Tag: atherosclerosis

Q10 and selenium protect the heart

Claus Hancke

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

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

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

Vitamin C against atherosclerosis (hardened arteries)

Claus Hancke

March 23, 2006

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

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

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

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

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

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

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

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

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

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

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

By: Vitality Council

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

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

Vitamin K against osteoarthritis and atherosclerosis

Claus Hancke

August 22, 2005

Researchers recommend Vitamin K supplementation. The need for this vitamin may be even greater than was previously supposed. Vitamin K deficiency leads to weaker bones and calcification of the arteries and vitamin K supplementation will both treat and prevent these problems.

Vitamin K “should be strongly considered as a dietary supplement” for women after menopause and for diabetics, groups which have high risks of developing both osteoarthritis and atherosclerosis. The vitamin is very non toxic and seems to be able to combat these ailments.

This is the very uncompromising conclusion put forth in a new scientific summary of vitamin K which has been published in the American Journal of Health-System Pharmacy, which is a serious but lesser known professional journal.

In spite of this journals lack of prominence, it’s very direct message regarding vitamin K will spread throughout the world. It was quickly published in its entirety by www.medscape.com the worlds largest website for doctors. Medscape has millions of readers worldwide.

Vitamin K is found almost exclusively in green vegetables. It is practically nonexistent in other foodstuffs. It was previously believed that the bacteria in our intestines hold us well supplied with the vitamin. This is not the case!

It is officially recommended (in the USA) that one has an intake of no less than 100 micrograms vitamin K daily, corresponding to about 75 grams green salad, spinach, etc. This is supposedly enough for the blood to coagulate properly.

But according to the article ensuring proper coagulation is far from enough. The vitamin is just as important for bones and arteries, and its optimal effect requires much more than officially recommended. In studies with vitamin K1, 10 times the official recommendation (10,000 micrograms) is typically used. This can be done worry free, there are no side effects. No effects have been reported, even when 45,000 micrograms K2 was used per day, 400-500 times recommended, for up to many years.

Vitamin K is responsible for making certain proteins able to bind to calcium. This occurs by the vitamin attaching mild acids (carboxyl groups) to the protein enabling it, like a type of crane, to pick up and move calcium to where it is needed. The protein which has this effect in bones is called osteocalcin and is produced with the aid of vitamin D. With the help of a weak acid osterocalcin can pick up calcium from the blood and place it in the bones. Vitamin K has long been used in Japan to counteract osteoarthritis.

In clogged arteries, for example the coronary arteries, the opposite occurs. It is believed that vitamin K counteracts the depositing of calcium in these vessels by adding a certain protein to the same acids. If the protein is missing or damaged and inaccessible to the acid, the blood vessel clogs quickly. This has been shown in animal studies. Normally the “crane” removes calcium from the arteries so they do not become clogged.

That there is a protein which prevents atherosclerosis and that vitamin K is necessary for its production is a very revolutionary theory. The theory is supported by Dutch research. In a three year long randomised study on older women, half received a daily dose of 1,000 micrograms vitamin K while the rest unknowingly received placebo.

The stiffness of the women’s carotid arteries was measured before and after the three years as a measure for the degree of arthrosclerosis. After the three year period this was unchanged in the women who received the vitamin K whereas nature had marched on in the rest of the women. Their arteries became 8% stiffer.

The strange phenomenon where calcium disappears from the bones and is accumulated in the arteries with age is called the “calcification paradox.” Aging phenomena are without a doubt a part of the explanation, but vitamin K deficiency is probably also contributory. It is without a doubt important to consider this paradox.

Important
If you receive strong blood thinning medicine such as Marevan, you should unfortunately avoid vitamin K supplements. Any such supplement can counteract your treatment and be life threatening.

By: Vitality Council

References:
1. Adams J, Pepping J. Vitamin K in the treatment and prevention of osteoporosis and arterial calcification. Am J Health-Syst Pharm 2005;62:1574-81.
2. Braam LA et al. Beneficial effects of vitamin D and K on the elastic properties of the vessel wall in postmenopausal women: A follow up study. J Thromb Haemosta. 2004;91:373-80.

www.ajhp.org
www.blackwellpublishing.com/journal.asp
www.iom.dk

Vitamin E Protects Against Blood Clots And Brain Haemorrhages

Claus Hancke

August 9, 2005

Healthy women over 65 can lower their risk of serious consequences of arthrosclerosis by 25 %. This is confirmed by the world’s longest study of vitamin E, so far.

