Diet and Inflammatory Bowel Disease

Review of Patient-Targeted Recommendations

Jason K. Hou; Dale Lee; James Lewisk


Clin Gastroenterol Hepatol. 2014;12(10):1592-1600. 

In This Article

Potential Mechanism of Action: Diet and Gut Inflammation

Various dietary components have been proposed to increase the risk of developing or exacerbating symptoms of IBD. One of the first dietary components associated with developing IBD was intake of sugar and refined carbohydrates.[6–9] However, an ecologic study in North America, Europe, and Japan failed to show an association between refined sugar intake and CD incidence rates.[10] There are consistent associations between both fatty acid and protein composition in the diet with the development of IBD in ecologic and prospective cohort studies.[11–14] Furthermore, dietary fiber intake has been associated with a lower risk of developing CD, but not UC (hazard ratio, 0.59; 95% confidence interval, 0.39–0.90).[15]

Two studies of patients who underwent ileocolonic resection provide the strongest evidence for the role of intestinal contents on the course of CD. Both studies demonstrated that recurrence of inflammation after ileal resection is dependent on exposure of the neoterminal ileum to the fecal contents. Inflammation recurred within 8 days of exposure to the luminal contents.[16,17] However, the fecal stream is a complex mixture of bacteria, other microorganisms, digested food content, and the metabolic products of digestion of food components by the host and microbiota. This makes it very challenging to identify the components of the luminal content that drive the underlying inflammation. Furthermore, these components are not independent of each other.

There is a potential link between diet and the composition of the gut microbiome. Long-term agrarian dietary patterns are associated with an enterotype characterized by Prevotella,[18] a genera more commonly observed in people from rural Africa where IBD and particularly CD is uncommon.[19]Prevotella and related bacteria are efficient at fermenting dietary fiber, thereby leading to higher concentrations of short-chain fatty acids,[20] which may protect against bowel inflammation.[21] In contrast, high-fat diets, through dietary-induced changes in the gut microbiota, may increase bowel permeability, a hallmark of CD.[22] High-fat diets also worsen dextran sodium sulfate–induced colitis in mice, possibly by increasing colonic epithelial nonclassical natural killer T cells and reducing Treg cells.[23] In animal models, consumption of milk-derived saturated fat alters bile acid composition, allowing for a bloom of sulfate-reducing bacteria, which in turn can produce greater amounts of the potentially mucosal toxic hydrogen sulfide.[24,25] A major source of hydrogen sulfide in the bowel is bacterial fermentation of sulfur amino acids, which are found in high-protein foods, such as meats.[26] Hydrogen sulfide has been proposed as contributing to bowel inflammation through a variety of mechanisms, including impaired use of short-chain fatty acids and direct toxic effects.[27,28] However, other research suggests that hydrogen sulfide has anti-inflammatory properties and contributes to mucosal healing.[29,30] These are but a few of the proposed mechanisms by which diet can affect the course of IBD. Unfortunately, it is currently unknown whether these findings in animal models translate to humans with IBD.

Observational Studies of Diet and the Natural History of Inflammatory Bowel Disease

There are surprisingly few observational studies examining the association of diet with the natural history of IBD. Jowett and coworkers[31] conducted a prospective study of patients with UC. They observed that patients who reported higher levels of meat, eggs, protein, and alcohol consumption were more likely to have a relapse of UC. Importantly, the association was much stronger for red and processed meats than for other meats and there was no association with fish consumption. Jowett and coworkers hypothesized that these dietary patterns resulted in higher intestinal concentration of sulfate, which in turn led to disease relapse. Another study found a correlation between sulfite consumption and endoscopic activity in UC.[32]

Dietary Intervention Studies to Alter the Course of Inflammatory Bowel Disease

In CD, exclusive enteral nutrition with elemental, semielemental, and defined formula diets has been widely studied for induction of remission and is considered first-line therapy in Europe.[33,34] Exclusive enteral nutritional therapy does not act by immunosuppression, but it has been shown to induce mucosal healing and prolong clinical remission of CD.[35] However, the practicality of maintaining exclusive enteral nutritional therapy over long periods of time is doubtful. In head-to-head randomized clinical trials, the degree of hydrolysis of proteins does not seem to impact the response rate with exclusive enteral nutrition therapy.[36] In general, response rates to enteral therapy exceed 80% among children with CD. For maintenance of remission, a diet in which half of the daily calories were from an elemental supplement resulted in a nearly 50% reduction in CD relapse rates compared with a regular diet.[37] Some evidence suggests that response rates are higher among those with small bowel disease. Furthermore, exclusive enteral nutrition has not been effective for UC.[38] The reason for this is uncertain but raises interesting hypotheses about the potential mechanism of action of exclusive enteral therapy.

Several small trials of diet restriction using regular food have also demonstrated improved disease activity and prolonged time to relapse.[39–41] In a recent uncontrolled trial, food-specific IgG4 levels were used to select which foods to exclude rather than excluding nearly all foods and gradually adding back selected foods.[42] Eggs and beef were the most common foods with high IgG4 antibody levels and were therefore excluded by the greatest number of patients. The 29 patients on the exclusion diet experienced a significant reduction in symptoms based on a modified Crohn's Disease Activity Index and reduction in the erythrocyte sedimentation rate compared with pretreatment levels. The major limitation of this study was the absence of a control group. In another small study (n = 22), Chiba and coworkers[43] demonstrated superiority of the semivegetarian versus an omnivorous diet to maintain clinical remission over 2 years (94% vs 33%). This study included patients with medically or surgically induced remission who received a lacto-ova-vegetarian diet in hospital. After discharge, the semivegetarian diet allowed for fish once weekly and meat once every 2 weeks. Eggs were allowed without limitation. It should be noted that this was not a randomized trial but rather allowed patients to choose whether or not to continue on the diet after discharge.

Other dietary intervention studies have not suggested a benefit. Omega-3 fatty acid supplements have been tested and were not effective in preventing CD relapse in 2 large placebo-controlled trials.[44] One of the largest dietary trials (n = 352) compared recommendations for a diet high in refined carbohydrates with one high in unrefined carbohydrates and low in sugar among patients with CD. Although there were differences in sugar and fiber intake between the study groups, rates of clinical deterioration were not statistically different.[45]