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Alzheimer’s disease: The third diabetes

Claus Hancke

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.

Vitamin D Could Prevent Every Third Cancer-related Death

Claus Hancke

April 21, 2006

Several of the World’s leading vitamin researchers advocate a much higher vitamin D-intake. They believe that up to every third death from cancer may be prevented.

“I challenge anyone to find a field or a nutritional substance or any other factor with as effective cancer-fighting properties as vitamin D.”

So said Edward Giovanucci, professor at Harvard University, last year in a speech to the American Society for Cancer Research.

More and more agree with Giovanucci, amongst them, several professors from well-renowned universities. A few months ago Cedric Garland, an absolute pioneer in the field, stated that it has been proved that the risk of cancer can be lowered dramatically with vitamin D. These are big words. Garland is a professor at the University of California in San Diego.

Giovanucci has together with six others, of these, no less than three are professors from Harvard, confirmed the claim further. In a quite laborious study they have confirmed the close connection between a vitamin D deficiency and cancer.

Since World War II it has been known that especially cancer in the alimentary canal is seen relatively seldom in southern countries. Since sunlight is the most important source of vitamin D, it has earlier been guessed that it was vitamin D and not the sun, which offers protection. In numerous studies the incidence of cancer has been found to be highest where sunlight is weakest, and where the content of vitamin D in the blood is lowest. We are children of the sun. At the same time laboratory research in recent years has shown that this vitamin inhibits the growth of abnormal cells, counteracts the spread of cancer and prevents the formation of blood vessels in tumorous masses.

Giovanucci now finds further proof of the connection. Earlier in humans there has only been found an indirect connection between vitamin D and cancer. There has been a lack of data from whole groups of the population, that have had their blood content of vitamin D measured, and have then been followed for a number of years. But Giovanucci has found something to substitute this data.

Mega doses of Vitamin D
They took 1095 men from the big population study “Health Professionals Follow-Up Study”. These 1095 men had had their vitamin D-status measured (this means the content of vitamin D in the blood). In addition, a lot of things were known about their personal habits etc. Would it be possible to go backwards and calculate their vitamin D-status from their personal habits? Yes! An estimation of the approximate vitamin D blood content could be made, when the individual’s skin colour (eg. race), body mass, height, place of residence (southern/northern in the USA), the amount of physical activity, time of year and the content of vitamin D in the test subject’s diet and possibly supplements was known.

In this manner the group worked out a point-system for the direct calculation of vitamin D status. What especially contributed to a low status was a northern place of residence, dark skin colour, overweight and lack of exercise. The calculations proved correct for the 1095 test subjects. But would they be correct for other people? They were checked for another group of men with known vitamin D status. They were consistent!

Every single subject, of the 47,800 men in Health Professionals Follow-Up Study now had their vitamin D status calculated. In the course of approximately four years, about one in ten got cancer. About half that died from it.

To find the significance of vitamin D, they chose to compare dead men whose plasma values for vitamin D (25(OH)D3) deviated by 25 nmol/L (nanomol/liter). It was found that the risk of dying from cancer was no less than 29 percent lower in men with a high vitamin D status. Concerning cancer of the alimentary canal – it was 45 percent lower for men, who were otherwise identical with regards to age, weight and level of physical activity.

If these results are correct, every third death from cancer may be prevented in the course of a few years. Also in the UK. This is nothing but a sensation. But if one wishes to increase the plasma level of vitamin D by 25 nmol/L, one must receive a supplement of no less than 1,500 units of vitamin D during the winter. This is achieved if a supplement of four vitamin D tablets of 10 mcg (micrograms) is taken daily from August until April.

1,500 units will probably shock many. Is it not toxic? No, it is quite certain that there is no risk, even with a permanent supplement of 2,000 units daily. For comparison, the skin produces 20,000 units during half an hour in the sun in the summer.

Garland, who was mentioned above, recommends 1,000 units (25 micrograms) a day. Others say 2,000. Giovanucci and his colleagues from Harvard strongly recommend 1,500.

Under any circumstances: If you want the full advantage of vitamin D, it seems that the need is far greater than what we have gotten used to believe. Maybe it is close to what stone-age people received naturally from their diet.

By: Vitality Council

References
1. Giovanucci E et al. Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. J Natl Cancer Inst 2006;98:451-9
2. 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]

jncicancerspectrum.oxfordjournals.org
www.ajph.org
www.iom.dk

Fish Oil – Still Indispensible!

