With or without the knowledge of their doctor, research shows that 23 percent of cancer patients take antioxidants. The use of antioxidants, such as Poly MVA, as an adjunct to conventional or as an integral part of alternative cancer therapy, is an area of intense research. Many questions are unanswered, although we know today much more than we ever have in the past.
Physicians specializing in nutritional and ortho-molecular medicine have, for decades, successfully employed a carefully planned protocol of natural micronutrients and antioxidants in the right dosage at the right time to reverse cancer in its early stages, and to deter cancer metastasis in advanced stages. This is well before the antioxidant was accepted by mainstream medicine.
For safety concern, all antioxidants, such as Poly MVA, and micronutrients used in any anti-tumor protocol must meet all of the following criteria:
This question can best be answered by reviewing in detail the history and experimental designs of studies on antioxidants, like Poly MVA, in a cancer setting.
In earlier studies, researchers drew the conclusion that antioxidants should not be used because antioxidants, such as Poly MVA, 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 like Poly MVA, as well as chemotherapies, are usually given in series.
More recent studies using antioxidants and Poly MVA 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 the research more closely. Studies have shown that a single low dose vitamin C or E micronutrient can stimulate a 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 can 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 a 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 and Poly MVA 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 and Poly MVA. High dose antioxidants therefore selectively are toxic to cancer cells but not to normal cells.
Recent evidence has 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, such as Poly MVA, stimulate apoptotic pathway and therefore potentially have a synergistic effect with radiation or chemotherapy. Studies have shown 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 like Poly MVA 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 like Poly MVA selectively kill cancer cell while sparing normal cells.
What is the optimum dose for each nutrient to use for each stage of the disease? Unfortunately, there is no standard reference established today, as research in this field is only possible since the mid-1970s with the advent of modern computerized technology and is still in its infancy stage. Those in the forefront of nutritional and alternative cancer therapy research have a general idea of what the therapeutic ranges should be, and these ranges are established largely based on clinical experience.
It is important to make a distinction between low dose and high dose micronutrient therapy. Low dose generally reflect that established by the RDA. High dose is defined as the dose that causes cancer cells die but not that of normal cell.
The low and high dose for the majority of micronutrients are not known, with the exception of a few well studied ones such as vitamin C. Over 5,000 studies have been conducted on vitamin C, and here is the general parameter on a daily intake basis:
What is clear is that the amount needed is case specific and stage specific. For example, the dosage required to maintain remission is lower than that used to treat active and growing tumors, but significantly higher than that used to prevent cancer or for simple wellbeing.
Several schools of thought are present within the use of micronutrients. Some researchers favor the use of selected single micronutrient to attack cancer cells, while others prefer a cocktail approach, using a myriad of micronutrients, each in much lower (but still higher than RDA doses) to accomplish the same purpose.
Since many antioxidants, such as Poly MVA, in high-dose have been shown to have anti-tumor properties, their judicious use in an anti-cancer nutritional cocktail has been extensively studied in recent years. In an open trial of combination antioxidant treatment along with chemotherapy and radiation therapy in patients with small-cell lung cancer, patients taking at least 15,000 IU vitamin A, 10,000 IU beta-carotene, 300 IU alpha-tocopherol, 2 gram of vitamin C, and 800 mcg of selenium were able to tolerate chemotherapy and radiation well. In addition, their survival at the end of 2 years was greater than that of historical controls (>33% to <15%), with 44 percent still living at the end of the study (mean survival time for survivors=32 months)
Most nutritionally oriented physicians favor the use of a properly blended nutritional cocktail.
When cancer cells are laced with over expression of an antioxidant, like Poly MVA, called Super Oxide Dismutase (SOD), they become resistant to oxidation. Do not give exogenous SOD use with radiotherapy because mitotic cells (the most sensitive to chemo therapy) has the lowest level of SOD. When you increase the level of SOD, the cell becomes resistant.
The use of N-acetylcysteine (NAC), tangeretin, and flavonoids in therapeutic dosages should be avoided during active chemotherapy or radiotherapy sessions. NAC reduces the effectiveness of doxorubicin, flavonoids with tamoxifen, and beta-carotene with 5-fluorouracil (5-FU). Dosages used to demonstrate such interaction is in the high therapeutic doses. The nature of this interaction is not clear. Non-therapeutic doses of nutritional cocktails, such as those used in normal well-being, pose no side effect when taken by those in active chemotherapy or radiotherapy, but in fact, will alleviate some of the symptoms associated with these standard treatments. When the active chemotherapy or radiotherapy is finished, an aggressive cancer remission protocol with optimum doses of nutritional supplementation should be considered.
