CoQ10 was first isolated by Dr. Frederick Crane in 1957 from the mitochondria of beef heart. During that same year Professor Morton, from Britain, also discovered CoQ10 in the livers of vitamin A deficient rats. During the following year researchers at Merck, Inc. determined its chemical structure and became the first to produce it.
It was neither the British nor the Americans that first found a practical use for the CoQ compounds. Professor Yamamura from Japan first used a related compound (CoQ7) in the treatment of congestive heart failure. Other practical uses then followed. CoQ6 was used as an effective antioxidant in the mid 1960s. In 1972 (in Italy) deficiency of CoQ10 was linked to heart disease. The Japanese, however, were the first to perfect the technology necessary to produce CoQ10 in sizeable enough quantities to make large clinical trials a reality and most of the pharmcological grade Co Q10 comes from Japan.
Coenzyme Q10 is a member of the ubiquinone family of compounds. All animals, including humans, can synthesize ubiquinones, hence, coenzyme Q10 cannot be considered a vitamin. The name ubiquinone refers to the ubiquitous presence of these compounds in living organisms and their chemical structure, which contains a functional group known as a benzoquinone.
Under normal conditions we produce all we need while we are young. But there are many factors that can contribute to CoQ10 deficiency. Among these are aging, disease, dietary deficiency, use of statin drugs and increasing tissue demands.
Mitochondrial ATP synthesis
The conversion of energy from carbohydrates and fats to adenosine triposphate (ATP), the form of energy used by cells, requires the presence of coenzyme Q in the inner mitochondrial membrane.
CoEnzyme Q10 serves as an antioxidant which neutralizes free radicals and helps protect our DNA and Lipids such as LDL from Oxidation.
Possible Role in the Aging Process
According to the free radical and mitochondrial theories of aging, oxidative damage of cell structures by reactive oxygen species (ROS) plays an important role in the functional declines that accompany aging . ROS are generated by mitochondria as a byproduct of ATP production. If not neutralized by antioxidants, ROS may damage mitochondria over time, causing them to function less efficiently and to generate more damaging ROS in a self-perpetuating cycle. Coenzyme Q10 plays an important role in mitochondrial ATP synthesis and functions as an antioxidant in mitochondrial membranes. Moreover, tissue levels of coenzyme Q10 have been reported to decline with age . One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle. It has been proposed that age-associated declines in tissue coenzyme Q10 levels may play a role in this decline and a recent study suggests Co Q10 may help relieve fatigue and help to improve exercise endurance and recovery.
Antifatigue effects of coenzyme Q10 during physical fatigue. Mizuno K et al Nutrition. 2008 Apr;24(4):293-9. Epub 2008 Feb 13
Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals. Cooke M,et al J Int Soc Sports Nutr. 2008 Mar 4;5:8
In recent studies, lifelong dietary supplementation with coenzyme Q10 did not increase the life spans of rats or mice ; however, one study showed that coenzyme Q10 supplementation attenuates the age-related increase in DNA damage . Presently, there is no scientific evidence that coenzyme Q10 supplementation prolongs life or prevents age-related functional declines in humans.
Life-long supplementation with a low dosage of coenzyme Q10 in the rat: effects on antioxidant status and DNA damage. Quiles JLet al Biofactors. 2005;25(1-4):73-86.
Because of the Antioxidant and Energy Production Functions of Co Q10, It may have usefulness for the following.
Protection against Heart Disease and Heart Failure
By blocking LDL oxidation and the the development of atherosclerosis.
By improving the function of the Failing Heart.
Various Neurologic Diseases. Parkinsons, Huntington's, Friereich's Ataxia
By virtue of the antioxidant qualities of Co Q10.
Inhibition by statins.
Coenzyme Q10 shares a common biosynthetic pathway with cholesterol. The synthesis of an intermediary precursor of Coenzyme Q10, mevalonate, is inhibited by some beta blockers, blood pressure-lowering medication, and statins, a class of cholesterol-lowering drugs. Statins can reduce serum levels of coenzyme Q10 by up to 40%. Some research suggests the logical option of supplementation with coenzyme Q10 as a routine adjunct to any treatment that may reduce endogenous production of coenzyme Q10, based on a balance of likely benefit against very small risk.