As I have reported previously, for a decade or more, the statins have very serious side effects and RRY carries the same risks.
One of the most overlooked side effects with the statin drugs is the depletion of CO Q 10. This article supports that loss in RRY as well.
While the effect may be less intense, the loss of Co Q 10 is a very serious nutritional depletion that may lead to sudden cardiac death and other health problems such as the cancer link.
This - IMHO - says that statins do not protect your heart.
So if you are using RRY to stave off the high priced Rx, do not fail to take CO Q 10 - minimally 100mg daily or more. This product may be order from us, just send a note and we'll be ahpy to provide the information.
Red Yeast Rice Depletes Coenzyme Q10 Levels in Mice - Safety Update
Author: Donald Brown, ND
Reference: Yang H-T, Lin S-H, Huang S-Y, et al. Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q10 levels in ICR mice. Br J Nutr 2005;93:131-5.
Summary: Eighty-eight adult ICR mice (a commonly used experimental breed of mice) were gavaged with a single dose of an average of 0.3 ml of red yeast rice (Monascus purpureus; China Chemical and Pharmaceuticals, Taipei, Taiwan), in a soybean oil emulsion, at concentrations of 1 g/kg body weight (low dose group) or 5 g/kg body weight (high dose group). A third group of mice, that did not receive red yeast rice, acted as the control.
After treatment, researchers observed the mice for 24 hours for mortality and signs of toxicity. The mice were then sacrificed and coenzyme Q10 (CoQ10) levels were analyzed in the heart, liver and kidney. Concentration of monacolin K (lovastatin) was analyzed in the liver only.
No deaths or toxicity were noted in either treatment group. Liver CoQ10 concentrations significantly decreased in the low- and high-dose groups 30 minutes after treatment (p < 0.01), was maximally depleted between 30 and 60 minutes (p < 0.05), and returned to baseline after 240 minutes. Heart CoQ10 levels were maximally reduced between 90 and 240 minutes in both groups; however, CoQ10 concentration in the high-dose group were 47% lower than in the low-dose group at 90 minutes (exact values not reported, p < 0.05). Heart CoQ10 levels did not return to normal during the study period in either group. Thirty minutes after treatment the hepatic monacolin K concentrations were 0.61 mg/g liver in the low-dose group compared to 1.62 mg/g liver in the high-dose group. At 30, 60, 90, 240 and 1440 minutes (24 hours), hepatic monacolin K levels were significantly higher in the high-dose group compared to the low-dose group (p < 0.05). Kidney CoQ10 levels did not change during the experiment. Furthermore, no histological or skin damage was detected.
Comments: Although this was an animal study testing high doses of red yeast rice, these results suggest that health care practitioners should advise patients taking red yeast rice products to routinely supplement CoQ10. Due to the presence of monacolins (especially monacolin K), the mechanism of action of red yeast rice has been attributed to the inhibition of HMG-CoA reductase. However, there has been debate about how aggressively red yeast rice inhibits the enzyme, especially when comparing the rather modest lipid-lowering results in humans compared to prescription statin drugs. These results suggest that the addition of CoQ10 may serve as an insurance policy against lowered production of CoQ10 in the body while taking red yeast rice. Hopefully, human trials will be completed to attempt to quantify the CoQ10-lowering effect of red yeast rice in humans.