Study Confirms Coq10 Decline In Statin Treated Patients

Study confirms CoQ10 decline in statin-treated patients

Longer telomeres linked to eating less fat, more fruit and vegetables

Friday, January 11, 2013. The January 8, 2013 issue of the Journal of the American College of Cardiology published the finding of Danish researchers of reductions in glucose tolerance and coenzyme Q10 (CoQ10) levels in men treated with simvastatin, one of several statin drugs commonly prescribed to lower high cholesterol. While the drugs are of benefit to millions of people at risk for cardiovascular events, their effect on coenzyme Q10, an important mitochondrial cofactor, has not been well publicized in mainstream medical media. (Mitochondria are the cells' energy-producing organelles.)

In their introduction to the article, Professor Flemming Dela of Copenhagen's Center for Healthy Aging and his associates remark that although statin drugs have a positive effect on heart muscle via the increase in antioxidant capacity and reduction of reactive oxygen species production, an adverse effect on skeletal muscle has been reported. Statin-associated muscle pain has been reported in approximately 10 percent of sedentary patients and in up to 75 percent of athletes. However, the incidence of myopathy in clinical trials of the drugs has been much lower, presumably due to a discrepancy in the definition of myopathy.

"A well-known side effect of statin therapy is muscle pain," Dr Dela explained. "Up to 75 percent of the physically active patients undergoing treatment for high cholesterol experience pain. This may keep people away from either taking their medicine or from taking exercise - both of which are bad choices."

The current study included ten men treated for high cholesterol with simvastatin for at least one year and ten healthy control subjects. Participants underwent oral glucose tolerance tests, muscle biopsies, and blood testing for numerous factors.

Four men in the simvastatin group reported muscle pain, compared to none of the controls. Among simvastatin-treated subjects, glucose levels were significantly higher during two-hour oral glucose tolerance testing in comparison with untreated men. When tissue biopsy results were compared, CoQ10 and the antioxidant enzymes catalase, manganese superoxide dismutase (MnSOD) and glutathione peroxidase were lower in those treated with the drug.

"The present study is to our knowledge the first to demonstrate a deleterious effect on the glucose tolerance in simvastatin-treated patients," the authors announce. "Furthermore, a decrease is found in Q10 protein content in skeletal muscle, accompanied by a limitation in maximal oxidative phosphorylation capacity in the patients treated with simvastatin. We suggest that these observations may be part of the explanation of the most common side effects of statin treatment: muscle pain and weakness."

"We have now shown that statin treatment affects the energy production in muscles," Dr Dela concluded. "We are working on the assumption that this can be the direct cause of muscle weakness and pain in the patients."

"The new study is the basis for a large planned research project, where we will focus broadly on patients undergoing statin treatment," he added. "We will look at statin consumption from a medical point of view, and will also investigate the media's influence on patients' acceptance or rejection of statins as a treatment option. Many contradictory views find their way into the public forum, and it can be difficult for patients to distinguish between fact and fiction."

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Findings in yeast shed light on calorie restriction

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The journal Nature published an article online on November 21, 2012 that provides new information on how calorie restriction extends life span.

Adam L. Hughes, PhD and Daniel Gottschling, PhD of Seattle's Fred Hutchinson Cancer Research Center report the results of their latest research involving yeast cells. They found that a structure within the cells known as the vacuole (whose animal counterpart is the lysosome) becomes less acidic early in the yeast cell's life span, resulting in a reduction in the ability of this organelle to store specific nutrients. These nutrients build up in the cell and overwhelm the mitochondria, which are the cell's power plants. When the mitochondria become exhausted by consuming the surplus, they become dysfunctional. "Until now, the vacuole's role in breaking down proteins was thought to be of primary importance," explained Dr Hughes, who is a postdoctoral fellow in Dr Gottschling's laboratory. "We were surprised to learn it was the storage function, not protein degradation, that appears to cause mitochondrial dysfunction in aging yeast cells."

"Normally, mitochondria are beautiful, long tubes, but as cells get older, the mitochondria become fragmented and chunky," noted Dr Gottschling, who is a member of the Fred Hutchinson Center's Basic Sciences Division. "The changes in shape seen in aging yeast cells are also observed in certain human cells, such as neurons and pancreatic cells, and those changes have been associated with a number of age-related diseases in humans."

"There has been a lot in the scientific literature and the general media lately about how what you eat affects the aging process, but it has been incredibly confusing," Dr Gottschling remarked. "Now we have a new paradigm for understanding how genetics and environment interact to influence lifespan, aging and age-related diseases. That's what I'm really excited about."

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