Intravenous Vitamin C

What is Intravenous Vitamin C cancer treatment?

Intravenous vitamin C refers to the method of administering vitamin C parenterally (i.e. to bypass the gut and liver), in order to achieve therapeutic levels in the blood, tissues and organs. By comparison, oral administration of vitamin C is dependant on absorption through the gut and must be processed by the liver before it enters the bloodstream and other tissues in the body. There are limits to the amount much vitamin C that can be absorbed through the gut and cannot alter the plasma (blood) levels of vitamin C to have an anti-tumour effect. Intravenous vitamin C is used clinically to achieve pharmacologic plasma levels of vitamin C.

Extensive research over the past 35 years provides compelling evidence that intravenous vitamin C (IVC), when infused at high doses and moderate frequency in conjunction with radiation or chemotherapy, kills cancer in the early stages. [1,2,3] In the case of late-stage cancer, IVC may improve the quality of life. [4,5]

There is a vast amount of literature that exists on the topic of ascorbic acid (vitamin C) and cancer. As early as 1949, ascorbate use was proposed for cancer therapy. [6] Pioneering work by scientist and two-time Nobel Prize recipient Linus Pauling laid the groundwork for much of the discovery around the therapeutic effect of vitamin C on cancer patients.[7] Since 1952, ascorbate has been proposed as a chemotherapeutic agent.[8,9] In the past 25 years, thousands of studies including cell, animal and human studies have added to the growing body of evidence for the clinical and scientific basis of vitamin C use in cancer.[10,11]

Linus Carl Pauling was an American chemist, biochemist, peace activist, author, and educator. He was one of the most influential chemists in history and ranks among the most important scientists of the 20th century Linus Carl Pauling was an American chemist, biochemist, peace activist, author, and educator. He was one of the most influential chemists in history and ranks among the most important scientists of the 20th century

 

Some of the most significant and compelling research has come from the Riordan Clinic Research Institute in Wichita, Kansas. Dr. Hugh Riordan, M.D. is largely responsible for carrying forward the work of Linus Pauling. He and his team of researchers are responsible for the groundbreaking work in defining the therapeutic range for IVC therapy as a chemotherapeutic and biologic response modifier.[12-15] The “Riordan IVC Protocol” forms the basis of the intravenous vitamin C treatments offered at our clinic.

How does intravenous vitamin C treatment work?

Evidence from both in vitro and in vivo studies have proven a multitude of anti-cancer effects from vitamin C when therapeutic levels (therapeutic range: 350-400 mg/dL) are achieved in the blood. The only method to achieve this pharmacologic dose is via intravenous infusion of vitamin C. Scientific and clinical data supports that, at therapeutic levels, vitamin C has the following actions:

  1. Direct cytotoxic (cell killing mediated by toxicity) effect on human cancer cells;[16-19]
  2. Induces apoptosis (cell death) in catalase-deficient cancer cells while sparing non-cancerous (healthy, non-catalase deficient) cells from oxidative damage;[20-23]
  3. Concentrates in cancerous cells due to the increased number of glucose receptors expressed by malignant cells (vitamin C has been shown to accumulate up to five times the concentration than in normal cells), selectively inducing apoptosis of cancer cells;[24-26]
  4. Similar to chemotherapy agents, vitamin C generates significant hydrogen peroxide (H202) which destroys cancer cells;[27-29]
  5. Promotes healthy mitochondria function;[30,3]
  6. Reduces oxidative damage to the tumor suppressor gene p53 caused by chemo and radiation;[31,32]
  7. Stimulates the immune system to increase production of agents such as interferon and natural killer (NK) cells that engage in the cancer-killing process as well as prevent the growth and spread of the tumor;[33-35]
  8. Decreases the production of inflammatory cytokines such as prostaglandin E2 (PGE2), C-reactive protein (CRP), TNF-alpha, IL-8 and others, thereby reducing the inflammatory response that is responsible for growth, spread and recurrence of the disease (inflammation and elevated CRP are associated with poor prognosis and decreased survival in many types of cancer);[36-38]
  9. Exerts direct and indirect anti-angiogenic effects on tumor (inhibits formation of blood vessels by the tumor used to support its growth, spread and invasion);[39]
  10. Protects higher oxygenated, non-cancerous tissues while simultaneously acting as a selective pro-drug in cancer tissue [40]

