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Coenzyme Q10
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[What is CoQ10? | Should I Take CoQ10? | What is the Dosage?]
[CoQ10 and Heart Failure | CoQ10 Deficiency]
[CoQ10 and Heart Disease | References]

 

Ubiquinol - NEW


Published with the exclusive permission of Peter H. Langsjoen, M.D.

What is CoenzymeQ10, otherwise known as CoQ10?
CoenzymeQ10 is a fat-soluble vitamin-like substance present in every cell of the body and CoQ10 serves as a coenzyme for several of the key enzymatic steps in the production of energy within the cell. Coenzyme Q10 also functions as an antioxidant which is important in its clinical effects. CoenzymeQ10 is naturally present in small amounts in a wide variety of foods but CoQ10 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 30 mg of CoQ10. Coenzyme Q10 is also synthesized in all tissues. In healthy individuals normal CoenzymeQ10 levels are maintained both by CoQ10 intake and by the body's synthesis of CoQ10. CoenzymeQ10 has no known toxicity or side effects.

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Should I take Coenzyme Q10 (CoQ10)?
This Coenzyme Q10 question can be asked in two ways. First, should a reasonably healthy person take CoQ10 to stay healthy or to become more robust? At present I do not believe anyone knows the answer to this question. Second, should a person with an illness such as congestive heart failure take Coenzyme Q10 (CoQ10)? As with any change in nutrition, diet, medication, or even activity, CoQ10 should be discussed with one's physician. As improvement in heart function occurs, a patient should have regular medical follow up with particular attention to concomitant drug therapy. The attached references will provide detailed information on the clinical use of CoenzymeQ10 (CoQ10) and can be obtained from any good medical library.

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What is the dosage of CoenzymeQ10?
The dosage of Coenzyme Q10 (CoQ10) used in clinical trials has evolved over the past 20 years. Initially, CoenzymeQ10 doses as small as 30 to 45 mg per day were associated with measurable clinical responses in patients with heart failure. More recent studies have used higher Coenzyme Q10 doses with improved clinical response, again in patients with heart failure. Most studies with CoQ10 involve the measurement of the level of Coenzyme Q10 (CoQ10) in blood. CoQ10 shows a moderate variability in its absorption, with some patients attaining good blood levels of CoQ10 on 100 mg per day while others require two or three times this amount of CoenzymeQ10 to attain the same blood level. All CoenzymeQ10 available today in the United States is manufactured in Japan and Coenzyme Q10 is distributed by a number of companies who place the CoQ10 either in pressed tablets, powder-filled capsules, or oil-based gelcaps. Coenzyme Q10 is fat-soluble and CoenzymeQ10 absorption is significantly improved when CoQ10 is chewed with a fat-containing food. Published data on the dosage of CoenzymeQ10 relates almost exclusively to the treatment of disease states. There is no information on the use of Coenzyme Q10 for prevention of illness. This is an extremely important question which, to date, does not have an answer.

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If Coenzyme Q10 (CoQ10) is so effective in the treatment of heart failure, why is Coenzyme Q10 not more generally used in this country?
The answer to this question is found in the fields of politics and marketing and not in the fields of science or medicine. The controversy surrounding CocoenzymeQ10 likewise is political and economic as the previous 30 years of research on Coenzyme Q10 have been remarkably consistent and free of major controversy. Although it is not the first time that a fundamental and clinically important discovery has come about without the backing of a pharmaceutical company, it is the first such discovery to so radically alter how we as physicians must view disease. While the pharmaceutical industry does a good job at physician and patient education on their new products, the distributors of Coenzyme Q10 are not as effective at this. This education is very costly and can only be done with the reasonable expectation of patent protected profit. CoenzymeQ10 is not patentable. The discovery of CoQ10 was based primarily on support from the National Heart Institute of NIH (National Institute of Health) at the Institute for Enzyme Research, University of Wisconsin.

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Coenzyme Q10 deficiency
Normal blood and tissue levels of CoenzymeQ10 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. Coenzyme Q10 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 CoenzymeQ10 dietary intake is presumed in chronic malnutrition and cachexia12. The relative contribution of Coenzyme Q10 biosynthesis versus dietary CoQ10 is under investigation. Karl Folkers takes the position that the dominant source of CoQ10 in man is biosynthesis. This complex, 17 step process, requiring at least seven vitamins (vitamin B2 - riboflavin, vitamin B3 - niacinamide, vitamin B6, folic acid, vitamin B12, vitamin C, and pantothenic acid) and several trace elements, is, by its nature, highly vulnerable. Karl Folkers argues that suboptimal nutrient intake in man is almost universal and that there is subsequent secondary impairment in Coenzyme Q10 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 CoenzymeQ10 deficiency "iceberg". HMG-CoA reductase inhibitors used to treat elevated blood cholesterol levels by blocking cholesterol biosynthesis also block Coenzyme Q10 biosynthesis13. The resulting lowering of blood CoQ10 level is due to the partially shared biosynthetic pathway of CoQ10 and cholesterol. In patients with heart failure, CoenzymeQ10 deficiency is more than a laboratory observation. CoenzymeQ10 deficiency has a significant harmful effect which can be negated by oral CoQ10 supplementation14. Increased body consumption of Coenzyme Q10 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 CoenzymeQ10, impaired CoQ10 biosynthesis, and excessive utilization of CoQ10) are operable to varying degrees in most cases of observed CoQ10 deficiency.

