Vitamin C inhibits cancer. But How?

September 18, 2007

New research sparks new theories about how vitamin C inhibits cancerous growth.

A great deal of research indicates that vitamin C has a considerable inhibitory effect on the growth of cancer cells.

The biochemical effect of high-dose treatment with vitamin C is reasonably understood; vitamin C acts as a pro-oxidant on cancer cells at such doses. This causes increased free radical strain on the cancer cells and thereby acts as a poison to the cancer.

In moderate doses, the kind of doses which we can get through our diets, vitamin C is an antioxidant. But even at these doses, vitamin C has shown an inhibitory effect on the growth of cancer cells.

It was therefore believed that vitamin C blocks the free radicals which cause the cancer forming mutations in the cells, and that the reason for its protective effects is that it protects the cells’ DNA.

This is presumably not the whole truth.

Many years ago a famous professor by the name of Warburg was among the first to maintain that cancer cells grow in oxygen poor tissue. Today this is common knowledge, but there lacks knowledge on how this occurs. Ten years ago Gregg Semenza of John Hopkins University found that cancer cells are dependent on a protein called HIF-1 (hypoxia induced factor), which helps the cells by compensating for lacking oxygen in the surrounding tissue and thus allows cancer cells to convert sugar to energy without oxygen. HIF-1 also catalyses the creation of new blood vessels so that hungry cancer cells can get fresh supplies of nutrients and oxygen. If a cancer grows aggressively, it quickly uses up its oxygen supply and becomes entirely dependent on HIF-1. The HIF-1 protein is dependent on the presence of free radicals, which are also necessary for many other processes in the body. A powerful antioxidant like vitamin C eliminates the surplus of free radicals, which causes HIF-1 to become ineffective and thus inhibits cancer growth.

This new theory is based on a study done by a research group at the centre of oncology at John Hopkins University in conjunction with Dean Felsher of Stanford.

They set out to study antioxidants’ roles in cancer growth and found, to their great surprise, that antioxidants destabilise the protein on which cancer cells are dependent. As professor Chi Dang from John Hopkins University wisely stated, “By uncovering the mechanism behind anti-oxidants, we are now better suited to maximize their therapeutic use.”

By: Claus Hancke, MD

Reference

HIF-Dependent Antitumorigenic Effect of Antioxidants In Vivo. Cancer Cell, Volume 12, Issue 3, 11 September 2007, Pages 230-238Ping Gao, Huafeng Zhang, Ramani Dinavahi, Feng Li, Yan Xiang, Venu Raman, Zaver M. Bhujwalla, Dean W. Felsher, Linzhao Cheng, Jonathan Pevsner et al.

www.cancercell.org

Smokers should get more vitamin C and E

April 1, 2006

Far too many people get too little vitamin E. The problem is especially large in smokers and can partially be solved by a supplement of vitamin C.

What do you do if you get too little vitamin E? Here is a suggestion: take more vitamin C.

Smokers have this problem more than any other group. They use vitamin E much faster than non-smokers. This is because tobacco smoke oxidizes and destroys the vitamin, which causes it to fail in the fight to protect the unsaturated fats of the body’s cells. Smokers therefore have a greater need for vitamin E than non-smokers. Because they have a greater need, it is easier for them to receive too little.

This is where vitamin C comes in. Vitamin C is easier to get a hold of than vitamin E. Because vitamin C is an antioxidant it can protect the vitamin E from oxidization by the free radicals of the tobacco smoke. This has long been believed, but, until recently, remained unproven in people. There has lately been a small scientific breakthrough in this field.

The study was done as a cooperative effort between a number of American universities and one Canadian university. 11 smokers and 13 non-smokers were given supplements of 50 mg vitamin E containing deuterium. By measuring the amount of deuterium in the blood the researchers were able to determine how fast the vitamin E disappeared from the smoker’s blood (plasma) and compare that to the changes in vitamin E levels in the non-smokers.

It disappeared, as expected, fastest in the smokers. In the course of 25 hours half of the marked vitamin E had disappeared. In the non-smokers this took 42 hours. But, when the smokers were given 500 mg vitamin C morning and evening, it took 34 hours for half of the marked vitamin E to disappear. The vitamin C protected the vitamin E reserves in the smokers, but did not bring them to the level of those in the non-smokers.

