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Summer sun prevents multiple sclerosis

Claus Hancke

April 10, 2007

Still more supports the theory that vitamin D can prevent multiple sclerosis. Enjoy the sun while its there.

Multiple sclerosis (MS) is a feared disease. Many believe that sclerosis is synonymous with a life in a wheelchair, and many have heard about tragic examples of how the disease can progress. It is worth remembering that even 20 years after the emergence of the disease, 75% of patients can walk unaided. Also, the death rate for those suffering from sclerosis is not much higher than that of the rest of the population.

On the other hand, MS affects especially younger people, primarily women. It is disquieting that the frequency of this disease has increased in the last 50 years and continues to increase. Over 80,000 people in the UK suffer from MS, which at a prevalence of over 140 people per 100,000 the highest in the industrialised world.

MS is an “autoimmune” disease, which is to say a disease where the body’s immune system turns against the body itself. In the case of MS the so called myelin sheaths which coat and isolate the nerves are attacked. On average, every fourth person with MS also suffers from another autoimmune disease, for example psoriasis, arthritis, or metabolism diseases.

Can one prevent MS? It is tempting to have this thought when one notices the enormous geographic variations. In England, Denmark, Norway, Sweden, Finland, Germany, and Canada the frequency is about the same. In Greece and Turkey it is about half as common while in northern Spain and Italy the frequency lies in between that of these areas.

These and other figures support a growing belief that MS has something to do with lack of sunlight; or more accurately, lack of vitamin D, of which the sun is the most important source. Vitamin D has in studies prevented an experimental form of MS (EAE, Experimental Autoimmune Encephalitis). In countries north of a latitude of 42, corresponding to Corsica, the sun is so low during the winter months that vitamin D practically cannot be produced in the skin. The result is widespread vitamin D deficiency.

Less than half the risk
Researches from Harvard University among others analyzed the problem in more detail. They studied 257 blood tests from military personnel who contracted MS between 1992 and 2004. The blood tests were taken and frozen before these people became sick. The question was whether they had remarkably little vitamin D in their blood when compared to people who did not contract MS.

It was shown that they did. 25-OH-D, the best measure for vitamin D status, was measured in both the sick and a large number of healthy people who were randomly chosen from 7 million personnel. It was found that “high circulating levels of vitamin D are associated with a lower risk of multiple sclerosis.” Low vitamin D levels were especially risky for people under 20 years of age.

How much vitamin D is enough? When the level of 25-OH-D was at least 99 nannomol/litre serum, the risk of MS was the lowest at about 40% average. The difference was statistically certain. For comparison, levels under 50 are indicative of insufficient levels of vitamin D. Such values can be found in most people during the winter.

The theory that vitamin D prevents MS is thus strengthened. One should attempt to distance oneself from vitamin D deficiency. This is easy during the summer, but from October to April it requires, for the majority of those in our latitudes, supplements.

By: Niels Hertz MD

References:
1. Munger L et al. Serum 25-Hydroxyvitamin D levels and risk of multiple sclerosis. JAMA 2006;296:2832-2838.
2. MS prevalence data for selected countries: http://www.mult-sclerosis.org/prev_tab.html
3. Newsletter from Vitalrådet dec. 27. 2006

jama.ama-assn.org

New slander against antioxidants

Niels Hertz

March 13, 2007

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

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

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

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

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

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

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

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

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

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

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

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

By: Niels Hertz MD

 

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

jama.ama-assn.org

Confusion about Omega-6

Claus Hancke

February 6, 2007

Confusion regarding the essential fatty acids is the rule rather than the exception while research regarding their good effects piles up. It’s hard to find head or tail in this subject, but the quick answer is: Eat more fish!

If you want to delve into the depths of this answer, then fasten your safety belt and read on!

There is general agreement that omega-3 fatty acids have a high health value in all of their sources, from linseed oils alpha-linolenic acid to fish’s docosahexaenoic acid and prostaglandin E3.

Is this true about the omega-6 fatty acids?

There is common confusion about the health benefits of essential fatty acids, and this has not been reduced by recent public warnings against the use of polyunsaturated omega-6 fatty acids.

