Nutrition 101Natural RemediesWeioht ManagementPhysician Education
Vitamins and MineralsNutrition and AgingNutrition and DiseaseResearch
HomeSite Search


Green Tea



St. John's wort

Chinese Red
Yeast Rice


Chinese Red Yeast Rice

There are 57 million Americans with cholesterol levels greater than 200 mg/dl who are at increased risk of heart disease, which remains the primary cause of mortality in the U.S. with 500,000 deaths per year due to heart attack. However, cholesterol-lowering drugs are only recommended for individuals with cholesterol levels above 240 mg/dl, and it is estimated that only 3 to 4 million Americans take these drugs currently. For 30 million Americans with cholesterol levels in the 200 to 240 mg/dl range, natural remedies combined with diet and lifestyle changes may offer a great public health benefit at reasonable cost and low risk. The botanical dietary supplement Monascus Purpureus Went yeast or Chinese red yeast rice contains a family of monacolins (polyketides) with the ability to inhibit cholesterol synthesis and lower plasma cholesterol levels independent of diet. One of the monacolins (Monacolin K) is identical in chemical structure to Lovastatin, which is widely sold as a prescription cholesterol-lowering drug, but the other monacolins in this botanical supplement may also have cholesterol-lowering activity. Evidence of the activity of multiple components of this yeast clearly will differentiate this product as a dietary supplement rather than a drug. Preliminary work has extensively characterized these potentially bioactive components of the yeast, and we have successfully conducted a recently published double-blind, placebo-controlled trial of this supplement in 80 individuals demonstrating a significant decrease in cholesterol levels from ca. 250 mg/dl to 210 mg/dl over 8 weeks independent of diet.

Chinese Red Yeast Rice

Red yeast rice is a traditional food consumed throughout Asia. Its food value and medicinal value is believed to date back more than a thousand years, with the first documentation of its use recorded in 800 A.D. The fungus Monascus isolated from red yeast rice first became known in Western society through the work of Dutch scientists, who noted its use by local populations in Java in 1884. A species isolated from red Koji or Honqu (as red rice yeast is known in East Asia) was named Monascus Purpureus Went in 1895, in recognition of the purple coloration. Today there are more than 30 Monascus strains on deposit with the American Type Culture Collection.

The traditional method of making red yeast rice is to ferment the yeast naturally on a bed of cooked non-glutinous whole rice kernels, and this method has been industrialized to produce a dietary supplement marketed in the United States (Cholestin, Pharmanex, Inc., Simi Valley, CA). The supplement contains only the rice and the Monascus fungus and the yeast in a capsule. There are a number of constituents in the natural product including pigments, fatty acids, and polyketides (monacolins). These monacolins are believed to account for the majority of the cholesterol-lowering activity of the yeast.

Lipid-Lowering Activity in Human Clinical Trials

We examined the cholesterol-lowering effects of Chinese red yeast rice supplement in an American population consuming a diet similar to the American Heart Association Step I diet using a double-blind placebo-controlled, prospectively randomized twelve-week controlled trial (32). Eighty-three healthy subjects (46 men, 37 women, aged 34-78) with hyperlipidemia (total cholesterol (TC) 204-338 mg/dL), LDL cholesterol (LDL) 128-277 mg/dL, triglycerides 55-246 mg/dL, and HDL cholesterol (HDL) 30-95 mg/dL) not being treated with lipid-lowering drugs participated. Subjects were treated with this supplement (2.4 g/day) or placebo and instructed on a diet providing 30% of energy from fat, less than 10 % saturated fat, and less than 300 mg of dietary cholesterol.

The total cholesterol (TC) level was significantly decreased between baseline and 8 weeks in the red yeast rice-treated group compared to the placebo treated group (p<0.05). TC levels at 8 and 12 weeks differed significantly (p< 0.05) between the two groups. At 8 weeks, mean TC was 208 ± 31 mg/dL in the red yeast rice-treated group compared to 254 ± 36 mg/dL in the placebo-treated group. Furthermore, TC at both 8 and 12 weeks differed significantly from baseline (p<0.05) in the red yeast rice-treated group. At 8 weeks, every patient in the red yeast rice-treated group experienced a reduction in TC, while there was no significant difference in TC at 8 and 12 weeks compared to baseline in the placebo-treated group. The difference between baseline and 12 weeks was 40 ± 21 mg/dL in the red yeast rice-treated group and 5 ± 20 mg/dL in the placebo-treated group.

