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The Natural Health Clinic - Vitamins Oklahoma

The 21st Century Wellness Center 
Home of Herb Power 21®-Our Registered Trademark 

Neuromuscular Therapy, Iridology, Cell Analysis, 
Hair Analysis, Weight-Loss,  Healthy food Parties.

Vitamin C

C Complex:


  • Detoxifies free radicals
  • Superior source of vitamin C
  • 10 times less acidic than ascorbic acid
  • Contains real antioxidants

C Complex is a 100% vegetarian Food supplement that is intended to supply 100% Food Vitamin C. Unlike some other so-called “whole food” vitamins, it does not contain any isolated ascorbic acid. Royal Lee claimed that ascorbic acid was not Vitamin C. Food Vitamin C is an antioxidant and has long been recognized as an important nutrient for supporting cardiovascular, immune, musculoskeletal, endocrine, and other systems. Studies have shown that FOOD Vitamin C has at least 17 times the antioxidant effect of USP ascorbic acid and is superior for optimal human health.

100% Pure Whole Food Supplements.

  • No Synthetics
  • No Toxins
  • No GMOs
  • Gluten-Free
  • Available in 60 or 180 Capsules
  • 100% Food Nutrients
  • Vegetarian Formula
  • Dietary Supplement

Suggested use: 1-3 tablets per day or as recommended by your health care professional. Adjust usage according to nutritional lifestyle requirements.

C Complex

Acerola is derived from acerola cherry, one of nature's highest sources of acerola vitamin C. The fruit can yield up to 3,000 mg of vitamin C per 100 grams of fresh weight, but on the average yields around 1,500 mg. acerola  Powder, is a 4:1 extract that yields 180 mg of vitamin C per teaspoon and tastes great! acerola extract, acrola cherry, acerola plus, acerola vitamin c, dhc acerola, acerola c 
Acerola is derived from acerola cherry, one of nature's highest sources of acerola vitamin C. The fruit can yield up to 3,000 mg of vitamin C per 100 grams of fresh weight, but on the average yields around 1,500 mg. acerola  Powder, is a 4:1 extract that yields 180 mg of vitamin C per teaspoon and tastes great! acerola extract, acrola cherry, acerola plus, acerola vitamin c, dhc acerola, acerola c 
Acerola is derived from acerola cherry, one of nature's highest sources of acerola vitamin C. The fruit can yield up to 3,000 mg of vitamin C per 100 grams of fresh weight, but on the average yields around 1,500 mg. acerola  Powder, is a 4:1 extract that yields 180 mg of vitamin C per teaspoon and tastes great! acerola extract, acrola cherry, acerola plus, acerola vitamin c, dhc acerola, acerola c 

 

Intravenous Vitamin C

 

Preparation of Sodium Ascorbate 
for IV and IM Use


ROBERT F. CATHCART III, M.D. 
ALLERGY, ENVIRONMENTAL & ORTHOMOLECULAR MEDICINE 
127 SECOND STREET, SUITE 4 
LOS ALTOS, CALIFORNIA 94022 
(650) 949-2822 
FAX (650) 949-5083

Note:  some of these solutions are labeled ascorbic acid which is confusing.  They are all buffered so as to really make them mostly sodium ascorbate.

Note: the following are excerpts from letters sent to physicians on the subject of IVC.

If one does not want to make their sodium ascorbate stock solutions from scratch like I recommend (and I can well understand why you might not): You can order from

Wholesale Nutrition 915 S. San Tomas Equino Road Campbell, CA 95008 order 800-325-2664 or FAX 408-867-6236
Merit Pharmaceuticals, 2611 San Fernando, Los Angeles, CA 90065, 
For CA orders: 800-696-3748 For Out-of State orders: 800-421-9657 

The Stock Bottle of Sodium Ascorbate                                                                      Sodium Ascorbate is a more bioavailable form of vitamin C that is an alternative to taking ascorbic acid as a supplement.

