Meta analysis outcome reveals significant decrease in plasma CoQ10 in association with statin therapy

Tuesday, October 13, 2015

The September 2015 issue of Pharmacological Research published the results of a meta-analysis of six trials which affirm an association between treatment with statin drugs and reduced plasma levels of coenzyme Q10 (CoQ10). Coenzyme Q10 is involved in the production of energy by the mitochondria and is found in nearly every cell of the body. While best known for its cardiovascular benefits, growing evidence has linked CoQ10's protective ability to other areas, including the brain and nervous system.

For their analysis, Maciej Banach of Poland's Medical University of Lodz and colleagues selected six placebo-controlled trials that investigated the impact of atorvastatin, pravastatin, rosuvastatin or simvastatin on serum or plasma CoQ10. Pooled analysis of the data uncovered an average reduction of 0.44 micromoles per liter CoQ10 following treatment with statin therapy. Analysis according to type of drug determined that the reduction in CoQ10 was significant for all four statins examined. Lipophilic statins, which include atorvastatin and simvastatin, and hydrophilic statins, that include rosuvastatin and pravastatin, were not associated with significantly different effects, and effects were significant for trials of more or less than 12 weeks duration.

"To our knowledge, this meta-analysis is the first to assess the effect of statins on plasma CoQ10 concentrations," the authors announce. "The biological consequences of statin-induced CoQ10 depletion may include: increased production of free radicals with consecutive damage of mitochondrial DNA, decrease of the mitochondrial oxidative phosphorylation capacity leading to mitochondrial dysfunction and the dysfunction or injury of skeletal muscle, [and] defective activity of cell division and apoptosis with increased tendency to malignancy."

They add that CoQ10 depletion associated with greater oxidative stress or inflammation has been reported in the elderly, and in patients with arterial hypertension, diabetes mellitus, periodontal disease, depression, chronic fatigue syndrome, Parkinson's disease and breast cancer. It has also been suggested as a factor in fibromyalgia.

"This meta-analysis showed a significant reduction in plasma CoQ10 concentrations following treatment with statins," Dr Banach and coauthors conclude."Further well-designed trials are required to confirm our findings and elucidate their clinical relevance."

What's Hot

Review summarizes benefits of CoQ10 supplementation

The March, 2013 issue of Nutrition Reviews published an article by Michael S. Pepper and his colleagues at the University of Pretoria in South Africa which provides an overview of coenzyme Q10 (CoQ10) supplementation in primary and secondary deficiency states. Primary CoQ10 deficiency occurs when the body's synthesis of this coenzyme is decreased due to mutations in specific enzymes involved in its production. Secondary deficiency is mainly observed among men and women who have been prescribed statin drugs which reduce a precursor in the pathway of CoQ10 synthesis, although there may be other causes.

In their review, the authors describe the CoQ10's benefits, including its antioxidant effect and its role in energy production and cell function. They note that CoQ10 has a remarkable safety profile as a supplement and has shown little in the way of adverse effects, which have not been observed to occur in greater frequency among those consuming relatively high doses in comparison with low doses. They add that no adverse effects have been demonstrated in association with amounts of up to 3,000 milligrams per day.

Supplementation is critical for those who are deficient in CoQ10, because of the minimal amount contributed by the diet. Although researchers do not yet agree upon routine supplementation to prevent adverse muscle events associated with statin-induced reductions in CoQ10, the authors of the review note that decreased coenzyme Q10 levels have been associated with consequences other than those that impact muscle, including an increased risk of mortality in heart failure patients. Monitoring patients who use statin drugs for plasma CoQ10 levels may be advisable, in addition to testing for a variation in a gene that is associated with statin intolerance.

"In patients in whom CoQ10 depletion is detected, appropriate supplementation should be administered at an optimal dose, using a formulation with proven superior bioavailability, to achieve normal plasma levels," the authors conclude. "In addition, a pharmacogenetic analysis may provide important information about the potential for statin-induced adverse effects in high-risk patients."

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Dermatologist's Corner

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Health Concern

Cholesterol management

Reduction of cellular cholesterol production is the most frequent strategy for reducing cardiovascular disease risk, with HMG-CoA reductase inhibitors (statins) being the most commonly prescribed cholesterol-lowering treatments. Statins inhibit the activity of the enzyme HMG-CoA reductase, a key regulatory step in cholesterol synthesis. Since cholesterol levels in cells are tightly controlled (cholesterol is critical to many cellular functions), the shutdown of cellular cholesterol synthesis causes the cell to respond by increasing the activity of the LDL receptor on the cell surface, which has the net effect of pulling LDL particles out of the bloodstream and into the cell. Statins may also reduce CHD risk by other mechanisms, such as by reducing inflammation.

Statins may induce serious side effects in some individuals; most common being muscle pain or weakness (myopathy). The prevalence of myopathy is fairly low in clinical trials (1.5-3.0%), but can be as high as 33% in community based studies and may rise dramatically in statin users who are active (up to 75% in statin-treated athletes.) Occasionally, statins may cause an elevation of the liver enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT). These enzymes can be monitored by doing a routine chemistry panel blood test. Additionally, by inhibiting HMG-CoA reductase (an enzyme not only required for the production of cholesterol, but other metabolites as well), statins may also reduce levels of the critically important antioxidant molecule CoQ10.