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

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.

Glusosamine is more that just glucosamine

March 2, 2006

Watch out. Read the declaration carefully, when you buy Glucosamine for your osteoarthrosis.

According to a new research study, Glucosamine did not help against osteoarthrosis of the knees. According to another study, glucosamine was so beneficially, that it ought to be standard treatment. Its important to know, that the Glucosamine in the two studies were not the same type.

If you are to believe the publicised GAIT-study, it is meaningless to take glucosamine for arthritis of the knees. It just doesn’t work.

The GAIT-study was both large and thorough. It encompassed 1,583 patients with arthritis and lasted for 24 months. The participants were on average 53 years old and 2/3 of them were women.

These many arthritis patients were organised into six groups by lottery. These groups receive the following treatment:

  1. 1,500 mg glucosamine daily
  2. 1,200 mg chondroitine sulphate (which is like glucosamine) daily
  3. A combination of the two first treatments
  4. 200 mg of the prescription medicine Celebra
  5. Placebo

No one knew what they received and all of the participants answered detailed questions about their pain, stiffness, walking distance, and so on before and after the 24 weeks. Each participant then received a score based on their answers which indicated the severity of their symptoms.

The goal of the study was to find out how many of the participants showed a 20% improvement after the 24 weeks, but the results were surprising. No fewer than 60% of those who received the placebo had a 20% or better improvement. The results were only slighty better in the other groups: 64% for the glucosamine group, 65% for the chondroitine sulphate group, 67% for the combination group, and 70% for the group taking the prescription medication. Only the last group differed from the placebo group enough to be statistically significant.

The combination treatment did work for a small group (354 of the participants) who related mild pain after the treatment as opposed to moderate-strong pain. 80% of these people were (at least 20%) better off.

But the glucosamine alone was not better than the placebo.

Protects the cartilage
Another study called the GUIDE study was presented in November at the yearly meeting of The American College of Rheumatology. It included 318 patients (88% women) who also had arthritis in their knees. They received daily supplements of:

  1. Placebo
  2. Glucosamine (1,500 mg per day)
  3. Paracetamol (1 gr. three times daily)

This study also lasted a half year, but this the groups which received paracetamol and glucosamine reported an improvement of 30% more than the placebo group, even though the study was structured the same way as the GAIT-study. There was also a tendency that the glucosamine was better than the pain relieving paracetamol.

Why was there such a large difference between GAIT and GUIDE? This can possibly be explained by an editorial in the New England Journal of Medicine, which originally published the GAIT-study.

The difference could be that glucosamine-hydrochloride was used in the GAIT study whereas GUIDE used glucosamine-sulfate. Sulfate is crucial for the effectiveness of glucosamine.

Two randomised studies have shown that glucosamine-sulfate puts the breaks on the development of arthritis in the knees. This could be proven using X-ray photographs.

Glucosamine sulphate counteracts the breakdown of cartilage!
The New England Journal of Medicine editorial comment on the GAIT study related the following: “Arthritis patients who wish to take dietary supplements… should… take glucosamine-sulfate, not glucosamine-hydrochloride.” The lead author of the GUIDE-study stated that, “1,500 mg glucosamine-sulfate once a day could become the preferred treatment for arthritis in the knees.” The studies ended differently, but their recommendations are the same!

So read the label carefully.
It should read: “500 mg Glucosamine-sulfate, corresponding to 400 mg Glucosamine.”

By: Vitality Council

1. Clegg DO et al. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med. 2006 Feb 23;354(8):795-808.
2. American College of Rheumatology Annual Scientific Meeting in San Diego, California. Press release.

Calcium supplements with vitamin D against colon cancer?

February 18, 2006

A large study attempted to show whether or not calcium and vitamin D prevent colon cancer. It was a strange study, using low doses over a short period.

There are probably those who believe that the latest study on calcium and vitamin D shows that neither is good for anything. But we should hesitate before going to that extreme. One can also believe that the study was not suited to draw this conclusion. Or, as it is stated in a leading editorial in “The New England Journal of Medicine:” the conclusion should be interpreted in light of the study was complicated and in light of the probability that the doses of calcium and vitamin D were too low.

The debate regards the insidious and widespread cancers of the colon and rectum. Half of a group of 36,282 American women between the ages of 50 and 79 took part in a seven year study where they received daily supplements of 1,000 mg calcium and 400 units vitamin D to see if reduced their risk of these diseases. The supplements given are the same as two normal calcium and vitamin D vitamin tablets, which many take to strengthen their bones. After the seven years the researchers assessed the number of women who developed colon and rectum cancer. The result was disheartening: Whether the women received supplements or placebo had not effect on the risk.

