Contradictions about vitamins

 April 26, 2012

One may wonder about the Danish newspapers’ poor interest in the latest vitamin report. First of all, the report predicts dead to those who take vitamin pills, secondly, the turn-over for vitamins is one and a half billion kroner a year. The subject must interest many.

Here the report itself will not be discussed. It is already commented. On the other hand, attention must be paid to a very serious issue concerning the marketing of the report: The contradictory statements that a prominent researcher has used the report to make.

The statements are from chief physician Christian Gluud from Rigshospitalet. He has previously said peculiar things. It’s hard to forget how he on television declared antioxidants (like vitamin E and vitamin C) to be carcinogenic, even when they occur in fruit and vegetables. However, in fruit and vegetables there was, he believed, “a lot of other substances that might either correct the potential damage caused by the antioxidants or that could completely neutralize them.”

You might consider this amusing statement the next time you eat broccoli. It is thus an antidote to vitamins, you are eating!

Currently, Gluud said on TV that his latest study, which combined the results of different trials, is based on trials with commonly recommended vitamin doses. And yet, in almost all trials, there were used from five to twenty times the recommended dose or more.

Gluud has further said (the news program Deadline 2.4.2012) that his group has revealed that, for example, the antioxidants Vitamin C and selenium are directly life threatening, as they increase mortality by 4%. And yet, his report frees both of the two antioxidants for this accusation.

In the TV2 news (22.3.2012) Gluud said that “it’s quite common vitamin pills in very common doses that give the increased mortality.” But in an interview with Medwatch.dk he said the opposite: He could not comment on that subject – that multivitamins increase mortality – because no one had studied it!

If you ask chief physician Gluud, you may obviously get the answer that his current state of mind indicates. One moment, common vitamin pills are dangerous poisons, the next, it is not known, and at one time, selenium and vitamin C are poisonous, but at another time and towards another audience – those who read the report – they are harmless.

The contradictions do not prevent Gluud from hoping that the report will have “a practical and industry related consequence,” as he says. What that means is easy to understand. Gluud is/has been chairman of a lobby group that has sought to influence the European Commission to prevent the free sale of vitamins. They must be made into drugs, which in practice will push small vitamin companies out of the lucrative market, which alone in Europe is more than $ 20 billion a year.

When a researcher is politicizing, he invariably throws a dubious light over his research, justly or not. Worse, however, is when the researcher is facing the public, on a topic of great importance, against better knowledge.

In doing so makes him disqualified.

By. Niels Hertz, M.D

Promising treatment for macular degeneration

December 22, 2007

New orthomolecular treatment named as the “first choice” for AMD, otherwise known macula degeneration.

In the November 28, 2006 edition of the Vitality Council Newsletter we reported on a study which indicated that eating eggs, which contain the antioxidants lutein and zeaxanthine, has positive effects on AMD.

Almost two years ago we described a maybe even more important study undertaken at the University of Rome. It showed that normal recommended doses of simple dietary supplements prevents the most common form of blindness, the age related degeneration of the retina otherwise known as “retinal calcification.” This is what medical professionals call AMD. About one in eight people over the age of 85 have AMD severe enough to cause vision loss.

This study has recently been published again, giving us grounds to discuss AMD in more detail.

One does not become completely blind due to AMD. Peripheral vision is still maintained, enabling one to orient themselves in a room or go for a walk. Even so, AMD does cause handicap. Central vision is lost, which means that the ability to see shapely is lost. Therefore reading is impossible, seeing the TV, cooking, using tools, working on the computer, and recognising friends and family is difficult. A grey dot in the middle of the field of vision replaces everyone’s faces.

Central sight is governed by a yellow spot on the eye’s retina where the highest concentration of colour registering cones is found. This is why one of the first things lost in AMD is colour vision.

The changes in AMD can be directly observed on the retina when one looks into the eye. In the early stages it is characterized by small or larger deposits of yellowish waste products in the eye. Every one of these deposits represents a hole in the field of vision. This is unnoticeable so long as these hoses are small. Almost everyone over the age of 50 has at least one of these deposits, but if there are many deposits of greater size, the risk for blindness is great.

Severe cases of AMD can be characterised by an accumulation of larger deposits alone. This is called dry AMD. Another, and more dangerous, form is the so called wet AMD. In this form “leaky” blood vessels grow in under the retina, possibly as the body’s effort to bring more energy to the retina. The result is that liquid seeps out of these vessels causing total destruction of central vision. This can occur very quickly, but with quick intervention of an ophthalmologist (eye doctor) the new blood vessels can be blocked with laser treatment and vision can be saved in many cases.

