CoEnzyme Q10 protects nerve cells
CoEnzyme Q10 has shown the ability to protect nerve cells and potentially lower the risk of various degenerative diseases.
Cells in the brain and nervous system depend on optimal mitochondrial function for energy. A research study published in the journal Neurobiology of Disease showed that oxidative stress causes mitochondria to produce excessive free radicals, leading to nerve cell damage and destruction. Due to its function in the mitochondrial energy process and its role as an antioxidant, researchers evaluated CoEnzyme Q10 for its ability to protect nerve cells.
The results of this study revealed that CoEnzyme Q10 inhibits the production of free radicals by the mitochondria and stabilizes the mitochondrial membrane when nerve cells are subjected to oxidative stress. CoEnzyme Q10 may therefore have a potential benefit in reducing the risk of various neurodegenerative diseases.
Neurobiol Dis. 2005 Apr;18(3):618-27
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The widespread use of statin drugs is of special concern because they can lower the endogenous levels of Coenzyme Q10, the naturally-occurring form of ubiquinone in humans. Ubiquinone is widely recognized as an essential component of energy metabolism in the electron-transfer system in mitochondrial membranes. At physiological concentrations it is also recognized as an effective lipid-soluble antioxidant. It is one of the end products of the mevalonate pathway where dolichol (a component of animal membranes) and cholesterol are synthesized. Both ubiqionone and dolichol are released by the liver cells into the blood circulation, but in much lower concentrations than that of cholesterol.
Ghirlanda et al(2) reported in a double-blind, placebo-controlled study a decrease of 50-54% of CoQ10 levels in the statin treatment groups, and similar results were reproduced by Watts et al(3).
Bliznakov and Wilkins reviewed studies of the effect of statins on the biosynthesis of Coenzyme Q10 and the clinical implication of CoQ10 deficiency.(4) The authors report that lovastatin, pravastatin and simvastatin lower the endogenous levels of Coenzyme Q10, as CoQ10 shares the common biosynthetic pathway with cholesterol.
Considering that Coenzyme Q10 is essential for mitochondrial function and antioxidant activity, and since oxidative mechanisms are important in atherogenesis, it can be assumed that a reduction in CoQ10 level may compromise coronary atherosclerosis despite optimal reduction in cholesterol levels by the use of statin drugs.
Furthermore, the reduction of ubiquinone levels might be associated with myopathy, a rare adverse effect associated with statin drugs. This "metabolic" myopathy is related to ubiquinone deficiency in muscle cell mitochondria, disturbing normal cellular respiration and causing adverse effects such as rhabdomyolysis, exercise intolerance, and recurrent myoglobinuria.(5)
It has also been suggested that CoQ10 deficiency can cause mitochondrial encephalomyopathies related to a primary or secondary ubiquinone deficient status, or even to an altered function of ubiquinone in the respiratory chain.(6) It is important to emphasize that Coenzyme Q10 supplementation does not interfere with the cholesterol-lowering effect of statin drugs(7) and therefore may be considered for all patients using such medications for an extended period of time.
Recognizing the importance of dietary supplementation with vitamins (E, C, B6, folate), and essential nutrients (CoQ10, L-arginine, propionyl L-carnitine) as an adjunct in the treatment of cardiovascular disease, we should pay attention to the potential adverse effect of drug-induced nutrient depletion affecting the aforementioned nutrients.
Pharmaceutical companies that market statin drugs should consider including the described CoQ10 potential depletion in their drug information materials provided to physicians and pharmacists, and they should encourage patients to consult their physician and pharmacist for appropriate supplementation.
Integration of nutritional medicine in the clinical practice of medicine can benefit for our patients using prescription medications for disease management and treatment.