Sterilize a 500 cc IV bottle along with a funnel, the rubber stopper, and a spoon. Then fill the bottle to the 300 cc line with sodium ascorbate fine crystals.  (I weighed the sodium ascorbate out one time and 250 gm came up to the 300 cc line.) Then add 1/3 of the 20 ml bottle (6.6 cc) of edetate disodium injection, USP 150 mg/ml. Then add water for injection q.s. 500 cc. Shake up the bottle and if there is 1 mm of crystals left on the bottom, add 1 mm of water to the top. It turns out that sodium ascorbate is soluble to almost exactly a 50% concentration at room temperature. I do not worry about the sterility of this because this is very bacteriocidal. Perhaps it should be filtered to get out particulate matter but I have never seen this to be a problem. The pH of this has always turned out to be 7.4. My nurse discovered recently that if you do not shake the mixture to make it go into solution until after you refrigerate it and are ready to use it that the solution is less yellow. I presume that this is good because sodium ascorbate is clear and dehydroascorbate is yellow. The made up solutions are always a little yellow but refrigeration before mixing results in a far less yellow mixture.

Preparation of the IV Bottle

I recommend that the above stock bottle solution be added to sterile water for injection such that 30 Gms (60 cc) to 60 Gms (120 cc) is added to a quantity of sterile water sufficient to make 500 cc of the final solution to be injected IV.  For patients with chemical or other sensitivity reactions, it is best that the sterile water be obtained in glass IV bottles rather than the plastic IV bottles.

IM Injections

IM injection material for infants is made from the stock solution diluted 50% in water giving a 25% solution. Generally, the size of the injection can be 2 cc in each buttocks. Ice may be applied if it hurts to much. This may be given every hour or so, frequently enough to bring the fever or other symptoms of excessive free radicals down rapidly.

General Comments

I have not had any trouble with these solutions. I hear all sorts of weird stories from patients who have gotten ascorbate elsewhere. I do not know if it is an acid problem (because ascorbic acid was used rather than sodium ascorbate) or whether some colleges get carried away with what other things they add to the intravenous solutions.

I think that there may be, at times minor troubles with commercially prepared solutions because of the following. I understand that the U. S. Pharmacopeia specifies that the solutions be made from ascorbic acid and then buffered with sodium hydroxide or sodium bicarbonate to a pH between 3.5 and 7.0. I worry that 60 grams of ascorbate at a pH of 3.5 is too acid. I know that Klenner (the first physician who used high dose intravenous ascorbate by vein) also made his solutions from sodium ascorbate powder despite the fact that he referred to the solutions in his papers as ascorbic acid.  (This fact comes from discussions with Annie Klenner, Fred Klenner's wife and nurse.).

I watch patients for hypocalcemia (although I have not seen it), hypoglycemia (I encourage patients to eat while taking the IV), and dehydration (I encourage water and slow the IV down.) I also see headaches afterward but not so much since I have been emphasizing the continuing high doses of oral ascorbic acid as soon as the IV is over. Actually I give oral ascorbic acid while the IV is going to get a double effect. Bowel tolerance goes up while the IV is running but one has to be careful to stop giving oral C about an hour before the IV stops or else you may get diarrhea as soon as the IV stops. The oral ascorbic acid is then started again 1/2 to 1 hour after the IVC stops.


Copyright (C) 1996,  Robert F. Cathcart, M.D.. Permission granted to distribute as long as distributed intact and with this attribution.


 

Subject: VITAMIN C KILLS CANCER CELLS
From: Orthomolecular Medicine News Service
Date: Thu, 22 Sep 2005 09:32:29 -0500
To: [email protected]