The deposits and new blood vessels lead to the creation of dents in the retina. In severe cases scars form and pull on the retina. This leads to vision where straight lines seem bent. Often, but not always, one can discover the beginnings of AMD by holding a piece of graph paper at a normal reading distance and looking at it one eye at a time. If the lines are curved, an eye doctor should be consulted immediately.

New methodology
The republished study mentioned earlier is a double blinded study that showed with statistical certainty an improvement in the sight of patients with early stage AMD after they received a combination of n-3 fatty acids, Q10, and L-carnitine. The improvement in sight, which was slight, was first present after 3-6 months, after which sight remained stable until the end of the study one year later. This effect lasted even longer in a following study. It was also observed that the number of deposits decreased! This is important and very promising. Improvement occurred primarily for those with mild cases, but also for some with more severe AMD. Early diagnosis is paramount.

The theory behind these finds is that AMD is a disease of the mitochondria, which means that it is a disease which affects energy production in the cells. This is supported by the fact that cells from AMD affected retinas have more damaged mitochondria than normal cells when viewed under and electron microscope. The logic behind the treatment used in the study is therefore the following:

The vitamin-like substance carnitine is necessary for mitochondrial fat uptake and metabolism.

The fat is added as n-3 fatty acids, like those found in fish oil. N-3 fats compose no less than 30% of the structure of the retina!

Q10 can be understood as the motor’s sparkplug. It optimises metabolism so that energy production can start. The body’s own Q10 production falls with age and because of this, and carnitine deficiency, there becomes less energy available. It is hardly coincidental that patients with wet AMD have less Q10 in their blood than normal.

This important study powerfully indicates that quick action can stop newly diagnosed AMD. The authors strongly believe that their treatment should be the treatment of choice for newly diagnosed AMD.

By: Vitality Council

References:
1. Feher et al. Metabolic therapy for early treatment of age-related macula degeneration. Orv Hetil 2007;148:2259-68.
2. Feher et al. Improvement of visual functions and fundus alterations in early age-related macular degeneration treated with a combination of acetyl-L-carnitine and coenzyme Q10. Ophtalmologica 2005;219:154-66
3. Feher et al. Mitotropic compounds for the treatment of age-related macular degeneration. The metabolic approach and a pilot study. Ophtalmologica 2003;217:351-7
4. Blasi et al. Does coenzyme Q10 play a role in opposing oxidative stress in patients with age-related macular degeneration? Ophtalmologica 2001;215:51-54.
5. Feher J et al. Mitochondrial alterations of retinal pigment epithelium in age-related macular degeneration. Neurobiol Aging 2005;June 22: 15979212.

New slander against antioxidants

March 13, 2007

A new article maintains that antioxidants cause death, but the article is based on a comparison of results from incomparable studies.

Once again a scientific article has created a commotion regarding antioxidants. It claims that they cause death. This has been heard, and disproved, before. Because of the common uncertainty regarding this subject, we are nonetheless forced to take a stand regarding this claim.

The man behind this claim is a Serbian professor from a university located in the town of Nis. One of the co-authors is a Danish physician who has, among other things, declared antioxidants to be poisonous and cancer causing on Danish TV. He even suggested that they are poisonous in the amounts found in vegetables.

The study is a so called Meta analysis. It combines as many old studies on antioxidants as possible and extracts a kind of average from their results. Small four week studies are blended up with larger studies which have gone on for up to 12 years. Studies where very small doses were used are blended up with studies on mega doses, studies using one antioxidant are blended up with studies on combinations of antioxidants (e.g. vitamin E, vitamin C, and selenium), and so on. Among the studies used, there are at least eight different combination treatments using vitamin E. This enormous mess alone causes the study to be somewhat questionable. One cannot calculate an average between apples and oranges.

This is not even the worst part. In an attempt to prove that vitamin E increases risk of death (the articles primary claim), the ignored studies where selenium was used together with vitamin E. The selenium studies often showed reduced mortality and lowered cancer risk. This was not good for the Meta analysis authors, it disturbed their theory. They eliminated 11 essential studies on vitamin E and selenium from the analysis.

