CoQ10 is a fat-soluble vitamin-like substance present in every cell of the body and serves as a coenzyme for several of the key enzymatic steps in the production of energy within the cell. It also functions as an antioxidant which is important in its clinical effects. It is naturally present in small amounts in a wide variety of foods but is particularly high in organ meats such as heart, liver and kidney, as well as beef, soy oil, sardines, mackerel and peanuts. To put dietary CoQ10 intake into perspective, one pound of sardines, two pounds of beef, or two and one half pounds of peanuts, provide 30mg of CoQ10. CoQ10 is also synthesized in all tissues and in healthy individuals normal levels are maintained both by CoQ10 intake and by the body's synthesis of CoQ10. It has no known toxicity or side effects.

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.

The dosage of CoQ10 used in clinical trials has evolved over the past 20 years. Initially, doses as small as 30-45mg per day were associated with measurable clinical responses in patients with heart failure. Additional studies have used higher doses with improved clinical response, again in patients with heart failure. Some patients attain good blood levels of CoQ10 on 100mg per day while others require two or three times this amount to attain the same blood level. All CoQ10 available today in the United States is manufactured in Japan and is distributed by a number of companies who place the CoQ10 either in pressed tablets, powder-filled capsules, or oil-based gelcaps. CoQ10 is fat-soluble and absorption is significantly improved when it is chewed with a fat-containing food. However, there is a new form of CoQ10 that will a greater response at a lower dose (see below).

There is no information on the use of CoQ10 for prevention of illness. This is an extremely important question which, to date, has not been answered.

The largest Japanese producer of CoQ10 has patented a novel form of coenzyme Q10 that increases human blood levels up to 8-times more efficiently than expensive CoQ10 products offered by commercial companies.

Coenzyme Q10 exists in both ubiquinol and ubiquinone forms, but they have very different roles to play in the body. For the first time, a stabilized ubiquinol form of CoQ10 is available in capsule form. When compared to conventional (ubiquinone) CoQ10 supplements, the benefits of ubiquinol are enormously superior.

For example, a recent peer-reviewed study measured the absorption in humans supplementing with 150 mg and 300 mg of this new ubiquinol form of coenzyme Q10. Far lower doses of ubiquinol produce about the same blood (plasma) levels compared with much higher doses of ubiquinone. In this study it takes 8-times more ubiquinone to increase CoQ10 blood levels to what can be achieved with much lower doses of ubiquinol.

What may also make this novel form of CoQ10 so much more effective than CoQ10 supplements on the market today is its ability to remain biologically active in the body much longer. In a study on aged rats, blood concentrations of this new ubiquinol CoQ10 was 3.75-fold greater after eight hours compared to the same amount of conventional coenzyme Q10. [Yan J, Fujii K, et al. Exp Gerontol. 2006 Feb;41(2):130-40]