High Dose Vitamin C IV Therapy

Story at a glance

  • Neurotransmitter synthesis, such as dopamine, serotonin, and adrenaline
  • Many hypothalamic and gastrointestinal peptide hormones
  • Required for growth and wound healing
  • An essential component of an enzyme system that “rewrites” and restores aberrant epigenetic changes associated with CFC formation back to normal
  • Required for iron absorption, activity, and metabolism
  • Required to synthesize L-carnitine necessary to utilize fat for energy.
  • Enhances T cell proliferation and function as well as NK cell proliferation (essential for immunity and specifically eradication of CFCs)
  • When high plasma levels of ascorbate are achieved through intravenous administration, the antioxidant activity of ascorbate, by acting on either iron or copper, produces highly reactive pro-oxidant molecules that directly destroy CFCs.
  • Selectively kill CFCs by targeting their unique metabolic vulnerabilities without harming healthy cells
  • Reduce the risk of recurrence and metastases by eliminating CFC stem cells
  • Enhance the immune system
  • Support the vitality of healthy cells and reduce the damage caused by conventional treatments

High Dose Vitamin C IV Therapy

Vitamin C, known as ascorbate, is an essential molecule in the biochemistry of life. The energy of life exists in the form of electricity, which represents the flow of electrons. The electrical pattern of an organ, such as the heart, reveals its health status based on the electrical waveforms, shapes, sizes, proximity to each other, activity rate, and different angles. These observations, discerned by trained experts, can reveal underlying issues and their origins. When the line is flat, i.e., no electron flow, then life is over. This principle applies to the brain, muscles, and all other organs.

Electrons flow through copper wires in our homes to power our houses and in the other machines and devices that we use daily, except for those that use different technology, such as Bluetooth, which requires no wires. In any case, the electrons need to be transferred in some sort of medium. In biological systems, there are molecules that “hand off” electrons called reductants (antioxidants), and those molecules that “pick up” or accept electrons are called oxidants. Therefore, life is an electronic current consisting of those molecules that pass them forward and those that “catch” them. Combining the words “reduction” and “oxidation” produces the word “redox” and that is the name of the biochemistry that permits life to exist.

As can be seen below, Fe2+ Iron in its “ferrous” form) loses an electron (oxidized) to become F3+ (“ferric” iron), whereas Ce (cerium) with 4 missing electrons to begin with gains an electron to become Ce3+ (reduced). The (+) means an electron is missing because electrons have a (-) sign, so 2+ means that 2 electrons are missing.

“Redox” reactions are the mechanisms by which electrons are transferred, hence flow and energize all life forms. One donates an electron, therefore reduced and the other gains one, hence oxidized: reduction-oxidation.

Transfer of Electrons Between Two Atoms or Molecules = redox

One of the most fundamental molecules in ‘redox’ biochemistry is ascorbate, an electron donor, or antioxidant. Nearly all forms of life, both plant and animal, either synthesize (produce) ascorbate and if they do not, then they must acquire it somehow to survive. 

Plants produce it in their chloroplasts, the organelles that produce glucose and oxygen from carbon dioxide and water. The energy for this reaction comes from sunlight, called photosynthesis. Light is said to be made of photons that are converted to electrons inside the chloroplasts of plants. Fish, amphibians, reptiles, and some older bird orders produce it in their kidneys, while all mammals except for the primates, fruit bats, guinea pigs, and some birds can produce ascorbate in their livers. The reason for this inability to produce an essential element of life is due to the lack of one specific enzyme, gulonolactone oxidase. That is our problem, too. We must therefore obtain it somehow to live. But, unlike the monkeys, great apes, guinea pigs, and fruit bats who eat their natural diet consisting of plant material with plenty of ascorbate, most humans eat food lacking in ascorbate.

Ascorbic acid, at physiological levels carried in the blood to all organs and cells, functions as an antioxidant and is an essential cofactor in 15 enzymes in all mammals, required for a diverse array of fundamental ‘redox’ reactions required for life. These reactions range from the absorption of iron to the production of neurotransmitters, such as dopamine, epinephrine and serotonin, collagen, and carnitine, to wound healing, to modification of genetic expression, to maintaining a healthy immune system (restores Th1 polarity necessary for eliminating CFCs, “viruses”, and other unwanted cells); and finally, it recycles vitamin E and glutathione, increases other antioxidant enzymes like catalase and superoxide dismutase (SOD), prolongs the life of peptides through a process called amidation, and is involved in the synthesis of bile acids for fat digestion, cholesterol metabolism, and cytochrome P-450 activity, a pivotal aspect of the liver’s ability to detoxify.

