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False Propaganda Against Vitamins

Niels Hertz

November 30, 2005

A frightening warning in an article in the Danish newspaper, Ekstra Bladet, claims that people will get sick from taking Vitamin B and injure their hearts by consuming Vitamin E. These claims are twisted and false.

Condescending evaluations of vitamin supplements are quite common. They rarely come from experts, but often from people who know something about something else and therefore think they know something about everything.

As a rule, it is stated that the vitamins only provide expensive urine and do not help against anything at all. Sometimes this message is spread rather too thickly.
The vitamins are poisonous! As the other day in a large published article in the newspaper Ekstra Bladet: You get sick from nutritional supplements, the headline stated. Further down, it became clear that you would not only get sick. You would die!

Whenever these kinds of statements appear, people get scared. They cannot imagine that anyone will write anything in Ekstra Bladet if it is not true. But unfortunately there are writers who don’t bother with that. This is evident from the mentioned article, which is mainly based on two gross, false claims. Here we comment on them in reverse order.

“The last new thing was the B vitamin folic acid, which should also be able to protect against heart disease. Recently, a large Norwegian study showed that folic acid did not make users less prone to heart disease. On the contrary, they got sick from the pills”.

Is that right? No. It is wrong. In the Norwegian randomised trial (it was called NORVIT), approx. 900 people who had had blood clots in the heart were supplemented with 0.8 mg of folic acid per day for 3-4 years. The table shows the relative mortality and incidence of heart clots in those who received folic acid and those who received inactive pills (placebo.)

……………………..………..……Folic acid……Placebo
Blood clot in the heart…….57,9…………….59,2
Total mortality………………….28,7…………….31,7

As seen, the overall mortality was 9% lower if folic acid was given instead of placebo. The risk of blood clots was also reduced. How does that agree with the fact that people “got sick (meaning heart disease) from the pills”? The answer is that it is not true. Admittedly, none of the differences were statistically significant. It was a trend. But that is not the same as the study showing the opposite of the trend.

And now to the first claim. It is about vitamin E. It was claimed that vitamin E should protect against heart disease, it says, but “when the major scientific studies came, it turned out that it… gave… heart failure, bleeding and an increased risk of dropping dead”.

Heart failure. That claim must come from the HOPE-TOO study, the only one of the many studies with a total of well over 100,000 participants in which heart failure has been found to be caused by vitamin E treatment.

4,000 people with severe atherosclerosis participated in HOPE-TOO. Those who received vitamin E (400 IU/day) had slightly more often weakened heart. The difference was statistically uncertain, i.e. that it could be accidental. The absence of heart failure in all the other studies suggests the same.

On the other hand, a slightly reduced risk of lung cancer was found in HOPE-TOO, and it was reliable. But since this has not been found in other studies either, it is unreasonable to mention it. It could be random anyway.

Another peculiarity of HOPE-TOO was that even though the participants were given 25 times the recommended amount of vitamin E, it could not be seen in the blood tests. On average, the participants had very little vitamin E in their blood, despite the large supplements. The concentration in the blood (17.6 mmol/l) was even at the lower end of the normal range (12-42 mol/l). Either the participants have not taken the vitamins, or they have e.g. taken them on an empty stomach so that they were not absorbed from the intestine. So where does the vitamin E study end up?

In other words: Here a single, guaranteed misleading, result from one small experiment is misused – as “fact”. It is cheating and distortion. And for the record: That you should start bleeding, let alone die from vitamin E in the mentioned doses, is out of thin air. In contrast, the vitamin prevents, in animal experiments, gastric bleeding caused by aspirin.

Professor Maret Traber, Oregon State University, is considered one of the world’s leading vitamin E researchers. She recommends vitamin E for a number of chronic health problems, including heart disease. Louis Ignarro, who received the Nobel Prize in 1998 for his research on blood vessels, unequivocally recommends vitamin E and C for the prevention of atherosclerosis. It works, he says.

Of course, what even such big celebrities think is no argument in itself. It is the substance that counts. Yet. If you are free to choose your advisers, you are likely to prefer the most knowledgeable – and the most reliable.