Selenium was ignored, but that wasn’t enough. The still couldn’t prove that vitamin E is harmful. The numbers wouldn’t work. To solve this, the article uses the fact that the antioxidant beta-carotene, the yellow colouring in carrots, increases death rates in smokers. This is commonly accepted (although not completely certain). In two of the largest studies conducted on antioxidants, a very slightly increased death rate was found due to a combination of beta-carotene and vitamin E.

More peculiarities
Common sense lends to the conclusion that beta-carotene is the villain in these studies. This was known in advance. Combinations of vitamin E with e.g. vitamin C and/or selenium do not increase mortality. More likely the opposite is true. In the large and very thorough French SU.VI.MAX study, death rates in men fell by over a third when they received vitamin E and vitamin C as well as selenium (besides zinc and beta-carotene!). This introduced a new era because this was the first time in our part of the world that a large array of antioxidants was used in study; which is what most people recommend. The antioxidants in our food are an orchestra, not solo instruments. They must play together to work. In a Chinese study from Linxian the same thing was found: lower mortality after supplements of vitamins E and C, selenium, beta-carotene, and vitamin A.

But the article in question maintains that vitamin E causes death. The claim is built, along with the discussed “manoeuvres,” on the two aforementioned studies, because the other vitamin E studies are insignificantly small in comparison. In these studies vitamin E was used with beta-carotene, and vitamin E was blamed in the Meta analysis for the poor results.

This is like claiming that mineral water is deadly if someone dies after drinking water mixed with arsenic. This conclusion is insane. The arsenic is deadly, not the water. Even though A+B is dangerous, it can naturally not be claimed that both A and B are dangerous alone.

There are other peculiarities in the article. Among other things, in at least two of the studies used, mortality was calculated many years after the end of the study. This is comparable to blaming a traffic accident for back pain when the pain became apparent eight years after the traffic accident. This type of measure was apparently necessary to get the desired results.

It is very easy to make these arguments in a scientific journal. If not for the press, it would be ignored. The article is based on a comparison of a number of incomparable articles, and this makes it hardly worth the effort it takes to make it better. It has also been exposed to sharp criticism. It has been clearly dismissed by two unrelated statisticians and by a professor of nutrition at Harvard University, Meir Stampfer. Stampfer is world renown and among the leading figures in nutrition studies encompassing over 300,000 people. He says that he will continue taking his vitamin supplements, unfazed by the article. But he adds that the article can lead to misinterpretation of the information that we have.

This is unfortunately an all too real possibility. Not in the least because the analysis’s authors insistently do the same.

By: Niels Hertz MD

 

References
1. Bjelakovic G, Nikolova D, Gluud LL et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention trials. JAMA 2007;297:842-857.
2. Virtamo J et al. ATBC Study Group. Incidence of cancer and mortality following alpha-tocoferol and beta carotene supplementation: A postintervention follow up. JAMA 2003;290:476-485.
3. Lee IM et al. Vitamin E in the primary prevention of cardiovascular disease and cancer. The Women’s Health Study. A randomized, controlled trial. JAMA 2005;294:56-65.

jama.ama-assn.org

Alzheimer’s disease: The third diabetes

May 4, 2006

According to a revolutionary theory, Alzheimer’s is caused by diabetes in the brain. The theory throws light on the need for antioxidants.

It has been one hundred years since the discovery of Alzheimer’s disease. Alzheimer’s is the most severe disease of dementia, and many of us will suffer from it if we become old enough. Those who get Alzheimer’s suffer from an unavoidable dementia which worsens until they loose contact with reality entirely. The brain shrinks and the spaces between the brain cells become filled with a peculiar substance called amyloid. A network of fibres is produced within the cells, decreasing the strength of the chemical signals that the cells use to communicate.

The medical treatment for Alzheimer’s is currently nothing to get exited about. Its function is to strengthen the chemical signals between the cells, but its effects are few. Now, one hundred years after the disease’s discovery, a surprising new theory has paved the way for new possibilities in the treatment of Alzheimer’s. According to the theory, Alzheimer’s is nothing more than a type of diabetes! The theory has such strong foundations that some already call Alzheimer’s “type 3 diabetes.”

Diabetics should not be alarmed by this find. Type 3 diabetes is in no way connected with either insulin requiring type 1 diabetes or the so called old age diabetes, type 2 diabetes. Type 3 diabetes only shows itself in the brain. How does it get there?

