Coenzyme Q10 belongs to a family of compounds known as ubiquinones. All animals, including humans, can synthesize ubiquinones, so coenzyme Q10 cannot be considered a vitamin (1). The name ubiquinone refers to the ubiquitous presence of these compounds in living organisms and their chemical structure, which contains a functional group known as a benzoquinone. Ubiquinones are fat-soluble molecules with anywhere from 1 to 12 isoprene (5-carbon) units. The ubiquinone found in humans, ubidecaquinone or coenzyme Q10, has a "tail" of 10 isoprene units (a total of 50 carbons) attached to its benzoquinone "head" (diagram) (2).
FUNCTION
Coenzyme Q is highly soluble in lipids (fats) and is found in virtually all cell membranes, as well as lipoproteins (2). The ability of the benzoquinone head group of coenzyme Q to accept and donate electrons is a critical feature in its physiological functions. Coenzyme Q can exist in three oxidation states (diagram): 1) the fully reduced ubiquinol form (CoQH2), 2) the radical semiquinone intermediate (CoQH·), and 3) the fully oxidized ubiquinone form (CoQ).
Mitochondrial ATP synthesis
The conversion of energy from carbohydrates and fats to adenosine triposphate (ATP), the form of energy used by cells, requires the presence of coenzyme Q in the inner mitochondrial membrane. As part of the mitochondrial electron transport chain, coenzyme Q accepts electrons from reducing equivalents generated during fatty acid and glucose metabolism and transfers them to electron acceptors. At the same time, coenzyme Q transfers protons outside the inner mitochondrial membrane, creating a proton gradient across that membrane. The energy released when the protons flow back into the mitochondrial interior is used to form ATP (2). 
Lysosomal function
Lysosomes are organelles within cells that are specialized for the digestion of cellular debris. The digestive enzymes within lysosomes function optimally at an acid pH, meaning they require a permanent supply of protons. The lysosomal membranes that separate those digestive enzymes from the rest of the cell contain relatively high concentrations of coenzyme Q. Recent research suggests that coenzyme Q plays an important role in the transport of protons across lysosomal membranes to maintain the optimal pH for cellular recycling (2, 3). 
Antioxidant functions
In its reduced form, CoQH2 is an effective fat-soluble antioxidant. The presence of a significant amount of CoQH2 in cell membranes, along with enzymes that are capable of reducing oxidized CoQ back to CoQH2, supports the idea that CoQH2 is an important cellular antioxidant (2). CoQH2 has been found to inhibit lipid peroxidation when cell membranes and low-density lipoproteins (LDL) are exposed to oxidizing conditions outside the body (ex vivo). When LDL is oxidized ex vivo, CoQH2 is the first antioxidant consumed. Moreover, the formation of oxidized lipids and the consumption of a-tocopherol (vitamin E) are suppressed while CoQH2 is present (4). In isolated mitochondria, coenzyme Q can protect membrane proteins and DNA from oxidative damage that accompanies lipid peroxidation (1). In addition to neutralizing free radicals directly, CoQH2 is capable of regenerating a-tocopherol. 
Nutrient Interactions 
Vitamin E: Alpha-tocopherol and coenzyme Q are the principal fat-soluble antioxidants in membranes and lipoproteins. When alpha-tocopherol (a-TOH) neutralizes a free radical, such as a lipid hydroperoxyl radical (LOO·), it becomes oxidized itself, forming the a-tocopheroxyl radical (a-TO·), which can promote the oxidation of lipoproteins under certain conditions in the test tube. When the reduced form of coenzyme Q (CoQH2) reacts with a-TO·, a-TOH is regenerated and the semiquinone radical (CoQH·) is formed. It is possible for CoQH· to react with oxygen (O2) to produce superoxide (O2·-), which is a much less oxidizing radical than LOO·. However, CoQH· can also reduce a-TO· back to a-TOH, resulting in the formation of fully oxidized coenzyme Q (CoQ), which does not react with O2 to form O2·- (See Reaction Scheme) (4, 5).
Vitamin B6: The first step in coenzyme Q10 biosynthesis (the conversion of tyrosine to 4-hydroxyphenylpyruvic acid) requires vitamin B6 in the form of pyridoxal 5'-phospate. Thus, adequate vitamin B6 is essential for coenzyme Q biosynthesis. A pilot study in 29 patients and healthy volunteers found significant positive correlations between blood levels of coenzyme Q10 and measures of vitamin B6 nutritional status (6). However, further research is required to determine the clinical significance of this association.
