Author: Claus Hancke

Vitamin D against atherosclerosis

Claus Hancke

January 28, 2008

Vitamin D counteracts the development of atherosclerosis and prevents fatal complications of high blood pressure – but vitamin D deficiency is very widespread.

We are not done with vitamin D. More and more information is streaming in about this amazing substance, which is actually not a vitamin but a hormone created in skin exposed to sunlight.

Now we will look at vitamin D’s effects on the heart and circulation. It seems as though the risks of blood clots in the heart and the brain are far lower in people who get enough vitamin D, which is to say people who get more than most. This “vitamin” is especially effective at lowering the risk in people with high blood pressure.

This find appears in a recent report from Farmingham, a little town in Massachusetts where the health and lifestyles of thousands of people (and their descendents) has been registered since 1948 in order to find lifestyle related reasons for cardiovascular disease. The Farmingham study is, without a doubt, the most famous of its kind. When we today take for granted that exercise, healthy diet, and aspirin prevents cardiac death it is the Farmingham project that we should thank.

The report in question is on a part of the study involving 1,739 people aged 50 – 70 who were free of cardiovascular disease at the beginning of the study. From 1996 to 2000 their vitamin D status was measured with blood tests after which their health was monitored for an average of 5.4 years (up to 7.6 years). Who suffered blood clots?

Those who had the least vitamin D in the blood! After seven years blood clots in the heart or the brain (stroke) was registered in one in ten with vitamin D levels over 37 nmol/l, but in no less than one in four of those with levels under 37. After correcting for differences within the group such as age, sex, cholesterol levels, smoking, diabetes, and so on, the group with the highest vitamin D levels still had a cardiovascular risk 60 % less than that of the group with the lowest levels. If these numbers are right, vitamin D is more important for cardiovascular health than aspirin or cholesterol medicine.

Strong immune system
The beneficial effects of vitamin D seem to be even greater for those with high blood pressure, which is the most important cause of cardiovascular disease. Among participants with high blood pressure the risk for those with vitamin D levels over 37 was half that of those with levels under 37.

This result is similar to that of other studies which have shown that low vitamin D status and high blood pressure and clogged cardiac arteries are related. The Farmingham has an even stronger message: If you lack vitamin D you are at risk of a heart attack within the foreseeable future.

Does this mean that vitamin D prevents atherosclerosis? Yes, this seems to be the case. This fits in well with other known effects including: that vitamin D counteracts an important hormone (renin) which is responsible for raising blood pressure and that when heart cells which normally use vitamin D are prevented from using vitamin D (through genetic manipulation) in experiments on mice, blood pressure rises quickly.

Without eating fatty fish is you get almost no vitamin D from October to May. Deficiency is therefore very widespread. In a European study of teenage girls more than one out of every three had severe anemia (blood percent of under 25 nmol/l). Over 90% of these girls would have, if they lived in Farmingham, ended up in the study group with severe atherosclerosis.

How much vitamin D is it wise to take? There is no rule of thumb, but it should be considered that a typical vitamin pill contains 200 units whereas one out of every two adult Americans need 1,000 units in order to have an “acceptable” vitamin D status (which is a concentration of 75 nmol/l – most American researchers recommend 75 – 150 nmol/l). It is also understood that it is completely safe to take up to 2,000 units daily.

Luz Tavera-Mendoza and John White, two molecular biologists from the American McGill University have shown that vitamin D causes the skin and the immune system to form antibiotics (cathelicidin and more) which kill bacteria, including tuberculosis bacteria. This is probably the explanation for the earlier idea that it is possible to cure tuberculosis with sunlight. These two researchers have written an easy to read summery of recent research and even reveal what they take as supplements during the dark months.

Luz, who is a younger woman, takes 1,000 unites (25 micrograms).
John, who is a younger man, takes 4,000 units (100 micrograms).

By: Niels Hertz, MD

References:
1. Wang TJ et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008;117:000-000.
2. Tavera-Mendoza L, White J. Celle defences and the sunshine vitamin. Scientific American 2007 (11):36-44.

circ.ahajournals.org
www.sciam.com

Never Calcium Without Magnesium

Claus Hancke

January 17, 2008

Calcium tablets as monotherapy increase the risk of blood clots in the heart and brain.

Last year, the British Medical Journal in their web version published a scientific article with the above-mentioned gloomy message.

1,471 healthy women over 55 years were randomly divided into two groups, one with 732, who took a supplement of calcium citrate for 5 years and a group of 739 who took placebo.

During these five years, they were examined every six months, and for each year, the distance between the two groups increased with statistic significance.

It was found that in the group who took calcium tablets, there was a significant increase in the risk of blood clots in both the brain and the heart.

The authors are surprised by the result and have reservations until the matter has been investigated further with more studies.

But do we have to wait five years for a new study of this result?

Is not it predictable?

Most people who have experience with the use of minerals for disease prevention are well aware that you should never take calcium without taking magnesium at the same time.