I’ve been told by my oncologist to avoid antioxidants. Will intravenous vitamin C interfere with my chemotherapy or radiation treatments?

dna-istock-rustycloudNo. Research has shown that using IVC concurrently with chemotherapy or radiation will not decrease the effectiveness of these treatments. In addition, studies performed at the Riordan Cancer Treatment & Research Center have concluded that the tumor cells become susceptible to high-dose vitamin C at plasma levels of 350-400 mg/dL, known as the ‘therapeutic range’. At this concentration in blood, vitamin C acts a pro-oxidant, rather than an anti-oxidant.[40,41,42] As a pro-oxidant, IVC appears to augment the effectiveness of chemotherapy and radiation. [14,42-46].

Results of a large-scale, multicentre study in Germany, published in 2011 in the journal In Vivo, concluded that complementary treatment of breast cancer patients with IVC enhanced tolerability and effectiveness of standard tumor-destructive therapies (in particular, this study looked at patients receiving radiation and/or chemotherapy) and reduced quality of life-related side effects from chemo and radiation. [46]

The pro-oxidant effect of IVC is similar to chemotherapy, in that it induces apoptosis (cell death) in cancer cells. However, unlike chemotherapy, the pro-oxidant effects of IVC spare non-cancerous (healthy) cells from oxidative damage. In essence, IVC acts as a pro-drug.[40] IVC does not interfere with the majority of chemo agents, as evidenced by in vitro (cell) and in vivo (animal and human) research in addition to clinical evidence.[14] The IVC protocol is not administered in conjunction with methotrexate chemotherapy.

It is well established that cancer cells can be resistant to the anti-cancer effects of radiation treatment.[47] When used concurrently with radiation therapy, IVC helps sensitize cancer cells to the anti-cancer effects of radiation therapy, effectively enhancing the outcome of treatment.[48-52] In addition, IVC provides support for the body’s immune system, thereby facilitating recovery and healing post-radiation, as well as minimizing the many side effects of radiation.

Based on extensive research conducted at the University of Kansas Hospital, physicians there recommend administering IVC on the same day as the chemotherapy and/or radiation treatment.[53,54] A phase I trial has been completed and a phase II trial is currently underway at the University of Kansas integrative medicine research center to evaluate the effects of IVC in combination with gemcitabine and erlotinib (chemo agents) in patients with metastatic pancreatic cancer. Conventional treatment approaches have had little impact on the course of pancreatic cancer, which has the highest fatality rate among cancers. Gemcitabine, the primary therapeutic agent for pancreatic carcinoma, produces minimal survival benefit as a single agent. The human trial was initiated after results of an animal model study conducted at the university found therapeutic levels of ascorbate (vitamin C) synergizes with gemcitabine in pancreatic cancer cell lines.[55] The phase I trial results (published Jan 2012) revealed no increased toxicity with the addition of IVC to the chemo protocol, and positive outcomes were observed in the combo treatment group.[56] The results are now being followed up with a longer, phase II trial.

