The Real Story of Vitamin C and CancerSteve Hickey Ph.D.;' Hilary Roberts, Ph.D.

IntroductionIn the last couple of weeks, vitamin C

and cancer has become a hot news topic.For people who have followed this mat-ter, the media's sudden interest comesas something of a surprise: tbe evidencethat vitamin C is a selective anticanceragent has been known for decades. Tbisstory is important, as it illustrates howthe bead-in-tbe-sand conventional view(tbat nutritional supplements are useless)can lead to restrictive legislation, reducedbealtb, and limited approacbes to tbetreatment of disease.

Tbe recent news story arose from astudy by researcbers at the US NationalInstitutes of Health (NIH).' Tbe NIH ex-periment sbowed tbat, wben injected intomice, vitamin C could slow tbe growtb oftumours. Tbe NIH paper presents its find-ings as new, ignoring tbe long bistory ofresearcb into vitamin C and cancer. Farfrom being novel, many of tbe findings re-ported in tbis paper bave been recognizedfor decades. Wbat is strange, bowever, istbat tbe media suddenly decided to reporta story tbey had ignored for so long.

A HistoryOne strand of tbis story begins witb

tbe work of an old friend. Dr. ReginaldHolman. In 1957, Holman publisbed apaper in Nature about bow bydrogenperoxide (tbe cbemical Marilyn Monroereportedly used on ber bair) destroyed orslowed tbe growtb of tumours in mice.^Reg Holman met witb some bostility fromtbe medical profession, wbicb slowed bisresearcb and clinical work over tbe follow-ing balf century. Nevertbeless, scientistsbave known tbat bydrogen peroxide killscancer cells for over fifty years.

1. FCET, Stañbrdhire University, Beaconside, Staf-ford, England, ST16 9DG. s.hickey@staffs.ac.uk

In 1969, wben man first walked on tbemoon, researcbers found tbat vitamin Cwould selectively kill cancer cells witboutbarming normal cells.^ Tbat finding meanttbat vitamin C was like an antibiotic forcancer: potentially a near perfect antican-cer drug. Before 1970, it was known tbatvitamin C was an example of a new classof anticancer substances. However, tbemedical researcb establisbment largelyignored tbese scientific results.

In tbe 1970s, some members of tbepublic and pioneering doctors experi-mented witb bigb doses of vitamin C totreat cancer. By 1976, double Nobel Prizewinner Linus Pauling and Scottisb sur-geon Ewan Cameron reported clinicaltrials, sbowing an unparalleled increasein survival times in terminal cancer pa-tients treated witb vitamin C ' However,by tbis time Pauling was considered aquack, baving claimed tbat vitamin Ccould prevent or cure tbe common cold,so tbese apparently amazing findingsmade little impact.

Cameron and Pauling publisbed asecond report in 1978.̂ Tbe Mayo Clinicresponded witb a study tbat suggestedvitamin C bad no effect, wbicb tbe medi-cal profession readily accepted, perbapsbecause it confirmed existing prejudices.However, despite tbe Mayo Clinic studybeing "considered definitive,"' it wasbigbly criticized from tbe start. In par-ticular, it used relatively low oral dosesfor sbort periods, ratber tban tbe lifetimecombination of bigb oral and intravenous(IV) doses in tbe Pauling and Cameronstudy. Tbe Mayo Clinic refused to providePauling witb tbeir data so be could cbeckit. Wben we emailed tbe Mayo Clinic witba similar request, we received no reply.

If Cameron and Pauling's work, backin tbe 1970s, bad been just a single study.

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it would have been interesting and sug-gestive. Such a large increase in survivaltime demands a proper scientific follow-up and, indeed, other studies soon backedup the findings. Japanese researchersfound similar survival times,** apparentlyconfirming Pauling's early results. Sub-sequently, Dr. Abram Hoffer, workingin Canada, provided more evidence thatvitamin C could enable cancer patients tolive much longer. We have analyzed theseresults and found them to be statisticallyvalid. They are not explicable by placeboeffect or by a simple biased selection oflong-lived patients. Moreover, over thelast three decades, a large number of clini-cal and anecdotal patient reports supportthe claims.

A long time before the NIH's mouseexperiment, Pauling also studied theeffects of vitamin C on cancer in mice.He worked with Dr. Art Robinson but,unfortunately, the two researchers fell outover their interpretations of the results.Robinson left the Linus Pauling Institute(which he had helped establish) andcompleted the experiment alone. It waseventually published in 1994.' The resultswere outstanding: mice with cancer thatwere given high dose vitamin C in the diet,or fed a diet of raw vegetables, lived up to20 times longer than controls. Translatedinto human terms, this might mean thata person with one year to live might getan extra 20. Importantly, Robinson andPauling had been inspired to do this ex-periment by claims from cancer sufferersin the popular literature.

