1. CoQ helps drive the mitochondrial energy production vital to all body functions. The functioning of all organs depends on each cell having adequate levels of CoQ to provide life-sustaining energy.

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2.  A year later, Dr. Karl Folkers and his coworkers at Merck & Co., Inc., had succeeded in establishing its structure. The structure of the Coenzyme Q molecule is that of a quinone with an isoprenoid side-chain, the number of isoprene units in the side chain varies with each species of animal or plant. Humans contain Coenzyme Q10, which has 10 isoprene units.
Coenzyme Q is one of a family of brightly colored substances (quinones) that are widely distributed in nature because they are essential for generating energy in living things that use oxygen. The name ubiquinone was derived from the ubiquitous nature of these quinones. Coenzyme Q is a true coenzyme. A coenzyme is a substance that is necessary for, or enhances, the function of an enzyme. Bioenergy enzymes are necessary for a cell to generate energy from its food substances. The cell then uses this energy for its life processes. Coenzyme Q is an essential coenzyme for several of these bioenergy enzymes
In cells, the process of generating energy takes place within the mitochondria, which are the energy-producing structures. In the mitochondria, molecules of coenzyme Q continually shuttle between bioenergy enzymes, transporting protons and electrons from one bioenergy enzyme to another. Cells in the body must continuously generate energy to support their function, and this process depends on each cell having adequate amounts of CoQ with which to generate this energy.
with such a fundamental role in energy production, it would be expected that deficiencies of CoQ would be detrimental to the bodies ability to function properly. Since CoQ is indispensably involved in the complex mechanism of respiration, including ATP formation, it is evident that a significant deficiency of CoQ in cellular respiration may have some detrimental effect upon the life processes dependent on energy, including mechanical, electrical, transport work, and biosynthesis. This deficiency could be reflected by one or more disease states, depending on the location and degree of the cellular deficiency of CoQ. Therefore, it is not surprising that CoQ deficiency has been linked to such diverse conditions as heart disease, heart failure, hypertension, muscular dystrophy, cancer, physical performance and athletics, diabetes, obesity, periodontal disease, aging, immune function, cellular antioxidant protection, and brain function.

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3.   However, it is not clear how much exogenous CoQ contributes to maintain the body stores of CoQ10. Since CoQ is found in many foods, and is biosynthesized within the human body, the question of whether a dietary source of CoQ is essential has been considered. CoQ is found in almost all foodstuffs, albeit in small quantities. Wheat germ and rice bran are fair sources of CoQ, as is soy and some other beans. Vegetables are fairly low in CoQ, although spinach and broccoli are good sources. The major sources of CoQ in the human diet, however, are meats, fish, and vegetable oils. Soybean, sesame, and rapeseed oils are high in CoQ10, while corn oil is high in CoQ9. The average person consumes approximately 5 milligrams a day of CoQ, a level insufficient to obtain sufficient CoQ for their needs. The remainder of the CoQ10 needed by the body is synthesized in the cells, especially within the liver.
The production of CoQ10 in the body is a complex process. At least 15 different reactions are necessary (each catalyzed by an enzyme), as well as a number of cofactor substances including vitamins B3, B5, B6, B12, C, and folate.

4.  In spite of its complex manufacture, most CoQ10 is made within the body. There is good evidence, however, that dietary CoQ contributes significantly to the endogenous body-pool of CoQ10. This has been shown in patients receiving total parenteral nutrition (TPN) that contains no CoQ. In these patients, who are dependent totally on endogenous CoQ10 synthesis, CoQ10 levels dropped by almost 50% within 1 week on a diet free of CoQ.

5. These levels remained depressed for the 12 weeks of the study. This represents good evidence that dietary sources are indeed a significant contributor to the body pool of CoQ10.

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5.  This paper was written to make known the clinical results published in Japan, from ten years of studying the administration of CoQ10 to cardiac patients. These 24 studies encompassed clinical data from 110 physicians in 41 medical institutions. The consensus from this decade of clinical research indicated a therapeutic benefit in about 75% of the patients having congestive heart failure. In addition, essential hypertension and angina pectoris appeared to have been improved by treatment with CoQ10. As a result of these studies, the Japanese government approved CoQ10 to treat congestive heart failure in 1974. By 1982, it was among the five most widely-used drugs in Japan. Despite a lack of interest in the US pharmaceutical industry, CoQ research began in earnest in the late 1970's with the availability of inexpensive, mass-produced CoQ10 from Japan. The vast majority of this research was conducted by independent researchers, as no US pharmaceutical company was interested in developing a non-patentable, natural compound like CoQ10, regardless of its potential.
In a 1985 review article, a total of 67 clinical studies involving some 1353 patients that had been treated for heart and blood vessel disease were presented. In these studies, CoQ10 was tested against heart muscle disease, arrhythmias, damage to the heart from drugs, high blood pressure, and stroke.

