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Ascorbic Acid Molecule in Orthomolecular Therapy and Prevention of Cancer. A Recent Review

by Guest on October 30, 2011


The following is a written report from Professor Badawi. He joined Natural Road recently and asked us to post this info which he had written. It is long and a bit technical and you might wish to read the entire article. I have highlighted (by red and bold) a few salient points. The highlights are mine and not Professor Badawi’s. I also made a couple of notes in blue.

Prof.Abdelfattah Badawi

Applied Surfactant Laboratory, Egyptian Petroleum Research Institute, Nasr City, Cairo, Egypt.

General secretary for International Society of Therapeutic, Experimental and Clinical Research (Bastia, France)


Ascorbic Acid (AA) plays an important role in oxidative stress control. AA in combination with other nutrients promote normal metabolism and interact with each other to facilitate absorption within the body. Most cancer patients die with nutritional imbalances that are difficult to correct by dietary intake alone. (Kim’s note:  this indicates that we need to make sure our bodies do not become nutritionally imbalanced – end note). AA questionnaire together with specific laboratory panels can be implemented for cancer patients. These tools may serve in providing data to assess the patient’s AA oxidative stress and clinical status, and directing AA intervention to treatment-related complications. This may result in improved quality of life, decreased morbidity, and prolonged survival.

This review will provide an update of peer-reviewed scientific data related to the impact and outcome of orthomolecular AA on cancer therapy and prevention.

Orthomolecular Oncology:

There are a wide variety of mechanisms by which AA prevents and inhibits malignant growth. The collective evidence supports the notion of increasing AA intake in patients suffering malignancies, specially provided by i.v. route. AA may produce benefits in both prevention and treatment of cancer, by inhibiting malignant cell proliferation, and inducing differentiation. (1)

The ideal anticancer agent is obviously one that specially interferes with tumor growth, prolongs survival time, and improves quality of life. There is evidence that AA might fit this description. Based on this evidence it is suggested, the use of i.v. AA as advent therapy in cancer treatment. (2)

Orthomolecular AA as Therapy for Human Cancer:

Mehdavi et al, (3) have determined the levels of oxidative stress, serum total antioxidants, and AA in a cohort of 57 cancer patients and 22 healthy participants. The level of oxidative stress was measured by malondialdehyde (end product of lipid peroxidation). Cancer patients as compared with controls, showed a significant increase in lipid peroxidation with a concomitant decrease in the antioxidant defence system. In addition, low serum levels of AA in spite of adequate daily intake may be because of increased use scavenging lipid peroxides as well as their sequestration by tumor cells.

The effect of chemotherapy alone versus a high dose of AA (6100mg/d) combined with vitamin E (1050mg/d) and B-carotine (60mg/d) in patients with advanced non-small-cell lung cancer (NSCLC) indicated a potential benefit for AA. (4)

Frei and Lawson reported the potential of AA as therapy for human cancer. (5) The authors are located at the Linus Pauling Institute and revitalized the interest in AA promoted by the investigations of Cameron and Noble prize Pauling that led to their conclusion “that treatment with AA in amounts of 10g/day or more is of real value in extending the life of patients with advanced cancer”. (6)

Frei and Lawson stressed the high statistical significance of the positive effect of AA and stated that “a series of case reports indicated that high-dose AA was associated with long-term tumor regression in three patients with advanced renal cell carcinoma, bladder carcinoma, or B cell lymphoma. (7)

AA with Nutrient Mixture Inhibits Human Bladder and Adenocarcinoma cell Lines:

A nutrient mixture (NM) of AA, lysine, proline, arginine and green tea extract was reported to inhibits the human bladder cancer cells and the human T-24 adenocarcinoma line 760-0. (8,9) The invasion of both human cancer cells was totally inhibited by (NM) at 1000 microgram/ml (NM). (Kim’s note – Ascorbate combined with magnesium, calcium and sodum, lysine and proline and green tea are in the MORE and the Arginine is in the RAANOW. We should be taking all the products – end note).

