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AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS Adapted from Crohn's and Colitis Foundation of America, Inc. http://www.ccfa.org/research/info/aboutcd Prevalence of Inflammatory Bowel Disease The Crohn’s and Colitis Foundation of American (CCFA) reports some alarming statistics. CCFA estimates that approximately one million Americans have IBD. This group is split almost evenly between individuals with Crohn's disease and ulcerative colitis. Crohn's disease affects both sexes fairly equally. People of all ages are affected, but the largest group is adolescents and young adults (ages of 15 to 35). Crohn's disease can occur in the 70+ age group and in young children. Only 10% of those affected are age 18 or younger. (4) A recent review by Head reports that Crohn's disease predominantly affects Caucasians, with a prevalence rate of 149 per 100,000. However, recent trends show that the prevalence of CD and UC is on the increase with African Americans. IBD is largely a disease of the industrialized nations, especially the US and Europe, and is especially in cities and northern climates. Crohn's disease is prevalent in developed countries especially white-collar workers with indoor, sedentary occupations. One theory is that sedentary jobs delay intestinal transit time, allowing increased contact between food antigens and the intestinal mucosa. (11). The incidence of IBD varies by population. Northern European populations such as the Irish, Norwegians, Scots and Fins, have a modest risk compared to those living in lower latitudes (12,13). The prevalence of IBD in Asians, Arabs, Africans and African Americans are absent or low (14-18). Risk Factors There are several risk factors for CD that range from adult appendectomy to the use of various substances, including nicotine (19-21), oral contraceptives, antibiotics and nonsteroidal anti-inflammatory agents (NSAIDs). Even second-hand smoke exposure has (ranging from mild to intense) and cramps following meals, as well as diarrhea. Fistulas may form. 88 2012 been shown to increase risk for developing CD (22,23). Other demographic factors such as economical, educational, geographical and occupational status can increase the risk of developing CD (24). Despite these risk factors, Ferguson (25) explains that ‚IBD is considered a genetic disease‛ as approximately 20% of people with one form of IBD have a blood relative also with IBD and 58% of monozygotic twins share the disease as compared to 4% of dizygotic twins (26,27). The Immune-Inflammatory Connection The gastrointestinal tract contains trillions of bacteria that are ideally in homeostasis with the host immune system (28). The gut contains most of the immune cells in the body and engages in a continuous fight with potentially pathogenic bacteria while leaving symbiotic bacteria largely unscathed (29). The presence of antibodies to microbial antigens in CD supports the theory that one aspect of CD pathology involves an abnormal immune response to otherwise normal intestinal flora resulting in inflammation and impaired intestinal permeability. For example, Crohn’s disease is characterized by elevations in anti- Saccharomyces cerevisiae (brewer’s yeast) antibodies in up to 60% of cases (30). Additionally, levels of antibodies, such as protein-bound IgG, have been found in the intestinal mucosa of patients with active CD to be significantly higher than patients with UC, irritable bowel syndrome, or non-specific IBD (31). One theory of immune regulation involves homeostasis between T-helper 1 (Th1) and T-helper 2 (Th2) activity (32). "Th1" and "Th2" cells are "important regulators of the class of immune response." (32) Alterations in the host gastrointestinal flora can have a significant influence on the Th1/Th2 balance of the gastrointestinal immune system (gut-associated lymphoid tissue or GALT). (33) Sometimes referred to as the innate immune system or the acquired or
AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS adaptive immune system respectively, balance of Th1/Th2 cytokines produced by the mucosa-associated lymphoreticular system (MALT) and the GALT plays a role in the stabilization of mucosal surfaces in the gut (34). These mucosal surfaces have multiple tasks that include absorption, macromolecule transfer and intestinal barrier and secretory functions. Large mucosal surfaces, such as the 300 square meters found in the human intestinal tract, are continuously exposed to millions of potentially harmful antigens from the environment, food and intestinal microbes. The mucosal surfaces possess a unique immune system that tightly controls the balance between responsiveness and nonresponsiveness. Loss of this immunological recognition of ‚friend vs foe‛ in the gut can result in activation of the inflammatory process (29). There is growing evidence that chronic inflammatory disorders in the mucosa, such as IBD, are due to the dysregulation of the mucosal immune system leading to a Th1 dominant inflammatory reaction and impairment of the barrier function of the gut. (34) Table 2. Susceptibility genes associated with IBD Name Of The Gene Gene Abbreviation Gene Variants (discussed in this Caspase-activated recruitment domain 15/nucleotide oligomerization domain 2 Autophagy-related 16like 1 Human beta defensins B2, B3 and B4 Major histocompatibility complex review) CARD15/NOD2 � Arg702Trp � Gly908Arg � 1007finsC or c.3020insC 89 2012 Genes/Gene Variants Associated With IBD – What Do We Know? Knowing the genes and gene variants associated with IBD can be useful for the practitioner once it is understood what genes are involved and how their variations are related to underlying mechanisms of IBD pathogenesis. Furthermore, evidence based nutrition intervention can be used to modulate genetic expression which can ultimately affect phenotypic outcome of the individual. While IBD appears to be of polygenic etiology, research strongly supports the assumption that susceptibility to IBD, especially Crohn’s disease, is inherited. It also indicates that IBD is not inherited as a Mendelian trait, but rather has a complex genetic basis with many contributing genes and at least nine susceptibility loci identified (34, 35). (See Fig 1). Table 2 is a classification of the susceptibility genes, their variants and areas genes affect (12,13,35,37- 42). Areas Genes Affect Affects bacterial recognition of the intestinal wall ATG16L1 Affects bacterial recognition of the HBD-2, HBD-3 and HBD-4 intestinal wall Affects bacterial recognition of the intestinal wall MHC Affects immune response Interleukin-23 receptor IL23R Affects immune response Toll-like receptors TLRs Affects immune response Sodium dependent SLC22A4/SLC22A5 � SLC22A4 Affects mucosal
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