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The Real Story o Vitamin C and Cancer

IntroductionIn the last couple o weeks, vitamin C

and cancer has become a hot news topic.For people who have ollowed this mat-ter, the medias sudden interest comesas something o a surprise: the evidencethat vitamin C is a selective anticanceragent has been known or decades. Thisstory is important, as it illustrates how

the head-in-the-sand conventional view(that nutritional supplements are useless)can lead to restrictive legislation, reducedhealth, and limited approaches to thetreatment o disease.

The recent news story arose rom astudy by researchers at the US NationalInstitutes o Health (NIH).1 The NIH ex-periment showed that, when injected intomice, vitamin C could slow the growth otumours. The NIH paper presents its nd-ings as new, ignoring the long history oresearch into vitamin C and cancer. Farrom being novel, many o the ndings re-ported in this paper have been recognizedor decades. What is strange, however, isthat the media suddenly decided to reporta story they had ignored or so long.

A HistoryOne strand o this story begins with

the work o an old riend, Dr. ReginaldHolman. In 1957, Holman published a paper in Nature about how hydrogenperoxide (the chemical Marilyn Monroereportedly used on her hair) destroyed orslowed the growth o tumours in mice.2Reg Holman met with some hostility romthe medical proession, which slowed hisresearch and clinical work over the ollow-ing hal century. Nevertheless, scientistshave known that hydrogen peroxide killscancer cells or over ty years.

In 1969, when man rst walked on themoon, researchers ound that vitamin Cwould selectively kill cancer cells withoutharming normal cells.3 That nding meantthat vitamin C was like an antibiotic orcancer: potentially a near perect antican-cer drug. Beore 1970, it was known thatvitamin C was an example o a new classo anticancer substances. However, the

medical research establishment largelyignored these scientic results.In the 1970s, some members o the

public and pioneering doctors experi-mented with high doses o vitamin C totreat cancer. By 1976, double Nobel Prize winner Linus Pauling and Scottish sur-geon Ewan Cameron reported clinicaltrials, showing an unparalleled increasein survival times in terminal cancer pa-tients treated with vitamin C.4 However,

by this time Pauling was considered aquack, having claimed that vitamin Ccould prevent or cure the common cold,so these apparently amazing indingsmade little impact.

Cameron and Pauling published asecond report in 1978.5 The Mayo Clinicresponded with a study that suggestedvitamin C had no eect, which the medi-cal proession readily accepted, perhaps

because it conrmed existing prejudices.However, despite the Mayo Clinic studybeing considered deinitive,1 it washighly criticized rom the start. In par-ticular, it used relatively low oral dosesor short periods, rather than the lietimecombination o high oral and intravenous(IV) doses in the Pauling and Cameronstudy. The Mayo Clinic reused to providePauling with their data so he could checkit. When we emailed the Mayo Clinic witha similar request, we received no reply.

I Cameron and Paulings work, backin the 1970s, had been just a single study,

Steve Hickey Ph.D.;1 Hilary Roberts, Ph.D.

1. FCET, Staordhire University, Beaconside, Sta-ord, England, ST16 9DG. [email protected]

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Journal o Orthomolecular Medicine Vol. 23, No. 3, 2008

it would have been interesting and sug-gestive. Such a large increase in survival

time demands a proper scientic ollow-up and, indeed, other studies soon backedup the indings. Japanese researchersound similar survival times,6 apparentlyconrming Paulings early results. Sub-sequently, Dr. Abram Hoer, workingin Canada, provided more evidence thatvitamin C could enable cancer patients tolive much longer. We have analyzed theseresults and ound them to be statisticallyvalid. They are not explicable by placebo

eect or by a simple biased selection olong-lived patients. Moreover, over thelast three decades, a large number o clini-cal and anecdotal patient reports supportthe claims.

A long time beore the NIHs mouseexperiment, Pauling also studied theeects o vitamin C on cancer in mice.He worked with Dr. Art Robinson but,unortunately, the two researchers ell out

over their interpretations o the results.Robinson let the Linus Pauling Institute(which he had helped establish) andcompleted the experiment alone. It waseventually published in 1994.7 The resultswere outstanding: mice with cancer thatwere given high dose vitamin C in the diet,or ed a diet o raw vegetables, lived up to20 times longer than controls. Translatedinto human terms, this might mean thata person with one year to live might get

an extra 20. Importantly, Robinson andPauling had been inspired to do this ex-periment by claims rom cancer suerersin the popular literature.

