expert opinion

Antioxidants Promote Tumor Cell Growth – Critical Notes on an In Vitro Experiment

November 1, 2009

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Prof. Dr. med. Hans K Biesalski, Institute for Biological Chemistry and Nutritional Science, University of Hohenheim, Stuttgart, Germany

 

“The headline ‘The dark sideof vitamin C’ recently appeared in the German newspaper service ‘Die Welt online,’ prompted by an American study showing that artificial antioxidants (N-acetyl cysteine and Trolox) support the metabolism of tumor cells that have become detached from the tumor and could thus promote metastasis (1). This applies particularly to cells that carry large amounts of the so-called anti-apoptotic receptor protein (erbB2) on their surface and which could therefore avoid apoptosis or cell death. On closer examination, it is hard to see quite how the study, by researchers from Harvard Medical School in Boston, could have given rise to the headline quoted above.

At no point does the original study refer to vitamin C or even natural antioxidants. For example, the statement in Die Welt’s online article that ‘antioxidants such as vitamin C, vitamin E or beta-carotene support the survival of detached tumor cells in the same way as erbB2’ is nowhere to be found in the original study and is on closer inspection even inaccurate. There are no studies on vitamin C in this context in scientific literature. Vitamin E has in fact been shown to have precisely the opposite effect, since it causes the death of precisely those cells with strong erbB2 expression.

This makes it all the more baffling that a scientist with such credentials as Professor Ristow of Jena could have been misled into stating that vitamin products, as this study is alleged to show, may cause damage. This statement not only contradicts the published study, but is also rejected by the authors of this research.

In a press release, one of the study authors stated that the scientists had originally thought that in order for cells to survive outside their normal environment, they would simply need to suppress apoptosis. Their studies indicated that this activity is not sufficient to prevent the demise of the cells since they are no longer able to sustain an energy supply. The researchers compared survival rates of cells carrying erbB2 on their surface with those of cells treated with synthetic antioxidants (N-acetyl cysteine and Trolox) which are not present in foods and food supplements. Surprisingly, metabolic function was restored in cells treated with the synthetic materials.

The authors caution against extrapolating too far from their data to the in vivo situation, since they were based on experiments in in vitro laboratory cell culture. They also emphasize that the experiments were not designed to mimic the effect of antioxidants introduced through supplements or food. What happens in the body to antioxidants introduced through food is much more complicated and was not the focus of the study.

Sweeping generalizations and questionable extrapolations of this kind are not helpful. Far from providing specific clarifications on the real benefits and risks of food supplements, they simply add to the longstanding uncertainty in this area. Ristow tries to put the claim into perspective by stating that fruit is healthy despite antioxidants, not because of them. It is true that the antioxidants mentioned are present naturally in fruit and indeed, depending on the variety, sometimes in quantities significantly above those found in food supplements. However, if there is any risk from the antioxidants named (vitamin E, C, beta-carotene), would there not also be a risk when they are consumed together with fruit? Cancer patients in particular are advised far too often and uncritically to take food supplements. This is an area where particular care is required according to the Nutrition and Cancer Commission of the German Cancer Society. There have been no investigations into whether this also applies to fruit and vegetables rich in antioxidants.

It would be preferable if information and press articles were based on greater objectivity rather than generating anxieties which ultimately lead patients to turn to even more questionable courses of action which might cause them real damage.”

Hohenheim, August 2009

References

  1. Schafer Z. T. et al. Antioxidant and oncogene rescue of metabolic de-fects caused by loss of matrix attachment. Nature. 2009; 461(7260):109–13 (Epub ahead of print).