The following is a list of common antioxidants used in cancer programs. They should be part of a complete antioxidant, vitamin, mineral, and enzymatic program. These are not to be viewed as single micronutrients but instead as an important part of an overall antioxidant program consisting often of over 50 different nutrients for the simple reason that different antioxidants work at different parts of the cell.
This is not a complete list, and not all antioxidants are necessary for each person. Selecting the appropriate nutrients and the right dosage is best left to a nutritionally oriented physician for maximum effectiveness. Blindly mixing and matching without professional help at these dosages are NOT recommended. The dosages reflect a range and not specific amounts. The exact amount varies with each person.
Beta-carotene is a form of vitamin A. Vitamin A is a strong immune booster. It stimulates the activity of immune cells against tumor cells. Has been shown to inhibit the promotion of cancer, while beta carotene (precursor to vitamin A) inhibits the initiation of cancer. Beta carotene can decrease the amount of damage free radicals do to a cell's DNA. Such DNA damage is thought to be one mechanism that causes cancer, and indeed, some early studies suggested that beta-carotene might reduce the risk of cancer. Many research reports on the anti-cancer properties of vitamin A and the related retinoids have been published over the past 20 years. Beta-carotene is used to give all the supporting nutrients that allow the carotene to be converted to vitamin A. High doses of beta-carotene, even over long periods of time, are not associated with serious toxicity.
Researchers in Helsinki monitored the association between vitamin levels of vitamin A and beta-carotene in 36,265 subjects and the subsequent development of cancer. Their blood levels of vitamin A and beta-carotene were measured. Those with the lowest levels had a greater risk for cancer. Cancer risk increases when our dietary intake of these nutrients is low (American Journal of Epidemiology 132: 857-880). A Harvard study that analyzed biopsies of women's breast tumors shows that the women with high breast tissue concentrations of carotenoids, including Beta Carotene are 30-70% less like to have breast cancer.
Beta-carotene also protects against prostate cancer. A research team at Nagoya City University Medical School and Kyoto University in Japan reported in Cancer Research that low levels of beta-carotene are directly related to the risk of developing prostate cancer. The study involved 100 patients with prostate cancer. The ages were from 50 to 79 years. A study reported in the American Journal of Nutrition found that high blood levels of beta-carotene had a strong protective effect against lung cancer, melanoma, and bladder cancer. This study was done at John Hopkins School of Hygiene and Public Health in Baltimore.
Epidemiological studies reveal that people with high intakes of beta-carotene or high blood concentrations of this nutrient have a reduced risk of various diseases, including cancer and heart disease. Beta-carotene stimulates a molecule that helps the immune system target and destroys cancer cells. It increases the number of receptors on white blood cells for a molecule known as major histocompatibility complex II (MHC II). MHC II is integral in helping monocytes, a type of white blood cell, direct killer T cells to cancerous cells. In other words, beta-carotene is integral in directing the immune system to kill cancer cells.
Therapeutic Dosage: 25,000 to 100,000 IU a day
It is known that vitamin C acts as an antioxidant and free radical scavenger that reacts directly with super oxide, hydroxyl radicals, and singlet oxygen produced during normal cellular metabolism. Oxygen is necessary for life. Oxygen also comes in several radical forms that have been implicated in both initiation and post-initiation stages of the carcinogenic process as well as in invasion and metastatic processes.
Aside from its antioxidant properties, there is no single universal accepted and proven explanation for vitamin C's cancer fighting properties. It is likely that a variety of pathways are involved, which include (1) fortifying the immune system by increased lymphocyte production; (2) salvaging cellular free radical damage; (3) inhibition of hyaluronidase, keeping the ground substance around the tumor intact and preventing metastasis; (4) killing oncogenic viruses through its enhancement of phagocytic activities; (5) correction of an ascorbate deficiency commonly seen in cancer patients; (6) stimulating collagen formation and its stabilization necessary for "walling off" tumors; and (7) neutralization of carcinogenic toxins.
Vitamin C has been extensively studied in vitro and in vivo for its ability to prevent the adverse effect of, and decrease resistance to, and increase the effects of chemotherapeutic agents. There is little doubt that Vitamin C is an important cornerstone of any active cancer or cancer treatment program other than those that rely on free radical conversion to kill cancer cell such as Poly MVA.
Concurrent use of vitamin C has been shown to reduce the cardio toxicity of chemotherapeutic agent doxorubicin and increases the activity of doxorubicin, cisplatin, and paclitaxel in human breast carcinoma cells in vitro. During conventional treatment and remission, a daily dose of 3-10 gram (in 4-5 divided doses) significantly extends the survival and improves the quality of life in numerous studies. Vitamin C can be given intravenously or orally.