In 1997 44 % of all American cardiologists regularly used antioxidants, especially vitamin E, to prevent coronary thrombosis and strokes. The confidence in vitamin E was so strong that it surpassed the confidence in aspirin, which was only used by 42 %.

The cardiologists relied on the universal theory that arthrosclerosis arises when cholesterol is oxidized and that vitamin E, amongst other things, prevents this oxidization. Unfortunately solid evidence that vitamin E truly protects against arthrosclerosis, and thereby prevents thromboses, has been lacking. Large randomized studies have been disappointing, but also encumbered by obvious faults. Everything is shrouded in doubt. But if the doctors have stopped using vitamin E in disappointment, maybe they will begin using it again now.

The occasion is the largest and longest randomized study up until now with vitamin E. It showed that when healthy women over 65 received vitamin E as a supplement, their risk of suffering a coronary thrombosis or a stroke decreased by 26 %. And not only was the incidence lowered, the diseases also became less dangerous. The total mortality rate was approximately halved (to 51 %).

Other studies of vitamin E have been relatively short, and have had participants who suffered from serious arthrosclerosis. However this study lasted ten years, and the participants were healthy. Exactly because they did not suffer seriously from arthrosclerosis from the beginning, it was hoped that it was not too late to prevent it. A total of 20,000 women received 600 units of natural vitamin E (alpha-tokoferol) every other day for ten years. Just as many other women were given a placebo (fake pills).

The women who were over 65 benefited. However, the large majority was younger than 65. They had no obvious benefits from the treatment. 18,000 women under 65 received vitamin E. 352 of these suffered a coronary thrombosis or a stroke, some with a fatal outcome. That number was eleven higher than amongst the 18,000 who received placebos. A small and random difference. Apparently vitamin E did not benefit the younger women.

For comparison only 2 times 2000 women over 65 participated. In the group receiving vitamin E, there were 130 cases of either cardiac thrombosis or stroke. In the placebo group there were 46 cases more. This difference is relatively large, and statistically quite certain.

But why does vitamin E not benefit the younger? The obvious answer is that maybe it does, but younger women more seldom suffer cardiac thrombosis, and the potential effect is difficult to measure. In the course of the ten years the study ran, less than two percent of those under 65 suffered a cardiac thrombosis or a stroke. Those older, of course had a bigger risk (about eight percent). One can speculate that despite the neutral numbers, the younger group did in fact become less atherosclerotic because of the vitamin E supplement. No one knows, since a direct measurement of the blood vessels was not conducted. The only measurement for the degree of arthrosclerosis was the rough numbers for cardiac thrombosis and stroke.

If seen under the same light, statistically there was only tendency towards benefit from vitamin E. It is a natural consequence of the fact that there were nine times as many young participants, as there were older. The researchers did however choose to conclude on the basis of this result. They believe that the study does not warrant a general recommendation of vitamin E for the prevention of cardio-vascular disease. With regards to those over 65, it is being said that the result deviates from “the total knowledge” and should be investigated further.

This is a somewhat weak comment. A more direct comment came from Maret Taber who is professor at the Linus Pauling Institute in California and one of the World’s leading vitamin E experts:

“Vitamin E has its clear value in the fight against cardiac disease and other degenerative sufferings. It is most important for smokers, persons suffering from hypertension and those who eat an unhealthy diet.”

By: Vitality Council

Reference:
Lee, I-Min. Vitamin E in the primary prevention of cardiovascular disease
and cancer. The Womens Health Study: A randomized controlled trial. JAMA
2005;294:56-65.

jama.ama-assn.org
www.iom.dk

Carnitine, a Stimulant for Heart, Brain, and Muscles

Claus Hancke

May 9, 2005

Carnitine creates energy in aged cells. The message from a new scientific congress is that supplementation of carnitine seems to help against both heart disease, arteriosclerosis, and dementia.

Are your memory failing or are you loosing strength, then perhaps carnitine is the remedy for rescue

Carnitine is an – undeservedly – overlooked dietary supplement that is on its way into the ‘scientific warmth’. A clear signal is that the New York Academy of Sciences dedicate a whole volume of its famous scientific annals to carnitine alone.