Research indicates that healthy levels of ascorbate in human plasma (blood) are between 50-70 μmol/l, < 23 μmol/l is considered deficient and levels < 11 μmol/l are considered to result in scurvy, a fatal condition resulting from a severe lack of ascorbate, or vitamin C.

When taken orally, humans are limited to a dosage of 200 mg at one time, and any more than that will result in it coming out in the urine. At doses of 500 mg or more, all ingested ascorbate is eliminated in the urine. It is for this reason that we recommend that people put 8 grams of pure sodium ascorbate powder in a liter of water and sip on it slowly for 10–12 hours. We call it, ”sip 7 to 7”.

Being an essential nutrient Vitamin C takes part in several vital functions in the body including maintenance of tissue structure, immune system, hormone production, and energy metabolism. While the recommended dose of vitamin C is sufficient in preventing deficiency symptoms, evidence suggests that higher intakes may be beneficial, especially for an optimal functioning immune system. It is well established in scientific studies that a diet high in fruits and vegetables is associated with a lower incidence of CFCs one mechanism possibly being high intakes of vitamin C. 

Intravenous high-dose vitamin C therapy allows the plasma ascorbate levels to reach as high as 350+ mg/dl, which can then eliminate CFCs by challenging their metabolic vulnerabilities without disrupting the function of healthy cells.

The effects of high-dose vitamin C on CFCs have been extensively researched and over ninety-one thousand published studies can be found on PubMed regarding this topic.

Fenton Reaction

In the diagram above, vitamin C donates an electron to ‘ferric’ iron and it becomes ‘ferrous’ iron, which is now activated and produces free radicals. The activity of vitamin C never changes, it is always donating electrons, however, if it donates to certain metal atoms, free radicals can be generated which is termed, the pro-oxidant effect. This well-known reaction that is necessary to produce neurotransmitters, for example, is called the Fenton Reaction.

While vitamin C functions as an antioxidant in physiological plasma levels achieved through oral intake, at higher plasma levels, it acts as a pro-oxidant which makes it toxic to CFCs when given in high doses intravenously. Vitamin C also accumulates more in CFCs than in healthy cells through glucose transporters (GLUTs) which CFCs have in abundance.

The therapeutic potential of vitamin C in treating CFCs was first discovered in the 1970s when studies done by Cameron, Pauling, and colleagues suggested that the administration of high doses of vitamin C may improve the survival of CFC patients.

Since then, numerous studies on the efficacy and mechanisms of action have confirmed that high-dose Vitamin C:

  • Eliminates CFCs specifically without harming healthy cells
  • Prevents metastases and kills CFC stem cells
  • Reduces side effects of chemotherapy

Vitamin C has been shown to eliminate CFCs by targeting several vulnerabilities in metabolic pathways characteristic of CFCs but absent in healthy cells. CFCs are deficient in many enzymes that healthy cells have in larger, adequate amounts. In addition, CFCs are not efficient at using oxygen to produce energy from glucose. These traits are universal to CFCs of every origin which makes high-dose IV Vitamin C a versatile therapy to use.

It must be kept in mind that only about 1-2% of the cells in a tumor are CFC stem cells and it is only stem cells that can successfully spread (metastasize) to another organ. However, chemotherapy, radiotherapy, and CFCs that produce cellular chemicals (cytokines) can cause what is known as epithelial-to-mesenchymal transition (EMT). In other words, mature cells that are not capable of metastasizing can be transformed back into stem cells and thereafter spread (metastasize) to other organs.

The Main Mechanisms through Which Vitamin C Has Been Proven To Eliminate CFCs:

Acting as a Pro-Oxidant

High doses of vitamin C increase the formation of hydrogen peroxide inside CFCs. Hydrogen peroxide is a normal byproduct of cellular metabolism, but in excessive amounts, it leads to excess free radical (oxidative) damage to cellular structures. Healthy cells regulate the presence of hydrogen peroxide by converting it into oxygen and water with an enzyme, called catalase. CFCs lack catalase since they do not use oxygen to produce energy and therefore do not need antioxidant enzymes to counteract the oxidative byproducts of aerobic (oxygen-requiring) energy metabolism. Since CFCs have no catalase to neutralize hydrogen peroxide, they are exposed to an insurmountable concentration of hydrogen peroxide (oxidative damage) and die off.