Claus Hancke

April 7, 2006

A British study claims that fishoil does not protect the heart. Formally, it is founded on the sum of all earlier studies. In reality it relies on only one, where the participants of the study probably cheated.

As time goes by, studies of all sorts of things pile up. At some point no one can keep track of them. Even people with a good memory remember only the studies they like. This calls for a meta-analysis – a calculation of a sort of average of what all reliable studies have shown.

This has now happened in a British study of fish oil. Does fish oil protect the heart? Does it prolong life? Yes, we know that it does!

At least, so we think. According to the new meta-analysis fish oil has “no clear effect on mortality, risk of heart attack or the incidence of cancer” – rest assured, you do not need to eat fish!

As far as cancer goes, one is hardly surprised, but what about the heart? Ever since the two Danish doctors’, Bang and Dyerberg’s, studies on Greenland 35 years ago, everyone has known that fish oil protects the heart. This is confirmed by numerous studies. How can all these studies amount to a big fat zero when summarized?

Of course they cannot. A meta-analysis can be just as subjective as everything else. This means that others, with the same starting point can arrive at the opposite result. This is the case in a new, far more comprehensive, American report. There is no doubt that fish oil is beneficial for the heart. In fact, it is stated in this report that everyone should be tested to see if they get enough of it. The two important fatty acids in fish oil, DHA and EPA, have “clear beneficial effects”. Everyone should ingest at least 1.5 grams of fish oil every day, in case of heart disease, double that. This will lessen the risk of dying from heart disease by 25 %.

That was the Americans. They thoroughly reviewed the extensive biochemical knowledge and conclusions from animal and human studies. From this they made a general conclusion. What did the British do?

The Test Subjects Cheated
They completely ignored all basic knowledge and concentrated on the incidence of heart disease and mortality in humans. But were they neutral?

They reviewed a total of 48 randomized studies. But they did something strange: Only fifteen of the studies were included in the mortality calculations. Why the remaining 33 studies were not included is not known. Maybe some were excluded because of suspicion of being biased. But, in nine of the fifteen studies included, there was “medium or high” risk of bias. For example because the test subjects knew whether they were given fish oil, or, because of the draw, were given something ineffective.

On top of this, an unknown number of the 48 studies were not even with fish oil but with alpha-linoic acid – which is found in flaxseed oil and in rape oil. These oils can be converted to “fish oil” in the human body.

Besides, the most famous study of linoleic acid is missing – the so-called Lyon experiment where rape oil (and a Mediterranean diet with olive oil) lowered the mortality in patients who had had a coronary thrombosis by 73 %.

When everything is boiled down, twelve randomized studies with fish oil remain. But of these, nine are very small and without relevance. This leaves three. The biggest of these three studies, (GISSI) show a massive reduction in mortality in twenty percent of persons who had had a coronary thrombosis. In the table it only says fourteen percent, apparently because of a misunderstanding.

Only one of the larger studies (Burr et al 2003) came out with a negative result. Here the mortality increased by fifteen percent in men with sclerotic coronary arteries, when they were given fish oil.

However, this study is at the least controversial, partly because the participants knew if they were given fish oil or not. Since they had a dangerous heart disease, many of them would have been tempted to take supplements on their own. This could have been checked through blood tests, but only a spot test was taken after six months. After this the study continued for three to nine years. The spot test showed that the difference between the two groups was remarkably small. Moreover, the participants explained that even if they were not in the group given fish oil, they ate so much fat fish (14 grams a day) that this alone would have provided them with the amount recommended in the American report. So, in fact, both groups received “enough”, and the value of this study must be questioned.

Still, it was printed in the news paper. However, you should believe the American report.

Fish is good – of course!

