Life Extension Update
Folic acid supplements shrink precancerous lesions
The results of a pilot study published early online in the American Cancer Society journal Cancer (which will appear in the July 15, 2006 issue) revealed that folic acid supplements regressed precancerous lesions of the larynx in the majority of subjects who used them. Folic acid is a B vitamin known as folate in its natural state, found in many fresh vegetables and fruits. The vitamin is more stable in its synthetic form, used in supplements and fortified foods. A deficiency of folic acid can lead to an elevation of homocysteine, an amino acid that has been linked with cardiovascular disease and the risk of some cancers when produced in the body in higher than normal levels.
Giovanni Almadori, MD and colleagues at the Università Cattolica del Sacro Cuore, Policlinico A. Gemelli in Rome administered 5 milligrams folic acid three times per day to 43 patients with a precancerous condition of the larynx known as glottic laryngeal leucoplakia. Progression of the disease was monitored every 30 days for six months.
At the end of the six month period, blood levels of folate had increased while homocysteine levels decreased significantly. Thirty-one participants experienced a 50 percent or more reduction in lesion size, and in 12 of these patients the original lesion was entirely eliminated.
Although vitamin A compounds known as retinoids showed even greater effectiveness against leucoplakia in earlier research, the drugs have a high potential for toxicity. No moderate or severe adverse effects were reported in association with folic acid supplementation.
The results of the study support the hypothesis that a folate deficiency is a risk factor for cancer progression. "Folate supplementation, alone or in combination with other chemopreventive drugs, could effectively reduce the risk of progression in an already genetically altered mucosa, especially in patients with hypofolatemia," the authors conclude.
Scientists have worked hard to understand why our homocysteine level increases throughout life, and how that impacts our health. Homocysteine level is affected by a number of influences, including lifestyle, dietary choices, and genetics. As we age, our ability to absorb nutrients decreases. As a result, less of the important B vitamins are available to help metabolize homocysteine. Homocysteine level is also increased by certain pharmaceuticals, an aging metabolism, smoking, drinking too much alcohol or coffee, lack of exercise, obesity, and stress.
Homocysteine levels are measured directly in the blood. An acceptable level of homocysteine depends partly on your age and gender. It is clear, however, that our homocysteine level rises as we age and that (above a certain level) homocysteine is dangerous. Conventional medicine classifies homocysteine levels as follows:
Management of hyperhomocysteinemia begins with folic acid, vitamin B6, and vitamin B12. To varying degrees, folic acid and vitamin B12 increase the remethylation of homocysteine back into SAMe. Vitamin B6 is necessary for the conversion of homocysteine into glutathione along the transsulfuration pathway.
As a reader of Life Extension magazine, you have a front row seat to a raging debate that could very well affect how many Americans will develop heart disease, stroke, osteoporosis, Alzheimer’s disease, blindness, depression, and other disorders associated with excess homocysteine.
Homocysteine was first theorized to cause vascular disease when autopsy results of young people revealed atherosclerotic plaque in those with very high homocysteine levels. Over a 37-year period, doctors uncovered startling evidence linking elevated homocysteine to increased risks of heart attack, stroke, and other disorders in aging adults.
In addition to human epidemiological data, scientists have identified specific mechanisms by which homocysteine causes the most common age-related diseases. One of the New England Journal of Medicine authors summed up these toxic mechanisms by stating:
“ . . . homocysteine is an atherogenic determinate that promotes oxidant stress, inflammation, thrombosis, endothelial dysfunction, and cell proliferation.”
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