clinical and experimental experiences

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Clinical and Experimental Experiences with Intravenous Vitamin C

For the p urp oses of this pap er referenceto a scorbic acid or v ita m in C refers to so-d ium ascorba t e . A ll i n v it ro s t ud i e s d e -scribed here in used sodium ascorbate . A l lintraven ou s vi tam in C referen ces herein re-fe r to t h e u se of v it a m in C for in ject io n p ro-du ced by Steri s Laboratories, or Am ericanRegen t la bora tories; b oth a re a scorb ic a cidbuf fered to a pH range of 5.5 to 7.0 by so-dium hydrox ide and /or sodium bicarbona te .

BackgroundVitamin C has potential as a chemo-

therapeutic agent. Rather than possessingadverse side effects as most chemotherapeu-tic drugs do, vitamin C has side benefits suchas increasing collagen production, and en-

hancing immune function.We began to study the effects of vita-

min C on cultured tumor cells in 1991. Wefound that vitamin C was preferentially toxicto tumor cellsit killed tumor cells beforekilling normal cells. This phenomenon firstcame to our attention through the work ofBenade et al in 1969.1 They theorized thatthe preferential toxicity was due to the rela-tive deficiency of catalase in tumor cells.This theory has since been validated by oth-ers.2 Our early findings on preferential vita-min C toxicity were published in 1994.3 Inthat paper we also described a so called se-rum effect; vitamin Cs toxicity was reducedby the presence of human serum. Serumsinhibitory effects led us to the conclusionthat the concentrations of vitamin C whichwere toxic to tumor cells in our early stud-

ies (5 to 50 mg/dL) would not necessarilybe toxic in vivo.

We therefore began a series of experi-ments in which we tried more closely tomimic the in v ivo tumor micro-environ-

ment. In particular we began testing fortoxicity of vitamin C toward cultured tumorcell lines using dense monolayers and hol-low fiber tumor models to mimic the threedimensionality of tumors. We used humansera as culture media to include the seruminhibitory activity seen in previous assays.Using these new culture conditions wefound that the cytotoxic concentration ofvitamin C for most human tumor cell lineswas indeed much higher than previouslydescribed. (Figure 1, p. 202).

Human Vitamin C Pharm acokineticsGiven the information that higher con-

centrations of vitamin C were required tobecome cytotoxic to tumor cells, we needed

to learn more about the pharmacokineticsof vitamin C. There were no data on theconcentrations of vitamin C that wereachievable in human beings after high-doseintravenous vitamin C. We therefore begana series of experiments to yield data formodeling pharmacokinetics of high dosesof vitamin C.

We gave a series of vitamin C infusionsto a 72 year old male who was in excellentphysical condition except for slowly pro-gressing, non-metastatic carcinoma of theprostate. Before the infusions, and at in-tervals thereafter, blood was drawn from aheparin lock (not the site of infusion). Theplasma was separated and analyzed forplasma vitamin C concentration using amicroplate-based 2,6-dichlorophenol-indo-phenol assay. Some of the results are given

in Figure 2, (p. 202). From this experimentwe observed that a 30 gram infusion wasnot adequate to raise plasma levels of vita-min C to a level that was toxic to tumorcells (>200 mg/dL for dense monolayersand >400 mg/dL for hollow fiber models).Infusion of 60 grams resulted in a brief (30

Clinical and Experimental Experienceswith Intravenous Vitamin C

Ne il H. Riordan , PA-C;1 Hug h D. Riordan, M.D.;1 Jo se ph P. Casc iari, Ph .D.1

1. Bio-Communications Research Institute, 3100 N. Hill-

side Ave, Wichita, KS 67219.


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Journal of Orthomolecular Medicine Vol. 15, No. 4, 2000

Figure 1. Vitamin C toxicity toward human colon cancer cells in different models.

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Figure 2. Effects of 15, 30, 60, and 65 grams of ascorbate infused over various times onplasma ascorbate concentration in a 72-year-old man.

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min) elevation of plasma levels of vitaminC above 400 mg/dL, while 60 grams infusedover 60 minutes immediately followed by

20 grams infused over the next 60 minutesresulted in a 240 minute period in whichthe vitamin C plasma concentration wasnear or above 400 mg/dL.

