Forleden skrev VG om en ny undersøkelse fra USA, om vitamin C og kreft. Fritt Helsevalg sendte en liten "korreks" til VG. Den samme nyheten har gått verden rundt, og dens profil er jo nærmest at "dette er interessant", men – i hvert fall foreløpig – ingen grunn til noe praktisk håp for kreftpasienter. Rent bortsett fra at forskningen ikke bringer noe nytt, så unnlater den å referere til all tidligere forskning – som i stor grad ligger utenfor "mainstream", og til den faktiske bruken av C-vitaminterapi i kreftbehandling. FHV gjengir derfor et tilsvar fra Steve Hickey og Hilary Roberts, via Alliance for Natural Health, som setter det hele i en mer korrekt historisk kontekst. De påpeker studien mangler. Og hva den ikke sier. Spennende lesning!

The Real Story of Vitamin C and Cancer

av

Steve Hickey PhD and Hilary Roberts PhD

Kilde: http://www.anhcampaign.org/files/080807_RealStoryOfVitaminCandCancer2_Hickey.pdf

via: http://www.anhcampaign.org/news/feature-real-story-vitamin-c-and-cancer

In the last couple of days, vitamin C and cancer has become a hot news

topic. For people who have followed this matter, the media’s sudden

interest comes as something of a surprise: the evidence that vitamin C is

a selective anticancer agent has been known for decades. This story is

important, as it illustrates how the head-in-the-sand conventional view

(that nutritional supplements are useless) can lead to restrictive

legislation, reduced health, and limited approaches to the treatment of

disease.

The recent news story arose from a study by researchers at the US

National Institutes of Health (NIH).1 The NIH experiment showed that,

when injected into mice, vitamin C could slow the growth of tumours. The

NIH paper presents its findings as new, ignoring the long history of

research into vitamin C and cancer. Far from being novel, many of the

findings reported in this paper have been recognized for decades. What is

strange, however, is that the media suddenly decided to report a story

they had ignored for so long.

A history

One strand of this story begins with the work of an old friend, Dr Reginald

Holman. In 1957, Holman published a paper in Nature about how

hydrogen peroxide (the chemical Marilyn Monroe reportedly used on her

hair) destroyed or slowed the growth of tumours in mice.2 Reg Holman

met with some hostility from the medical profession, which slowed his

research and clinical work over the following half century. Nevertheless,

scientists have known that hydrogen peroxide kills cancer cells for over

fifty years.

In 1969, when man first walked on the moon, researchers found that

vitamin C would selectively kill cancer cells without harming normal cells.3

That finding meant that vitamin C was like an antibiotic for cancer:

potentially a near perfect anticancer drug. Before 1970, it was known that

vitamin C was an example of a new class of anticancer substances.

However, the medical research establishment largely ignored these

scientific results.

In the 1970s, some members of the public and pioneering doctors

experimented with high doses of vitamin C to treat cancer. By 1976,

double Nobel Prize winner Linus Pauling and Scottish surgeon Ewan

Cameron reported clinical trials, showing an unparalleled increase in

survival times in terminal cancer patients treated with vitamin C.4

However, by this time Pauling was considered a quack, having claimed

that vitamin C could prevent or cure the common cold, so these

apparently amazing findings made little impact.

Cameron and Pauling published a second report in 1978.5 The Mayo Clinic

responded with a study that suggested vitamin C had no effect, which the

medical profession readily accepted, perhaps because it confirmed

existing prejudices. However, despite the Mayo Clinic study being

“considered definitive”,1 it was highly criticised from the start. In

particular, it used relatively low oral doses for short periods, rather than

the lifetime combination of high oral and intravenous (IV) doses in the

Pauling and Cameron study. The Mayo Clinic refused to provide Pauling

with their data so he could check it. When we emailed the Mayo Clinic

with a similar request, we received no reply.

If Cameron and Pauling’s work, back in the 1970s, had been just a single

study, it would have been interesting and suggestive. Such a large

increase in survival time demands a proper scientific follow-up and,

indeed, other studies soon backed up the findings. Japanese researchers

found similar survival times,6 apparently confirming Pauling’s early

results. Subsequently, Dr Abram Hoffer, working in Canada, provided

more evidence that vitamin C could enable cancer patients to live much

longer. We have analysed these results and found them to be statistically

valid. They are not explicable by placebo effect or by a simple biased

selection of long-lived patients. Moreover, over the last three decades, a

large number of clinical and anecdotal patient reports support the claims.

