Inflammatory bowel disease epidemiology

Sandler RS, Wurzelmann JI, Lyles CM. Oral contraceptive use and the risk of inflammatory bowel disease. Epidemiology 1992 3(4) 374-8. 

Andres PG, Friedman LS. Inflammatory bowel disease. Epidemiology and the natural causes of inflammatory bowel disease. Gastroenterol Clinics 1999 28 255-281. 

Loftus, E.V., Clinical epidemiology of inflammatory bowel disease Incidence, prevalence, and environmental influences, Gastroenterology, 126, 1504, 2004. 

In conclusion, phytic acid forms soluble complexes with Ca2+ at intestinal pH under a variety of conditions and fails to inhibit Ca2 bioavailability to mice in our experimental system. Despite the hazard in direct extrapolation of results obtained with animals kept on a well-defined dietary regimen to humans consuming a complex diet, many elements of which affect Ca2+ bioavailability, our data demonstrate the need for a reevaluation of the putative antinutritional properties of dietary phytate. Our further contention that adequate levels of dietary phytate may actually be beneficial due to its food preserving properties and its protection against colonic cancer will warrant a prospective epidemiological human study designed to assess the longterm effects of dietary phytate on mineral bioavailability and inflammatory bowel diseases. 

Timmer A (2003) Environmental influences on inflammatory bowel disease manifestations. Lessons from epidemiology. Dig Dis 21(2) 91-104... 

The causal connection between NSAIDs and large bowel inflammation needs to be confirmed by appropriate epidemiological studies. Many publications have associated NSAID and colonic inflammation (SEDA-10, 77) (SEDA-15, 95), but the differential diagnosis between colonic inflammation arising de novo and exacerbation of underlying inflammatory bowel disease can be difficult, and the role of NSAIDs in aggravating ulcerative colitis or Crohn s disease or other inflammatory bowel disease is controversial (SEDA-10, 76) (SEDA-15, 95). A case-control study showed no association between appendi-cectomy for acute appendicitis and the use of NSAIDs (SEDA-22, 111). 

Sandler RS. Epidemiology of inflammatory bowel disease. In Targan SR, Shanahan F, eds. Inflammatory Bowel Disease From Bench to Bedside. Baltimore, Williams Wilkins, 1994 5-30. 

Whelan G. Epidemiology of inflammatory bowel disease. Med Clin North Am 1990 74 1-12. 

There is an epidemic of immune-mediated disease in highly-developed industrialized countries. Such diseases, like inflammatory bowel disease, multiple sclerosis and asthma increase in prevalence as populations adopt modem hygienic practices. These practices prevent exposure to parasitic worms (helminths). Epidemiologic studies surest that people who carry helminths have less immune-mediated disease. Mice colonized with helminths are protected from disease in models of cohtis, encephalitis. Type 1 diabetes and asthma. Clinical trials show that exposure to helminths reduce disease activity in patients with ulcerative colitis or Crohn s disease. This chapter reviews some of the work showing that colonization with helminths alters immune responses, against dysregulated inflammation. These helminth-host immune interactions have potentially important implications for the treatment of immune-mediated diseases. 

---