The long term goal of this project is to clarify how interactions between dietary factors and epigenetic mechanisms influence the development of inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) and Crohn's disease (CD). UC is linked primarily to inflammation of the colonic mucosa extending from the rectum in a uniform manner to involve part of, or the entire, colon. Conversely, CD involves inflammation of the entire gastrointestinal tract, but it most commonly affects the terminal ileum and proximal colon. During the last two decades there has been a measurable increase in the incidence of adult and pediatric IBD in Western countries. In the U.S. alone, ~1.4 million adults suffer from IBD. However, genetic factors account for only a modest proportion of the disease ranging from ~14% for CD to ~7.5% for UC. These observations highlight the importance of exogenous factors, including diet, in the pathogenesis of IBD. Therefore, the intriguing possibility arises epigenetic influences may largely account for the development of IBD.Epigenetics refers to regulation of gene expression in the absence of changes in DNA sequence. For example, dietary exposures to various fats during pregnancy and postnatal life have been shown to impact epigenetic reprogramming and affect metabolic pathways in children. Certain epigenetic modifications become part of the cellular memory and contribute to IBD. Importantly, epigenetic modifications are reversible. Therefore, clarifying whether or not epigenetic changes contribute to the etiology of IBD may provide novel targets for dietary prevention and treatment.