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Allergens , Dysbiosis and Immune Dysregulation : Case studies on Inflammatory Bowel Disease

Daniel Lukaczer, ND, Robert H. Lerman, MD, PhD

Inflammatory bowel disease (IBD) is a general term for a group of chronic inflammatory disorders of the bowel, usually divided into two major categories: Crohn’s disease (CD) and ulcerative colitis (UC). Crohn’s disease most commonly affects the distal ileum and colon, but may occur in any part of the gastrointestinal (GI) tract. Ulcerative colitis is limited to the colon. The two disease categories may present with similar symptoms of frequent diarrhea associated with abdominal pain, cramping, and fever. Blood in the stool is more characteristic of UC although it may sometimes be seen in patients with CD. The prevalence of IBD in the United States is approximately 100 cases per 100,000 population.1 Considerable debate has centered on the underlying etiology of IBD. Genetic predisposition plays a significant role in disease occurrence, as demonstrated by the fact that 10-20% of IBD patients have a relative with either UC or CD.2 Additionally, with childhood IBD, the likelihood of another family member with the disease is greater than 40%.1 And recently, a relationship with the NOD2 gene was found in patients with CD.3,4 Homozygosity for the NOD2 gene was associated with a 20-fold increase in CD incidence. However, there is mounting evidence suggesting that IBD results from a combination of genetic and environmental factors. For example, environmental influences such as gastrointestinal infection, subtle floral imbalances, and dietary antigens, have all been proposed as precipitating or triggering agents in the development of IBD.

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