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Preventing Colon Cancer with the B-Vitamin, Folic Acid
James Meschino DC, MS, ROHP
Colon and rectal cancers continue to represent the second leading cause of cancer death when you combine statistics for men and women. Although a genetic component is well established the evidence suggests that as much as 80-90% of colorectal cancers are produced by faulty nutrition and lifestyle factors. This is based on differences in cancer rates between countries, changes in colon cancer rates over time and migration studies.
To date the research implicates diets high in animal fat or red meat and alcohol, low in fiber, fruits and vegetables as nutritional factors that encourage colorectal cancer development. More recently evidence has become more convincing that calcium and vitamin D may reduce risk of colon cancer. The same is true for vitamin E supplementation and vitamin C.
In addition to these dietary agents an abundance of research now suggests that the B-vitamin, folic acid is also important in the prevention of colorectal cancer.
Folic acid is required to help the body convert homocysteine to methionine. Once formed methionine is readily converted to S-adenosylmethionine, which is necessary to form the DNA that makes up our genetic blueprints for life.
If folic acid levels become sub-optimal, then the amount of S-adenosylmethionine declines. This results in an inability to properly produce DNA as cells replace themselves from one generation to the next. The danger is that genetic errors become more common and genetic linkages become more fragile and prone to breakage with resulting mutations.
These alterations to genetic structure provide the foundation for cancerous changes to occur in our genes.
A low level of folic acid during pregnancy is a well-established risk factor for neural tube defects, such as spina bifida. The inability to provide the necessary building blocks of DNA results in defects in developing tissues. It has been estimated that 50% of spinal birth defects would not occur if all women of childbearing age ingested 400 mcg. of folic acid per day.
The same appears to be relevant to prevent of colorectal cancer according to available research.
Giovannucci et al assessed dietary intake for a 1-year period for women of the Nurses’ Health Study and for men of the Health Professional Follow-up study – using a semi-quantitative and food frequency questionnaire. Of the 25,474 subjects 895 developed adenomatous polyps of the left colon or rectum.
A major finding of the study was that high folic acid intake was protective against colorectal cancer. Women in the top 20% intake level of folic acid demonstrated a 34% decreased risk of colorectal cancer compared with women in the bottom 20% intake level of folic acid. For men a 37% reduction in risk was observed for the highest 20% intake of folic acid versus the lowest 20% intake group.
Users of multiple vitamins demonstrated the greatest reduction in risk of colorectal cancer in this study. Much of this protective effect was shown to be due to folic acid. These findings are consistent with other epidemiological evidence indicating that folic acid reduces the risk of colorectal cancers.
In other studies low folic acid intake and/or blood levels has been linked to an increase cancer or pre-cancerous lesions on the cervix, in the bronchial tubes and other sites. For example, Butterworth et al found the cervical dysplasia risk from human papillomavirus (HPV) to be limited to those with low folic acid status.
Reversal of cervical dysplasia and bronchial dysplasia (two pre-cancerous states) has been attained through the administration of folic acid and vitamin B12 supplementation.
As indicated by Giovannucci et al more intensive efforts to improve the poor folic acid status present in large segments of the population should be undertaken.
The use of a multiple vitamin and mineral containing at least 400 mcg. of folic acid is a simple step to ensure that adequate levels of folic acid and other important micronutrients are maintained.
Through its unique effects as a methyl donor, folic acid is vital to the prevention of cancer, heart disease, and neural tube defects. It also participates in liver detoxification and the production of brain chemicals known as neurotransmitters. Lastly, folic acid is an essential ingredient that ensures your DNA is perfectly duplicated from one generation of cells to the next without genetic errors occurring.
Sub-optimal intake of folic acid is very common. As a means to prevent colorectal cancer, as well as a host of other degenerative problems, many authorities now advise individuals to consume at least 400 mcg. of folic acid per day, (up to 1,000 mcg) by way of supplementation.
- Giovannucci et al: Folate, methionine, and alcohol intake and risk of colorectal adenoma. J. Natl Cancer Inst. 1993; 85; 11: 875-83
- Doll R, Peto R: The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. JNCI 66:1191-1308, 1981
- Willet W: The search for the causes of breast and colon cancer. Nature 338:398, 394, 1989
- Haenszel W, Kurihara M: Studies of Japanese migrants. I. Mortality from cancer and other diseases among Japanese in the United States. J Natl Cancer Inst 40:43-68, 1968
- McKeown-Eyssen GE, Bright-See E: Dietary factors in colon cancer: International relationships, Nutr Cancer 6:160-170, 1984
- Potter JD, McMichael AJ: Diet and cancer of the colon and rectum: A case-control study. JNCI 76:557-569, 1986
- Graham S, Dayal H, Swanson M, et al: Diet in the epidemiology of cancer of the colon and rectum. J Natl Cancer Inst 55:15-18, 1978
- La Vecchia C, Negri E, Decarli A, et al: A case-control study of diet and colo-rectal cancer in northern Italy, Int J Cancer 41:492-498, 1988
- Nyce J, Weinhouse S, Magee PN: 5-Methylcytosine depletion during tumor development: An extension of the miscoding concept, Br J Cancer 48:463-475, 1983
- Hoffman RM: Altered methionine metabolism, DNA methylation and oncogene expression in carcinogenesis. Biochim Biophys Acta 738:49-87, 1984
- Shivapurkar N. Poirer LA: Tissue levels of S-adenosylmethionine and S-adenosylhomocysteine in rats fed methyl-deficient diets for one to five weeks. Carcinogenesis 4:1052-1057, 1983
- Wainfan E, Dizik M, Stender M, et al: Rapid appearance of hypomethylated DNA in livers of rats fed cancer-promoting, methyl-deficient diets. Cancer Res 49:4094-4097, 1989
- Wainfan E, Poirier LA: Methyl groups in carcinogenesis: Effects of DNA methylation and gene expression. Cancer Res 52:2071s-2077s, 1992
- Cravo ML, Mason JB, Dayal Y, et al: Folate deficiency enhances the development of colonic neoplasia in dimethylhydrazine-treated rats. Cancer Res 52:5002-5006, 1992
- Feinberg AP, Vogelstein B: Hypomethylation distinguishes genes of some human cancers from their normal counterparts. Nature 301:89-92, 1983
- Goelez SE, Vogelstein B, Hamilton SR, et al: Hypomethylation of DNA from benign and malignant human colon neoplasms. Science 228:187-190, 1985
- Feinberg AP, Gehrke CW, Kuo KC, et al: Reduced genomic 5-methylcytosine content in human colonic neoplasia. Cancer Res 48:1159-1161, 1988
- Freudenheim JL, Graham S, Marshall JR, et al: Folate intake and carcinogenesis of the colon and rectum, IntJ Epidemiol 20:368-374, 1991
- Lashner BA, Heidenreich PA, Su GL, et al: Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. A case-control study, Gastroenteral 97:255-259, 1989
- MRC Vitamin Study Research Group: Prevention of neural tube defects: results of the medical research council vitamin study. Lancet 338:131-137, 1991
- Sauberlich HE: Evaluation of folate nutrition in population groups. In: Folic Acid Metabolism in Health and Disease (Picciano MF, Stokstad ELR, Gregory JF, eds). New York: Wiley-Liss, 1990, pp211-235