Abstract:Diet has been speculated to be a factor in the pathogenesis of inflammatory bowel disease and may be an important factor in managing disease symptoms. Patients manipulate their diet in attempt to control symptoms, often leading to the adoption of inappropriately restrictive diets, which places them at risk for nutritional complications. Health professionals struggle to provide evidence-based nutrition guidance to patients due to an overall lack of uniformity or clarity amongst research studies. Well-designed d… Show more
“…Families stated a preference for nutritional support as dietary advice instead of MEN. Young people and parents reported an increased interest in their diet after diagnosis, similar to previous findings . Engaging young people with CD in the co‐design of studies on healthy diet and lifestyle choices may positively impact clinical and nutritional outcomes in adulthood and as a patient‐led practice may improve quality of life .…”
Patients' perception of the usefulness of MEN differs to professionals. This study highlights the extensive practice of MEN after EEN in clinical remission, which may not be nutritionally indicated. Patient preference is for dietary advice rather than MEN.
“…Families stated a preference for nutritional support as dietary advice instead of MEN. Young people and parents reported an increased interest in their diet after diagnosis, similar to previous findings . Engaging young people with CD in the co‐design of studies on healthy diet and lifestyle choices may positively impact clinical and nutritional outcomes in adulthood and as a patient‐led practice may improve quality of life .…”
Patients' perception of the usefulness of MEN differs to professionals. This study highlights the extensive practice of MEN after EEN in clinical remission, which may not be nutritionally indicated. Patient preference is for dietary advice rather than MEN.
“…Our results indicate that diet is a critical factor affecting development of IL-23-driven experimental IBD, and suggest that it does so by modifying the microbiota. Dietary constituents have been shown to affect the immune response and the inflammatory status, in part by modulating the microbiota 22,50 Our studies showed a marked reduction in alpha diversity as function of the diet change.…”
Section: Discussionmentioning
confidence: 68%
“…Mice bearing specific gene alterations develop colitis, but a significant number of them do not develop colitis when raised in germ-free conditions, suggesting a critical role for genes and the microbiota in promoting disease 4,20 . Other animal studies suggest a critical role of dietary components in the onset and severity of colitis [21][22][23] . Yet, the development of relapsingremitting disease models has not been reported.…”
A wealth of experimental data points to immunological and environmental factors in the pathogenesis of inflammatory bowel disease (IBD). Here we study the role of IL-23, the microbiome, and the diet in the development of colitis. To promote IL-23 expression in vivo,we generated a mouse model in which IL-23 was conditionally expressed by CX 3 CR1 + myeloid cells, upon cyclic administration of tamoxifen in a specific diet (diet 2019). IL-23 expression induced an intestinal inflammatory disease that resembled ulcerative colitis in humans with cycles of acute disease and remission. The relapses were caused by the diet switch from the conventional diet used in our facility (diet 5053) to the diet 2019, and were not dependent on tamoxifen after the first cycle. The switch in the diet modified the microbiota, but did not alter the levels of IL-23. Colitis induction depended on the microbiota and required CD4 T lymphocytes. Colitis-inducing CD4 + T cells were found in the mesenteric lymph node and large intestine during remission and were able to trigger disease when transferred to lymphopenic mice, but only upon diet modification. The CD4 TCR repertoire in the diseased recipient Rag -/-mice had reduced diversity associated with the expansion of dominant T cell clones. These findings reveal a critical role for IL-23 in generation of a CD4 + T cell population in mice that is sensitive to a modification of intestinal bacterial flora subsequent to a dietary manipulation. Dietary changes occurring in the context of altered IL-23 expression may contribute to the onset and progression of IBD.
“…23) Haskey et al showed that a high protein intake, especially from animal protein, resulted in a 3.3 time increased risk of IBD, suggesting that a diet high in animal protein was a major risk factor. 23) With respect to the intake of dietary fats, a high n3 polyunsaturated fatty acid (PUFA) to n6 PUFA ratio is reportedly inversely associated with the risk of IBD. 2325) Several studies have shown the influence of certain components contained in food on epithelial cell permeability.…”
Inflammatory bowel disease (IBD) is a chronic relapsing im munemediated disease of the intestinal tract. Although its pre valence is reportedly lower in Asia than in Western countries, the rapid increase in the incidence of IBD has drawn attention to its etiology, including genetic susceptibility and environmental factors. Specifically, recent studies concerning dietary treatments and intestinal microbiota suggest that these factors may interact with the immune system, and the imbalance of this relationship may lead to immune dysregulation in IBD. Changes in diet or alterations in the composition of the intes tinal microbiota may be associated with the increasing incidence of IBD in Asia. Here, we aim to review recent studies on the role of diet and intestinal microbiota in IBD pathogenesis and the results of the investigations performed to modulate these factors.
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