Calcium from supplements offers best protection against colorectal tumors
In a large study reported in the November 2004 issue of The American Journal of Clinical Nutrition, it was revealed that participants in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial had a lower incidence of the colorectal tumors known as adenomas when their intake of calcium, particularly from calcium supplements, was high. Colorectal tumors known as adenomas are a type of polyp that are precursors of invasive tumors, in contrast with hyperplastic polyps, which are not considered to be premalignant.

Researchers from the Division of Cancer Epidemiology and Genetics at the National Cancer Institute compared the participants’ supplemental and dietary calcium intake as reported via food frequency questionnaires. Sigmoidoscopic examination detected adenomas of the descending colon, sigmoid colon or rectum in 3,696 participants. The control group consisted of 34,817 subjects in whom no suspicious lesions were found.

The research team found that participants whose calcium intake was in the top fifth (greater than 1,767 milligrams calcium per day) had a 12 percent lower incidence of colorectal tumors than those whose calcium intake was the lowest, at less than 731 milligrams per day. Individuals who took more than 1200 milligrams calcium per day in supplement form for up to two years prior to enrollment in the study experienced a 27 percent lower risk than subjects who did not use calcium supplements. Calcium supplement use five years before enrollment also lowered adenoma risk. Among food sources, nondairy intake of calcium offered greater protection than dairy sources of the mineral. Calcium offered more protection from tumors of the colon than those located in the rectum.

This large study confirms of the findings of other studies that have found a protective benefit for calcium against the risk of developing colorectal adenomas, and ultimately, colorectal cancer.

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).

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

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