FOR IMMEDIATE RELEASE  Orthomolecular Medicine News Service, September 22, 2005  Intravenous Vitamin C is Selectively Toxic to Cancer Cells  (OMNS) National Institutes of Health scientists have confirmed the concepts that vitamin C is selectively toxic to cancer cells and that tumor-toxic levels of vitamin C can be attained using intravenous administration.  The article, published in the September 12, 2005 issue of the Proceedings of the National Academy of Sciences (1) concluded, These findings give plausibility to intravenous ascorbic acid in cancer treatment   Orthomolecular  medical researchers, including Nobel laureate Linus Pauling, have long recognized the great importance of vitamin C in fighting cancer. (2)  Scientists associated with the Bio-Communications Research Institute (BRCI) in Wichita, Kansas have published 20 scientific articles on the subject. (3)  BCRI researchers first reported in 1995 that vitamin C in sufficient amounts is selectively toxic to tumor cells. The authors concluded that tumor-toxic levels of vitamin C could be achieved only by giving the vitamin intravenously. Subsequent research from BCRI, published in the British Journal of Cancer in 2001 (4), was the first to describe in detail the pharmacokinetics of high doses of intravenous vitamin C.    “It is gratifying to have our research on vitamin C and cancer confirmed by scientists at the prestigious National Institutes of Health,said Neil Riordan, Ph.D.,Research Director. The findings reinforce our goal and commitment to pursue cutting edge cancer research,” added Michael Gonzalez, Ph.D., D.Sc. of the University of Puerto Rico.   
vitamin C research was headed by its founder Hugh D. Riordan, M.D.  The research team includes Dr. Xiaolong Meng, Dr. Joseph Casciari, Dr. Nina Mikirova, Dr. Jie Zhong, Dr. James A. Jackson, Dr. Don Davis, Dr. Jorge Miranda, Dr. Michael Gonzalez, Dr. Neil Riordan, and Mr. Paul Taylor.   What is Orthomolecular Medicine?  Linus Pauling defined orthomolecular medicine as "the treatment of disease by the provision of the optimum molecular environment, especially the optimum concentrations of substances normally present in the human body." Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org   Take the Orthomolecular Quiz at http://www.orthomolecular.org/quiz/index.shtml   The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.   Editorial Review Board:  Abram Hoffer, M.D. Harold D. Foster, Ph.D. Bradford Weeks, M.D. Carolyn Dean, M.D. N.D. Eric Patterson, M.D. Thomas Levy, M.D., J.D.  OMNS Editor: Andrew W. Saul, Ph.D. Email: [email protected] . BCRI contact person: Renee Olmstead: [email protected]  To subscribe at no charge: http://orthomolecular.org/subscribe.html  References:  [1] Chen Q, Espey MG, Krishna MC, Mitchell JB, Corpe CP, Buettner GR, Shacter E, Levine M. Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a pro-drug to deliver hydrogen peroxide to tissues. Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13604-9. Epub 2005 Sep 12.   [2] Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A. 1976 Oct;73(10):3685-9. The original paper is posted at http://profiles.nlm.nih.gov/MM/B/B/K/Z/_/mmbbkz.pdf  Also: Cameron E, Pauling L, Leibovitz B. Ascorbic acid and cancer: a review.  Cancer Res. 1979 Mar;39(3):663-81.   [3] Full text papers listed and accessible at no charge at  http://brightspot.org/cresearch/index.shtml   [4] Casciari, J.J., Riordan NH, Schmidt, T.L., Meng, X.L., Jackson JA, Riordan HD. Cytotoxicity of ascorbate, lipoic acid, and other antioxidants in hollow fibre in vitro tumours. British J Cancer. 2001, 84(11), 1544-1550.  -------------------------------------- Update Your Information:  http://www.orthomolecular.org/12all/p_m.php?mi=32&nl=1&ei=ZG9jY0Bkb2NjLmNvbQ==&eid=MjA2MTc=  Forward To A Friend:  http://www.orthomolecular.org/12all/p_f.php?mi=32&nl=1&ei=ZG9jY0Bkb2NjLmNvbQ==&eid=MjA2MTc=  View the Complete OMNS Press Release Archive:  http://orthomolecular.org/resources/omns/index.shtml   --------------------------------------------------------------------

shows the responses to increasing doses of ascorbate of four human tumor cell lines grown in dense monolayers in a medium of human serum.

Figure 1 Caption:
Response to sodium ascorbate (mean of 12 samples) of tumor cell lines Mia PaCa-2 (human pancreatic carcinoma). SK-MEL-28 (human melanoma), SW-620 (human colon carcinoma), and U-2-OS (human osteogenic sarcoma), all from ATCC, Rockville, MD. Results reflect total viable cells. Maintenance medium was DMEM High-glucose culture medium (Irvine Sci.) wf 10% heat-inactivated fetal calf serum + antibiotics + Fungizone, 5% CO2 humidified incubator at 37 degrees C. Experimental medium was human serum from patients with diagnoses of respective human tumors. Cultured for 3 days after supplementation of ascorbate. Seeded with 24,000 celIs Avell in 96-well culture plates (Nune). Absolute quantitation of live cells determined using previously described microplate fluorometer method (16).