Far too few get enough
One can therefore see a normalising of vitamin E in smokers with the help of vitamin C. This is of course only true if the smokers receive enough vitamin E in the first place, which can be said of far too few.

To conclude the summary of this research is should be mentioned that only 8% of men and 2.4% of women receive the recommended 12 mg vitamin E (alpha-tocopherol) per day. This is highly likely no better in the U.K. The first and most important recommendation made is that smokers received the recommended amounts (for smokers) of both vitamins C and E (125 mg vit. C and 15 mg vit. E). The second recommendation is that more research be undertaken regarding whether other antioxidants can protect against the degradation of vitamin E. This is important.

But is it true that one needs 12 mg vitamin E per day? Yes it is! An earlier study has shown that the bodily tissue of healthy, young people uses about 5 mg vitamin E (alpha-tocopherol) per day.

Because one on average only absorbs about one third of ones food intake in the intestine, should one take a little bit more than the aforementioned 12 mg. But if one eats an especially light diet more should be taken. If breakfast is only cornflakes and low fat milk, taking a vitamin E supplement won’t do much good. Only a tenth of it will be absorbed.

Even young, healthy smokers should receive more vitamin E than others. Older people have an even greater need and it is apparent that most people don’t get enough.

By: Vitality Council

References
1. Bruno R S et al. Human vitamin E requirements assessed with the use of apples fortified with deuterium-labeled α-tocopheryl acetate. Am J Clin Nutr 2006;83:299-304
2. Bruno R S et al. α-Tocopherol acetate disappearance is faster i9n cigarette smokers and is inversely related to their ascorbic acid status- Am J Clin Nutr 2005;81:95.103.
3. Bruno R S et al. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radical Biology & Medicine 2006;40:689-97

Vitamin C against atherosclerosis (hardened arteries)

March 23, 2006

So far a British research study is showing that C vitamin fights inflammation. Therefore it is very possible that it also fights hardened arteries and blodclots.

If one compares peoples’ eating habits with their risk of blood clots in the heart, one gets the impression that vitamin C prevents blood clots. So far it has been hard to prove through randomised trails that vitamin C supplements protect high risk patients from blood clots. This is how it has been up to now, even though one can claim that many of the studies have been lacking.

Whatever the objections, it is widely believed that the debate over.

It is currently said that vitamin C does not protect against atherosclerosis, but is it true? A recent summary could indicate that the debate is long from over. It shows that vitamin C counteracts inflammation, which is to say infection-like reactions. There is also widespread agreement that atherosclerosis is due to inflammation. Does vitamin C therefore protect against atherosclerosis?

In order to understand the problem it is necessary to take a little detour in this discussion:
Until 20-30 years ago, atherosclerosis was believed to be a process which was roughly due to the depositing of cholesterol in the walls of the blood vessels followed by the build up of calcium. Today it is understood the vessel walls are composed of living cells, and that both the build up of cholesterol and the thickening of the vessel walls are related to inflammation. The same is true for the bursting of the surface against the blood stream, with the emptying of cholesterol and cell products, which causes the platelets (etc.) to clump together, causing a blood clot.

Inflammation appears, curiously enough, to be a part of the sales success of the cholesterol lowering medications, the so called statins. It cannot be denied that they save lives, but is it because they lower the blood’s cholesterol level?

Vitamin C lowers CRP
Here there is doubt. Statins do not only lower cholesterol, but also reduce inflammation. This can be directly measured by a simple blood test (CRP) which hundreds of thousands of Danes get taken when their doctors what to know if they have infection in their bodies. The two effects of statins, the lowering of CRP and the reduction of cholesterol, are not necessarily related, but the risk of blood clots in the heart is more related to CRP than to cholesterol levels. In a study where statins were shown to reduce the risk of heart disease by ca. 30%, their favourable effect was statistically shown to be related to CRP levels, regardless of the cholesterol level! It looks like CRP is more important than cholesterol!

With this we can return to vitamin C. Does vitamin C reduce CRP, just like statins?

