Do Cholesterol-Lowering Drugs Cause Heart Failure? – Coenzyme Q10
25 Jan 2004
What is causing the epidemic of heart failure in North America? The usual answer is an aging population. Old hearts eventually get tired and stop beating. But at a meeting in London, England, several researchers suggested a surprising new reason for heart failure, cholesterol-lowering drugs (CLDs). Ironically, the very medication prescribed to prevent heart disease may in fact be causing it! And 12 million Japanese may have the answer to this dilemma, coenzyme Q10 (Co-Q10).
There’s no doubt that high blood cholesterol is a proven risk factor for heart disease. It’s also known that CLDs such as Lipitor, Zocor, Pravachol, Mevacor and others are effective in lowering cholesterol. But, as always, there’s a price to pay for medication.
CLDs work by inhibiting an enzyme required for the production of cholesterol. Unfortunately this enzyme is also needed in the manufacture of Co-Q10 an important nutrient for normal cardiac function.
Co-Q10 has been called the “sparkplug of our motors” and we know what happens when sparkplugs fail to function in automobiles.
Studies show that CLDs, used for one year, can decrease the body’s Co-Q10 by as much as 40 per cent. This is like draining the gas tank that fuels the car. In this case, sapping energy away from the heart and other muscles. Some researchers believe it’s this lack of Co-Q10 in the heart’s muscle that is responsible for the epidemic of heart failure.
Printed matter distributed to patients using CLDs outlines several potential side effects such as muscle weakness, soreness, and liver enzyme elevation. But there is no mention that these problems may be related to the decrease of Co-Q10. Or that a decrease in C0-Q10 could be detrimental to the heart and liver.
One CLD was taken off the market two years ago because it was linked to several deaths from rhabdomyolysis. This problem results from a breakdown of muscle tissue sometimes resulting in kidney failure and death. However, current drugs being used to lower cholesterol are also capable of causing this same effect.
The question is whether these deaths could have been prevented by the use of Co-Q10. And why so little has been said about the importance of Co-Q10
Currently 15 published articles show that CLDs lower C0-Q10 in humans and how this affects cardiac function. In addition, the higher the dose of CLD the greater the effect on C0-Q10.
Dr. Khursheed Jeejeebhoy, Professor of Nutrition, at the University of Toronto, reports that the heart muscles of patients suffering from heart failure show decreased levels of Co-Q10. And that Co-Q10 therapy improves cardiac performance.
Another report in the American Journal of Cardiology showed that a daily dose of 150 milligrams of C0-Q10 decreased the incidence of angina by 50 per cent. It’s believed that Co-Q10 allows the heart to work harder before oxygen lack causes angina.
Other research shows that as we age the body’s ability to extract C0-Q10 from food decreases. Not too surprising as all our organs work less efficiently with the passage of time.
In 1974 the Japanese government, due to all these findings, approved the use of C0-Q10 for the treatment of heart failure. Today over 12 million Japanese are taking this medication to both prevent and treat heart disease.
Several doctors at the meeting in London, England, questioned why pharmaceutical companies have been so silent about the importance of C0-Q10. Why have they failed to mention that CLDs decrease the heart’s supply of this nutrient? And why have they not recommended its use to counteract the effects of CLDs?
Dr. Julian Whitaker, a prominent US physician, claimed that patents have been assigned for a drug combination that includes a CLD and Co-Q10. And that Merck pharmaceutical company has owned this patent for years.
The question is why hasn’t Merck produced a combination drug. One reason may be they don’t want to increase public anxiety. And this year sales of CLDs will top 30 billion dollars. With such a massive amount of profit why rock the boat? Or am I just a skeptical medical journalist?
