Abstract
Inflammatory bowel disease (IBD) is a chronic relapsing–remitting systemic disease of the gastrointestinal tract, characterized by an inflammatory process that requires lifelong treatment. The underlying causes of IBD are still unclear, as this heterogeneous disorder results from a complex interplay between genetic variability, the host immune system and environmental factors. The current knowledge recognizes diet as a risk factor for the development of IBD and attributes a substantial pathogenic role to the intestinal dysbiosis inducing an aberrant mucosal immune response in genetically predisposed individuals. This review focused on the clinical evidence available that considers the impact of some nutrients on IBD onset and the role of different diets in the management of IBD and their effects on the gut microbiota composition. The effects of the Specific Carbohydrate Diet, low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet, gluten free diet, anti-inflammatory diet and Mediterranean diet are investigated with regard to their impact on microbiota and on the evolution of the disease. At present, no clear indications toward a specific diet are available but the assessment of dysbiosis prior to the recommendation of a specific diet should become a standard clinical approach in order to achieve a personalized therapy.
Highlights
Inflammatory bowel disease (IBD) is a chronic relapsing–remitting systemic disease of the gastrointestinal tract, characterized by an inflammatory process that requires lifelong treatment
We focused on various nutritional approaches, specific food components and microbiome to identify a possible link between them that could influence the evolution of IBD, with the aim of determining a personalized diet for patients affected by ulcerative colitis (UC) or Crohn’s Disease (CD)
The low FODMAP diet involves, similar to Specific Carbohydrate Diet (SCD), a reduction in poorly absorbed and highly fermentable carbohydrates, with the difference that monosaccharide intake is favored in SCD, while it is discouraged in FODMAP; the premise underlying the two diets is similar, i.e., that carbohydrates that are poorly absorbed may lead to large intestine dysbiosis, inflammation, fermentation, water secretion and lumen distension [134,135,136]
Summary
Inflammatory bowel disease (IBD) is a heterogenous set of inflammatory diseases, mediated by the immune system, which affect the gastrointestinal tract. Most of these IBD susceptibility genetic polymorphisms are associated with host mucosal barrier function and are involved in host–microbiome interactions [12,13,14,15,16,17] These findings support the hypothesis that alterations of the gut microbiome are essential in triggering chronic inflammation and not merely a consequence [18,19]. Microbiota influences the activation of some genes associated with hypomethylated active regulatory regions, inducing the expression of genes associated with colitis and IBD [77]
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