In a couple of small randomised studies it was examined whether or not this is the case. In both studies the daily dose of vitamin C was about 500 mg. In the first (with smokers as the participants) CRP was markedly reduced, in the second nothing happened. The contradictory results have now been explained by a study with 3258 reasonably cardio-vascular healthy men between the ages of 60-79.

The primary result was that the more vitamin C that the men had in their blood (serum), the lower their CRP. The quarter of the participants who had the highest level of vitamin C in their blood (with or without consideration of supplements), had the lowest CRP values. The difference was overwhelmingly statistically certain. Concurrently, other measurements indicated that the likelihood for “irritability” of the vessel walls (endothelial dysfunction) was also the lowest in the highest vitamin C group. There is common agreement that this “irritability” mirrors a tendency for atherosclerosis.

Vitamin C is therefore believed to lower CRP, which is an important indicator for inflammation, and therefore the risk of dying of a blood clot. The debate rages on!

By: Vitality Council

References:
1. Ridker et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med 2005;352:20-8
2. Ridker PM, C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005 Jan 6;352(1):20-8
3. Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83(Suppl):456S-60S
4. Goya S et al. Associations of vitamin C status, fruit and vegetable intakes, and markers of inflammation and hemostasis. Am J Clin Nutr 2006;83:567-74
5. Ishwarlal J et al. Is vitamin C an anti-inflammatory agent? Am J Clin Nutr 2006;83:525-6
6. Mora S Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)–can C-reactive protein be used to target statin therapy in primary prevention?Am J Cardiol. 2006 Jan 16;97(2A):33A-41A. Epub 2005 Dec 1.
7. Bruunsgaard H, Long-term combined supplementations with alpha-tocopherol and vitamin C have no detectable anti-inflammatory effects in healthy men. J Nutr. 2003 Apr;133(4):1170-3.
8. Block G Plasma C-reactive protein concentrations in active and passive smokers: influence of antioxidant supplementation. J Am Coll Nutr. 2004 Apr;23(2):141-7.

content.nejm.org
www.ajcn.org
www.nutrition.org

High Dose Intravenous Vitamin C Fights Cancer

September 28, 2005

This was the New York Times’ headline two weeks ago.

The United States National Institute of Health (NIH) has publicized a laboratory study (1) which shows that when cancer cells are exposed to high doses of vitamin C, which can only be achieved though intravenous injection, the cancer cells die without the normal cells being effected.

The NIH pronounced,”These findings give plausibility to i.v. ascorbic acid in cancer treatment.” They rightly add that much separates laboratory studies from human treatment.

Meanwhile this study is an affirmation of similar results of many earlier studies. In 2004 researchers indicated that “the role of vitamin C in cancer treatment should be re-examined” because intravenous doses of vitamin C can give concentrations which have anti-tumour effects (2)

In 1993 a study showed that vitamin C is deadly or cytotoxic to fast growing malignant cells while being non-toxic to non-malignant cells. Supplementary studies showed that ascorbate’s effects on cell growth are due to its direct lethal effect on cancer cells contrary to a cytostatic effect (3).

Earlier it had been proven that vitamin C has a growth inhibiting effect on cancer cells, but only in large concentrations. The addition of the antioxidant catalase to the growth media completely suppressed this growth inhibiting effect.

The authors of this study believed that this indicates that an overproduction of hydrogen peroxide in involved in the mechanisms responsible for vitamin C’s inhibitory effect of tumour cell growth (4).

The authors of the more recent study lean towards this hypothesis from 1989, which is that high dose vitamin C’s toxic effect on cancer cells is due to subsequent high concentrations of peroxide. Normal cells have an intact antioxidant defence in the form of catalase. This is lacking in cancer cells. This is why vitamin C harms cancer cells and not normal cells, which is exactly the finding of the 2005 study.

Vitamin C’s potential in cancer treatment was also shown in two large studies from 1994, where large doses of ascorbic acid had strong cytotoxic (cell poisonous) effects on a wide range of cancer cell types grown in test tubes (5).

The authors of the second 1994 study also argue that ascorbic acids acts as a pro-oxidant in cancer cells, and they recommend the use of ascorbic acid in the treatment of neuroblastoma (6).

