Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder of the gastrointestinal tract, with increasing prevalence, and its pathogenesis remains unclear. Accumulating evidence suggested that gut microbiota and bile acids play pivotal roles in intestinal homeostasis and inflammation. Patients with IBD exhibit decreased microbial diversity and abnormal microbial composition marked by the depletion of phylum Firmicutes (including bacteria involved in bile acid metabolism) and the enrichment of phylum Proteobacteria. Dysbiosis leads to blocked bile acid transformation. Thus, the concentration of primary and conjugated bile acids is elevated at the expense of secondary bile acids in IBD. In turn, bile acids could modulate the microbial community. Gut dysbiosis and disturbed bile acids impair the gut barrier and immunity. Several therapies, such as diets, probiotics, prebiotics, engineered bacteria, fecal microbiota transplantation and ursodeoxycholic acid, may alleviate IBD by restoring gut microbiota and bile acids. Thus, the bile acid–gut microbiota axis is closely connected with IBD pathogenesis. Regulation of this axis may be a novel option for treating IBD.

Inflammatory bowel disease (IBD) is a result of a complex interplay between genes, host immune response, gut microbiota, and environmental factors. As one of the crucial environmental factors, diet plays a pivotal role in the modulation of gut microbiota community and the development of IBD. In this review, we present an overview of dietary patterns involved in the pathogenesis and management of IBD, and analyze the associated gut microbial alterations. A Westernized diet rich in protein, fats and refined carbohydrates tends to cause dysbiosis and promote IBD progression. Some dietary patterns have been found effective in obtaining IBD clinical remission, including Crohn’s Disease Exclusion Diet (CDED), Mediterranean diet (MD), Anti-Inflammatory Diet (AID), the low-“Fermentable Oligo-, Di-, Mono-saccharides and Polyols” (FODMAP) diet, Specific Carbohydrate Diet (SCD), and plant-based diet, etc. Overall, many researchers have reported the role of diet in regulating gut microbiota and the IBD disease course. However, more prospective studies are required to achieve consistent and solid conclusions in the future. This review provides some recommendations for studies exploring novel and potential dietary strategies that prevent IBD.

Inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC) are common diseases of the digestive system. Vitamin deficiencies and gut microbiota dysbiosis have a close relationship with the risk, development, and progression of IBD and CAC. There is a strong link between vitamins and the gut microbiome. Vitamins are extremely crucial for maintaining a healthy gut microbiota, promoting growth and development, metabolism, and innate immunity. Gut microbiota can not only influence the transport process of vitamins, but also produce vitamins to compensate for insufficient food intake. Emerging evidence suggests that oral vitamin supplementation can reduce inflammation levels and improve disease prognosis. In addition, improving the diet structure and consuming foods rich in vitamins not only help to improve the vitamin deficiency, but also help to reduce the risk of IBD. Fecal microbiota transplantation (FMT) and the application of vitamin-producing probiotics can better assist in the treatment of intestinal diseases. In this review, we discuss the interaction and therapeutic roles of vitamins and gut microbiota in IBD and CAC. We also summarize the methods of treating IBD and CAC by modulating vitamins. This may highlight strategies to target gut-microbiota-dependent alterations in vitamin metabolism in the context of IBD and CAC therapy.