Low density lipoprotein (LDL) cholesterol levels at 8 and 12 weeks differed significantly (p<0.001) between the two groups. At 12 weeks, mean LDL cholesterol in the red yeast rice-treated group was 135 ± 27 mg/dL compared to 175 ± 33 mg/dL in the placebo-treated group. Furthemore, LDL levels at 8 and 12 weeks within the red yeast rice-treated group differed significantly (p<0.001) from baseline levels. At 8 weeks, all but one of the red yeast rice-treated subjects experienced a drop in LDL cholesterol. On the other hand, in the placebo-treated group there was no significant difference between baseline and 8 weeks or between baseline and 12 weeks. The difference in the red yeast rice-treated group between baseline and 12 weeks 39 ± 19 mg/dL compared to 5 ± 22 mg/dL in the placebo-treated group (Table 1).

Table 1

Cholesterol (mg.dL)

Triglycerides (mg/dL)

HDL (mg/dL)



254 + 29

143 + 46

46 + 10

Red Yeast

250 + 30

133 + 48

50 + 13

Week 8


254 + 36

142 + 52

46 + 10

Red Yeast

208 + 31

118 + 41

50 + 13

Week 12


250 + 36

146 + 47

46 + 11

Red Yeast

210 + 31

124 + 44

50 + 14

Triglyceride levels at 8 and 12 weeks differed significantly (p<0.05 and p<0.05, respectively) between the two groups. At 12 weeks, mean triglyceride levels in the red yeast rice-treated group were 124 ± 44 mg/dL compared to 146 ± 47 mg/dL in the placebo-treated group. Mean triglyceride levels within the red yeast rice-treated group differed from baseline at 8 weeks (p<0.05), but not at 12 weeks (p<0.054). On the other hand, in the placebo-treated group there was no significant difference between baseline and 8 weeks or baseline and 12 weeks. The difference in the red yeast rice-treated group between baseline and 12 weeks was 9 ± 30 mg/dL and for the placebo-treated group it was 3 ± 36 mg/dL.

HDL cholesterol levels did not differ significantly within or between the groups at baseline, 8 weeks, or 12 weeks.

There were no significant differences in dietary intake within or between groups at 8 weeks. Blood lipid differences between the red yeast rice-treated and placebo-treated groups were already evident at a time (8 weeks), when there were no differences in dietary intake. Differences in dietary intake cannot, therefore, account for the observed decrease in cholesterol. Furthermore, there were no differences in body weight between or within groups at any time. At 12 weeks, the treatment group reported reduced intake of total calories, saturated fat, monounsaturated fat, and fiber intake compared to baseline, but not when compared to the placebo-treated group. Reported total fat intake and polyunsaturated fat intake were lower than reported at baseline, as well as when compared to the placebo-treated group.

There were no serious adverse effects in any of the 88 subjects randomized. In the placebo-treated group, three subjects reported minor adverse effects, including: 1) development of a rash which responded to prednisone and antihistamine; 2) headaches; and 3) concurrent development of pneumonia while on study. There were no reported adverse events in the red yeast rice-treated group, except for one subject who reported an intercurrent hospitalization for musculoskeletal chest pain at his 12th week visit. He continued the dietary supplement while hospitalized and had a normal electrocardiogram stress treadmill performed by his outside doctor. His chest pain resolved and was not related to the dietary supplement.

Liver function tests were measured at baseline and 12 weeks. There were no significant differences between the groups at baseline or 12 weeks. Within treatment groups, BUN and GGTP differed significantly between baseline and 12 weeks. Both were lower at 12 weeks than at baseline. There were no abnormal liver function or renal function tests obtained at any time in any subject under study.

In this double-blind randomized, placebo-controlled prospective study, red yeast rice significantly reduced cholesterol levels beyond effects that could be accounted for by diet alone, and without significant adverse effects. The content of Monacolin K is only 0.2%, or about 5 mg. Therefore, 5 mg is the relevant comparison to 20 to 40 mg of lovastain. At this level, the mixture of monacolins and other substances present in the red yeast may have some effect on cholesterol biosynthesis not explained by the Monacolin K content. It is unlikely to be due solely to a single species of Monacolin, but rather to result from a combination of actions of monacolins and other substances in the red yeast rice.

Studies in humans have been conducted in China with both greater and lesser concentrated extracts of the red yeast rice than in our red yeast rice-treated group. In 324 hypercholesterolemic subjects treated with Xuezhikang (1.2 g/day containing 13.5 mg total monacolins) for 8 weeks, serum cholesterol levels decreased by 23 %, triglycerides reduced by 36.5 %, and HDL cholesterol levels increased by 19.6%. Two to four weeks before the initiation of this study, subjects were instructed to cease taking all medications and were provided dietary counseling. In a second study, an earlier version of the red yeast rice supplement containing 10 to 13 mg total monacolins was given to 101 hypercholesterolemic subjects. Total cholesterol decreased by 19.5 % and triglycerides decreased by 36.1% in the treated group. HDL cholesterol levels increased by 16.7% in this study. These and other Chinese studies were similar to this study in showing a marked effect of the constituents of this traditional seasoning on cholesterol levels. However, there were differences in the ethnicity and serum lipid levels of the populations studied. Furthermore, a rice placebo was used in the present study conducted in a double-blind fashion, while the Chinese studies used different natural preparations in the comparison group rather than a matched placebo capsule.

