Combat-training stress and high pro-inflammatory markers in soldiers linked to increased intestinal permeability and gastrointestinal symptoms

combat training stress

A study published in the February 2013 issue of Alimentary Pharmacology and Therapeutics reports that soldiers participating in as little as 6 weeks of combat training had high stress; anxiety and depression levels combined with gastrointestinal (GI) symptoms, pro-inflammatory immune activation and increased intestinal permeability.

Gastrointestinal symptoms in soldiers are among the most common causes of front-line clinic visits; and data from the Gulf, Iraq and Afghanistan conflicts have highlighted the significance of GI symptoms on military efficiency and manpower loss on the front lines. However, underlying mechanisms, apart from infectious diarrhea, have not been extensively investigated. Also, the stress responses related to the GI-tract have been mainly characterized using animal models, and little is known about the long-term effects of stress in the battlefield.

In this prospective, longitudinal study, Li and colleagues from the Neurogastroenterology Research Unit, Department of Medicine, National University of Singapore, Singapore, demonstrate that protracted combat-training stress induced GI symptoms associated with increased upper and lower intestinal barrier permeability and elevated systemic levels of interleukin (IL)-6, and tumor necrosis factor (TNF)-α. Notably, the subgroup that had suffered the most GI symptoms also scored higher in anxiety, depression and stress.

This human study indicates that protracted and intense physical and psychological stress in soldiers may alter GI permeability and thus, may elicit clinical GI symptoms. The authors suggest that the responsiveness of an individual’s stress–neuroimmune axis at rest, and during stress, influences downstream GI permeability changes and related GI symptoms and vice versa. One possible mechanism is that the increased intestinal permeability is most likely due to stress-driven neuroimmune activation, with subsequent increases of systemic or local production of   TNF-α and IL-6. This, in turn, leads to disruption of intestinal barrier integrity and further release of inflammatory mediators.

According to the authors, the identification of a subgroup of individuals with greater propensity for GI adverse events, may allow selection of those at-risk of long-term effects of stress, such as functional GI disorders, as well as the development of protective measures.

Source: Aliment Pharmacol Ther. 2013, 37:799. doi: 10.1111/apt.12269. Epub 2013 Feb 24.

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