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More on calcium and colorectal cancer: Meta-analysis finds increased calcium intake associated with lower colorectal cancer risk
Readers of the June 21 issue of Life Extension Update will recall the results of a study published in the Journal of the National Cancer Institute (JNCI) which found that supplementation with calcium appears to offer protection against advanced colon polyps, which are a type of polyp that is strongly associated with the development of invasive colon cancer. Further evidence concerning calcium’s protective benefit against colorectal cancer appeared in the July 7 2004 issue of the JNCI in which a meta-analysis of ten studies concluded that higher calcium consumption is associated with a reduced risk of the disease.
Eunyoung Cho, ScD, of Brigham and Women's Hospital and Harvard Medical School in Boston, and colleagues analyzed ten studies involving 534,536 people, among whom 4,992 individuals were diagnosed with colorectal cancer during the follow-up periods. The studies examined provided data on dietary consumption, including supplements. The research team found that calcium intake was inversely related to the risk of developing colorectal cancer. Participants whose calcium intake from diet was in the highest one-fifth had a 14 percent lower risk of developing colorectal cancer than those whose intake was in the lowest fifth. When calcium from diet and supplements combined was examined, the risk of developing colorectal cancer in those whose intake was highest was 22 percent lower than that of the group consuming the least. Of all food sources of calcium, only milk consumption was similarly inversely associated with colorectal cancer risk. The relative risk of being diagnosed with colorectal cancer was lowest for those whose vitamin D and total calcium intake were in the highest third of participants compared to the lowest third.
The authors conclude that increasing calcium to 1000 milligrams per day or greater could result in 10 percent fewer cases of colorectal cancer among men, and 15 percent fewer cases in women. They write, "These data, in combination with the previous experimental studies documenting a salutary effect of calcium supplementation on colonic epithelial cell turnover and colorectal adenoma recurrence, support the concept that moderate milk and calcium intake reduces the risk of 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.
Folic Acid + Vitamin B12 capsules
A deficiency of folate can result in impaired cell division and protein synthesis. With diminished replacement of healthy red blood cells and intestinal cells, anemia and a decline in GI tract function ensue. The systemic need for folate increases in certain disease states in which increased cell multiplication is needed. Chronic use of medications such as aspirin and antacids can interfere with the natural synthesis of folate.
Calcium Citrate with Vitamin D
Calcium is a major essential mineral that is often inadequately supplied, inefficiently absorbed, or excreted faster than it is being assimilated. The citrate salt of calcium has been documented to be well absorbed and utilized by the body. Calcium is important in maintaining bone mineral density and in blocking the absorption into the bloodstream of free radical generating iron.
Vitamin D3 is included to enhance calcium absorption and utilization.
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