This question can best be answered by reviewing in detail the history and experimental designs of studies on antioxidants in a cancer setting.
In earlier studies, researchers drew the conclusion that antioxidants should not be used because antioxidants protect cancer cells during chemotherapy. This hypothesis was based on experimental designs where cancer cells were given a single low dose micronutrient (like 65 mg. of vitamin C) just before the commencement of a series of conventional chemotherapy or radiotherapy. Cancer cells exposed to a single low dose micronutrient showed resistance to chemo and radiological therapeutic agent. It is extrapolated from this experimental observation that antioxidants will protect all cancer cells against conventional therapy and therefore should not be used. This conclusion is flawed in two ways: it assumes that cancer cell react the same to low dose as well as high dose antioxidant therapy. Secondly, it assumes that only one dose of antioxidant is given, while in real life, antioxidants as well as chemotherapies are usually given in series.
More recent studies using antioxidants in the appropriate high and repeated doses showed that they actually improve the efficacy of tumor response to chemotherapy and radiological therapy. This is the total opposite of the earlier researches mentioned above. These later studies showed that antioxidants at high doses selectively inhibit the growth of cancer cells without affecting the normal cells. This hypothesis is now well tested in many cell cultures and in clinical trials and is widely accepted by nutritionally minded physicians.
Let us look at these researches more closely. Studies have shown that a single low dose vitamin C or E micronutrient can stimulate growth of normal cells and some cancer cells. In the famous beta-carotene trial, where low dose beta-carotene is given to heavy smokers (whose body's cells are exposed from free radical damage and oxidative stress from the cigarette smoke and therefore cells are pre-cancerous), it is demonstrated that in fact, low dose beta-carotene increase the incidence of lung cancer. This is totally consistent with the fact that both cancer and normal cells strive in an environment of a low dose antioxidant that is beneficial for all cell types.
Normal and cancer cells respond in the same way to low dose antioxidant therapy because both cell types require antioxidants in low doses for optimum function. In an environment of high dose of antioxidants, however, the picture is quite different. Normal cells have a mechanism to protect themselves when exposed to high doses of antioxidants while cancer cells do not. In other words, cancer cells have not yet adapted to the new insult and they suffer damage from the antioxidants. High dose antioxidants therefore selectively are toxic to cancer cells but not to normal cells.
Recent evidences shown that radiotherapy and chemotherapy often harm DNA to a minor extent, which causes the cells to undergo apoptosis rather than necrosis. High dose antioxidants stimulate apoptotic pathway and therefore potentially have a synergistic effect with radiation or chemotherapy. Studies have showed that a cancer cell's defense mechanism may be impaired, making tumor cells unable to use the extra high dose antioxidant in a repair capacity. Supplying extra antioxidants through nutritional support will allow the cell to go thru a self-repair process. Most human tumor cell lines studies are low in an enzyme call catalase by 10-100 times compare to normal cells. Vitamin C administration to these cells would cause a build up of hydrogen peroxide, which leads to cell death. The cytotoxic effects of vitamin C were eliminated by addition of catalase to the cell culture.
It is clear now that repeated high dosage of antioxidants selectively kill cancer cell while sparing normal cells.
Antioxidants and cancer
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