A possible mechanism of vitamin C to destroy CFC stem cells was revealed in a study on liver CFCs. Vitamin C was uptaken by the cells through SVCT2 receptors causing oxidative stress leading to DNA damage, ATP depletion, and cell death. It was discovered that CFC stem cells had SVCT2 receptors along with genes usually found in stem cells (stemness-related genes). Treatment with vitamin C significantly reduced tumor growth and decreased (downregulated) the expression of stemness-related genes. The study used liver tumor samples from people treated with vitamin C revealing a significant association between IV vitamin C administration and enhanced survival in people with SVCT2 receptors as well as the expression of stemness-related genes in the tumor.

Intracellular Redox Stress

The oxidized form of vitamin C, Dehydroascorbate (DHA), structurally resembles a glucose molecule and can enter the cell via glucose transporter 1 (GLUT1). For CFCs to be able to fulfill their requirements of glucose, they have high amounts of GLUT1 receptors on their cell membranes and can, therefore, pick up DHA rapidly. Accumulated DHA causes oxidative stress (increases free radical production), which depletes the antioxidant enzyme glutathione and the cell dies from oxidative damage.

Downregulation of the Hypoxic Phenotype

CFC metabolism creates distinct conditions in its surroundings such as nutrient and oxygen deprivation (hypoxia). Lack of oxygen activates a transcription factor called hypoxia-inducible factor-1 (HIF-1) in the cell which leads to the expression of several genes involved in processes that enable the cell to adapt to low oxygen (hypoxic) conditions such as energy production by fermentation (glycolysis), glucose uptake and growth of new blood vessels (angiogenesis). Activation of these genes is essential for invasion, metastasis, generation of stem cells, metabolic reprogramming, and resistance to chemo- and radiotherapies. Vitamin C prevents activation of HIF-1 by acting as a co-factor for hydroxylase enzymes that lead to the degradation of HIF-1. In this way, vitamin C can turn off the fundamental driver of CFC progression.

The effects of vitamin C on tumor development were studied in humans with colorectal CFCs. Higher vitamin C levels in tumor tissues were associated with lower activity of HIF-1 and its target genes as well as decreased tumor size and significantly improved survival.

And yet, another study on human endometrial (uterine) CFCs also found that lower vitamin C levels in tumors were associated with higher HIF-1 activity, elevated expression of proteins VEGF (blood vessel growth factor) and GLUT-1 (glucose transporter) that are regulated by HIF-1 and higher tumor growth rate. In other words, lower levels of vitamin C, unable to regulate HIF-1 activity, allowed it to increase. This, in turn, led to an increase in tumor blood vessel growth and the number of receptors for glucose uptake at a faster rate, ultimately resulting in an accelerated rate of tumor growth.

Epigenetic Modulation

The fully functioning mature CFC (phenotype) is mostly the result of reversible non-genetic (epigenetic) gene regulation that is determined by signals from the environment outside the cell. Reprogramming of genes that drive CFC progression is mostly triggered by low oxygen (hypoxia) and oxidative stress (too many free radicals) in the tumor microenvironment.

Vitamin C has been shown to reverse several epigenetic changes in CFCs including:

  • Restores activity of TET (ten-eleven translocase) proteins, which has been decreased by the CFCs. Hence, this gene regulation mediated by TET is decreased (downregulated) in most CFCs leading to altered mature forms (phenotype) which includes CFC stem cell production.
  • Upregulates p53 Transcription
    Activation of p53 is the most essential cellular pathway to induce cell death in response to various stressors. It is known as the “guardian of the genome” and is referred to as a “tumor suppressor” gene. In CFCs however, p53 is often inactivated and the cell does not die appropriately, hence, one of the reasons for the immortality of CFCs. Vitamin C reactivates p53 hence allowing cell death to occur.
  • Decreases Ras Transcription
    The Ras-mediated pathway is often activated in CFCs, and it regulates genes that are involved in metabolic programming including glucose uptake via GLUT1 receptors. Vitamin C inhibits this pathway by detaching Ras protein from the cell membrane. This diminishes GLUT1 production and the cell dies from glucose and energy deprivation.  
  • Inhibits Nuclear Factor kappa-Beta (NF-kB)
    NF-kB is a transcription factor that regulates major signaling pathways responsible for multiple aspects of CFC development and progression. NF-kB is activated by a variety of stressful stimuli such as environmental carcinogens, oxidative stress, hypoxia, and inflammatory cytokines and the following gene regulation leads to suppressed apoptosis, increased cell proliferation, invasion, metastasis, chemo and radiotherapy resistance, stem cell survival and renewal, and inflammation. Vitamin C has been shown to interfere with all these processes by inactivating NF-kB.

