Hyperlipidemia and associated conditions such as renal damage, cardiovascular disease, and prevention of and recovery from myocardial infarction.
Mechanism of Action
Monascus purpureus acts act as a natural HMG-CoA reductase inhibitor.1,2,3 It regulates serum triglycerides, total cholesterol, and LDL-cholesterol (LDL-C) as well as the expression of inflammatory transcription factors. It up-regulates high-density lipoprotein-cholesterol. Animal studies have shown it to protect the vasculature by reducing the expression levels of the inflammatory transcription factors such as tumor necrosis factor-α and interleukin (IL)-6.4
Several studies have found M. purpureus to be moderately effective at improving lipid profiles, particularly for lowering LDL-C levels.5 In several random controlled trials to study its effects on lipid profiles in human subjects, M. purpureus was found to be superior to placebo. Over a dozen randomized, placebo-controlled trials containing 804 participants have been conducted to evaluate its effects on cholesterol, and all have reported it to be effective in lowering LDL-C.6 One study used 1200 or 2400 mg daily and found that both dosages were effective in lowering cholesterol in roughly 50% of those receiving the serum.7 Another large randomized controlled study from China found that
M. purpureus significantly reduced the risk of major adverse cardiovascular events and overall survival in patients after myocardial infarction.8
A short-term study compared 10 mg of isolated monacolins (an active constituent) to placebo for effects on C-reactive proteins in addition to lipids. After 4 weeks, monacolins were shown to improve lipids as well as lower C-reactive proteins.9 Animal models of hyperlipidemia have shown M. purpureus to repair renal damage associated with elevated lipids.4
Safety in Pregnancy and Breastfeeding
There are no published studies regarding the safety of M. purpureus in pregnancy and lactation.
Monascus purpureus lowers cholesterol without elevating creatine kinase, a finding associated with myopathy and a potential consequence of statin drugs owing to their interference with coenzyme Q10 (CoQ10) synthesis. Monascus purpureus is the natural source of statin drugs; lovastatin was derived from monacolin K. One study found no depletion of CoQ10 and the related ubiquinones in rat hearts 30 days of use10; however, other researchers have reported that it will deplete muscles of CoQ10 with long-term use.11 Animal studies have shown liver and heart levels of CoQ10 to decline dramatically with the use when it is dosed at roughly 5 times the human dose in a single dose. CoQ10 levels were shown to drop within 30 min and to remain reduced 24 h later. A lower dose of 1 g/kg body weight in mice causes less CoQ10 reduction, but it was found to suppress heart, liver, and cardiac CoQ10 production.12 In humans, it would be prudent to take CoQ10 when taking M. purpureus just as it is with HMG-CoA reductase inhibitor medications or statins. A systematic review and meta-analysis of 20 studies found
M. purpureus significantly lowered LDL-C at a rate similar to statin therapy; 1.02 mmol/L. Liver and kidney damage and muscle symptoms were 0%–5% or the same as in the placebo treatment arm.13
A study using 2400 mg of M. purpureus to evaluate its effects on cholesterol reported the medication to be safe and well tolerated, with minor GI irritation as the most commonly reported adverse event.14 No subject experienced myopathy or markedly elevated liver transaminases or creatine kinase, as may occur with statin drugs. A meta-analysis of 13 randomized, placebo-controlled trials involving 804 participants was analyzed and found that M. purpureus usage resulted in no serious side effect symptoms or abnormal blood serum results.6 The Italian Surveillance System of Natural Health Products from 2002 to 2015 found 52 reports of 55 adverse events from M. purpureus. Myalgia or elevated creatinine phosphokinase occurred in 19 people, rhabdomyolysis in one, liver injury in 10, gastrointestinal reaction in 12, cutaneous reactions in 9, and other reactions in 4, with 70% of the cases being women. Of these cases, 13 were hospitalized and 28 were on other medications that could be a factor in their reaction to M. purpureus. Causality was rated as certain in 1.8% (1 case), probable in 56% (31 cases), and possible in 34% (18 cases).15
Monascus purpureus is a type of red yeast used in traditional Chinese medicine as early as the Tang Dynasty, at least 300 BC, to promote circulation. The traditional preparation is rice fermented with this yeast, and the resulting food is consumed as part of the diet of patients with heart disease. The principle constituents are monacolins. Monacolin K is the compound from which lovastatin and the statin medications for dyslipidemia are derived. Monascus purpureus is traditionally used to make red rice vinegar, Peking duck, and Korean rice wine. Monacolins are also found in oyster mushrooms (Pleurotus ostreatus).16
Curr Ther Res. 1997;58(12):964–78. Multicenter clinical trial of the serum lipid-lowering effects of a Monascus purpureus rice preparation from traditional Chinese medicine. Wang J, Lu Z, Wang W, et al.
