Soy extract may help prevent colon cancer
The May 2004 issue of the Journal of Nutrition (http://www.nutrition.org) published the results of a study showing that a substance found in soy helped prevent colon cancer in mice. The compound is soy glucosylceramide, known as soy GlcCer, a type of sphingolipid. Al Merrill, of Georgia Tech University, along with colleagues from Emory University and the Karmanos Cancer Institute, had previously conducted research which found that milk sphingolipids suppress tumor formation in the colon of experimental animals, and their latest research is the first to establish that a plant sphingolipid can do the same.

In the current study, mice who were administered the colon carcinogen DHM were provided with diets containing 0.025 percent or 0.1 percent soy GlcCer: amounts comparable to that found in soybeans. The investigators found that the compound reduced colonic cell proliferation in the upper half of the crypts by 50 percent when compared to animals who did not receive the compound. (Crypts are the indentations in the walls of the colon in which cells grow and replicate.) Aberrant crypt foci, which are an early marker of colon cancer, were reduced by 38 percent in the mice who received diets containing 0.025 percent soy GlcCer and 52 percent in those who received the 0.1 percent diet.

When mice bred to develop gastrointestinal cancer were administered the soy GlcCer enhanced diets, tumor formation was reduced by 22 percent in those who received the lower concentration and 37 percent in those who received the higher concentration of the compound.

Unlike many nutrients that are broken down in the digestive tract, soy GlcCer survives digestion which enables it to exert its cancer-fighting mechanism in the colon. Its mechanism of action appears to be that of lowering beta-catenin, a protein involved in cell growth.

Dr Miller commented, “Soy is known to have a number of health benefits, including the suppression of cancer. Based on our results, some of this benefit may be due to a group of molecules known as sphingolipids. We are looking for even more potent forms of these molecules that might be effective for cancer treatment. If naturally occurring sphingolipids like soy GlcCer suppress cancer in humans, this has the potential to allow the public to select their diets in a more rational way.”

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 (De et al. 1997) 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% (Barron 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 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 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. 1999). 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). Intervention trials have found a beneficial effect of selenium supplementation (Lipman et al. 1998). There is an association between iron exposure and colorectal polyps (Bird et al. 1996).

https://www.lifeextension.com/protocols/cancer/colorectal

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