6.  In those patients with heart muscle disease, approximately 75% showed meaningful clinical improvement. In fact, a study published in 1990 showed that CoQ10 significantly improved the survival of cardiomyopathy patients compared to treatment with traditional drugs.

7. After 3 years, 24% of the patients on conventional treatment were alive, while 75% of the CoQ10 patients were alive. In addition, most patients with mild cardiomyopathy became normal on CoQ10 therapy. These studies also indicated that CoQ10 could successfully treat patients with arrhythmias, angina, ischaemic heart disease, stroke, and high blood pressure. In an animal model of cardiomyopathy, CoQ10 was found superior to digoxin, a traditional drug of choice, in attenuating disease progression.

8.  Additionally, a recently published study showed that heart failure patients who were candidates for a heart transplant, and were instead treated with CoQ10, improved significantly.

9.  All patients improved, with many requiring no conventional drugs and having no limitations on life-style.
Although CoQ10 has proven to be an effective treatment for congestive heart failure, two other nutrients have proven to be synergistic with CoQ10 in the treatment of congestive heart failure. These nutrients, carnitine and taurine, are similar to CoQ10 in being consumed in the diet, and produced by the body. Carnitine has been shown to be synergistic and complementary to CoQ in energetic metabolism, providing improvements in energy production that CoQ10 or carnitine alone are incapable of.

10.  Taurine, on the other hand, resulted in improvements in congestive heart failure that were not observed in CoQ10 treated patients, although both groups improved.

11.  These results with taurine are particularly interesting, as it has been known for some time that taurine deficiency in cats results in dilated cardiomyopathy, and cat food is now supplemented with taurine to prevent this affliction. There seems little doubt that in the case of heart failure, the utilization of CoQ10, carnitine, and taurine would be a useful and effective combination.
Beyond its well researched and approved (in Japan, Italy, Sweden, Denmark, and Canada) indication for congestive heart failure, CoQ10 is an important component in other aspects of cardiovascular health. To begin with, CoQ10 treatment reduces blood viscosity in patients with ischaemic heart disease.

12. This is something that more dangerous blood- thinning drugs are usually used for. Additionally, dietary supplementation with CoQ10 results in increased levels of CoQ10 within circulating lipoproteins, and increased resistance of human low-density lipoprotein (LDL) to the initiation of lipid peroxidation.

13.  This may have far reaching implications for the development and progression of atherosclerosis, as oxidized LDL has been directly implicated in the pathogenesis of artery blockage and coronary artery disease
The rationale for the use of CoQ10 treatment to provide protection for the heart in ischaemic cardiovascular syndromes was initially provided by animal studies which showed that CoQ10 pretreatment provided significant protection to the ischaemic myocardium (heart muscle).

14.  Based on these positive results in animal studies, human clinical trials were initiated. A number of clinical trials using CoQ10 in chronic stable angina have been reported. The results of a double-blind study comparing oral CoQ10 to placebo showed that exercise time before distress was significantly increased in the CoQ10 treated group.

15.  Another study showed that CoQ10 caused a significant reduction in cumulative exercise-induced electrocardiogram (ECG) abnormalities when compared to placebo.

16.  In this study, CoQ10 also caused a reduction in exercise-induced systolic blood pressure from placebo values. It appears that CoQ10 treatment may allow ischaemic tissue to reach higher levels of energy expenditure before the onset of symptoms or exercise-induced ECG changes. The conclusion of these studies is that CoQ10 has a favorable effect on exercise tolerance with minimal adverse reactions.
One of the serious complications of cardiac surgery is the damage caused to the myocardium. During many cardiac surgical procedures the heart tissue is rendered ischaemic, due to lack of blood flow during surgery. Subsequently, the heart is reperfused when blood flow is resumed. It is during this reperfusion phase that much of the damage to the heart muscle takes place. The consequence of this damage is usually manifested by post-reperfusion arrhythmias and low cardiac output. It has been demonstrated that both damage secondary to reperfusion and post-reperfusion arrhythmias can be inhibited by pretreatment with CoQ10.

