More evidence that a lack of Vitamin D allows the occurrence of inflammatory bowel disease
Ulcerative colitis and Crohn's disease are the two most common forms of inflammatory bowel disease. Emerging evidence is linking the pathology cause of inflammatory bowel disease to a deficiency of Vitamin D.
In this study researchers from the University of Chicago compared mice who normally use Vitamin D with mice who have a genetic disturbance in their ability to use vitamin D. Both groups of mice were fed dextran sulfate sodium (DSS) an irritant that can cause intestinal damage. The mice that can use Vitamin D were basically resistant to the irritant effects of lower doses of DSS. However, mice that genetically lack the ability to use Vitamin D in their intestines developed severe damage and soon died when exposed to the same dosage of DSS. They quickly developed severe diarrhea, rectal bleeding, and severe weight loss leading to death within 2 weeks. Histological examination revealed extensive ulceration and impaired wound healing in the colon lining of these animals. Vitamin D deficiency may compromise the lining of the intestines leading to increased susceptibility to damage and increased risk of inflammatory bowel disease. The study is published in the October 25th. 2007 issue of the American Journal of Physiology; Gastrointestinal and Liver Physiology.
Adding Riboflavin to Folic Acid increases the colon protecting effect in patients genetically susceptible to colon cancer who have polyps
Folic Acid decreases the risk of colon cancer but some people with polyps have a genetic inability to adequately use this vitamin. However scientists from Ireland and the United Kingdom have determined that adding Riboflavin (Vitamin B2) to Folic Acid boosts the protective effect Folic Acid has in patients with colon polyps, further decreasing their risk of developing colon cancer even when they have this genetic defect. In their study 106 patients with colorectal polyps and 98 healthy people were randomly given either 400 mcg of Folic Acid, 1,200 mcg of Folic Acid, 400 mcg of Folic Acid plus 5 mg of riboflavin, or inactive placebo daily for 6 to 8 weeks. Giving Riboflavin along with Folic Acid improved the activity of Folic Acid in the colon tissue of patients with a genetic inability to efficiently use the Vitamin. The study is published in the October 1st 2007 issue of Cancer Epidemiology, Biomarkers and Prevention.