A similar randomized phase I/IIa pilot trial was conducted to assess the safety and benefit of administering high-dose IVC in combination with chemotherapy (first line carboplatin and paclitaxel) in newly diagnosed advanced stage III ovarian cancer or stage IV ovarian cancer. Ovarian cancer represents the leading cause of death from all gynecological malignancies and remains the fifth leading cause of cancer-related deaths among women. Due to the lethality of ovarian cancer and the need fro improved treatment options, this population was selected to evaluate IVC in combination with standard treatment to explore the benefits on outcome. Results revealed the combination treatment is remarkably safe and suggested a trend to benefit on outcomes, warranting further study of greater magnitude in the future.[57]

The belief of some oncologists that vitamin C as an ‘antioxidant’ may reduce the effectiveness of chemotherapy and radiation was due in part to an article published by Agus et al in 1999, in which they described how cancer cells acquire and concentrate vitamin C.[58] The authors suggested that this increased intracellular concentration of vitamin C might provide malignant (cancerous) cells with a metabolic advantage. Despite the significant misunderstanding of the detailed biochemistry of ascorbic acid in cancer cells with the conclusions drawn from this one study, some medical practitioners have embraced and held on to the belief that vitamin C in cancer may be harmful.

In actual fact, cancer cells use glucose as a main energy for fuel.[11] This has been the premise for much of the recent evidence for how low-glycemic (low carbohydrate) and calorie-restricted diets improve survival in cancer patients, reduce the rate of recurrence and overall lower the risk of cancer.[59,60] Because vitamin C has a similar molecular structure as glucose, the glucose transporters that are more heavily expressed (4-6 fold) on cancer cells, facilitate the entry and concentration of vitamin C intracellularly.[11,61] Once heavily concentrated inside the cell, vitamin C is cytotoxic (toxic to the cancer cells) and thereby acts a pro-oxidant drug, effectively killing the cancer cells and reducing tumor burden.[40]

To address the concern about use of antioxidants with cancer treatments, it’s important to recognize that a vast body of literature exists on this topic and an overwhelming majority of studies have demonstrated that antioxidants, when prescribed appropriately, enhance the effects radiation and chemotherapy.[48-51,62-63]

In 2007, Dr. Keith Block, MD and others led a systematic review of evidence gathered from MEDLINE, Cochrane and other esteemed medical and scientific databases. The study was published in Cancer Treatment Review and found that, of the 845 trials meeting inclusion criteria for the review, none of the trials reported evidence of significant decreases in efficacy from antioxidant supplementation during chemotherapy. In fact, the authors concluded “many of the studies indicated that antioxidant supplementation resulted in either increased survival times, increased tumor responses, or both, as well as fewer toxicities than controls”. [64]

It must be emphasized here that the type of antioxidants, dosage and frequency must be carefully assessed on a case-by-case basis and depends largely on the type of disease and specific treatment(s). Some antioxidants can interfere with the effectiveness of radiation and certain chemotherapy. If you take antioxidants, you must be under the care and guidance of a naturopathic or medical physician specially trained in integrative cancer care.

If I take oral vitamin C (ascorbate) will it provide the same results?

No. Oral vitamin C is an antioxidant with limited absorption. Most individuals cannot absorb more than 8 grams per day of vitamin C. In addition, with oral ascorbate we cannot attain blood levels of vitamin C high enough to kill cancer cells. Ascorbate is more efficient when administered intravenously than when given orally because it bypasses the gut and higher circulating levels are achieved for longer periods of time. Furthermore, the therapeutic target of plasma vitamin C levels (described above) can only be attained through the intravenous route, on average with 50 grams or more of vitamin C per infusion.[11,13,14]

However, we advise patients take oral vitamin C (at least 3 grams daily) in order to maintain the serum vitamin C levels between treatments. Oral supplementation of vitamin C also helps prevent a possible vitamin C “rebound effect” on days when IVC infusion is not given.[14] In addition, oral vitamin C supplementation (and other antioxidants) has been used to help prevent cancer onset and its recurrence. [11]

What types of cancer will benefit from intravenous vitamin C treatment?

