• Atorvastatin
  
• Cerivastatin
  
• Fluvastatin
  
• Lovastatin
  
• Pravastatin
  
• Simvastatin
  

Statins lower levels of coenzyme Q10 by inhibiting HMG-CoA reductase, the rate-limiting enzyme in the synthesis of mevalonate, a precursor of CoQ10 (ubiquinone), and cholesterol, a carrier for CoQ10 (Bargossi et al. 1994; Belichard et al. 1993; Bliznakov and Wilkins 1998; De Pinieux et al. 1996; Folkers et al. 1990; Ghirlanda et al. 1993; Laaksonen et al. 1994; Mortensen et al. 1997). Specifically, lovastatin, pravastatin, and simvastatin significantly deplete plasma and platelet levels of CoQ10 (Hanaki et al. 1993; Kaikkonen et al. 1999). Simvastatin may cause a dose-dependent decrease in CoQ10 levels that is greater than the reduction in cholesterol (Watts et al. 1993). Although it has not been reported, atorvastatin, cerivastatin, and fluvastatin could theoretically have similar effects on CoQ10 levels.

Although CoQ10 is manufactured by the body, deficiencies occur in some physiological and pathological conditions (Artuch et al. 1999). CoQ10 deficiency may be related to certain conditions such as gingivitis (Nakamura et al. 1974); breast cancer (Jolliet et al. 1998); congestive heart failure (Munkholm et al. 1999); angina pectoris (Kamikawa et al. 1985); acute myocardial infarction (Singh et al. 1998); mitochondrial encephalomyopathies (Chan et al. 1998); hypertension, and cardiac function (Singh et al. 1999). In addition, CoQ10 depletion may contribute to aging and photoaging (Hoppe et al. 1999). Low levels of CoQ10 may also compromise immune function (Folkers et al. 1993) and play a role in male infertility (Overvad et al. 1999).

Daily doses of coenzyme Q10 as high as 200 mg for periods of 6 to 12 months or 100 mg for up to 6 years have not been associated with reports of serious adverse effects in clinical studies (Overvad et al. 1999). Concomitant administration of CoQ10 (100 mg) and simvastatin (20 mg) to hypercholesterolemic patients for 6 months prevented reductions in both plasma and platelet CoQ10 levels without affecting the cholesterol-lowering effect of the drug (Bargossi et al. 1994). Similarly, CoQ10 supplementation can reverse the CoQ10-lowering effect of lovastatin (Loop et al. 1994). In one study, supplementation with CoQ10 during lovastatin treatment restored depleted LDL CoQ10 levels, but did not improve LDL antioxidative capacity (Palomaki et al. 1998). 

This information is intended to serve as a concise reference for healthcare professionals to identify substances that may be depleted by many commonly prescribed medications. Depletion of these substances depends upon a number of factors including medical history, lifestyle, dietary habits, and duration of treatment with a particular medication. The signs and symptoms associated with deficiency may be nonspecific and could be indicative of clinical conditions other than deficiency. The material presented in these monographs should not in any event be construed as specific instructions for individual patients.

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Kamikawa T, Kobayashi A, Yamashita T, et al. Effects of coenzyme Q10 on exercise tolerance in chronic stable angina pectoris. Am J Cardiol. 1985;56(4):247-251.

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Mortensen SA, Leth A, Agner E, Rohde M. Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors. Mol Aspects Med. 1997; 18(Suppl);S137-S144.

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Nakamura R, Littarru GP, Folkers K, Wilkinson EG. Study of CoQ10-enzymes in gingiva from patients with periodontal disease and evidence for a deficiency of coenzyme Q10. Proc Natl Acad Sci USA. 1974;71(4):1456-1460.

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Singh RB, Niaz MA, Rastogi SS, et al. Effect of hydrosoluble coenzyme Q10 on blood pressure and insulin resistance in hypertensive patients with coronary heart disease. J Hum Hypertens. 1999;13(3):203-208.

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