By: Niels Hertz  MD

References:
1. A. Astrup. Du bliver syg af kosttilskud. Sund og Slank. Ekstra Bladet. 26.11.05.
2. The HOPE and HOPE-TOO Trial Investigators. Effects of long-term vitamin E supplementation on cardiovascular events and cancer. JAMA 2005;293:1338-47.
3. Bonaa KH. NORVIT: Randomized trial of homocysteine-lowering with B-vitamins for secondary prevention of cardiovascular disease after acute myocardial infarction. Program and Abstracts from the European Society of Cardiology Congress 2005; September 3-7, 2005; Stockholm, Sweden. Hot Line II. Iflg. Linda Brooks. NORVIT: The norwegian vitamin trial. Medscape Sept. 2005. (Not published in printed media.)

Selenium May Prevent Degenerative Joint Disease

Claus Hancke

November 24, 2005

For the first time ever, researchers have studied the correlation between selenium deficiency and osteoarthritis, which correlation is surprisingly strong and indicates that selenium supplementation may prevent the Western World’s most common cause of mobility-impairment.

There is a general agreement that selenium is a mineral which western Europeans get less and less of through their diets. Modern agricultural methods and the acidification of the soil has have caused a lowered amount of this vital antioxidant I crops, and thereby a lowered amount of selenium in our bodies. The deficiency is severe enough that, as early as the 1980’s, it widespread problems in Danish pigs so severe that, after some political tug-of-war, supplements were added to their feed. But does this deficiency mean anything for people?

So far the only answer is “probably.” Large population studies in Finland etc. have shown that members of the group which gets the least selenium via diet have the greatest risk of getting cancer.

Just as importantly, in an American randomised study with 1,300 participants undertake nine years ago, it was found that supplements of selenium halved the frequency of new cancer cases. The less selenium presents in the blood beforehand, the greater the positive effect with the supplement. The result was so certain that the study was stopped early for ethical reasons and is being repeated on a larger scale. If selenium prevents cancer so effectively, we should be absolutely certain of its effects.

Meanwhile, researchers from North Carolina’s university in cooperation with the American Center for Disease Control (CDC) discovered another relationship: Selenium deficiency causes an increased risk of arthritis of the knees. The risk of arthritis of the knees increases by 15-20% every time that the body’s selenium content is reduced by 10 micrograms (per kilo body weight). For comparison, the blood of the average Dane contains about 80 microgram/litre while the blood of the average American contains 110.

Among the nearly 900 people who were followed for 15 years, the risk was 40% lower in the third who received the most selenium. If they developed arthritis anyway, there was a tendency that it was to a lesser degree.

This is just a statistical relationship. It has not yet been published in the press, but has been presented in a congress (15.11.05) in San Diego for American arthritis doctors and can be read in an official press release from North Carolina’s university.

Nevertheless, the study’s leader, professor Joanne Jordan, has declared that the group is very excited about their findings. It could indicate that there is a possibility of preventing arthritis in the knee and possibly in other joints. In other words, it might be possible to prevent the most common reason for activity reduction in the western world. In China it is known that extreme selenium deficiency can cause severe cartilage injury in joints as early as during childhood. Does this point in the same direction?

Maybe, but it is not known for certain. According to Joanne Jordan, the next step in to study selenium’s effect on cartilage in the laboratory. The obvious hypothesis is that this effect is due to selenium’s function as an antioxidant. Clinical studies, in other words randomised studies, should be undertaken to find out whether selenium supplements effect pain and the level of function in people with arthritis.

The new finds are not final, but it is the first time that anyone has studied the correlation between arthritis and selenium. It is very surprising that the relationship is so apparent.

By: Vitality Council

References:
1. Rayman M. The importance of selenium to human health. The Lancet 2000:;356:233-41.
2. News Release. Study links low selenium levels with higher risk of osteoarthritis. The University of North Carolina at Chapel Hill: http://www.unc.edu/news/archives/nov05/jordan111005.htm
3. Clark LC. et al. Effect of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. JAMA 1996;276:1957-63.

www.thelancet.com
www.unc.edu/news/archives/nov05/jordan111005.htm
jama.ama-assn.org
www.iom.dk

New Theory on the origin of the flu

Claus Hancke

November 15, 2005

A recent theory claims that one does not catch the flu from contagious people, but by the activation of a dormant virus activated by vitamin D deficiency.