 

Figure 2 Caption:
Plasma ascorbate concentrations during infusion of 65 grams ascorbic acid in 500 ml sterile water at a rate of one gram AA per minute. Whole blood was taken via a heparin lock from the antecubital vein of the arm contraleral to the arm receiving the IV infusion. Plasma AA concentrations were determined using high performance liquid chromatograpy. Patient I was a 74-year-old male who had a diagnosis of non-metastatic prostate carcinoma, who had received more than 30 IAA infusions in the two years prior to the study. Patient 2 was a 50-year-old male with a diagnosis of non-Hodgkin's lymphoma who had received l6 IAA infusions prior to study. Patient 3 was a 69 year old male with a diagnosis of metastatic carcinoma of the jejunum who had received 16 IAA infusions prior to study.

Figure 2 depicts plasma ascorbate levels of three representative patients given 65 grams of ascorbate over 65 minutes. Patient 1 with localized prostate cancer was clinically well and had received IAA in the past; he achieved a peak plasma concentration of 702 mg/dL. Patients 2 and 3, had diagnoses of non-Hodgkin's lymphoma, and metastatic carcinoma of the jejunum, respectively. Both had received several IAA infusions at the time of study, yet achieved lower plasma AA concentrations of 309 mg/dL (patient 3), and 396 mg/dL (patient 2).

From the data in both Figures 1 and 2, one can see that the concentrations required to kill tumor cells can be achieved at least briefly in human plasma. Figure 2 suggests the need to measure post-IAA plasma ascorbate concentrations to determine if patients are achieving what we expect are adequate concentrations.

Infusion Protocol

Treatment choice
Treatment of cancer with IAA should never be considered to replace an effective, proven treatment. It should only be considered in: 

Cases of treatment failure using proven methods cases with no known effective treatments; and, 

Cases in which it is used as an adjunct to proven treatments. 

Because IAA treatment is experimental an appropriate informed consent form should be read, understood, and signed by the patient.

Precautions and side effects
The side effects of IAA in our experience are rare. However, there are contraindications and potential side effects to be considered.

1. Although it has been reported only once in the literature, tumor necrosis, hemorrhage, and subsequent death after a single intravenous 10 gram dose of AA, as reported by Campbell and Jack (10), should be the highest priority concern for the safety of IAA for cancer patients. For this reason, we always begin with a small dose (see Infusion).

2. Another report described acute oxalate nephropathy in a patient with bilateral ureteric obstruction and renal insufficiency who received 60 gram IAA (11). We have also heard one case report of a patient with colon carcinoma, receiving daily IAA, who developed nausea and vomiting and was hospitalized for dehydration (12). Both cases show the need to ensure that patients have adequate renal function, hydration, and urinary voiding capacity. To these ends, our baseline lab tests include a serum chemistry profile and urinalysis.

3. Hemolysis can occur in patients with a red cell glucose-6-phosphate dehydrogenase (G6PD) deficiency. We therefore test G6PD on all patients before beginning IAA infusions.

4. Localized pain at the infusion site can occur if the infusion rate is too high. This is usually corrected by slowing the rate.

5. Because ascorbate is a chelating agent, some individuals may experience shaking due to low serum calcium. This is treated by a slow (1 cc per minute) intravenous push of 10 cc's of calcium gluconate.

6. Rivers (13) reported that high dose IAA is contraindicated in renal insufficiency, chronic hemodialysis patients, unusual forms of iron overload, and oxalate stone formers. However, oxalate stone formation may be considered a relative contraindication. Two groups of researchers (14,15) demonstrated that magnesium oxide (300 rng/d orally) and vitamin B6 (10 mg/d orally) inhibited oxalate stone formation in stone formers.

