Fluvastatin is a member of the HMG-CoA reductase inhibitor family of drugs that blocks the body’s production of cholesterol. Fluvastatin is used to lower high cholesterol and to slow or prevent hardening of the arteries.
In a randomized, double-blind trial, blood levels of coenzyme Q10 (CoQ10) were measured in 45 people with high cholesterol treated with lovastatin or pravastatin (drugs related to fluvastatin) for 18 weeks.1 A significant decline in blood levels of CoQ10 occurred with either drug. One study found that supplementation with 100 mg of CoQ10 prevented declines in CoQ10 when taken with simvastatin (another HMG-CoA reductase inhibitor drug).2 Many doctors recommend that people taking HMG-CoA reductase inhibitor drugs such as fluvastatin 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.
A synthetic molecule related to beta-sitosterol, sitostanol, is available in a special margarine and has been shown to lower cholesterol levels. In one study, supplementing with 1.8 grams of sitostanol per day for six weeks enhanced the cholesterol-lowering effect of various statin drugs.4
none
A supplement containing red yeast rice (Monascus purpureas) (Cholestin) has been shown to effectively lower cholesterol and triglycerides in people with moderately elevated levels of these blood lipids.5 This extract contains small amounts of naturally occurring HMG-CoA reductase inhibitors such as lovastatin and should not be used if you are currently taking a statin medication.
A study of 37 people with high cholesterol treated with diet and HMG-CoA reductase inhibitors found blood vitamin A levels increased during two years of therapy.6 Until more is known, people taking HMG-CoA reductase inhibitors, including fluvastatin, should have blood levels of vitamin A monitored if they intend to supplement vitamin A.
Niacin is the form of vitamin B3 used to lower cholesterol. Fluvastatin and niacin used together have been shown to be more effective than either substance alone.7 Ingestion of large amounts of niacin along with HMG-CoA reductase inhibitors such as fluvastatin may cause muscle disorders (myopathy) that can become serious (rhabdomyolysis).8 , 9 Such problems appear to be uncommon.10 , 11 Nonetheless, individuals taking fluvastatin should consult with their doctor before taking niacin.
1. 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):S137–44.
2. 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.
3. Glueck CJ, Budhani SB, Masineni SS, et al. Vitamin D deficiency, myositis-myalgia, and reversible statin intolerance. Curr Med Res Opin 2011;27:1683–90.
4. Goldberg AC, Ostlund RE Jr, Bateman JH, et al. Effect of plant stanol tablets on low-density lipoprotein cholesterol lowering in patients on statin drugs. Am J Cardiol2006;97:376–9.
5. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr 1999;69:231–6.
6. Muggeo M, Zenti MG, Travia D, et al. Serum retinol levels throughout 2 years of cholesterol-lowering therapy. Metabolism 1995;44:398–403.
7. Jacobson TA, Chin MM, Fromell GJ, et al. Fluvastatin with and without niacin for hypercholesterolemia. Am J Cardiol 1994;74:149–54.
8. Garnett WR. Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors. Am J Health Syst Pharm 1995;52:1639–45.
9. Yee HS, Fong NT. Atorvastatin in the treatment of primary hypercholesterolemia and mixed dyslipidemias. Ann Pharmacother 1998;32:1030–43.
10. Jacobson TA, Amorosa LF. Combination therapy with fluvastatin and niacin in hypercholesterolemia: a preliminary report on safety. Am J Cardiol 1994;73:25D–9D.
11. Jokubaitis LA. Fluvastatin in combination with other lipid-lowering agents. Br J Pract Suppl 1996;77A:28–32.
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