Enzymes are compounds in the body that are absolutely essential for the many processes necessary to keep us alive and our bodies functioning properly. Mitochondrial enzymes are those particular enzymes that are essential for the production of the high-energy phosphate ATP (adenosine triphosphate) upon which all cellular function depends. Without it our bodies shut down at the cellular level. Coenzyme Q10 is the cofactor upon which at least three mitochondrial enzymes depend. By logical inference then ATP functioning depends upon CoQ10. In short, all human cellular function depends on ATP. And ATP function depends on CoQ10.
As was already said, the production of CoQ10 occurs within our body tissues. Its biosynthesis from the amino acid tyrosine is a complex multistage process requiring several vitamins and trace elements. 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. Before we get to CoQ10 deficiencies, however, it is well to look at the history of CoQ10 research.
History
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.
After Peter Mitchell won the Nobel Prize in 1978 for defining the biological energy transfer that occurs at the cellular level (for which CoQ10 is essential) there was a considerable increase in the number of clinical studies performed in relation to CoQ10 usefulness. This was due in part to the large amounts of pharmaceutical grade CoQ10 that was now available from Japan and the ability to measure CoQ10 in blood and body tissues. CoQ10 since has become known for its importance as a powerful antioxidant and free radical scavenger and as a treatment in many chronic illnesses, especially heart disease.
Coenzyme Q10 Deficiency
The usefulness of CoQ10 as a medical treatment has largely been approached from the perspective that when a chronic disease is present (especially in the case of heart disease) CoQ10 is often grossly deficient. For example, a person suffering from congestive heart failure often demonstrates extreme CoQ10 deficiency. Normal blood and tissue levels of CoQ10 have been well established. Significantly low levels of CoQ10 have been linked to a vast variety of diseases in both animal and human studies.
But if CoQ10 is biosynthesized in our bodies why do we often suffer from deficiency? There are at least three causes. The first is an insufficient diet. Dietary intake of CoQ10 is an important factor in total blood and tissue levels of the compound. If we do not consume enough of the foods that contain CoQ10 then the body must make up the difference. Further, the biosynthesis of Coenzyme Q10 is a complex 17-step process involving a whole string of B vitamins, vitamin C and pantothenic acid. Diets deficient in these compounds make CoQ10 synthesis impossible. This is not the place to discuss the condition of the average diet and the vitamin deficient nature of many of our food sources. Suffice it to say that most of us do not get nearly enough CoQ10 or the other vitamins necessary for optimal synthesis.
The second cause of deficiency is linked to the first, and that is impairment of CoQ10 biosynthesis. In addition to inadequate intakes of the compounds necessary to make CoQ10 there are other biological reasons for inadequate production of it. These might include physiological conditions and chronic diseases that cause failure in production. The treatments of diseases can also be a factor. For instance the use of statins to control cholesterol levels has been implicated in the depletion of CoQ10 levels. The catch-22 is, in treating heart disease we use drugs that deplete natural compounds that in turn are necessary to fight heart disease.
The third cause of CoQ10 deficiency is excessive use of the compound by the body. This again can be related to medications, aging or other causes such as excessive exertion, hypermetabolism, and acute shock states.
The real cause of CoQ10 deficiency is usually a combination of these three influences. It is likely that the average CoQ10 levels which have been observed in humans are suboptimal. In other words, the normal levels of CoQ10 that have become the standard for comparisons are very likely less than optimal. That would mean that the extremely low levels observed in connection with chronic diseases are just the worse case scenarios and that other less serious maladies are connected with lesser levels of deficiency.
If this sounds too much like laboratory theory, it isn’t. Patients who suffer from chronic diseases and also demonstrate extreme low levels of CoQ10 are not laboratory specimens. They are people who, in many cases, have been greatly helped by CoQ10 supplementation. If chronic disease is only the tip of the iceberg when it comes to CoQ10 deficiency one is forced to wonder what better diets and CoQ10 supplementing could do for the eradication of diseases and other chronic conditions.
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