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CoQ10 and Selenium Supplementation Shown to Reduce Cardiovascular Disease Deaths by 50% in Older Subjects

James Meschino DC, MS, ROHP

The September 2013 edition of the International Journal of Cardiology in September included a remarkable cardiovascular study that followed 443 Swedish Citizens for over 5 years, with re-evaluation of all subjects every 6 months during the study period. The study subjects were 70-88 years of age at the beginning of the study. The study was a 5-year randomized double-blind placebo-controlled clinical trial, whereby half the subjects were given 200 mg of coenzyme 200 mg and 200 mcg selenium as supplements throughout the trial.  The other half of the subjects were given a placebo.

The study showed that after 5 years, the group given the CoQ10 and selenium had 50% fewer deaths from cardiovascular disease.  The group receiving the CoQ10 and selenium supplements also showed lower levels of a marker for congestive heart failure (NT-proBNP) and showed better heart function according electrocardiograph (ECG) evidence.  At the end of the 5-yr period 12.6% of the placebo group had died of cardiovascular disease, while only 5.9 percent of those taking the supplements had died. That’s greater than a 50% reduction in cardiovascular disease deaths in those following the supplement routine. The researchers concluded, “long-term supplementation of selenium/CoQ10 reduces cardiovascular mortality. The positive effects could also be seen in NT-proBNP levels and on electrocardiography”.

So, how might CoQ10 and selenium Cut the Risk of Cardiovascular Disease? We have known for a long time that the body makes less CoQ10 as we age. CoQ10 is required to convert food into energy in our cells, including heart muscle cells. Thus, lower CoQ10 levels in the heart muscle result in a weakened heart pump due to an energy power shortage. Putting CoQ10 back into the body as you age helps to maintain more optimal CoQ10 levels in the heart muscle, enabling the heart muscle to generate adequate energy for its pumping action, and preventing a weakening of the heart muscle. The net result is a reduced risk of heart failure. That appears to be the primary mechanism.

Selenium plays a key role in preventing free radical damage to the heart muscle. Previous studies have shown that low selenium levels increase risk of a type of heart failure known as Keshan Disease, which is reversed and prevented by optimizing selenium nutritional status.

My feeling has been to start taking low doses of CoQ10 by age 45 – about 30 mg per day, as a means to support heart muscle performance. By age 60 you may want to up the dosage to 60-90 mg per day. The study in the International Journal of Cardiology provided 200 mg per day of CoQ10 to 70-88 year olds. I’m not sure that doses that high are required for prevention, especially keeping in mind that CoQ10 is quite expensive. However, it’s important to know that cholesterol-lowering statin drugs (like Lipitor) decrease Co10 synthesis in the body and thus, at least 90 mg of CoQ10 should be taken by those using these cholesterol-lowering medications to compensate for the CoQ10 depletion imposed by these drugs.

As for selenium, many multiple vitamins contain 100-200 mcg of selenium, and I think its best to ingest selenium along with other vitamins and minerals in this form as opposed to a stand alone selenium supplement. Selenium works synergistically with other nutrients and that is why I would suggest taking it as part of high-potency multiple vitamin.

This 5-year study is very eye-opening and continues to support the view that in addition to a prudent diet, exercise, not smoking, stress management, and other lifestyle factors, that targeted supplements, such as CoQ10 and selenium, may also play a role in the prevention of cardiovascular disease.


Alehagan U, Johansson P, et al. Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: A 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. Int J Cardiology, 2013, 167(5):1860-1866



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