Doctors Hugh Riordan, Ron Hun-ninghake, Jim Jackson, Jorge Miranda-Massari, Michael Gonzalez and others inthe Center for the Improvement of HumanFunctioning, Inc., did the core researchon vitamin C and cancer. They repeatedand extended the early work, which hadshowed vitamin C would selectively killcancer cells. They have years of experienceof treating cancer patients with high dose

vitamin C. Their work is consistent wdthresults from independent researchers anddoctors worldwide.̂

The authors of this article recentlyreviewed the literature on vitamin C andcancer, in our book Cancer: Nutrition andSurvival.^ We found 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 generatingfree radicals and killing the abnormalcells. Furthermore, an understanding ofits 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 form a populationof varying cells that compete with eachother for survival. It was immediately clearthat oxidation could explain how cancerstarts; following which Darwin's theory ofevolution takes over. Given enough time,cells divide and the "fittest" are selected.In this context, the fittest to survive arethose cells that grow rapidly to form an in-vasive cancer. Cancer is not a mysteriousdisease but is a result of straightforwardbiological processes.

This microevolutionary model forcancer makes highly specific predictions.One is that high dose vitamin C shouldprevent cancer and even higher dosesshould kill cancer cells. The model alsopredicts that there could be thousandsof selective anticancer drugs. Animals,and especially plants, will contain thesesubstances, because they evolved in thepresence of cancer and had to developways to control it. If such predictionsare correct, we should find a multitudeof safe anticancer agents in food. Check-ing against medical databases, we im-mediately found numerous examples,such as curcumin from turmeric, alpha-lipoic acid, and vitamin D3. Everywherewe looked, we found substances with thepredicted properties. Unfortunately, many

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are the very supplements the Alliance forNatural Health (ANH) is trying to protectfrom being banned!

To conclude our history, the NIHpaper was essentially a repeat of previousanimal experiments. Despite this, the NIHauthors appear not to have referencedmany ofthe scientists who did the originalwork on vitamin C and hydrogen perox-ide in cancer. Instead, they present theirwork as standing alone, in an informa-tional vacuum: with the exception of theCameron and Pauling clinical trial, theoriginal scientists' work is not mentionedin the NIH text. Wrongly, a reader mightgain the impression that the NIH's workwas fundamentally original, rather thanrepeating the work of others. This mightmislead the media into ascribing creditfor the work on vitamin C and cancer tothe NIH, which would be unfair to the realpioneers of this subject.

Intravenous or Oral?Dr. Mark Levine of the NIH claims

that "When you eat foods containing morethan 200 milligrams of vitamin C a day-for example, 2 oranges and a serving ofbroccoli-your body prevents blood levelsof ascorbate from exceeding a narrowrange."' This statement is demonstrablyfalse (the NIH's own data refutes it) andis an artefact of 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 for injection, as vitaminC (ascorbic acid) can cause local inflam-mation at the injection site. The resultsthey obtained are suggestive of a response,but do not show the same large effectsreported by Robinson. Robinson fed hismice dietary vitamin C, in very highdoses. Thus, the NIH's suggestion thatonly intravenous vitamin C is useful asan anticancer agent does not appear to fit

the animal data. Likewise, the idea thatonly intravenous vitamin C is effectiveagainst cancer does not fit the clinicaldata. Abram Hoffer, for example, used oraldoses and obtained essentially the sameresults as Cameron and Pauling.

The NIH's insistence that the body has"tight controls," which prevent oral vita-min C from functioning as an anticanceragent, is wrong. In our book Ascorbate:The Science of Vitamin C, we have shownthat the NIH claims for blood "saturation"at a low level (70 |i M/L) are incorrect.'"The NIH authors never admitted this er-ror, despite a long email correspondencebetween Hickey and Levine. However,they have changed the wording they use,from "saturated" to "tight controls," andincreased the level by about three times(to 200 \iM/L). It would appear thatthey are holding onto an outdated ideaabout how vitamin C acts in the body.As an alternative, we have proposed adynamic now model, in which, at highdoses, vitamin C flows through the body,providing antioxidant support, potentiallypreventing cancer growth and killing can-cer cells."

Dynamic FlowDr. Mark Levine claims:

"Clinical and pharmacokinetic stud-ies conducted in the past 12 years showedthat oral ascorbate levels in plasma andtissue 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 effect."'

As we have explained, there is noevidence for such tight control. The sug-gestion that the legendary scientist. Dr.Linus Pauling, or consultant surgeon,Ewan Cameron, did not know the dif-ference between oral and intravenousadministration'^ is bizarre and, again.

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demonstrably incorrect." The differencebetween oral and intravenous vitamin Cis, 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 ofcancer. There is a fair case for suggestingthat high dose oral administration couldbe more effective.

At low intakes, the body preventsvitamin C from being lost through theurine; if this were not the case, we wouldall be at risk of acute scurvy. The bodytries to retain a minimum of about70 \M/L of vitamin C in blood plasma.This level can be maintained with anintake as low as 200 mg a day. At higherdoses, the body can afford 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. If dietary vitaminC is in plentiful supply, there is no needfor our bodies to retain it all. So, at highdoses, vitamin C flows through the body,being taken in from the gut and excretedin the urine. With such high intakes, thebody has a reserve that it can call uponin times of need.