2 Am J Clin Nutr. 1999;69:69-231–6. Cholesterol-lowering effects of a proprietary Chinese red-yeast rice dietary supplement. Heber D, et al.
3 Nat Med Assoc Sci Assem. 1998. A monascus purpureus rice preparation reduces serum cholesterol and triacylglycerols in elderly with primary hyperlipidemia: a randomized double-blind clinical trial. New Orleans LA. Qin SC.
4 Exp Ther Med. 2014;8(6):1737–44. Red yeast rice repairs kidney damage and reduces inflammatory transcription factors in rat models of hyperlipidemia. Ding M, Si D, Zhang W, Feng Z.
5 BMC Complement Altern Med. 2013;13:178. Red yeast rice lowers cholesterol in physicians - a double blind, placebo controlled randomized trial. Verhoeven V, Lopez Hartmann M, Remmen R, Wens J, Apers S, Van Royen P.
6 PLoS One. 2014;9(6):e98611. A meta-analysis of red yeast rice: an effective and relatively safe alternative approach for dyslipidemia. Li Y, Jiang L, Jia Z, Xin W, Yang S, Yang Q, Wang L.
7 J Clin Lipidol. 2014;8(6):568–75. Effects of Xuezhikang in patients with dyslipidemia: a multicenter, randomized, placebo-controlled study. Moriarty PM, Roth EM, Karns A, et al.
8 Mo Med. 2013;110(4):349–54. Red yeast rice for dysipidemia. Shamim S, Al Badarin FJ, DiNicolantonio JJ, Lavie CJ, O’Keefe JH.
9 Nutr Res. 2013;33(8):622–8. Red yeast rice improves lipid pattern, high-sensitivity C-reactive protein, and vascular remodeling parameters in moderately hypercholesterolemic Italian subjects. Cicero AF, Derosa G, Parini A, et al.
10 Can J Physiol Pharmacol. 2014;92(6):481–9. Red yeast rice and coenzyme Q10 as safe alternatives to surmount atorvastatin-induced myopathy in hyperlipidemic rats. Abdelbaset M, Safar MM, Mahmoud SS, Negm SA, Agha AM.
11 J Am Geriatr Soc. 2006;54(4):718–20. Chinese red rice depletes muscle coenzyme Q10 and maintains muscle damage after discontinuation of statin treatment. Vercelli L, Mongini T, Olivero N, Rodolico C, Musumeci O, Palmucci L.
12 Br J Nutr. 2005;93(1):131–5. Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. Yang HT, Lin SH, Huang SY, Chou HJ.
13 Atherosclerosis. 2015;240(2):415–23. Traditional Chinese lipid-lowering agent red yeast rice results in significant LDL reduction but safety is uncertain—a systematic review and meta-analysis. Maaike CG, Ruben JT, Huixin Y, Koks CHW, Gerdes VEA.
14 Br J Clinical Pharmacol. 2017;83(4):849–908. Adverse reactions to dietary supplements containing red yeast rice. Massanti G, Moro PA, Raschi E, Da Cas R, Menniti-Ippolito F.
15 Mayo Clinic. 2017. Red yeast rice. https://www.mayoclinic.org/drugs-supplements-red-yeast-rice/art-20363074 Accessed October 30, 2017.
16 Drugs.com. 2017. Red yeast rice. https://www.mayoclinic.org/drugs-supplements-red-yeast-rice/art-20363074 Accessed October 30, 2017.