Let’s look into this:

The most common misconception is that it is possible to generalize about all omega-6 fatty acids. It is not. In the industrialized world the problem is that we are inundated with cheap linoleic acid, which is an omega-6 fatty acid that is found in e.g. corn and sunflower oil. Linoleic acid alone is not that healthy either. If you eat too much of it, you build up deposits of NEFA (which has nothing to do with bicycle lights!) but means that linoleic acid builds up as a non-esterized fat, which can lead to sudden cardiac arrest (1).
The ratio between our consumption of omega-6 to omega-3 fatty acids should be close to 2:1, but unfortunately it is closer to 20:1. The problem with linoleic acid is that we get too much of it because it is cheap.

Linoleic acid must be converted to gamma linolenic acid (GLA), followed by DGLA and prostaglandin E1, before we have the equivalent of healthy omega-3 fatty acids. The first conversion (to GLA) requires an enzyme called delta-6-desaturase. There are many people this enzyme. These people are primarily people with allergies and people with diabetes. When you lack this enzyme the only way to avoid getting too much linoleic acid is to take supplementary GLA. GLA is found in evening primrose oil or borage seed oil.

If you do not lack delta-6-desaturase, the best thing to do is to limit linoleic oil intake and increase fish oil consumption.

If we eat fatty fish and fish oil we save more of the enzyme needed to convert linoleic acid to GLA. Therefore, if we balance our linoleic acid consumption with fish oil then we will not suffer as many harmful effects from unconverted omega-6 fatty acid.

Another way of reducing the amount of accumulated linoleic acid is by taking the amino acid L-Carnitine. L-Carnitine functions as a kind of oil pipeline which transports the linoleic acid directly into the cells power plant (the mitochondria), where, with the help of Q10, it is made into energy. This reduces the amount of freely circulating linoleic acid in the blood.

As explained in the above, we should avoid too much linoleic acid, whereas its converted product, GLA, is healthy and good. So the health value of omega-6 fatty acids is dependent on which omega-3 fatty acid is being discussed.

In a large summary article in Current Pharmaceutical Biotechnology (2), the authors assess a long list of illnesses where GLA has an amazing effect. These include inflammatory conditions such as rheumatoid arthritis, autoimmune diseases, and cancers. GLA has been shown to be able to inhibit osteonectin, which is a protein connected cancer metastasis. GLA also has been shown to increase nerve impulse speed in diabetics.

Therefore, omega-6 fatty acids cannot be seen as either all bad or all good. This is especially true when comparing GLA with linoleic acid. Supplementation of both fish oil and GLA is a good idea.

By: Vitality Council

References:
1. Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population. Xavier Jouven, MD, PhD; Marie-Aline Charles, MD; Michel Desnos, MD; Pierre Ducimetière, PhD. Circulation. 2001;104:756.
2. Gamma linolenic acid: an antiinflammatory omega-6 fatty acid. Kapoor R, Huang Y-S, Current Pharmaceutical Biotechnology, 2006; 7(6): 531-4.

Early old age without vitamins and minerals

Niels Hertz

January 15, 2007

Without sufficient vitamins and minerals, old age comes too early. This is because the organism ignores the future when resources are limited. If it needs to, it does what is best for the present.

Keep an eye on Bruce Ames, the American biochemist and professor from Berkeley University. He is the man behind the worldwide renown Ames test, a quick method of establishing whether or not substances in food and the environment are cancerous, which is to say whether or not they cause mutation. He is also the author of uncountable numbers of scientific articles and has proposed some very important hypothesises in the field of nutrition. In 1999 President Clinton handed him the “American Nobel prise,” the National Medal of Science, for his contributions. At an age of 78, Ames is still extremely active.

Ames is among those who insist that there is, in uncountable ways, relationships between shortages of vitamins and minerals and cancer, mutations, and aging. But earlier than others, he also sought to explain these relationships bio chemically. It is highly important that we turn to long term studies involving thousands of people for these biomechanical mechanisms to be tested. When Ames invented his mutation test, he simplified detection of cancerous substances with one blow. Long term animal studies became unnecessary. Now he also wants to make long term human studies unnecessary in the study of nutritional deprivation.

The relationship between nutritional deprivation and cancer has been documented with extensive references in last November’s Proceedings of the National Academy of Science. For example, mutations, cancer, and early aging are seen early in association with magnesium deficiency. Vitamin D deficiency is believed to be the reason for 29% of all cancer in men. There is a relationship between deficiency of n-3 fatty acids from fish oil and malignant melanoma (skin caner), between selenium deficiency and cancer, and between potassium deficiency and heart disease. Lack of the B vitamin folic acid, vitamin B12, thiamine, and niacin also are associated with mutations and cancer. Even iron deficiency leads to mutations.