Here you can read more than 197 pages from all 18 contributions given at a two-day conference on carnitine held by the academy in March 2004. The contributions are, among other things, about the importance of carnitine for the burning of fat, for the functioning of the muscles and the heart and about its promising role in the fight against a weakened memory.

Carnitine is an essential nutrient that we mainly get from red meat and dairy products. The body only produces small amounts, and vegans in particular are at risk of deficiency. Carnitine is necessary for the mitochondria – the energy factories of the cells – to burn fat. First, it enables fatty acids to enter the mitochondria, then it promotes their combustion, thereby preventing the harmful accumulation of fatty acid residues, while at the same time supplying the cells with energy.

With age, the transfer of fatty acids to the mitochondria slows down. In addition, the mitochondria become less able to get rid of incompletely broken down fatty acids. This leads to their accumulation of free radicals, a main reason why they degenerate. But without mitochondria, there is no life. Degeneration of the mitochondria is a central phenomenon in the aging process.

Anti-Aging
Many therefore believe that carnitine is an extremely obvious ally in the fight against aging. In a summary by Charles Rebouche from Iowa University, it is stated that carnitine supplementation appears to inhibit aging in rats, just as in humans it both combats age-related memory decline and mitigates the deterioration of Alzheimer’s.

That carnitine as a supplement can really replace missing carnitine function is evident from experiences with children who, for genetic reasons, have difficulty transferring carnitine to the mitochondria. Untreated, they develop severe heart and muscle diseases, but with the help of carnitine supplements, children with these rare disorders have survived to more than 30 years of age – and are still doing well.

However, many more people can benefit from Italian studies that have shown that it is possible to limit the damage that occurs to the heart when a blood clot cuts off the blood supply to parts of the heart muscle. Carnitine reduces the deformation of the heart that would otherwise occur, and during long-term treatment, carnitine-treated patients can work longer and harder, and their fitness is better.

This is an extremely exciting result, which is consistent with the finding that patients with intermittent claudication – walking pain due to calcification, and thus narrowing, of the arteries in the legs – improved their performance on a treadmill when they received a supplement of two grams of carnitine daily.

After the congress, experiments have shown that carnitine also helps against the type of diabetic neuropathy that causes pain. In both rats and humans, a significant effect has been found on this neuropathy, which is often a painful companion to undertreated diabetes. The dose was ½-1 gram three times daily.

Nerves, muscles and heart are major consumers of energy. Carnitine supplies energy. When the brain, heart or muscles weaken with age, it seems wise to think about Carnitine.

By: Vitality Council

Reference:
Salvatore Alesci et al. (Eds.). Carnitine: The Science behind a Conditionally Essential Nutrient. Annals of The New York Academy of Sciences 2005, vol. 1033.

www.annalsnyas.org
www.iom.dk

Deficiency in B-vitamin Causes Dementia

Claus Hancke

April 18, 2005

According to one American study, folic acid weakens the memory of the elderly. According to another study, the opposite happens. Nearly all studies, however, indirectly indicate that folic acid prevents both arteriosclerosis and dementia.

It is a well-known fact that the B-vitamin folic acid prevents congenital neural tube defects. However, it can also lower the blood’s content of homocysteine; a biproduct in human metabolism that promotes atherosclerosis, among other things. Having an increased level of homocysteine is just as dangerous as cholesterol: Up to 40% of all individuals with premature atherosclerosis have increased blood levels of homocysteine.

The fact that homocysteine also damages the brain is indicated by more than 20 different studies. It has been found with almost unerring certainty that demented old people have more homocysteine in their blood than others and that the ones who score highest on memory tests are the ones with the least homocysteine in their blood. This is a clear argument for taking folic acid.

However, completely unexpectedly, a fly in the ointment has now appeared. A study at Rush University in Chicago has shown that the exact opposite might be the case. If you are elderly and you get more than the typical 0.4mg. of folic acid a day, your memory will decline more rapidly.

A total of 3,718 trial subjects over 65 years of age were followed for five to six years after having reported their eating habits. They were then mentally tested three times during the course of the 5 – 6 years. The results were the same whether they got folic acid from their diet or from dietary supplements: In the people taking folic acid, memory declined more rapidly than in the others.

Are these results the result of a coincidence? Anyhow, it does make you wonder that the 20% who got the most folic acid (0.7 mg. a day) did far better on the mental tests than the rest. Granted, their memory deteriorated more rapidly, but they obviously had a better memory to begin with. Why was that so, if folic acid is actually harmful?