Serious medical journals do not often engage themselves with what private individuals think. In the latest issue of “The British Medical Journal” an exception is made on the journal’s last page, which is written regularly by the pretty named but anonymous female doctor, “Minerva.” Minerva has given her readers interesting scientific news, great and small, every week for decades.

This time she has pointed out a “blog” (an internet forum) with a gripping story on the virtues of vitamin D and why the flu sets in during the winter. She relates that the blog’s author is a member of “The vitamin D council,” a non-profit organisation which wishes to combat vitamin D deficiency.

Minerva recounts that he may be just another person who has hopped aboard the flu bandwagon. But could he possibly have found something important?

The blog is written by the Californian Dr. John Cannell. He explains, including many citations, first and foremost his theory about how the flu arises. The theory states that the flu is not so much the result of contagion, but more the activation of a dormant virus which we already have in our bodies. This virus can be activated and cause the flu when we are weakened by vitamin D deficiency during the winter. It is similar to the mechanisms behind cold sores, where the virus is dormant but can be activated causing a break out.

Does this sound like nonsense? In 2003, a department in the United State’s Center for Disease Control (CDC) disclosed that they had been unable to find any English language documentation for the flu being able to be infectious from person to person.

The recently dead epidemiologist, Edward Hope-Simpson discovered that when the elderly get shingles, it is caused by the same virus which causes chickenpox as a child. It becomes dormant in the body but can cause shingles when one is weakened by age.

Hope-Simpson became interested in the well known, but quite strange, fact that the flu only arises when the sun weakens during the winter. In the tropics, one gets the flu during the rainy season. He found that influenza outbreaks with exactly the same virus occurred year after year at almost exactly the same time in two far separated places, Prague and his English home town, Cirencester. With the help of old church records he found that, despite our faster daily lives, flu epidemics arise at the same time of year as they have for the last 400 years. This is true even in isolated towns; in such places the flu comes at the same time as in big cities.

Therefore, Hope-Simpson believed that flu epidemics are not cause by infection, but by a weakened state caused by the absence of sunlight. Canning now adds that vitamin D has a meaningful effect on the immune system and that the Japanese, as far back as 1945, found that it can protect rats against the flu. The well known vitamin D deficiency during the winter could be the reason for the weakened state that Hope-Simpson postulated.

Canning proposes that we should stock up on capsules of 50,000 units vitamin D in the event of a bird flu pandemic. He does not know if this will do any good, but says that it might save your life.

In any event, as Minerva also believes, his blog (as Minerva also believes) gives us something to think about.

By: Vitality Council

References:
1. www.knowledgeofhealth.com/report.asp?story=Why%20Flu%20Epidemics%20Occur%20in%20Winter
2. Minerva. British Medical Journal 2005;331:1152.

www.knowledgeofhealth.com/report.asp
bmj.bmjjournals.com
www.iom.dk

Dietary Supplement Strengthens Immuno-Therapy Against Breast Cancer

Claus Hancke

November 7, 2005

An American study has shown that the pioneering cancer medicine against breast cancer, Herceptin, can be made 30-40 times more effective when used in conjunction with a harmless dietary supplement: gamma-linolenic acid (GLA). The study’s results are preliminary but calls for further investigation.

Every year, almost 3,500 Danish women get breast cancer. Approx. every fifth of them have a particularly aggressive form of cancer, which you may fear in particular, if you find cancer in the lymph nodes of the armpit during surgery. The aggressive cancer is due to a gene in the affected women which is particularly active and forms large amounts of HER2, a protein. When HER2 adheres to the surface of a breast cell, it reacts with growth agents in the blood that can transform the cell into a cancerous cell and stimulate it to growth.

However, since 1998, there have been medicine available that, in the same way as an antibody, have been able to block HER2 and thus weaken the growth stimulation. The name of the drug is Herceptin® (Trastuzumab) and so far only women have been offered this, who in addition to being “HER2 positive”, have had recurrence of breast cancer that has spread.

More recently, however, research has shown that Herceptin also helps when it is given much earlier, namely as soon as it is known after the operation that the woman is HER2-positive. In Denmark, the treatment can be relevant for approx. 450 women annually. In an experiment with approx. In 3,350 women who received Herceptin for one year, the risk of recurrence of the disease was halved and mortality was reduced by a third. In a Belgian trial with just over 5,000 women, the risk of relapse was also halved – to approx. 6%. Overall mortality was also reduced in this trial, but only slightly and not statistically significantly.