7. Given the amount of fluid which is used as a vehicle for the ascorbate and the sodium hydroxide/sodium bicarbonate used to adjust the pH, any condition which could be adversely affected by increased fluid or sodium is relatively contraindicated. For example: congestive heart failure, ascites, edema, etc.

8. As with any intravenous site, infiltration is always possible.

9. Ascorbate should only be given by intravenous drip. It should never be given IV push, as the osmolality of high doses are capable of sclerosing peripheral veins, nor should it be given intramuscularly or subcutaneously. There is always a trade-off between fluid volume and osmolality. We have found an osmolality of less than 1200 milliOsmal to be tolerated well by most patients (Table 1, which may be seen in the original paper). 

Baseline work-up
Prior to administering large quantities of ascorbate, we gather the following information for a baseline and as a way to monitor therapy: 

 Serum chemistry profile with electrolytes 
 Complete blood count with differential 
 Red blood cell G6PD 
 Urinalysis 
 Patient weight 
 Tumor type/staging 
 Appropriate serum tumor markers 
 Appropriate CT, MRL, bone scans, and x-ray imaging

Table 1 Caption:
Osmolality of various amounts of sodium ascorbate/ascorbic acid in sterile water and Ringer's Lactate (mOsm; isotonic = 300 mOsm). Hypotonic mixtures are underlined: useful mixtures from isotonic to 1200 mOsm are in bold. An equal volume of IV solution is removed from the bag or bottle, prior to adding concentrated sodium ascorbate/ascorbic acid solution (500 mg/mL).

Infusion solution
In high-dose ascorbate therapy, many intravenous solutions are hypertonic. This does not seem to present a problem as long as the infusion rate is low enough and the tonicity does not exceed 1200 milliOsmal (mOsm). We generally infuse AA mixed with Ringer's lactate (RL) solution for AA amounts up to 15 gram, and in sterile water for larger amounts of AA. We presently use a sodium ascorbate/ascorbic acid mixture Containing 0.91 moles of sodium per mole of ascorbate (500 mg AA/mL, pH range 5.5-7.0, Merit Pharmaceuticals, Los Angeles, California, and Maclaskey Pharmaceuticals, Wichita, Kansas). Table I shows the osmolalities of commonly prepared solutions.

Infusion
As indicated in the precautions, a small starting dose of 15 gram AA in 250 mL RL over 1 hr is recommended. The patient is watched closely for any adverse effects. The dose can then be gradually increased over time. The infusion rate should not exceed 1 gram AA per minute; 0.5 gram/mm is well tolerated by most patients. Although there is variability due to scheduling and tolerance, a typical protocol will consist of the following infusions: 

Week 1: 1 x 15 g infusion per day, 2-3 per week 
Week 2: 1 x 30 g infusion per day, 2-3 per week 
Week 3: 1 x 65 g infusion per day, 2-3 per week 

The dose is then adjusted to achieve transient plasma concentrations of 400 mg/dL, 2-3 infusions per week.

According to our working hypothesis, the goal of the infusions is to raise plasma ascorbate concentration above the tumor-cytotoxic level for as long as possible. Because the ascorbate is so readily cleared by the kidney, the optimal infusion rate will result in tumor-cytotoxic plasma levels of ascorbate for the longest time periods--and hopefully, maximum tumor cell killing.

We advise patients to orally supplement with 4 grams ascorbate daily, especially on the days when no infusions are made, to help prevent a possible scorbutic "rebound effect."

Case histories
We have seen patients with almost every type of solid tumor in our clinic. Many of them have received IAA, with various degrees of success. Our cases include a patient with cancer of the head of the pancreas who lived for 3.5 years with IAA as sole therapy, resolution of bone metastases in patients with breast cancer, many patients with non-Hodgkin's lymphoma (none of whom have died from their disease), resolution of primary liver carcinoma tumors, resolution of and reduction in size of metastatic colon carcinoma lesions, and resolution of metastatic lesions and over 3-year survival in patients with widely metastatic ovarian carcinoma. We plan to present a full compilation of cases in another communication.