Doctors Hugh Riordan, Ron Hun-ninghake, Jim Jackson, Jorge Miranda-Massari, Michael Gonzalez and others inthe Center or the Improvement o HumanFunctioning, Inc., did the core researchon vitamin C and cancer. They repeated

and extended the early work, which hadshowed vitamin C would selectively killcancer cells. They have years o experienceo treating cancer patients with high dose

vitamin C. Their work is consistent withresults rom independent researchers and

doctors worldwide.8

The authors o this article recentlyreviewed the literature on vitamin C andcancer, in our bookCancer: Nutrition andSurvival.8 We ound solid evidence thatvitamin C, in high enough doses, acts asa selective anticancer drug. In healthytissues, vitamin C is an antioxidant, whilein cancer it acts as an oxidant generatingree radicals and killing the abnormalcells. Furthermore, an understanding o

its action provides insight into the can-cer development process. Oxidants, suchas hydrogen peroxide, are able to makecells grow and divide erroneously. So, asthe cells divide, they orm a populationo varying cells that compete with eachother or survival. It was immediately clearthat oxidation could explain how cancerstarts; ollowing which Darwins theory oevolution takes over. Given enough time,

cells divide and the ttest are selected.In this context, the ttest to survive arethose cells that grow rapidly to orm an in-vasive cancer. Cancer is not a mysteriousdisease but is a result o straightorwardbiological processes.

This microevolutionary model orcancer makes highly specic predictions.One is that high dose vitamin C should prevent cancer and even higher dosesshould kill cancer cells. The model also

predicts that there could be thousandso selective anticancer drugs. Animals,and especially plants, will contain thesesubstances, because they evolved in the presence o cancer and had to develop ways to control it. I such predictionsare correct, we should nd a multitudeo sae anticancer agents in ood. Check-ing against medical databases, we im-mediately ound numerous examples,

such as curcumin rom turmeric, alpha-lipoic acid, and vitamin D3. Everywherewe looked, we ound substances with thepredicted properties. Unortunately, many

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are the very supplements the Alliance orNatural Health (ANH) is trying to protect

rom being banned!To conclude our history, the NIHpaper was essentially a repeat o previousanimal experiments. Despite this, the NIHauthors appear not to have reerencedmany o the scientists who did the originalwork on vitamin C and hydrogen perox-ide in cancer. Instead, they present their work as standing alone, in an inorma-tional vacuum: with the exception o theCameron and Pauling clinical trial, the

original scientists work is not mentionedin the NIH text. Wrongly, a reader mightgain the impression that the NIHs work was undamentally original, rather thanrepeating the work o others. This mightmislead the media into ascribing creditor the work on vitamin C and cancer tothe NIH, which would be unair to the realpioneers o this subject.

Intravenous or Oral?Dr. Mark Levine o the NIH claimsthat When you eat oods containing morethan 200 milligrams o vitamin C a dayor example, 2 oranges and a serving obroccoliyour body prevents blood levelso ascorbate rom exceeding a narrowrange.9 This statement is demonstrablyalse (the NIHs own data reutes it) andis an arteact o the way the NIH groupinterpret their experiments.

In their mouse paper, the NIH usedintravenous vitamin C, rather than oral.To be more accurate, the NIH used in-travenous ascorbate. Sodium ascorbateis normally used or injection, as vitaminC (ascorbic acid) can cause local infam-mation at the injection site. The resultsthey obtained are suggestive o a response,but do not show the same large eectsreported by Robinson. Robinson ed his

mice dietary vitamin C, in very highdoses. Thus, the NIHs suggestion thatonly intravenous vitamin C is useul asan anticancer agent does not appear to t

the animal data. Likewise, the idea thatonly intravenous vitamin C is eective

against cancer does not t the clinicaldata. Abram Hoer, or example, used oraldoses and obtained essentially the sameresults as Cameron and Pauling.

The NIHs insistence that the body hastight controls, which prevent oral vita-min C rom unctioning as an anticanceragent, is wrong. In our bookAscorbate:The Science of Vitamin C,we have shownthat the NIH claims or blood saturationat a low level (70 M/L) are incorrect.10

The NIH authors never admitted this er-ror, despite a long email correspondencebetween Hickey and Levine. However,they have changed the wording they use,rom saturated to tight controls, andincreased the level by about three times(to 200 M/L). It would appear thatthey are holding onto an outdated ideaabout how vitamin C acts in the body.As an alternative, we have proposed a

dynamic fow model, in which, at highdoses, vitamin C fows through the body,providing antioxidant support, potentiallypreventing cancer growth and killing can-cer cells.11

Dynamic FlowDr. Mark Levine claims:

Clinical and pharmacokinetic stud-ies conducted in the past 12 years showedthat oral ascorbate levels in plasma and

tissue are tightly controlled. In the caseseries, ascorbate was given orally andintravenously, but in the trials ascorbatewas just given orally. It was not realizedat the time that only injected ascorbatemight deliver the concentrations neededto see an anti-tumor eect.9

As we have explained, there is noevidence or such tight control. The sug-gestion that the legendary scientist, Dr.