Studies (human and animal) on intravenous vitamin C have shown benefit in every type of cancer, including breast, ovarian, colon, lung, kidney, prostate, liver, pancreatic, skin, thyroid, gastric, brain and blood-borne cancers such as leukemia’s and lymphomas.[65] However, there are many factors that will determine the degree of effectiveness of any given therapy. This includes epigenetic factors (i.e. diet, smoking and other lifestyle factors will influence the effectiveness of therapies), other treatments used synergistically with intravenous vitamin C, individual genetic mutations and variation, as well some unique characteristics of the primary cancer cells and cancer stem cells (CSC’s) or circulating tumor cells (CTC’s).[66-68]

Specialized tests we use at our clinic (from international research centers and laboratories) have been extremely helpful in identifying which treatments in particular (both natural substances and pharmacologic agents) will specifically target the CTC’s and CSC’s in a given patient.

How frequently are the intravenous vitamin C treatments administered?

We begin patients with a low dose (15 grams) and raise the dose incrementally with subsequent infusions, until the therapeutic level is attained. We measure post IVC plasma levels to ensure that these levels are being maintained at the recommended frequency. Average frequency of treatments is 2-3 per week. Each infusion takes between 1-3 hours, depending on the amount of IVC administered.

Based on a large and growing body of evidence, the following conclusions about the clinical use of vitamin C are firmly established:

  1. IVC can be effective as a stand-alone therapy, but is most commonly used in combination with conventional chemotherapeutic and radiation regimens.
  2. Concurrent IVC with chemo/radiation may reduce side effects and enhance quality of life.
  3. Concurrent IVC helps to preserve immunocompetence (critical functional anti-cancer capabilities of the immune system) during chemotherapy and radiation.
  4. Peer reviewed scientific and clinical literature reveals over 8000 patients who have benefited from either IVC therapy or other concurrent antioxidant regimens

Can IVC treatments be used to treat other conditions?

Many chronic illnesses can benefit from IVC. We have had great results with IVC as part of a successful treatment plan for patients suffering with Lyme disease, chronic fatigue, arthritis and chronic or recurrent infections. [38,69-72]

IV nutrient therapy is routinely administered to our patients to protect from the undesirable and hazardous consequences of certain dental procedures. Many dental procedures will consequently result in a substantial release of toxins and pathogenic microbes into the blood stream and surrounding tissues.[73-75] Vitamin C and glutathione are critical components to assist the body with removal of hazardous toxins and bacteria, thereby offering protection to the systems that are most vulnerable and likely to be harmed in the process: the immune system, heart, lungs, liver, kidneys and brain.[76] Vitamin C and glutathione have a molecular composition whereby they are able to chelate (bind) toxins – including heavy metals.[77] In these situations, low-dose vitamin C is administered (as an anti-oxidant, not a pro-oxidant), coupled with other vitamins and antioxidants to support the body’s immune and detoxification capabilities.

To learn more about intravenous vitamin C and the cancer care offered at our clinic, please call (604) 949-0077 to speak with one of our care coordinators.

 References:

  1. Cameron E. Pauling L. Leibovitz B. Ascorbic acid and cancer: a review. Cancer Research. 1979; 39:663-681. [Pub Med]
  2. Tamayo C, Richardson MA. Vitamin C as a cancer treatment: state of science and recommendations for research. Altern Ther Health Med. 2003; 9(3):41-141. [Pub Med]
  3. Gonzalez MJ, Miranda-Massari JR, Mora EM, Riordan NH, et al.. Orthomolecular oncology review: ascorbic acid and cancer 25-years later. Integr Cancer Ther. 2005; 4(1):32-44. [Pub Med]
  4. Murata A, Morishige F, Yamagushi H. Prolongation of survival time of terminal cancer patients by administration of large doses of ascorbate. Int J Vitam Nutr Res Suppl. 1982; 23:103-113. [Pub Med]
  5. Chang HY, Gyou CJ, Keun JS. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007; 22:7-11. [Pub Med]
  6. Klenner FR. The treatment of polyomyelitis and other virus diseases with vitamin C. South Med Surg. 1949;3:7-12. [Pub Med]
  7. Cameron E, Pauling L, Leibovitz B. Ascorbic acid and cancer: a review. Cancer Res. 1979; 39:663-681. [Pub Med]
  8. McCormick WJ. Ascorbic acid as a chemotherapeutic agent. Arch Pediat. 1952;69:151-155. [Pub Med]
  9. Riordan NH, Riordan HD, Meng X, Li Y, Jackson JA. Intravenous ascorbate as a tumor cyto-toxic chemotherapeutic agent. Medical Hypothesis. 1995; 44:207-213. [Pub Med]
  10. Padayatty SJ, Katz A, Wang Y, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22:18-35. [Pub Med]
  11. Gonzalez MJ, Miranda-Massari JR, Mora EM, Riordan NH, Casciari JJ, Jackson JA, Roman-Franco A. Orthomolecular oncology review: ascorbic acid and cancer 25-years later. Interg Cancer Ther. 2005; 4(1): 32-44. [Pub Med]
  12. Riordan HD, Jackson JA, Schultz M. Case study: high-dose intravenous vitamin C in the treatment of a patient with adenocarcinoma of the kidney. J Orthomolec Med. 1990;5:5-7.
  13. Jackson JA, Riordan HD, Hunninghake RE, Riordan NH. High dose intravenous vitamin C and long time survival of a patient with cancer of the head of the pancreas. J Orthomolec Med. 1995;10:87-88.
  14. Riordan NH, Riordan HD, Casciari JJ. Clinical and experimental experiences with intravenous vitamin C. J Orthomolec Med. 2000; 15:201-213.
  15. Casciari JJ, Riordan NH, Schmidt TL, Meng XL, Jackson JA, Riordan HD. Cytotoxicity of ascorbate, lipoic acid and other antioxidants in hollow fiber in vitro tumours. Br J Cancer. 2001;84:1544-1550. [Pub Med]
  16. Gonzalez MJ, Miranda-Massari JR, Mora EM, et al. Orthomolecular oncology: a mechanistic view of intravenous ascorbate’s chemotherapeutic activity. PR Health Sci J. 2002; 21(1): 39-41. [Pub Med]
  17. González MJ, Mora E, Riordan NH, Riordan HD, Mojica P. Rethinking vitamin C and cancer: an update on nutritional oncology. Cancer Prev Int. 1998;3:215-224.
  18. Yamamoto K, Takahashi M, Niki E. Role of iron and ascorbic acid in the oxidation of methyl linoleate micelles. Chem Lett. 1987;1:49-52.
  19. Rowly DA, Halliwell B. Superoxide-dependents and ascorbate- dependent formation of hydroxy radicals in the presence of copper salts: a physiologically significant reaction? Arch Biochem Biophys. 1983;225:279-284.
  20. Punnonen K, Ahotupa M, Asaishi K, Hyoty M, Kudo R, Punnonen R. Antioxidant enzyme activities and oxidative stress in human breast cancer. J Cancer Res Clin Oncol. 1994; 120: 374-377. [Pub Med]
  21. Jaruga P, Olinste R. Activity of antioxidant enzymes in cancer diseases. Postepy Hig Med Dosw. 1994;48:443-455. [Pub Med]