A long time before the NIH’s mouse experiment, Pauling also studied the

effects of vitamin C on cancer in mice. He worked with Dr Art Robinson

but, unfortunately, the two researchers fell out over their interpretations

of the results. Robinson left the Linus Pauling Institute (which he had

helped establish) and completed the experiment alone. It was eventually

published in 1994.7 The results were outstanding: mice with cancer that

were given high dose vitamin C in the diet, or fed a diet of raw

vegetables, lived up to 20 times longer than controls. Translated into

human terms, this might mean that a person with one year to live might

get an extra 20. Importantly, Robinson and Pauling had been inspired to

do this experiment by claims from cancer sufferers in the popular

literature.

Doctors Hugh Riordan, Ron Hunninghake, Jim Jackson, Jorge Miranda-

Massari, Michael Gonzalez and others in the Brightspot Center for the

Improvement of Human Functioning, did the core research on vitamin C

and cancer. They repeated and extended the early work, which had

showed vitamin C would selectively kill cancer cells. They have years of

experience of treating cancer patients with high dose vitamin C. Their

work is consistent with results from independent researchers and doctors

worldwide.8

The authors of this article recently reviewed the literature on vitamin C

and cancer, in our book “Cancer: Nutrition and Survival”.8 We found solid

evidence that vitamin C, in high enough doses, acts as a selective

anticancer drug. In healthy tissues, vitamin C is an antioxidant, while in

cancer it acts as an oxidant generating free radicals and killing the

abnormal cells. Furthermore, an understanding of its action provides

insight into the cancer development process. Oxidants, such as hydrogen

peroxide, are able to make cells grow and divide erroneously. So, as the

cells divide, they form a population of varying cells that compete with

each other for survival. It was immediately clear that oxidation could

explain how cancer starts; following which Darwin’s theory of evolution

takes over. Given enough time, cells divide and the “fittest” are selected.

In this context, the fittest to survive are those cells that grow rapidly to

form an invasive cancer. Cancer is not a mysterious disease but is a result

of straightforward biological processes.

This microevolutionary model for cancer makes highly specific predictions.

One is that high dose vitamin C should prevent cancer and even higher

doses should kill cancer cells. The model also predicts that there could be

thousands of selective anticancer drugs. Animals, and especially plants,

will contain these substances, because they evolved in the presence of

cancer and had to develop ways to control it. If such predictions are

correct, we should find a multitude of safe anticancer agents in food.

Checking against medical databases, we immediately found numerous

examples, such as curcumin from turmeric, alpha-lipoic acid, and vitamin

D3. Everywhere we looked, we found substances with the predicted

properties. Unfortunately, many are the very supplements the Alliance for

Natural Health (ANH) is trying to protect from being banned!

To conclude our history, the NIH paper was essentially a repeat of

previous animal experiments. Despite this, the NIH authors appear not to

have referenced many of the scientists who did the original work on

vitamin C and hydrogen peroxide in cancer. Instead, they present their

work as standing alone, in an informational vacuum: with the exception of

the Cameron and Pauling clinical trial, the original scientists’ work is not

mentioned in the NIH text. Wrongly, a reader might gain the impression

that the NIH’s work was fundamentally original, rather than repeating the

work of others. This might mislead the media into ascribing credit for the

work on vitamin C and cancer to the NIH, which would be unfair to the

real pioneers of this subject.

Intravenous or oral?

Dr Mark Levine of the NIH claims that "When you eat foods containing

more than 200 milligrams of vitamin C a day — for example, 2 oranges

and a serving of broccoli — your body prevents blood levels of ascorbate

from exceeding a narrow range."9 This statement is demonstrably false

(the NIH’s own data refutes it) and is an artefact of the way the NIH

group interpret their experiments.

In their mouse paper, the NIH used intravenous vitamin C, rather than

oral. To be more accurate, the NIH used intravenous ascorbate. Sodium

ascorbate is normally used for injection, as vitamin C (ascorbic acid) can

cause local inflammation at the injection site. The results they obtained

are suggestive of a response, but do not show the same large effects

reported by Robinson. Robinson fed his mice dietary vitamin C, in very

high doses. Thus, the NIH’s suggestion that only intravenous vitamin C is

useful as an anticancer agent does not appear to fit the animal data.

Likewise, the idea that only intravenous vitamin C is effective against

cancer does not fit the clinical data. Abram Hoffer, for example, used oral

doses and obtained essentially the same results as Cameron and Pauling.