Linus Pauling, or consultant surgeon,Ewan Cameron, did not know the di-erence between oral and intravenousadministration12 is bizarre and, again,

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demonstrably incorrect.8 The dierencebetween oral and intravenous vitamin C

is, however, more complex than suggestedby the NIH. Contrary to their conclusions,it is not clear that intravenous vitamin Cnecessarily provides an advantage overoral supplements in the treatment ocancer. There is a air case or suggestingthat high dose oral administration couldbe more eective.

At low intakes, the body preventsvitamin C rom being lost through theurine; i this were not the case, we would

all be at risk o acute scurvy. The bodytries to retain a minimum o about70 M/L o vitamin C in blood plasma.This level can be maintained with anintake as low as 200 mg a day. At higherdoses, the body can aord to let some vi-tamin C escape in urine. This saves energy,which the kidneys would otherwise use tokeep pumping the vitamin C moleculesback into the blood. I dietary vitamin

C is in plentiul supply, there is no needor our bodies to retain it all. So, at highdoses, vitamin C fows through the body,being taken in rom the gut and excretedin the urine. With such high intakes, thebody has a reserve that it can call uponin times o need.

A single 5 gram dose o vitamin C cangenerate blood levels o about 250 M/L;this is above the NIH papers claimedmaximum o 200 M/L. Moreover, re-

peated large doses can sustain these levels.We have achieved vitamin C plasma levelsabove 400 M/L, ollowing a single dose ooral liposomal vitamin C.13 It seems thatthe claimed tight control concept willneed revising again soon.

People vary in their responses to vi-tamin C. In some people, a single 2 gramoral dose o vitamin C may have a laxativeeect. Our collaborator, Dr. Robert Cath-

cart, described this as the bowel tolerancelevel. Strangely, bowel tolerance has beenobserved to increase dramatically whena person is ill, say with the fu. A person

with a laxative eect at, say, 2 grams, maybe able to tolerate 100 times more i they

become ill. This increased bowel tolerancealso occurs in cancer suerers. It suggeststhat at times o stress or illness, the bodyabsorbs extra vitamin C. When promotingintravenous vitamin C, the NIH authorshave not considered the possibility o suchincreased bowel tolerance to oral doses.

To achieve the maximum bloodplasma levels possible with oral vitaminC, a typical healthy person may need atotal intake o about 20 grams, spread

throughout the day (say 3 or 4 grams everyour hours). However, cancer patients mayrequire ar more. Such massive intakesresult in consistently high blood levels,which tumour tissues absorb, and whichthen generate the hydrogen peroxide thatkills the cancer cells.

Other possible mechanisms or howvitamin C kills cancer cells14 are notcovered by the NIH study. The NIH base

their work on laboratory studies o mice,in which vitamin C kills cancer cells overthe course o, perhaps, a couple o hours.Lower levels o vitamin C may simply takelonger to kill the cells, which is a standarddose response relationship. Sustainedoral doses can increase plasma vitaminC consistently, over periods measured inmonths or years: this may, in the end, bemore eective that the short, sharp shocko intravenous therapy. Sustained levels

also reduce the likelihood o tumoursdeveloping resistance to the therapy(analogous to bacterial resistance to an-tibiotics.)

Redox synergyWhen combined with alpha-lipoic

acid, selenium, vitamin K3, or a rangeo other supplements, vitamin C is a armore powerul anticancer agent than

when used alone. Experimental data romRiordan and others shows that the cancerdestroying eect o such combinations ismuch higher. We have described some o

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these combinations in a recent book TheCancer Breakthrough.15 Strong scientic

reasons suggest that such combinations,given orally, could provide cancer suer-ers with a large increase in liespan andincreased quality o lie.

Just as your doctor advises you totake a whole course o antibiotics continu-ously, until all inection is gone, vitamin Cbased redox therapy needs to be continu-ous. Like bacterial inections, cancers canrapidly become resistant to intermittenttreatments. Typically, intravenous ascor-

bate is given at intervals, whereas oralascorbate can maintain blood levels con-tinuously and indenitely. This is a validmedical reason to preer an oral regime.Also, patients preer the oral route, as theyhave greater control, lower cost, and aremore involved in their treatment.