If all of this, and more, is an expression of a causal relationship, then nutrient deficiency should naturally be combated. Deficiency is, as we all know, extremely widespread. We receive large amounts of carbohydrates and fats, but few vitamins and minerals. One in every two Americans receive less magnesium than recommended, 90% receive too little vitamin E, 30% receive too little vitamin C, and so on… and so on.

Mutations can wait
If these many nutrient deficiencies are really the reasons for cancer, aging, and mutation, than what is the explanation? According to Ames, cells, and therefore the organs that they compose, prioritise when they temporarily or permanently lack something. A cell which as a result of a deficiency cannot accomplish all of its tasks, choose, for example, to prioritise the production of energy over the reparation of mutations. Correspondingly, scarce resources cause the organism to prioritise the production of red blood cells over the production of white blood cells, which is to say over immune system maintenance. The principle behind this is the same as when blood is directed to vital organs, such as the heart and lung, after blood loss. The organism must survive now, even though the price is weakening in the long term.

Prioritising is nonetheless only one reason for mutation and aging. A more direct connection is that nutrient deficiencies cause problems for the cells’ energy factories, the mitochondria. They are weakened by vitamin B (biotin) deficiency, pantoic acid deficiency, riboflavin deficiency, B6 deficiency, among others. Without these nutrients, the mitochondria cannot produce the enzymes necessary for energy production. Without energy nothing works in the cell, including the defence against mutation

Ames and others are now trying to find out how much nutrients we need to hold the number of mutations to a minimum and to keep the our mitochondria intact. This is not easy, but it is easier than undertaking expensive, and in many ways, uncertain, decade(s) long population studies. Also, who would finance such expensive studies?

In recent years we have seen a number of studies of supplementary vitamins E and C, selenium, beta-carotene, and vitamin A. Many of these were poorly done, more have been misinterpreted, and some have been proven. Few have become wiser. Is this the way forward? Or has Ames again shown a better shortcut?

While we wait for better knowledge, we should, according to Ames, take reasonable supplements of vitamins and minerals. Everything points towards that this is wise. And there are no risks.

By: Niels Hertz, MD

Reference:
Ames B. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. PNAS 2006; 103:17589-94.

www.pnas.org

Magnesium benefits asthmatics

Niels Hertz

January 8, 2007

Almost everyone gets far less magnesium in their diet than people got in the past. It seems that this greatly worsens life for asthmatics. But the problem has hardly been investigated.

One has to take magnesium seriously. It is a vital mineral, but many people get far less than the 3-400 milligrams a day that are considered adequate. Before the industrialization, we got an average of approx. 500 mg a day (some have said 1,000). Today, many get less than 250.

Several reports in recent years have linked magnesium deficiency to asthma and allergies. In 1994, for example, an English study showed that the more magnesium asthmatics got, the better their lung function. Those who received 500 mg a day had 25% better lung function than those who received 400 – judged by the amount of air you can exhale in one second.

Asthma was not very common in the past. Today, it is a fearsome widespread disease. Approx. every tenth Danish school child has asthma. In Aberdeen and Philadelphia, every fourth child at the age of eight has it. The frequency in Denmark has more than tripled since the 1970s, and no one has any reasonable explanation. What if magnesium deficiency is part of the cause?

During an asthma attack, the bronchi contract so that the air can neither get out nor in – especially not out. But as early as 1912, the famous physician Trendelenburg – it was he who suggested that you should have your legs up in the air if the blood pressure drops – showed that magnesium has the opposite effect. It dilates the bronchi. It was on cows, but in 1936 it was also detected on humans.

Still, only two randomized studies have actually been made to investigate the effect on asthma. One (from 1997) showed that magnesium reduces symptoms. The second (from 2003) showed nothing, which was probably due to the patients receiving so much medication that there was nothing to improve.

Less allergy
Now a team of Brazilian doctors has made a third attempt. They studied 37 children and adolescents (7-19 years) with persistent moderate asthma and allergies. All received medical treatment in the form of an asthma spray with a bronchodilator in addition to adrenal cortex hormone. In addition, they had an acute-acting spray for use in aggravation.