In addition to this, doctors from the UCLA in February 2005 published results stating the exact opposite. Among 499 well-functioning 70 – 79 year-olds, most folic acid was found in the blood of the ones who had the best memory. And equally importantly: Seven years later, they were in better posession of all their faculties.

No explanation
What is true, then? If the truth lies in the Chicago study, it might be based on the co-operation between vitamin B12 and folic acid. Both vitamins reduce blood levels of homocysteine and the major task of both of them is to produce small, chemical units – which only contain a single carbon atom – for building other molecules.

Folic acid delivers its units to vitamin B12 which are then further delivered to – homocysteine. In this way, homocysteine is neutralized and is transformed into a harmless amino acid and the blood level of homocysteine will drop.

Whether you lack vitamin B12, folic acid, or both, the transport of the single-carbon units will be complicated. In all three cases, the result will be a specific type of anaemia (pernicious anaemia) which is characterized by the red blood cells being abnormally large.

However, the symptoms in vitamin B12 deficiency and folic acid deficiency are not quite similar. In folic acid deficiency, neuritis – i.e. nerve damage – will not occur. In vitamin B12 deficiency, it will. The anaemia in vitamin B12 deficiency can be removed by taking folic acid, but the neuritis cannot. Vitamin B12 has an affect on nervous tissue that folic acid cannot imitate.

In up to 30% of all elderly people, vitamin B12 deficiency can be demonstrated. Imagine large amounts of folic acid enhancing the B12 deficiency in the nervous system by blocking the small amounts of vitamin B12 with single-carbon compounds. This could correlate to another finding in the Chicago study: Memory declined by 25% less in the ones with the largest consumption of vitamin B12.

The leader of the study, Martha Clare Morris, believes that folic acid might mask the very common vitamin B12 deficiency in the elderly. This is more or less the same thing. In both cases, the consequence should be that the elderly get more vitamin B12 and not less folic acid which can have a protective effect in other areas.

This is the message – that is if you do not choose to believe that the new finding is a coincidence and that the truth is the exact opposite – which is actually also quite likely!

For the time being, however, Morris’ conclusion is simple: “We don’t know yet what is going on,” she says.

Up to every third elderly person may have demonstrable signs of mild vitamin B12 deficiency. If the results of the Chicago study are truthful, elderly persons possibly should not reduce their folic acid intake but rather focus on getting enough vitamin B12.

By: Vitality Council

References:
1. Morris MC et al. Dietary folate and vitamin B12 and cognitive decline among community-dwelling older persons. Arch Neurol 2005;62:641-5
2. Austin RC et al. Role of hyperhomocysteinemia in endothelial dysfunction and atherthrombotic disease. Cell Death and Differentiation 2004;11:S56-S64
3. Morris MS. Homocysteine and Alzheimers disease. Lancet Neurol 2003;2:425-8
4. Kado DM et al. Homocysteine versus the vitamins folate, B6, and B12 as predictors of cognitive function and decline in older high-functioning adults: Mac Arthur Studies of Successfull Aging. Am J Med 2005;118:161-7
5. Garcia A et al. Homocysteine and cognitive function in elderly people. CMAJ, Oct. 12, 2004; 171 (8).

archneur.ama-assn.org
www.nature.com/cdd/index.html
www.thelancet.com
www.sciencedirect.com
www.cmaj.ca
www.iom.dk

Vitamin E or false product description

Claus Hancke

November 12, 2004

Calculations on the basis of old studies leads to claim of increased mortality by antioxidants and vitamin E, but is in reality based on studies with beta-carotene.

Recently, researchers published a study on beta-carotene, but called it antioxidants. Now there is a new study of beta carotene, but this time it is called vitamin E. Both studies are so-called meta-analyzes, ie. calculations of previous research.

The two studies claim to show that respectively antioxidants and vitamin E increase mortality, but they are both based on the results of old beta-carotene tests. Since 1994, it has been known that beta-carotene can cause cancer and increase mortality in at least male smokers.

The latest meta-analysis originates from Johns Hopkins University in the USA. Here, the mortality rate in a total of 19 old treatment trials with vitamin E was investigated. Apparently, doses above 400 units per day slightly increased mortality, although it was decreased in the trial where the dose was the highest (2,000 units/day). There were 11 trials where more than 400 units were used per day. At a lower dose, there was a tendency for decreased mortality.