The NIH’s insistence that the body has “tight controls”, which prevent oral

vitamin C from functioning as an anticancer agent, is wrong. In our book

Ascorbate: The Science of Vitamin C, we have shown that the NIH claims

for blood “saturation” at a low level (70 μM/L) are incorrect.10 The NIH

authors never admitted this error, despite a long email correspondence

between Hickey and Levine. However, they have changed the wording

they use, from “saturated” to “tight controls”, and increased the level by

about three times (to 200 μM/L). It would appear that they are holding

onto an outdated idea about how vitamin C acts in the body. As an

alternative, we have proposed a dynamic flow model, in which, at high

doses, vitamin C flows through the body, providing antioxidant support,

potentially preventing cancer growth and killing cancer cells.11

Dynamic flow

Dr Mark Levine claims:

"Clinical and pharmacokinetic studies conducted in the past 12 years

showed that oral ascorbate levels in plasma and tissue are tightly

controlled. In the case series, ascorbate was given orally and

intravenously, but in the trials ascorbate was just given orally. It was not

realized at the time that only injected ascorbate might deliver the

concentrations needed to see an anti-tumor effect."9

As we have explained, there is no evidence for such tight control. The

suggestion that the legendary scientist, Dr Linus Pauling, or consultant

surgeon, Ewan Cameron, did not know the difference between oral and

intravenous administration12 is bizarre and, again, demonstrably

incorrect.8 The difference between oral and intravenous vitamin C is,

however, more complex than suggested by the NIH. Contrary to their

conclusions, it is not clear that intravenous vitamin C necessarily provides

an advantage over oral supplements in the treatment of cancer. There is

a fair case for suggesting that high dose oral administration could be

more effective.

At low intakes, the body prevents vitamin C from being lost through the

urine; if this were not the case, we would all be at risk of acute scurvy.

The body tries to retain a minimum of about 70 μM/L of vitamin C in

blood plasma. This level can be maintained with an intake as low as 200

mg a day. At higher doses, the body can afford to let some vitamin C

escape in urine. This saves energy, which the kidneys would otherwise

use to keep pumping the vitamin C molecules back into the blood. If

dietary vitamin C is in plentiful supply, there is no need for our bodies to

retain it all. So, at high doses, vitamin C flows through the body, being

taken in from the gut and excreted in the urine. With such high intakes,

the body has a reserve that it can call upon in times of need.

A single 5 gram dose of vitamin C can generate blood levels of about 250

μM/L; this is above the NIH paper’s claimed maximum of 200 μM/L.

Moreover, repeated large doses can sustain these levels. We have

achieved vitamin C plasma levels above 400 μM/L, following a single dose

of oral liposomal vitamin C.13 It seems that the claimed “tight control”

concept will need revising again soon.

People vary in their responses to vitamin C. In some people, a single 2

gram oral dose of vitamin C may have a laxative effect. Our collaborator,

Dr Robert Cathcart, described this as the bowel tolerance level. Strangely,

bowel tolerance has been observed to increase dramatically when a

person is ill, say with the flu. A person with a laxative effect at, say, 2

grams, may be able to tolerate 100 times more if they become ill. This

increased bowel tolerance also occurs in cancer sufferers. It suggests that

at times of stress or illness, the body absorbs extra vitamin C. When

promoting intravenous vitamin C, the NIH authors have not considered

the possibility of such increased bowel tolerance to oral doses.

To achieve the maximum blood plasma levels possible with oral vitamin C,

a typical healthy person may need a total intake of about 20 grams,

spread throughout the day (say 3 or 4 grams every four hours). However,

cancer patients may require far more. Such massive intakes result in

consistently high blood levels, which tumour tissues absorb, and which

then generate the hydrogen peroxide that kills the cancer cells.

Other possible mechanisms for how vitamin C kills cancer cells14 are not

covered by the NIH study. The NIH base their work on laboratory studies

of mice, in which vitamin C kills cancer cells over the course of, perhaps,

a couple of hours. Lower levels of vitamin C may simply take longer to kill

the cells, which is a standard dose response relationship. Sustained oral

doses can increase plasma vitamin C consistently, over periods measured

in months or years: this may, in the end, be more effective that the short,

sharp shock of intravenous therapy. Sustained levels also reduce the

likelihood of tumours developing resistance to the therapy (analogous to

bacterial resistance to antibiotics.)

Redox synergy

When combined with α-lipoic acid, selenium, vitamin K3, or a range of

other supplements, vitamin C is a far more powerful anticancer agent

than when used alone. Experimental data from Riordan and others shows

that the cancer destroying effect of such combinations is much higher. We

have described some of these combinations in a recent book “The Cancer

Breakthrough”.15 Strong scientific reasons suggest that such

combinations, given orally, could provide cancer sufferers with a large

increase in lifespan and increased quality of life.

Just as your doctor advises you to take a whole course of antibiotics

continuously, until all infection is gone, vitamin C based redox therapy

needs to be continuous. Like bacterial infections, cancers can rapidly

become resistant to intermittent treatments. Typically, intravenous

ascorbate is given at intervals, whereas oral ascorbate can maintain blood

levels continuously and indefinitely. This is a valid medical reason to

prefer an oral regime. Also, patients prefer the oral route, as they have

greater control, lower cost, and are more involved in their treatment.

