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Putting the “C” in Cancer

Decades ago, seminal research looked at vitamin C cancer benefits ... then research stopped. Researchers are back at it, with this trial looking at vitamin C for specific types of lung and brain cancer.

Study under review: O2·- ,– and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate

Introduction

In 1972, Ewan Cameron proposed in a brief letter[1] to The Lancet that ascorbic acid, also known as vitamin C, could be useful in suppressing cancer. In 1976[2], he famously teamed up with Linus Pauling to investigate this matter, publishing a clinical trial finding that 10 grams of ascorbic acid given intravenously for around 10 days, followed by 10 grams per day orally, prolonged the survival of terminal cancer patients. However, follow up research in the late ‘70s[3] and ‘80s[4] using 10g oral ascorbic acid failed to replicate this effect. These failures reduced interest in ascorbic acid’s effects on cancer.

In the mid-1990s, researchers argued[5] that this reduced interest was premature. They hypothesized that intravenous ascorbic acid could reach levels toxic to cancer cells. They also cited a host of evidence suggesting that ascorbic acid would not be harmful to normal cells due to metabolic differences with cancer cells involving hydrogen peroxide generation. Since ascorbic acid could potentially kill cancer cells selectively, they thought that intravenous ascorbic acid’s effect on cancer should be investigated.

In 2004, their arguments were bolstered[6] by research that found a reason for the failure to replicate Cameron and Pauling’s initial paper. These researchers found that oral vitamin C was unable to reach concentrations high enough in the plasma to have antitumor activity. However, intravenous dosing could, in theory, reach such levels. The Cameron and Pauling study may have worked because they started out with intravenous treatment. The replications, however, used only oral ascorbic acid, which can’t reach levels high enough to kill cancer cells.

This finding renewed interest in ascorbic acid’s effect on cancer, and research again picked up. In vitro test tube research found that ascorbic acid can kill pancreatic cancer cells[7] with a mechanism dependent on hydrogen peroxide production. A similar effect, also dependent on hydrogen peroxide, was seen in ovarian cancer[8].

The pieces of the puzzle started falling into place. Ascorbic acid seemed to selectively kill cancer cells over normal cells through a hydrogen peroxide-dependent mechanism. But some questions remain. How could this mechanism explain the selectivity? And would high dose intravenous vitamin C be safe and possibly effective in humans with cancer? The goal of a recently published study was to explore these questions through a series of preclinical and clinical experiments.

Linus Pauling and others found that ascorbic acid (vitamin C) improved outcomes in terminal cancer patients. Replications of these experiments failed, though. This may have been due to the early experiments using intravenous ascorbic acid, which is the only way to elevate vitamin C to levels toxic to cancer cells. The later experiments used oral ascorbic acid. Recently, interest in ascorbic acid’s effect on cancer has been renewed. While it’s known that ascorbic acid’s selective cancer-killing involves hydrogen peroxide production, the details of the mechanism aren’t well-understood.

Who and what was studied and what were the findings?

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