioning. Elevations in cortisol, for example, suppress immune function, and Sternberg and colleagues have offered the hypothesis that some autoimmune conditions such as RA are a consequence of an insufficient cortisol response. Other stressrelated hormones are likely to be involved as well. Moderate increases in prolactin promote immune activation. This pituitary hormone is often elevated during stress and has been found higher in RA than osteoarthritis patients with comparable pain. Although the focus of most studies has typically been on the HPA system, there is also evidence of sympathetic nervous system involvement.

Chronically stressful situations may also reduce the sensitivity of the receptors on immune cells to the anti-inflammatory actions of hormones like cortisol. Coping responses that fail to resolve the stressful situation may lead to chronic distress with accompanying feelings of helplessness and depression. Persons with clinical depression have elevations in proinflammatory cytokines such as Il-6, which are also elevated in some autoimmune conditions such as RA, suggesting that affective disturbance is a key cofactor in disease course (Maes, Song, Lin, et al., 1998). These influences may be reversible through interventions that elevate positive affect and provide means to better regulate negative emotions. Early evidence of such relationships has been found in studies that manipulated positive emotion and found a reduction in levels of proinflammatory cytokines. It is important to keep in mind, however, that models of unidirectional cause and effect relationships often must give way to bidirectional relationships to fully capture the processes that underlie relationships between immune function and human emotion.

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