Primary Anticancer Mechanism
The primary anticancer mechanism of vitamin C (Vc, also called ascorbic acid) is hydrogen peroxide (H2O2) generation in cells. Normal cells have 10-100 folds of catalase (convert H2O2 to water and oxygen) higher than tumor1. Therefore, normal cells have higher tolerance of H2O2 toxicity than cancer cells.
Other Anticancer Functions of Vitamin C
- Vc is essential to ensure the efficient working of immune system, including of immunoglobulin synthesis, increasing the migration and chemotaxis of the leukocytes, activating phagocytosis and enhancing interferon production.
- Inactivation of carcinogens through the mixed function oxidases and protection against nitrate induced carcinogens.
- Balancing the disturbed sodium/potassium in cancer by removal of sodium via urine.
- Inhibiting prostaglandins of the 2-series to decrease the cancer cell proliferation.
- Stabilizing cancer suppressor gene, p53, to stop the cancer cell proliferation.
Figure 2: In vitro studies: Our previous study showed that Vc presented doseresponse to four human cancer cell lines in vitro: Mia PaCa-2 (pancreatic carcinoma), SKMEL-28 (melanoma), SW-620 (colon carcinoma), and U-2-OS (osteogenic sarcoma). Results reflect total viable cells. At 400 mg/dL, Vc kills about 90% or more cancer cells2.
Figure 3: Tumor inhibition effect of Vc on melanoma mice. 700 mg/kg Vc (equivalent to 50g on 70 kg person) was injected intraperitoneally, thrice a week for 3 weeks. Tumor inhibition was 57% at the end of the test.
Figure 4: The effect of survival time of Vc on sarcoma mice. 700 mg/kg Vc (equivalent to 50g on 70 kg person) was injected intraperitoneally every day for 64 days. Vc increased the lifespan for 46% comparing with control group.
Vc by oral and intravenous administrations in healthy people3:
Figure 5: For the maximum tolerated oral dose of 3 g every 4 hours (6 times/day), pharmacokinetic model predicted peak plasma vitamin C concentrations of 220 μmol/L (3.87 mg/dL), while 13,400 μmol/L (235.84 mg/dL) for a 50g IVC dose.
Peak predicted urine concentrations of Vc from IVC were 140-fold higher than those from maximum oral doses. Therefore, IVC instead of oral Vc administration is the way to reach the plasma level to kill cancer cells.
1 mmol/L = 1000 μmol/L = 17.6 mg/dL;
1 μmol/L = 0.0176 mg/dL; 1 mg/dL= 56.82 μmol/L. The plasma Vc level reached by intravenous vitamin C (IVC).
Figure 6: Showed Mean ± 2SD of plasma Vc level after different amount of Vc infusion. After 15 g Vc infusion, the plasma Vc level can reach 100 mg/dL in average. After 65g IVC, plasma Vc reached 400 mg/dL, which is high enough to kill the cancer cells.
Plasma Vc response on cancer patients by IVC
- Cancer patients often have below-normal plasma vitamin C4,6. In one of our studies, 14 out of 24 patients were ascorbate deficient prior to therapy, with 10 patients having no detectable vitamin C in their plasma6.
- In most cases, plasma Vc levels increased to near maximum in 1 to 2 weeks of IVC on cancer patients.
Figure 7: Showed the plasma Vc levels during infusion of 65g Vc at a rate of 1g Vc per minute on three cancer patients. Vc reached 300-700 mg/dL peak after 16 IVCs.
- Case 1: In September 1995, shortly after diagnosis of a primary tumor in the left kidney of a 52-year-old white female, a nephrectomy was performed. Histology confirmed renal cell carcinoma. In September 1996, a chest x-ray film revealed 4 1- to 3-cm masses in her lungs. One month later there were 8 1- to 3-cm masses in her lungs (7 in right lung, 1 in left). No new medical, radiation, or surgical therapies were performed prior to her visit to our clinic in October 1996, when she began IVC therapy. Her initial dose was 15 g, which increased to 65 g after 2 weeks, two per week. She was also started on: N-acetyl cysteine, 500 mg 1 p.o., QD; beta-1,3- glucan (a macrophage stimulator), 2.5 mg 3 p.o. QD; fish oil (300 mg eicosatetraenoic acid, 200 mg docosahexaenoic acid), 1 p.o. TID; vitamin C, 9 g p.o. QD; betacarotene, 25,000 lU. 1 p.o. BID; L-threonine, 500 mg p.o. QD (for a deficiency revealed by laboratory testing of serum); Bacillus laterosporus, 280 mg, 2 p.o. QD for intestinal Candida albicans, inositol hexaniacinate complex (500 mg niacin, 100 mcg chromium) 2 p.o. QD, and a no-refined-sugar diet. She continued IAA treatments until June 1997 when another chest x-ray film revealed resolution of 7 of the 8 masses, and reduction in the size of the 8th. According to the medical imaging report, “The nodular infiltrates seen previously in the right lung and overlying the heart are no longer evident and the nodular infiltrate seen in left upper lung field has shown marked interval decrease in size and only vague suggestion of an approximately 1 cm density.” The patient discontinued IAA treatments in June 1997. She has continued on an oral nutritional support program since that time, and 4 years later was well with no evidence of progression2.
