Named for its prevalence in most living cells, ubiquinone or coenzyme Q10 (CoQ10) was discovered in the 1950s as a part of beef heart mitochondria. Since then, it has become apparent as a vital part of the electron transport chain, a critical part of the energy production process. In this capacity, CoQ10 helps move fats and carbs across the mitochondrial membrane to help produce adenosine triphosphate (ATP), which is used by body cells as energy. Due to this cellular role, scientists have looked into various health effects attributable to CoQ10.
While the electron transportation is fairly efficient, there are some leaks of electrons during the process, which contribute to the formation of free radicals such as super oxide. CoQ10 can serve as an antioxidant, protecting against damage from these free radicals.
The body naturally produces CoQ10 from other, lower-numbered ubiquinones and can further reduce CoQ10 to ubiquinol. However, this ability to reduce or convert CoQ10 to ubiquinol diminishes with age. Up to the age of 20, most healthy people have optimal ability to convert ubiquinone to ubiquinol; however, production of ubiquinol begins to decline after the age of 20, resulting in about a one-third loss of ubiquinol in vital organs, such as the heart, kidney and liver.
Organs like the heart have high energy demands; thus, ubiquinol is important for sustained output. This is why CoQ10 has been subjected to substantial research in the area of heart health. In fact, CoQ10 has proven useful in cardiovascular disease (CVD) based on two mechanisms, antioxidant and energy production.
Oxidized cholesterol, especially low-density lipoprotein (LDL) cholesterol, is a big factor in the development of atherosclerosis. In one trial, administration of 3 mg/d of CoQ10 (Q-Gel®, from Tishcon) in rabbits with high trans fat levels inhibited oxidative damage and atherosclerosis development.1 On the other hand, a combination of CoQ10 and vitamin E, as alpha-tocopherol, was shown to increase plasma levels of vitamin E and beneficial high-density lipoprotein (HDL) cholesterol in one trial,2 and reduce atherosclerosis at the aortic root and descending thoracic aorta in another trial.3
Targeting cholesterol control from another angle, CoQ10 has increasingly shown itself a necessity in people taking statin drugs. These drugs affect hydroxymethylglutaryl (HMG)-CoA reductase conversion which, in turn, affects coQ10 synthesis. Noting statin treatment generally results in lower plasma levels of CoQ10 due possibly to lowered levels of LDL, scientists reported a decrease of CoQ10 seen in the platelets and lymphocytes relative to statin use, suggesting CoQ10 synthesis itself may be inhibited.4
Intervention studies have all but confirmed this consequence. A Japanese open study examining the impact of pitavastatin or atorvastatin on plasma levels of CoQ10 in patients with hypercholesterolemia found the drugs not only reduced total and LDL cholesterol and increased HDL cholesterol, but they also significantly reduced plasma levels of CoQ10.5 Atorvastatin lowered CoQ10 (-26.1 percent) more so than pitavastatin (-7.7 percent). In an Italian study, three months of statin therapy dose dependently reduced total cholesterol, as well as levels of both ubiquinol and ubiquinone in plasma.6 In fact, the researchers suggested CoQ10 be taken along with statin therapies to mitigate the side effects of the drugs.