Ascorbate Pharmacokinet icsUsing data from the above experi-

ments we designed a two-compartmentmodel with four adjustable parameters (VP,KX, K1, K2) to fit the data. The model sche-

matic and the data fit are shown in theaccompanyingFigure 3 (below). The pa-rameter KX represents the rate of excre-tion of ascorbate out of the blood (renalexcretion), while parameter K1 representsthe rate of diffusion of ascorbate from theblood into tissue and K2 represents the dif-fusion rate for return of ascorbate to theblood stream from the tissue compart-

ment.We used this two compartmentmodel to obtain kinetic parameters fromeach of the in vivo vitamin C experimentswhere sufficient time-concentration datawere obtained. We first fitted all four pa-rameters, then fixed the blood plasmavolume at 30 dL (near the average valuefor all experiments) and floated the threeK values. Results are given in Table 1

(p.204). The average parameter values for

all experiments are shown in Table 2 (p.204) To see if there was any systematicvariation in Table 2 parameter values over

time, the parameter KX, and the ratio K2/K1 for each experiment were plottedagainst time. The excretion constant, KX,was remarkably uniform, as was the ratioK2/K1 (Figure 4, p. 205). The tissue up-take rate constant, K1, did vary, but not ina systematic way. We use the ratio K2/K1to point out that while K2 also varies, itsvariation merely compensates for varia-tions in K1. We conclude from this analy-

sis that the pharmacokinetic parametersof the subject did not change over a onemonth period of regular ascorbate infu-sions.

Other Pharm acokinetic Stu diesWe plotted data points from three re-

cent studies (over a three month period)against the theoretical curve obtained us-

ing the average parameter values givenabove. The results are shown in (Figure 5,p. 205). Clearly, there was excellent agree-ment between the theoretical curve andthe recent data, suggesting the ascorbatepharmacokinetics for this subject were thesame over the three month treatment pe-riod. This further supports the conclusionthat the ascorbate transport parametersfor a given subject remain relatively con-

stant during the time of treatment.

Injection

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K2 K1

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VP, CP(t)

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Figure 3. Two compartment model.


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Computer Protocol SimulationsA program was then constructed to

predict the plasma ascorbate levels in vari-ous protocols based on the pharmaco-ki-netic parameters obtained above. Threeprotocols were simulated:

A) 1 hour at 60 g/hrB) 2 hours at 60 g/hrC) 1 hour at 60 g/hr, then 6 hours at 10 g/hr

Predicted plasma ascorbate levelsfor these protocols are shown in Figure 6(p.206). Prolonged infusions at higher

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Dose (g) 15 30 60 30 60 65 65 65 65

Infusion 45 80 160 40 80 60 60 60 60

min

Kx(min -1) 0.026 0.027 0.024 0.025 0.022 0.025 0.022 0.023 0.027

excretion

K1(min-1) 0.195 0.214 0.653 0.307 0.124 0.447 0.200 0.150 0.884

tissue adsorb

K2(min-1) 0.066 0.060 0.165 0.091 0.038 0.141 0.062 0.040 0.235

tissue efflux

K2/K1 0.337 0.279 0.253 0.296 0.302 0.317 0.310 0.265 0.266

efflux/adsorb

Max CP 125.7 186.1 285.3 233.3 417.8 458.4 495.0 472.8 397.2

mg/dL

Ave. (1-8hr) 37.3 70.6 150.1 76.0 165.4 167.6 185.4 221.5 151.9

CP mg/dL

Table 2. Average parameter values.

Table 1. Ascorbate pharmacokinetics in v ivo.

Kx 0.025 0.002K1 0.353 0.261K2 0.100 0.067K2/K1 0.292 0.028

Parameter Mean SD


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doses obviously give the highest peak val-ues, while a trickle infusion can be used

to maintain plasma levels at a desired level.This computer simulation can be auseful tool for examining what plasmalevels we can expect from variousprotocols, once the pharmacokinetics fora given subject are known from an ini-tial experiment.

Effects of Human Serum Obtained fromSubject Receiving Intravenous Vitamin C

on Tum or Cell GrowthTo study more closely the probabilityof in vivo cytotoxic effects of intravenousvitamin C we planned and performed thefollowing experiment. Dense monolayersof human prostate tumor cells (PC-3 fromATCC) were created in microplates. A pa-

Figure 4. Pharmacokinetic variation in parameter values over time.

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Figure 5. Plotted data points from three recent studies against thetheoretical curve based on figure four values.