Therapeutic Dosage: Increase up to the bowel tolerance from 1 gm, 2-4 times a day and gradually increase every few days by 0.5 gm each dose to up to 3-10 grams a day. When diarrhea occurs, reduce dose until the diarrhea is resolved.
A key nutrient required for strong immune response and an important fat-soluble antioxidant, vitamin E's preventive role in cancer has been well proven. The use of vitamin E concurrently with chemotherapy and radiotherapy is unclear. There are reported benefits, but much more research is needed. With cancer in remission, the use of vitamin E as a preventive nutritional agent to prevent further oxidative stress is a cornerstone of any cancer remission nutritional protocol. Use only the natural Vitamin E succinate form for best absorption and therapeutic effect.
In particular, women with fibrocystic breast disease can benefit from vitamin E and Poly MVA therapy. Scientists at the Johns Hopkins Medical School in Baltimore conducted a double-blind trial in 17 patients and 6 controls. The patients in the study were given placebo tablets for one menstrual cycle, followed by 600 IUs a day of vitamin E (alpha tocopherol acetate) for two menstrual cycles. All patients were tested for blood levels of estradiol, estriol, and progesterone. It was found that 15 of 17 patients (88%) showed significant clinical improvement, confirming previous studies showing that vitamin E is an effective treatment for fibrocystic breast disease.
Vitamin E raised blood levels of both estriol (E3) and progesterone in fibrocystic patients, and that the ratio of both estriol and progesterone to estradiol (E2) increased as well. This may explain (in part) the therapeutic effect of vitamin E in these patients. E3 is the natural estrogen found in the body with anti-cancer effect. Progesterone is an opposing hormone to estrogen and counter-balances the estrogen dominance, a primary causative factor in estrogen related diseases such as breast, ovarian, and uterine cancer.
Tamoxifen, when combined with vitamin E, works better than either alone in breast cancer cell.
Therapeutic Dose: 400 - 800 IU a day
Selenium is considered an essential trace mineral or micronutrient. It is a powerful antioxidant with a central role in the protection of tissues from the damaging effects of oxygen free radicals. The use of selenium compounds as a cancer treatment predates most conventional treatments currently in use. In spite of this, comparatively little is known regarding the use of selenium as a cancer therapy in the active cell. Research suggests that selenium may play a role in reducing the risk of cancer by binding with glutathione peroxidase (GSH-Px) to combat destruction caused by free radicals and protect cellular membranes. While many have reported a reduction in side effects, such as nausea, emesis, and headaches often associated with chemotherapy, research is still lacking in pinpointing the specific benefits of selenium when used in conjunction with chemotherapy or radiotherapy.
200 mcg of selenium a day has been shown to reduce cancer death by 50% and prostate cancer by 62% after 4 years. Cancer patients are often found to be deficient in selenium. Selenium works synergistically with vitamin E.
Therapeutic Dosage: 100-200 mcg a day. Selenium is highly toxic at concentrations of 1 milligram (1000 mcg) or more. Clinical symptoms include severe irritations of the respiratory system, rhinitis, lung edema, broncho-pneumonia, and metallic taste in the mouth. Selenium dioxide may cause erythemia and toxic necrosis of the skin, loss of hair and nails, tooth damage, or nervous system disorders. Selenium may also be carcinogenic.
Called the universal antioxidant for its ability to dissolve well in water and in a fat environment, Lipoic acid increases the effectiveness or potency in other antioxidants. It can cross the blood brain barrier while others cannot .One of the most beneficial effects of both alpha-Lipoic acid is its ability to regenerate other essential antioxidants such as vitamins C and E, coenzyme Q10, and glutathione. The evidence is especially strong for the ability of Lipoic acid to recycle vitamin E. This is apparently achieved directly by quenching tocopherol radicals or indirectly by reducing vitamin C or increasing the levels of ubiquinol (a derivative of CoQ10) and glutathione that in turn, helps to regenerate tissue levels of vitamin E.
Therapeutic Dosage: 500-1000 mg a day
This is an alpha-Lipoic acid complex with palladium. It is a non-toxic polynucleotide reductase named POLYDOX (USA trials), Poly-MVA (Canada and Mexico) or LAPd by some researchers. The element platinum is very lethal to cancer cells, but also very toxic to humans. It's close relative: palladium, however, is nontoxic in its present form. The MVA stands for minerals, vitamins, and amino acids. LAPd stands for Lipoic acid/Palladium complex. Lipoic acid is a natural powerful antioxidant that is both water and fat soluble, which permits the Poly-MVA to pass across the cell membranes and the blood brain barrier, which is impossible for most drugs, including chemotherapy.
