To Prevent IBD in Children, Let the Sunshine in?

Abstract

n this edition of the Journal of Pediatric Gastroenterology and Nutrition, Holmes et al (1) describe an association between I higher exposure to sunlight and decreased risk of pediatric inflammatory bowel disease (IBD), based on a matched case-control study. The authors delineate the strengths and limitations of their methodology, including the possibility of recall bias from estimating cumulative exposure to sunshine with a questionnaire. Nonetheless, this study may offer the best possible data to examine whether sunshine protects against IBD. The alternative, which is to follow a large group of children prospectively for many years to address this question, is highly impractical. So, should we let our children run in the sun to protect them from developing IBD? To answer this question, we would first like to discuss possible reasons for a protective effect of sun exposure on IBD risk. First, sunlight increases the cutaneous synthesis of vitamin D. Vitamin D may then decrease IBD risk. We discuss supportive evidence for this possibility in more detail below. Alternatively, sunshine may exert a vitamin D-unrelated effect on the skin that mitigates IBD risk. For example, ultraviolet radiation upregulates the expression of adrenocorticotropin hormone, which stimulates the synthesis of cortisol, a known immune modulator (2). Additionally, an activity or behavior performed outdoors, such as exercise, may protect from developing IBD. Along these lines, the Nurses’ Health Study found that exercise is associated with a decreased risk of developing Crohn disease (3). As well, higher exposure to sunlight may be a marker of a lifestyle that reduces the risk of IBD for reasons that are unrelated to sunshine per se, such as diet. Cutaneous vitamin D synthesis induced by ultraviolet radiation may decrease the risk of IBD via several possible mechanisms. For example, multiple in vitro studies have shown that vitamin D stimulates innate immune activity and dampens adaptive immune function (4). If the same occurs in vivo, vitamin D may decrease the likelihood of developing IBD by affecting the immune system. In mouse studies, vitamin D supplementation decreases the severity of dextran sodium sulfate (DSS)-induced colitis (5). Overexpression of human vitamin D receptor (hVDR) in mice reduces the severity of experimental colitis, possibly because of the reduction of intestinal epithelial cell apoptosis (6). VDR knockout mice develop severe gastrointestinal inflammation, suggesting a role for VDRmediated signaling in gastrointestinal immune function (7). In another