The Danish Cancer Society is now calling on women who have had surgery for breast cancer to find out whether they are HER2-positive and should have the treatment. But unfortunately it is not as risk-free as it sounds. HER2 also plays a role in the heart, and chemotherapy along with blocking HER2 is a cocktail that can cause heart failure. This happens in up to 20%, many of whom have to stop the treatment. How they fare in the long term is not known.

GLA and Herceptin collaborate
All this is mentioned only to say that HER2 can apparently – sensationally – also be attacked from a completely unexpected angle. The vital fatty acid gamma-linolenic acid (GLA), used by many as a dietary supplement, also (in laboratory experiments) inhibits HER2, but by a different mechanism than Herceptin. According to researchers from Northwestern University in the USA, GLA enhances the effect of Herceptin no less than 30-40 times, without affecting healthy cells. The combination means that many more cancer cells die, while others are inhibited in their growth.

The way it works is complicated. The experiments suggest that GLA stimulates the formation of a protein (PEA3), which in turn inhibits the gene that must produce HER2. Since GLA and Herceptin therefore intervene separately – one blocks the formation of HER2, the other blocks the effect – they reinforce each other. Previous experiments have shown that GLA can also independently inhibit cancer in the laboratory.

If even a little of this applies to living people, it is a sensation. But it must be emphasized that these are only laboratory experiments at the cellular level. Further extensive research is needed. It is, as the authors write, on the other hand required. What women with HER2-positive breast cancer must do here and now is, among other things, for now up to the individual.

By: Vitality Council

References:
1. Piccart-Gebhart et al. Trastuzumab after adjuvant chemotherapy in HER2-positive breast cancer. N Engl J Med 2005;353:1659-72.
2. Romond EH et al. Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N Engl J Med 2005;353: 1673-84.
3. Menendez JA et al. Effect of gamma-linolenic acid on the transcriptional activity of the Her2/neu (erbB-2) oncogene. J Natl Cancer Inst 2005;97:1611-15.

content.nejm.org
jncicancerspectrum.oxfordjournals.org
www.iom.dk

Vitamin B12 And Folic Acid Reduce The Risk Of Blood Clots In The Brain

Claus Hancke

October 31, 2005

After Americans enriched their diet with folic acid in 1996, the frequency of blood clots in the brain was reduced by 15%. Now research shows that added supplementation of Vitamin B12 will markedly lower this risk even further.

Immediately, it sounds simple: People with high levels of the amino acid homocysteine in the blood have an increased risk of blood clots in the brain and in the heart. You also know that you can lower homocysteine with folic acid and, to a lesser extent, with B6 and B12 vitamins. When the Americans began to enrich cereal products with folic acid from 1996, both the average American’s homocysteine and the rate of blood clot in the brain decreased by about 15% in three years.

“The money fits”, and then the result is almost obvious in advance, if you want to conduct a lottery experiment, where every other participant gets folic acid, B6 and B12 vitamins. Of course, they get fewer blood clots in the brain.

But the reality is more varied. In Norway, such an experiment (NORVIT) was conducted with 3,750 patients who had just survived a blood clot in the heart. For 3.5 years, they were supplemented with either folic acid (0.8 mg), vitamin B6 (40 mg), both or blind tablets (placebo). Among those who only received folic acid, mortality decreased approx. 10%, but not statistically certain. But in the other two groups the death tolls were increased, not statistically certain either.

Perhaps it is too late to start taking supplements when you are already severely calcified. Or, as will appear, perhaps it was more decisive that the Norwegians “forgot” to give the participants vitamin B12.

An experiment has also been carried out in the USA (VISP). It was with people who had recovered from a blood clot in the brain, but had an increased risk of a new one. Admittedly, the Americans did not initially find any effect either. Supplementation of folic acid (2.5 mg), vitamin B6 (25 mg) and vitamin B12 (0.4 mg) did not reduce or improve mortality or risk of blood clots in the brain. Therefore, the experiment was simply stopped after two years. It was useless, they thought.