In 18 of the children, this treatment was supplemented with 300 mg of magnesium daily for two months. The rest received placebo (“calcium pills”). Who got what, was decided by secret drawing of lots.

Magnesium helped. Those who received magnesium had significantly fewer days of asthma exacerbation during the two months (12 and 17, respectively). Despite this, they also had significantly fewer days in which to resort to the acute-acting spray (7 and 12, respectively). Although the experiment was small, the differences were statistically extremely reliable. In addition, those who were treated responded far less to the traditional skin prick tests used to examine for allergies. They actually became less allergic! Finally, one could directly measure that their bronchial mucosa was far less irritable.

The conclusion is obvious: Trendelenburg’s old discovery holds water with great certainty. But magnesium is a very cheap mineral (a prolonged-release tablet with 360 mg costs a little over a penny), which no one can patent. Who will pay for further research?

Niels Hertz, MD


Referencer:
1. Gontijo-Amaral C et al. Oral magnesium supplementation in asthmatic children: A double-blind placebo controlled trial. European Journal of Clinical Nutrition 2007: 61:54-60.
2. Britton J et al. Dietary magnesium, lung function, wheezing, and airway hyperreactivity in a random adult population. Lancet 1994;344:357-62

www.nature.com/ejcn/index.html
www.thelancet.com

Remember your daily egg

Claus Hancke

November 28, 2006

Two new studies indicate that important nutrients, contained in, among other things, egg, play a part in the prevention of the most common type of age related blindness.

Macular degeneration, otherwise known as retinal calcification, is the degeneration of retinal cells in the eye’s macula (a yellow spot in the middle of the eye which is the centre of the visual field and has a high concentration of cells responsible for colour vision). Because the macula is in the centre of the eye, if one looses cells in the macula, one also looses sight in the centre of the eye. This means that peripheral vision is retained. With macular degeneration, it is possible to become oriented in, for example, a room, but it is difficult to see what lies directly ahead, including faces, the TV, or a newspaper. One retains ones sense of space, but is functionally blind. It is very irritating for sufferers because they cannot recognize their children or close friends it they meet them on the street. They cannot see their faces, only a black dot.

The first sign of macular degeneration is that straight lines aren’t seen as being straight, but bend so that text and the blinds in front of the window “bulge.” The next sign is the loss of colour vision, because the macula has the highest concentration of colour discerning cells (cones) in the eye.

Earlier studies have shown that it is possible to reduce the risk of macular degeneration with certain antioxidants. Recent studies are interesting because thy have shown that natural measures can be used to in increase the retina’s contents of important chemicals, thereby decreasing the risk of macular degeneration.

At the University of Wisconsin in Madison, USA, an analysis of 1,700 older women from the huge Women’s Health Initiative (a study over what it now a period of 15 years including 161,000 women of the ages 50 – 79) showed that their density of macula pigment was positively correlated with the amount of carotenoids such as lutein and zeaxanthin in the diet and negatively correlated with diabetes and obesity.

A coinciding intervention study was undertaken at the University of New Hampshire, USA, where a group of 24 women, aged 24-59, ate 6 eggs weekly over a period of 12 weeks.

Both lutein and zeaxanthin is found in eggs yolks from which they are readily absorbed into the blood and thereafter concentrated in the retina.

One group received eggs with 331 micrograms lutein and zeaxanthin per yolk. Another received eggs with 964 micrograms lutein and zeaxanthin per yolk and a third group received a daily sugar pill, which they were told contained lutein and zeaxanthin.

I both of the groups which ate the daily egg their levels of lutein and zeaxanthin increased. The same was not true of the group which received the sugar pill. This effect was known from earlier studies with eggs, but this study went one step further and measured the participants density of macula pigment as well as serum – cholesterol and triglycerides at the start of the study and after 4, 8, and 12 weeks.

Serum – cholesterol was not increased in either of the groups which received eggs, but both cholesterol and triglyceride levels increased significantly in the participants who received sugar pills.

Conversely, serum zeaxanthin (not lutein) as well as, importantly, the retina’s content of sight pigment increased in the eggs groups, but not in the sugar group.

Even though there are significantly more carotenoids in vegetables, such as spinach, the authors of the study prefer eggs because of their high bioavailability of lutein and zeaxanthin.