So far so good; but remember that researchers from the NIH mention that there is much separating laboratory studies and the treatment of people.

Vitamin C is meanwhile so non-toxic that some have already undertaken large studies on people.

As early as 1936, a young Danish doctor published an article in the Danish medical weekly “Ugeskrift for Læger” outlining a study where vitamin C was used in the treatment of two leukaemia patients where both showed improvement. This young doctor, named Preben Plum later became a renowned professor or paediatrics.

40 years later a study including 1,100 patients suffering from terminal cancer showed that those who were treated with i.v. vitamin C lived considerably longer than those who were not treated (7).

Ten years ago Riordan et. al. showed that ascorbic acid levels in the plasma can reach levels toxic to tumour cells if given intravenously. The authors believe that ascorbic acid’s cytotoxic properties should qualify it to be considered as a chemotherapeutic drug.

These few examples of a large amount of vitamin C studies fit together like pieces of a puzzle.

This has awakened considerable interest in the media and could strengthen the scientific foundation of clinics where i.v. vitamin C treatment for cancer is already used.

By: Vitality Council

References:
1. Chen et al. Proceedings of the National Academy of Sciences 20. Sept. 2005;102:13604-9.
2. Annals of Internal Medicine 2004;140: 533-37.
3. P.Y. Leung, et al. Cytotoxic Effect of Ascorbate and its Derivatives on Cultured Malignant and Nonmalignant Cell Lines, Anticancer Research, 13(2), March-April 1993, p. 475-480.
4. V. Noto, et al., Effects of Sodium Ascorbate (Vitamin C) and 2-methyl-1,4-Naphthoquinone Treatment on Human Tumor Cell Growth in Vitro. I. Synergism of Combined Vitamin C and K3 Action, Cancer, 63(5), March 2, 1989, p. 901-906.
5. M. A. Medina, et al. Ascorbic Acid is Cytotoxic for Pediatric Tumor Cells Cultured in Vitro, Biochem Mol Biol Int, 34(5), November 1994, p. 871-874.
6. S.L. Baader, et al., Uptake and Cytotoxicity of Ascorbic Acid and Dehydroascorbic Acid in Neuroblastoma (SK-N-SH) and Neuroectodermal (SK-N-LO) Cells, Anticancer, 14(1A), January-February 1994 p. 221-227.
7. Cameroun, Proc Natl Acad Sci 1976;73:3685-9.
8. N.H. Riordan, et. al. Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent, Medical Hypotheses, 44(3), March 1995, p. 207-213.

www.nih.gov
www.pnas.org
www.annals.org
www.iiar-anticancer.org/research/research_index.htm
www.cancer.org/docroot/home/index.asp
www.med.unibs.it/biblioteca/pubmed2/biomol6.htm
www.sciencedirect.com
www.cancer.gov
www.nytimes.com
www.iom.dk

On-time “Delivery” with Vitamin C

June 28, 2005

Vitamin C is necessary for the creation and maintenance of connective tissue. Therefore, it protects pregnant women against damage to the fetus membrane so that the uterine fluid in which the fetus floats does not leave the uterus prematurely. The typical Danish diet contains much too little Vitamin C for pregnant women.

It is well-known that pregnant women should take folic acid – even before the conception of the fetus – to prevent the birth of children with Spina Bifida. Now it seems that Vitamin C is important for the pregnant in another area: It protects against premature birth.

By: Vitality Council

Reference:
Casanueva E, Ripoll C, Tolentino M, Morales RM, Pfeffer F, Vilchis P, Vadillo-Ortega F Vitamin C supplementation to prevent premature rupture of the chorioamniotic membranes: a randomized trial. Am J Clin Nutr. 2005 Apr;81(4):859-63.

New Type of Antioxidant Protects Against Sunburns

June 6, 2005

A new type of antioxidant protects against sunburns and is thought to have other, additional health benefits. Similarly, vitamins C and E have been found to work too.

French researchers have created an innovative substance, incorporating a special form of the important antioxidant/enzyme SOD (Super Oxide Dismutase), that can be taken orally without fear of the SOD being destroyed in the stomach prior to assimilation.