By: Vitality Council

References:
1. Hooper et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: Systematic review. BMJ online 24.3.06: BMJ, doi:10.1136/bmj.38755.366331.2F
2. Wang C et al. Agency for Health Care Research and Quality. US Department of Health Care Rsearch and Human Services. www.abrq.gov . Evidence report/technology assessment Number 94. Effects of omega -3 fatty acids on cardiovascular disease. March 2004.
3. Burr ML, Ashfield-Watt PA, Dustan FD, . , et al.: Lack of benefit of dietary advice to men with angina: results of a controlled trial. Eur J Clin Nutr 2003, 57: 193-200.

bmj.bmjjournals.com
www.ahrq.gov
www.nature.com/ejcn/index.html

Smokers should get more vitamin C and E

Claus Hancke

April 1, 2006

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

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

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

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

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

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

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

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

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

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

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

By: Vitality Council

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

Vitamin C against atherosclerosis (hardened arteries)

Claus Hancke

March 23, 2006

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

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

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

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

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

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

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

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

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

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

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

By: Vitality Council

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

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

Children with ADHD lack magneisum

Claus Hancke

March 17, 2006

A majority of restless ADHD children were lacking in magnesium. All children improved when given magnesium and B6-vitamin supplements.

In almost all kindergarten classes there are one or two so-called ADHD-children giving the teacher a hard time with their continuous restlessness, running about, violent behaviour and inattentiveness. (ADHD stands for Attention Deficit, Hyperactivity Disorder).

Two studies – the only ones conducted – have now shown that a combination of magnesium and vitamin B6 helps.

Why should magnesium help? In a French study 52 children, all diagnosed with ADHD, were examined. The children were typically six years old. If the serum level of magnesium was measured in a normal blood test, normal values were seen. But since almost all magnesium in the body is found inside the cells, this says nothing. It is inside the cells that we must look.

On average, the children only had 4/5 of the amount of magnesium in the cells (in this case, the red blood cells) present in normal adults. They were deficient in magnesium!

Therefore they were given a daily supplement of 6 mg. of magnesium and 0.8 mg. Vitamin B6 per kilo body mass for one to six months. After this, no less than all the children got better. For example, at the beginning of the experiment 26 of the children were deemed physically aggressive. After four months, only six. At the same time their ability to concentrate and their attention span improved (evaluated in an approved manner). Statistically, these results were quite credible.

A weakness in the French study was that it was a so-called open study. There was no untreated control group and the treatment was not blind. This leaves room for coincidence and over-interpretation. On the other hand, the study showed exactly the same as a similar study from 1997. Also, the improvements occurred at the same time as the measurable magnesium deficiency disappeared. When this had happened, treatment was stopped.

Magnesium in the Diet
If it works, it may not be that surprising. The same course of treatment seems to have helped women suffering from irritability and imbalance due to PMS (PreMenstrual Syndrome) in several studies. On top of this comes the generally sedative effect on nerves (magnesium can be used as a local anaesthetic). Magnesium has a relaxing effect on muscles. Does magnesium also have a calming effect on the central nervous system?

Another question is why ADHD-children apparently are deficient in magnesium. The French suggest that genetic factors play a role, but in a majority of the parents, it was not just one, but both of them who were deficient in the mineral. This suggests that nutrition is more important.

A British evaluation indicates that foodstuffs’ content of magnesium has decreased in the past 60 years. It is estimated that today there is 24 and 16 percent less magnesium in vegetables and fruit, respectively, than in 1940. On top of this is an increase in the consumption of sugar. Those who dauntlessly claim that 10 percent of the calories in the diet can be contributed by sugar, are also saying that you can easily omit 10 percent of the diet’s magnesium. Furthermore, less physical work means a decreased need for food generally, thereby decreasing the amount of magnesium we consume. A typical magnesium consumption rate today (3-400 mg. a day) is probably half of what it was 100 years ago.

Something else to consider also is that there is a row of more or less confirmed observations of connections between behavioural disorders in children and teenagers (and criminals) and an unhealthy diet. Is this purely coincidence?
It will take several months to rectify a magnesium deficiency, but it might be worth it to try.

By: Vitality Council

References:
1. Mousain-Bosc et al. Magnesium VitB6 intake reduces central nervous system hyperexcitability in children. J Am Coll Nutrition 2004;23:545S-548S
2. Starobrat-Hermelin et al. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactive disorder (ADHD). Magnes Res 1997;10:143-8

www.jacn.org

Antioxidants against macular degeneration and blindness

Admin

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.

content.karger.com/ProdukteDB/produkte.asp
jama.ama-assn.org

Glusosamine is more that just glucosamine

Admin

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

References:
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.

content.nejm.org

Calcium supplements with vitamin D against colon cancer?

Admin

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

References:
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!

Admin

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

References:
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.