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Crohn’s disease and its association with dietary vegetable and fruit consumption

Crohn’s disease (CD) is a chronic, relapsing disease resulting from inflammation of the gastrointestinal tract. Of unknown etiology, the disease is thought to result from complex interactions between genetic, environmental and immunological factors. Genetic susceptibility is well established and numerous genes associated with disease have been identified. The delineation of putative environmental factors such as diet has however been difficult and less successful. In spite of extensive research over nearly three decades, evidence for a link between dietary foods/nutrients and CD remains controversial. Given the relative rarity of disease, diet-CD associations have been most commonly studied using the case-control methodology. Implementing such designs in particular for CD is challenging as there can be substantial delays from symptom-onset to disease diagnosis. Given that patients are likely to modify their diets with the onset of disease, it is unclear whether the dietary information captured is “pre-illness” diet or “post-illness” diet. It is thus not surprising that reports of association between specific dietary elements such as vegetables, fruits and fats and CD have been quite inconsistent.

Children are increasingly susceptible for CD. In Canadian children the incidence of CD is about 8.3/105, numbers that seem to approach those in adults (13.4/105)(1). Children affected with CD pose major public health challenges in particular as most children are affected during adolescence and consequently, growth delay is a major complication. Based on suggestions that Canadian children do not consume recommended amounts of fruits and vegetables(2, 3), we investigated whether these imbalances could predispose to CD. We examined(4) whether diet during the 12 month prior to disease diagnosis was associated with disease. We utilized the case-control design based on newly-diagnosed cases, excluded those who reported changes in diet prior to disease diagnosis and assessed diet within 1 month of diagnosis. We assessed food consumption using a foodfrequency questionnaire specifically validated in children. After controlling for potential confounding variables, we observed that consuming high amounts of vegetables and fruits was associated with significantly lower risks for CD. A dose-response relationship was evident indicating a trend for increasing risks with decreasing consumption.

Assessment of associations between individual foods and/or nutrients vis-à-vis risk for disease has both advantages and disadvantages. On one hand the putative dietary elements that are protective or riskconferring can be tracked out; however, assessing dietary patterns is likely to be more beneficial with regards to prevention and clinical intervention. This is because individuals tend to eat foods in combination and interactions between these foods are likely to underlie disease etiopathogenesis. Thus, in a follow-up to the above study in an enhanced cohort of subjects we first examined the characteristic dietary patterns prevalent in Canadian children and secondly, we evaluated whether any particular pattern was associated with the development of CD(5). We observed that by and large, two dietary patterns were common between boys and girls: a traditional western pattern, characterized by meat, fried foods, fast foods, snacks and desserts, and a prudent pattern characterized by vegetables, fruits, dairy products, eggs, olive oil, dark breads, grains, fish and nuts. In both boys and girls, the prudent pattern was associated with significant reductions in risk for CD, whereas, the western pattern was associated with significantly elevated risks for CD, particularly in girls. We further analyzed whether the protection offered by the prudent pattern was related to consumption of vegetables and fruits using multivariate regression modeling. We observed that in girls much of the protective effects of a prudent pattern were related to vegetable consumption, but not fruits. However in boys, neither vegetables or fruits contributed to the protective effects associated with this pattern. These findings are extremely interesting and highlight the complex relationship between dietary consumption and CD pathogenesis.

Findings from our two studies seem to suggest that both vegetables and fruits individually or a prudent pattern heavily comprised of vegetables may provide protection from chronic diseases such as CD. We have speculated on the mechanisms whereby vegetables can provide this protection(6). Constituents of vegetables are known to modify the levels and activities of detoxifying enzymes. Therefore, higher consumption may enhance and facilitate the clearance of toxic metabolites (viz. reactive oxygen species) that are routinely generated in body tissues including the gut. The latter can prevent recurrent gut injury and modify inflammatory processes that are characteristic of CD. Additional studies, preferably with prospectively ascertained dietary information, are required to shed further light on the associations between vegetables and fruits in CD etiopathogenesis.

  1. Bernstein CN, Wajda A, Svenson LW et al. The epidemiology of inflammatory bowel disease in Canada: a population-based study. Am J Gastroenterol. 2006;101(7):1559-68.
  2. Starkey LJ, Johnson-Down L, Gray-Donald K. Food habits of Canadians: comparison of intakes in adults and adolescents to Canada’s food guide to healthy eating. Can J Diet Pract Res. 2001;62(2):61-69.
  3. Veugelers PJ, Fitzgerald AL, Johnston E. Dietary Intake and Risk Factors for Poor Diet Quality among Children in Nova Scotia. Can J Pub Health. 2005;96:212-216.
  4. Amre DK, D’Souza S, Mack D et al. Imbalances in dietary consumption of fatty acids, vegetables and fruits are associated with risk for Crohn’s disease in children. Am J Gastroenterol. 2007;102(9):2016-2025.
  5. D’Souza S, Levy E, Mack D et al. Dietary patterns and risk for Crohn’s disease in children. Inflamm Bowel Dis 2007 (Epub ahead of print).
  6. Amre DK, Seidman EG. Etiopathogenesis of pediatric Crohn’s disease. Biologic pathways based on interactions between genetic and environmental factors. Med Hypotheses 2003; 60(3):344–350.
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