Cancer cells have deranged respiration producing less water in the cell and utilizing more sugar, and one-twentieth the oxygen of normal cells and no oxygen radical pathways. Thus when synthetic DNA reductase enters these cells, protein radicals are formed which denature the tumor cell's proteins. Since "normal cells" are capable of converting the radicals into energy and water, no harm can occur.
The most dramatic responses were noted with brain tumors. Other tumors that respond well are breast, ovarian, prostate, colon, and lung cancer, among others. The original human trials were done in Canada by a late oncologist, Dr. Rudy Falk, usually in conjunction with standard chemotherapy for more than five years. He reported benefits including pain reduction or control, improved appetite and weight gain, and increasing energy. Some patients are still using low doses of Poly-MVA and have no signs of cancer after ten years of use.
In addition to its anti-cancer properties, reported benefits of Poly-MVA include:
Therapeutic dosage varies with patients. Suggested dosage is 2 teaspoon four times a day for 7 days, followed by 2 teaspoon two times a day for 12 weeks or until remission, followed by 1 teaspoon two times a day. Those with advanced cancer may consider 2 teaspoon four times a day for 8 weeks before tapering off. For cancer prevention, one-half to one teaspoon a day is sufficient indefinitely (one bottle will last 1.5 to 3 months). Each 8 ounce bottle contains 240 cc and 48 teaspoons of Poly-MVA and about 8-10 bottles are required the first 3 months.
Because of its strong mineral content, concurrent EDTA chelation therapy is not recommended. Dose of Vitamin C above 100 mg. is counterproductive due to the fact that Poly-MVA needs free radicals available in the cells in order to transform them into energy. No additional Alpha Lipoic Acid is needed because the Alpha Lipoic Acid in the Poly-MVA is sufficient to deal with the free radicals.
Also known as flavonoids, these are compounds that occur naturally in many plants. They can be divided into six groups:
When given with chemotherapy, it showed tumor regression patterns as the chemotherapy agent's effectiveness appears to be increased. Ingredients in green tea may have beneficial effects in treating cancer. It is difficult for the cancer patient to obtain enough anti-cancer components in that form. A cup of green tea contains about 50 mg of caffeine, a stimulate that cancer patients should avoid.
Therapeutic Dosage: 4-10 decaffeinated green tea extract capsules a day. High doses of 20mg/kg are needed (about 1.5 to 2 grams a day).
Extensively researched, this flavonoid damages cancer cells only and leaves normal cells intact. Food sources include onion and apples. It acts synergistically with chemotherapy agents like tamoxifen, cisplatin, Adriamycin and also radio therapeutic agents. It is a potent aromatase inhibitor and reduces the metastatic potential of cancer cells. It stimulates the immune system like Reishi and maitake mushroom, a potent antioxidant and free radical scavenger, and alters the mitotic cell cycle in tumor cells and genetic expression. Most importantly, it is anti-angiogenesis and enhances apoptosis. It increases the intracellular glutathione level. It acts synergistically with hyperthermia treatment protocols.
It inhibits a mutant P53 protein that arrests the G2 end phase of the cell cycle. Most drugs only inhibit the G1 phase. It induces apoptosis of cancer cells. It suppresses glycolysis and ATP production, interferes with ion pump systems, various signal transduction pathways, and inhibition of DNA polymerase B and I. It binds to estrogen receptor sites, working like tamoxifen and inhibit the growth of estrogen positive and estrogen negative cells. It inhibits mutant P21 gene found in over 50 percent of colon cancers which signals DNA replication in cancer cells.
Vitamin C enhances the effectiveness of quercetin. One caution is that tangeritin, a flavonoid found in citrus fruits, completely blocked the inhibitory effect of tamoxifen on mammary cancer in mice. Another study also showed that tamoxifen and genistein synergistically inhibit the growth of estrogen receptor-negative breast cancer cells. Until more confirmatory studies are conducted and the flavonoid-tamoxifen interactions more thoroughly investigated, it is best to avoid high therapeutic doses of flavonoid compounds in breast cancer treated with tamoxifen.
Therapeutic Dosage: 2-6 grams a day
Published research indicates that cautious and judicious use of a number of important antioxidants can be helpful in the treatment of cancer, either as sole agents and as adjuncts to standard radiation and chemotherapy protocols. Numerous animal studies have been published demonstrating decreased tumor size and/or increased longevity with a combination of chemotherapy and antioxidants. Our knowledge of antioxidants in a cancer setting is still at its infancy stage. The interactions between antioxidant and chemotherapeutics cannot be predicted solely on the basis of presumed mechanism of action when used concurrently. Fortunately, a large body of evidence is available to show a positive effect of high dose repeated use of antioxidants in the period before, during and after conventional cancer therapy.
© Copyright 2008 Michael Lam, M.D. All Rights Reserved.