Protocol Colorectal cancer Oral calcium supplementation has been proposed as a dietary intervention for individuals at high risk of colorectal cancer because calcium can reduce the growth rate of rectal and colonic epithelial cells both directly and by binding bile acids and fatty acids in the stool, resulting in compounds that are less likely to adversely affect the colon (Rozen et al. 1989). Calcium reduces the risk of colorectal cancer but its effects may occur only in individuals who have a low level of fat intake and may also be site-specific within the colon (Cats et al. 1995). However, oral calcium supplementation reduced benign epithelial tumor (adenoma) formation by 19% (Baron et al. 1999) and was shown to cause a minor nonstatistically significant reduction of epithelial cell proliferation in the rectum (Cats et al. 1995). Folate is a potentially protective agent against colorectal cancer. Folate depletion in experimental studies increases the risk of tumor formation and also reduces DNA methylation by reducing methyl group availability. Low folate intake, especially when combined with alcohol consumption and a low-protein diet, has been implicated in increased colorectal cancer risk (Kato et al. 1999). Alcohol consumption increases the need for folate intake. Dietary folate influences DNA methylation, synthesis, and repair. Abnormalities in these DNA processes may enhance carcinogenesis, particularly in rapidly growing tissues such as the colorectal mucosa. DNA methylation abnormalities may influence the expression of cancer-related genes, and inadequate levels of folate may lead to uracil misincorporation into DNA and to DNA damage (chromosomal breaks) (Feinberg et al. 1983; Lengauer et al. 1997). An increasing number of epidemiologic studies indicate that higher intakes of folate either from dietary sources or from supplements may lower the risk of colorectal adenoma and cancer (Giovanucci 2002). After supplementing with folate-containing multivitamins for 15 years a reduced risk of colon cancer was observed (Giovannuci et al. 1998) whereas the contribution of dietary folate was modest. Increased vitamin D intake has been associated with reduced risk for colon carcinoma (Garland et al. 1999). Vitamin D3 causes differentiation of colon cancer cells. Cancer cells that are well differentiated are close to the original normal healthy colon cells in nature and are usually less aggressive cancer cells. Poorly differentiated cells have changed more from the normal healthy cells and are usually more aggressive cancer cells. Total vitamin D intake was inversely related to colorectal cancer incidence (Martinez et al.1996), meaning the higher an individual’s intake of vitamin D the lower the rate of colorectal cancer. In high-risk individuals, the use of multivitamins has been shown to reduce the risk of adenoma formation (Whelan et al.1999). A reduced risk of colon cancer is associated with the use of vitamin C (Howe et al. 1992). Vitamins C, E, and A showed protection against the risk of developing colorectal cancer (Newberne et al. 1990). Low levels of selenium correlated with the presence of adenomas (benign tumors), whereas increased levels were associated with reduced risk of adenomas (Russo et al. 1997). http://www.lef.org/protocols/prtcl-148.shtml Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.