The benefits of statin drugs on the primary prevention of heart disease and in the secondary prevention of recurrent heart disease have been demonstrated in several large prospective clinical trials. These studies have increased interest in the use of statins for heart disease prevention, such as for individuals with hypercholesterolemia and modest cholesterol elevations. While it is acknowledged that side effects with statins are rare and are dose-related, there are data indicating that some statins may cause liver function abnormalites, and under certain circumstances rhabdomyolysis.

A clinical trial in 5608 men and 997 women with average cholesterol levels demonstrated that Lovastatin reduced the risk for a first acute major coronary event. The authors suggested a "need for reassessment of the national Cholesterol Education Program guidelines regarding pharmacological intervention." However, an accompanying editorial raised concerns regarding the economic impact of using cholesterol-lowering drugs, if used in the general population with average cholesterol levels. The currently available Chinese red yeast rice preparation used in the present study costs $20-$30/mo, while cholesterol-lowering drugs cost $120-$300/mo, with an average cost of $187/mo (32) . When considering a population-based public health approach to lowering cholesterol and preventing coronary artery disease, the reduced costs of the red yeast rice dietary supplement compared to prescription drugs could provide a new and novel approach for the maintenance of healthier cholesterol levels.


1. Heber D, Yip I, Ashley JM, Elashoff DA, Elashoff RM, and Go, VLW. Cholesterol-lowering effects of a proprietary Chinese red yeast rice dietary supplement. Am J Clin Nutrition 1999;69:231-236.

2. Wang HL, Fang SL. "Indigenous fermented foods of non-Western origin" in Hesseltine CW, Wang HL (eds) Mycologia Memoirs pp. 317-344.

3. Sung R-H. "Tien-Kung K’ai-Wu" Chinese Technology in the Seventeenth Century. Pennsylvania State University Press. 1966, pp. 292-294.

4. Tieghem Van . P. Monascus, genre nouveau de l’ordre des Ascomycetes. Bull. Soc. Fr. 1884; 31:226-231.

5. Went FAFC. Monascus purpureus le champignon de l’angquac une nouvelle thelebolee. Ann Soc Nat Bot. 1895; 8:1-17.

6. Lucas J, Schumacker J, Kunz B. Solid state fermentation of rice by Monascus Purpureus. J. Korean Society of Food Sciences. 1993;9:149-159.

7. Martinkova L, Juzlova P, Vesely D. Biological activity of polyketide pigment production by fungus Monascus. J. Appl. Bacteriology 1995;79:609-616.

8. Endo A. Monacolin K, a new hypocholesterolemic agent produced by Monascus sp. J. Antibiotics 1979;8:23-28.

9. Li C, Zhu Y, Wang Y, Zhu J-S, Chang J, Kritchevsky D. Monascus purpureus fermented rice (red yeast rice): a natural food product that lowers blood cholesterol in animal models of hypercholesterolemia. Nutrition Research 1998;18:71-78.

10. Alberts AW, Chen J, Kuron G, Hunt V, Huff J, et al. Mevinolin: a highly potent competitive inhibitor of hydroxymethylglutaryl coenzyme A reductase and a cholesterol-lowering agent. PNAS 1980;77:3957-3961.

11. Pentikainen PI, Saheimo M, Schwartz JI, Amin RD, Schwartz MS, Brunner-Ferber F, Rogers JD. Comparative pharmacokinetics of lovastatin, simvastatin, and pravastatin in humans. J Clin Pharmacol 1992;32:136-140.

12. Duggan DE, Chen I-W, Bayne WF, Halpin RA, Duncan CA, Schwartz MS, Stubbs RJ, Vickers S. The physiological disposition of lovastatin. Drug Metabolism and Disposition 1989; 17: 166-173.

13. Brown MS, Goldstein JL. A receptor-mediated pathway for cholesterol homeostasis. Science 1986;232:34-47.

14. Sinensky M. In; Regulation of HMG CoA Reductase ed. B. Preiss Academic Press, Orlando, Fla. 1985 pp. 201-220.

15. Magana MM, Lin SS, Dooley KA, Osborne TF. Sterol regulation of acetyl coenzyme A carboxylase promoter requires two interdependent binding sites for sterol regulatory binding proteins. J. Lipid Res. 1997;38:1630-1638.

16. Edwards PA, Ericsson J. Signalling molecules derived from the cholesterol biosynthetic pathway: mechanisms of action and possible roles in human disease. Current Opinions in Lipidology 1998;9:433-440.

