The urban diet and Crohn's disease: is there a relationship?

The aetiology and pathogenesis of Crohn's disease (CD) remain to be elucidated. In addition to genetic influences and immune mediated cytokine gene activation, various specific and non-specific environmental factors are considered to be associated with the induction and/or exacerbation of inflammatory bowel disease (IBD). The incidence of CD is higher in urban areas than in the rural environment. Patients with CD have a higher dietary intake of sucrose, refined carbohydrates and omega -6 fatty acids, and reduced intake of fruit and vegetables. Elemental and exclusion diets are known to be effective in CD. However, patients relapse on returning to a normal diet, which suggests that there is something in an ordinary diet which, on penetrating the mucosal defence mechanism of the terminal ileum, generates a pathogenic immune process. It has been suggested that the urban diet contains large quantities of inert inorganic non-nutrient microparticles, such as natural contaminants (soil and dust), food additives and anti-caking agents which may combine with intestinal luminal components such as bacterial cell wall lipopolysaccharides, to form antigenic particles. When these are taken up by mucosal mononuclear cells they can mediate immune reactions both locally in the mucosa and in the systemic circulation. In a study published in this issue of the journal, CD patients allocated to a low microparticle diet experienced a significant reduction in CD activity and the requirement for corticosteroids, when compared with the control group on a normal diet. The main advantage of the microparticle free diet, when compared with elemental and exclusion diets, is its enhanced tolerance by the patients and its relatively low cost. The preliminary results may give an explanation for the rising incidence of the disease in urban society. The results of an on-going multi-centre trial by the authors are awaited with interest. Eur J Gastroenterol Hepatol 13: 93-95 (C) 2001 Lippincott Williams & Wilkins.