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Co-Enzyme Q10 and Carnitine Deficiency

Co-Enzyme Q10 levels in blood and heart tissue (myocardial cells obtained from a catheter biopsy) were obtained from normal individuals and from patients with Class I (essentially asymptomatic) through Class IV (symptoms of heart failure at rest) cardiomyopathy. As you can see, as the severity of heart failure increases, heart muscle Co-Q levels fall. Blood Co-Q levels fall in tandem. This makes sense, as the heart is the greatest consumer of Co-Q in the body. The still viable cells of the failing heart run out of Co-Q, as they are overworking, trying to make enough ATP to generate a normal cardiac output. Without Co-Q, however, they are overworking in vain, as without Co-Q, ATP cannot be generated from the energy stored in sugar and fat, so heart function continues to deteriorate. Heart failure and Co-Q deficiency go hand in hand. Heart failure can cause Co-Q deficiency, and Co-Q deficiency can cause heart failure

When an individual with coronary insufficiency exercises, the heart muscle served by the blocked artery will experience oxygen deficiency. Energy production will be deranged, free radical stress will occur, the adenine nucleotide pool will deplete (more on this in the Ribose section), and Co-Q will be used up. Individuals with coronary insufficiency develop myocardial Co-Q deficiency, and as with the cardiomyopathy patients, their blood Co-Q levels will fall. One of Co-Q's jobs is to prevent oxidation of the LDL particle. LDL cholesterol is essentially harmless, while oxidized LDL is readily incorporated into arterial plaque. With less Co-Q, LDL oxidation is more likely to occur, and plaque deposition is more likely to progress. Free radical stress and Co-Q deficiency, as a consequence of coronary disease, lead to more coronary disease, which leads to more free radical stress and Co-Q deficiency, in a vicious cycle that we can block with supplementation.

These and other studies have shown that Co-Q deficiency is associated with heart disease, and that heart disease is associated with Co-Q deficiency. The chart to your left shows that the same principle holds with Carnitine; the worse the CHF, the lower the myocardial Carnitine level. Similar relationships have been shown for other nutrients involved in cardiac energy metabolism. Conversely, bioenergetic supplementation has been shown to increase blood and myocardial levels of Co-Q and Carnitine in the patient with CHF or coronary insufficiency. Energy metabolism is improved, and with this we see an improvement in cardiac performance (in the studies, average ejection fraction will rise or heart chamber size decreases), while symptoms will lessen (exercise capacity increases and NTG requirement falls).

James C. Roberts MD FACC
1/01/07