Q10 and selenium protect the heart

April 23, 2023

Supplementation of Q10 and Selenium over a 4-year period
could halve cardiovascular mortality.

A  short  time ago a very important scientific article was published.

The article was an offshoot of the sensational article by researcher Dr. Urban Alehagen and colleagues from 2015, who showed massive cardiovascular protection with supplementation of Q10 in combination with selenium.
Alehagen and colleagues then carried out a follow-up of this study, but not only that. They have also sought to dig into the actual cause of this positive effect, which was a halving of cardiovascular mortality after 4 years of supplementation.

The logic is straight to the point. The vast majority of cardiovascular diseases are caused by atherosclerosis, and this is caused by a combination of inflammation, i.e. a local response to tissue damage and oxidation (here rancidity). Without these two factors, atherosclerosis does not occur.

Briefly, the mechanism is that oxidation turns LDL3 cholesterol rancid, which is thereby “eaten” by a type of white blood cells called monocytes via a structure on the cell surface called a “scavenger receptor”. This means that LDL cholesterol is directed around the usual LDL receptor, which could otherwise easily block intake. But the scavenger receptor cannot stop its intake of LDL cholesterol if it is oxidized, because LDL in this form acts as a free radical. And that is exactly what the scavenger receptor is designed to let into the monocyte. However, since the intake cannot stop, even though the monocyte is probably so crowded, it swells up and is seen under the microscope as a large white blob. And when there are many of these monocytes together, it looks like foam. Therefore, these “overfed” monocytes are called “foam cells”.
Oxidation is thus required for a monocyte to become a foam cell.
When the monocyte circulates in the bloodstream, it will react if it finds an area, e.g. the blood vessel wall, where there is inflammation, e.g. due to high blood pressure. The monocyte will search for the inflamed area, penetrate the vessel wall (into the subendothelial layer), where it will perish and leave behind a fatty layer of oxidized LDL3 cholesterol. This will increase inflammation and attract even more foam cells, which in turn perish, leaving behind more of the rancid fat, which is gradually consolidated by fibrin and finally stabilized by calcium, which is the last step in atherosclerosis.

The entire above process will not take place unless there is both increased inflammation and oxidation.
And precisely selenium and Q10 inhibit both inflammation and oxidation. Therefore, it is perhaps not so strange that they prevent cardiovascular disease and reduce the risk of dying from it.

Q10
The body’s cells produce energy in order to function, and this energy requires Q10 in the cells’ internal power plant, the mitochondria.
Unfortunately, there is a natural decline in the body’s production of Q10 as we age, and it is therefore natural to supplement this.
Q10 is a substance that the body produces in almost the same way as it produces cholesterol. Q10 and cholesterol are actually sister molecules that look very similar. So when you take a cholesterol-lowering medication, you also lower the production of Q10. You should therefore be aware that you often lack Q10 if you take cholesterol-lowering medication.

Selenium
Selenium is a substance that we absolutely must not lack, and numerous studies have confirmed over the years that selenium deficiency can lead to, among other things, heart failure, cancer, metabolic disorders, arthritis, childlessness, atherosclerosis, increased inflammation and a number of immunological failures, which were particularly relevant in the corona era.
There are thousands of articles that cement heavy research into selenium, such as a study of selenium deficiency related to cardiovascular disorders and inflammatory conditions. Since cardiovascular disorders are also initiated by inflammation, it is natural to investigate this together.
Previous studies have also shown that low selenium in the blood was the cause of increased inflammation, increased risk of cardiovascular disease and early death.

The current study mentioned above is also primarily aimed at finding the biochemical mechanism behind this effect.

As mentioned above, it is based on Alehagen and colleagues’ article from 2015, and it is evidence with a very high degree of reliability, as it was a double-blind, randomized, prospective study. The participants were healthy elderly with an average age of 76 years. 165 received 200µg Selenium + 200mg Q10 daily, and 161 received placebo. The treatment lasted 4 years, after which various parameters were measured.
They were particularly interested in measuring the change in Sirtuin1, an enzymatic protein (deacetylase), which is important for the survival of cells when they are exposed to oxidative stress, because Sirtuin1 increases the effect of certain antioxidants.
But not only that. Sirtuin1 also inhibits the so-called NFκB signal, which is a substance that otherwise produces a strong inflammatory response.
So if you can increase Sirtuin1, you will thereby be able to inhibit inflammation and oxidation, – in other words, the two factors, which are mainly responsible for, among other things, cardiovascular diseases.
After a 4-year intervention period, the SIRT1 concentration was found to be significantly increased (from 252 to 469 ng/ml) in the active group and decreased (from 269 to 190 ng/ml) in the placebo group.
In a 10-year follow-up period, 25 in the active group and 52 in the placebo group died of cardiovascular disease, and the 77 who died had significantly lower SIRT1 concentration than the rest.
A small wrinkle in the study is that the so-called microRNA is also affected in a direction that inhibits the aging of the cardiovascular system. Micro-RNA contributes to the regulation of the gene activity. This has very far-reaching consequences for epigenetics, that is different modifications of DNA, which can turn genes on or off, and will of course be explored intensively in the future.

In this scientific trial, Alehagen and colleagues have shown that just 4 years of Selenium and Q10 supplementation inhibits oxidation and inflammation, and halves cardiovascular mortality over a 10-year period.

