Inflammatory Bowel Disease: Nutritional Considerations

Western diets high in animal protein and fat and low in fruit, vegetables, and fiber have been associated with the onset of IBD.^9,10 Dietary changes may modify the risk for IBD or act as an adjunct to the anti-inflammatory treatments used to control disease activity.

Research studies have adduced several factors that may play a role in the risk of developing IBD:

Breast-feeding. Breast-feeding may protect against IBD by protecting against gastrointestinal infection during infancy; by stimulating the early development, maturation, and immunologic competence of the gastrointestinal mucosa; and by delaying exposure to cow's milk (see below).¹¹ A meta-analysis found that the risk for ulcerative colitis was 25% lower and the risk for Crohn's disease 35% lower in individuals who were breast-fed.¹²

A Western dietary pattern. Western diets that are relatively high in meat, dairy products, and sugar, and low in fiber and other plant constituents, compared to diets that are traditional in other regions of the world, have been associated with a higher risk of IBD. It is difficult to identify specific aspects of the diet that are responsible for this pattern. Candidates that have been studied are discussed below. However, it may be that interventions to reduce risk need to address the overall dietary pattern, rather than its components.

Animal protein. Dietary data from Japan suggest that the westernization of traditional Asian diets is associated with increased risk for IBD. When the incidence of Crohn's disease and the daily intake of various dietary components were compared annually from 1966 to 1985, animal protein intake emerged as the strongest independent risk factor.¹³

Animal protein contributes significantly to the colonic sulfur pool, resulting in the generation of hydrogen sulfide. Hydrogen sulfide may increase disease activity in ulcerative colitis through a direct toxic effect on intestinal mucosa, and by interfering with butyrate oxidation, an important anti-inflammatory fatty acid produced from dietary fiber.¹⁴

Among patients with ulcerative colitis, meat intake per se more than triples the rate of relapse. Consumption of the highest, compared with lowest, intake of red meat and processed meat (172 g/day, compared with 124 g/day) increases the rate of relapse more than 5-fold.¹⁵ Conversely, a pilot study restricting animal protein and other dietary sources of sulfur resulted in a complete absence of IBD relapse, compared with an expected relapse rate of 22% to 26% with medication alone.¹⁶ Further studies are needed to confirm these effects.

On diets that provide vegetable sources of protein, fecal sulfide content is much lower than that of meat-based diets.¹⁷ This may help explain why epidemiological studies have found an inverse relationship between Crohn's disease prevalence and vegetable protein intake.¹³

Dairy products. Individuals with IBD reveal symptoms of sensitivity to cow's milk far more often than controls, and those who had documented cow's milk allergy developed ulcerative colitis at an earlier age than did people with this disease who were free of milk allergy. Patients with IBD have antibodies to cow's milk protein, and these correlate with disease activity in Crohn's disease.¹¹ Studies also indicate that cow's milk increases both intestinal permeability and production of proinflammatory cytokines, both of which are involved in IBD.¹⁸ Preliminary data indicate that allergies to foods other than dairy products might be involved in IBD,¹⁹ but further study is required before hypoallergenic diets are established as an effective IBD treatment.

Some evidence suggests that a milk-borne pathogen may play an etiological role in Crohn's disease. Mycobacterium avium subsp. paratuberculosis (MAP) is commonly found in milk products, survives pasteurization, and causes a Crohn's-like illness (Johne's disease) in dairy cows and other ruminants. MAP has been found with far greater frequency in patients with Crohn's disease than in those with ulcerative colitis or controls.²⁰ However, the pathogen has not yet been proven to be a causative agent in Crohn's, and the benefit of eradicating MAP with antibiotic therapy has not been established.²⁰

High-fat diet. Fat intake may affect IBD through conversion of omega-6 fatty acids (found in animal products and vegetable oils (eg, corn, safflower and sunflower oil) to proinflammatory eicosanoids (eg, leukotriene B₄).²¹ Diets that are high in fat, particularly animal fat, and cholesterol, have been associated with significant increases in the risk for IBD.^9,10 The intake of foods containing partially hydrogenated fats is also associated with IBD risk. In countries where margarine consumption has increased, a rise in the rate of Crohn's disease followed.¹¹ Persons eating fast foods (ie, foods high in hydrogenated oils) at least twice per week had 3 times the risk for Crohn's disease and 4 times the risk for ulcerative colitis, compared with those who avoided these foods.²²