  22. Sun Y, Colburn NH, Oberley LW. Depression of catalase gene expression after immortalization and transformation of mouse liver cells. Carcinogenesis. 1993;14:1505-1510. [Pub Med]
  23. Bozzi A, Mavelli I, Mondovi B, Strom R, Rotilio G. Differential sensitivity of tumor cells to externally generated hydrogen per- oxide: role of glutathione and related enzymes. Cancer Biochem Biophys. 1979;3:135-141.
  24. Moss RW. Questioning Chemotherapy. New York, NY: Equinox Press; 1995.
  25. Spielholz C, Golde DW, Houghton AN, Nualart F, Vera JC. Increased transport of dehydroascorbic acid without changes in sodium dependent ascorbate transport in human mela- noma cells. Cancer Res. 1997;57:2529-2537. [Pub Med]
  26. Younes M, Lechago LV, Somoano JR, Mosharaf M, Lechago J. Nude expression of the human erythrocyte glucose trans- porter Glut-1 in human cancers. Cancer Res. 1996;56:1164- 1167.
  27. Halliwell B. Vitamin C: antioxidant or pro-oxidant in vivo? Free Radic Res. 1996;25:439-454. [Pub Med]
  28. Asano K, Satoh K, Hosaka M, et al. Production of hydrogen peroxide in cancerous tissue by intravenous administration of sodium 5,6 benzylidene-L-ascorbate. Anticancer Res. 1999;19:229-236. [Pub Med]
  29. Jonas SK, Riley PA, Willson RL. Hydrogen peroxide cytotoxicity. Biochem J. 1989;264:651-655. [Pub Med]
  30. LiY, Cobb CE ,HillKE, BurkRF, MayJM. Mitochondrialuptake and recycling of ascorbic acid. Arch Biochem Biophys. 2001;387:143-153. [Pub Med]
  31. Kim J, Lee SD, Chang B, Jin DH, et al. Enhanced antitumor activity of vitamin C via p53 in cancer cells. Free Radical Biol Med. 2012; 53(80):1607-15. [Pub Med]
  32. Ludke A, Sharma AK, Bagchi AK, Singal PK. Subcellular basis of vitamin C protection against doxorubicin-induced changes in rat cardiomyocytes. Mol Cell Biochem. 2012; 360(1-2):215-24. [Pub Med]
  33. Huwyler T., Hirt A, Morell A. Effect of ascorbic acid on human natural killer cells. Immunol Lett. 1985; 10(3-4):173-6. [Pub Med]
  34. See D, Mason S, Roshan R. Increased tumor necrosis factor alpha (TNF-alpha) and natural killer cell (NK) function using an integrative approach in late stage cancers. Immunol Invest. 2002; 31(2): 137-53. [Pub Med]
  35. Dahl H, Degre M. The effect of ascorbic acid on production of human interferon and the antiviral activity in vitro. Acta Pathol Scand Sect B. 1976;84:280-284. [Pub Med]
  36. El Attar TMA, Lin HS. Effect of vitamin C on prostaglandin synthesis by fibroblasts and squamous carcinoma cells. Prostaglandins Leukot Essent Fatty Acids. 1992;47:253-257. [Pub Med]
  37. Beetens JR, Hermen AG. Ascorbic acid and prostaglandin for- mation. Int J Vitam Nutr Res. 1983;24(suppl):131s-144s.
  38. Mikirova N, Casciari J, Taylor P, Rogers A. Effects of high-dose intravenous vitamin C on inflammation in cancer patients. J Transl Med. 2012; 10:189. [Pub Med]
  39. Mikirova NA, Ichim TE, Riordan N. Anti-angiogenic effect of high dose ascorbic acid. J Transl Med. 2008; 6(50) doi:10.1186/1479-5876-6-50. [Pub Med]
  40. Chen Q, Espey MG, Krishna MC, Mitchell JB, Corpe CP, Buettner GR, Shacter E, Levine M. Ascorbic acid at pharmacologic concentrations selectively kills cancer cells: ascorbic acid as a pro-drug for hydrogen peroxide delivery to tissues. Proc Natl Acad Sci, USA. 2005; 102: 13604-13609. [Pub Med]
  41. Gonzalez MJ, Miranda-Massari JR, Mora EM, Jimenez IZ, et al.. Orthomolecular oncology: a mechanistic view of intravenous ascorbate’s chemotherapeutic activity. P R Health Sci J. 2002; 21(1):39-41. [Pub Med]