There was a single positive find buried in the data. The women who had the least vitamin D in their blood during the study had with statistical certainty the greatest probability of developing colon cancer. This could indicate that vitamin D has a positive effect. There was also a tendency, but only a tendency, that these women had the greatest benefit from the supplements.

Quite a lot of things contribute to that this conclusion be taken with a grain of salt. This is partially due to that the study was very complex.

Possibly the most important objection is that it “only” lasted seven years. It is believed that colon cancer takes 10-20 years to develop before it is diagnosed. It the supplements prevent a new cancer from forming it is clear that for this reason no effects will be found as early as after seven years. This has been considered: Participants in the study will be monitored further for the next five years.

Strong objections
If the goal was to show a difference within the seven year period, those responsible should have at least ended the study by examining the intestines of all of the participants in order to find early cancer stages, or polyps. This did not occur. There was neither the money nor the resources necessary to do over 35,000 intestinal examinations. It was only possible to establish that the number of independently undertaken intestinal exams and the number of discovered cancers in the two groups were about the same. But maybe nothing more can be expected.

One confusing detail is that the study participants were allowed to continue taking the supplements that they had taken before the study along with the supplements that they received as a part of the study. On average they received 1,100 mg calcium and 350 units vitamin D, both close to the recommended dosages, before the study began. Many of them therefore must have received very large doses of calcium, over 2,000 mg, per day. Is it reasonable to guess that this is the reason for the slightly increased frequency of self-reported kidney stones? 2.4% of those who received supplements and 2.1% of those who received placebo, got kidney stones during the seven years.

Also, the average age was relatively low (62), which reduced the risk of cancer, and therefore weakened the study. It was further weakened by the fact that more than one out of four participants did not finish the study. Whether this dropout rate is because calcium pills can cause constipation is not considered in the article.

Just as important, the dose of vitamin D, as referred to in the editorial, may have been too low. Recently it has been estimated that about 1,000 units daily is necessary for most people in order to achieve any supposed cancer preventing effect. This amount of vitamin D (or more accurately 25-(OH)-vitamin D) is necessary to achieve a serum concentration of over 30 nano-grams per litre (75 nanomols per millilitre). Nevertheless, only a minority of the study participants received this amount.

What can be concluded from this? The editorial gives some suggestions for new studies. Much indicates that vitamin D, and maybe calcium, prevents cancer. But we still lack sufficient knowledge.

By: Vitality Council

1. Wactawski-Wende J et al. Calcium plus vitamin D supplementation and the risk of colorectal cancer. N Engl J Med 2006;354:684-96.
2. Forman M C et al. Calcium plus vitamin D3 supplementation and colorectal cancer in women. N Engl J Med 2006;354:752-4.
3. Garland C F et al. The role of vitamin D in cancer prevention. Am J Publ Health 2006;96:9-18.

By all Means: Enjoy a great Sauce!

February 11, 2006

One of the know-it-all expert councils has turned out to be wrong – again! A diet without fat does not benefit health.

When it comes to nutrition, the word from on high should be reconsidered. There are many who preach old advice with enthusiasm, sometimes without spouting a glimmer of truth. Nutrition is a question of religion. But it has been ten years since margarine was pushed off its pedestal, two years since sugar fell, and now the end is near for light products.

For years we have been brainwashed to believe that we must eat lean foods in order to be healthy and thin. Even though it seems obvious, this dogma has received some criticism in recent years; including from the results of multitudes of studies where fatty foods replaced easily absorbable carbohydrates. Despite these results, supporters of the old dogma recently had wind in their sails when a well known American nutrition expert misinterpreted a study and claimed that there was proof that when one eats pasta, potatoes and bread, one becomes thin.

Nobody noticed that the study had proven the opposite. Even when one eats lean foods for seven years, there is only a 400 g weight loss. Pasta and bread were not what it took to achieve this miniscule weight loss. In the study more fruit and vegetables made the food light, whereas intake of pasta and corn products was reduced by 20%.

We are used to being led astray, but now we can set the fact that in practice one does not become thinner by avoiding fat in stone. But that isn’t all; three other parts of the same study (Women’s Health Initiative) have now shown that one does not become healthier by avoiding fat.

In any event, a healthy woman between the ages 50 and 79 years cannot count on avoiding breast cancer, colon cancer, stroke, or coronary disease by reducing fat intake by 25% for eight years. Nor does it play a role for her to simultaneously increase fruit and vegetable intake from four to five portions daily.