B12 is useful if it is absorbed
A close explanation could be the aforementioned enrichment of cereal products with folic acid. After all, the average homocysteine had already fallen by approx. 15% in the Americans. During the trial, it only dropped a further 2%.

But the Americans have since studied the numbers more closely. In doing so, they discovered one important source of error in particular: Many of the 3,680 elderly participants had reduced absorption of vitamin B12 from the gut and therefore had relatively little B12 in their blood (less than 250 pmol/l). This is often seen in the elderly, and it is now known that these elderly need supplements of at least 1,000 micrograms of vitamin B12 per day. But the participants had only received 400.

What would it look like if you now disregarded these participants and concentrated on those with normal B12 uptake? It was decided to investigate. At the same time, participants with reduced kidney function were disregarded, as they also respond sluggishly to these supplements. Finally, participants who were previously receiving medical treatment with B12 were naturally disregarded.

There remained 2,155 people who had no problems absorbing B12. In this large group, the supplements both lowered homocysteine further and reduced the overall risk of death, blood clot in the heart or blood clot in the brain – by 21%! The treatment helped anyway; even a lot when the ability to absorb B12 was intact.

As stated, it appears that the fortification of cereal products with folic acid has reduced the Americans’ risk of blood clots in the brain by approx. 15%. Now it seems that a solid supplement of vitamin B12 on top of that can reduce it significantly more – but the many elderly people, who absorb vitamin B12 poorly, presumably need larger supplements.

This is the result at the moment. It must be verified before it is approved. But the indications are there.

By: Vitality Council

References:
1. Toole JF, et al. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA. 2004 Feb 4;291(5):565-75.
2. Bonaa KH. NORVIT: Randomized trial of homocysteine-lowering with B-vitamins for secondary prevention of cardiovascular disease after acute myocardial infarction. Program and Abstracts from the European Society of Cardiology Congress 2005; September 3-7, 2005; Stockholm, Sweden. Hot Line II. Iflg. Linda Brooks. NORVIT: The norwegian vitamin trial. Medscape sept. 2005. (Ikke publiceret i trykt medie)
3. Spence DJ et al. Vitamin intervention for stroke prevention trial. An efficacy analysis. Stroke 2005;36:2404-2409.

jama.ama-assn.org
www.medscape.com
stroke.ahajournals.org
www.iom.dk

Children Get Smarter From Taking Fish Oil

Claus Hancke

October 24, 2005

The omega-3 fatty acid DHA in fish oil is an important building block for the brain. DHA deficiency in the first years of life may impact the normal development of the child’s brain.

Are children getting smarter from eating fish? Recent studies suggest that fatty acids in fish oil can help certain children with ADHD or dyslexia. But what about infants?

From the last third of fetal life to the end of the second year of life, children’s brains grow so strongly that one speaks of a brain growth spurt. During this period, a lack of a number of vital nutrients, such as fish oil, will affect brain function. The American Journal of Clinical Nutrition recently published a comprehensive review of what is known about fish and young children’s brains.

As a starting point, it is known that the polyunsaturated n-3 fatty acid DHA (docosahexaenoic acid) is highly concentrated in the cell walls of nerve cells. DHA is one of the two important n-3 fatty acids in fish oil. The other is EPA (eicosa-pentaenoic acid). EPA can be converted to DHA, and to a certain extent they can both be formed from the n-3 fatty acid alpha-linolenic acid in e.g. linseed oil.

But does it form enough in a child who is not breastfed or gets oily fish? The question is relevant. It is known that breast-fed babies have up to 40% more DHA in the brain’s gray matter than bottle-fed babies. In addition, it is known that young animals and probably also infants, even if they are neither near-sighted nor far-sighted, will see a little less sharply if they lack n-3 fatty acids. The significance of this is debated.

The importance of DHA has been investigated e.g. by comparing bottle-fed babies with breast-fed babies who got DHA from breast milk. Bottle babies have also been compared with other bottle babies who have received n-3-enriched formula. The children have been tested for intellectual and motor development, attention, etc.

Greater attention
In these kinds of experiments, it has been shown that breast-fed babies fare slightly better on average than bottle-fed babies. But is the difference due to DHA? Nursing mothers may function slightly better than non-nursing mothers, and may have better social relationships, etc. When you correct for this, the differences diminish. Furthermore, there are many other differences between milk substitute and mother’s milk other than the DHA content.