A single 5 gram dose of vitamin C cangenerate blood levels of about 250 |xM/L;this is above the NIH paper's claimedmaximum of 200 \iM/L. Moreover, re-peated large doses can sustain these levels.We have achieved vitamin C plasma levelsabove 400 fjM/L, followdng a single dose oforal liposomal vitamin C.'-* 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 of vitamin C may have a laxativeeffect. 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 flu. A person

with a laxative effect at, say, 2 grams, mayhe able to tolerate 100 times more if theybecome ill. This increased bowel tolerancealso occurs in cancer sufferers. It suggeststhat at times of stress or illness, the bodyabsorbs extra vitamin C. When promotingintravenous vitamin C, the NIH authorshave not considered the possibility of suchincreased bowel tolerance to oral doses.

To achieve the maximum bloodplasma levels possible with oral vitaminC, a typical healthy person may need atotal intake of about 20 grams, spreadthroughout the day (say 3 or 4 grams everyfour hours). However, cancer patients mayrequire far 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 for howvitamin C kills cancer cells'"* are notcovered by the NIH study. The NIH basetheir work on laboratory studies of mice,in which vitamin C kills cancer cells overthe course of, perhaps, a couple of hours.Lower levels of 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 effective that the short, sharp shockof intravenous therapy. Sustained levelsalso reduce the likelihood of tumoursdeveloping resistance to the therapy(analogous to bacterial resistance to an-tibiotics.)

Redox synergyWhen combined with alpha-lipoic

acid, selenium, vitamin K3, or a rangeof other supplements, vitamin C is a farmore powerful anticancer agent thanwhen used alone. Experimental data fromRiordan and others shows that the cancerdestroying effect of such combinations ismuch higher. We have described some of

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these combinations in a recent book "TheCancer Breakthrough".^^ Strong scientificreasons suggest that such combinations,given orally, could provide cancer suffer-ers with a large increase in lifespan andincreased quality of life.

Just as your doctor advises you totake a whole course of antibiotics continu-ously, until all infection is gone, vitamin Cbased redox therapy needs to be continu-ous. Like bacterial infections, cancers canrapidly become resistant to intermittenttreatments. Typically, intravenous ascor-bate is given at intervals, whereas oralascorbate can maintain blood levels con-tinuously and indefinitely. This is a validmedical reason to prefer an oral regime.Also, patients prefer the oral route, as theyhave greater control, lower cost, and aremore involved in their treatment.

People often ask us what we would do,if we developed the disease. In the eventthat one of us developed a malignancy,we would opt for 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 n M/L, together with alpha-lipoicacid, selenium, and other synergistic nutri-ents.'^ While we realize malignant cancerwould place us at high risk of death, wewould expect to live a greatly extendedlife. While the assessment of increasedlongevity could be inaccurate (the data isnot definitive), the risks are small and thepotential benefits substantial.

ConclusionsMark Levine claims that the "NIH's

unique translational environment, whereresearchers can pursue intellectual high-risk, out-of-the-box thinking with highpotential payoff, enabled us to pursuethis work."'

However, the recent NIH study, whileinteresting, adds little to the studies it

replicates. More interesting is the lack ofhistorical perspective, which may detractfrom the people, such as Hugh Riordan,Abram Hoffer, or Linus Pauling, who de-serve the credit for carrying out originalresearch, despite conventional medicineactively suppressing their work. Theground breaking work of doctors such asthose in the British Society for EcologicalMedicine, who have risked their careersto provide vitamin C based treatmentsfor cancer and other conditions should berecognized. These pioneering doctors areoften well aware of the scientific evidenceand should not be described as "comple-mentary" or "alternative". Perhaps, oneday, the media will realize the true storyof vitamin C and cancer, and patients willhave the opportunity to benefit.

The Alliance for Natural Health isdefending our right to supplements. Overthe last century, we have benefited froma large increase in life expectancy andfreedom from many diseases. Much ofthat benefit has arisen directly from nu-trition.'^' We need access to supplements,which provide the possibility of diseaseprevention without significant risk. Ifthis basic right is removed by CodexAlimentarius, or similar legislation—forexample, the draconian regulatory mea-sures the natural health sector is facingin Europe—even pioneering doctors willfind it difficult to progress the nutritionaltreatment of disease. The health of most ofus will suffer. We will get more illnesses,more often, and options for medical treat-ment of major killers, such as cancer,heart disease, and stroke, will decline.

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2. Holman RA: A method of 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 of Ehrlich ascites carcinoma cells byascorbate and 3-amino-l, 2,4, -triazole. Oncol-ogy, 1969; 23:33-43.

4. Cameron E, Pauling L: Supplemental ascor-bate in the supportive treatment of cancer:Prolongation of survival times in terminal hu-man cancer. Proc NatlAcad Sei USA, 1976; 73:3685-3689.

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9. NIH News: Vitamin C Injections Slow TumorGrowth in Mice, Embargoed for Release, Mon-day, August 4, 5:00 p.m. EDT. 2008.

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12. Padayatty SJ, Levine M: Réévaluation of ascor-bate in cancer treatment: Emerging evidence,open minds and serendipity, 7/Im Coll Nutr,2000; 19(4): 423-425.

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