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Nutrition and cancer: A review of the evidence for an anti-cancer diet

Michael S Donaldson

Nutrition Journal 2004, 3:19  doi:10.1186/1475-2891-3-19

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Obvious or erroneous?

Steve Hickey   (2007-02-12 00:07)  Manchester Metropolitan University

Michael Donaldson’s paper includes erroneous and misleading points on vitamin C. The first is his assertion that oral intakes of vitamin C, even in multiple divided doses, are not as effective as intravenous (IV) administration for the treatment of cancer. There is insufficient data to support this statement.

Donaldson references Padayatty et al (2004), who provide limited evidence, based on plasma levels. These data do not show oral doses to be less therapeutically effective than IV. Donaldson has extrapolated from the results of in vitro experiments, over periods of hours, to oral treatments, lasting months. [1] A principle benefit of non-toxic redox therapies, based on vitamin C, is that patients can take them continuously for months, or even years. [2] To put it simply, just because a given level of vitamin C kills cancer cells quickly in a test tube, does not mean that a sustained, lower level will not be effective inside the human body.

Donaldson states that the amounts required for therapeutic effects are “obviously” beyond dietary intakes. This is not an obvious conclusion; it is an unjustified extrapolation, based on limited data. When measured over a period of hours, 200-250 microM/L vitamin C can be selectively cytotoxic to some cancer cells. This level can be built up using repeated (say, three hourly) oral dosing, to achieve a pharmacological steady state. Even if Donaldson’s conclusions were ultimately shown to be true for oral ascorbic acid, it is possible that liposomal formulations, given orally, could reach cytotoxic concentrations in plasma.

Furthermore, Donaldson’s assertion does not take into account possible combinations of vitamin C with other anti-cancer agents. For example, a synergistic combination of vitamin C with vitamin K3, or r-alpha-lipoic acid, is known to be many times more effective as an in vitro anticancer agent than vitamin C alone. Such a combination, taken orally, could reach therapeutic levels. Similarly, vitamin C, at an orally-achievable level of only 50-100 microM/L, drives motexafin gadolinium (a quinone drug, similar to vitamin K3) producing cytotoxicity and complete inhibition of proliferation over a 24 hour period. [3]

Another problem with Donaldson’s assertion relates to treatment resistance. The use of IV ascorbate typically provides a high plasma concentration, but in a series of pulses. Although this may shrink a tumour more quickly than is possible with oral doses (this has yet to be demonstrated), IV administration could ultimately be less effective at prolonging lifespan than oral dosing, which allows sustained plasma levels. [1] With standard chemotherapy, treatment becomes less effective with repeated courses of treatment, as cancer cells are selected for resistance. The same could happen with IV vitamin C.

Consider antibiotic therapy: the problems of resistant bacteria are minimised by providing a continuous selection pressure until the bacteria are gone. In practice, this means making sure the patient takes the full course. Intermittent pulses of antibiotic treatment would rapidly select for resistant organisms. Similarly, intermittent use of chemotherapy, or IV vitamin C, could favour treatment-resistant cancer cells. Until we have adequate experimental data, it is reasonable to combine intravenous vitamin C with maximal dynamic flow level oral dosing. This prevents the more resistant cancer cells having a treatment break, during which to regenerate.

Extrapolation from test tube studies to the living body ignores physiological actions. For example, tumours can absorb ascorbate, especially when glucose is restricted, concentrating it to levels above those of the plasma. By focusing on plasma levels, Donaldson runs the risk of underestimating the anti-tumour effects of vitamin C. [4] There are numerous anecdotal and clinical reports of the effectiveness of oral ascorbate in cancer.[5] However, current trials typically use inappropriate doses, both in magnitude and methodology.[6]

Assuming our choice was limited either to IV doses of ascorbate or oral doses (in association with a synergistic, redox-active agent, such as alpha-lipoic acid), it is certainly not “obvious” that intravenous ascorbate would be a more effective treatment for cancer patients. Indeed, one could make a strong argument that a suitable oral regime might offer a longer lifespan, with less chance of the disease recurring. In reality, we could choose to supplement dynamic flow level oral doses with intravenous ascorbate, thus gaining the advantages of each.

Current evidence suggests that ascorbate given alone is a relatively weak anticancer agent, but also that it is highly synergistic with other redox active nutrients. Appropriate research on the anticancer effects of vitamin C and related nutrients has been hindered by prejudice, for too long. It is time for a dispassionate examination of the science.

1. Hickey S Roberts H. (2005) Cancer: Nutrition and Survival, Lulu press.

2. Hickey S. Roberts H. Cathcart R (2005) Dynamic flow, a new model for ascorbate, Journal of Orthomolecular medicine, 20(4), 237-244.

3. Evens A.M. Lecane P. Magda D. Prachand S. Singhal S. Nelson J. Miller R.A. Gartenhaus R.B. Gordon L.I. (2005) Motexafin gadolinium generates reactive oxygen species and induces apoptosis in sensitive and highly resistant multiple myeloma cells, Blood, 105(3), 1265-1273. Epub 2004 Sep 23.

[4]. Hickey S. Roberts H. (2007) Selfish Cells, JOM, in press.

[5]. Gonzalez M.J. Miranda-Massari J.R. Mora E.M. Guzman A. Riordan N.H. Riordan H.D. Casciari J.J. Jackson J.A. Roman-Franco A. (2005) Orthomolecular oncology review: ascorbic acid and cancer 25 years later, Integr Cancer Ther, 4(1), 32-44.

6. Hickey S, Roberts H (2005) Misleading Information on the Properties of Vitamin C. PLoS Med 2(9): e307

Competing interests

No competing interests

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