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tient with carcinoma of the prostate wasgiven 65 grams of intravenous vitamin C(in 500 cc sterile water for injection) over65 minutes. Serum separator blood tubeswere drawn before the infusion and at in-tervals thereafter from a heparin lock sepa-rate from the infusion site. The final blooddraw was five hours after the infusion be-gan. Some of the collected serum was thentested for vitamin C concentration, and therest was heat-inactivated and used as cul-ture media for the prostate tumor cells. Thecells were incubated for five days when thenumbers of viable tumor cells were deter-

mined using a previously describedcarboxy-fluorescein diacetate/microplatefluorometer viable cell determinationmethod. The results of the experiment aregraphed in Figure 7 (p.207). Greater than97% cytotoxicity was observed for the serumsamples taken at 35, 65, and 95 minutes af-

ter the beginning of the IV vitamin C. Dur-ing those periods the serum concentrationwas greater than 400 mg/dL. After that timethe toxicity decreased. The last sampletaken (vitamin C concentration 213 mg/dL)resulted in 64% inhibition compared to thecontrols.

Potentiation of Preferential Toxicity ofVitam in C

Because plasma concentrations of vita-min C of greater than 200 mg/dL are prob-lematic to maintain, we began looking forways to increase the sensitivity of tumor cells

to vitamin C. During experimentation wefound that lipoic acid (a water and lipid solu-ble antioxidant that recycles vitamin C) canenhance the tumor toxic effects of vitaminC. Figure 8(p.208) illustrates dose responseof tumor cells in a hollow fiber tumor modelexposed to vitamin C with and without lipoic

Figure 7. Effects of human serum removed from patient before and at intervalsafter intravenous infusion of vitamin C (60 grams) on cultured human

prostate tumor cells.

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acid. Lipoic acid decreased the dose of vita-min C required to kill 50% of the tumor cellsfrom 700 mg/dL to 120 mg/dL.

Effects of High-Dose Vitamin C onTumor Cell Collagen Production

It is well known that vitamin C is re-quired for the hydroxylation of proline, andthat low levels of vitamin C can be a lim-iting factor in the production of colla-

gen. Because many tumor cells producecollagenase and other proteolytic en-zymes, we wanted to determine if vita-min C supplementation would increasecollagen production by tumor cells,thereby having a balancing effect on col-lagenase. In an experiment, we supple-

mented cultured tumor cells with vita-min C concentrations that are achievablewith oral supplementation (2 and 4 mg/dL) and measured the collagen producedusing a well-known method.5 We foundthat indeed, these concentrations of vi-tamin C greatly increased the productionof collagen. Data are summarized in Fig-ure 9,p.209. It is interesting to note thatwhen we performed cytotoxicity assays

of vitamin C against the PC-3 humanprostate carcinoma cell lines using con-centrations as high as 300 mg/dL, wewere unable to detach remaining live cellsfrom the tissue culture flasks usingtrypsin/EDTA. In some cases severaldays of treatement with high concentra-

Figure 8. Effect of lipoic acid on ascorbate efficiency: SW620 human coloncarcinoma cells grown as hollow fiber solid in vitro tumors exposed for 48 hours to

sodium ascorbate alone or in combination with lipoic acid sodium (combo 10:1).

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tions of collagenase were required todetach the cells. One of us remembersliterally chipping cells off the plasticflasks. Prostate tumor cells are very re-sistant to high doses of vitamin C. It maybe that they are so rapidly using the vita-min C for collagen production that itdoesnt have as much residence time as inother cell lines, and is therefore less toxic.Of clinical note is that we have several pa-tients diagnosed with prostate cancer whohave taken continuous large oral doses ofvitamin C for many years and do notprogress to metastatic disease, despite arelatively large intracapsular tumor bur-den. Perhaps their tumor cells are gluingthemselves in place by high collagen pro-

duction.

Clinical ExperiencesWe have not observed toxic reactions

to high-dose intravenous vitamin C. Allpatients are pre-screened for glucose-5-phosphate dehydrogenase deficiency.

