intravenous vitamin c cancer study

intravenous vitamin c cancer study

intravenous vitamin c cancer nih

Intravenous Vitamin C Cancer Study

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The IP address used for your Internet connection is part of a subnet that has been blocked from access to PubMed Central. Addresses across the entire subnet were used to download content in bulk, in violation of the terms of the PMC Copyright Notice. Use of PMC is free, but must comply with the terms of the Copyright Notice on the PMC site. For additional information, or to request that your IP address be unblocked, For requests to be unblocked, you must include all of the information in the box above in your message.Vitamin C, when administered in high doses by intravenous (I.V.) infusions, can kill cancer cells. Vitamin C interacts with iron and other metals to create hydrogen peroxide. In high concentrations, hydrogen peroxide damages the DNA and mitochondria of cancer cells and shuts down their energy supply and kills them outright. Best of all — and unlike virtually all conventional chemotherapy drugs that destroy cancer cells — it is selectively toxic. No matter how high the concentration, Vitamin C does not harm healthy cells.




Do not attempt to use this treatment by yourself. This treatment must be used under the direction of cancer experts who are based at a clinic. The Vitamin C by I.V. treatment is generally used for cancer, but it can also be used to cure MDM-1, NDM-1, and Ebola. Two-time Nobel Prize winner Linus Pauling, along with Dr. Ewen Cameron of Scotland, did a scientific study proving that 10 grams of Vitamin C, given by I.V., could extend the life of advanced cancer patients six-fold. However, there is currently an entire field of research called orthomolecular medicine which is devoted to natural treatments, especially Vitamin C, and their effect on disease. “Vitamin C is thought to act as a pro-oxidant inside the cell in high concentration, and some hydrogen peroxide is formed which is rapidly disposed of by catalase in a normal cell,” said Dr. William Wassell. “Since cancer cells have a deficiency or lack entirely of catalase the peroxides kill the [cancer] cell.” There are several clinics in the United States that use this treatment.




Bright Spot For Health, a large research clinic in Wichita, Kansas, was the home of a great deal of research on Vitamin C by I.V. The original research was done by the late Dr. Hugh Riordon. In cancer, Riordan et al. (1995) demonstrated the likelihood that Vitamin C was an effective anti-tumor therapy as long as high enough concentrations of it could be achieved inside the tumor(s). These researchers also concluded that oral Vitamin C supplementation was unlikely to produce blood levels of Vitamin C high enough to have a direct killing effect on a given tumor. Later, in studying a certain line of cancer cells and the ability of Vitamin C to kill those cancer cells, Casciari et al. (2001) elegantly demonstrated this point. They showed that the rapid intravenous infusion of Vitamin C as sodium ascorbate in combination with alpha-lipoic acid was effective in reaching Vitamin C levels that were toxic to the cancer cells. They also showed that a fat-soluble analogue of Vitamin C, phenyl-ascorbate, was able to kill cancer cells effectively at a dose roughly three times lower than seen with unaltered Vitamin C.




Vitamin C was first suggested as a tool for cancer treatment in the 1950s. Its role in collagen production and protection led scientists to hypothesize that ascorbate replenishment would protect normal tissue from tumor invasiveness and metastasis (McCormick, 1959; Cameron, et al., 1979). Also, since cancer patients are often depleted of vitamin C (Hoffman, 1985; Riordan, et al., 2005), replenishment may improve immune system function and enhance patient health and well-being (Henson, et al., 1991). Cameron and Pauling observed fourfold survival times in terminal cancer patients treated with intravenous ascorbate infusions followed by oral supplementation (Cameron & Pauling, 1976). However, two randomized clinical trials with oral ascorbate alone conducted by the Mayo clinic showed no benefit (Creagan, et al., 1979; Moertel, et al., 1985). Most research from that point on focused on intravenous ascorbate. The rationales for using intravenous ascorbate infusions (IVC) to treat cancer:




If large amounts of Vitamin C are presented to cancer cells, large amounts will be absorbed. In these unusually large concentrations, the antioxidant Vitamin C will start behaving as a pro-oxidant as it interacts with intracellular copper and iron. This chemical interaction produces small amounts of hydrogen peroxide. Because cancer cells are relatively low in the intracellular antioxidant enzyme catalase, the high dose Vitamin C induction of peroxide will continue to build up until it eventually lysis the cancer cell from the inside out. This effectively makes high dose IVC a non-toxic chemotherapeutic agent that can be given in conjunction with conventional cancer treatments. Based on the work of several Vitamin C pioneers before him, Dr. Riordan was able to prove that Vitamin C was selectively toxic to cancer cells if given intravenously. This research was reproduced and published by Dr. Mark Levine at the National Institutes of Health. Only markedly higher doses of Vitamin C will selectively build up as peroxide in the cancer cells to the point of acting in a manner similar to chemotherapy.




