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Review
, 54 (10), 1481-91

Psychological Stress in IBD: New Insights Into Pathogenic and Therapeutic Implications

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Review

Psychological Stress in IBD: New Insights Into Pathogenic and Therapeutic Implications

J E Mawdsley et al. Gut.

Abstract

Psychological stress has long been reported anecdotally to increase disease activity in inflammatory bowel disease (IBD), and recent well designed studies have confirmed that adverse life events, chronic stress, and depression increase the likelihood of relapse in patients with quiescent IBD. This evidence is increasingly supported by studies of experimental stress in animal models of colitis. With the evolving concept of psychoneuroimmunology, the mechanisms by which the nervous system can affect immune function at both systemic and gut mucosal levels are gradually becoming apparent. Recent data suggest that stress induced alterations in gastrointestinal inflammation may be mediated through changes in hypothalamic-pituitary-adrenal (HPA) axis function and alterations in bacterial-mucosal interactions, and via mucosal mast cells and mediators such as corticotrophin releasing factor (CRF). To date, the therapeutic opportunities offered by stress reduction therapy remain largely unexplored, in part because of methodological difficulties of such studies. This paper reviews recent advances in our understanding of the pathogenic role of psychological stress in IBD and emphasises the need for controlled studies of the therapeutic potential of stress reduction.

Figures

Figure 1
Figure 1
Pathways mediating the effects of stress on the gastrointestinal tract. (The effects of activation of the enteric nervous system on the gut in inflammatory bowel disease are shown in fig 2 ▶.) ACTH, adrenocorticotrophic hormone; CRF, corticotrophin releasing factor.
Figure 2
Figure 2
Pathways by which the enteric nervous system (ENS) is likely to mediate stress induced increases in inflammatory bowel disease (IBD) symptomatolgy and disease activity. CRF, corticotrophin releasing factor; SP, substance P; IL, interleukin.

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