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 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.