  42. Gonzalez MJ, Miranda-Massari JR, Mora EM, Guzman A, et al.. Orthomolecular oncology review: Ascorbic acid and cancer 25 years later. Int Cancer Ther. 2005; 4(1);32-44
  43. Shinozaki K, Hosokawa Y, Hazawa M, et al.. Ascorbic acid enhances radiation-induced apoptosis in an HL60 human leukemia cell line. J Radiat Res. 2011; 52(2):229-37.
  44. Park JH, Davis KR, Lee G, Jung M, et al.. Ascorbic acid alleviates toxicity of paclitaxel without interfering with the anticancer efficacy in mice. Nutr Res. 2012; 32(11):873-83.
  45. Riordan HD, Hunninghake RB, Riordan NH, et al.. Intravenous ascorbic acid: protocol for its application and use. P R Health Sci J. 2003; 22(3):287-90.
  46. Vollbracht C, Schneider B, Leendert V, Weiss G, Auerback L, Beuth J. Intravenous vitamin C administration improves quality of life in breast cancer patients during chemo-/radiotherapy and aftercare: Results of retrospective, multicentre, epidemiological cohort study in Germany. In Vivo. 2011; 25(6):983-990.
  47. Lundholm L, Haag P, Zong D, Juntti T. Mork B, et al..Resistance to DNA-damaging treatment in non-small cell lung cancer tumor-initiating cells involves reduced DNA-PK/ATM activation and diminished cell cycle arrest. Cell Death Dis. 2013;4:e478.
  48. Lamson DW, Brignall MS. Antioxidants in cancer therapy: their actions and interactions with oncologic therapies. Alt Med Rev. 1999;4:304-329.
  49. Lamson DW, Brignall MS. Antioxidants in cancer therapy II: quick reference guide. Altern Med Rev. 2000;5:152-163.
  50. Lamson DW, Brignall MS. Antioxidants in cancer III. Altern Med Rev. 2000;5:196-208.
  51. Prasad KN, Kumar A, Kochupillai V, Cole WC. High doses of multiple antioxidant vitamins: essential ingredients in improving the efficacy of standard cancer therapy. J Am Coll Nutr. 1999;18:13-25.
  52. Moss RW. Antioxidants Against Cancer. New York, NY: Equinox Press; 2000.
  53. Padayatty SJ, Sun AY, Chen Qm Espey MG, Drisko J, Levine M. Vitamin C: intravenous use by complementary and alternative medicine practitioners and adverse effects. PLoS One. 2010; 5(7):e11414.
  54. Espey MG, Chen Q, Levine M. Comment re: Vitamin C antagonizes the cytotoxic effects of chemotherapy. Cancer Res. 2009; 69(22):8830.
  55. Espey MG, Chen P, Chalmers B, Drisko J, Sun AY, et al.. Pharmacologic ascorbate synergizes with gemcitabine in preclinical models of pancreatic cancer. Free Radic Biol Med. 2011. 1;50(11):1610-9.
  56. Monti DA, Mitchell E, Bazzan A, Littman S, Zabrecky G, Yeo C, et al.. Phase I evaluation of intravenous ascorbic acid in combination with gemcitabine and erlotinib in patients with metastatic pancreatic cancer. PLoS One. 2012; 7(1)e29794.
  57. Ma Y, Drisko J, Polireddy K, Chen Q. Synergistic effects of ascorbatewith carboplatin against human ovarian cancer in vitro and in vivo. Society for Integrative Oncology 8th International Conference, Cleveland, Ohio, Nov. 10-12, 2011.
  58. Agus DB, Vera JC, Golde DW. Stand allocation: a mechanism by which tumors obtain vitamin C. Cancer Res. 1999;59:4555- 4558.
  59. Belle FN, Kampman E, McTiernan A, Bernstein L, et al.. Dietary fiber, carbohydrates, glycemic index, and glycemic load in relation to breast cancer prognosis in the HEAL cohort. Cancer Epidemiol Biomarkers Prev. 2011; 20(5):890-9.