It becomes somewhat clearer when you compare bottle babies, where only half receive extra n-3 supplements. Here the results have been mixed, but on one point a difference has been seen quite consistently: Infants who receive n-3 supplements have a greater capacity for visual attention, i.e. to follow the things they see. This important result has also been obtained in experiments with monkeys.

In animal experiments with rodents, the clearest differences have been found. This is due, among other things, to the fact that these experiments can be set up, so that the difference in brain DHA becomes particularly large. Animals that are starved of n-3 fat become less agile, find it harder to find their way around a maze, etc. Even if there are only minor differences in brain DHA, the animals that do not get fish oils are weakened. Roughly speaking, this is what is known.

So what can be concluded? The authors do not claim that children should demonstrably have n-3 supplementation during the brain spurt. But they claim, after sifting through 258 scientific papers, that the need cannot be ruled out.

– Small differences in brain DHA, which most likely occur between bottle-fed babies with and without n-3 supplementation, may have effects that are currently difficult to detect but could be important, it says. Or to put it more simply: Remember to give babies and toddlers fatty fish or fish oil! They seem to be getting wiser from it.

By: Vitality Council

Reference:
Mc Cann J C, Ames, Bruce N. Is docosahexaenoic acid, an n-3 long chain polyunsaturated fatty acid, required for development of normal brain function? An overview of evidence from cognitive and behavioural tests in humans and animals. Am J Clin Nutr 2005;82:281-95

www.ajcn.org
www.iom.dk

You Must Plug The Hole Before The Boat Sinks

Claus Hancke

October 11, 2005

A Norwegian study has shown that if you have already experienced an acute myocardial infarction, the risk of another such infarction will not be reduced by taking folic acid, Vitamin B6, and Vitamin B12, even if homocysteine levels are lowered thereby.
If you get a great deal of folic acid, the blood content of the amino acid homocysteine will be relatively low. So much is certain. When the content is low, the risk of blood clots in the heart or brain hemorrrhage – other things being equal – is also low. It is also safe, but both are statistics only.

With these facts in the bag, one is tempted to think that supplementation with folic acid must be a good idea. As you know, folic acid is the B vitamin that young women should take to avoid having children with spina bifida. One can agree with the American Heart Association, which advises everyone to get 0.4 mg of folic acid a day, the same dose that women should take as a supplement.

In Tromsø in Norway, the so-called NORVIT trial (Norwegian Vitamin Trial) was the first to test whether supplements also help heart patients who have already had a blood clot in the heart. If the media is to be believed, it ended with a scare.

The results, which were presented in September at this year’s congress of the European Society of Cardiology (ESC), led directly to warnings against folic acid in the press: B vitamins could be dangerous for heart patients, it said, and our own Danish heart association was quick to announce, that folic acid is “still” not recommended for heart patients – even though the month before was said something close to the opposite.

But, as is so often the case, the reports were misleading. Strictly speaking, the Norwegian trial did not show that folic acid is dangerous. If you want to argue that it showed anything at all, it was that the risk of heart attack, stroke, or death decreased—albeit by only a few percent—in those who took 0.8 milligrams of folic acid a day for 3.5 years . However, this was not statistically certain.

The fact is that there were in fact not one, but three trials, with a total of 3,750 people, all of whom had had blood clots in the heart. One showed that a combination of folic acid, vitamin B6 and B12 led to approx. 20% more cases of blood clots in the heart than placebo (cheat pills). The second – the only one where only folic acid was used – showed no difference in reality. There was also no difference in the third trial, where the participants only received vitamin B6.

In one area, the experiments turned out to be successful: those who received folic acid achieved a drop in the blood homocysteine content of approx. 30%. Enough so that one could hope for a nice drop in the number of new blood clots. Which did not appear.

But the questions arise: Is it appropriate for heart patients to be careful about taking folic acid, vitamin B6 and vitamin B12 at the same time?
Or are we talking about completely different anatomical conditions with secondary prophylaxis than there are with primary prophylaxis? After all, you have had a blood clot.

Also at the congress, the ESC’s designated commentator, Ian Graham, doubted the result. He believed that the experiment might have been too small and too complicated to be credible.