The human body itself creates SOD, an essential enzyme. So far, it has only been possible to supply SOD by injection. But thanks to a combination of the enzyme with the wheat protein gliadin, this difficulty has now been overcome. The product (Glisodin) can be bought in Denmark.

By. Vitality Council

(Shortened)

References:
1. CARD (Annual Congress of Dermatological Research) meeting in Brest on May 28th 2005, (report).
2. Placzek M et al. Ultraviolet B-induced DNA damage in human epidermis is modified by the antioxidants ascorbic acid and D-alpha-tocopherol. J Invest Dermatol. 2005 Feb;124(2):304-7.
3. Bialy TL et al. Dietary factors in the prevention and treatment of nonmelanoma skin cancer and melanoma. Dermatol Surg 2002;28:1143-52.

www.blackwell-synergy.com/loi/jid
www.blackwellpublishing.com/journal.asp
www.iom.dk

No Danger from Vitamin E and C

May 23, 2005

Many of the worlds reknown scientist state that vitamin E and C are safe to take, even in high dosages. At the same time, the theory that the two vitamins prevent chronic illnesses, is still very much alive.

A number of world-leading researchers in vitamin E and vitamin C have concluded that the two antioxidants are completely safe over a very wide dose range. Thus, they reject claims to the opposite which are expressed in particular to the public, and to a lesser degree to the scientific community.

………………………………………

By: Vitality Council

Reference:
Hathcock JN et al. Vitamins E and C are safe across a broad range of intakes. Am J Clin Nutr 2005;81:736-45.

www.ajcn.org
www.iom.dk

Depressed Due to Vitamin Deficiency?

April 11, 2005

Several reports show a connection between depression and Vitamin E deficiency. There is a similar relation between depression and lack of Vitamin C and selenium. So far this gives food for thought.

Could it be that lack of vitamin E plays a role in depression? Something in that direction according to a preliminary Australian survey.

By: Vitality Council

References:
1. Owen AJ et al. Low plasma vitamin E levels in major depression: Diet or disease? Eur J Clin Nutr 2005;59:304-6.
2. Tiemeier H et al. Vitamin E and depressive symptoms are not related. The Rotterdam Study. J Affect Disord 2002;72:79-83.
3. Maes M et al. Lower seriúm vitamin E concentration in major depression. Another marker of lowered antioxidant defense in that disease. J Affect Disord 2000;58:241-6.
4. Benton D et al. The impact of selenium supplementation on mood. Biol Psychiatry 1991;29:1092-8.

www.nature.com/ejcn/index.html
www.sciencedirect.com
www.iom.dk

Listen to this: Vitamins Preserve the Hearing!

February 3, 2005

Studies with guinea pigs and American soldiers show that large doses of the vitamins C and E prevent chronic hearing impairment caused by noise. The conclusion is important, as every tenth grown-up has impaired hearing.

Do you have difficulties hearing? If so, the cause might be a vitamin deficiency. This is the result of a study carried out at the renowned Karolinska University Hospital in Stockholm, Sweden – the hospital is known throughout the world for being the place in which the staff scientists decide who gets the annual Nobel Prize for medicine.

The study showed that if the guinea pigs were given large doses of the vitamins C and -E before and after a violent noise impact, they would avoid the chronic hearing impairment that would otherwise be the result. Studies of American soldiers at target practice have shown similar results.

Impaired hearing is more common than you would probably think. 10% of all adults have so serious hearing difficulties that it affects their everyday communication. The prevalence increases with age, but many people become hearing impaired when they are young if they have a liking for violent music or if they have some sort of genetic predisposition for being sensitive to noise.

Professor Mats Ulfendahl from The Center for Hearing and Communication Research at the Karolinska University Hospital is behind the study. It was based on the knowledge that noise produces free oxygen radicals in the sensory cells of the inner ear and that these radicals are responsible for destroying the sensory cells.

For this reason, it was logical to try to limit the damage by supplying antioxidants to the guinea pigs. Ulfendahl presented the results at a congress about hearing impairment at the Karolinska University Hospital in September 2004.