It is nice to, one more time, establish that eggs are good. And they don’t taste too bad either!

By: Vitality Council

References:
• Mares JA, Larowe TL, et al. Predictors of optical density of lutein and zeaxanthin in retinas of older women in the Carotenoids in Age-Related Eye Disease Study, an ancillary study of the Women’s Health Initiative. Am J Clin Nutr., 2006, 84(5): 1107-1122.
• Wenzel AJ, Gerweck C, et al. A 12-wk egg intervention increases serum zeaxanthin and macular pigment optical density in women. J Nutr., 2006; 136(10): 2568-2573.

www.ajcn.org
jn.nutrition.org/contents-by-date.0.shtml

Fish oil is good for the heart and the brain

Claus Hancke

August 21, 2006

There is no doubt that fish oil is good for the heart. This has been shown by a new extensive survey on the subject. But no one knows how much is ideal.

The scientific interest for fish oil is enormous. Since September of last year, almost 800 articles about fish oil have been publicised in established journals.

This is with very good reason. Notably, fish oil contains two types of fatty acid, both of which are attributed with having a positive effect against many serious chronic diseases. If this is even in part true, it should be considered very imprudent not to receive fish oil every day. The primary disease that it is believed to prevent is cardiovascular disease, but there is also good reason to believe that fish oil works against, for example, depression, dementia, arthritis, and diabetes, even though there is no concrete evidence as of yet in these areas.

The two fatty acids are called EPA (eicosapentic acid) and DHA (docosahexaenoic acid). Together they compose one third of the contents of fish oil and two thirds of the concentrated fish oil products, which can be found in capsule form.

Much attention has been given to DHA which, contrary to EPA, is found in large amounts in the brain (14% of the cerebral cortex’s fat content) and in even greater amounts in the retina (22%). Breast fed children have much higher concentrations of DHA in their brains than bottle fed children (babies cannot produce DHA themselves). It is hard to believe that there are no consequences of receive too little.

There are an incredible number of adults who take supplements of fish oil daily to maintain their cardiac health.

But does it work?

Six months ago a group of English researchers maintained that it does not. They had looked at all of the relevant studies and then calculated the averages of their results. In their opinion, the results showed that fish oil neither protects the heart nor lengthens life span. This is just the opposite of what was previously believed.

This meta-analysis was strongly criticized and, as discussed in another of The Danish Vitality Council’s newsletters (“Fish Oil – Still indispensible”) there were so many question raised by the analysis that it lacked credibility.

Doubts regarding the dosage
This is now supported by a summary article from the distinguished American Journal of Clinical Nutrition. According to the head authors, a group of researchers undertook an extensive survey, taking “a large step forward” in spreading light into the darkness. There is no longer much doubt that fish oil reduces the overall risk of premature death and the risk of death due to a blood clot in the heart, and that it possibly reduces the risk of stroke.

Completing this survey was an extensive project. The researchers first read summaries of 8,039 scientific articles. They then picked 842 relevant articles from these to be read in their entirety. 46 articles of these 842 met the strict quality requirements and were studied further. The researches requirements regarded the length of the studies (at least one year), the dose of the fish oil given, and proper documentation.

How big are the advantages and how much fish oil should one take? This actually cannot be answered with certainty! The studies surveyed were too different regarding the dose given, the type of participants, the time taken, and so on to answer such questions. It is simply bad form to establish any averages, as the English researchers did. But if one wants to draw conclusions anyway, it is safe to guess that the overall risk of premature death and the risk of death due to cardiac disease can be reduced by 15-20% or more.

It is however nearly certain that fish oil helps those who have had a blood clot in the heart and wish to avoid another. But what about the dose, how much should one take?

Until more information surfaces, we should rely on the American Heart Association’s recommendations, which are based on estimates. Heart patients should receive 1 gr. EPA + DHA daily. This is the equivalent of about two large capsules of 1 gr. concentrated fish oil. Everyone else should receive at least half this amount. This can be achieved by eating fatty fish for dinner 1-2 times weekly.

There is a lot of knowledge lying in wait, not just about fish oil and the heart. More results will surface in the next year. While we wait we wait in the knowledge that it is important to get enough.