Patients with Renal Cell CarcinomaTreated with Intravenous Vitamin C

One of us (HDR) reported positive ef-fects of vitamin C therapy in a patient withadenocarcinoma of the kidney in 1990.4

This report described a 70-year-old whitemale diagnosed with adenocarcinoma ofhis right kidney. Shortly after right ne-phrectomy, he developed metastatic le-sions in the liver and lung. The patientelected not to proceed with standard meth-ods of treatment. Upon his request, hebegan intravenous vitamin C treatment,starting at 30 grams twice per week. Sixweeks after initiation of therapy, reportsindicated that the patient was feeling well,his exam was normal, and his metastases

were shrinking. Fifteen months after ini-tial therapy, the patients oncologist re-ported the patient was feeling well with ab-solutely no signs of progressive cancer. Thepatient remained cancer-free for 14 years.He died of congestive heart failure at theage of 84. A second case study, published

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in 1998,5 described another complete remis-sion in a patient with metastatic renal cellcarcinoma. The patient was a 52-year-oldwhite female from Wisconsin diagnosedwith non-metastatic disease in September1995. In October 1996, eight metastaticlung lesions were found: seven in the rightlung and one in the left (measuring be-tween 1-3 cm). The patient chose not to

undergo chemotherapy or radiation treat-ments. The patient was started on intra-venous vitamin C and specific oral nutri-ent supplements to correct diagnosed de-ficiencies and a broad-spectrum oral nu-tritional supplement in October, 1996. Theinitial dose of intravenous vitamin C was15 grams, subsequently increased to 65grams after two weeks. The patient was

given two infusions per week. Intravenousvitamin C treatments were continued un-til June 6, 1997. An x-ray taken at that timerevealed resolution of all but one lungmetastases. The patient discontinued intra-venous vitamin C infusions at that time andcontinued taking the broad-spectrum oral

nutritional supplement. A radiology reporton a chest x-ray taken January 15, 1998, statedthat no significant infiltrate was evident, andthere was resolution of the left upper lobelung metastasis. In February, 1999 a chest x-ray showed no lung masses, and the patientreported being well at that time.

Combined Intravenous Vitamin C and

Chemotherapy in a Patient with Stage IVColorectal Carcinoma

In April, 1997, a 51-year-old white malefrom Wichita, Kansas was first seen at ourcenter. He was well other than having typeII diabetes until the previous fall when hedeveloped painless bright red rectal bleed-ing. A work-up demonstrated the presenceof a distal colon lesion. On December 31,

1997 he underwent an anterior colon re-section and appendectomy at a local hos-pital. The colon tumor penetrated throughthe bowel wall and into the surroundingpericolonic adipose tissue. Two large he-patic metastases were discovered at thetime of surgery; one was biopsied. Pathol-

Figure 9. Effects of Vitamin C supplementation on collagen production bytumor cells.

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ogy revealed that the colon lesion was amoderately differentiated adenocarcinoma,and the liver biopsy was metastatic adeno-carcinoma. Following surgery he receivedchemotherapy with weekly 5-FU and leu-covorin for twelve cycles with a decreasein his CEA from 90.2 to 67.7. The patientand his wife, who is an R.N., asked thechemotherapist about getting intravenousvitamin C along with the chemotherapy.The oncologist informed them that vitaminC would not be of any value.

The patient was then seen at PittsburgUniversity hospital on May 13, 1997 wherehe underwent liver resection to segmentsthree and five. During surgery, the stom-

ach was mobilized off the inferior surfaceof the liver and a frozen section of this areawas taken and confirmed metastatic ad-enocarcinoma. The pathology reportshowed metastatic carcinoma consistentwith colon primary within the desmoplas-tic tissue and adjacent hepatic parenchyma

from the stomach wall and liver. Segmentsthree and five both contained multiple nod-ules. His CEA was 9.8 post surgery. ThePittsburg University oncologist informedhim his prognosis was very poor and thathe should go home and begin chemotherapyagain. He and his wife asked this oncologistif he should use intravenous vitamin C. Heresponded, I know of no studies whichshowed that this [vitamin C] would eradi-cate or delay progression of cancer.

In spite of the two no-confidence rec-ommendations for the use of intravenousvitamin C, The patient returned to ourcenter for infusions after recovering fromsurgery in June, 1997. He also began re-

ceiving weekly 5-FU (1100 mg) and Leu-covorin (1300 mg) treatments adminis-tered by his local oncologist. His first vita-min C infusion was 15 grams over one hour.The dose was gradually increased duringbi-weekly infusions. On September 9, 1997,a post-intravenous vitamin C (100 gram in

Figure 10. Patient with cancer of the pancreas.