SOURCES
Biosynthesis
Coenzyme Q10 is synthesized in most human tissues. The biosynthesis of coenzyme Q10 involves three major steps: 1) synthesis of the benzoquinone structure from the amino acids, tyrosine or phenylalanine, 2) synthesis of the isoprene side chain from acetyl-coenzyme A (CoA) via the mevalonate pathway, and 3) the joining or condensation of these two structures. The enzyme hydroxymethylglutaryl (HMG)-CoA reductase plays a critical role in the regulation of coenzyme Q10 synthesis as well as the regulation of cholesterol synthesis (1, 7).
Food Sources
Based on food frequency studies the average dietary intake of coenzyme Q10 in Denmark was estimated to be 3-5 mg/d (7, 8). Most people probably have a dietary intake of less than 10 mg/d of coenzyme Q10. Rich sources of dietary coenzyme Q10 include mainly meat, poultry, and fish. Other relatively rich sources include soybean and canola oils, and nuts. Fruits, vegetables, eggs, and dairy products are moderate sources of coenzyme Q10. Approximately 14-32% of coenzyme Q10 was lost during frying, but the coenzyme Q10 content of vegetables and eggs did not change when boiled. Some relatively rich dietary sources and their coenzyme Q10 content in milligrams (mg) are listed in the table below (9-11).

*A 3-ounce serving of meat or fish is about the size of a deck of cards.

Supplements

CoQ10's key role is in producing adenosine triphosphate (ATP), needed for energy production in every cell of the body. 

Coenzyme Q10 is available without a prescription as a dietary supplement in the U.S. Supplemental doses for adults range from 30-60 mg/d, although this is considerably higher than normal dietary coenzyme Q10 intake. Therapeutic doses for adults generally range from 100-300 mg/d, although doses as high as 1200 mg/d have been used to treat early Parkinson's disease under medical supervision (12). Absorption decreases as the dose increases, and is likely less than 10% in humans. Coenzyme Q10 is fat-soluble and is best absorbed with fats in a meal. Doses higher than 100 mg/d are generally divided into two or three doses throughout the day (8, 13). 
Does oral coenzyme Q10 supplementation increase tissue levels? Oral supplementation with coenzyme Q10 is known to increase plasma and lipoprotein concentrations of coenzyme Q10 in humans (2, 14). However, it is not clear whether oral supplementation increases coenzyme Q10 concentrations in other tissues of individuals with normal endogenous coenzyme Q10 synthesis. Oral coenzyme Q10 supplementation of young healthy animals has not generally resulted in increased tissue concentrations, other than in the liver, spleen, and blood vessels (15, 16). Supplementation of healthy men with 120 mg/d for 3 weeks did not increase muscle concentrations of coenzyme Q10 (17). However, supplementation may increase coenzyme Q10 levels in tissues that are deficient. For example, oral supplementation of aged rats increased brain coenzyme Q10 concentrations (18), and a study of 24 older adults supplemented with 300 mg/d of coenzyme Q10 or placebo for at least 7 days prior to cardiac surgery found that the coenzyme Q10 content of atrial tissue was significantly increased in those taking coenzyme Q10, especially in those over 70 years of age (19). Clearly, this is an area of research that requires further investigation.
DEFICIENCY
No coenzyme Q10 deficiency symptoms have been reported in the general population, so it is generally assumed that normal biosynthesis and a varied diet provides sufficient coenzyme Q10 for healthy individuals (7). It has been estimated that dietary consumption contributes about 25% of plasma coenzyme Q10, but there are currently no specific dietary intake recommendations for coenzyme Q10 from the Food and Nutrition Board or other agencies (8). The extent to which dietary consumption contributes to tissue coenzyme Q levels is not clear. 
Genetic defects of coenzyme Q10 biosynthesis appear to be quite rare, since only four cases have been reported in the medical literature. Coenzyme Q10 levels have been found to decline gradually with age in a number of different tissues (1, 20), but it is unclear whether this age-associated decline constitutes a deficiency (see Disease Prevention). Decreased plasma levels of coenzyme Q10 have been observed in individuals with diabetes, cancer, and congestive heart failure (see Disease Treatment). Lipid lowering medications (statins) that inhibit the activity of HMG-CoA reductase, a critical enzyme in cholesterol and coenzyme Q10 synthesis, have been found to decrease plasma coenzyme Q10 levels (see Drug Interactions).