By: Vitality Council

References:
1. Wang C et al. n-3 fatty acids from fish or fish-oil supplements, but not á-linolenic acid, benefit cardiovascular disease outcome in primary- and secondary-prevention studies: A systematic review. Am J Clin Nutr 2006;84:5-17.
2. Deckelbaum R et al. n-3 fatty acids and cardiovascular disease: navigating toward recommendations. Am J Clin Nutr 2006;84:1-2.
3. Distribution, interconversion, and dose response of n-3 fatty acids in humans. Am J Clin Nutr 2006;83(suppl):1467S-76S.

www.ajcn.org

Again, uneasiness regarding the pill

Claus Hancke

July 31, 2006

The pill (contraception in pill form) drains the body of the antioxidants, vitamin E and Q10. This could mean that a supplement would make it much safer to take the pill.

More than 100 million women worldwide use the pill as contraception. The pill is believed to be remarkably safe, and it is easy to forget that it can have serious side effects. According to a Dutch report from 2003, users of the pill have a 3-6 times higher risk of developing blood clots in the veins, which is a dangerous condition. In addition, they have a 2-5 times higher risk of developing blood clots in the heart or of suffering from stroke. These numbers are the same for the modern forms of the pill, which have few other few side effects.

If the risk of disease is low, (because of being young and otherwise healthy) than a low percentage increased in risk does not so important. But why is there any increase at all? Light has been thrown on this question by researchers of the Albert Einstein College of Medicine in New York. They have proven that users of the pill have lower vitamin E and Q10 levels in their blood than women who do not take the pill. Vitamin E and Q10 are well known antioxidants.

This is nothing new. Already 15 years ago, researchers believed that vitamin E could reduce the risks associated with the pill. It was also known that the pill drains the body of antioxidants, which can be directly linked to an increased risk of blood clot formation. When one lacks vitamin E, the fats in the blood become oxidized, thereby stimulating the platelets to stick together causing the formation of blood clots. Logically, it was suggested that vitamin E should be combined with use of the pill.

The pill uses up the body’s vitamin E and Q10 reserves. This has been proven again, this time in a study where 15 users of the pill in their forties were compared with women in the same age group who did not take the pill. The differences found were statistically valid, and although this was a small study there were no doubts regarding the results. These results were known before the study was completed; the problem was that nobody had been paying any attention to them.

Unsolved problems
Why does the pill strain the bloods vitamin E and Q10 contents? The pill raises the body’s oestrogen levels. This is why the ovaries go into hibernation so that ovulation is inhibited. The body registers a hormone level high enough that the ovaries can take a break. Even normal (physiologic) levels of oestrogen stimulate the formation of free radicals and therefore cause an increased use of antioxidants. This has been shown in an American study of the cells which compose the inner walls of the blood vessels (endothelium cells). They also showed that free radicals resulting from the presence of oestrogen caused the cells to grow, causing the blood vessels to thicken. It is believed that this increases the risk of blood clots. It also indicates that antioxidants could prevent such side effects.

For practical purposes, women with an increased risk for side effects are advised not to take the pill. This includes women over the age of 35, women with high blood pressure, and so on. All women with an increased risk of blood clots should refrain from using the pill. This causes some amount of contemplation. Who knows if they are in the high risk group? Is their risk so low that a five fold increase in risk is acceptable?

Aside from these problems it is important to know that if you use the pill, your defence against the formation of free radicals is weakened. Even though this is well known, no one has, until recently, thought to reduce this risk with the use of antioxidants.

An important question follows: What is the long term prognosis for women who took the pill for many years when they were young? During the many years they took the pill, they had reduced levels of vitamin E and Q10 in their blood. In the short term, this increased the oxidation of the blood’s fats which increased the risk of blood clots. But does it cause problems in the long term like smoking and high blood pressure? As yet, we can only guess.