17. Jackson SM, Ericsson J, Edwards PA. Signalling molecules derived from the cholesterol biosynthetic pathway. In Bittman R ed. Subcellular biochemistry vol. 28: cholesterol: Its functions and metabolism in biology and medicine. New York: Plenum Press: 1997. pp. 1-21.

18. Paigen B, Morrow A, Brandon C, Mitchell D, Holmes P. Variation in succeptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 1985; 57:65.

19. Zhang SH, Reddick RL, Piedrahita JA, Maeda N. Spontaneous hypercholesteolemia and arterial lesions in mice lacking apo E. Science 1992;258:468.

20. Plump AS, Breslow JL. Apolipoprotein E and the apoliporotein deficient mouse. Ann. Re. Nutr. 1995, 15:495-518

21. Nakashima Y, Plump AS, Raines EW, Breslow JL, Ross R. Apo E deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree. Arterioscl. Thromb. 1994;14:133-40.

22. Van Vlijem GJ, Pearce NJ, Bergo M, Staels B, Yates JW, Gribble AD, Bond BC, Hofker MH, Havekes LM, Groot PH. Apolipoprotein E3-Leiden transgenic mice as a test model for hypolipidemic drugs. Arzneimittelforschung 1998;48:396-402.

23. Zhu Y, Li CL, Wang YY, Zhu JS, Chang J, and Kritchevsky D. Monascus Purpureus (red yeast): a natural product that lowers blood cholesterol in animal models of hypercholesterolemia. Nutrition Research, accepted for publication.

24. Wang J, Su M., Lu Z, et al. Clinical trial of extract of Monascus Purpureus (red yeast)in the treatment of hyperlipidemia. Chinese Journal of Experimental herapeutics for Prepared Chinese Medicine 1995;12:1-5.

25. Shen Z, Yu P, Su M, et al. A prospective study on Zhitai capsule in the treatment of primary hyperlipidemia. National Med. J. China 1996; 76:156-7.

26. Mei F. Red yeast flavored duck. In "Fang Mei’s illustrated cookbook of regional Chinese cuisine". Guangxi, China, Guangxi National Press, 1990;177-88.

27. Shepherd J, Cobbe SM, Ford I, et al., for the West Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. New Engl. J. Med. 1995; 333:1301-7.

28. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344:1383-

29. Sacks FM, Pfeffer MA, Moye LA, et al., for the Cholesterol and Recurrent Events Trial Investigation. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. New Engl J Med. 1996; 335:1001-9.

30. Bradford RH, Shear CL, Chremos AN, et. al. Expanded Clinical Evaluation of Lovastatin (EXCEL) study results: Two-efficacy and safety follow-up. American Journal of Cardiology 1994;74:667-73.

31. Downs JR, Clearfield M, Weis S, et al. Primary prevention of acute coronary events with Lovastatin in men and women with average cholesterol levels. JAMA 1998;279:1615-22.

32. Pearson TA. Commentary: Lipid-lowering therapy in low-risk patients. JAMA 1998;279:1659-61.

33. Inoue J; Sato R; Maeda M. Multiple DNA elements for sterol regulatory element-binding protein and NF-Y are responsible for sterol- transcription of the genes for 3-hydroxy-3-methylglutaryl coenzyme A synthase and squalene synthase. J Biochem (Tokyo) 1998 Jun;123(6):1191-8.

34. Lowenstein JM, Brunengraber H, Wadke M. Measurement of rates of lipogenesis with deuterated and tritiated water. Methods Enzymol. 1975; 34:279-287.

35. Lee WNP, Bassilian S, Ajie HO, Schoeller DA, Edmond J, Bergner A, Byerley LO.

In vivo measurement of fatty acids and cholesterol synthesis using D2O and mass

isotopomer analysis. 1994; Am. J. Physiol. 266:E699-E708.

36. Qiao J-H, Xie P-Z, Fishbein MC, Kreuzer J, Drake TA, Demer LL, Lusis AJ. Pathology of atheromatous lesions in inbred and genetically engineered mice. Arterioscler Thromb 1994;14:1480-97.

37. Bisgaier CL, Essenburg AD, Auerbach BJ, Pape ME, Sekerke CS, Gee A, Wolle S, Newton RS. Attenuation of plasma low density lipoprotein cholesterol by select 3-HMGCoA reductase inhibitors in mice devoid of low density lipoprotein receptors. J. Lipid Research 1997; 38:2502-2515.

38. Pentikainen PI, Saraheimo M, Schwartz JI, Raju DA, Schwartz MS, Brunner-Ferber F, and Roger JD. Comparative pharmacokinetics of lovastatin, simvastatin, and pravastatin in humans. J. Clin Pharmacol 1992;32:136-140.







Nutrition 101 - Natural Remedies - Weight Management - Physician Education
Vitamins & Minerals - Nutrition & Aging - Nutrition & Disease - Research