The explanation is simple when one knows a few facts about diabetes and insulin: With classic diabetes one lacks insulin, which is normally produced in the pancreas. This is unfortunate because insulin is necessary for the sugar I the blood to enter the cells, where it can be used for energy. The brain is especially dependent on insulin, because it can only metabolise blood sugar (fructose and glucose), not fat as in other tissues.

Therefore the brain needs insulin. But where does it get it? The new theory is based on new knowledge. The brain makes its own insulin! This occurs in the temporal lobes and in deep lying areas of the brain, namely the hippocampus and the hypothalamus. Insulin produced in the brain only affects blood sugar locally as it cannot leave the brain. Likewise, insulin produced by the pancreas cannot enter the brain. One can thus have diabetes in the brain without having it in the rest of the body and the reverse.

Q10 protects the brain
Multitudes of data have shown that there are signs of defect in the brain’s sugar metabolism already in the early stages of Alzheimer’s. Is this due to type 3 diabetes, seen as a lack of insulin and therefore sugar within the cells? A solid argument for this new theory is based on a recent animal study where the effect of insulin in the brains of the animals was blocked chemically by an injection of a special insulin toxin (streptozotocin). The animals not only became demented due to the resulting brain diabetes, but also produced fewer neurotransmitters, produced deposits of amyloid, and produced fibres within the nerve cells; just like one finds in Alzheimer’s.

Alzheimer’s could thus be the result of the brain lacking the energy it needs to perform its functions. According to a very prominent researcher in this field, Suzanne de la Monte from Brown University, lack of insulin in the brain causes the production of free radicals (causing oxidative stress) because the weakened cells cannot neutralize them because, for example, they cannot produce the necessary enzymes. The amassed free radicals cause the amyloid deposits, and fibre formation, and so on. They also kill the brain cells.

But if the free radicals are the central reason for the nervous damage, antioxidants should help. Is this the case? Yes; in another recent animal study utilizing the same insulin poison, the animals (rats) were given large doses of Q10 for three weeks following the injection of the poison. The treated animals were much better off in all of the subsequent tests. Their brain cells produced more energy, they were better able to find their way in a labyrinth, and they produced more signalling chemicals in their brains.

It is not unreasonable to mention here that there have been many studies which have shown that long time users of vitamins C and E have a considerably reduced risk of getting Alzheimer’s; or that there is a statistical link between low blood levels of selenium and the quick development of dementia. Vitamins E and C, as well as selenium and Q10, are antioxidants.

Is this comparison valid? This can be considered; studies using human subjects will take shape in the coming years.

By: Vitality Council

References:
1. Ishrat T et al. Coenzyme Q10 modulates cognitive impairment against intracerebroventricular injection of streptozotocin in rats. Behav. Brain Res. 2006; Apr 16;(Epub ahead of print)
2. Lester-Coll N et al. Intracerebral streptozotocin model of type 3 diabetes: Relevance to sporadic Alzheimer disease. J Alzheimers Dis. 2006;9:13-33.

Antioxidants against macular degeneration and blindness

March 9, 2006

Antioxidants can delay the most common cause of blindness in Denmark. It looks like they also can prevent it. Other supplements can possibly directly improve the sight – if they are taken early enough.

The most common cause of blindness in the U.K. is macular degeneration, also known as AMD. AMD is the age related degeneration of the area of the eye (retina) where light is collected, like rays hitting a magnifying glass, causing sharp sight. This degeneration thereby causes blurred sight. Thousands of people in the U.K. are affected by AMD each year. Many more suffer from other forms of poor sight.

The more mild forms of AMD are quite common. With these forms, sight is reduces to such a small degree that the loss is normally not noticed. Optometrists can ascertain such mild forms of AMD with the finding of small yellow spots on the retina under an eye exam. These defects are composed of accumulated waste products. Almost everyone over the age of 50 has at least one such defect. Small defects are unimportant, even when there are many. But, if they are larger there is a risk of serious AMD. About 30% of those with larger defects will have advanced AMD within five years.

Therefore it created a sensation when, in 2001, an American study showed that this five year risk could be reduced to 20%, meaning by a third, with the supplement of zinc and antioxidants. The doses given in the study were: 500 mg vitamin C, 400 units vitamin E, 15 micrograms beta-carotene as wall as no less than 80 mg zinc per day. Treatment with antioxidants alone appeared to be just as effective, but could not be proven statistically.

