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Chapter: Basic & Clinical Pharmacology : Dietary Supplements & Herbal Medications

Coenzyme Q10

Coenzyme Q10, also known as CoQ, CoQ10, and ubiquinone, is found in the mitochondria of many organs, including the heart, kidney, liver, and skeletal muscle.




Coenzyme Q10, also known as CoQ, CoQ10, and ubiquinone, is found in the mitochondria of many organs, including the heart, kidney, liver, and skeletal muscle. After ingestion, the reduced form of coenzyme Q10, ubiquinol, predominates in the systemic circulation. Coenzyme Q10 is a potent antioxidant and may have a role in maintaining healthy muscle function, although the clini-cal significance of this effect is unknown. Reduced serum levels have been reported in Parkinson’s disease.

Clinical Uses


A. Hypertension


In early clinical trials, small but significant reductions in systolic and diastolic blood pressure were reported after 8–10 weeks of coenzyme Q10 supplementation. The exact mechanism is unknown but, if correct, might be related to the antioxidant and vasodilating properties of coenzyme Q10. In three well-designed randomized, placebo-controlled trials, coenzyme Q10 was reported to significantly lower systolic blood pressure and dia-stolic blood pressure by 11 mm Hg and 7 mm Hg, respectively, as compared with no change in the placebo groups. Whether coenzyme Q10 can be used to lower blood pressure remains unclear. Since all three clinical trials have shown a benefit, it is possible that publication bias may be present. Furthermore, an exaggerated treatment effect may occur as adequate randomiza-tion, blinding, and concealment of allocation have been ques-tioned for these studies.

B. Heart Failure


Low endogenous coenzyme Q10 levels have been associated with worse heart failure outcomes, but this association is likely because low levels are a marker for more advanced heart failure, rather than a predictor of disease. Despite these findings, coenzyme Q10 is often advocated to improve heart muscle function in patients with heart failure. According to the most recent meta-analysis, coenzyme Q10 was shown to improve ejection fraction by 3.7% with a more significant effect being observed in patients not receiving angiotensin-converting enzyme inhibitors. It is unclear whether the improvements in ejection fraction are appli-cable to all patients with heart failure, as more research is required to assess the role of coenzyme Q10 in heart failure and its impact on disease severity.

C. Ischemic Heart Disease


The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theo-retical basis for such benefit could be metabolic protection of the ischemic myocardium. Double-blind, placebo-controlled trials have demonstrated that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein a, high-density lipoprotein cholesterol, exercise toler-ance, and time to development of ischemic changes on the electro-cardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%).


D. Prevention of Statin-Induced Myopathy


Statins reduce cholesterol by inhibiting the HMG-CoA reductase enzyme . This enzyme is also required for synthe-sis of coenzyme Q10. Initiating statin therapy has been shown to reduce endogenous coenzyme Q10 levels, which may block steps in muscle cell energy generation, possibly leading to statin-related myopathy. It is unknown whether a reduction in intramuscular coenzyme Q10 levels leads to statin myopathy or if the myopathy causes cellular damage that reduces intramuscular coenzyme Q10 levels. In one of the largest studies, when rosuvastatin was used in patients with heart failure, there was no association between statin-induced low coenzyme Q10 levels and a worse heart failure outcome. Furthermore, the study found no observable difference in the incidence of statin-induced myopathy regardless of endog-enous coenzyme Q10 levels. More information is needed to deter-mine which patients with statin-related myopathy might benefit most from coenzyme Q10 especially as it relates to the specific statin, the dose, and the duration of therapy.


Adverse Effects


Coenzyme Q10 is well tolerated, rarely leading to any adverse effects at doses as high as 3000 mg/d. In clinical trials, gastrointes-tinal upset, including diarrhea, nausea, heartburn, and anorexia, has been reported with an incidence of less than 1%. Cases ofmaculopapular rash and thrombocytopenia have very rarely been observed. Other rare adverse effects include irritability, dizziness, and headache.


Drug Interactions


Coenzyme Q10 shares a structural similarity with vitamin K, and an interaction has been observed between coenzyme Q10 and warfarin. Coenzyme Q10 supplements may decrease the effects of warfarin therapy. This combination should be avoided or very carefully monitored.




As a dietary supplement, 30 mg of coenzyme Q10 is adequate to replace low endogenous levels. For cardiac effects, typical dosages are 100–600 mg/d given in two or three divided doses. These doses increase endogenous levels to 2–3 mcg/mL (normal for healthy adults, 0.7–1 mcg/mL).


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