A large and very thorough interventions study has shown this. It has been called the “Rolls Royce” of studies and it has been so expensive (three billion dollars) that it probably will never be repeated. The conclusions that we must make must therefore be taken from this study.

48,836 American women have participated. Of these 40% were placed on a diet while the rest were used as controls. Typically the women were slightly overweight but, even though they set their fat intake down from 38% to 29% of their caloric intake, they lost very little weight (waist measurement was reduced by an average of 0.8 cm). Blood pressure and cholesterol fell just as little, and the risks of falling ill with the aforementioned diseases did not change.

What was not studied
“The results for all three studies is a complete nothing,” declared leading researcher Michael Thun of the American Caner Society.

“The results must be taken seriously. Diet does not protect at all,” stated statistician David Freedman of Berkeley University. He added: “We in the scientific community often give conclusive advice based on weak groundwork. There we must do experiments.”

But does all this mean that what we eat is not important. Not even close – of course not! One must consider everything that the study did not take into account.

In the first place, there was no focus placed on the use of fish. The Italian intervention study, GISSI, which included 12,000 participants, showed a few years ago that just three grams fish oil daily reduced cardiac death in a high risk group by 30%. It is not the amount, but the kind of fat that is important.

Neither was there focus put on antioxidants. But according to a large American randomised study from 1996, supplements of the antioxidant selenium (200 microgram per day) reduce the risk of many forms of cancer by up to 50%.

That antioxidants are interesting was also seen in the seven year French SUVIMAX study form 2004. Here a fall in mortality was seen in men who received a number of antioxidants (selenium, zinc, vitamins C and E, zinc, and beta carotene) in moderate doses.

Nor was there focus on vitamin D, which is believed to have a future in the prevention of prostate cancer, enlarged prostate, breast cancer, arthritis, among others. Folic acid, which is believed to prevent breast cancer, osteoporosis, and more, was also lacking from the study.

The list could easily be longer. The important find of the study is that the dietary advice that experts have given out for years, without any doubts at all, has been disproved! It has only benefited the lucrative industry of light products.

This should be a wake up call in all camps. When is one an expert?

A study involving an increased fat intake has actually not been made. Therefore results of eating in this way are as yet unknown. Maybe we should just concentrate on eating fat of a higher quality that we are used to. Let us enjoy good butter and healthy olive oil.

By: Vitality Council

1. Prentice R et al. Low fat dietary pattern and risk of invasive breast cancer. JAMA 2006;295:629-42.
2. Buzdar A U. Dietary modification and risk of breast cancer. JAMA 2006;295:691-2.
3. Kolate G. Low-fat diet does not cut health risks, study finds. The New York Times 8.2.06.
4. Beresford S A A et al. Low-fat dietary pattern and risk of colorectal cancer. JAMA 2006;295:643-54.
5. Howard B V. Low-fat dietary pattern and risk of cardiovascular disease. JAMA 2006;295:655-66.
6. Appel L A. Dietary modification and CVD prevention. JAMA 2006;295:693-5
7. Howard B V. Low-fat dietary pattern and weight change over 7 years. JAMA 2006;295:39-49.

Greater need for vitamin B-12

February 1, 2006

Middle-aged and elderly women’s need for Vitamin B-12 is with great certainty 2,5 times higher than previously believed. A daily vitamin tablet is often not enough.

How is the need for a vitamin determined? Earlier it was determined based on how much is necessary to avoid acute deficiencies. This is sometimes still the case. For example, the current recommendations for vitamin C are still based on a World War II study on 20 English military objectors. Half of them came down with scurvy and two were close to death. But this study found that scurvy can be avoided with 12 mg vitamin C per day.

This kind of research is brutal by today’s standards. But it is also antiquated because it does not take other deficiency symptoms into account, including those which arise after longer periods and are not coupled with bruising of the skin, brittle bones, paralyses, and other acute symptoms. Today, instead of merely recording with a study participant becomes deathly ill, we follow the processes that the vitamins in question are involved in and determine whether or not they function as they should. This methodology was used by the American, Mark Levine when he proved that our need for vitamin C is closed to 200 mg per day than the normally recommended 60 mg. If one makes due with 60 mg it is believed that the vitamin C dependant reactions become slow and that there is an significantly increased risk of cardiovascular disease and cancer.