Low-fiber diet. Compared with persons consuming small amounts of fiber, those eating 15 grams or more per day had half the risk for developing Crohn's disease.²² Fruit intake in particular appears more strongly associated with reduced risk of IBD compared with cereals.¹¹ Individuals eating high-fiber diets were more likely to remain in remission, or had significantly fewer and shorter hospitalizations and required less intestinal surgery, than a control group.²³

Most high-fiber foods are also high in naturally occurring antioxidant vitamins, minerals, carotenoids, and flavonoids. These help to limit oxidative stress, a condition found in individuals with IBD as a result of intestinal inflammation,²⁴ even in persons with low indices of disease activity while taking medication.²⁵

High sugar intake. Studies have consistently found an association between higher intakes of sugars and the development of IBD.^9,11 However, these associations may merely reflect lifestyle patterns common in populations with IBD. A biological mechanism has not been established for sugar's effect in IBD, and larger clinical trials have not documented significant benefits of a diet low in refined carbohydrates. Further studies are required to determine if such a diet helps to prevent or treat IBD.

In addition, the following dietary factors may play a role in clinical treatment:

Dietary supplements. Some patients with IBD may have significant malabsorption of nutrients. Others may have an increased need for certain antioxidants due to oxidative stress. Serum concentrations of several nutrients (beta-carotene, vitamin C, vitamin E, selenium, and zinc) were also significantly lower or outright deficient in IBD patients, as were antioxidant status and serum concentrations of magnesium and vitamin D.^23,26 These deficiencies indicate a need for micronutrient-dense foods and a multiple vitamin-mineral supplement. Other types of dietary supplements, including fatty acids, botanicals, and probiotics, appear to be promising adjunctive approaches to IBD. Clinicians should consider prescribing the following nutrients for individuals with IBD:

B-vitamin supplements and plasma homocysteine. Many individuals with IBD have elevated levels of plasma homocysteine. In turn, recent evidence indicates that homocysteine plays a pathogenic, pro-inflammatory role in IBD.²⁷ Lower levels of folate,^28,29 vitamin B₁₂,^30,31 and vitamin B632 have been found in patients with IBD and elevated homocysteine. Clinical trials to assess benefits of lowering homocysteine levels with B vitamins in IBD have not yet been published. However, the folate-depleting effects of sulfasalazine may be involved with intestinal dysplasia, an abnormality preventable by folate supplementation.²⁴

Vitamin K status is often poor in patients with Crohn's disease and is associated with higher levels of uncarboxylated osteocalcin and a greater rate of bone turnover.^33,34 No evidence currently indicates that supplementation with vitamin K improves these indices. However, a high intake of vegetables containing vitamin K (eg, green leafy vegetables) is advised.

Omega-3 fatty acids. Some investigators have speculated that long-chain omega-3 fatty acids may decrease disease activity in IBD by reducing leukotriene B₄ (LTB4) and other indices of immune overreactivity.^23,24 Studies have suggested advantages of omega-3 supplementation in patients with ulcerative colitis,³⁵ for reducing the rate of relapse in Crohn's disease,³⁶ or as an adjunct to mesalazine for maintaining remission in pediatric patients with Crohn's disease.³⁷ However, a review of omega-3 fatty acid supplementation studies found insufficient evidence to support conclusions about their effects on clinical, endoscopic, or histologic scores, or on remission or relapse rates.³⁸

Probiotic therapy. Treatment with lactobacilli, streptococci, bifidobacteria, Saccharomyces boulardii, and certain E coli subspecies is based on several lines of evidence. These include: abnormal proliferation of harmful bacteria in the gut; the ability of "friendly" bacteria to augment lactic acid production, thereby reducing the luminal content pH and inhibiting growth of putrefactive or harmful bacteria; and a bacteriostatic effect against harmful bacteria. A number of clinical trials indicate reductions in disease activity and longer remission in patients with IBD who were treated with single or combined probiotics.²⁴

Orders

See Basic Diet Orders chapter.

What to Tell the Family

Research is suggestive, but has not yet established whether IBD is to some degree preventable through avoidance of a typical Western diet high in animal protein, animal fat, hydrogenated oils, and sugar, or through the addition of high-fiber foods. Evidence suggests that, in persons with established disease, these steps may improve the length of disease remission achievable with standard medical treatment, thus reducing the need for hospitalization and surgery.