Experimental stress in inflammatory rheumatic diseases: a review of psychophysiological stress responses

Abstract

IntroductionStressful events are thought to contribute to the aetiology, maintenance and exacerbation of rheumatic diseases. Given the growing interest in acute stress responses and disease, this review investigates the impact of real-life experimental psychosocial, cognitive, exercise and sensory stressors on autonomic, neuroendocrine and immune function in patients with inflammatory rheumatic diseases.MethodsDatabases Medline, PsychINFO, Embase, Cinahl and Pubmed were screened for studies (1985 to 2009) investigating physiological stress responses in inflammatory rheumatic diseases. Eighteen articles met the inclusion criteria.ResultsResults suggest that immune function may be altered in response to a stressor; such alterations could contribute to the maintenance or exacerbation of inflammatory rheumatic diseases during stressful events in daily life.ConclusionsThis review emphasizes the need for more experimental research in rheumatic populations with controlled stress paradigms that include a follow-up with multiple evaluation points, simultaneous assessment of different physiological stress systems, and studying factors contributing to specific physiological responses, such as stress appraisal.

The role of psychological factors in inflammatory rheumatic diseases: From burden to tailored treatment

“…2) nervous system (ANS), which includes the sympathoadrenal medullary (SAM) axis that secretes adrenaline and noradrenaline, and the neuroendocrine system, which includes the hypothalamicepituitaryeadrenal (HPA) axis that secretes cortisol, a major stress regulatory parameter. Because both pathways are connected with the immune system, influencing these pathways through psychological factors may influence disease processes in immune-mediated rheumatic diseases [23,26,27]. …”

“…However, causality cannot be ascertained as prospective associations could also be due to factors that are associated with both the risk or resilience factor and the change in quality of life or disease impact. Although the laboratory setting is not a natural environment, which may limit the generalizability of the findings to daily life settings, experimental studies that manipulate a psychological factor and examine its effect on functioning while controlling other key factors enable true causal conclusions [26]. Although not all psychological factors can (easily) be manipulated (e.g., personality characteristics) and not much experimental research has been conducted in patients with inflammatory rheumatic diseases, the following paragraphs will provide the current knowledge base in this or related fields (e.g., pain stimulation in healthy participants or other chronic pain populations).…”

“…These stressors have shown to induce stress-related SAM, HPA, and immune responses in patients with inflammatory rheumatic diseases, with the strongest effects shown in response to psychosocial stressors [26,27]. In inflammatory rheumatic diseases, immune responses that are similar to those in experimental stress in healthy individuals have been found; the exceptions are a lower Natural Killer (NK) cell cytotoxicity after stress in patients than in controls, potentially because of chronic immune activation due to the inflammatory disease [26], and an increased proinflammatory cytokine increase in response to a psychosocial stressor after controlling for elevated baseline levels of proinflammatory cytokines in patients with rheumatoid arthritis [56]. The link between real-life psychosocial stressors and psychophysiological and immune reactivity suggests a potential role of stressors in the maintenance or exacerbation of inflammatory rheumatic diseases, which is in line with the prospective evidence of a link between stressors and disease outcome [26,27].…”

The Pathogenetic Link Between Stress and Rheumatic Diseases

“…Recent advances in psychoneuroimmunology have provided insight into the complex mechanisms by which stressors might affect the homeostasis and the body's immune system (de Brouwer et al, 2010). Stress challenges the organism's homeostatic mechanisms, triggering a cascade of events that should, normally, maintain or allow a return to equilibrium (Pêgo et al, 2010).…”

“…It was shown that psychological stress is also thought to contribute to the aetiology, maintenance and exacerbation of rheumatic diseases (de Brouwer et al, 2010). Stress has been studied in several autoimmune rheumatic diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) (Cutolo & Straub, 2006).…”