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Vitamin C (ascorbic acid) has been proposed to have anti-cancer effects since the 1940s. Linus Pauling and Ewan Cameron pioneered research into vitamin C and cancer with their study reporting that terminal cancer patients treated with intravenous and oral vitamin C lived longer than those treated with standard care alone (Cameron & Pauling, 1976).
How Vitamin C Works With Cancer
Laboratory studies have shown that high concentrations of vitamin C can kill cancer cells without harming normal cells via production of cytotoxic levels of hydrogen peroxide that normal cells can neutralise (Ohno, et al., 2009). Ascorbic acid also down-regulates hypoxia-inducible factor 1 (HIF-1) and promotes apoptosis via regulation of caspases and the mitochondrial membrane potential. Furthermore, ascorbic acid inhibits cell proliferation by inducing cell-cycle arrest in the quiescent phase (Fromberg, et al., 2011).
Intravenous Vitamin C (IVC) Therapy
Vitamin C has been used to help people with cancer for over 30 years, not just for its cytotoxic effect and potential life-prolongation, but also because there have been some reports of remission (Riordan, et al., 2004) and changes to health-related quality of life such as improvements in physical, emotional and cognitive function, as well as a reduction in fatigue, nausea, vomiting, pain and loss of appetite (Yeom, Jung, & Song, 2007).
People with cancer tend to have a low vitamin C concentration in their blood. Oral supplementation can increase blood levels slightly, but due to tight regulation of vitamin C absorption from the gut, not high enough to reach cytotoxic levels – to achieve such levels would require intravenous administration (Padayatty, et al., 2004). In vitro studies have found that vitamin C concentrations of 20mM (350mg/dL) were cytotoxic to many types of cancer cells but not to normal cells (Chen, et al., 2005). Lipoic acid may enhance the effect of vitamin C and reduce the concentration needed to kill cancer cells (Riordan, Riordan, & Casciari, 2000; Casciari, Riordan, & Schmidt, 2001).
Intravenous doses of up to 1.5g/kg body weight have been given to humans with few adverse events (Hoffer, et al., 2008; Padayatty, et al., 2010). Most adverse events associated with IVC are transient and mild, such as diarrhoea, headache and fatigue. However, for people with glucose-6-phosphate dehydrogenase (G6PD) deficiency, high doses of vitamin C may cause hemolysis so should be avoided (Campbell, Steinberg, & Bower, 1975). At Integrated Health Options we insist on testing for G6PD deficiency before administering higher doses of IVC.
There have been concerns that high doses of vitamin C may increase the risk of kidney stones, since one of the byproducts of vitamin C metabolism is oxalic acid which can form calcium oxalate deposits (Massey, Liebman, & Kynast-Gales, 2005). However, some studies may have exaggerated the risk by using analysis methods that cause conversion of vitamin C to oxalate. When people with normal renal function receive IV vitamin C and urine samples are processed appropriately, less than 0.5% of the vitamin C is converted to oxalic acid (Robitaille, et al., 2009). As a precaution we carefully monitor our clients with impaired renal function or a history of stone formation.
The information provided here is only for general reference and cannot replace personalised professional medical advice from a doctor. You are welcome to discuss any points during your consultation with our doctors.
- Cameron E, Pauling L. (1976). Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. PNAS. 1976;73:3685-3689.
- Campbell GD, Steinberg MH, Bower JD. (1975). Letter: Ascorbic acid-induced hemolysis in G-6-PD deficiency. Ann Intern Med. 82:810.
- Casciari JJ, Riordan NH, Schmidt TL, et al. (2001). Cytotoxicity of ascorbate, lipoic acid, and other antioxidants in hollow fibre in vitro tumours. Br J Cancer. 84:1544-1550.
- Chen Q, Espey MG, Krishna MC, et al. (2005). Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues. PNAS. 102:13604-13609.
- Fromberg A, Gutsch D, Schulze D, et al. (2011). Ascorbate exerts anti-proliferative effects through cell cycle inhibition and sensitizes tumor cells towards cytostatic drugs. Cancer Chemother Pharmacol. 67:1157-1166.
- Hoffer, LJ, Levine M, Assouline S, et al. (2008). Phase I clinical trial of i.v. ascorbic acid in advanced malignancy. Ann Oncol. 19:1969-1974.
- Massey LK, Liebman M, Kynast-Gales SA. (2005). Ascorbate increases human oxaluria and kidney stone risk. J Nutr. 135:1673-1677.
- Ohno S, Ohno Y, Suzuki N, et al. (2009). High-dose vitamin C (ascorbic acid) therapy in the treatment of patients with advanced cancer. Anticancer Res. 29:809-816.
- Padayatty SJ, Sun H, Wang Y, et al. (2004). Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med. 140:533-537.
- Padayatty SJ, Sun AY, Chen Q, et al. (2010). Vitamin C: intravenous use by complementary and alternative medicine practitioners and adverse effects. PLoS One. 5:e11414.
- Riordan NH, Riordan HD, Casciari JJ. (2000). Clinical and experimental experiences with intravenous vitamin C. J Orthomol Med. 15:201-213.
- Riordan HD, Riordan NH, Jackson JA, et al. (2004). Intravenous vitamin C as a chemotherapy agent: a report on clinical cases. P R Health Sci J. 23:115-118.
- Robitaille L, Mamer OA, Miller WH, et al. (2009). Oxalic acid excretion after intravenous ascorbic acid administration. Metabolism. 58:263-269.
- Yeom CH, Jung GC, Song KJ. (2007). Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 22:7-11.