Magnesium is the key
(If you think it becomes too biochemical, then just read the conclusion at the end).
Magnesium sits like a bolt in the calcium channel of the cell membrane.

The moment calcium wants to enter a cell, magnesium closes the door and when calcium wants leave the cell, magnesium will open up. It’s the opposite in bone cells.

Therefore, the cells in the soft tissues are almost empty of calcium. The calcium concentration outside of a cell is about 10,000 times as high as within a cell. Thanks to magnesium.

If we lack magnesium, the calcium channels will open.

This means that through the open calcium channels, calcium flows into the cells, causing the cell to cramp and, in the long term, (hours) destroy its mitochondria.

The cramp causes immediate contraction of the blood vessels due to the smooth muscle cells around the small arteries, resulting in increasing blood pressure and risk of brain hemorrhage and destruction of calcification plaque and thus risking a blood clot in the heart. At the same time, the energy production of the cell is minimized due to the destruction of the energy-producing mitochondria with their vital content of coenzyme Q10.

This not only results in less energy production in the cells, but also a smaller consumption of oxygen absorbed in the cell, which in turn means that a greater proportion of this oxygen are then used to produce harmful free radicals, IF there is iron present as a catalyst for this process, and this is precisely the case in this group of women who no longer menstruate.

Then the roulette runs with destruction of the cell membrane and the surrounding cells from within, because now the cell has suddenly had its own little “Chernobyl meltdown”.

If we lack magnesium, we have no control over the distribution of calcium, and it is distributed more or less evenly throughout the cell phase, ie. both in bone cells and in soft tissue cells, muscle cells, skin cells, connective tissues, etc.

But are we lacking magnesium?
Yes we are. More than 70% of the population do not even get the recommended daily allowance of 300 mg of magnesium.

Why not?

The food has gradually become more and more low in magnesium. In part, the industrialization of the diet has resulted in a large loss of magnesium in the finished product, and we eat less vegetables where we find this magnesium and when we cook the vegetables, we pour the magnesium out with the boiling water.

Furthermore, many elderly people loses magnesium because they take diuretic medicine or because they drink too much coffee.

70% of research participants with low intracellular magnesium are more than sufficient to explain the significant increased risk associated with calcium intake as monotherapy.

There is therefore no surprise in the achieved result, and it should not be necessary to wait a lot of years to take extra magnesium along with ones calcium supplement. This will not only benefit muscles, heart, brain and bones, but also a variety of processes in the body that rely on the more than 300 enzymes for which magnesium is required.

So: Never take calcium without magnesium!

By: Claus Hancke, M.D.

 

References

Mark J Bolland, P Alan Barber, Robert N Doughty, Barbara Mason, Anne Horne, Ruth Ames, Gregory D Gamble, Andrew Grey, Ian R Reid. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ published online 15 Jan 2008;doi:10.1136/bmj.39440.525752.BE

Promising treatment for macular degeneration

Claus Hancke

December 22, 2007

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

By: Vitality Council

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

Vitamin C inhibits cancer. But How?

Claus Hancke

September 18, 2007

New research sparks new theories about how vitamin C inhibits cancerous growth.

A great deal of research indicates that vitamin C has a considerable inhibitory effect on the growth of cancer cells.

The biochemical effect of high-dose treatment with vitamin C is reasonably understood; vitamin C acts as a pro-oxidant on cancer cells at such doses. This causes increased free radical strain on the cancer cells and thereby acts as a poison to the cancer.

In moderate doses, the kind of doses which we can get through our diets, vitamin C is an antioxidant. But even at these doses, vitamin C has shown an inhibitory effect on the growth of cancer cells.

It was therefore believed that vitamin C blocks the free radicals which cause the cancer forming mutations in the cells, and that the reason for its protective effects is that it protects the cells’ DNA.

This is presumably not the whole truth.

Many years ago a famous professor by the name of Warburg was among the first to maintain that cancer cells grow in oxygen poor tissue. Today this is common knowledge, but there lacks knowledge on how this occurs. Ten years ago Gregg Semenza of John Hopkins University found that cancer cells are dependent on a protein called HIF-1 (hypoxia induced factor), which helps the cells by compensating for lacking oxygen in the surrounding tissue and thus allows cancer cells to convert sugar to energy without oxygen. HIF-1 also catalyses the creation of new blood vessels so that hungry cancer cells can get fresh supplies of nutrients and oxygen. If a cancer grows aggressively, it quickly uses up its oxygen supply and becomes entirely dependent on HIF-1. The HIF-1 protein is dependent on the presence of free radicals, which are also necessary for many other processes in the body. A powerful antioxidant like vitamin C eliminates the surplus of free radicals, which causes HIF-1 to become ineffective and thus inhibits cancer growth.

This new theory is based on a study done by a research group at the centre of oncology at John Hopkins University in conjunction with Dean Felsher of Stanford.