Decreases Epithelial-Mesenchymal Transition (EMT) and hence metastases

A key step for CFCs to migrate from the primary tumor and invade distant tissues is EMT, a process where epithelial cells (mature cells) tightly adhered to each other are transitioned to mesenchymal-like cells (stem cells). Mesenchymal-like cells lack adhesion protein E-cadherin and are free to detach from neighboring cells and metastasize. Vitamin C has been found to prevent EMT by suppressing TGF-β1 mediated signaling pathway. 

Enhances Immune Function

Vitamin C is vital for several types of immune cells, and it plays a role in the development, proliferation, differentiation, and activation of these cells. A dysregulated and suppressed immune system is a major contributor to CFC development and progression and therefore restoring its function is necessary for reversing the CFC process.

Natural killer (NK) cells are lymphocytes that are responsible for immune surveillance against CFCs. They can recognize and directly kill CFCs independent of specific molecular elements (antigens). Most CFCs downregulate (cause to lessen) major histocompatibility complex 1 (MHC-I) molecules on their cell surface and therefore can escape from CD8+T lymphocyte (activated lymphocytes) recognition and an immune response against the tumor. NK cells are therefore essential in anti-tumor immunity and low levels of NK cells are linked to CFC development as well as a poor prognosis. Vitamin C has been shown to increase NK cell number and activity against CFCs. NK cells are susceptible to oxidative stress of the tumor microenvironment which suggests that vitamin C as an antioxidant protects NK cells and maintains their motility and anti-tumor function.

T-lymphocytes play an essential role in the immune response against tumors, and they include CD4+ T helper cells (Th1), and CD8+ cytotoxic T cells (Tc). CD4+ T cells can differentiate into different subsets such as Th1, Th2, and T Regulatory cells (Treg). Th1 cells participate in antitumor immune response. However, the tumor microenvironment causes infiltrating CD4+ T cells to differentiate into Th2 cells, which are not able to eliminate CFCs, and into Treg cells, which are lymphocytes that turn off the ability of activated CD8+ cells to kill the CFCs. A tumor microenvironment dominated by the Th2 cell type is associated with tumor-supporting immunity and metastases. Vitamin C promotes the differentiation of CD4+ T cells into Th1 cells and increases CD8+ cytotoxic T cells. Hence it is essential for healing from CFCs.


Vitamin C (ascorbate), like all other molecules, produces different effects depending upon the immediate chemical environment in which they are reacting. So, it is the environment that supports and requires a certain action to occur. In chemistry, the ‘environment’ usually relates to the pH and the temperature, which are fundamental aspects of the physical world. With microorganisms, this concept is known as polymorphism, meaning that they change shape and form depending on the environment in which they find themselves. 

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Abdel-Latif M., Raouf A., Sabra K., Kelleher D., Reynolds J. Vitamin C enhances chemosensitization of esophageal cancer cells in vitro. Journal of Chemotherapy. 2005 Oct;17(5):539-49. doi: 10.1179/joc.2005.17.5.539. https://pubmed.ncbi.nlm.nih.gov/16323444/

Aguilera O., Muñoz-Sagastibelza M., Torrejón B., Borrero-Palacios A., Del Puerto-Nevado L., Martínez-Useros J., Rodriguez-Remirez M., Zazo S., García E., Fraga M., Rojo F., García-Foncillas J. Vitamin C uncouples the Warburg metabolic switch in KRAS mutant colon cancer. Oncotarget. 2016 Jul 26;7(30):47954-47965. doi: 10.18632/oncotarget.10087. https://pubmed.ncbi.nlm.nih.gov/27323830/

