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The Many Potential Benefits of Coenzyme Q10Coenzyme Q10 belongs to a family of compounds known as ubiquinones, ubiquitous compounds in living organisms containing benzoquinone. The specific ubiquinone found in humans is coenzyme Q10. Coenzyme Q10 is highly soluble in lipids (fats) and is found in virtually all cell membranes and lipoproteins. The production of energy thorough conversion of carbohydrates and fats into adenosine triphosphate (ATP) requires the presence of coenzyme Q in the cellular mitochondria. Since coenzyme Q is fat-soluble, it is best absorbed in a meal with fats. In individuals with normal coenzyme Q levels, oral supplementation may not increase tissue concentrations. However, supplementation may increase coenzyme Q levels in specific tissues when they are deficient. A study of 24 older adults taking 300 mg/d of coenzyme Q10 or placebo prior to cardiac surgery found that atrial tissue levels of coenzyme Q10 were significantly increased in those taking coenzyme Q10. Coenzyme Q10 is an effective fat-soluble antioxidant that has been found to inhibit lipid peroxidation when cell membranes and low-density lipoproteins (LDL) are exposed to oxidizing conditions. Coenzyme Q may protect membrane proteins and DNA from oxidative damage that accompanies lipid peroxidation. In addition to neutralizing free radicals directly, Coenzyme Q is capable of regenerating the antioxidant activity of vitamin E. Aging Oxidative damage to cellular structures from free radicals may play an important role in aging. Free radicals are generated as a byproduct of ATP production and if not neutralized by antioxidants may, over time, damage the mitochondria, contributing to decline in aging. Since tissue levels of coenzyme Q10 decline with age, the age-related decline in tissue coenzyme Q10 levels may play an important role in the decline of aging. Atherosclerosis Coenzyme Q10 may inhibit the progression of cardiovascular diseases. Oxidation of low-density lipoproteins (LDL) in artery walls is thought to lead to the development of atherosclerosis. Coenzyme Q10 inhibits the oxidation of LDL in vitro and works together with vitamin E to inhibit LDL oxidation. Animal studies have found that coenzyme Q10 supplementation significantly inhibits the formation of atherosclerotic lesions. Congestive Heart Failure Impairment of the heart's ability to pump sufficient blood to meet the body's needs is known as congestive heart failure. The accumulation of atherosclerotic plaque in the coronary arteries may prevent parts of the heart muscle from receiving adequate circulation, resulting in impaired pumping ability. Myocardial Infarction also damages the heart muscle, resulting in heart failure. It has been found that myocardial tissue coenzyme Q10 levels are lower in patients with severe heart failure than in those with milder heart failure. A number of studies have shown improvement in cardiac function when congestive heart failure patients received 100-200 mg of coenzyme Q10 daily for 1-3 months. Angina Pectoris Myocardial ischemia may lead to chest pain known as angina pectoris. People with angina often experience symptoms when the demand for oxygen exceeds the capacity of their coronary circulation to deliver it. Five small, placebo-controlled studies have examined the effects of oral coenzyme Q10 supplementation (60-600 mg/d) as an adjunct to medical therapy in patients with chronic stable angina. In most of these studies, coenzyme Q10 supplementation improved exercise tolerance and reduced or delayed myocardial ischemia compared to placebo. Hypertension Coenzyme Q10 supplementation may result in moderate blood pressure reduction in hypertensive individuals. The addition of 120 mg/d of coenzyme Q10 to medical therapy for 8 weeks in patients with hypertension and coronary artery disease decreased systolic blood pressure by an average of 12 mm Hg and diastolic blood pressure by an average of 6 mm Hg compared to a placebo. Healthy function of the inner lining of blood vessels (the vascular endothelium) allows blood vessel dilation and plays an important role in reducing hypertension. Atherosclerosis impairs vascular endothelial function, compromising the ability of blood vessels to relax (vasodilate). Statin Therapy Coenzyme Q10 supplementation may replace diminished endogenous production during statin therapy. Statins are widely used cholesterol-lowering medications that may also decrease the endogenous synthesis of coenzyme Q10. Statin drugs inhibit HMG-CoA reductase, an enzyme that plays a critical role in the regulation of coenzyme Q10 synthesis, in addition to cholesterol synthesis. Studies have found decreased plasma or serum coenzyme Q10 in people on statin therapy. These statements have not been evaluated by the FDA.
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