We have seen only two cases of metastatic renal cell carcinoma, considered a uniformly untreatable disease. Because the results were so dramatic, people with this disease could potentially benefit the most from IAA treatment. 

Following are those two cases.

Case 1
A 52-year-old white female with a history of renal cell carcinoma was seen in our clinic for the first time in October, 1996.In September 1995, shortly after diagnosis of a primary tumor in her left kidney, a nephrectomy was performed. Histology confirmed renal cell carcinoma. No evidence of metastases was found at that time. In March 1996, metastases to the lungs were found on chest x-ray film. In September 1996, a chest x-ray film revealed 4 1- to 3-cm masses in her lungs. One month later there were 8 1- to 3-cm masses in her lungs (7 in right lung, 1 in left).No new medical, radiation, or surgical therapies were performed prior to her visit to our clinic in October 1996, when she began IAA therapy. Her initial dose was 15 g, which increased to 65 g after 2 weeks, two per week. She was also started on: N-acetyl cysteine (Vitamin Research Products, Carson City, NV), 500 mg 1 p.o., QD; beta-1,3- glucan (a macrophage stimulator, NSC-24, Nutrition Supply Corp., Carson City, NV), 2.5 mg 3 p.o. QD; fish oil (Super-EPA, Bronson Pharmaceuticals, St. Louis, MO; 300 mg eicosatetraenoic acid, 200 mg docosahexaenoic acid), 1 p.o. TID; vitamin C, 9 g p.o. QD; beta-carotene (Beta Carotene 25, Miller Pharmacal Group, Inc., Carol Stream, IL), 25,000 lU. 1 p.o. BID; L-threonine (The Solgar Vitamin Co, Inc., Lynbrook, NY), 500 mg p.o. QD (for a deficiency revealed by laboratory testing of serum); Bacillus laterosporus (Lateroflora, International Bio-Tech U.S.A., San Marcos, CA), 280 mg, 2 p.o. QD for intestinal Candida a/b icans, inositol hexaniacinate complex (Niaplex, Karuna Corp., Novato, CA; 500 mg niacin, 100 mcg chromium) 2 p.o. QD, and a no-refined-sugar diet.

She continued IAA treatments until June 1997 when another chest x-ray film revealed resolution of 7 of the 8 masses, and reduction in the size of the 8th. According to the medical imaging report, "The nodular infiltrates seen previously in the right lung and overlying the heart are no longer evident and the nodular infiltrate seen in left upper lung field has shown marked Interval decrease in size and only vague suggestion of an approximately I cm density."

The patient discontinued IAA treatments in June 1997. She has continued on an oral nutritional support program since that time, and at this writing (December 1997) is well with no evidence of progression.

Case 2
In December 1985, a mass occupying the lower pole of the right kidney was discovered in a 70- year-old white male. Pathology of the mass after a radical nephrectomy confirmed renal cell carcinoma. He was followed by an oncologist at another clinic. Approximately three months after surgery, the patient's x-ray film and CT scan showed "multiple pulmonary lesions and lesions in several areas of his liver which were abnormal and periaortic lymphadenopathy."

In March 1986 the patient was seen in our clinic (1). He decided not to undergo 
chemotherapy. Vie requested and was started on IAA, 30 g twice per week. In April 1986, six weeks after the x-ray film and CT scan studies, the oncologist's report stated, 

". . . the patient returns feeling well. His exam is totally normal. His chest x-ray shows a dramatic improvement in pulmonary nodules compared to six weeks ago. The periaortic lymphadenopathy is completely resolved..., either he has had a viral infection with pulmonary lesions with lymphadenopathy that has resolved or (2) he really did have recurrent kidney cancer which is responding to your vitamin C therapy." 

The oncology report in July 1996 stated, "there is no evidence of progressive cancer. He looks well . . . chest x-ray today is totally normal. The pulmonary nodules are completely gone. There is no evidence of lung metastasis, liver metastasis or lymph node metastasis today, whatsoever."

In 1986 the patient received 30 g infusions twice-weekly for 7 months. The treatments were then reduced to once per week for 8 more months. For an additional 6 months he received weekly, 15 g IAA infusions. During and after treatments, the patient reported no toxicities, and his blood chemistry profiles and urine studies were normal.  The patient continued well, and was seen periodically at our clinic until early 1997 when he died, cancer-free, at age 82, 12 years after diagnosis.

