Posted to MediaSyndicate.com (Nov 19, 2009 - 05:57 PM) : Many of you may be gawking at the recent headline and squirming at the very remote possibility that the folic acid and B-12 vitamin that you are taking may be the single cause of your possibly developing lung cancer. Let’s decipher the recent study that has once again caused chaos as the medical and nutritional world bunt heads.



According to today’s issue of JAMA (Journal of the American Medical Association), researchers combined the results of two Norwegian trials of vitamin B supplementation in approximately 7000 patients with known heart disease. The original intent of the studies was to determine whether or not taking b vitamins improves cardiovascular health. It is important to note that about ¾ of the subjects were current or former smokers. The subjects were in one of four groups:

1. 0.8mg of folic acid + 0.4 mg of B12 + 40mg of B6 daily
2. Folic acid + B12 daily
3. B6 only daily
4. Placebo

After 78 months, it was shown that the risk for developing cancer in the groups that included folic acid was 21% greater than in those not taking folic acid. Another way to look at this is: 341 patients who took folic acid and B12 got cancer and 288 patients who did not take folic acid or B12 got cancer. The type of cancer of greatest incidence was found to be lung cancer. 94% of those who developed lung cancer were current of former smokers. The authors of the study point out, however, that prior “epidemiologic studies have demonstrated no associations between intakes of folate or folic acid and lung cancer risk.”
It is interesting to note that the rates of total cancer incidence declined from 2001 to 2005 in the setting of mandatory folic acid fortification, which began in 1998. We have seen drastic reductions in lung cancer over the last two decades. Certainly, however, this reduction is not solely due to folic acid fortified foods.

It is difficult to apply this study to the general population, being that the study included only patients with heart disease, as the original intent of the study was to weight the benefits of b vitamins on heart disease.
Note that the accompanying editorial also states that “the findings do not nullify the potential long term benefits that folic acid fortification may have on population health.”


This is not folic acid’s first time being in the cancer limelight. A previous study in 2007 showed that folic acid supplementation was associated with a nonsignificant trend toward a more high-grade colorectal adenoma.

A study following 643 men for 7 years found that of the 34 patients who were diagnosed with prostate cancer, 25 patients were taking folic acid and 9 were taking placebo. This study brought to light that perhaps not all middle aged men should be on folic acid supplementation.


There is a biochemical rationale behind why folic acid may promote cancer. First, folic acid is necessary for the synthesis of nucleotides that are needed for the growth of cancer cells. Second, cancer cells have an exaggerated amount of folate receptors. Both of these factors should stimulate further research on folic acid supplementation and cancer.


Low-folate status, however, has been associated with increased risks of several cancer types, suggesting also a chemopreventive role of folate. There is also some evidence that a more bioavailable for of folate, metyl-tetra-hydro-folate may be less of an issue with regard to cancer as compared to regular folic acid.


The jury is still out on this one. In the meantime, make sure that you and your physician are familiar with this research. There is plenty of room for further study here. Being that folate comes in prescription form, perhaps some of the studies will be industry sponsored and actually take place on a large scale.

www.advanced-medicine.com

Cole, B. and Baron, J. "Folic Acid for the Prevention of Colorectal Adenomas." The Journal of the American Medical Association 297.21 (6 Jun. 2007): 2351-2359.

Ebbing M et al. Cancer Incidence and Mortality After Treatment with Folic Acid and Vitamin B12. JAMA 2009 Nov 18; 302:2119