Vitamin C is a powerful antioxidant, protecting cells from free radicals, DNA damage, and cellular stress. It plays an important role in supporting the immune system, collagen production, and iron absorption, and has been recently researched as a potent anti-cancer agent.
Intravenous vitamin C for cancer was originally studied by Dr. Linus Pauling and Dr. Ewan Cameron who published clinical trials reporting increased survival rates among patients treated with pharmacological doses (10g) of vitamin C. Similar results were not found upon oral administration of the same dose. This could be because blood plasma concentrations of vitamin C only reached 0.22 mmol/L from oral intake, while IV administration produced blood plasma levels at >6 mmol/L. When taken orally, vitamin C must pass through the digestive system and is dependent on intestinal and kidney absorption. This is unlike intravenous administration which enters the blood directly. This distinction between oral and IV treatment could explain why vitamin C infusion has been historically overlooked as a potential therapy for cancer. Dr. Mark Levine, a prominent researcher at the National Institutes of Health, conducted studies finding that an infusion of 100g of vitamin C could produce blood levels from 25-30 mmol/L, and previous studies have demonstrated that a blood concentration of 10 mmol is adequate to kill cancer cells.
Dr. Levine and his team also discovered the mechanism by which vitamin C kills cancer. While low doses of vitamin C produce an antioxidant effect, high doses produce a pro-oxidant effect. Vitamin C reacts with the oxygen in cancer cells to produce hydrogen peroxide, an oxidative agent that is cytotoxic to cancerous tissue. Hydrogen peroxide is naturally produced in healthy cells, for example in the conversion of thyroid hormones from T4 to T3. Its inflammatory effects are mitigated by the enzyme, catalase, which breaks down hydrogen peroxide into one oxygen molecule and two water molecules. Most cancer cells lack the enzyme catalase, making them susceptible to the toxic effects of hydrogen peroxide, while surrounding healthy tissues remain unaffected.
The redox potential of vitamin C for metals such as iron, which is elevated in cancerous tissue, is responsible for this oxidative damage. For instance, the conversion of iron Fe3+ to its more bioavailable form Fe2+ produces hydrogen peroxide. The increased levels of Fe2+ in tumors also react with hydrogen peroxide, producing the hydroxyl (OH) radical and damaging the cell. GLUT1, a protein that helps facilitate the transport of carbohydrates and vitamin C, is increased in cancer cells as well. GLUT1 mediates the cellular uptake of oxidized vitamin C which is reduced in the process, depleting other antioxidants including glutathione (GSH). Because of their dysfunctional mitochondria, cancer cells are already susceptible to high levels of oxidative stress. Vitamin C may also mitigate metastasis by promoting the synthesis of collagen. Collagen has been demonstrated to stabilize the extracellular matrix, which effectively prevents tumor cells from penetrating surrounding tissues.
Vitamin C IV is not necessarily effective in all cancer cases. Some cancers overgrow the circulatory system’s ability to provide oxygen to cells, which is needed for hydrogen peroxide production. Some cells can produce catalase, mitigating hydrogen peroxide. If cells do produce catalase, vitamin K3 along with vitamin C can be used in infusions to increase the production of hydrogen peroxide.
While vitamin C acts as an antioxidant at low doses, it is a powerful oxidative agent when administered as an IV at pharmacological doses. Patients do not usually experience side effects from this therapy, and it is especially effective because it does not target or harm healthy tissues. As research emerges we continue to discover mechanisms of this powerful anti-tumor agent.
1 PMID: 34717701
2 Intravenous High Dose Vitamin C
3 PMID: 34717701