In part 1 of this article [Jan. 29 DC], I highlighted the research pertaining to the use of nutritional supplements in the management of Crohn's disease.
During flare-up periods, it is advised that patients be taken off all supplements and managed by strict adherence to dietary strategies outlined by the patient's registered dietician and/or attending physician, as certain supplements may irritate the intestinal wall during an exacerbated state.
Etiological Factors in Crohn's Disease
The question on the minds of many patients and practitioners is, what causes Crohn's disease to develop in the first place? The increased concordance of Crohn's disease in identical twins has provided strong evidence that genetic factors are important in its pathogenesis. More specifically, family history investigations have revealed that mutations within the NOD2/CARD15 gene are strongly associated with the development of Crohn's disease. NOD2/CARD15 gene is on chromosome 16 and is present in 17 percent to 27 percent of patients with Crohn's disease. This gene encodes an intracellular receptor involved in the innate immune system that regulates the immediate response to microbial pathogens.
Approximately one-third of all Crohn's disease patients display polymorphism of the NOD2/CARD15 gene. However, not all individuals with this genetic trait develop Crohn's disease or any other inflammatory bowel disease. Thus, the gene mutation alone is not the sole culprit, but rather appears to create susceptibility.
Researchers indicate that environmental factors clearly play a role in the development of Crohn's disease, based on the increasing incidence of Crohn's disease in recent decades, the changing incidence of inflammatory bowel diseases in migrant populations (e.g., increased inflammatory bowel disease in Asians after emigrating to England), and the incomplete concordance in monozygotic twins (identical twins). At present, the most widely-held hypothesis among researchers is that Crohn's disease (and ulcerative colitis) is primarily a manifestation of a dysregulated immune response to intraluminal antigens, conceivably dietary, but may also include common enteric bacteria. In this regard it is thought that immune cells overreact to the intraluminal antigen load and, in turn, produce a chronic inflammatory process in which tissue injury is mediated by specific immune cells.
Dietary Antigens and Toxins Triggering Crohn's Disease
To date, no specific dietary toxin or antigen has been determined as the principal triggering agent in Crohn's disease. Some case-control studies of Crohn's disease patients, compared to healthy individuals, have shown that pre-illness intake of higher amounts of refined sugars correlate with a greater risk of future onset of Crohn's disease. However, some studies show only a weak correlation. Other studies show that inflammatory bowel disease patients have circulating antibodies to milk protein. However, this may result from a damaged intestinal membrane allowing intact milk proteins to leak into the bloodstream (from the gut), with subsequent development of antibodies against those proteins.
Other dietary features of significance include the fact that breast-fed infants have a reduced risk of developing Crohn's disease, according to some research. Smokers are also at an increased risk of developing Crohn's disease. A Japan-based study showed that increased intake of animal protein, total fat, and animal fat, especially n-6 polyunsaturated fatty acids relative to n-3 fatty acids, were associated with a greater risk of developing Crohn's disease, within this largely homogeneous population..
Ginsberg and Albert, along with others researchers, report that wheat and dairy products are the two foods most likely to shift Crohn's disease from a state of low-grade disease or remission into an exacerbated state, as evidenced by food detection and elimination studies. It appears to be milk itself, not lactose, to which many of these patients are intolerant. There is also evidence that the intestinal tract of Crohn's patients has increased permeability to various-sized sugars, which may further serve to exacerbate the condition when refined sugars are ingested beyond a certain threshold level.
Long-Term Dietary Management
- Once identified, eliminate any food that appears to be a trigger in the patient's particular case.
- Consume a low-animal-fat, low-total-fat, low-trans-fat and low-cholesterol diet, with the exception of fish, which is high in omega-3 fats.
- Limit refined sugars.
- Avoid alcohol completely.
- Avoid all dairy products.
- Use grains other than wheat and consider moving to a gluten-free diet as a more extreme measure.
- Avoid raw vegetables. Steam or cook them to make them less of an intestinal irritant.
- Avoid foods that are very high in total fiber, as too much roughage may trigger diarrhea in these susceptible individuals.
- Use olive oil and canola oil to saute vegetables or to brown chicken or turkey breast.
- Avoid pan-fried and deep-fried foods.
- Dilute fruit juices with two-thirds water to one-third juice.
When Crohn's disease is in remission or in a more low-grade state, any dietary plan proposed to the patient should factor in these considerations. In addition to the supplementation program outlined in my previous article, the nutritional interventions outlined above should also be considered in the long-term management of Crohn's disease.
- Shils ME, et al. Modern Nutrition in Health and Disease. Lippincott, Williams & Wilkins 2006: pp. 1213-1214.
- Hugot JP, Chamaillard M, Zouali H, et al. Association of NOD2 leucinerich repeat variants with susceptibility to Crohn's disease. Nature, 2001;411:599-603.
- Ogura Y, Bonen DK, Inohara N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature, 2001;411:603- 606.
- Harris ML, Bayless TM. "Dietary Antigens as Aggravating Factors in Crohn's Disease" (editorial). Digestive Diseases and Sciences, 1989;34(10):1613-1614.
- Hanauer SB. Inflammatory bowel disease: epidemiology, pathogenesis, and therapeutic opportunities. Inflamm Bowel Dis, 2006;12(1):S3-S9.
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