17.  Because of its ability to protect myocardial tissue during ischaemic reperfusion, CoQ10 has been evaluated in patients undergoing cardiac surgery. CoQ10 pretreatment significantly reduced the incidence of low cardiac-output postoperatively.

18.  CoQ10 has also been evaluated in patients undergoing coronary- artery bypass surgery. It was found that the CoQ10 treated group had significantly higher cardiac output, lower requirements for post-surgical drug support, and significantly lower levels of creatine phosphokinase-MB (an indicator of heart tissue damage).

19.  Several different classes of pharmaceuticals have side-effects that include negative impacts on heart function. Some of these drugs, such as doxorubicin (a powerful anti-cancer drug) have cardiovascular effects so severe that they are strictly limited in their use by the extent to which the patients heart-function deteriorates while taking the drug. Others, like some psychotropics such as phenothiazine neuroleptics and tricyclic antidepressants, have a less severe effect on heart function; this cardiac side-effect, however, often makes their continued use dangerous or impossible. Even drugs such as beta-blockers, which are used to lower blood pressure and protect the cardiovascular system, have been shown to interfere with the production and function of CoQ10, and detrimentally effect heart function. In the case of doxorubicin, it was shown that the negative effects of this drug on heart function was due to its inhibitory effects on CoQ10-dependent enzyme systems.

20.  Subsequent to this discovery, it was shown in cancer patients treated with doxorubicin that patients pretreated with CoQ10 had a reduction in doxorubicin's cardiotoxicity.

21.  Interestingly, the use of CoQ10 with doxorubicin results in a two-fold increase of anti- tumor activity, in addition to CoQ10's ability to reduce side-effects.

22.  In fact, this combination therapy may allow larger, and thus more effective, doses of doxorubicin to be administered before cardiotoxicity becomes a problem.
Undesirable cardiac effects have often been reported from the clinical use of phenothiazine neuroleptics and tricyclic antidepressants.

23.  ECG abnormalities and arrhythmias appear to be the predominant cardiac abnormalities caused by these drugs, although heart failure and infarction are not uncommon. Furthermore, there have been increasing reports of sudden unexplained death with the administration of psychotropic drugs. CoQ10 reversed most effectively the inhibition of CoQ10-dependent enzymes caused by phenothiazines and most tricyclic antidepressants, and improved electrocardiographic changes in patients on psychotropic drugs.

23.  One of the most commonly used classes of drugs in medicine are the beta-blockers. These drugs, used for the control of high blood pressure, are generally considered to be safe and effective. These drugs, however, are known to have antagonistic activities for CoQ10-dependent enzymes.

24.  Since CoQ10 also lowers blood pressure in hypertensive patients, it would seem logical that the combination of beta-blockers with CoQ10 would be a particularly effective treatment, both for better control of blood pressure and the prevention of CoQ10 inhibition by the beta-blocker. In fact, this combined modality has been extensively reviewed, and found to be successful.

24. Of all the drugs that have been found to lower the activity of CoQ10-dependent enzymes, none is more troubling than a class of drugs known as HMG-CoA reductase inhibitors. In recent years, these drugs have gained wide clinical acceptance as safe and effective treatments for elevated cholesterol. One of the more popular drugs in this category is known as lovastatin, although there are numerous others being developed as pharmaceuticals both in the US and abroad. These drugs work by inhibiting an enzyme known as HMG-CoA reductase, and they are very effective in lowering cholesterol levels. However, this enzyme is responsible not only for the production of cholesterol, but also for the production of CoQ10. Thus, the cholesterol lowering effect of these drugs is mirrored by an equivalent lowering of CoQ10. In patients with existing heart failure, lovastatin causes increased cardiac disease.

25.  This deterioration was life-threatening for some patients. Interestingly, those patients given oral supplements of CoQ10 along with lovastatin had an improvement of cardiac function when compared to the patients given only lovastatin. There is evidence, however, that HMG-CoA reductase inhibitors cause morphological and physiological changes in cells that are not prevented by the replacement of CoQ10.

26.  Indeed, the long-term effects of this class of drugs may indeed be very negative, keeping in mind the detrimental effects of lowering the body's CoQ10 levels. Not surprisingly, known side effects of these drugs include liver dysfunction and heart failure. Ironically, supplements of CoQ10 have been shown to lower cholesterol levels by feedback inhibition of HMG-CoA reductase.

27.  Although the cholesterol lowering effect of CoQ10 awaits definitive proof in controlled studies, it may someday prove to be an interesting and healthful alternative to currently available cholesterol-lowering drugs.