DISEASE PREVENTION
Aging
According to the free radical and mitochondrial theories of aging, oxidative damage of cell structures by reactive oxygen species (ROS) plays an important role in the functional declines that accompany aging (21). ROS are generated by mitochondria as a byproduct of ATP production. If not neutralized by antioxidants, ROS may damage mitochondria over time, causing them to function less efficiently and to generate more damaging ROS in a self-perpetuating cycle. Coenzyme Q10 plays an important role in mitochondrial ATP synthesis and functions as an antioxidant in mitochondrial membranes. Moreover, tissue levels of coenzyme Q10 have been reported to decline with age (20). One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle. It has been proposed that age-associated declines in tissue coenzyme Q10 levels may play a role in this decline (22). Although one study in the 1970's found that weekly coenzyme Q10 injections increased the lifespan of mice, those results have not been replicated. In more recent studies, lifelong dietary supplementation with coenzyme Q10 did not increase the life spans of rats or mice (15). Presently, there is no scientific evidence that coenzyme Q10 supplementation prolongs life or prevents age-related functional declines in humans. 
Cardiovascular diseases
Oxidative modification of low-density lipoproteins (LDL) in artery walls is thought to represent an early event leading to the development of atherosclerosis. Reduced coenzyme Q10 (CoQH2) inhibits the oxidation of LDL in the test tube (in vitro) and works together with a-tocopherol (a-TOH) to inhibit LDL oxidation by reducing the a-tocopheroxyl radical (a-TO·) back to a-TOH. In the absence of a coantioxidant such as CoQH2 (or vitamin C), a-TOH can, under certain conditions, promote the oxidation of LDL in vitro (4). Supplementation with coenzyme Q10 increases the concentration of CoQH2 in human LDL (14). Studies in apolipoprotein E-deficient mice, an animal model of atherosclerosis, found that coenzyme Q10 supplementation significantly inhibited the formation of atherosclerotic lesions (23). Interestingly, cosupplementation of these mice with a-tocopherol and coenzyme Q10 was more effective in inhibiting atherosclerosis than supplementation with either a-tocopherol or coenzyme Q10 alone (24). Another important step in the development of atherosclerosis is the recruitment of immune cells known as monocytes into the blood vessel walls. This recruitment is dependent in part on monocyte expression of cell adhesion molecules (integrins). Supplementation of 10 healthy men and women with 200 mg/d of coenzyme Q10 for 10 weeks resulted in significant decreases in monocyte expression of integrins, suggesting another potential mechanism for the inhibition of atherosclerosis by coenzyme Q10 (25). Although coenzyme Q10 supplementation shows promise as an inhibitor of LDL oxidation and atherosclerosis, more research is needed to determine whether coenzyme Q10 supplementation can inhibit the development of atherosclerosis in humans.
DISEASE TREATMENT
Mitochondrial encephaloymopathies
Mitochondrial encephalomyopathies represent a diverse group of genetic disorders resulting from numerous inherited abnormalities in the function of the mitochondrial electron transport chain. Coenzyme Q10 supplementation has resulted in clinical and metabolic improvement in some patients with various types of mitochondrial encephalomyopathies (26). Neuromuscular and widespread tissue coenzyme Q10 deficiencies have been found in a very small subpopulation of individuals with mitochondrial encephalomyopathies (27, 28). In those rare individuals with genetic defects in coenzyme Q10 biosynthesis, coenzyme Q10 supplementation has resulted in substantial improvement (29). 
Cardiovascular diseases 
Congestive heart failure: Impairment of the heart's ability to pump enough blood for all of the body's needs is known as congestive heart failure. In coronary artery disease, the accumulation of atherosclerotic plaque in the coronary arteries may prevent parts of the heart muscle from getting adequate circulation, ultimately resulting in damage and impaired pumping ability. Myocardial infarction (MI) may also damage the heart muscle, resulting in the development of heart failure. Because physical exercise increases the demand on the weakened heart, measures of exercise tolerance are frequently used to monitor the severity of heart failure. Echocardiography is also used to determine the left ventricular ejection fraction, an objective measure of the heart's pumping ability (30). The finding that myocardial coenzyme Q10 levels were lower in patients with more severe heart failure than in those with milder heart failure led to a number of clinical trials of coenzyme Q10 supplementation in heart failure patients (31). A number of small intervention trials have demonstrated improvement in some measure of cardiac function when congestive heart failure patients were supplemented with 100-200 mg of coenzyme Q10 daily for 1-3 months in addition to conventional medical therapy (32). However, two of the most recent placebo-controlled trials found that the addition of 100-200 mg/d of oral coenzyme Q10 supplementation to conventional medical therapy did not result in significant improvements in left ventricular ejection fraction or exercise performance in heart failure patients (33, 34). Although there is some evidence that coenzyme Q10 supplementation may be of benefit, large well-designed intervention trials are needed to determine whether coenzyme Q10 supplementation has value as an adjunct to conventional medical therapy in the treatment of congestive heart failure. 
