The use of CoQ10 may be of benefit in several disorders. When supplementing with CoQ10, however, it is possible that a pre-existing CoQ10 deficiency may be necessary for any benefits to be seen. Measurement of plasma CoQ10 concentrations can assist in detecting deficiency states and thus serve as a dosage guide when oral supplementation is indicated.
Normal blood and tissue levels of CoQ10 have been well established by numerous investigators around the world. Significantly decreased levels of CoQ10 have been noted in a wide variety of diseases in both animal and human studies.
CoQ10 deficiency may be caused by insufficient dietary CoQ10, impairment in CoQ10 biosynthesis, excessive utilization of CoQ10 by the body, or any combination of the three.
Decreased dietary intake is presumed in chronic malnutrition and wasting conditions. The relative contribution of CoQ10 biosynthesis in the human body versus dietary CoQ10 is under investigation. This complex production process requires at least seven vitamins and several trace elements. It is argued that suboptimal nutrient intake in man is almost universal and that there is subsequent secondary impairment in CoQ10 biosynthesis. This would mean that average or "normal" levels of CoQ10 are really suboptimal and the very low levels observed in advanced disease states represent only the tip of a deficiency "iceberg".
HMG-CoA reductase inhibitors (all the "statin" drugs) that are used to treat elevated blood cholesterol levels by blocking cholesterol synthesis also block CoQ10 synthesis. The resulting lowering of blood CoQ10 level is due to the partially shared biosynthetic pathway of CoQ10 and cholesterol. In patients with heart failure they have a significant harmful effect which can be negated by oral CoQ10 supplementation. Increased body consumption of CoQ10 is the presumed cause of low blood CoQ10 levels seen in excessive exertion, hypermetabolism, and acute shock states. It is likely that all three mechanisms (insufficient dietary CoQ10, impaired CoQ10 biosynthesis, and excessive utilization of CoQ10) are operable to varying degrees in most cases of observed CoQ10 deficiency.
Internationally, there have been at least nine placebo-controlled studies on the treatment of heart disease with CoQ10. All nine of these studies have confirmed the effectiveness of CoQ10 as well as its remarkable safety. Treatment with CoQ10 significantly improves heart muscle function while producing no adverse effects or drug interactions.
The largest study to date involved 2,664 patients with heart failure. Diastolic dysfunction – one of the earliest identifiable signs of myocardial failure – is often found in mitral valve prolapse, hypertensive heart disease and certain fatigue syndromes. Diastolic dysfunction is seen early in the course of many common cardiac disorders and can be demonstrated by echocardiography. The heart muscle stiffening found here returns towards normal with supplemental CoQ10 along with clinical improvement of symptoms. It is important to note that in all of the above clinical trials, CoQ10 was used in addition to traditional medical treatments, not to their exclusion. Hypertension is reduced when diastolic function improves.
HMG-CoA reductase inhibitors ("statin" drugs) used to treat elevated blood cholesterol levels by blocking cholesterol synthesis also block CoQ10 synthesis. The resulting lowering of blood CoQ10 level is due to the partially shared biosynthetic pathway of CoQ10 and cholesterol.
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