Tag: heart disease

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 E May Be Diabetic’s Saviour

Claus Hancke

December 20, 2005

About one out of every two diabetics has a five times larger than average risk of dying from heart disease. This risk can be cut in half by vitamin E. This is a well justified theory which is now being tested in a large Israeli study.

It is well known that the heart’s of diabetics become easily atherosclerotic, often causing them to die due to blood clots in the heart. Therefore, health officials work hard to combat atherosclerosis in diabetics. For example, diabetics are encouraged to take cholesterol reducing medicine, even when their cholesterol levels are very low. Diabetics’ blood pressure should also be low.

If one believes the Israeli researcher, Andrew Levy, the lives of even more diabetics can be saved by taking 400 units of vitamin E daily. Levy’s theory is now being tested in Israel in a large randomised study with 5,000 middle aged diabetics. Half of them will receive vitamin E for the next four years while the other half will not. If it goes as is hoped, the result will have enormous significance for public health.

It is optimistic to implement such an expensive study with vitamin E. As every (Danish, ed.) TV watcher knows, vitamin E doesn’t work against anything. Why would Levy and his co-workers from the Israeli Technion Technical Institute, where many Nobel prise winners can be found, go against the flow?

The explanation involves an antioxidant which few non-experts know of. It is called haptoglobin and is a protein which is created in the body. Haptoglobin binds the blood’s colouring agent, the iron rich haemoglobin, if it becomes detached from the red blood cells. In this way it prevents iron poisoning and therefore against overloading of free radicals in a long list of conditions where red blood cells die.

Disregarded effects of vitamin E
Levy and his co-workers have shown time and time again that haptoglobin works as an antioxidant. There is more to the story; haptoglobin is found in two forms, which are not equally effective antioxidants. Type 1 haptoglobin works much better than type 2. If one has type 2 haptoglobin (like 40% of the Israeli diabetics) the risk of death due to heart disease is five times higher than normal! In other words, a very large part of diabetics’ high death rate due to heart disease is because one out of every two of them has an insufficiency defence against oxidation because of ineffective haptoglobin.

The logical consequence of this enormous difference is, according to Levy, that the poorly protected diabetics with type 2 haptoglobin should take supplementary antioxidants. This is where the vitamin E study comes in. Vitamin E should be able to help. On the other hand, if it does help, why have other studies with vitamin E not previously shown this effect?

Levy believes that this is presumably because they have not been analysed with this effect in mind. He studied serum from a large sample of the ca. 10,000 participants in the Canadian HOPE study, where atherosclerotic participants received 400 units of vitamin E daily. The people behind the HOPE study found no effect of the vitamin E. But what about the 1,000 diabetics in the study? About a year ago, Levy proved that vitamin E reduced the risk of heart disease by 50% in the diabetic participants who had type 2 haptoglobin.
This surprising result was hidden in the HOPE study and was apparently unknown. This is quite educational. If the most threatened diabetics’ very high risk of heart disease can be halved with a cheap, harmless, vitamin E pill, the signification is very large.

Until 2010 we only have these results. There are no other results to turn to. It is not even possible to find out which kind of haptoglobin you have. If you wish to prevent heart disease, you have to do it in the dark. It is however risk free.

By: Vitality Council

References:
1. Andrew P. Levy et al. The Effect of Vitamin E Supplementation on Cardiovascular Risk in Diabetic Individuals With Different Haptoglobin Phenotypes. Diabetes Care 27:2767, 2004.
2. Levy AP et al. Strong Heart Study. Haptoglobin phenotype is an independent risk factor for cardiovascular disease in individuals with diabetes: The Strong Heart Study. J Am Coll Cardiol. 2002 Dec 4;40(11):1984-90.
3. Suleiman M, et al. Haptoglobin polymorphism predicts 30-day mortality and heart failure in patients with diabetes and acute myocardial infarction. Diabetes. 2005 Sep;54(9):2802-6.
4. A survey of the study can be found at Clinical Trials.gov: www.clinicaltrials.gov/ct/gui/show/NCT00220831.

care.diabetesjournals.org
www.cardiosource.com/jacc/index.asp
www.clinicaltrials.gov/ct/gui/show/NCT00220831
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

Decisive Agreement About Fish Oil Has Now Been Reached

Claus Hancke

January 10, 2005

For the first time, there is agreement about chronic lack of fish oil increasing the risk of coronary heart disease. An official American report sets a recommended intake for all adults.

It looks like there is now decisive agreement among experts that there is a connection between coronary heart disease and a chronic lack of the fatty acids in fish oil. This is the conclusion of a report published in Current Atherosclerosis Reports which was prepared at the request of the federal health authorities of the USA.

According to the report, the indications for a connection between a lack of fatty acids and death caused by coronary heart disease have become stronger year by year. It is the two N-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) that are significant. According to the report, DHA and EPA have “clear heart-protective effects.”

It also states that both national American and international experts now recommend larger intakes of N-3 fatty acids. The recommended daily intake is 450 mg. a day (EPA + DHA), but for persons with recognized coronary heart disease, the recommendation is 1000 mg. a day. This equals 1.5 g. of ordinary fish oil for healthy persons and 3 g. in case of heart disease, respectively; this is half the contents of a concentrated fish oil capsule.

The report underlines that according to both cellular- and animal tests, the N-3 fatty acids are capable of preventing irregular heartbeat and that this has now also been confirmed in tests on humans; this fact is also mentioned elsewhere on this site. In particular, the fatty acids can counteract the extremely common and often uncomfortable atrial fibrillation. All in all, the risk of death as a result of coronary heart disease is reduced by 25% when taking sufficient amounts of fish oil, as mentioned.

The strength of this evidence is now so comprehensive that the report encourages measuring people’s blood content of fatty acids just as measuring the blood pressure, checking the cholesterol, etc. is being done at present to estimate the risk of coronary heart disease. Likewise, it is now appreciated that it must become a national priority to see to it that everyone gets a sufficient intake of fish oil.

By: Vitality Council

Reference:
Harris WS. Are omega-3 fatty acids the most important nutritional modulators of coronary heart disease risk? Curr atheroscler Rep. 2004;6:447-52.

lansbury.bwh.harvard.edu/docosahexaenoic_acid_reviews_L.htm