By: Vitality Council

References:
1. Palan PR Magneson AT, Castillo M, Dunne J, Mikhail MS. Effects of menstrual cycle and oral contraceptive use on serum levels of lipid soluble antioxidants. Am J Obstet Gynecol. 2006 May;194(5):e35-8. Epub 2006 Apr 21
2. Felty Q. Estrogen-induced DNA synthesis in vascular endothelial cells is mediated by ROS signaling. BMC Cardiovasc Disord 2006 Apr 11;6:16
3. Ciavatti M, Renaud S. Oxidative status and oral contraceptive. Its relevance to platelet abnormalities and cardiovascular risk. Free Radic Biol Med. 1991;10(5):325-38
4. Saha A, Roy K, De K, Sengupta C. Effects of oral contraceptive norethindron on blood lipid and lipid peroxidation parameters. Acta Pol Pharm. 2000 Nov-Dec;57(6):441-7.
5. Tanis BC, Rosendaal FR. Venous and arterial thrombosis during oral contraceptive use: Risks and risk factors. Semin Vasc Med. 2003 Feb;3(1):69-84
6. Crook D, Godsland I. Safety evaluation of modern oral contraceptives. Effect on lipoprotein and carbohydrate metabolism. Contraception. 1998 Mar;57(3):189-201

An end to the old weakling

Claus Hancke

July 14, 2006

The deficiency of an important antioxidant enzyme seems to be the most important reason that the elderly develop weak muscles. This paves the way for interesting perspectives.

The most striking sign of aging is that muscle strength is reduced and movement becomes slower. Even the most persistent exerciser cannot avoid it. The weakening of the muscles is the most important reason that old people become frail.

Why does this happen? We know that with age more and more signs of oxidation by free radicals can be found in muscles and other tissue. But is this why the muscles weaken?

A group of 12 researchers from both Texas and Stanford University in U.S.A. have undertaken an unusual and very detailed study which indicates that this is precisely the reason. According to them, the age related muscle weakness is due to strain from free oxygen radicals. This can shine light on possible ways to slow this process and maintain mobility longer.

Aging mice are a reliable model for age related muscle weakness in humans. But the American study was just possible because they had a special genetically manipulated mouse which lacked the ability to produce SOD (superoxide dismutase), a very important anti-oxidative enzyme.

In order to understand this it is necessary to know that free radicals are broken down in a chain reaction. SOD is necessary in the first step. In this step “active oxygen” (superoxide anions) is converted to less dangerous hydrogen peroxide. Without SOD this occurs very slowly, but with SOD this occurs at breakneck speed. In the next step hydrogen peroxide, which is also dangerous, is converted to harmless water. This occurs with the help of a selenium rich enzyme. This is one of the best known reasons that selenium, which we get too little of, is necessary for life.

Vital SOD
Back to SOD. It is also necessary to know that there are many forms of SOD. One of them is found in the mitochondria, which are the small power plants of the cells where cell metabolism occurs. If a mouse lacks SOD here, it dies after no more than three weeks. The power plants are destroyed by the free radicals which they produce. Another form of SOD is found outside the mitochondria, but still inside the cells. If the mice lack this type they can survive, but their lifespan is shortened by about 30%.

The researchers worked with mice which lacked the latter SOD form. They saw that the mice already started to develop weakened muscles while young. When the mice were 29 months old, they lacked half of their muscle mass in their hindquarters, whereas normal mice of the same age retain all of their youthful muscle. The so called fast type II muscle fibres were the most affected. The mice were left with slower type I fibres. Heart muscle remained undamaged.

The strength and speed of the muscles were not the only things affected. The mice also became less curious and less willing to engage in exhausting exercises like running in a mouse wheel. When they become old, they shook slightly in their weakened muscles.

It is hard to contest that this damage was caused by oxygen radicals. SOD has no other function other than being an antioxidant. As always it can be added that more research is necessary. This was only a study on mice. But if the results can be transferred to humans it can be argued that it is beneficial to increase the body’s production of SOD. SOD production is decreased with age.

Because SOD is an enzyme, which is to say a protein, it cannot be eaten without being destroyed in the stomach unless given as a special preparation. In combination with other antioxidants and possibly vitamin D (but that’s another story) the effect is supposedly more pronounced. This is not certain, but it is interesting.

By: Vitality Council

References:
1. Muller, Florian L et al. Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy. Free Radical Biology & Medicine 2006;40:1993-2004
2. Jackson Malcolm J. Lack of CuZnSOD activity: A pointer to the mechanisms underlying age-related loss of muscle function, a commentary on “Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy”. Free Radical Biology & Medicine 2006;40:1900-01

Vitamin D Can Be Used As Heart Medicine

Claus Hancke

May 23, 2006

The warnings against direct sunlight in the summer should be taken with a grain of salt. The vitamin D synthesized in the skin in the wonderful sunshine, prevents, amongst other things, weakening of the heart, if we look at the latest research.