But how does one know if one has the early stages of AMD? Because the loss of sight in such cases is minimal, one might not go to an eye doctor. Therefore it is recommended that everyone over the age of 55 undergo an eye exam so they can consider whether or not they should take supplements. Because beta-carotene has been reported to cause lung cancer in smokers, this advice is only relevant to non-smokers.

Antioxidants can also inhibit the development of AMD, but this use is not often considered. The question however remains whether antioxidants can prevent AMD from occurring in the first place. A new Dutch study implies that they can.

Sharper sight
In this study 6,000 residents of Rotterdam were followed starting from the years 1990-93. In 2004 560 of them had AMD, but it was not entirely random who developed AMD. Both a high intake of zinc and vitamin E lowered the risk, but only a little. If one received high doses of both vitamins C and E, beta-carotene and zinc, the risk of developing AMD was reduced an impressive 35%.

An Italian randomised study published last year showed even more intriguing results. In this study 106 patients with an early form of AMD were treated over the course of a few years with a combination of fish oil (n-3 fatty acids), the antioxidant Q10, as well as the dietary supplement, carnitine. The goal was to improve the fatty acid metabolism of the retina. Carnitine advanced the metabolizing of fat such that the depositing of waste products was counteracted. This is important in the retina seeing that the concentration of n-3 fatty acids is even richer than in brain tissue. 30% of the matter in the retina is composed of n-3 fatty acids as opposed to 20 % in the brain.

The result, with regards to light sensitivity in centre of the eye, visual acuity (measured with a normal eye chart), and perceptual changes in the retina, was not only the progress of the disease was stopped, but that there was also a direct improvement! The area of the eye where defects could be seen was not just unchanged, but had shrunken! All of this was statistically sound.

With advanced AMD one is both blind and can see. One cannot read, watch TV, or recognize faces. But peripheral vision is retained. One can see out of the corner of the eye, so it is still possible to orientate oneself in space and walk, with care. This functional blindness can, in many cases, be improved by antioxidants and, according to the above mentioned research; the condition can even be improved by simple dietary supplements, if they are taken in time.

By: Vitality Council

References:
1. Age-Related Eye Disease Study Research Group.Arch Ophthalmol. 2001 Oct;119(10):1417-36. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8.
2. Feher J et al. Ophthalmologica. 2005 May-Jun;219(3):154-66.Improvement of visual functions and fundus alterations in early age-related macular degeneration treated with a combination of acetyl-L-carnitine, n-3 fatty acids, and coenzyme Q10.
3. van Leeuwen R et al. JAMA. 2005 Dec 28;294(24):3101-7. Dietary intake of antioxidants and risk of age-related macular degeneration.

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jama.ama-assn.org

Antioxidants Halve The Damage Of Brain Hemorrhage

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.

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By: Vitality Council

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

Green Diet And Antioxidants Act Against Prostate Cancer

August 16, 2005

A radically changed lifestyle together with antioxidant supplementation seems to stop the growth of early prostate cancer, while the blood becomes eight times more capable of fighting cancer cells.

Some studies with humans and numerous animal trials and population surveys have indicated that antioxidants counteract cancer. Nevertheless, only a few researchers have examined whether they help against cancer in humans when the disease is a reality. An American trial now shows that this may be the case, at least by cancer in the prostate.

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By: Vitality Council

References:
Ornish D et al. Intensive lifestyle changes may affect the progression of prostate cancer. The Journal of Urology 2005;174:1065-70.
Ornish D et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA 1998;280:2001-7.

Antioxidants Prolong Life

May 17, 2005

An antioxidant enzyme that protects cellular energy production has been found to prolong the lifespan of mice by 20%. A world-renowned researcher thinks that this same method may also be used for humans.

Antioxidants prolong life. If you manipulate with the genes of mice to form extra much of the antioxidant enzyme catalase, the mice will live on average 20% longer.

At the same time they age more slowly, as seen by a lower tendency to cataracts as well as less age-related weakening of the heart muscle. Something similar can be achieved with human beings, though manipulation with human genes is not an option.

………………………………..