Of current interest, there is news regarding the need for vitamin B12. The current recommendation in England has been set to 1 microgram per day. A Danish study has recently shown that the need for vitamin B12 is six times as much (6 micrograms). This was determined in a study of 98 Danish women with an average age of 60. Such a large need meanwhile created a problem; the women typically only received 4.6 micrograms via their diet.

Even though they supplemented their intake with a normal vitamin pill (1 microgram B12), half of them received too little vitamin B12. Stronger pills are needed.

Increasing recommendations
For the last 50 years B12 status has been determined by measuring the blood’s B12 content. Findings in recent years have shown that a “normal” B12 value does not necessarily mean that there is enough. Even with a normal B12 value, build op of metabolism products which B12 normally removes can occur (these include homocysteine and MMA, otherwise known as methylmalonic acid). Therefore the amount of these substances present is measured when trying to determine whether or not there is a deficiency.

Recently a third indirect measure for B12 deficiency has been put into focus: holotranscobalamin, a B12 containing protein, seems to be able to replace the above-mentioned method and may even be more sensitive to B12 deficiency. It is very important to get enough of this protein. It is responsible for delivering B12 to the cells, almost like the paperboy who delivers the paper to your door. Without the paperboy, there is no paper.

The Danish study showed that the values for Holotranscobalamin, MMA, and homocysteine no longer indicated deficiency only when a B12 intake of over 6 micrograms per day was achieved. If B12 intake is less than 6 micrograms, there is sand in the B12-works.

The researchers conclude with conviction:
”…our results, together with those of others, strongly suggest that the RDA of 2.4 micrograms/day should be increased.”
This can also been said about many other vitamins. Experience from recent years indicates that the recommendations for not only vitamin B12, but also vitamins C and E and the minerals selenium, chromium, and magnesium, should also be increased, and in some cases greatly increased. Increased intake of many of the other B vitamins as well as iodine should also be considered.

This is especially true about vitamin D, on which we at the Danish Vitality Counsel have focused. The recommended daily dosage of vitamin D should be doubled for those of us who live in northern climes.

The official recommendations have as a whole not followed developments in research, even though there are strong arguments for new recommendations. According to some, there is need for more evidence. But this is contrary to the supposition that new recommendations could prevent serious chronic disease.

The dilemma is strengthened by the fact that it is difficult or impossible to get higher doses of vitamins and minerals though our modern diet. Some suggest that it might be possible with a Stone Age diet, but we surely will not have another Stone Age.

By: Vitality Council

1. Mustafa Vakar Bor et al. A daily intake of approximately 6 {micro}g vitamin B-12 appears to saturate all the vitamin B-12-related variables in Danish postmenopausal women. Am J Clin Nutr. 2006 Jan;83(1):52-8.
2. Zouë Lloyd-Wright et al. Holotranscobalamin as an Indicator of Dietary Vitamin B12 Deficiency. Clinical Chemistry 49: 2076-2078, 2003;10.1373/clinchem.2003.020743.

Lipoic Acid. Perhaps The Medicine Of The Future?

January 25, 2006

Lipoic acid is a simple fatty acid which is produced in all human cells. It is considered to be the ideal antioxidant and it may actually be highly beneficial against diabetes, neurological damage, and more. However, it is banned in Denmark.

Is lipoic acid the medicine of the future? There are many who believe this is so. One of the worlds leading experts in the field of antioxidants, Lester Packer of Southern California University, has emphasized that lipoic acid is the ideal antioxidant and a recent article by Polish researchers cautiously comes to the same conclusion.

Packer maintains that “from a therapeutic viewpoint, few natural antioxidants are ideal.” He continues by indicating that an ideal antioxidant should fulfil many demands: It should be absorbable by the intestines, occur in a form useful to the cells and have many antioxidant effects (including interaction with other antioxidants) in both cell membranes and the organism’s aqueous phase. It also must be completely non-toxic. Packer believes that lipoic acid is unique among antioxidants because it fulfils these demands. Lipoic acid is a potentially very effective medicine in many situations where free oxygen radicals are implicated.

Lipoic acid is a small sulphur containing fatty acid. It was discovered in 1950, but its special anti-oxidative properties were first noticed during the 1980’s. It is a very strong antioxidant, considerably stronger than vitamin C. It is also both fat and water soluble, which means that it can enter and have effects both outside and inside the cells. When other antioxidants such as vitamins E and C are used up, they can be “recharged” by lipoic acid so that they can be used again. It is also necessary for the cells’ metabolism and for a period it was considered to be a vitamin, but when laboratory animals did not suffer damage from lipoic acid deficiency, this idea was dropped.