People oten ask us what we would do,i we developed the disease. In the eventthat one o us developed a malignancy,

we would opt or a vitamin C based redoxtherapy as our primary approach to treat-ment. This would be based on oral intakes:we would consider intravenous ascorbateonly as an adjunct. We might use liposo-mal vitamin C to sustain blood levels at400-500 M/L, together with alpha-lipoicacid, selenium, and other synergistic nutri-ents.15 While we realize malignant cancer would place us at high risk o death, we would expect to live a greatly extended

lie. While the assessment o increasedlongevity could be inaccurate (the data isnot denitive), the risks are small and thepotential benets substantial.

ConclusionsMark Levine claims that the NIHs

unique translational environment, whereresearchers can pursue intellectual high-risk, out-o-the-box thinking with high

potential payo, enabled us to pursuethis work.9However, the recent NIH study, while

interesting, adds little to the studies it

replicates. More interesting is the lack ohistorical perspective, which may detract

rom the people, such as Hugh Riordan,Abram Hoer, or Linus Pauling, who de-serve the credit or carrying out originalresearch, despite conventional medicineactively suppressing their work. Theground breaking work o doctors such asthose in the British Society or EcologicalMedicine, who have risked their careersto provide vitamin C based treatmentsor cancer and other conditions should berecognized. These pioneering doctors are

oten well aware o the scientic evidenceand should not be described as comple-mentary or alternative. Perhaps, oneday, the media will realize the true storyo vitamin C and cancer, and patients willhave the opportunity to benet.

The Alliance or Natural Health isdeending our right to supplements. Overthe last century, we have beneted roma large increase in lie expectancy and

reedom rom many diseases. Much othat benet has arisen directly rom nu-trition.16 We need access to supplements, which provide the possibility o disease prevention without signiicant risk. Ithis basic right is removed by CodexAlimentarius, or similar legislationorexample, the draconian regulatory mea-sures the natural health sector is acingin Europeeven pioneering doctors willnd it dicult to progress the nutritional

treatment o disease. The health o most ous will suer. We will get more illnesses,more oten, and options or medical treat-ment o major killers, such as cancer,heart disease, and stroke, will decline.

References1. Chen Q, Espey MG, Sun AY, et al: Pharmaco-

logic doses o ascorbate act as a prooxidantand decrease growth o aggressive tumorxenograts in mice, PNAS, 2008; 105(32):

1110511109.2. Holman RA: A method o destroying a ma-

lignant rat tumour in vivo, Nature, 1957;179(4568):1033.

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3. Benade L, Howard T, Burk D: Synergistickilling o Ehrlich ascites carcinoma cells byascorbate and 3-amino-1, 2, 4, -triazole, Oncol-

ogy, 1969; 23: 3343.4. Cameron E, Pauling L: Supplemental ascor-

bate in the supportive treatment o cancer:Prolongation o survival times in terminal hu-man cancer.Proc Natl Acad Sci USA, 1976; 73:36853689.

5. Cameron E, Pauling L: Supplemental ascor-bate in the supportive treatment o cancer:Reevaluation o prolongation o survival timesin terminal human cancer,Proc Natl Acad SciUSA, 1978; 75: 45384542.

6. Murata A, Morishige F, Yamaguchi H: Prolonga-

tion o survival times o terminal cancer patientsby administration o large doses o ascorbate,IntJ Vit Nutr Res, Suppl, 1982; 23: 101-113.

7. Robinson AR, Hunsberger A, Westall FC:Suppression o squamous cell carcinoma inhairless mice by dietary nutrient variation,Mech Aging Devel, 1994; 76: 201-214.

8. Hickey S, Roberts H: Cancer: Nutrition andSurvival, 2005; Lulu Press.

9. NIH News: Vitamin C Injections Slow Tumor

Growth in Mice, Embargoed or Release, Mon-day, August 4, 5:00 p.m. EDT. 2008.

10. Hickey S, Roberts H:Ascorbate: the Science ofVitamin C, 2004, Lulu Press.

11. Hickey S, Roberts H, Cathcart RF: Dynamicfow,J Orthomol Med, 2005; 20(4), 237-244.

12. Padayatty SJ, Levine M: Reevaluation o ascor-bate in cancer treatment: Emerging evidence,open minds and serendipity, J Am Coll Nutr,2000; 19(4): 423-425.

13. Hickey S, Roberts H, Miller NJ: (2008) Pharma-cokinetics o oral ascorbate liposomes,JNEM,

2008, (in press).14. Toohey JI: Dehydroascorbic acid as an anti-

cancer agent, Canc Lett, 2008; 263: 164169.15. Hickey S, Roberts HJ: The Cancer Break-

through, 2007, Lulu press.16. Wootton D:Bad Medicine, 2007, Oxord Uni-

versity Press.

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