Conclusion
We believe that IAA has potential as a chemotherapeutic agent. We hope our protocols for mixing and infusion of IAA, precautions to be taken before and during its use, and clinical case reports will justify further clinical trials and research with IAA for patients with metastatic disease. We do not believe it is a cure for all cancers. Although it shows promise as a sole therapy, particularly in renal cell carcinoma, it should be used primarily as an adjunct to other effective therapies.

Support
Our research is funded solely through donations from individuals. We have neither sought nor received funding from government agencies. We encourage readers to support our research. All donations to our 501 (C) 3 organization are tax-deductible.

Neil H. Riordan, PA-C
Hugh D. Riordan, M.D.
Ronald E. Hunninghake, M.D.

The Center for the Improvement of Human Functioning, International, Inc.
3100 N. Hillside Ave., Wichita, Kansas 67219

Acknowledgments: 
We would like to thank the Bio-Communications Research Institute scientific staff who contributed to this research: Neil Riordan, P.A.-C., Xiaolong Meng, MB.; Paul Taylor, B.S.; Jei Zhong, MB.; Kevin Alliston, MS.; and Joseph Casciari, Ph.D. We thank Don R. Davis, Ph.D., for editing this manuscript.

References
1. 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 Ortho Med 1990; 5: 5-7.

2. Riordan N, Jackson JA, Riordan HD. Intravenous vitamin C in a terminal cancer patient. J Ortho Med 1996; 11: 80-82.

3. Riordan NH, Riordan HD, Meng X, Li Y, Jackson JA. Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent. Med Hypotheses 1 995; 44: 207-2 13.

4. Cohen MH, Krasnow SH. Cure of advanced Lewis lung carcinoma (LL): A new treatment strategy. Proceedings of AA CR I 987; 28: 416.

5. Lupulesco A. Vitamin C inhibits DNA, RNA and protein synthesis in epithelial neoplastic cells. mdl Vit Nutr Res 1991; 61: 125-129.

6. Varga JM, Airoldi, L. Inhibition of transplantable melanoma tumor development in mice by prophylactic administration of Ca-ascorbate. Life Sciences 1983 ; 32: 1559-1564.

7. Pierson HE, Meadows GG. Sodium ascorbate enhancement of carbidopa-levodopa methyl ester antitumor activity against pigmented B-16 melanoma. Cancer Res 1983; 43: 2047-205 I.

8. Chakrabarti RN, Dasgupta PS. Effects of ascorbic acid on survival and cell-mediated immunity in tumor bearing mice. IRCS Med Sci 1984; 12: 1147-1 148.

9. Tsao CS, Dunham WB, Ping, YL. In vivo antineoplastic activity of ascorbic acid for human mammary tumor. In vivo 1988; 2: 147-150.

10. Campbell A, Jack T. Acute reactions to mega ascorbic acid therapy in malignant disease. Scot Med J 1979; 24: 151.

11. Wong K, Thomson C, Bailey RR, McDiarmid S, Gardner J. Acute oxalate 
nephropathy after a massive intravenous dose of vitamin C. Aust NZ J Med 1994: 24.

12. Hanson, J. Personal communication, December 1, 1997.

13. Rivers JM. Safety of high-level vitamin C ingestion. In: Third Conference on AA. Ann NY Acad Sci 1987; 498: 95-102.

14. Rattan V, Sidhu H, Vaidyanathan 5, Thind SK, Nath R. Effect of combined 
supplementation of magnesium oxide and pyridoxine in calcium-oxalate stone formers. (Irol Res 1994; 22: 161-5.

15. Prien EL, Gershoff S F. Magnesium oxide-pyridoxine therapy for recurrent calcium oxalate calculi. J Urol 1974; l 12: 509-512.

16. Riordan HD, Riordan NH, Meng X, Zhong Z, and Jackson JA. Improved microplate fluorometer counting of viable tumor and normal cells. Anticancer Res 1994: 927-932. 

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