Diabetes and nerve damage
The question of whether or not it is a good idea to take lipoic acid supplements should be addressed. The previously mentioned Polish researchers analysed some of the as yet very limited knowledge in this area and found that lipoic acid may be especially interesting for diabetics. Studies on animals with type II diabetes have shown strong improvement of their diabetes with lowered blood sugar levels and better utilization of their bodies own insulin with lipoic acid supplements. Many studies have shown that lipoic acid improves nerve function in diabetics with nervous inflammation.

Just as interesting, lipoic acid may be an effective weapon against the protein damage caused by heightened blood sugar. In a process called protein oxidation the proteins change structure in a way which is similar to what happens when an egg is boiled. This oxidation is an important part of the explanation for diabetics’ tendency to get cataracts, where the lens of the eye becomes clouded. In animal studies this is counteracted by lipoic acid.

The apparent nerve protective properties have lead to studies in Alzheimer’s treatment. In two studies it was found that the disease was halted by lipoic acid, but these results should be considered as provisional. The same result has been found in studies of Parkinson’s disease.

Does lipoic acid prevent cancer? The Polish researchers are uncertain. Their tissue studies indicate that small doses promote growth, while large doses inhibit growth. Dare we claim that this effect speaks for supplementation? We produce small doses of lipoic acid without help.

Only about 1,000 articles on lipoic acid can be found in the medical database, Medline. Research is still in its infancy. Even so, entering lipoic acid into Google gives over two million links (search “lipoic acid”).

By: Vitality Council

Bilska A et al. Lipoic acid – the drug of the future? Pharmacological Review 2005;57:570-77.

Selenium, A Potent Substance Against Cancer

January 18, 2006

Studies from all angles support the idea that selenium works against cancer. Even though there is need for more research, an optimal dose can be suggested.

Selenium prevents cancer. This is common knowledge which is only awaiting conclusive confirmation. It received recognition when, in 1996, an American researcher (Clark) showed in a randomised study that the frequency of cancer fell by 38%, and that the fatality rate of those with cancer fell by 50%, in participants who received daily supplement of 200 micrograms selenium.

The supposition that selenium is preventative for cancer is in fact much more extensively backed. This has been shown by a leading selenium expert, Margret Rayman from the University of Surrey in England, in a thorough, but also complicated, summary. She has also illuminated who selenium prevents cancer and, even more importantly, how much is needed.

Rayman reviews the many geographical studies that have, since the 1960’s, consistently shown that the populations who received the least amount of selenium also had the highest cancer rates. Animal studies are also discussed. If one gives selenium to a male dog, not only is there less damage to the DNA of prostate cells, but the damaged cells that remain also die normally instead of living on as cancer cells.

A certain pattern emerges when one looks at studies where the blood concentration of selenium is compared to the cancer rate in groups of people. In a French study of this type from 2005, the death rate from cancer after nine years was four times greater in the 25% of the study-group who received the least selenium than in those who received the most selenium. Typically the French receive as little selenium in their diets as the British. Many studies from many countries have shown similar results for lung cancer (a 26% lower risk of cancer was reported in those with diets rich in selenium), oesophagus cancer, stomach cancer, and not in the least, prostate cancer as well as possibly cancer of the large intestine.

How much is enough
The best evidence can always be found in randomised studies where neither the patients nor the doctors know who receives what. A Chinese study of this type has shown that selenium has an especially effective against liver cancer. As mentioned before, Clark’s study had similar results. It is intriguing that, even though Americans receive an average of 200 micrograms more selenium daily than us, an additional 200 micrograms was beneficial to most. The effects were nevertheless minimal in those who received the most selenium beforehand. These individuals already received close to the optimal dose. But third of the population who received the least beforehand, had their cancer risk halved, and their prostate cancer risk decreased by 86%, after taking supplementary selenium.

Typical Europeans receive too little selenium while Americans receive double as much and Japanese receive almost three times as much. It has become apparent that 70 micrograms of selenium is needed in the daily diet to maintain levels of the selenium based antioxidant GSHpx in the body. The Japanese and most Americans receive this amount in their diets while we do not. But why is their cancer risk reduced when they receive supplementary selenium? The reason cannot be GSHpx and may not even be the anti-oxidizing effects alone.

Rayman examines many possible explanations. One is that high doses of selenium lead to the formation of the simple selenium compound methylselenol; which can kill cancer cells, counteract the formation of blood vessels (which the cancer cells need to survive) and can inhibit cancer in other ways. But selenium is naturally an antioxidant, an immune system stimulant, an activator for cancer inhibiting genes, an inhibitor for growth factors, etc. There is not one, but many, mechanisms of action.