Agus D., Vera J., Golde D. Stromal Cell Oxidation: A Mechanism by Which Tumors Obtain Vitamin C. Cancer Research (1999) 59 (18): 4555–4558. https://aacrjournals.org/cancerres/article/59/18/4555/505443/Stromal-Cell-OxidationA-Mechanism-by-Which-Tumors

Block G., Patterson B., Subar A. Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence. Nutrition and Cancer. 1992;18(1):1-29. doi: 10.1080/01635589209514201. https://pubmed.ncbi.nlm.nih.gov/1408943/

Cameron E., Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer. PNAS. 1976 Oct;73(10):3685-9. doi: 10.1073/pnas.73.10.3685. https://pubmed.ncbi.nlm.nih.gov/1068480/

Chen Q., Espey M., Sun A., Lee J., Krishna M., Shacter E., Choyke P., Pooput C., Kirk K., Buettner G., Levine M. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. PNAS. 2007 May 22; 104(21): 8749–8754. doi: 10.1073/pnas.0702854104 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885574/

Chen Q., Espey M., Sun A., Pooput C., Kirk K., Krishna M., Beneda Khosh D., Drisko J, Levine M. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. PNAS. 2008 Aug 12; 105(32): 11105–11109. doi: 10.1073/pnas.0804226105 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2516281/

Doseděl M., Jirkovský E., Macáková K., Kujovská Krčmová L., Javorská L, Pourová J, Mercolini L, Remião F., Nováková L., Mladěnka P. Vitamin C—Sources, Physiological Role, Kinetics, Deficiency, Use, Toxicity, and Determination. Nutrients. 2021 Feb; 13(2): 615. doi: 10.3390/nu13020615 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918462/

Du J, Martin SM, Levine M, Wagner BA, Buettner GR, Wang SH, Taghiyev AF, Du C, Knudson CM, Cullen JJ. Mechanisms of ascorbate-induced cytotoxicity in pancreatic cancer. Clin Cancer Res. 2010 Jan 15;16(2):509-20. doi: 10.1158/1078-0432.CCR-09-1713. Epub 2010 Jan 12. PMID: 20068072; PMCID: PMC2807999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807999/

Gregoraszczuk EL, Zajda K, Tekla J, Respekta N, Zdybał P, Such A. Vitamin C supplementation had no side effect in non-cancer, but had anticancer properties in ovarian cancer cells. Int J Vitam Nutr Res. 2021 Jun;91(3-4):293-303. doi: 10.1024/0300-9831/a000634. Epub 2020 Feb 3. PMID: 32008465. https://pubmed.ncbi.nlm.nih.gov/32008465/

Hagel A., Albrecht H., Dauth W., Hagel W., Vitali F., Ganzleben I., Schultis H., Konturek P., Stein J., Neurath M., Raithel M. Plasma concentrations of ascorbic acid in a cross section of the German population. Journal of International Medical Research. 2018 Jan;46(1):168-174. doi: 10.1177/0300060517714387. https://pubmed.ncbi.nlm.nih.gov/28760081/

Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discov. 2022 Jan;12(1):31-46. doi: 10.1158/2159-8290.CD-21-1059. PMID: 35022204.. https://pubmed.ncbi.nlm.nih.gov/35022204/

Kuiper C., Dachs G., Munn D., Currie M., Robinson B., Pearson J. Vissers M. Increased Tumor Ascorbate is Associated with Extended Disease-Free Survival and Decreased Hypoxia-Inducible Factor-1 Activation in Human Colorectal Cancer. Frontiers in Oncology. 2014; 4: 10. doi: 10.3389/fonc.2014.00010 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3912592/

Kuiper C., Molenaar I., Dachs G., Currie M., Sykes P., Vissers M. Low ascorbate levels are associated with increased hypoxia-inducible factor-1 activity and an aggressive tumor phenotype in endometrial cancer. Cancer Research. 2010 Jul 15;70(14):5749-58. doi: 10.1158/0008-5472.CAN-10-0263. https://aacrjournals.org/cancerres/article/70/14/5749/559387/Low-Ascorbate-Levels-Are-Associated-with-Increased

