Vitamin C IV Therapy in Cancer Treatment Benefits and Dangers

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"A Short History Review of IV Vitamin C Therapy as a Cancer Treatment
Over 60 years ago, physician William McCormick observed that many cancer patients had low serum vitamin C levels, which made him believe that vitamin C might be used against cancer.
In 1972, Ewan Cameron, a Scottish physician, hypothesized that ascorbate could inhibit a group of enzymes that can catalyze the degradation of hyaluronic acid, resulting in an enhanced extracellular matrix and a reduced risk of tumor metastasis.
In 1976, Cameron and Linus Pauling published a study of 100 cancer patients who were treated with ascorbate. Although lacking a control group, the study results showed that vitamin C therapy improved quality of life and resulted in a four-fold increase in the patients" mean survival time. Also, their follow-up study showed that over 20% of patients treated with vitamin C had more extended survivorship for more than a year compared to the percentage of patients in the control group, which was only 0.4%. A similar result was reported from a clinical trial in Japan. (Intravenous High-Dose Vitamin C in Cancer Therapy - NCI, n.d.)
The Controversy
Even though these promising findings spurred an interest in vitamin C as a cancer therapy, the later Mayo Clinic's randomized clinical trials (RCTs) led by Charles Moertel failed to show the benefits of high-dose vitamin C therapy in treating cancer. To understand this discrepancy, we need to look at a couple of crucial factors:
The RCTs at Mayo Clinic administered vitamin C therapy for only 2.5 months of use, and then the patients got switched to standard chemotherapy when they presented signs of tumor progression. In contrast, the vitamin C therapy in Pauling and Cameron trials lasted for the entire study period or longer for up to twelve years.
The Mayo Clinic administered a daily dose of 10 g ascorbate to patients orally, whereas the Cameron and Pauling trials applied it both orally and intravenously.
When administered orally, the plasma concentration of vitamin C is tightly controlled in the body through several processes, such as GI absorption, tissue accumulation, renal reabsorption/excretion, etc. But if administered intravenously, this tight control is bypassed, resulting in a pharmacologic plasma level of vitamin C and further leading to cell death in cancer cell lines. (Verrax & Calderon, 2009) This means the outcome of the Mayo Clinic"s RCTs doesn"t provide sufficient evidence to rule out the therapeutic potential of high-dose vitamin C as a cancer treatment. With this realization, an interest in new research on this topic has been rekindled.
Over the past decade, more clinical trials have tested the efficacy and safety of vitamin C as a cancer therapy. What"s encouraging is that pretty much all these studies showed improved quality of life with fewer side effects and more protection of normal tissues from toxicity induced by standard treatments. Moreover, vitamin C therapy showed synergistic effects when combined with chemo and radiation therapies. However, these studies were not large-scale RCTs; therefore, the efficacy of high-dose vitamin C therapy as a cancer therapy remains inconclusive. (Intravenous High-Dose Vitamin C in Cancer Therapy - NCI, n.d.)
Observed Benefits
Over half of colorectal cancers (CRCs) are associated with KRAS or BRAF gene mutations. These oncogenic mutations can contribute to the Warburg effect by upregulating glucose transporter (GLUT1), allowing cancer cells to efficiently uptake glucose. This suggests that targeting KRAS or BRAF mutant cancer by exploiting the expression of GLUT1 and the cancer cell"s increased dependence on glycolysis should be a strategy. Recent studies have shown that high-dose vitamin C could selectively kill KRAS or BRAF mutant CRC cells by targeting these distinct characteristics.
What"s also fascinating is that GLUT1 transports both glucose and the oxidized form of vitamin C called dehydroascorbic acid (DHA). It was observed that KRAS or BRAF mutant CRC cells increased the uptake of DHA via GLUT1; consequently, it increased the production of oxidative stress and ROS in the cancer cells. Through its conversion to DHA, ascorbic covertly promoted intracellular ROS production after entering cancer cells via GLUT1, ultimately killing the cancer cell. Because KRAS and BRAF mutations are not limited to CRC, high-dose vitamin C may also benefit other types of KRAS and/or BRAF mutant cancers. (Intravenous High-Dose Vitamin C in Cancer Therapy - NCI, n.d.)
Reported Downsides
High-dose IV ascorbic acid is generally well tolerated; however, the following warnings and incidents have been given and reported:
Renal failure in patients with renal disorders
Fluid overload
Not suitable for those with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency due to the risk of developing hemolysis
Possible interference with certain laboratory tests, such as strip-based glucose measurement, causing false elevations."

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