Antioxidant supplementation

According to the free radical theory of aging, disease occurs because cells accumulate free radical damage over time. The free radical theory of aging implies that antioxidants such as vitamin A, vitamin C, vitamin E, and glutathione will slow disease by preventing free radicals from oxidizing sensitive biological molecules or reducing the formation of free radicals.

Evidence supporting the efficacy of antioxidants against disease is limited.

Supplementation with antioxidants beyond the Recommended Daily Intake is contraindicated for Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. (MP) patients. One exception is quercetin. Quercetin has well-defined molecular actions, and is used by MP patients for its palliative effects.

Problematic and unknown molecular actions

Antioxidants have widespread effects throughout the body, a number of which are not well documented or quantified. Researchers are beginning to suspect that the body may actually need free radicals, which help kill cancerous cells, ensure optimal immune function, and regulate blood sugar.

It seems safe to say that one's body has all the necessary requirements to carry on these functions in the presence of a balanced diet. Placing additional chemistry into the mix is unwise and could be a deterrent to the positive outcome a patient is striving for on the MP.

Interference with apoptosis

Apoptosis, or regulated cell suicide, eliminates unwanted and damaged cells, including precancerous and cancerous cells. Reactive oxygen species (ROS) are chemically-reactive molecules containing oxygen, which act to neutralize antioxidants, regulate apoptosis1). In their 2000 study, Salganki et al. reasoned that since ROS act as essential apoptotic mediators, increasing the ROS level might enhance apoptosis and thereby slow down tumor growth.2) Provocatively, that team showed that tumor growth was inhibited in mice fed an antioxidant-depleted diet while an antioxidant-rich diet had no impact on tumor growth. This work, while preliminary, offers one mechanism how megadoses of antioxidants are not protective against cancer and may actually exacerbate unchecked cell growth.

Evidence against supplementation

Though the free radical theory of aging and disease has existed for over 50 years, there is no in vivoA type of scientific study that analyzes an organism in its natural living environment. evidence to support the efficacy of antioxidants against chronic disease:

Since the early 1990s scientists have been putting antioxidants through their paces, using double-blind randomised controlled trials - the gold standard for medical intervention studies. Time and again, however, the supplements failed to pass the test. True, they knock the wind out of free radicals in a test tube. But once inside the human body, they seem strangely powerless. Not only are they bad at preventing oxidative damage, they can even make things worse. At worst, antioxidants may even have the opposite effect, promoting the very problems they are supposed to stamp out.

Lisa Melton, New Scientist


In 1992 researchers at the US National Cancer Institute set about testing beta carotene. They recruited more than 18,000 people at high risk of developing lung cancer, either because they smoked or had been exposed to asbestos, and gave around half of them beta carotene supplements.3) The trial was supposed to run for six years, but the researchers pulled the plug two-thirds of the way through after discovering, to their surprise and horror, that those taking supplements were faring worse than the controls. Their lung cancer rate was 28 per cent higher, and the overall death rate was up 17 per cent. “It was a shock. It not only did no good but had the potential to do harm,” Halliwell says.

Lisa Melton, New Scientist

Vitamin E

It's a similar story with the world's most popular antioxidant…. Several [vitamin E studies] found no protective effect and one even concluded that vitamin E increased the risk of heart failure.

Lisa Melton, New Scientist

Vitamin C

Vitamin C is another disappointment. “People are still trying to defend it, but you don't get an effect on free radical damage unless you start with people with a vitamin C deficiency,” says Halliwell. “I think it is a lost cause.” In fact, results from a vast US trial probing the links between diet and health, called the Women's Health Study, suggest that vitamin C supplements may accelerate atherosclerosis in some people with diabetes.

Lisa Melton, New Scientist

Researchers at Memorial Sloan-Kettering Cancer Center studied the effects of vitamin C on cancer cells.4) As it turns out, the vitamin seems to protect not just healthy cells, but cancer cells, too. “The use of vitamin C supplements could have the potential to reduce the ability of patients to respond to therapy,” said Dr. Mark Heaney, an associate attending physician at the cancer center.