Highly metastatic melanoma is resistant to existing therapies. The mice supplemented with NM not only showed less tumor growth in the spleen as the control mice, but also drastically reduced metastasis to the liver. (10)

Strenthening of collagen and connective tissue can be achieved naturally through the synergistic effects of NM. This NM has exhibited a potent anticancer activity in vivo and in vitro in a low dosen cancer cell lines. Its anti-cancer effects include inhibition of metastasis tumor growth, matrix metalloproteinase (MMP) secretion, invasion, angiogenesis, and cell growth as well as induction of apoptosis. (11)

AA administered i.v. as Cancer Therapy:

The history of AA and cancer has been marked with controversy. Clinical studies evaluating AA in cancer outcome continue to the present day. However, the wealth of data suggesting that AA may be highly beneficial in addressing cancer-associated inflammation, particularly progression to systemic inflammatory response syndrome (SIRO) and multi organ failure (MOF), has been largely overlooked. Patients with advanced cancer are generally deficient in AA. Once these patients develop septic symptoms, a further decrease in ascorbic acid levels occurs. Given the known role of ascorbate in: a) maintaining endothelial and suppression of inflammatory markers; b) protection from sepsis in animal models; and c) direct antineoplastic effects, we propose the use of ascorbate as an adjuvant to existing modalities in the treatment and prevention of cancer-associated sepsis. (12)

AA and Vitamin K3 as Cancer Therapy:

A combination of AA and a quinine was used as a supplemental treatment for an ovarian cancer patient. The combination may be administered before, during and after the patient undergoes a conventional cancer treatment protocol. The combination may be administered orally, intravenously, or intraperitoneally. Oral administration may be in the form of capsules containing a predetermined ratio of AA to Vitamin K3. The supplemental treatment is effective to inhibit metastases of cancer cells and inhibit tumor growth. The ratio the AA to Vitamin K3 is in the range of about 50 to 1 to about 250 to 1. A method for evaluating the effectiveness of the supplemental treatment includes monitoring the patient’s serum DNase activity throughout the course of treatment. (13)

AA and Metal Ions as Catalytic Therapy of Cancer:

In catalytic therapy (CT) most often the combination of AA, as a substrate, and phthalocyanine dyes containing transition metal ions, as catalysts, is used. Mechanisms underlying the antitumor action of CT are similar to X-ray therapy and Photodynamic Therapy (PDT) cancer treatments, in that CT’s actions are dependent on the production of Reactive Oxygen Species (ROS), which subsequently induces oxidative degradation of critical cellular molecules and organelles. (14-17) Compared to traditional chemotherapy and PDT, CT has the potential to become a preferred treatment for an array of diverse malignancies.

It has been found that a combination of cobalt or iron phthalocanine and sodium ascorbate has high antitumor activity. This system is highly effective, with a success rate similar to that of PDT. The effectiveness of CT has been demonstrated in in vitro experiments with porphyrin-like moieties (vitamin B12) and its derivatives, as catalysts, and with ascorbate as a substrate. (18-20) Several in vivo experiments with the same CT systems have also been reported. (21-24) A combination of teraphthal (cobalt (II) octa-4,5-carboxyphthalocyanine) and AA has been approved for Phase II clinical trials in Russia.(25) AA is currently considered the most suitable substrate for CT. It has been well recognized that some human tumors accumulate AA more than normal tissues do. It has also been demonstrated that AA may be a pre-drug for the formation of H2O2 in tumor cell. (26) In addition, formation of H2O2 and OH- by photosensitizers such as methylene blue, hematoporphyrin, and texaphyrines in the presence of AA and without light has been observed. (27,28) While PDT is limited to regions of the body accessible to light illumination, CT does not require light, thereby making it more flexible and adaptable for treatment of poorly accessible neoplasms. In cancer treatment, CT functions by various mechanisms including direct cell killing, damage to the tumor vasculature, and stimulation of inflammation and nonspecific or specific immune effector cells. (29)