Unchecked amounts of selenium should not be taken. Studies indicate that sufficiently high doses of selenium can increase the risk of cancer as much as insufficient amounts. Clark’s study, as well as others, suggests that a daily supplement of 200 micrograms is optimal.

The reward can be large, but more research is needed. Currently a large clinical trail (called SELECT) is being undertaken in the U.S.A., but a study in the more selenium poor Europe would be better. Rayman believes that such a study should be undertaken. But who wants the placebo!?

By: Vitality Council

1. Rayman M P. Selenium in cancer prevention: A review of the evidence and mechanism of action. Proceedings of the nutrition society. 2005;64:527-42.
2. Clark LC et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer study group. JAMA 1996;276:1957-63.
3. Akbaraly NT et al. Selenium and mortality in the elderly: Results from the EVA study. Clin Chem. 2005;51:2117-23.

Vitamins against aging

January 9, 2006

The need for many vitamins increases with age. A deficiency can be compared to radiation exposure, which causes mutations, decreased energy production, cancer, and age-related changes in the body, according to one of the World’s leading nutrition scientists.

When Bruce Ames was 70, President Clinton surprised him with U.S.A.’s highest scientific recognition, The National Medal of Science, for his research in nutrition, cancer, and aging.

Today he is 77, but still an almost incomprehensibility active researcher and professor at the famous Berkeley University in California. He is also the man behind the world renown Ames test, a lightning fast method to find out whether a specific chemical can cause mutations, and thereby cancer.

This introduction shows that Ames it a researcher to be listen to, and therefore we have decided to discuss one of Ames’s latest and most important scientific articles.

The article was published in a periodical for the European organization of molecular biologists (EMBO reports). It describes how it is possible to reduce the tendency for cancer and aging by taking more than the recommended dose of diverse vitamins and other important substances.

How does it do this? In his study Ames found that deficiencies of vitamins C, E, B6, and B12 as well as of folic acid and zinc can have exactly the same effect on cells as radioactivity. This means that such deficiency causes mutations, for example as a result of breakage of the chromosomes.

Folic acid deficiency causes such breakage because it leads to the introduction of a wrong substance (uracil) in uncountable places along the DNA molecules. These mutations affect the cells the same way as a virus affects a computer. In the worst cases, the system beaks down.

But deficiency does not only lead to mutations. Another result is weakening of the energy producing mitochondria, otherwise known as the cells’ power plants. In order for the mitochondria to function, they must have access to certain enzymes, which can be regarded as the power plant’s machinery. The enzymes work together so that the product from one “machine” is processed further by the next in a chain of reactions which result in the conversation of oxygen and hydrogen into water, and the production of energy. But where do the enzymes come from? Without the necessary building blocks they do not exist at all!

Ames has among other things proven that deficiencies of zinc or the B vitamins biotin and pantothenic acid weaken the fourth reaction in this chain of reactions. They are the building blocks of the “machines” which carry out this step in the process. Not only is the production of energy reduced by such deficiency, but oxygen is also insufficiently converted to water. As a result the mitochondria empty free radicals into the surrounding cell where they can cause mutations, cancer, and weakness.

More Energy
Why does Ames believe that it is necessary to take more vitamins than recommended? This is as a result of the third and last point in his thought process. It regards the consequence of the uncountable mutations which by the aforementioned methods unavoidably arise during ones life. These mutations cause the cells to produce less effective enzymes that bind less effectively to the vitamins which they need to aid their function. Ames maintains that this poor binding can be overcome simply by increasing the amount of vitamins. This makes the enzymes work again.

A particular problem in this regard is the weakening of the mitochondria which occurs with age. Without energy, nothing functions within the cell and the degeneration of the mitochondria is central to what we call aging. But Ames emphasizes that it is possible to make old rats faster by giving them supplements of the two vitamin-like substances lipoic acid and carnitine.

Both substances are important intermediates for energy production in the mitochondria. With age they bind poorly to the enzymes which cause the mitochondria to function poorly. But this poor binding can also be overcome with supplements. As well as making the rats faster it was possible to measure that their mitochondria once again functioned normally. Clinically such treatment has been able to result in improvement in people with mild Alzheimer’s.

The unique thing about Ames is that his arguments are based on biochemistry. This means that he refers to elementary chemical reactions which are demonstrable in the organism. Many others base their views of more or less uncertain clinical trails, sometimes without knowledge of the biochemistry behind them. It might not be coincidental that The Nobel Prise in medicine typically is given to a biochemist.