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Treatment of heart disease with Coenzyme Q10
CoenzymeQ10 is known to be highly concentrated in heart muscle cells due to the high energy requirements of this cell type. For the past 14 years, the great bulk of clinical work with CoQ10 has focused on heart disease. Specifically, congestive heart failure (from a wide variety of causes) has been strongly correlated with significantly low blood and tissue levels of Coenzyme Q1015.

The severity of heart failure correlates with the severity of CoenzymeQ10 deficiency16. This Coenzyme Q10 deficiency may well be a primary etiologic factor in some types of heart muscle dysfunction while in others it may be a secondary phenomenon. Whether primary, secondary or both, this deficiency of CoQ10 appears to be a major treatable factor in the otherwise inexorable progression of heart failure.

Pioneering trials of CoenzymeQ10 in heart failure involved primarily patients with dilated weak heart muscle of unknown cause (idiopathic dilated cardiomyopathy). CoQ10 was added to standard treatments for heart failure such as fluid pills (diuretics), digitalis preparations (Lanoxin), and ACE inhibitors. Several trials involved the comparison between supplemental CoQ10 and placebo on heart function as measured by echocardiography. Coenzyme Q10 was given orally in divided doses as a dry tablet chewed with a fat containing food or an oil based CoenzymeQ10 gel cap swallowed at mealtime. Heart function, as indicated by the fraction of blood pumped out of the heart with each beat (the ejection fraction), showed a gradual and sustained improvement in tempo with a gradual and sustained improvement in patients' symptoms of fatigue, dyspnea, chest pain, and palpitations. The degree of improvement was occasionally dramatic with some patients developing a normal heart size and function on CoenzymeQ10 alone. Most of these dramatic cases were patients who began CoQ10 shortly after the onset of congestive heart failure. Patients with more established disease frequently showed clear improvement but not a return to normal heart size and function.

Internationally, there have been at least nine placebo controlled studies on the treatment of heart disease with CoenzymeQ10: two in Japan, two in the United States, two in Italy, two in Germany, and one in Sweden17,18,19,20,21,22,23,24,25. All nine of these Coenzyme Q10 studies have confirmed the effectiveness of CoenzymeQ10 as well as CoQ10 remarkable safety. There have now been eight international symposia on the biomedical and clinical aspects of Coenzyme Q10 (from 1976 through 199326,27,28,29,30,31,32,33). These eight CoenzymeQ10 symposia comprised over 300 papers presented by approximately 200 different physicians and scientists from 18 different countries. The majority of these Coenzyme Q10 scientific papers were Japanese (34%), with American (26%), Italian (20%) and the remaining 20% from Sweden, Denmark, Germany, United Kingdom, Belgium, Australia, Austria, France, India, Korea, Netherlands, Poland, Switzerland, USSR, and Finland. The majority of the CoenzymeQ10 clinical studies concerned the treatment of heart disease and were remarkably consistent in their conclusions: that treatment with CoQ10 significantly improved heart muscle function while producing no adverse effects or drug interactions.

It should be mentioned that a slight decrease in the effectiveness of the blood thinner, coumadin, was noted in a case by a Norwegian clinician34. This possible drug - Coenzyme Q10 interaction has not been observed by other investigators even when using much higher doses of CoQ10 for up to seven years and involving 25 patients treated with coumadin concomitantly with CoQ10 (this is still, as of this date, unpublished data).

The efficacy and safety of CoenzymeQ10 in the treatment of congestive heart failure, whether related to primary cardiomyopathies or secondary forms of heart failure, appears to be well established35,36,37,38,39,40,41,42. The largest Coenzyme Q10 study to date is the Italian multicenter trial, by Baggio et al., involving 2664 patients with heart failure43. The most recent work in heart failure examined the effect of CoQ10 on diastolic dysfunction, one of the earliest identifiable signs of myocardial failure that is often found in mitral valve prolapse, hypertensive heart disease and certain fatigue syndromes44,45. Diastolic dysfunction might be considered the common denominator and a basic cause of symptoms in these three diagnostic groups of disease. Diastole is the filling phase of the cardiac cycle. Diastolic function has a larger cellular energy requirement than the systolic contraction and, therefore, the process of diastolic relaxation is more highly energy dependent and thus more highly dependent on CoQ10. In simpler terms, it takes more energy to fill the heart than to empty it. Diastolic dysfunction is a stiffening of the heart muscle which interferes with the heart's ability to function as an effective pump. It is seen early in the course of many common cardiac disorders and is demonstrable by echocardiography. This stiffening returns towards normal with supplemental CoQ10 in tempo with clinical improvement. It is important to note that in all of the above clinical trials, Coenzyme Q10 was used in addition to traditional medical treatments, not to their exclusion.

In one study by Langsjoen et al46, of 109 patients with essential hypertension, 51% were able to stop between one and three antihypertensive drugs at an average of 4.4 months after starting CoenzymeQ10 treatment while the overall New York Heart Association (NYHA) functional class improved significantly from a mean of 2.40 to 1.36. Hypertension is reduced when diastolic function improves. In another Coenzyme Q10 study39, there was a gradual and sustained decrease in dosage or discontinuation of concomitant cardiovascular drug therapy: Of 424 patients with cardiovascular disease, 43% were able to stop between one and three cardiovascular drugs with CoQ10 therapy. The authors conclude that the vitamin-like substance, Coenzyme Q10, "may be ushering in the new era of cellular/biochemical treatment of disease, complementing and extending the systems-oriented, macro and microscopic approach that has served us well to this point".

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