Red Yeast Rice

Akasha Naturals Support -

Cholesterol is produced in the liver and is essential to several physiological processes in the body including hormone production, cell membrane integrity, and bile acid synthesis. Cholesterol and other fat soluble compounds, such as triglycerides, vitamin E, carotenoids, and CoQ10 are circulated and delivered to various organs and tissues throughout the body by transport vesicles called VLDLs and LDLs. When tissues become saturated with cholesterol they prevent the delivery of more cholesterol from the LDL vesicles and these vesicles continue to circulate throughout the body. If LDLs are circulating for too long without being able to deliver their compounds to various tissues or return them back to the liver, these compounds may become oxidized over time and create inflammation in the arteries. By slowing down the liver's production of cholesterol it will up-regulate LDL receptor cites on the cell surface and allow circulating LDLs to deliver their compounds back to the liver. The mevalonate biochemical pathway is responsible for producing cholesterol in the liver. When this pathway gets an overload of mevalonate compounds the activity of the HMG-CoA reductase enzyme gets inhibited and the entire pathway is slowed down and will not manufacture cholesterol. The conversion of HMG-CoA to the mevalonate compound by the HMG CoA reductase enzyme constitutes the committed step in the biosynthesis of cholesterol in this pathway [5]. When this step gets inhibited and cholesterol levels in the liver decrease up-regulation of more LDL receptors on the cell surface will allow for intake of cholesterol from circulating LDLs. Red Yeast Rice contains mevalonate like compounds which are able to slow down the activity of the HMG-CoA reductase enzyme. When the HMG-CoA reductase enzyme gets inhibited it not only slows the production of cholesterol in the liver but slows down the production of CoQ10 as well. Figure 1: Shows the Mevalonate biochemical pathway of cholesterol and CoQ10 (Ubiquinone) in the liver.

Graph
Figure 1: Cholesterol Synthesis Pathway

 

 

1. Herber D, Yip I, Ashley JM, Elashoff DA, Elashoff RM, Liang W Go V. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. American journal of Clinical Nutrition, 1999 Feb; 69(2): 231-236.

http://www.ajcn.org/content/69/2/231.full.pdf+html

*Quick Summary of Study: Red yeast rice significantly reduces LDL cholesterol, and total triacylglycerol concentrations, compared with placebo, and provides a new novel, food-based approach to lowering cholesterol in the general population.

Abstract

�“Background: We examined the cholesterol-lowering effects of a proprietary 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 12-wk controlled trial at a university research center.
Objective: We evaluated the lipid-lowering effects of this red-yeast-rice dietary supplement in US adults separate from effects of diet alone.
Design: Eighty-three healthy subjects (46 men and 37 women aged 34�78 y) with hyperlipidemia [total cholesterol, 5.28�8.74 mmol/L (204�338 mg/dL); LDL cholesterol, 3.31�7.16 mmol/L (128�277 mg/dL); triacylglycerol, 0.62�2.78 mmol/L (55�246 mg/dL); and HDL cholesterol 0.78�2.46 mmol/L (30�95 mg/dL)] who were not being treated with lipid-lowering drugs participated. Subjects were treated with red yeast rice (2.4 g/d) or placebo and instructed to consume a diet providing 30% of energy from fat, <10% from saturated fat, and <300 mg cholesterol daily. Main outcome measures were total cholesterol, total triacylglycerol, and HDL and LDL cholesterol measured at weeks 8, 9, 11, and 12.
Results: Total cholesterol concentrations decreased significantly between baseline and 8 wk in the red-yeast-rice�treated group compared with the placebo-treated group [(x � SD) 6.57 � 0.93 mmol/L (254 � 36 mg/dL) to 5.38 � 0.80 mmol/L (208 � 31 mg/dL); P < 0.001]. LDL cholesterol and total triacylglycerol were also reduced with the supplement. HDL cholesterol did not change significantly.
Conclusions: Red yeast rice significantly reduces total cholesterol, LDL cholesterol, and total triacylglycerol concentrations compared with placebo and provides a new, novel, food-based approach to lowering cholesterol in the general population.”[1]

2. Liu J, Zhang J, Shi Y, Grimsgaard S, Alraek T, F�nneb� V. Chinese red yeast rice (Monascus purpureus) for primary hyperlipidemia: a meta-analysis of randomized controlled trials. Chin Med. 2006 Nov 23; 1(4).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1761143/?tool=pubmed

*Quick Summary of Study: Extracts of RYR have been clinically shown to contain several active ingredients, including lovastatin, and this constituent may have lipid-lowering effects. These effects seemed to be similar to other popular statin drugs and RYR had no adverse side effects.