- Case 2: In December 1985, a mass occupying the lower pole of the right kidney was discovered in a 70-year-old white male. Pathology of the mass after a radical nephrectomy confirmed renal cell carcinoma. In March 1986 the patient was seen in our clinic. He was started on IVC, 30 g twice per week. In April 1986, six weeks after the x-ray film and CT scan studies, the oncologist’s report stated, “… the patient returns feeling well. His exam is totally normal. His chest x-ray shows a dramatic improvement in pulmonary nodules compared to six weeks ago. The periaortic lymphadenopathy is completely resolved… either he has had a viral infection with pulmonary lesions with lymphadenopathy that has resolved or (2) he really did have recurrent kidney cancer which is responding to your vitamin C therapy.” The oncology report in July 1996 stated, “there is no evidence of progressive cancer. He looks well . . . chest x-ray today is totally normal. The pulmonary nodules are completely gone. There is no evidence of lung metastasis, liver metastasis or lymph node metastasis today, whatsoever.” In 1986 the patient received 30 g infusions twice-weekly for 7 months. The treatments were then reduced to once per week for 8 more months. For an additional 6 months he received weekly, 15 g IAA infusions. The patient continued well, and was seen periodically at our clinic until early 1997 when he died, cancer-free, at age 82, 12 years after diagnosis.
- Case 3: A 55 year old woman with stage-IIIC papillary adenocarcinoma of the ovary and an initial CA-125 of 999. underwent surgery followed by six cycles of chemotherapy (paclitaxel, carboplatin) combined with oral and parenteral ascorbate. Ascorbate infusion began at 15 grams twice weekly and increased to 60 twice weekly. Plasma ascorbate levels above 200 mg/dL were achieved during infusion. After six weeks, ascorbate treatment continued for year, after which patient reduced infusions to once every two Patient also supplemented with vitamin E, coenzyme Q10, vitamin beta-carotene, and vitamin A. After over 40 months from initial diagnosis and remains on ascorbate infusions, the patient’s all CT and PET are negative for disease, and her CA-125 levels remain normal.
Figure 8: In our study of IVC for 24 late-stage cancer patients, blood creatinine, BUN and uric acid concentrations were decreased or remained stable during therapy, suggesting that IVC did not adversely affect renal functions6. Other blood counts also showed that IVC is safe on cancer patients.
- IVC has been used for three decades here at The Center. There have been no serious complications. The most common adverse events reported were nausea, edema, and dry mouth or skin; and these were generally minor5,6.
- Although many physicians worry that large doses of vitamin C may cause kidney stones, we have rarely seen the phenomenon5. Kidney stones are formed mostly in alkaline urine (calcium oxalate), while high dose of ascorbate infusion make the urine acidic, thus preventing stone formation. There are various studies found no evidence of ascorbate increasing the risk of kidney stone formation1. However, for those patients with kidney stone history, more care should be taken on IVC treatment6.
- For people with glucose-6-phosphate dehydrogenase (G6PD) deficiency, high dose of Vc may be at risk of developing hemolysis. Therefore, we also check our patients for G6PD deficiency before IVC at the Center5,6.
- Because vitamin C enhances iron absorption, iron overload must be ruled out5.
- Because ascorbate is a chelating agent, some individuals may experience shaking due to low serum calcium. This is treated by a slow (1 cc per minute) intravenous push of 10 cc’s of calcium gluconate2.
- Another concern of IVC is a rapid tumor hemorrhage and necrosis. This can be avoided by starting the small dose first. A typical protocol will consist of the following infusions: Week 1: 15g, 25g, 50g infusion, 3 times/week, according to plasma C level. Week 2 and later: 25g or 50g infusion per day, 3 times/week, according to plasma C level.
The dose is then adjusted to achieve transient plasma concentrations near 400 mg/dL, 3 infusions per week2.
References
- Michael J. Gonz‡lez et al: Orthomolecular Oncology Review: Ascorbic Acid and Cancer 25 years Later. Integrative Cancer Therapies 4(1); 2005 pp.32-44
- Padayatty SJ: Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med. 2004 Apr 6;140(7):533-7.
- Anthony et al, Br J Cancer 46 : 354, 1982
- Cancer
- Hugh D. Riordan et al: A Pilot Clinical Study of Continuous Intravenous Ascorbate in Terminal Cancer Patients. PR Health Sci J. 2005; 24(4):269-276.
- Drisko JA, Chapman J, Hunter VJ. The use of antioxidants with first-line chemotherapy in two cases of ovarian cancer. Am J Coll Nutr 22: 118- 123 (2003).