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1000 cc sterile water infused over 2 hours)plasma concentration of vitamin C was 355mg/dL. He was then started on intrave-

nous vitamin C, 100 grams, twice weekly. Hiswife gave most of these infusions at home.In addition to the vitamin C, he was givenrecommendations for oral vitamin and min-eral supplementation to increase levels ofnutrients that he was found to be low in.

He kept up his vitamin C infusions untilFebruary, 1998 when he traveled to Floridafor a vacation. While on vacation he con-tinued the 5-FU/Leucovorin injections. Af-

ter a two weeks hiatus from the vitamin Cinfusions he began to experience nausea,diarrhea, stomach pain, and stomatitis; com-mon side effects of 5-FU. The side effectsstopped when he restarted intravenous vi-tamin C. He continued on chemotherapyand 100 gm bi-weekly intravenous vitaminC until April 1, 1998. Other than the briefperiod of side-effects mentioned above, he

had no other side effects during the year ofchemotherapy. He never experiencedleukopenia, thrombocytopenia, or anemia.

During April, 1998 we began to taperhis intravenous vitamin C. The doses were:75 grams, one time per week for 2 months;then 75 grams, one time every other weekfor 2 months; then 75 grams, on time everymonth for two months; and then 50 grams,one time per month for 6 months. The

patients CEA dropped into the normalrange on July 31, 1997, and has remainednormal (


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active again. The evidence also suggestthat intravenous vitamin C was workingindependently of the chemotherapy given

the CA-19-9 level continued to decreaseafter chemotherapy was discontinued.This patient died at home on July 4th,1998.

Resolut ion of non -Hodgkins Lym-phom a with Intravenou s Vitamin C-2Cases

A 66 year old white female was diag-nosed with a large peri-spinal (L4-5) ma-

lignant, non-Hodgkins lymphoma (diffuselarge cleaved cell of B-cell lineage) in Janu-ary, 1995. Her Oncologist recommendedlocalized radiation therapy andAdriamycin-based chemotherapy. She be-gan localized radiation therapy five daysper week for five weeks on 1/17/95, butrefused chemotherapy. On 1/13/95 shewas started on intravenous vitamin C, 15

grams in 250 cc Ringers Lactate two timesper week which she continued after com-pleting the radiation therapy. She alsobegan taking several oral supplements toreplace those found to be deficient bylaboratory testing, and empirical co-en-zyme Q10, 200 mg BID. She was also suc-cessfully treated at that time for an intes-tinal parasite. On May 6, 1995 she returnedto her oncologist with swelling and pain-

ful supraclavicular lymph nodes. Onelymph node was removed and found tocontain malignant lymphoma cells. Inspite of recommendations for chemo-therapy and more radiation, she refusedand continued with her intravenous vita-min C and oral regimen. Within six weeksthe supraclavicular nodes were barely no-ticeable. She continued intravenous vita-

min C infusions until December 24, 1996.She has been followed with regular physi-cal exams and has had no recurrence.During a telephone follow-up on 3/23/99she was well without recurrence. Com-ment: This case is rarethe patient re-fused chemotherapy, which in all likeli-

hood would have been curative. She alsohad a so-called recurrence of her lym-phoma during intravenous vitamin C

therapy months after her radiationtherapy had ended. The possibility existsthat the lymphoma cells in her lymphnodes were there at the initial diagnosisand the adenopathy occurred during im-mune recognition of those cells. Also ofnote is the fact that this patient receivedonly 15 grams of vitamin C per infusion.According to our model, this in not a highenough dose to achieve cytotoxic concen-

trations of vitamin C in the blood. There-fore, any effect of vitamin C could only beattributed to its biological response modi-fication characteristics.

In Fall 1994 a 73-year-old white malefarmer from Western Kansas was diagnosedwith wide-spread non-Hodgkins lym-phoma. Biopsies and CT-scan revealed bi-lateral tumor involvement in his anterior

and posterior cervical, inguinal, axillary andmediastinal lymph node beds. Bone mar-row aspirate was negative for malignantcells. He was treated with chemotherapy for8 months that resulted in remission. In July,1997 he began losing weight (30 lbs). He re-turned to his oncologist and a CT-scan atthat time showed recurrence. He was placedon chemotherapy in September, 1997. In De-cember, 1997 he developed leukopenia and

then extensive left sided Herpes Zoster. Asa result the chemotherapy was stopped. InMarch, 1998 he became a patient at ourCenter and began receiving intravenous vi-tamin C and oral nutrient supplements in-cluding lipoic acid. His vitamin C dose wasescalated until he was receiving 50 gramsin 500 cc sterile water two times per week.He continued on that dose for 11 months.