One can go a step further and think that the result is purely due to chance. In any case, it is not supported by any theory.
It is more likely that folic acid is simply not suitable for preventing blood clots in severely arteriosclerotic patients. – In other words secondary prophylaxis.

There is a lot of evidence that folic acid – and low homocysteine – slows the development of atherosclerosis in healthy people – i.e. primary prophylaxis. But the usefulness of this function diminishes when the calcification is already very advanced. The bottom plug must be inserted before the boat is sunk.

If folic acid is to prevent blood clots, you probably have to start in good time. On the other hand, the vitamin has other benefits. Among other things. experiments convincingly indicate that it helps to keep the brain young, even in the elderly.

By: Vitality Council

Reference:
Bonaa KH. NORVIT: Randomized trial of homocysteine-lowering with B-vitamins for secondary prevention of cardiovascular disease after acute myocardial infarction. Program and Abstracts from the European Society of Cardiology Congress 2005; September 3-7, 2005; Stockholm, Sweden. Hot Line II. Iflg. Linda Brooks. NORVIT: The Norwegian vitamin trial. Medscape Sept. 2005. (Not published in a printed media).

www.medscape.com/viewprogram/4494_pnt
www.iom.dk

Antioxidants Halve The Damage Of Brain Hemorrhage

Claus Hancke

October 6, 2005

Countless animal studies have shown that the brain injury following a brain hemorrhage can be reduced dramatically with antioxidants. Several clinical human studies are now being conducted.
Next to heart disease and cancer, brain hemorrhage is the most common cause of death in Western countries. Among those who survive, many will face severe difficulties in the years ahead with chronic brain injuries and paralysis. But more and more people will experience a brain hemorrhage because of an increasing number of old people.

Can this gloomy perspective be mitigated? Numerous trials have shown that antioxidants can both prevent brain hemorrhage and reduce subsequent brain injury if the accident nevertheless occurs. This fascinating topic has just been elucidated in a robust overview of researchers from the pharmacological laboratory at the Rene Descartes University in Paris.

Contrary to popular belief, a brain hemorrhage is rarely a hemorrhage. It is far more often a blood clot, which either forms on the inside of one of the brain’s large arteries – in the same way as a blood clot in the heart – or is supplied with the blood. Regardless of the language confusion, the result is the same: parts of the brain on the blocked side get no oxygen and perish, while the victim becomes more or less paralyzed on the opposite side.

This is where the antioxidants come in. They fight free oxygen radicals, which are responsible for the majority of brain damage. The free radicals are formed during a lack of oxygen, but paradoxically, it is not an absolute advantage when the organism breaks down the blood clot itself – or when it is broken down medically, which can more or less be done up to three hours after the first symptoms. The renewed blood supply – this is called reperfusion – unfortunately leads to a massive production of free radicals – and thus further brain damage.
Regardless of whether the blood supply resumes or not, things can go wrong.

Why do these free radicals occur in tissues that do not receive blood or that have only temporarily been lacking blood? The article reviews the possibilities. Certain enzymes e.g, which normally inactivate free radicals, stop functioning. In addition, the weakening of the mitochondria – the energy factories of the cells i.a. – play a role. It is the mitochondria that process the oxygen, and when they weaken, the free (oxygen) radicals leak. It has been proven that the more free radicals are formed, the worse the brain damage.

It is therefore logical to believe that antioxidants can limit the damage. This is also true of a large number of experiments on animals. Here, damage has been reduced by more than 50% by pre-treating the animals with antioxidants such as NAC (n-acetyl-cysteine), resveratrol (the colorant in red wine), lipoic acid (a beneficial and harmless food supplement that is banned in Denmark) or melatonin ( also beneficial, harmless and forbidden for Danes).

With vitamin E, it has also been possible to halve the damage – or more. Of course, it worked best when the treatment was started quickly. Quick help is double help.

There are now several clinical trials on humans, but the difficulty is that you cannot predict when or if a person will have a brain haemorrhage. In the trials, the treatment is only started when the brain haemorrhage has occurred. There are no reliable results yet, and the antioxidants that are tested are unfortunately synthetic substances, which can be patented (and later sold as expensive drugs): Tirilazad, Ebselen, Edavaron and NXY-059. Edavaron is recognized as a treatment in Japan.