Abstract

�“Extracts of Chinese red yeast rice (RYR, a traditional dietary seasoning of Monascus purpureus) contains several active ingredients including lovastatin, and several trials of its possible lipid-lowering effects have been conducted. This meta-analysis assesses the effectiveness and safety of RYR preparations on lipid modification in primary hyperlipidemia. We included randomized controlled trials testing RYR preparation, compared with placebo, no treatment, statins, or other active lipid-lowering agents in people with hyperlipidemia through searching PubMed, CBMdisk, TCMLARS, the Cochrane Library, and AMED up to December 2004. Ninety-three randomized trials (9625 participants) were included and three RYR preparations (Cholestin, Xuezhikang and Zhibituo) were tested. The methodological quality of trial reports was generally low in terms of generation of the allocation sequence, allocation concealment, blinding, and intention-to-treat. The combined results showed significant reduction of serum total cholesterol levels (weighted mean difference -0.91 mmol/L, 95% confidence interval -1.12 to -0.71), triglycerides levels (-0.41 mmol/L, -0.6 to -0.22), and LDL-cholesterol levels (-0.73 mmol/L, -1.02 to -0.043), and increase of HDL-cholesterol levels (0.15 mmol/L, 0.09 to 0.22) by RYR treatment compared with placebo. The lipid modification effects appeared to be similar to pravastatin, simvastatin, lovastatin, atorvastatin, or fluvastatin. Compared with non-statin lipid lowering agents, RYR preparations appeared superior to nicotinate and fish oils, but equal to or less effective than fenofibrate and gemfibrozil. No significant difference in lipid profile was found between Xuezhikang and Zhibituo. RYR preparations were associated with non-serious adverse effects such as dizziness and gastrointestinal discomfort. Current evidence shows short-term beneficial effects of RYR preparations on lipid modification. More rigorous trials are needed, and long-term effects and safety should be investigated if RYR preparations are to be recommended as one of the alternative treatments for primary hyperlipidemia.” [2

3.Deichmann R, Larie C, Andrews S. Coenzyme Q10 and Statin-Induced��� ��Mitochondrial Dysfunction. Ochner J. 2010 Spring; 10(2):16-21.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096178/?tool=pubmed

*Quick Summary of Study: Statin drugs often result in reduced synthesis of coenzyme Q10 which may lead to statin-induced myopathic syndrome. By adding adequate levels of CoQ10 to statin type supplements the user may offset the effects of neurologic and myopathic sydromes.

Abstract

�“Coenzyme Q10 is an important factor in mitochondrial respiration. Primary and secondary deficiencies of coenzyme Q10 result in a number of neurologic and myopathic syndromes. Hydroxyl-methylglutaryl coenzyme A reductase inhibitors or statins interfere with the production of mevalonic acid, which is a precursor in the synthesis of coenzyme Q10. The statin medications routinely result in lower coenzyme Q10 levels in the serum. Some studies have also shown reduction of coenzyme Q10 in muscle tissue. Such coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies. However, coenzyme Q10 supplements have not been shown to routinely improve muscle function. Additional research in this area is warranted and discussed in this review.”[3]

4. Mohr D, Bowry VW, Stocker R. Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. Biochim Biophys Acta. 1992 Jun 26;1126(3):247-54.

http://www.ncbi.nlm.nih.gov/pubmed?term=1637852

*Quick Summary of Study: Oral supplementation of CoQ10 may increase resistance to LDL oxidation.

Abstract

“Ubiquinol-10 (CoQH2, the reduced form of coenzyme Q10) is a potent antioxidant present in human low-density lipoprotein (LDL). Supplementation of humans with ubiquinone-10 (CoQ, the oxidized coenzyme) increased the concentrations of CoQH2 in plasma and in all of its lipoproteins. Intake of a single oral dose of 100 or 200 mg CoQ increased the total plasma coenzyme content by 80 or 150%, respectively, within 6 h. Long-term supplementation (three times 100 mg CoQ/day) resulted in 4-fold enrichment of CoQH2 in plasma and LDL with the latter containing 2.8 CoQH2 molecules per LDL particle (on day 11). Approx. 80% of the coenzyme was present as CoQH2 and the CoQH2/CoQ ratio was unaffected by supplementation, indicating that the redox state of coenzyme Q10 is tightly controlled in the blood. Oxidation of LDL containing various [CoQH2] by a mild, steady flux of aqueous peroxyl radicals resulted immediately in very slow formation of lipid hydroperoxides. However, in each case the rate of lipid oxidation increased markedly with the disappearance of 80-90% CoQH2. Moreover, the cumulative radical dose required to reach this 'break point' in lipid oxidation was proportional to the amount of CoQH2 incorporated in vivo into the LDL. Thus, oral supplementation with CoQ increases CoQH2 in the plasma and all lipoproteins thereby increasing the resistance of LDL to radical oxidation.”[4]

