The engine that powers the activity of virtually every cell in the body is the mitochondria. Because it is ubiquitous, and found everywhere in the body, a crucial factor to fuel that engine is called ubiquinone, otherwise known as coenzyme Q10, or better yet simply as CoQ10. CoQ10 helps spark the process of moving the electrons in the mitochondria to create adenosine triphosphate (ATP), the natural gasoline or “battery” that powers our body at a microscopic level. Of all of the cells in the body, the heart contains the most mitochondria, but the brain needs impressive amounts of CoQ10, too
Regardless of the “ubiquitous” nature of CoQ10, deficiencies are fairly common. CoQ10 levels decline with age, intensive and regular physical activity or stress, prolonged illness, and statin use. In fact, one of the ways of tracking whether statin drugs are being metabolized in the liver is by noting a reduction in CoQ10 levels. One of the reasons this happens is because CoQ10 is carried by lipids – that is, it is a fat-soluble nutrient. Most of the foods that are considered rich in CoQ10 have some elements of natural fats or fatty acids that transport it into the body. After it is ingested, CoQ10 or “ubiquinone” becomes “ubiquinol” in the body.
This review finds that the effects of CoQ10 can help overcome depletion from statin use, reduce brain aging inflammation and oxidative stress, and overall, help fuel the microscopic engines throughout the body.
As a supplement, CoQ10 is available as ubiquinone and ubiquinol – often referred to as an “active” or “reduced” CoQ10. Either supplemental form is beneficial, and getting CoQ10 at meaningful levels is as simple as adding it to a daily regimen.
Hernández-Camacho JD, Bernier M, López-Lluch G, Navas P. Coenzyme Q<sub>10</sub> Supplementation in Aging and Disease. Front Physiol. 2018;9:44.
Coenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and an antioxidant in plasma membranes and lipoproteins. It is endogenously produced in all cells by a highly regulated pathway that involves a mitochondrial multiprotein complex. Defects in either the structural and/or regulatory components of CoQ complex or in non-CoQ biosynthetic mitochondrial proteins can result in a decrease in CoQ concentration and/or an increase in oxidative stress. Besides CoQ10 deficiency syndrome and aging, there are chronic diseases in which lower levels of CoQ10 are detected in tissues and organs providing the hypothesis that CoQ10 supplementation could alleviate aging symptoms and/or retard the onset of these diseases. Here, we review the current knowledge of CoQ10 biosynthesis and primary CoQ10 deficiency syndrome, and have collected published results from clinical trials based on CoQ10 supplementation. There is evidence that supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics. Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10. There is a need for further studies and clinical trials involving a greater number of participants undergoing longer treatments in order to assess the benefits of CoQ10 treatment in metabolic syndrome and diabetes, neurodegenerative disorders, kidney diseases, and human fertility.
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