Coenzyme Q10 supplements have been purported to be effective for treating a variety of disorders,1,2 in particular hypertension and statin-induced myalgia.
Several studies3–7 found that coenzyme Q10 supplementation significantly lowered blood pressure in hypertensive patients. Moreover, some trials have demonstrated that statin therapy reduces serum or muscle levels of coenzyme Q10,8–14 prompting investigations to determine whether coenzyme Q10 deficiency is related to statin-induced muscle pain.15–17
In this review, we discuss the efficacy and safety of coenzyme Q10 supplementation in patients with hypertension and those taking statins, and some of the caveats about using supplements that are not approved by the US Food and Drug Administration (FDA), as well as the bioavailability and quality of available formulations.
WHAT IS COENZYME Q10?
Coenzyme Q10, also known as coenzyme Q, ubidecarenone, and ubiquinone, is found in all human cells, with the highest concentrations in the heart, liver, kidney, and pancreas.1,2 It is a potent antioxidant, a membrane stabilizer, and an integral cofactor in the mitochondrial respiratory chain, helping to generate adenosine triphosphate, the major cellular energy source.1,2,18 It may also regulate genes associated with cell metabolism.19
RATIONALE FOR SUPPLEMENTATION
Coenzyme Q10 supplementation has been used, recommended, or studied in heart failure, hypertension, parkinsonism, mitochondrial encephalomyopathies, and other ailments.
Depending on the class, various antihypertensive drugs can have adverse effects such as depression, cough, and cardiac and renal dysfunction. 20,21 Furthermore, many patients need to take more than one drug to control their blood pressure, increasing their risk of side effects. Some researchers believe coenzyme Q10 supplementation may reduce the need to take multiple antihypertensive drugs.5
Coenzyme Q10 appears to lower blood pressure. The exact mechanism is not known, but one theory is that it reduces peripheral resistance by preserving nitric oxide.21 Nitric oxide relaxes peripheral arteries, lowering blood pressure. In some forms of hypertension, superoxide radicals that inactivate nitric oxide are overproduced; coenzyme Q10, with its antioxidant effects, may prevent the inactivation of nitric oxide by these free radicals. Alternatively, coenzyme Q10 may boost the production of the prostaglandin prostacyclin (PGI2) a potent vasodilator and inhibitor of platelet aggregation, or it may enhance the sensitivity of arterial smooth muscle to PGI2, or both.1,22
In patients taking statins
Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), first-line agents for lowering cholesterol levels to prevent cardiovascular disease, are some of the most commonly prescribed medications.23,24 However, statin therapy carries a risk of myopathy, which can range from muscle aches to rhabdomyolysis. 23,24
In a clinical advisory,25 the American College of Cardiology, the American Heart Association, and the National Heart, Lung, and Blood Institute recommend that patients on statin therapy who experience muscle soreness, tenderness, or pain with serum creatine kinase levels 3 to 10 times the upper limit of normal should have their creatine kinase level checked weekly. If the level is 3 to 10 times the upper limit of normal, statin therapy may be continued, but if it exceeds 10 times the upper limit, then statins and other potential offending agents (eg, niacin, fibrate) need to be discontinued.
Statins inhibit the synthesis of cholesterol by reducing the production of mevalonate, a precursor of both cholesterol and coenzyme Q10. Since both cholesterol and coenzyme Q10 are produced by the same pathway, it is not surprising that statins have been reported to reduce serum and muscle coenzyme Q10 levels.9–14 However, one study did not report a significant reduction of coenzyme Q10 levels in muscle tissue in patients treated with simvastatin 20 mg for 6 months.26
Nonetheless, researchers have hypothesized that a reduction in coenzyme Q10 levels in muscle tissue causes mitochondrial dysfunction, which could increase the risk of statininduced myopathy,13–17 and some believe that treatment with coenzyme Q10 may reduce myalgic symptoms and allow patients to remain on statin therapy.13,24
Researchers have investigated the potential of coenzyme Q10 supplementation to reduce or prevent statin-induced myopathy.15–17 (More on this below.)
Interestingly, a randomized, placebo-controlled trial27 found that 6 months of daily therapy with simvastatin (Zocor) 20 mg or pravastatin (Pravachol) 40 mg lowered systolic and diastolic blood pressure significantly in patients with no documented history of cardiovascular disease or diabetes. A possible mechanism of statin-induced blood pressure reduction is the up-regulation of endothelial nitric oxide synthetase, a potent vasodilator. Coenzyme Q10 levels were not assessed during this study. Whether coenzyme Q10 supplementation used to treat statin-induced myalgia enhances or inhibits the antihypertensive effects of statins is not yet known.