However, of the 11 trials, the so-called Heart Protection Study (HPS) from the year 2000 is by far the largest. In fact, so large that it completely dominates the calculation. In HPS, almost twice as many died as in all the other 10 trials combined – and more than four times as many as in the other trials with increased mortality. The problem with this is that in HPS, in addition to vitamin E, the treatment consisted of vitamin C and beta-carotene!

Of course, one cannot comment on the risk of vitamin E based on an experiment in which both vitamin E and C and beta-carotene were used. You can only comment on vitamin E and C and beta-carotene!

Also, in the trial in question (HPS), synthetic vitamin E was used. It consists of eight different chemical compounds, only one of which is found in nature. That makes it even more difficult to comment on vitamin E, which most people buy in its natural form.

There are many other objections to the new meta-analysis. If you e.g. arrange the numbers just a little differently, but still fairly, the excess mortality disappears entirely. That happens if you ignore the misleading HPS study and include trials using over 300 units instead of just over 400. That would be entirely plausible.

This and much else may be why several independent statisticians told the New York Times that they did not believe the conclusion.

One can debate whether there is a real need for these sometimes arbitrary concoctions of old experiments, which easily lead to misinterpretations. Far greater is the need for large-scale investigations into whether, for example, a combination of natural vitamin E and C prevents atherosclerosis in people who are not overwhelmingly atherosclerosis already. This is where one can expect an effect, but these experiments have not been carried out.

Sales of vitamin E are increasing in the United States, where many doctors in particular take it. The combination of vitamin E and C can be seen i.a. as a competitor to the tremendous expensive, but almost ineffective, prescription drugs for Alzheimer’s. According to a report earlier this year – also from Johns Hopkins – users of both of these vitamins have approx. 80% reduced risk of getting Alzheimer’s – compared to those who get only one of them or none at all.

Most recently, the Nobel laureate Louis Ignarro, based on his own experiments, strongly recommended the same combination as prevention against atherosclerosis.

By: Vitality Council

 

References:
1) Metaanalysis: High-dosage vitamin E supplementation may increase all-cause mortality. Ann Int Med 2004;142.
2) Bjelakowic G, Nikolova D, Simonetti R G, Gluud C. Antioxidant supplements for prevention of gastrointestinal cancers: a systematic review and meta-analysis. The Lancet 2004;364:1219-28.
3) Ignarro L J et al. “Long Term Beneficial Effects of Physical Training and Metabolic Treatment on Atherosclerosis in Hypercholesterolemic Mice. PNAS 2004 (May 24).
4) Zandi PP et al. Reduced risk of Alzheimer disaease in users of antioxidant vitamin supplements. Arch Neurol 2004;61:82-88.
5) Gina Kolata: Large Doses of Vitamin E May Be Harmful. New York Times 11.11.04.

Fish Oil for the Heart

Claus Hancke

March 7, 2003

Essential oils in fish oil can prevent heart disease in elderly people. Quite many consumers and doctors have good experiences with this, but now it has also been confirmed by a study, recently published in the American Journal of Clinical Nutrition.

The trial included 360 persons at the age of 65, and the researchers found that a high concentration of the fatty acids DHA and EPA is associated with a lower risk of dying of blood clots in the heart.

– “Again, this is a good example of a preventive measure with natural substances such as fish oil, pays off” says Claus Hancke, chairman of the Vitality Council.

–  Fish oil reduces the risk of both blood clots and atherosclerosis, so there is common sense in taking fish oil, especially if you do not eat as much fish.

– Research results of this type unfortunately receive far too little attention in Denmark, on the contrary, we have often been told that dietary supplements are not useful at all. As a consumer, therefore, it can be difficult to know what to believe.

– Therefore, I believe that a sober-minded information about dietary supplements such as fish oil should be one of the obvious tasks for a future Council for Exercise and Nutrition, says Hancke, who is a specialist in general medicine and General Manager of the Department of Orthomolecular Medicine in Lyngby.

Science today knows very little about the link between heart disease in the elderly and the body’s content of these fatty acids, and therefore studies like this are welcomed by the doctors who work with orthomolecular medicine on a daily basis, popularly speaking: Biological medicine.

By Vitality Council

Reference:
American Journal of Clinical Nutrition, Vol. 77, No. 2, 319-325, February 2003.

www.ajcn.org
www.iom.dk