By: Vitality Council

1. Bruce N Ames. Increasing longevity by tuning up metabolism. EMBO reports 2005;6:S20- S23.
2. Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and/or R-a-lipoic acid. J. Liu et al. Proc Natl Acad Sci USA.2002;99:2356-61.
3. B N Ames et al. High-dose vitamins stimulate variant enzymes with decreased coenzyme-binding affinity (increased Km): Relevance to genetic diseases and polymorphisms. Am J Clin Nutr 2002;75:616-58.

Vitamin D Prevents Cancer

December 30, 2005

A new and much discussed analysis, has shown that nearly every other cancer case can be prevented by D vitamin, if everyone is getting the suffient dosage, which almost no one is.

It has now been proven that the frequency of cancer can be reduced dramatically by increasing the population’s vitamin D intake.

This is the claim of the American researcher Cedric Garland, who is a professor of epidemiology at the University of Southern California, San Diego. He is behind the largest analysis of vitamin D research and cancer to date. 63 studies from 1962-2004 were analysed.

As a whole they strongly indicate that if the population’s intake of vitamin D is set up to 1,000 units per day, the frequency of colon cancer would be halved while the number of breast cancers and ovarian cancers would be reduced by a third. The 1,000 units of vitamin D (25 micrograms) would be, with certainty, without side effects. This is the same as five times the normally recommended dose, which only few receive.

Garland, who has studied vitamin D for 25 years, is very certain of his results. In a statement given to the BBC and The Independent he declared that there is now such an overwhelming amount of indications from the best observational studies, that governmental action is warranted.

It is worth noticing that these internationally respected media concerns both came with detailed reports, which also were followed by a leading editorial in The Independent. The study itself was published in the February 2006 issue of the American Journal of Public Health. The results were also published beforehand online in an extensive statement on the university’s (UCSD) official homepage.

Garlands interest for vitamin D was awakened when he noticed in the 1980’s that the risk of colon cancer and breast cancer in the northern United States was double that of the risk in the Southern states. He and others started a 12 year study, which lead to a hypothesis that the reason behind this phenomenon is sunlight’s ability to create vitamin D in the skin. This theory has subsequently been tested in many ways. It also fits with the increased cancer frequency in cities, when air pollution containing sulphur dioxide blocks the vitamin D producing short ultraviolet solar radiation.

This also fits with the diet and cancer studies on workers in Chicago and with the low frequency of breast cancer in Japan, where though there is little sunlight, the diet is largely fish based. Fatty fish are just about the only regular source of vitamin D outside of the summer months in Japan, Chicago, and Northern Europe. Additionally, the theory fits well with the fact that the many people, who for genetic reasons utilize vitamin D poorly, are strongly overrepresented among those who suffer cancers of the colon, breast, prostate, and more.

More and more indications
The faithful subscribers to this newsletter may remember our accounts of the studies of the last year which have shown that women with low vitamin D status have much more frequently lumps in their breasts than others. This is a relationship which fits with a higher risk of cancer.

They may also remember that an American (as well as a large Norwegian) study showed that the possibility of beating many cancer forms is best when the cancer is found during the summer, when vitamin D status is highest.

This indicates that the vitamin not only prevents cancer, but also inhibits cancer growth. Concordantly with Garland’s claim, African Americans have a lower chance of recovery form breast cancer than Anglo Saxon individuals. This may be due to a reduced vitamin D status brought on by the reduced ability to absorb vitamin D which comes with dark skin colour.

These results and others are strengthen by animal studies where it has been proven that vitamin D promotes cell death in abnormal cells in the process called apoptosis and has a general dampening effect on cell growth. This last principle is utilized by psoriasis salves, which contain a vitamin D – like substance which inhibits the overwhelming growth and lack of cell maturation which characterises this skin disease.

The optimal daily vitamin D dose, especially during the winter months between October and May, is according to Garland about 1,000 units (or 25 micrograms) per day. This recommendation is based on a study from October 2005. The 1,000 units lead to a concentration of the vitamin D precursor 25-OH-vitamin D of about 80 nmol/l (nanomol per litre), which Garland found to lead to the lowest risk of colon cancer.

Much also indicates that Garland is correct that vitamin D supplements could save thousands of lives. If this is the case, than any media claim that we get superfluous vitamins is contrary to public health.