  60. Hardin J, Cheng I, Witte JS. Impact of consumption of vegetable, fruit, grain, and high glycemic index foods on aggressive prostate cancer risk. Nutr Cancer. 2011; 63(6):860-72.
  61. Bartella V, De Marco P, Malaguarnera R, Belfiore A, Maggiolini M. New advances on the functional cross-talk between insulin-like growth factor-I and estrogen signaling in cancer. Cell Signal. 2012; 24(8):1515-21.
  62. Simone C, Simone N, Simone V, et al.. Antioxidants and other nutrients do not interefere with chemotherapy or radiation therapy and can increase kill and increase survival, Part I. Altern Ther. 2007; 13(1):22-28.
  63. Simone C, Simone N, Simone V, et al.. Antioxidants and other nutrients do not interefere with chemotherapy or radiation therapy and can increase kill and increase survival, Part II. Altern Ther. 2007; 13(2):40-47.
  64. Block KI, Koch AC, Mead MN, Tothy PK, Newman RA, Gyllenhaal C. Impact of antioxidant supplementation on chemotherapeutic efficacy: a systematic review of the evidence from randomized controlled trials. Cancer Treat Rev. 2007; 33(5):407-18.
  65. Riordan HD, Hunnighake RB, Riordan NH, et al.. Intravenous ascorbic acid: protocol for its application and use. PRHSJ. 2003; 22(3);287-290.
  66. Kim MY, Oskarsson T, Acharyya S, Nguyen DX, Zhang XH, Norton L, Massagué J. Cell. Tumor self-seeding by circulating tumor cells. Cell. 2009;139(7):1315-26.
  67. Lianidou ES, Markou A. Circulating tumor cells as emerging tumor biomarkers in breast cancer. Clin Chem Lab Med. 2011; 49(10):1579-90.
  68. Swaby RF, Cristofanilli M. Circulating tumor cells in breast cancer: A tool whose time has come of age. BMC Medicine. 2011; 9(43): 1741-7015.
  69. Mikirova N, Rogers A, Casciari J, Taylor P. Effect of high dose intravenous ascorbic acid on the level of inflammation in patients with rheumatoid arthritis. Modern Research Inflammation. 2012; 1(2):26-32.
  70. Gonzalez MJ, Rosario-Perez G, Guzman AM, et al.. Mitochondria, energy and cancer: The relationship with ascorbic acid. J Orthomol Med. 25(1):29-38.
  71. Mikirova N, Casciari J, Hunninghake R, Riordan N. Assessment of the energy metabolism in patients with chronic fatigue syndrome. Alternative Therapies. 2012, 18(1):36-40.
  72. Mikirova N, Jackson JA, Riodan NH. The effect of high dose IV vitamin C on antioxidant capacity and level of oxidative stress in cancer patients and healthy subjects. J Orthomol Med. 2007; 22(3):153-160.
  73. Gupta SK, Saxena P, Pant VA, Pant AB. Release and toxicity of dental resin composite. Toxicol Int. 2012; 19(3):225-34.
  74. Geir DA, et al. A significant relationship between mercury exposure from dental amalgams and urinary porphyrins: a further assessment of the Casa Pia children’s dental amalgam trial. Biometals. 2011; 24:214-224.
  75. Richardson GM. Inhalation of mercury-contaminated particulate matter by dentists: An overlooked occupational risk. Human and Ecolog Risk Assess. 2003; 9:1519-1531.
  76. Jones, DP. The health dividend of glutathione. The Natural Medicine Journal. 2011; http://www.naturalmedicinejournal.com/article_content.asp?article=18
  77. Falcone G, Foti C, Gianguzza A, Giuffrè O, Napoli A, Pettignano A, Piazzese D. Sequestering ability of some chelating agents towards methylmercury(II). Anal Bioanal Chem. 2013; 405(2-3):881-93.

 

Learn more information about early cancer detection tests referred to as the ONCOblot test, or the CTC’s referred to as circulation tumour cell test, and cancer biomarker testing by clicking on the words.