Mats Ulfendahl is among the world’s leading researchers in hearing impairment and, among other things, he has demonstrated that there are stem cells in the inner ear that can develop into mature auditory- and neve cells. He believes that this discovery can imply that during the next 10 – 20 years, people suffering from aquired deafness can have their hearing restored. If he is right, it is hardly unlikely that his colleagues at the Karolinska University Hospital will nominate him for the Nobel Prize.

At present, there is no method for repairing damaged auditory cells in humans. Birds, however, automatically regenerate their hearing when they become deaf as a result of a noise injury. The thought of restoring hearing, therefore, is not fundamentally impossible. If you are considering some kind of prophylaxis before going to a disco, for example, it would probably be a good idea to consider taking a megadose vitamin supplement.

By: Vitality Council

References:
This time we do not refer to a scientific article, but an online introduction by a Swedish professor and a speech (in Swedish), which you may listen to directly at the web addresses below:
1) Can vitamins really soothe impaired hearing? ( Kan verkligen vitaminer lindra hörselnedsättning? ) http://www.hrf.se/templates/Page2x1____3855.aspx
2) Take a vitamin pill and then listen! ( Ta en vitamin och hör sen! )
http://www.karolinska.se/templates/Page.aspx?id=39736

www.hrf.se/templates/Page2x1____3855.aspx
www.karolinska.se/templates/Page.aspx
www.iom.dk

New Knowledge on the Spreading of Cancer

January 5, 2005

Research at the Finsen Institute explain how cancer tumours metastasize. The results may be of vital importance to the treatment of cancer and could give e.g. Vitamin C a central role.

A fundamental and unpleasant characteristic of cancer tumours is their ability to make metastases; cancer cells work loose from the original tumour and wander with the lymph or blood to the liver, lungs, bones, or brain. Here, they will settle and make new, independent tumours. Of course, this unfortunate process makes it incredibly difficult to completely cure the disease.

So – how can the metastasizing be prevented? More than ten years ago, the German-American M.D. Matthias Rath and the Nobel prize winner Linus Pauling made a joint hypothesis on this subject. They believed that a condition for metastases to be made was that the cancer cells should first make enzymes which break down the material and connective tissue that surrounds all cells like mortar around bricks.

The enzymes are necessary for both the ability of the cancer cells to break away from the original tumour and for them to penetrate healthy cells and install themselves in another organ.

The two scientists were particularly fastened upon a precursor (uPA) to the enzyme plasmin which partly breaks down the protein substance fibrinogen, and parly is involved in indirectly breaking down connective tissues etc.

They claimed that cancer patients could greatly benefit from particularly large doses of vitamin C, supplements of the amino acid Lysine, and the antioxidants (Epigallocatechin) in green tea. According to the two scientists, all these things would reduce the formation of uPA and thereby counteract metastasizing.

Now, at least the first part of the theory seems to hold water according to studies at the Danish Finsen Institute in Copenhagen. For more than five years, they have had a special interest in the very uPA enzymatic system, albeit without entering into the mentioned possibilities in regard to medical treatment. At least 15 articles regarding uPA have been published from this institute since 1999.

Most recently, a study of mice that was published in the International Journal of Cancer has aroused international interest. In six cases out of seven, it showed that genetically modified mice who had been made incapable of producing uPA did not form any metastases. The mice were doing fine without the enzyme. It seems, therefore, that the cancer needs this enzyme far more than does the healthy organism.

The perspective is, of course, that by inhibiting the uPA system, the cancer can be kept under control and medicine with strong side effects can be avoided. Both domestic and foreign research now carry conviction that the first part of the theory of Matthias Rath and Linus Pauling holds water. It strengthens the presumption – but unfortunately does not give proof – of the second part of the theory being right as well.

By: Vitality Council

References:
1) http://www4.dr-rath-foundation.org/NHC/aids/study/study01.htm
2) Almholt K, Johnsen M. Stromal cell involvement in cancer. Recent Results Cancer Res. 2003;162:31-42.
3) Rockway TW, Giranda VL. Inhibitors of the proteolytic activity of urokinase type plasminogen activator. Curr Pharm Des. 2003;9(19):1483-98.

www4.dr-rath-foundation.org/NHC/aids/study/study01.htm
cancerres.aacrjournals.org
www.iom.dk