Review Article | Published:

The role of diet in the aetiopathogenesis of inflammatory bowel disease

Nature Reviews Gastroenterology & Hepatology (2018) | Download Citation


Crohn’s disease and ulcerative colitis, collectively known as IBD, are chronic inflammatory disorders of the gastrointestinal tract. Although the aetiopathogenesis of IBD is largely unknown, it is widely thought that diet has a crucial role in the development and progression of IBD. Indeed, epidemiological and genetic association studies have identified a number of promising dietary and genetic risk factors for IBD. These preliminary studies have led to major interest in investigating the complex interaction between diet, host genetics, the gut microbiota and immune function in the pathogenesis of IBD. In this Review, we discuss the recent epidemiological, gene–environment interaction, microbiome and animal studies that have explored the relationship between diet and the risk of IBD. In addition, we highlight the limitations of these prior studies, in part by explaining their contradictory findings, and review future directions.

Key points

  • Epidemiological studies have identified a number of potential dietary risk factors for Crohn’s disease and ulcerative colitis.

  • Early results from dietary intervention studies in Crohn’s disease and ulcerative colitis have been promising, particularly in paediatric patients, but high-quality randomized trials are needed to assess efficacy.

  • Preliminary gene–environment and microbiome studies have demonstrated an interaction between diet, host genetics and the gut microbiota in the aetiopathogenesis of Crohn’s disease and ulcerative colitis.

  • Large-scale studies are needed to prospectively examine the role of diet in the aetiopathogenesis of Crohn’s disease and ulcerative colitis in the context of host genetics and the gut microbiota.

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H.K. is funded by the US National Institute of Diabetes and Digestive and Kidney Diseases (K23 DK099681 and R03). A.T.C. is funded by the US National Institutes of Health (NIH) grant K24 DK098311, a Stuart and Suzanne Steele Massachusetts General Hospital (MGH) Research Scholar Award and a Senior Investigator Award from the Crohn’s and Colitis Foundation.

Author information


  1. Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA

    • Hamed Khalili
    • , Paul Lochhead
    • , Ashwin N. Ananthakrishnan
    •  & Andrew T. Chan
  2. Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA

    • Hamed Khalili
    • , Ashwin N. Ananthakrishnan
    •  & Andrew T. Chan
  3. Department of Medicine, Norwich Medical School, University of East Anglia, Norwich, UK

    • Simon S. M. Chan
    •  & Andrew R. Hart
  4. Department of Gastroenterology, Norfolk and Norwich University Hospital NHS Trust, Norwich, UK

    • Simon S. M. Chan
    •  & Andrew R. Hart
  5. Channing Division of Network Medicine, Harvard Medical School, Boston, MA, USA

    • Andrew T. Chan
  6. Broad Institute, Cambridge, MA, USA

    • Andrew T. Chan


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H.K., S.S.M.C. and A.N.A. made substantial contributions to discussion of the content. H.K., P.L. and A.R.H. wrote the article. All authors reviewed and/or edited the manuscript before submission.

Competing interests

H.K. has received consulting fees from AbbVie and Samsung Bioepis. H.K. also receives funding from Takeda. S.S.M.C. has received consulting fees from AbbVie and Ferring Pharmaceuticals. P.L. is supported by a career development grant by the Crohn’s and Colitis Foundation (CCF). A.N.A. is a member of the scientific advisory board for Exact Sciences, AbbVie and Cubist Pharmaceuticals. A.T.C. has served as a consultant for Bayer Healthcare, Pfizer and Takeda. A.R.H. declares no competing interests.

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Correspondence to Andrew T. Chan.

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