AA in Cancer Prevention:

Breast Cancer: Plasma levels of AA were significantly lower while platelet levels were higher in a group of recently diagnosed breast cancer patients when compared to a matched group of controls. (30) Epidemiological studies appear to point to ascorbate as a possible chemopreventive for breast cancer. In the Iowa Women’s Health Study, women who reported consuming at least 500mg AA daily has a relative risk of developing breast cancer of 0.79 (not statistically significant), compared with women who did not supplement with AA.(31) Rohan et al., reported a small, statistically insignificant decrease in risks with AA consumption (as assessed by dietary reporting). (32) In a Spanish study comparing AA intake among breast cancer patients and matched controls, the patients reported significantly lower intakes of dietary AA than controls. (33)

A meta-analysis of 12 studies and a number of different nutrients and their relationship to breast cancer found “AA intake has the most consistent and statistically significant inverse association with breast cancer risk. (34) Verhoeven et al found no significant association between AA supplementation and decreased breast cancer risk. To make the claim as they did, however, that supplementation with AA does not confer protection from breast cancer, is erroneous since their “higher doses” were an average of 165.3mg daily. (The group was divided according to supplemental intake as reported on a questionnaire into quintiles with the average reported intake of AA daily ranged from 58.6mg in the lowest quintile to 165.3mg in the highest). (35)

Cervical Cancer: A Latin American study compared nutrient intake and dietary patterns of 748 cervical cancer patients with 1.411 controls. The result supported a protective affect of AA against invasive cervical cancer. Other researchers have found a similar inverse relationship between cervical neoplasia and dietary AA. (36,37) A review article examining a number of studies concluded that in many, but not all studies, an inverse relationship between AA status and risk for cervical dysplasia was observed. (38)

Colorectal Cancer: Colonic polyps are recognized as a frequent precursor to colorectal cancer. In a group of 36 patients with polyps, 19 received 3 grams AA daily and 17 received placebo. The researchers noted a decrease in polyp area after nine months of treatment with ascorbate but not placebo. In addition, a trend toward decrease in polyp number was noted. Other researchers have used antioxidants to prevent recurrence of polyps in patients who had undergone surgical removal of their polyps. Patients were divided into three groups receiving either lactulose, a combination of vitamins A, C, and E, or nothing. Among 209 patients, polyps recurred in 5.7 percent of those given the vitamins, in 14.7 percent of those receiving lactulose, and in 35.9 percent of the untreated control. (39)

An Australian study examining dietary habits and incidence of colorectal cancer found AA but not vitamin A to be protective. A similar study on patients of a major health plan in Los Angeles found a weak inverse relationship between supplemental and dietary AA and incidence of colorectal cancer. (40)

Cancer cells are the result of multiple genetic defects resulting from exposure to environmental, dietary and infectious agents. The dietary carcinogens such as N-nitroso compounds polycyclic aromatic hydrocarbons and heterocyclic amines are present in cured or spoiled foods and crude oil contaminated diet. The level of exposure of the cell DNA to those and other carcinogens depends largely on the general quality of diet, the presence of bioactivated dietary constituents, including antioxidant vitamins found in abundance in fruits and vegetable. In addition, normal cellular metabolizing enzymes which convert particular chemicals to more water-soluble compounds that can be excreted in the urine. (41)

Oxidative stress induction by crude oil was indicated by increased lipid peroxidation and decrease in superoxide dismutase and catalase activities. However, pre-treatment of the diet with AA and E exhibited a protective role on the toxic effect of crude oil. The order of protection was vitamin E + C > vitamin E > vitamin C. (42)

Humans are exposed to performed N-nitroso compounds (NOCs) and endogenous NOCs. Several NOCs are potential human carcinogens including N-nitrosodimethylamine (ND MA). There was a significant interaction between plasma AA concentration and dietary NDMA intake on cancer incidence. Plasma AA may modify the relation between NDMA exposure and cancer risk. (43)

By Prof. Abdelfattah Badawi

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