Coenzyme Q10, or CoQ10, is found in the mitochondria of all cells and is particularly enriched in tissues of the heart, liver, kidney and pancreas. CoQ10 functions as part of the cellular system that generates energy from oxygen (in the form of ATP) for bodily processes. CoQ10 can also act as an antioxidant to help prevent cellular damage from free radicals created during exercise and during the generation of energy.
Dietary supplements containing CoQ10 (often suspended in soybean oil or other oil base for better absorption) are generally marketed with claims of increasing energy and endurance levels, supporting heart function, reducing blood pressure, and improving overall heart strength.
Because coenzyme Q10 is part of the respiratory chain as an electron/proton carrier, it functions in the production of adenosine triphosphate (ATP) in the mitochondria of the cell. CoQ10 has also been shown to exhibit activity as a free radical scavenger and antioxidant. The theory of CoQ10 supplementation posits that consumption of CoQ10 increases tissue and mitochondrial CoQ10 levels and supports ATP production as well as serving an antioxidant function.
For athletes, the data do not consistently support the use of supplemental CoQ10 as an ergogenic performance aid. As a general “energetic” dietary supplement, as in the case of reducing fatigue and alleviating symptoms of Chronic Fatigue Syndrome, the effectiveness of CoQ10 supplementation is largely unsupported. As an antioxidant, especially in combination with other antioxidants such as vitamins C and E, CoQ10 appears to be beneficial. For heart patients, CoQ10 appears to be especially indicated, particularly in those patients who may be taking cholesterol-lowering medications (HMG-CoA reductase inhibitors in the class of “statin” medications that includes lovastatin (Mevacor) simvastatin (Zocor), pravastatin (Pravachol), and fluvastatin (Lescol)).
Since CoQ10 levels peak around age 20 and decline with age, it seems logical that supplemental CoQ10 might be beneficial in older adults. The antioxidant effects of CoQ10 are well-established. A number of studies have shown that CoQ10 reduces the initiation and propagation of lipid peroxidation (free radical damage) in cell membranes and in lipoprotein fractions (Taggart et al. 1996). Additionally, combined supplementation of CoQ10 plus vitamin E produces a synergistic antioxidant effect on lipoproteins and "spares" the vitamin E (Kucharska et al. 1996).
In heart disease, CoQ10 has shown benefits in patients with heart failure – with 50mg daily for 4 weeks resulting in improvements in dyspnea, heart rate, blood pressure, and ankle edema (Hoffman-Bang et al. 1995). In most studies of heart failure, a significant reduction in hospitalizations and episodes of pulmonary edema and cardiac asthma are generally observed (Khatta et al. 2000). Cardiac patients supplemented with CoQ10 prior to heart surgery tend to recover sooner and maintain blood and tissue levels of CoQ10 better than patients not receiving supplements. In a one study, 144 patients suffering from acute MI benefited from 28 days of CoQ10 at 120mg/day when compared to placebo by decreasing incidence of angina, arrhythmias, and poor left ventricular function (Soja et al. 1997). A handful of studies have suggested reductions in systolic and diastolic blood pressure of 7-10mmHg after 8-10 weeks of CoQ10 supplementation (Sacher et al. 1998, Singh et al. 1998). In addition, individuals taking cholesterol-lowering medications (HMG-CoA reductase inhibitors – also known as “statin” drugs) may benefit from CoQ10 supplements because these medications can reduce blood levels of CoQ10 (Langosjoen and Langosjoen 1999). In several studies, CoQ10 levels have been shown to be significantly reduced with simvastatin and related statin medications, resulting in an accompanying reduction in ejection fraction response to exercise, myocardial reserve, and myocardial contractile function (Langosjoen and Langosjoen 1999, Knontush et al. 1997). CoQ10 was approved in 1974 in Japan for the treatment of congestive heart failure and at least one formulation (UbiQGel), has received FDA Orphan Drug Status for treating mitochondrial disorders (Greenberg and Frishman 1990).
The one area in which data is most conflicting is for CoQ10 as an ergogenic aid for athletic performance. Because of its role in ATP synthesis, it is logical that supplemental CoQ10 may support the process of cellular energy production. Research in this area has been conflicting, however, with some studies showing a benefit and others showing no effect (Weston et al. 1997).
CoQ10 has a good safety profile and daily doses of 50-100mg are well tolerated. Reported side effects are rare, but tend to be various forms of epigastric distress (heartburn, nausea, stomachache) which can be prevented by consuming the supplement with a meal. Intakes of 100-200mg per day have been studied with no apparent adverse side effects, but muscle damage has been noted in at least one study (Kucharska et al. 1998) of 120mg per day over 20 days (perhaps due to a pro-oxidant effect and free radical damage in the muscle).
Smoking is known to deplete CoQ10 levels in blood and tissues. Several medications can reduce blood and tissue levels of CoQ10, including those for controlling cholesterol (statins, including a theoretical reduction in CoQ10 levels with use of red yeast rice supplements, which contain natural lovastatin), blood pressure (beta-blockers, by inhibiting CoQ10-dependent enzymes), and blood sugar (some oral hypoglycemic agents), suggesting that CoQ10 supplements may be warranted in patients taking these medications. HMG-CoA reductase inhibitors can reduce CoQ10 concentrations by approximately 32 to 47% by blocking the synthesis of mevalonic acid, a precursor of coenzyme Q-10.
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EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.