By: Vitality Council

1. Garland CF et al. The Role of Vitamin D in Cancer Prevention. Am J Public Health. 2006;96(2):9-18. 2005 Dec 27; [Epub ahead of print].
2. Gorham ED et al. Vitamin D and prevention of colorectal cancer. J Steroid Biochem Mol Biol. 2005 Oct;97(1-2):179-94. Epub 2005 Oct 19.
3. Garland CF et al. Serum 25-hydroxyvitamin D and colon cancer: eight-year prospective study. Lancet. 1989 Nov 18;2(8673):1176-8.
4. Jeremy Laurance, Health Editor. Revealed: the pill that prevents cancer. The Independent 28.12.05.

Vitamin E May Be Diabetic’s Saviour

December 20, 2005

About one out of every two diabetics has a five times larger than average risk of dying from heart disease. This risk can be cut in half by vitamin E. This is a well justified theory which is now being tested in a large Israeli study.

It is well known that the heart’s of diabetics become easily atherosclerotic, often causing them to die due to blood clots in the heart. Therefore, health officials work hard to combat atherosclerosis in diabetics. For example, diabetics are encouraged to take cholesterol reducing medicine, even when their cholesterol levels are very low. Diabetics’ blood pressure should also be low.

If one believes the Israeli researcher, Andrew Levy, the lives of even more diabetics can be saved by taking 400 units of vitamin E daily. Levy’s theory is now being tested in Israel in a large randomised study with 5,000 middle aged diabetics. Half of them will receive vitamin E for the next four years while the other half will not. If it goes as is hoped, the result will have enormous significance for public health.

It is optimistic to implement such an expensive study with vitamin E. As every (Danish, ed.) TV watcher knows, vitamin E doesn’t work against anything. Why would Levy and his co-workers from the Israeli Technion Technical Institute, where many Nobel prise winners can be found, go against the flow?

The explanation involves an antioxidant which few non-experts know of. It is called haptoglobin and is a protein which is created in the body. Haptoglobin binds the blood’s colouring agent, the iron rich haemoglobin, if it becomes detached from the red blood cells. In this way it prevents iron poisoning and therefore against overloading of free radicals in a long list of conditions where red blood cells die.

Disregarded effects of vitamin E
Levy and his co-workers have shown time and time again that haptoglobin works as an antioxidant. There is more to the story; haptoglobin is found in two forms, which are not equally effective antioxidants. Type 1 haptoglobin works much better than type 2. If one has type 2 haptoglobin (like 40% of the Israeli diabetics) the risk of death due to heart disease is five times higher than normal! In other words, a very large part of diabetics’ high death rate due to heart disease is because one out of every two of them has an insufficiency defence against oxidation because of ineffective haptoglobin.

The logical consequence of this enormous difference is, according to Levy, that the poorly protected diabetics with type 2 haptoglobin should take supplementary antioxidants. This is where the vitamin E study comes in. Vitamin E should be able to help. On the other hand, if it does help, why have other studies with vitamin E not previously shown this effect?

Levy believes that this is presumably because they have not been analysed with this effect in mind. He studied serum from a large sample of the ca. 10,000 participants in the Canadian HOPE study, where atherosclerotic participants received 400 units of vitamin E daily. The people behind the HOPE study found no effect of the vitamin E. But what about the 1,000 diabetics in the study? About a year ago, Levy proved that vitamin E reduced the risk of heart disease by 50% in the diabetic participants who had type 2 haptoglobin.
This surprising result was hidden in the HOPE study and was apparently unknown. This is quite educational. If the most threatened diabetics’ very high risk of heart disease can be halved with a cheap, harmless, vitamin E pill, the signification is very large.

Until 2010 we only have these results. There are no other results to turn to. It is not even possible to find out which kind of haptoglobin you have. If you wish to prevent heart disease, you have to do it in the dark. It is however risk free.

By: Vitality Council

1. Andrew P. Levy et al. The Effect of Vitamin E Supplementation on Cardiovascular Risk in Diabetic Individuals With Different Haptoglobin Phenotypes. Diabetes Care 27:2767, 2004.
2. Levy AP et al. Strong Heart Study. Haptoglobin phenotype is an independent risk factor for cardiovascular disease in individuals with diabetes: The Strong Heart Study. J Am Coll Cardiol. 2002 Dec 4;40(11):1984-90.
3. Suleiman M, et al. Haptoglobin polymorphism predicts 30-day mortality and heart failure in patients with diabetes and acute myocardial infarction. Diabetes. 2005 Sep;54(9):2802-6.
4. A survey of the study can be found at Clinical