These tumor-toxic dosages can only be obtained by intravenous administration.Maybe Linus Pauling was on to something after all. Decades ago the Nobel Prize–winning chemist was relegated to the fringes of medicine after championing the idea that vitamin C could combat a host of illnesses, including cancer. Now, a study published online today in Science reports that vitamin C can kill tumor cells that carry a common cancer-causing mutation and—in mice—can curb the growth of tumors with the mutation. If the findings hold up in people, researchers may have found a way to treat a large swath of tumors that has lacked effective drugs. "This [could] be one answer to the question everybody's striving for," says molecular biologist Channing Der of the University of North Carolina, Chapel Hill, one of many researchers trying to target cancers with the mutation. The study is also gratifying for the handful of researchers pursuing vitamin C, or ascorbic acid, as a cancer drug. Maybe people will finally pay attention," says vitamin C researcher Mark Levine of the National Institute of Diabetes and Digestive and Kidney Diseases.




In 1971, Pauling began collaborating with a Scottish physician who had reported success treating cancer patients with vitamin C. But the failure of two clinical trials of vitamin C pills, conducted in the late 1970s and early 1980s at the Mayo Clinic in Rochester, Minnesota, dampened enthusiasm for Pauling’s idea. Studies by Levine’s group later suggested that the vitamin must be given intravenously to reach doses high enough to kill cancer cells. A few small trials in the past 5 years—for pancreatic and ovarian cancer—hinted that IV vitamin C treatment combined with chemotherapy can extend cancer survival. But doubters were not swayed. "The atmosphere was poisoned" by the earlier failures, Levine says. A few years ago, Jihye Yun, then a graduate student at Johns Hopkins University in Baltimore, Maryland, found that colon cancer cells whose growth is driven by mutations in the gene KRAS or a less commonly mutated gene, BRAF, make unusually large amounts of a protein that transports glucose across the cell membrane.




The transporter, GLUT1, supplies the cells with the high levels of glucose they need to survive. GLUT1 also transports the oxidized form of vitamin C, dehydroascorbic acid (DHA), into the cell, bad news for cancer cells, because Yun found that DHA can deplete a cell’s supply of a chemical that sops up free radicals. Because free radicals can harm a cell in various ways, the finding suggested “a vulnerability” if the cells were flooded with DHA, says Lewis Cantley at Weill Cornell Medicine in New York City, where Yun is now a postdoc. Cantley’s lab and collaborators found that large doses of vitamin C did indeed kill cultured colon cancer cells with BRAF or KRAS mutations by raising free radical levels, which in turn inactivate an enzyme needed to metabolize glucose, depriving the cells of energy. Then they gave daily high dose injections—equivalent to a person eating 300 oranges—to mice engineered to develop KRAS-driven colon tumors. The mice developed fewer and smaller colon tumors compared with control mice.




Cantley hopes to soon start clinical trials that will select cancer patients based on KRAS or BRAF mutations and possibly GLUT1 status. His group’s new study "tells you who should get the drug and who shouldn't," he says. Cancer geneticist Bert Vogelstein of Johns Hopkins University, in whose lab Yun noticed the GLUT1 connection, is excited about vitamin C therapy, not only as a possible treatment for KRAS-mutated colon tumors, which make up about 40% of all colon cancers, but also for pancreatic cancer, a typically lethal cancer driven by KRAS. “No KRAS-targeted therapeutics have emerged despite decades of effort and hundreds of millions of dollars [spent] by both industry and academia,” Vogelstein says. Others caution that the effects seen in mice may not hold up in humans. But because high dose vitamin C is already known to be safe, says cancer researcher Vuk Stambolic of the University of Toronto in Canada, oncologists “can quickly move forward in the clinic." One drawback is that patients will have to come into a clinic for vitamin C infusions, ideally every few days for months, because vitamin C seems to take that long to kill cancer cells, Levine notes.