By: Vitality Council

References:
1. Science (DOI 10.1126/science.1106653).
2. Rudolph RE, Vaughan TL, Kristal AR, Blount PL, Levine DS, Galipeau PC, Prevo LJ, Sanchez CA, Rabinovitch PS, Reid BJ Serum selenium levels in relation to markers of neoplastic progression among persons with Barrett’s esophagus. J Natl Cancer Inst. 2003 May 21;95(10):750-7.

www.sciencemag.org
jncicancerspectrum.oupjournals.org
www.iom.dk

Antioxidants Relieve the Adverse Effects of Chemotherapy

November 15, 2004

Children suffering from leukaemia tend to be more ill and be hospitalized longer if they are not given antioxidants.

The primary effect of chemotherapy is not through free radical activity but it does strain the organism with free radicals. Free radicals are combatted by antioxidants like vitamin C and -E. This piece of information is important, because not taking enough antioxidants while going through chemoterapy will result in more adverse effects and the treatment results can be delayed.

American doctors from several universities have published these results after having studied 103 children receiving chemotherapy for leukaemia. An evaluation of the children’s diet showed that they usually only got 1/3 – 2/3 of the recommended or normal amounts of various antioxidants. The reason for this is probably the treatment causing general malaise and reduced appetite.

The children who got the most vitamin C were hospitalized for a significantly shorter period and the children who got the most vitamin E suffered fewer infections and fewer adverse effects of the chemotherapy. The doctors conclude that a low intake of antioxidants results in more negative effects of the treatment.

The results can be related to a study of 49 American women who received chemotherapy for breast cancer and were asked about their use of dietary supplements. Multivitamins and vitamin E were the preferred supplements among the 35 women who did use supplements.

The women who took these vitamins maintained a better immune defence during the treatment – i.e. the number of white blood cells in their blood was less reduced during treatment compared to the women who did not use vitamin supplements. On the other hand, the number of white blood cells was more reduced in women taking relatively large amounts of the vitamin B9, folic acid.

It is very common for cancer patients to use dietary supplements. More than every other cancer patient at a hospital clinic in London used supplements, but less than half of them had told their GP about it.

By: Vitality Council

Source:
Kennedy DD, Tucker KL, Ladas ED, et al. Low antioxidant vitamin intakes are associated with increases in adverse effects of chemotherapy in children with acute lymphoblastic leukemia. Am J Clin Nutr (United States), Jun 2004, 79(6) p1029-36.

www.ajcn.org
www.iom.dk

Not All Antioxidants Prevent Cancer

October 1, 2004

The Cochrane Institution is very well-respected for its objective consideration of medical issues. The last report from The Lancet today does not actually reveal anything truly new, despite a very useful summary of results from earlier prevention studies made with antioxidants. The results are listed after each antioxidant and after each type of cancer in the gastrointestinal tract.

The good news is that it looks as if selenium may very effectively prevent cancer diseases in the gastrointestinal region, as selenium both halves the frequency of cancer as well as the rate of death in the group of people taking selenium compared with the group taking placebo.

The disappointing news is that certain other antioxidants do not have any cancer-preventive effect in the studies mentioned and in some cases they even have harmful effects – mainly attributed to beta-carotene. This is a well-known fact.

The authors are inclined to think that the ones who might be harmed by antioxidants are people who are not very strained by the harmful free radicals in the first place. However, the authors will not warn against taking moderate doses of antioxidants or eating fruits and vegetables, and they thereby recognize the importance of getting moderate amounts of these antioxidants.

The study should be a memento for the authorities who prevent the public from being informed with fair and useful information on effects as well as side effects of dietary supplements. This censorship conceals positive as well as negative research results to the consumer who is left only to pure speculation about the use and dosage of the antioxidants which could be very beneficial if used correctly.

Antioxidants prevent atherosclerosis with great probability, but, naturally, this must happen before the atherosclerosis is far advanced. Based on his own research, the Californian Nobel Prize Winner Louis Ignarro, one of the world’s leading experts in vascular surgery, has recently in very clear terms encouraged anyone who want to avoid having blood clots to take supplements of vitamin C and -E.

In the last three months alone, the Vitality Council have posted at least six press releases about new scientific research regarding antioxidants; all involving important – in some cases essential – new knowledge from the leading research centres around the world.

By: Vitality Council

Reference:
Goran Bjelakovic, Dimitrinka Nikolova, Rosa G Simonetti, Christian Gluud Antioxidant supplements for prevention of gastrointestinal cancers: a systematic review and meta-analysis Lancet 2004; 364: 1219-28.

www.lancet.com
www.cochrane.dk/index.htm
www.iom.dk

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