Sooner or later in the course of the summer a dermatologist will appear on television to warn against direct exposure to the sun. It may lead to skin cancer and also threatening is the feared, deadly birthmark cancer, the incidence of which has risen dramatically in step with more and more people desiring a tan. This is partly true.

On the other hand it is prudent to be skeptical when someone advices us to act against what is natural. Can it really be true that the sun is so dangerous when people in our part of the world have been far more exposed to the sun through thousands of years?

Vitamin D is made in the skin when it is in the sunlight, but not from September till May, when the sun is too low on the horizon to be used for this in our part of the world. Since our diet only contains minimal amounts of this vitamin, in the wintertime we use the vitamin which has been built up in the skin in the course of the summer. During the winter approximately 85 % of the daily D-vitamin usage is taken from reserves, even in cases where the diet is rich in D-vitamin. All in all, approximately 100 mcg. is used in a day.

But what happens if the reserves are too small?

In the past half-year a number of studies have shed light over the mysteries of vitamin D. According to one study, the vitamin can help against tuberculosis, which we know was a widespread disease in the 19th and beginning of the 20th century, when many people lived under dire conditions in the cities.

Another study of over 14,000 Americans showed that the people with the largest D-vitamin reserves generally had far better lung function than those with the smallest stores. The difference is as big as the difference between ex-smokers and people who have never smoked before. A possible explanation is that the D-vitamin secures the necessary repairs of worn-out cells.

At about the same time, one of the veterans of vitamin-D research, the American Cedric Garland, concluded that now the proof that vitamin D protects against cancer (especially breast cancer, cancer of the colon and prostate cancer) was very strong. Strong enough to make him regard the connection as definite. He has reviewed all relevant research done since 1966.

Weak Heart and Arthritis
His claims can be compared to the fact that David Feldman of Stanford University now wants to conduct an experiment with calcitriol (the active form of vitamin D, which is made in body from vitamin D in the skin or the food) and ordinary arthritis medication against prostate cancer. In laboratory studies he has found that calcitriol slows the growth of prostate cancer by 25 %, while the combination with arthritis medication slows it by 70 %. A true break-through if it is true.

Everyone knows that vitamin D is necessary for the bones, but it is also necessary for the muscles. A deficiency leads to both muscle pain, weak muscles and for example, a tendency to fall in the elderly. But what about the heart? The heart is also a muscle, and weakening of the heart (cardiac insufficiency) because of atherosclerosis or increased blood pressure occurs in as many as 50,000 Danes. It is a dangerous condition with a high mortality rate.

A German study of 123 patients with a weak heart showed that on average they had quite small amounts of vitamin D in their blood stream, close to a deficiency in the traditional sense. Half of them were given supplements of 50 mcg. D3-vitamin each day for nine months. This is five times as much as the elderly are traditionally recommended given, and is also the upper limit, of what is not dangerous to ingest.
The study was too small to show a difference in mortality, but it did show something interesting. It concerns the protein TNF-alpha, which is produced by the white blood cells in connection with inflammation. TNF-alpha is meant to be a major cause of weakening of the heart. In the patients left untreated, the blood’s content of this protein increased by 5 %. In those treated, there was no worsening. This indicates a stabilizing effect on the inflammation.

This is especially interesting for another reason. TNF-alpha is an important cause of pain and swelling in arthritis. So important that new types of arthritis medication, which blocks TNF-alpha, fittingly, are considered wonder-drugs. If vitamin D decreases the effect of TNF-alpha on the weakened heart, maybe the same happens in arthritic joints. This would also confirm the old assumption that vitamin D protects against arthritis.

When in the sun, one should be sensible and avoid sunburns. Stay in the shadow if the sun is very strong and do not lie about for hours in the sun all covered up in greasy sun lotion.

Also important to know is that it is a risk rather than a virtue to stay out of the sun in the summer.

By: Vitality Council

References
1. Schleithof S S et al. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: A double blind randomized placebo-controlled trial. Am J Clin Nutr 2006;83:754-9
2. Heaney R et al. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr 2003;77:304-10.
3. Moreno J, Krishnan AV, Feldman D. Molecular mechanisms mediating the anti-proliferative effects of Vitamin D in prostate cancer. J Steroid Biochem Mol Biol. 2004 Nov;92(4):317-25

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