The role of stress on physiologic responses and clinical symptoms in irritable bowel syndrome

Abstract

Studies support the concept that irritable bowel syndrome (IBS) is a biopsychosocial disorder that can be explained by a neurobiological model which postulates stress-induced alterations in central stress and arousal circuits and activation of parallel motor outputs from brain regions that can affect bodily function and behavior. Sustained stress can result in chronic overactivity or underactivity of allostatic (or adaptive) systems, including the hypothalamic-pituitary-adrenal (HPA) axis, autonomic nervous system, metabolic, and immune systems, can occur. Animal and human studies have demonstrated that chronic or sustained stress is associated with the onset and exacerbation of symptoms of IBS. Chronic stress is also an independent predictor of developing post-infectious IBS. IBS patients specifically show stress-induced alterations in gastrointestinal motility, rectal perception, autonomic tone and HPA axis responses, although these findings are not entirely consistent among studies. This can be in part due to differences in study methodology or to various factors that can affect these physiologic responses. A greater recognition and understanding of the effects of stress in IBS may help identify targets for future drug development and also help guide more effective management of IBS symptoms.

Figure 1. Physiologic and pathologic responses to stress

An adult’s resilience or vulnerability to stress can be determined by genetic inherence and early life experiences. Activation of the central stress response sets in motion the HPA axis, ANS and other adaptive systems. Stress-induced changes in GI function occur and these can in turn result in perceived symptoms of IBS. (Adapted from Lightman, 200884)