Levine M., Rumsey S. C., Daruwala R., Park J. B., Wang Y. Criteria and recommendations for vitamin C intake. JAMA. 1999 Apr 21;281(15):1415-23. doi: 10.1001/jama.281.15.1415. https://pubmed.ncbi.nlm.nih.gov/10217058/

Levine M., Conry-Cantilena C., Wang Y., Welch R., Washko P., Dhariwal K., Park J., Lazarev A., Graumlich J., King J., Cantilena L. Vitamin C pharmacokinetics in healthy volunteers: evidence for a recommended dietary allowance. PNAS. 1996 Apr 16;93(8):3704-9. doi: 10.1073/pnas.93.8.3704. https://pubmed.ncbi.nlm.nih.gov/8623000/

Lu Y., Wu Q., Chen D., Chen L., Wang Z., Ren C., Mo H., Chen Y., Sheng H., Wang Y., Wang Y., Lu J., Wang D., Zeng Z., Wang F., Wang F., Li Y., Ju H., Xu R. Pharmacological Ascorbate Suppresses Growth of Gastric Cancer Cells with GLUT1 Overexpression and Enhances the Efficacy of Oxaliplatin Through Redox Modulation. Theranostics. 2018; 8(5): 1312–1326. doi: 10.7150/thno.21745 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835938/

Lv H., Wang C., Fang T., Li T, Lv G., Han Q., Yang W., Wang H. Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2. NPJ Precision Oncology. 2018 Jan 8;2(1):1. doi: 10.1038/s41698-017-0044-8. https://pubmed.ncbi.nlm.nih.gov/29872720/

Ma Y., Chapman J., Levine M., Polireddy K., Drisko J., Chen Q. High-dose parenteral ascorbate enhanced chemosensitivity of ovarian cancer and reduced toxicity of chemotherapy. Science Translational Medicine. 2014 Feb 5;6(222):222ra18. doi: 10.1126/scitranslmed.3007154. https://pubmed.ncbi.nlm.nih.gov/24500406/

Massagué J., Ganesh K. Metastasis-Initiating Cells and Ecosystems. Cancer Discovery. 2021 Apr;11(4):971-994. doi: 10.1158/2159-8290.CD-21-0010. https://pubmed.ncbi.nlm.nih.gov/33811127/

Nishikimi, R. Fukuyama, S. Minoshima, N. Shimizu, K. Yagi. Cloning and chromosomal mapping of the human nonfunctional gene for L-gulono-gamma-lactone oxidase, the enzyme for L-ascorbic acid biosynthesis missing in man. Journal of Biological Chemistry, 269 (1994), pp. 13685-13688. https://www.sciencedirect.com/science/article/pii/S0021925817368849

Shenoy N., Bhagat T., Nieves E., Stenson M., Lawson J., Choudhary G., Habermann T., Nowakowski G., Singh R., Wu X., Verma A., Witzig T. Upregulation of TET activity with ascorbic acid induces epigenetic modulation of lymphoma cells. Blood Cancer Journal. 2017 Jul; 7(7): e587. doi: 10.1038/bcj.2017.65 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5549257/

van Gorkom G., Wolterink R., Van Elssen C., Wieten L., Germeraad W., Bos G. Influence of Vitamin C on Lymphocytes: An Overview. Antioxidants (Basel). 2018 Mar 10;7(3):41. doi: 10.3390/antiox7030041. https://pubmed.ncbi.nlm.nih.gov/29534432/

Wilkes J., O’Leary B., Du J., Klinger A., Sibenaller Z., Doskey C., Gibson-Corley K., Alexander M., Tsai S., Buettner G., Cullen J. Pharmacologic ascorbate (P-AscH−) suppresses hypoxia-inducible Factor-1α (HIF-1α) in pancreatic adenocarcinoma. Clinical and Experimental Metastasis. 2018 Feb; 35(1-2): 37–51. doi: 10.1007/s10585-018-9876-z https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959274/

Zeng L., Wang Q., Feng L., Ke Y., Xu Q., Wei A., Zhang C., Ying R. High-dose vitamin C suppresses the invasion and metastasis of breast cancer cells via inhibiting epithelial-mesenchymal transition. OncoTargets and Therapy. 2019 Sep 10:12:7405-7413. doi: 10.2147/OTT.S222702. https://pubmed.ncbi.nlm.nih.gov/31571901/

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