Dr. Heaney and his colleagues tested five different chemotherapy drugs on cancer cells in the laboratory. Some of the cells were first treated with vitamin C. In each case and in dose-dependent fashion, chemotherapy did not work as well if cells had been exposed to vitamin C. The chemotherapy agents killed 30 to 70 percent fewer cancer cells when the cells were treated with the vitamin.

A second set of experiments implanted cancer cells in mice. They found that the tumors grew more rapidly in mice that were given cancer cells pretreated with vitamin C. The researchers found that just like healthy cells, cancer cells also benefit from vitamin C. The vitamin appeared to repair a cancer cell’s damaged mitochondria, the energy center of cells. When the mitochondria is injured, it sends signals that force the cell to die, but vitamin C interrupts that process.

“Vitamin C appears to protect the mitochondria from extensive damage, thus saving the cell,” Dr. Heaney said. “And whether directly or not, all anticancer drugs work to disrupt the mitochondria to push cell death.”


A food frequency questionaire administered to 7,182 women in Northern Italy found that increased dietary selenium intake was associated with an increased risk of type 2 diabetes.5)

Other compounds

In the last few years, other compounds like glutathione and phenols, have been touted as having disease-inhibiting properties, but studies are lacking and there's no reason to think that the trend will change. Clearly whatever is behind the health benefits of a diet rich in whole foods, one cannot reproduce it by taking purified extracts or vitamin supplements.

Read more

* Vitamin C May Interfere With Cancer Treatment

===== Notes and comments =====

“It may well be that the only one benefiting from supplements is the one making the profits.”

Joyful: IMO, your addition strays from the tone we are aspiring for. We don't want to question motives as others so often question ours. Best to stick to discussions of the evidence and take the high road, IMO. — Paul Albert 07.05.2010

  • Legacy content
    • This whole article is awkward reading. Can some of the block quotes be worked into text blocks or the sources be made more evident? — Joyful 06.29.2009
    • I see your point, but the New Scientist article is too well-written not to quote from. I changed things around so it's hopefully less awkward. Does this improve things? — Paul Albert 06.09.2010
    • Yes, good work, Paul! — Joyful 06.10.2010

Another important mechanism involved in the host response to infection is oxidative stress, which plays a major role in the systemic inflammatory response in bacterial(16178750) and viral infections.(15944946)(Olteanu, see EndNote)

===== References =====

Simon HU, Haj-Yehia A, Levi-Schaffer F. Role of reactive oxygen species (ROS) in apoptosis induction. Apoptosis. 2000 Nov;5(5):415-8. doi: 10.1023/a:1009616228304.
[PMID: 11256882] [DOI: 10.1023/a:1009616228304]
Salganik RI, Albright CD, Rodgers J, Kim J, Zeisel SH, Sivashinskiy MS, Van Dyke TA. Dietary antioxidant depletion: enhancement of tumor apoptosis and inhibition of brain tumor growth in transgenic mice. Carcinogenesis. 2000 May;21(5):909-14. doi: 10.1093/carcin/21.5.909.
[PMID: 10783311] [DOI: 10.1093/carcin/21.5.909]
Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, Keogh JP, Meyskens FL, Valanis B, Williams JH, Barnhart S, Hammar S. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996 May 2;334(18):1150-5. doi: 10.1056/NEJM199605023341802.
[PMID: 8602180] [DOI: 10.1056/NEJM199605023341802]
Heaney ML, Gardner JR, Karasavvas N, Golde DW, Scheinberg DA, Smith EA, O'Connor OA. Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs. Cancer Res. 2008 Oct 1;68(19):8031-8. doi: 10.1158/0008-5472.CAN-08-1490.
[PMID: 18829561] [PMCID: 3695824] [DOI: 10.1158/0008-5472.CAN-08-1490]
Stranges S, Sieri S, Vinceti M, Grioni S, Guallar E, Laclaustra M, Muti P, Berrino F, Krogh V. A prospective study of dietary selenium intake and risk of type 2 diabetes. BMC Public Health. 2010 Sep 21;10:564. doi: 10.1186/1471-2458-10-564.
[PMID: 20858268] [PMCID: 2949772] [DOI: 10.1186/1471-2458-10-564]
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