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Vitamin C Treatment

Vitamin C, or ascorbic acid, is a potent water-soluble antioxidant in humans. The body cannot form this vitamin, therefore, it has to be ingested for survival.

Studies in the 1970's and 1980's by Nobel price laureate Linus Pauling and colleagues suggested that very large doses of vitamin C were helpful in increasing the survival time and improving the quality of life of terminal cancer patients.

Only recently, in 2006, researchers at the US National Institutes of Health published an article in the peer-reviewed Canadian Medical Association Journal that called for a reassessment of the effectiveness of vitamin C as a cancer treatment. Vitamin C treatment is currently still considered an alternative medicine. Lead researcher Sebastian J. Padayatty found high concentrations of vitamin C to be toxic to cancer cells, but not to healthy cells.

In 2005, another group of researchers at the US National Institutes of Health, led by M. Levine, came to the same conclusion.

In the August 4–8, 2008 issue of the Proceedings of the National Academy of Sciences, researcher and co-author of the study, Mark Levine, M.D., chief of the US National Institutes of Health’s Molecular and Clinical Nutritional Section, found that intravenous vitamin C produced hydrogen peroxide, which proceeded to reduce cancerous tumors in mice by 43 to 51 %. The mice had ovarian, pancreatic and brain cancer. According to the researchers it is possible to intravenously boost levels of vitamin C in humans to the levels used in the mice. The results also indicate that at pharmacologic levels, vitamin C elicits hydrogen peroxide-dependent cytotoxicity only toward cancer cells, leaving normal cells unscathed. [Proc Natl Acad Sci USA 2008.]

The high concentrations of vitamin C in the blood needed to kill cancer cells cannot be achieved orally, but only by intravenous infusions.

* Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues.

Chen Q, Espey MG, Krishna MC, Mitchell JB, Corpe CP, Buettner GR, Shacter E, Levine M.

Molecular and Clinical Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Human pharmacokinetics data indicate that i.v. ascorbic acid (ascorbate) in pharmacologic concentrations could have an unanticipated role in cancer treatment. Our goals here were to test whether ascorbate killed cancer cells selectively, and if so, to determine mechanisms, using clinically relevant conditions. Cell death in 10 cancer and 4 normal cell types was measured by using 1-h exposures. Normal cells were unaffected by 20 mM ascorbate, whereas 5 cancer lines had EC(50) values of <4 mM, a concentration easily achievable i.v. Human lymphoma cells were studied in detail because of their sensitivity to ascorbate (EC(50) of 0.5 mM) and suitability for addressing mechanisms. Extracellular but not intracellular ascorbate mediated cell death, which occurred by apoptosis and pyknosis/necrosis. Cell death was independent of metal chelators and absolutely dependent on H(2)O(2) formation. Cell death from H(2)O(2) added to cells was identical to that found when H(2)O(2) was generated by ascorbate treatment. H(2)O(2) generation was dependent on ascorbate concentration, incubation time, and the presence of 0.5-10% serum, and displayed a linear relationship with ascorbate radical formation. Although ascorbate addition to medium generated H(2)O(2), ascorbate addition to blood generated no detectable H(2)O(2) and only trace detectable ascorbate radical. Taken together, these data indicate that ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2), and that blood can be a delivery system of the pro-drug to tissues. These findings give plausibility to i.v. ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where H(2)O(2) may be beneficial.

Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13604-9. Epub 2005 Sep 12.
PMID: 16157892 [PubMed - indexed for MEDLINE] [Link to the Article]

DISCLAIMER: The extent of the response to treatment varies from patient to patient, even with similar diagnosis as the internal bodily environment is unique to each individual patient.

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