IBD and Diet, the Role of Foods, and Genetics

A recent article in Medscape (Expert Rev Clin Immunol. 2013;9(8):735-747.) looked at the role of foods in the management of IBD. The author Lynette Ferguson summarised some of the key areas, and this summary is a synopsis of her paper.

Inflammatory bowel disease includes ulcerative colitis and Crohn’s disease, which are both inflammatory disorders of the gastrointestinal tract. Both types of inflammatory bowel disease have a complex aetiology, resulting from a genetically determined susceptibility interacting with environmental factors, including the diet and gut microbiota. Genome Wide Association Studies have implicated more than 160 single-nucleotide polymorphisms in disease susceptibility. Consideration of the different pathways suggested to be involved implies that specific dietary interventions are likely to be appropriate, dependent upon the nature of the genes involved. Epigenetics and the gut microbiota are also responsive to dietary interventions. Nutrigenetics may lead to personalized nutrition for disease prevention and treatment, while nutrigenomics may help to understand the nature of the disease and individual response to nutrients.

Epigenetics provides a mechanism for regulating otherwise heritable changes in gene expression, but without changes to the coding DNA sequence

Diet has a significant impact on the development and progression of IBD. However, it is apparent that no single dietary regime is beneficial to all patients with the disease. The most prudent dietary advice is likely to relate to genotype. By 2010, it was apparent that more than 90 genetic variants were involved in disease susceptibility, and a number of these had clear mechanistic associations with diet. Important developments since 2010, especially involving the development of a highly focused gene chip for autoimmune diseases such as IBD (the immunochip) have increased this number to more than 160 genes, and also increased our understanding of the number of pathways likely to be involved in disease susceptibility. Again specific dietary recommendations may associate with these newly discovered genes. For example, vitamin D and VDR polymorphisms are being increasingly recognized as important in IBD pathogenesis.

As well as genetic variants, two other factors are becoming increasingly apparent from the recent literature. IBD susceptibility, especially in animal models, has emerged after epigenetic changes. Epigenetics, as DNA methylation, is known to be modulated by micro-nutrients interacting in one carbon metabolism. Histone deacetylase (HDAC) inhibition is also recognised as a key target, which may be responsive to various phytochemicals in the diet. Modulation of the gut microbiota may be especially important among the various effects of dietary manipulation. Although there have been some interesting results on UC and a mixed probiotic, most studies considering effects of probiotics and prebiotics on IBD have proved generally disappointing. It would appear that modulation of macro- and micronutrients, and dietary phytochemicals, may produce more sustainable effects.

Key Issues

Epigenetics & IBD

Epigenetics research may be essential to understanding the potential role of environment, including diet, in IBD. Jenke and Zilbauer reviewed the results of recent studies on epigenetic events in IBD, considering both the challenges and also the opportunities for future research. They summarized the accumulating evidence that epigenetics may modulate some of the effects of genetic predisposition, as well as environment and intestinal microbiota on the pathogenesis of IBD.[1]


IBD is a complex illness, increasing in frequency and requires careful consideration in terms of nutrient support and intervention. Without gene assays it can be a trial and error strewn approach, but cautious evolution of food selection and micro-nutrient supplementation can provide significant improvements in functionality.


[1] Jenke AC, Zilbauer M. Epigenetics in inflammatory bowel disease. Curr Opin Gastroenterol. 2012 Nov;28(6):577-84. doi: 10.1097/MOG.0b013e328357336b. Review. View Abstract

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