Now that selenium and Q10 are effective in inhibiting oxidation and inflammation, it is not surprising that they can halve the risk of dying from cardiovascular disease.
It is more strange that this is not standard advice from the medical profession when the evidence is so solid.

Take care of yourself and others.

Claus Hancke MD
Specialist in general medicine

Q10 increases survival in heart failure

May 24, 2022

New review article highlights ubiquinone/Q10 as a first choice for heart failure.

Heart failure is a relatively common disorder, and often occurs as a result of a blood clot in the heart, which has left a scar in the heart muscle. This scar tissue is connective tissue that does not have the normal muscle function of the myocardium, and if a large part of the muscles of the left ventricle in particular is out of order, it is clear that the heart can no longer pump as efficiently.

The most common symptom is dyspnoea, which means that you breathe faster with physical exertion, because the oxygen concentration in the blood can not be maintained when the heart has reduced its ability to pump blood to oxygenate the lungs.

This condition is clinically classified in the so-called “NYHA” groups 1-4, which were once defined by the New York Heart Association, hence the name.

Roughly speaking, in class 1 you have no problems with normal activity, in class 2 you can not run, only walk, in class 3 only sit, and in class 4 you are largely bedridden.

All this is precisely limited by dyspnoea.

The heart failure is diagnosed and graded by ultrasound-Doppler examination and especially the “stroke volume” / EF (Ejection Fraction) of the left ventricle is measured, which is usually around 60% and satisfactory at 50%.

(The volume of the heart is a bit like with the lungs. You can not completely empty it of blood, just as you can not completely empty the lungs of air. Therefore, it is satisfying if the heart can pump out half of its contents at each heart rate.)

The heart muscle can be weakened by many things other than a blood clot, and by any of the transient conditions, such as eg. inflammation of the heart muscle (myocarditis), the pump function can also be restored afterwards.

But after a blood clot, it is difficult because the scar tissue that is formed after the blood clot will never actively pump again.
However, there is hope because the part of the heart muscle that is not damaged may well become stronger.

This is the focus of rehabilitation after a blood clot, but there is also something else that can be done. -You can optimize the energy production in the cells of the myocardium.

Treatment of heart failure
The usual treatment for heart failure was once limited to diuretics and digoxin, but has been under constant development and is today complemented with ACE inhibitors, Procoralan, SGLT-2 inhibitors and even beta-blockers, which were once contraindicated in heart failure. .

This is how the treatments develop continuously, and the idea with the treatment is primarily to relieve the heart and prevent arrhythmias or prevent that you get a blood clot again.

There are also patients with heart failure who benefit from a pacemaker, and if the situation it is completely bad, then a heart pump or a transplant.

Stop for a moment
Before we go off at a tangent maybe we should just try to get a little overview. What exactly do we want to achieve?

We want to achieve that a person with heart failure lives as well as possible for as long as possible.

So should we not try the least invasive treatment so that we avoid many of the heavy side effects following all the above treatments?

All the common treatments are intended to relieve the heart. But there are also options to make the heart stronger so that it pumps better with the remaining muscle tissue. As mentioned, exercise is one of the options, but you can also increase energy production in every single heart muscle cell.

Ubiquinon/Q10
Last week, a review article was published in Journal of Cardiovascular Development and Disease , which reviews 22 scientific articles (20 RCTs) on Q10 used against heart failure.

In the 16 articles, they found significant improvement in pump function (EF) or survival or both. In all cases, there was an inverse correlation between the blood concentration of Q10 and the worsening of the symptoms in patients with heart failure, just as the concentration of Q10 was an indicator of longevity.

In other words, those who had the lowest content of Q10 in the blood had a rapid worsening of the symptoms, just as they lived for a shorter time.
In line with this, it was similarly found that supplementation with Q10 improved the pumping function of the heart and increased the life expectancy of these patients.

The article also focuses on the inappropriate effect of statins, which not only lower cholesterol production but also the production of coenzyme Q10, as these form a common synthetic route from AcetylcoA over mevalonate to farnesyl pyrophosphate. This synthesis requires i.a. the enzyme HMG-CoA reductase and this enzyme is inhibited by statins.

Often, statins are actually prescribed to patients with heart failure, although this should be contraindicated according to the above.
It is noted very laconic that Q10 has at least as good a documentary weight as the treatment that is today considered the gold standard for treating heart failure. Exercise is extremely well documented, whereas digoxin and SGLT-2 inhibitors are poorly documented. Here we must say that Q10 is significantly better documented.

Given the solid evidence and the absence of interactions and side effects with ubiquinone/Q10, it is an obvious first-line treatment for heart failure, and should be implemented throughout the public health system.

 

Claus Hancke
Specialist in general medicine

Ref.

2022 Maj 16, Krzysztof J. Filipiak et al: Heart Failure, -Do We Need New Drugs or Have Them Already? A Case of Coenzyme Q10, J. Cardiovasc. Dev. Dis. 2022, 9, 161

Vitamin D against atherosclerosis

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

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

Folic acid for stroke – and to remember

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

Fish oil is good for the heart and the brain

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

Vitamin D Can Be Used As Heart Medicine

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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Fish Oil – Still Indispensible!

April 7, 2006

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Fish is good – of course!

By: Vitality Council

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

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Vitamin C against atherosclerosis (hardened arteries)

March 23, 2006

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

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

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

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

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

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

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

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

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

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

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

By: Vitality Council

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

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