Three months after beginning vitamin Ctherapy a CT-scan showed no evidence tomalignancy. Another CT-scan in February,1999 was also clear and he was declared tobe in complete remission by his oncologist.Also of note is that this patient was ad-dicted to sleeping pills when first seen at


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our center. After three months of intrave-nous vitamin C therapy he replaced thesleeping pills with Kava tea.

Intravenous Vitamin C in a Patient withEnd-Stage Metastatic Breast Carcinoma

In 1995 a hospitalized 68 year oldwomen with widely metastatic end-stagebreast cancer was seen.6 Her latest bonescan showed metastases to nearly everybone in her skeleton. She was experienc-ing bone pain which was not controlledwith narcotics. At the time of her first con-sultation she had blood clots in both sub-

clavian veins, and shortly thereafter con-tracted cellulitis in her left arm and handsecondary to an errant arterial blood draw.After the blood clots were treated withActivase R, she was placed on intravenousvitamin C, 30 grams per day intially, in-creasing to 100 grams per day over fivehours. Within one week, the once bed-bound patient began walking the halls of

the hospital. Several hospital staff reportedthat she looked like a new person. Her cel-lulitis cleared, and she was discharged fromthe hospital. At home she received 100grams of intravenous vitamin C three timesper week. Three months after starting thevitamin C therapy a bone scan revealedresolution of several skull metastases. Sixmonths after starting the vitamin C, she fellwhile shopping at a mall, and subsequently

died of complications from pathologicalfractures.

ConclusionWe have presented evidence that vita-

min C may be useful in the treatment ofcancer. In particular we have produced thefollowing evidence: Vitamin C is toxic totumor cells. Concentrations of vitamin C

that kill tumor cells can be achieved inhumans using intravenous vitamin C infu-sions. Infusion of a bolus of vitamin C fol-lowed by slow infusion can result in sus-tained concentrations of vitamin C in hu-man plasma. Modeling of vitamin C phar-macokinetics can accurately predict

plasma concentrations of vitamin C usingvaried infusion protocols. Lipoic acid en-hances vitamin C induced tumor cell tox-

icity. Vitamin C in blood concentrationsachievable through oral supplementation iscapable of increasing collagen productionby tumor cells. Vitamin C in doses up to 50grams per day, infused slowly, are not toxicto cancer patients. Some cancer patientshave had complete remissions after high-dose intravenous vitamin C infusions. Con-centrations of vitamin C that kill mosttumor cells are not achieved after infusionof 30 grams of vitamin C. Therefore, re-missions in patients treated with this doseof vitamin C are likely to have occurred asa result of vitamin C induced biologicalresponse modification effects rather thanits cytotoxic effects.

References1. Benade L, Howard T, Burk D: Synergistic kill-

ing of Ehrlich ascites carcinoma cells by ascor-bate and 3-amino-1, 2, 4-triazole. Oncology ,1969; 23: 33-43.

2. Maramag C, Menon M, Balaji KC, Reddy PG,Laxmanan S: Effect of vitamin C on prostatecancer cells in vitro: effect on cell number, vi-ability, and DNA synthesis. Prostate, 1997; 32:188-95.

3. Riordan NH, et al: Intravenous ascorbate as atumor cytotoxic chemotherapeutic agent. M edHyp ot h , 1994; 9: 207-213.

4. Riordan HD, Jackson JA, Schultz M: Case study:

High-dose intravenous vitamin C in the treat-ment of a patient with adenocarcinoma of thekidney. J Or th om ol M ed , 1990; 5: 5-7.

5. Riordan HD, Jackson JA, Riordan NH, SchultzM: High-dose intravenous vitamin C in thetreatment of a patient with renal cell carcinomaof the kidney. J Or th om ol M ed , 1998; 13: 72-73.

6. Riordan N, Jackson JA, Riordan HD: Intravenousvitamin C in a terminal cancer patient. JOrthom ol Med , 1996; 11: 80-82.

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