5. Mabuchi H, Higashikata T, Kawashiri M, Katsuda S, Mizuno M, Nohara A, Inazu A, Koizumi J,Kobayashi J.Reduction of serum ubiquinol-10 and ubiquinone-10 levels by atorvastatin in hypercholesterolemic patients. J Atheroscler Thromb. 2005;12(2):111-9.

http://www.jstage.jst.go.jp/article/jat/12/2/111/_pdf

*Quick Summary of Study: Statin drugs act as a HMG-CoA reductase inhibitor that leads to not only the reduction of cholesterol synthesis but also the reduction of serum CoQ10 levels which may have associated risks.

Abstract

Reduction of serum cholesterol levels with statin therapy decreases the risk of coronary heart disease. Inhibition of HMG-CoA reductase by statin results in decreased synthesis of cholesterol and other products downstream of mevalonate, which may produce adverse effects in statin therapy. We studied the reductions of serum ubiquinol-10 and ubiquinone-10 levels in hypercholesterolemic patients treated with atorvastatin. Fourteen patients were treated with 10 mg/day of atorvastatin, and serum lipid, ubiquinol-10 and ubiquinone-10 levels were measured before and after 8 weeks of treatment. Serum total cholesterol and LDL-cholesterol levels decreased significantly. All patients showed definite reductions of serum ubiquinol-10 and ubiquinone-10 levels, and mean levels of serum ubiquinol-10 and ubiquinone-10 levels decreased significantly from 0.81 +/- 0.21 to 0.46 +/- 0.10 microg/ml (p < 0.0001), and from 0.10 +/- 0.06 to 0.06 +/- 0.02 microg/ml (p = 0.0008), respectively. Percent reductions of ubiquinol-10 and those of total cholesterol showed a positive correlation (r = 0.627, p = 0.0165). As atorvastatin reduces serum ubiquinol-10 as well as serum cholesterol levels in all patients, it is imperative that physicians are forewarned about the risks associated with ubiquinol-10 depletion.

 

6. Becker DJGordon RYHalbert SCFrench BMorris PBRader DJ. Red yeast rice for dyslipidemia in statin-intolerant patients: a randomized trial. Ann Intern Med. 2009 Jun 16;150(12):830-9, W147-9.

http://www.ncbi.nlm.nih.gov/pubmed/19528562

Abstract

“BACKGROUND:

Red yeast rice is an herbal supplement that decreases low-density lipoprotein (LDL) cholesterol level.

OBJECTIVE:

To evaluate the effectiveness and tolerability of red yeast rice and therapeutic lifestyle change to treat dyslipidemia in patients who cannot tolerate statin therapy.

DESIGN:

Randomized, controlled trial.

SETTING:

Community-based cardiology practice.

PATIENTS:

62 patients with dyslipidemia and history of discontinuation of statin therapy due to myalgias.

INTERVENTION:

Patients were assigned by random allocation software to receive red yeast rice, 1800 mg (31 patients), or placebo (31 patients) twice daily for 24 weeks. All patients were concomitantly enrolled in a 12-week therapeutic lifestyle change program.

MEASUREMENTS:

Primary outcome was LDL cholesterol level, measured at baseline, week 12, and week 24. Secondary outcomes included totalcholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride, liver enzyme, and creatinine phosphokinase (CPK) levels; weight; and Brief Pain Inventory score.

RESULTS:

In the red yeast rice group, LDL cholesterol decreased by 1.11 mmol/L (43 mg/dL) from baseline at week 12 and by 0.90 mmol/L (35 mg/dL) at week 24. In the placebo group, LDL cholesterol decreased by 0.28 mmol/L (11 mg/dL) at week 12 and by 0.39 mmol/L (15 mg/dL) at week 24. Low-density lipoprotein cholesterol level was significantly lower in the red yeast rice group than in the placebo group at both weeks 12 (P < 0.001) and 24 (P = 0.011). Significant treatment effects were also observed for total cholesterol level at weeks 12 (P < 0.001) and 24 (P = 0.016). Levels of HDL cholesterol, triglyceride, liver enzyme, or CPK; weight loss; and pain severity scores did not significantly differ between groups at either week 12 or week 24.

LIMITATION:

The study was small, was single-site, was of short duration, and focused on laboratory measures.

CONCLUSION:

Red yeast rice and therapeutic lifestyle change decrease LDL cholesterol level without increasing CPK or pain levels and may be a treatment option for dyslipidemic patients who cannot tolerate statin therapy.” [6]

 

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