Does Diet Influence the Disease Course in Patients with IBD?

The pathogenesis of IBD is complex and involves both genetic and environmental factors. Among the environmental factors associated with IBD, diet and the intestinal microbiota would seem the most likely to be modifiable, making them potential targets for disease prevention and treatment. Also, in the past five years, researchers have learned much about the effects of diet on the mucosal immune system, epithelial barrier function and gut microbiota. While these relationships are complex and not fully elucidated, it is clear that dietary nutrients can directly regulate immune function as well as modify the composition of the gut microbiota and its production of metabolites, which can have subsequent effects on the host.

Now, we know that the incidence of IBD is highest in industrialized nations; and in developing nations, where IBD was once rare, the incidence has increased as these nations have become more industrialized. This has led to the hypothesis that increased IBD incidence is associated with westernization, particularly the consumption of a western diet. There are in fact epidemiologic data associating dietary patterns consistent with a western lifestyle with an increase in disease risk. For example, high dietary intake of total fats, polyunsaturated fatty acids, omega-6 fatty acids and meat has been associated with an increased risk of both Crohn’s disease and ulcerative colitis. We have also learned from the Nurses’ Health Study, a large cohort of registered nurses in the U.S., that longterm intake of dietary fiber is associated with a decreased risk of developing Crohn’s disease. These findings support the hypothesis that diets high in fruits and vegetables, and low in meats and fats, may reduce the risk of developing IBD. The notion that diet, particularly the western diet, may be involved in the pathogenesis IBD has also been demonstrated by studies suggesting that dietary milk fat and more recently, dietary emulsifiers — which are additives found in most processed foods — can exacerbate colitis in a mouse model of IBD.

“What should I eat?” is one of the most commonly asked questions by patients and is also one of the most difficult to answer.

We know that diet is important to patients who have IBD. “What should I eat?” is one of the most commonly asked questions by patients and is also one of the most difficult to answer. Patients often identify foods that cause increased symptoms and subsequently follow self-imposed restricted diets. However, for the most part, there is not clear evidence for a direct link between these dietary alterations and the reduction in inflammation. The available evidence suggests that diet may play an important role in disease pathogenesis, but can diet alter the disease course once the IBD diagnosis has been made?

I am convinced that the answer is “yes” and the strongest evidence to support this belief is the success of defined formula diets for the treatment of Crohn’s disease. In Crohn’s disease, exclusive enteral nutrition with various formulas has been utilized for nearly four decades and is considered first-line therapy for the induction of remission in many parts of the world. Exclusive enteral nutrition has been shown to promote mucosal healing in Crohn’s disease and there are obvious additional benefits, such as the lack of serious adverse events that can be associated with corticosteroids and other pharmacologic therapies, as well as the positive impact on nutrition and bone health. While the majority of the evidence supports a role in the induction of remission in Crohn’s disease, there is also some evidence to suggest that specific enteral nutritional therapy protocols may be efficacious in the maintenance of remission and preventionof post-operative recurrence. Although the mechanism of action of enteral nutritional therapy has not been well-characterized, hypotheses involve reduction in luminal antigens secondary to food exclusion (i.e., excluding something potentially harmful from the typical diet) and modulation of the gut microbiota. Newer exclusion diets — such as Chiba and colleagues’ semivegetarian diet to prevent relapse, and Levine and colleagues’ Crohn’s Disease Exclusion Diet to induce remission — have demonstrated efficacy in small populations of Crohn’s patients, providing additional support for the notion that there is something harmful in the typical diet that leads to inflammation or dysbiosis andexacerbating IBD.

The Crohn’s Disease Exclusion Diet, for example, excludes foods that are commonly thought of as being more prevalent in the western diet and also foods which have been shown to be pro-inflammatory in animal models of IBD. It is important to note that these and other exclusion diets, such as the specific carbohydrate diet, have not been sufficiently studied. But it is reasonable to hypothesize that diets that are less restrictive than exclusive enteral nutrition may alter the disease course and may soon be a part of our treatment armamentarium. Going forward, we need to improve our methods for studying diet in IBD and we also need to better understand the mechanism of action of exclusive enteral nutrition, which will inform the development of new dietary therapies to control these diseases.

Dr. Albenberg has no conflicts to disclose.

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