What can ordinary people do? The review concludes that antioxidants are “certainly some of the most promising agents against cerebral hemorrhage” and that they are of “great interest” in combination with the medical breakdown of blood clots used today.
You have to choose yourself. But it is worth noting that a solid intake of antioxidants seems to be able to prevent – perhaps tragic – consequences of a brain haemorrhage.

By: Vitality Council

Reference:
Isabelle Margaill et al. Antioxidant strategies in the treatment of stroke. Free Radical Biology and Medicine 2005;39:429-43.

High Dose Intravenous Vitamin C Fights Cancer

Admin

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

Breast Cancer Cannot Tolerate Iron Deficiency

Claus Hancke

September 21, 2005

Breast cancer is fought just as effectively by utilising the body’s iron deposits as by using chemotherapy. This has been shown in an American animal study.

TV and radio sometimes gives the impression that researchers have lost interest in antioxidants. Meanwhile, research in this field continues.

The following describes a study which has recently been published in the worlds leading journal for research in the field of free radicals. Free radicals are neutralised by antioxidants such as vitamins E and C etc.

The journal is called Free Radicals in Biology and Medicine. It comes out every 14 days with about 125 large pages which contain summary articles as well as 10-12 descriptions of new research. It has an editorial staff with nine members and an international review board with 73 members, all of whom are university-researchers. It is unfortunately written in such technical, biologic-biochemical, language that it is not understandable for normal nutrition experts and doctors. But the size and format of the journal is an expression of the intense international research which is still producing new information for the understanding of the roles of antioxidants and free radicals in disease.

The study in question has special interest for doctors who treat atherosclerosis with EDTA. EDTA is given intravenously and binds the bloods heavy metals as well as iron. Because both iron (excess) and heavy metals strain the organism with free radicals, EDTA works as an antioxidant.

In the study, mice were given a human form of breast cancer. The mice did not receive EDTA, but a related substance called desferal (desferoxamine) which is an old medication which removes iron from the blood. The question was whether the mice would be better off after, thanks to the desferal, they were drained of their iron deposits. They were!

Desferal halved the cancer growth and was just as effective as the much more poisonous chemotherapy (in this case, doxorubicin, which is commonly used against breast cancer). When the mice received both desferal and the chemotherapy, the cancer inhibiting effect was slightly larger than with each of the two treatments alone.

Antioxidants support chemotherapy
The method of action is unknown. It is known that an excess of iron can create free radicals and that desferal, like EDTA, can be regarded as an antioxidant. But some conditions of the study showed that that was not the determining factor. The explanation is more rather that the fast growing cancer cells need more iron than normal cells. Desferal starves them of iron which stops their growth.

Contrary to the expected, the study said nothing about the combination of chemotherapy and antioxidants. Cancer doctors in Denmark advise against this combination. They believe that chemotherapy works by creating free radicals and that the treatment therefore is ruined by antioxidants such as vitamins E and C, selenium, Q10, etc.

This is rejected by the article as an antiquated way of thinking. Typical chemotherapy (doxorubicin, cisplatin, etc.) does not work by creating free radicals, but by blocking vital enzymes with difficult names such as topoisomerase etc. This has been proven by a number of researchers (see ref.)

It is actually more probable that antioxidants support chemotherapy. In any case, studies have shown that chemotherapy can be weakened by adding free radicals (hydrogen peroxide). It therefore seems wise to get rid of them with antioxidants, and thereby both streamline chemotherapy and make it less poisonous.

The American researchers who published the study (and who, in addition, work for the American Food and Drug Administration) showed, sensationally, that breast cancer cells can be held in check if they are starved of iron. They also believe, based on their own research as well as the research of others, that cancer doctors should sooner ban free radicals than antioxidants.

This is just basic research. In the future there will be clinical trails which may show that this method works on humans.

By: Vitality Council

References:
1. Hoke E.M et al. Desferal inhibits breast tumor growth and does not interfere with the tumoricidal activity of doxorubicin. Free Radical Biology & Medicine 2005;39:403-11.
2. Senturker S et al. Induction of apoptosis by chemotherapeutic drugs without generation of reactive oxygen species. Arch Biochem Biophys 2002;397:262-72.