They set out to study antioxidants’ roles in cancer growth and found, to their great surprise, that antioxidants destabilise the protein on which cancer cells are dependent. As professor Chi Dang from John Hopkins University wisely stated, “By uncovering the mechanism behind anti-oxidants, we are now better suited to maximize their therapeutic use.”

By: Claus Hancke, MD

Reference

HIF-Dependent Antitumorigenic Effect of Antioxidants In Vivo. Cancer Cell, Volume 12, Issue 3, 11 September 2007, Pages 230-238Ping Gao, Huafeng Zhang, Ramani Dinavahi, Feng Li, Yan Xiang, Venu Raman, Zaver M. Bhujwalla, Dean W. Felsher, Linzhao Cheng, Jonathan Pevsner et al.

www.cancercell.org

Folic acid for stroke – and to remember

Claus Hancke

June 12, 2007

You must remember your folic acid, otherwise you forget it.
This sounds like nonsense, but its not.

Folic acid helps keep the brain in good shape, and if you don’t get enough you might have problems thinking clearly and remembering when you get older.

Folic acid is the vitamin that fertile women should take (0.4 mg per day) unless they are 100% sure that they will not become pregnant. Far from all do this, even though folic acid prevents children from being a lifelong invalids due to spinal chord herniation (spina bifida) and reduces the risk of cleft lip and palate! That it is preventative is so called new knowledge (1) which is to say that it was pointed out, but ignored, over twenty years ago.

But folic acid also helps the memory and thought ability. Who do we know this? The English neurologist Edward Reynolds demonstrated it 40 years ago in hi article in The Lancet. He showed that 26 epilepsy patients who suffered folic acid deficiency due to their medicine improved when they received folic acid (2). This has since been forgotten.

Now there are new studies. One had negative results. Its authors concluded that folic acid has no effect on cognitive function, which did not improve for study participants who received 0.4 mg folic acid daily (without vitamin B12, in which they were mildly deficient) (3).

There is a simple explanation for this: the only lasted 24 weeks. This is not long enough, which will be explained below, but first a couple of other results.

An issue of the American Journal of Clinical Nutrition from last February included an article which outlined that the more pronounced folic acid deficiency in elderly people, the poorer (statistically) their cognitive function. The likelihood of decreasing cognitive function was more than doubled in those with a deficiency of folic acid (4). There are many people with folic acid deficiency because folic acid is primarily found in liver and leafy vegetables, which many people push to the side if their plates.

20% fewer strokes
Lack of folic acid is shown roughly by finding increased blood levels of the substance, homocysteine. It is an amino acid which is poisonous to the blood vessels (among other things) and which is believed to lead to atherosclerosis, but that the body nonetheless creates. Normally it is neutralised in part by folic acid. If you lack folic acid, you homocysteine levels rise.

A link between lowered cognitive function and homocysteine has been shown in Sweden (5). There it was shown that elderly people with documented memory problems often had high levels of homocysteine. This was only true with the poor memory was found along with atherosclerosis, which homocysteine is believed to promote!

In addition, Dutch researchers recently showed in a randomised trail that a supplement of folic acid (o.8 mg daily) for 50 – 70 year olds not only reduced their levels of homocysteine, but also statistically improved the “brain functions which have a tendency to decline with age.” Memory, reaction time, and the ability to speak quickly and fluently were bettered. The study lasted for three years, which is a necessary time period (6).

If that is not enough, a comprehensive study of eight randomised studies has recently shown that the risk of stroke resulting from atherosclerosis generally is reduced by 20% when taking folic acid supplements. The studies which lasted longer than three years showed the best results. Participants who had already had a stroke were less protected and if those who were lucky enough to live in a country where food is enriched with folic acid (USA, Canada) showed fewer effects.

We should remember our folic acid. The daily dosage should be between 0.4 and 0.8 mg daily.

By: Vitality Council

 

References:
1. Bille C et al. Folic acid and birth malformations. BMJ 2007;334:433-34.
2. Reynolds E. Folate and aging. Lancet 2007;;369:1601.
3. Eussen SJ et al. Effect of oral vitamin B12 with or without folic acid on cognitive function in older people with mild vitamin B-12 deficiency: A randomized, placebo-controlled trial. Am J Clin Nutr 2006;84(2):361-70.
4. Haan M et al. Homocysteine, B-vitamins, and the incidence of dementia and cognitive impairment: Results from the Sacramento area latino study on aging. Am J Clin Nutr 2007;85:511-7.
5. Nilsson K et al. Plasma homocysteine is elevated in elderly patients with memory complaints and vascular disease. Dement Geriatr Cogn Discord 2007;23(5):321-6.
6. Durga J et al. Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: A randomised double blind controlled trial. The Lancet 2007;369:208-16.
7. Xiaobin Wang et al. Efficacy of folic acid supplementation in stroke prevention: a meta-analysis. The Lancet 2007;369:1876-82.

www.bmj.com
www.thelancet.com
www.ajcn.org

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

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.

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