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Simvastatin

Also indexed as: Zocor®

Simvastatin is a member of the HMG-CoA reductase inhibitor family of drugs that blocks the body’s production of cholesterol. Simvastatin is used to lower elevated cholesterol and to reduce the risk of heart attack and death.

Interactions with Dietary Supplements

Coenzyme Q10
In patients with high cholesterol, simvastatin therapy results in decreased serum coenzyme Q10 (CoQ10) levels.1 2 Several trials, including double-blind trials, have confirmed this effect of simvastatin and other HMG-CoA reductase inhibitors, such as lovastatin and pravastatin.3 4 5 Supplementation with 100 mg6 per day or 10 mg three times daily7 of CoQ10 has been shown to prevent reductions in blood levels of CoQ10 due to simvastatin. In the latter study, people taking CoQ10 along with simvastatin increased their blood CoQ10 concentration by 63%. Many doctors recommend that people taking HMG-CoA reductase inhibitor drugs such as simvastatin also supplement with approximately 100 mg CoQ10 per day, although lower amounts, such as 10–30 mg per day might conceivably be effective in preventing the decline in CoQ10 levels.

The omega-3 fatty acid EPA, present in fish oil, may improve the cholesterol and triglyceride-lowering effect of simvastatin. In a preliminary trial, people with high cholesterol who had been taking simvastatin for about three years were able to significantly lower their triglyceride levels and raise their levels of HDL (“good”) cholesterol by supplementing with either 900 mg or 1800 mg of EPA for three months in addition to simvastatin.8 The authors of the study concluded that the combination of simvastatin and EPA may prevent coronary heart disease better than simvastatin alone.

Niacin
Niacin is the form of vitamin B3 used to lower cholesterol. High-dose niacin taken with lovastatin (a drug closely related to simvastatin) or with simvastatin itself may cause muscle disorders (myopathy) that can become serious (rhabdomyolysis).9 10 Such problems appear to be uncommon.11 12 Moreover, niacin has been successfully combined with statin drugs to reduce cholesterol more effectively than using these drugs without niacin.13 14 People taking both simvastatin and niacin should be monitored for muscle disorders by the prescribing physician.

Vitamin A
A study of 37 people with high cholesterol treated with diet and HMG-CoA reductase inhibitors found blood vitamin A levels increased over two years of therapy.15 Until more is known, people taking HMG-CoA reductase inhibitors, including simvastatin, should have blood levels of vitamin A monitored if they intend to supplement vitamin A.

Vitamin E
In a study of seven patients with hypercholesterolemia, eight weeks of simvastatin plus vitamin E 300 IU improved markers of blood vessel elasticity more than simvastatin alone.16

Interactions with Foods and Other Compounds

Food
Simvastatin may be taken with or without food.17

Summary of Interactions for Simvastatin

Depletion or interference Coenzyme Q10
Adverse interaction Vitamin A*
Side effect reduction/prevention None known
Supportive interaction Fish oil (EPA)
Vitamin E*
Reduced drug absorption/bioavailability None known
Other (see text) Niacin

For the convenience of the reader, the information in the summary is categorized as follows: “Depletion or interference” indicates the drug may deplete or interfere with the absorption or function of the supplement or herb. “Adverse interaction” indicates that the supplement or herb used together with the drug may result in undesirable effects. “Side effect reduction/prevention” indicates the supplement or herb may reduce the likelihood and/or severity of a potential side effect caused by the drug. “Supportive interaction” indicates the supplement or herb may support or aid the function of the drug. “Reduced drug absorption/bioavailability” indicates that the supplement or herb may decrease the absorption and/or activity of the drug in the body. An asterisk (*) next to an item in the summary indicates that the interaction is supported only by weak, fragmentary, and/or contradictory scientific evidence.

References:

1. Laaksonen R, Jokelainen K, Sahi T, et al. Decreases in serum ubiquinone concentrations do not result in reduced levels in muscle tissue during short-term simvastatin treatment in humans. Clin Pharmacol Ther 1995;57:62–6.

2. Laaksonen R, Ojala JP, Tikkanen MJ, et al. Serum ubiquinone concentrations after short- and long-term treatment with HMG-CoA reductase inhibitors. Eur J Clin Pharmacol 1994;46:313–7.

3. Ghirlanda G, Oradei A, Manto A, et al. Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study. J Clin Pharmacol 1993;33:226–9.

4. Watts GF, Cummings MH, Umpleby M, et al. Simvastatin decreases the hepatic secretion of very-low-density lipoprotein apolipoprotein B-100 in heterozygous familial hypercholesterolaemia: pathophysiological and therapeutic implications. Eur J Clin Invest 1995;25:559–67.

5. Folkers K, Langsjoen P, Willis R, et al. Lovastatin decreases coenzyme Q levels in humans. Proc Natl Acad Sci USA 1990;87:8931–4.

6. Bargossi AM, Grossi G, Fiorella PL, et al. Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors. Molec Aspects Med 1994;15(suppl):s187–93.

7. Miyake Y, Shouzu A, Nishikawa M, et al. Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. Arzneimittelforschung 1999;49:324–9.

8. Nakamura N, Hamazaki T, Ohta M, et al. Joint effects of HMG-CoA reductase inhibitors and eicosapentaenoic acids on serum lipid profile and plasma fatty acid concentrations in patients with hyperlipidemia. Int J Clin Lab Res 1999;29:22–5.

9. Garnett WR. Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors. Am J Health Syst Pharm 1995;52:1639–45.

10. Yee HS, Fong NT. Atorvastatin in the treatment of primary hypercholesterolemia and mixed dyslipidemias. Ann Parmacother 1998;32:1030–43.

11. Jacobson TA, Amorosa LF. Combination therapy with fluvastatin and niacin in hypercholesterolemia: a preliminary report on safety. Am J Cardiol 1994;73:25D–9D.

12. Jokubaitis LA. Fluvastatin in combination with other lipid-lowering agents. Br J Pract Suppl 1996;77A:28–32.

13. Davignon J, Roederer G, Montigny M, et al. Comparative efficacy and safety of pravastatin, Nicotinic acid and the two combined in patients with hypercholesterolemia. Am J Cardiol 1994;73:339–45.

14. Jacobson TA, Jokubaitis LA, Amorosa LF. Fluvastatin and niacin in hypercholesterolemia: a preliminary report on gender differences in efficacy. Am J Med 1994;96(suppl 6A):64S–8S.

15. Muggeo M, Zenti MG, Travia D, et al. Serum retinol levels throughout 2 years of cholesterol-lowering therapy. Metabolism 1995;44:398–403.

16. Neunteufl T, Kostner K, Katzenschlager R, et al. Additional benefit of vitamin E supplementation to simvastatin therapy on vasoreactivity of the brachial artery of hypercholesterolemic men. J Am Coll Cardiol 1998;32:711–6.

17. Threlkeld DS, ed. Diuretics and Cardiovasculars, Antihyperlipidemic Agents, HMG-CoA Reductase Inhibitors. In Facts and Comparisons Drug Information. St. Louis, MO: Facts and Comparisons, Sep 1998, 172.