People often ask us what we would do, if we developed the disease. In

the event that one of us developed a malignancy, we would opt for a

vitamin C based redox therapy as our primary approach to treatment.

This would be based on oral intakes: we would consider intravenous

ascorbate only as an adjunct. We might use liposomal vitamin C to

sustain blood levels at 400-500 μM/L, together with α-lipoic acid,

selenium, and other synergistic nutrients.15 While we realise malignant

cancer would place us at high risk of death, we would expect to live a

greatly extended life. While the assessment of increased longevity could

be inaccurate (the data is not definitive), the risks are small and the

potential benefits substantial.

Conclusions

Mark Levine claims that the "NIH''s unique translational environment,

where researchers can pursue intellectual high-risk, out-of-the-box

thinking with high potential payoff, enabled us to pursue this work."9

However, the recent NIH study, while interesting, adds little to the studies

it replicates. More interesting is the lack of historical perspective, which

may detract from the people, such as Hugh Riordan, Abram Hoffer, or

Linus Pauling, who deserve the credit for carrying out original research,

despite conventional medicine actively suppressing their work. The

groundbreaking work of doctors such as those in the British Society for

Ecological Medicine, who have risked their careers to provide vitamin C

based treatments for cancer and other conditions should be recognised.

These pioneering doctors are often well aware of the scientific evidence

and should not be described as “complementary” or “alternative”.

Perhaps, one day, the media will realise the true story of vitamin C and

cancer, and patients will have the opportunity to benefit.

The ANH is defending our right to supplements. Over the last century, we

have benefited from a large increase in life expectancy and freedom from

many diseases. Much of that benefit has arisen directly from nutrition.16

We need access to supplements, which provide the possibility of disease

prevention without significant risk. If this basic right is removed by Codex

Alimentarius, or similar legislation—for example, the draconian regulatory

measures the natural health sector is facing in Europe—even pioneering

doctors will find it difficult to progress the nutritional treatment of

disease. The health of most of us will suffer. We will get more illnesses,

more often, and options for medical treatment of major killers, such as

cancer, heart disease, and stroke, will decline.

1 Chen Q. Espey M.G. Sun A.Y. Pooput C. Kirk K.L. Krishna M.C. Khosh D.B. Drisko J.

Levine M. (2008) Pharmacologic doses of ascorbate act as a prooxidant and decrease

growth of aggressive tumor xenografts

in mice, PNAS, 105(32), 11105–11109.

2 Holman R.A. (1957) A method of destroying a malignant rat tumour in vivo, Nature,

179(4568), 1033.

3 Benade L. Howard T. Burk D. (1969) Synergistic killing of Ehrlich ascites carcinoma

cells by ascorbate and 3-amino-1, 2, 4, -triazole, Oncology, 23, 33–43.

4 Cameron E. Pauling L. (1976) Supplemental ascorbate in the supportive treatment of

cancer: Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA,

73, 3685–3689.

5 Cameron E. Pauling L. (1978) Supplemental ascorbate in the supportive treatment of

cancer: Reevaluation of prolongation of survival times in terminal human cancer, Proc

Natl Acad Sci USA, 75, 4538–4542.

6 Murata A. Morishige F. Yamaguchi H. (1982) Prolongation of survival times of terminal

cancer patients by administration of large doses of ascorbate, International Journal for

Vitamin and Nutrition Research, Supplement, 23, 101-113.

7 Robinson A.R. Hunsberger A. Westall F.C. (1994) Suppression of squamous cell

carcinoma in hairless mice by dietary nutrient variation, Mechanisms of Ageing and

Development, 76, 201-214.

8 Hickey S. Roberts H. (2005) Cancer: Nutrition and Survival, Lulu Press.

9 NIH News (2008) Vitamin C Injections Slow Tumor Growth in Mice, Embargoed for

Release, Monday, August 4, 5:00 p.m. EDT.

10 Hickey S. Roberts H. (2004) Ascorbate: the Science of Vitamin C, Lulu Press.

11 Hickey S. Roberts H and Cathcart R.F. (2005) Dynamic flow, JOM, 20(4), 237-244.

12 Padayatty S.J. Levine M. (2000) Reevaluation of ascorbate in cancer treatment:

Emerging evidence, open minds and serendipity, Journal of the American College of

Nutrition, 19(4), 423-425.

13 Hickey S. Roberts H. Miller N.J. (2008) Pharmacokinetics of oral ascorbate liposomes,

JNEM, in press.

14 Toohey J.I. Dehydroascorbic acid as an anti-cancer agent, Cancer Letters 263 (2008)

164–169.

15 Hickey S. Roberts H.J. (2007) The Cancer Breakthrough, Lulu press.

16 Wootton D. (2007) Bad Medicine, Oxford University Press.