To the Editor: We thank Eppinga and Peppelenbosch for their interest in our article and their observations with dietary triggers, exacerbating symptoms in patients with inflammatory bowel disease (IBD). Their finding, particularly with certain food groups, such spicy and fatty foods, fruits and vegetables, alcohol, dairy products, and sugary foods exacerbating symptoms, corroborates our observations. We agree that further research is required, before such findings and others from restriction diets, largely popularized by anecdotal evidence, can be applied to advising patients with IBD. Research in the role of diet in IBD is limited by difficulty in accurately capturing dietary intake, the proportion of food intake relative to other dietary components, the potential for complex interactions between food groups, variable food metabolism among individuals, and inherent differences in food products (preparation, preservation, processing, and packaging). Diet is a factor within the complex “exposome” of IBD and may need to be considered separately from its role in IBD pathogenesis. There are multiple putative mechanisms by which food components may affect the gut and induce symptoms, such as satiety signaling in the brain-gut axis, chemostimulation of gut receptors, neuroendocrine influences, and psychosocial factors. Therefore targeted approaches in research must consider elimination diets, exclusion of specific inflammatory mediators, inclusion of anti-inflammatory mediators, and the effect of diet on the microbiota and immune system. For example, exacerbation of symptoms through ingestion of insoluble fiber in fruit and vegetables is a likely result of metabolic fermentation and water retention in the colon with consequent accelerated movement of food through the intestine. Furthermore, the striking observation that patients noted onion and cabbage among exacerbating factors might relate to FODMAP (Fermentable, Oligosaccharides, Disaccharides, Monosaccharides and Polyols) intake and an osmotic effect from fermentation by intestinal bacteria, so is independent of inflammation. A similar explanation may hold true for sugar and other carbohydrate rich foods. Eppinga and Peppelenbosch reported that diets with high fat consumption exacerbated symptoms in patients with IBD. Fatty acids may promote inflammation through diverse mechanisms including cytokine signaling, affecting intestinal permeability, and a direct effect on immune cells and Toll-like receptors. A high fat diet may be associated with endotoxemia and a low-grade inflammatory state even in healthy subjects. The evidence for exclusive enteral nutrition in reducing symptoms and mucosal inflammation in IBD holds promise for the therapeutic benefit for certain diets and derived supplements. These observations may serve to optimize clinical studies through identification of nocebo effects and proinflammatory food groups to gain deeper mechanistic insights into the effects of food on the microbiota and the immune system. It is plausible that in unraveling the mysteries of microbiome, diet, and immune system interactions, we may discover what “we are” through what we eat.
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