Myocardial infarction and cardiac surgery: The heart muscle may become oxygen-deprived (ischemic) as the result of myocardial infarction (MI) or during cardiac surgery. Increased generation of ROS when the heart muscle's oxygen supply is restored (reperfusion) is thought to be an important contributor to myocardial damage occurring during ischemia-reperfusion. Pretreatment of animals with coenzyme Q10 has been found to decrease myocardial damage due to ischemia-reperfusion (35, 36). Another potential source of ischemia-reperfusion injury is aortic clamping during some types of cardiac surgery, such as coronary artery bypass graft (CABG) surgery. Three out of 4 placebo-controlled trials found that coenzyme Q10 pretreatment (60-300 mg/d 7-14 days prior to surgery) provided some benefit in short-term outcome measures after CABG surgery (19, 37). In the placebo-controlled trial that did not find preoperative coenzyme Q10 supplementation to be of benefit, patients were treated with 600 mg of coenzyme Q10 twelve hours prior to surgery (38), suggesting that preoperative coenzyme Q10 treatment may need to commence at least one week prior to CABG surgery in order to realize any benefit. Although the results are promising, these trials have included relatively few people and have only examined outcomes shortly after CABG surgery. 
Angina pectoris: Myocardial ischemia may also lead to chest pain known as angina pectoris. People with angina pectoris often experience symptoms when the demand for oxygen exceeds the capacity of the coronary circulation to deliver it to the heart muscle, e.g., during exercise. Five small placebo-controlled studies have examined the effects of oral coenzyme Q10 supplementation (60-600 mg/d) in addition to conventional medical therapy in patients with chronic stable angina (32). In most of the studies, coenzyme Q10 supplementation improved exercise tolerance and reduced or delayed electorcardiographic changes associated with myocardial ischemia compared to placebo. However, only two of the studies found that symptom frequency and nitroglycerin consumption decreased significantly with coenzyme Q10 supplementation. Presently, there is only limited evidence suggesting that coenzyme Q10 supplementation would be a useful adjunct to conventional angina therapy. 
Hypertension: The results of several small, uncontrolled studies in humans suggest that coenzyme Q10 supplementation could be beneficial in the treatment of hypertension (37). More recently, two short-term placebo-controlled trials found that coenzyme Q10 supplementation resulted in moderate blood pressure decreases in hypertensive individuals. The addition of 120 mg/d of coenzyme Q10 to conventional medical therapy for 8 weeks in patients with hypertension and coronary artery disease decreased systolic blood pressure by an average of 12 mm Hg and diastolic blood pressure by an average of 6 mm Hg compared to a placebo containing B-complex vitamins (39). In patients with isolated systolic hypertension, supplementation with 120 mg/d of coenzyme Q10 and 300 IU/day of vitamin E for 12 weeks resulted in an average decrease of 17 mm Hg in systolic blood pressure compared with 300 IU/day of vitamin E alone (40). Further research is needed to determine whether coenzyme Q10 supplementation can provide significant long-term benefit in the treatment of hypertension.
Vascular endothelial function (blood vessel dilation): Normal function of the inner lining of blood vessels, known as the vascular endothelium, plays an important role in preventing cardiovascular diseases (41). Atherosclerosis impairs vascular endothelial function, compromising the ability of blood vessels to relax (vasodilate). Endothelium-dependent vasodilation is known to be impaired in individuals with elevated serum cholesterol levels, coronary artery disease, and diabetes. One placebo-controlled trial found that supplementation with coenzyme Q10 (200 mg/d) for 12 weeks improved endothelium-dependent vasodilation in diabetic patients with abnormal serum lipid profiles, although it did not restore vasodilation to levels seen in nondiabetic individuals (42). However, in a study of individuals with high serum cholesterol levels who were otherwise healthy, supplementation with 150 mg/d did not affect endothelium-dependent vasodilation (43). 
Diabetes mellitus 
Diabetes mellitus is a condition of increased oxidative stress and impaired energy metabolism. Plasma levels of reduced coenzyme Q10 (CoQH2) have been found to be lower in diabetic patients than healthy controls when normalized to plasma cholesterol levels (44). However, supplementation with 100 mg/d of coenzyme Q10 for 3 months neither improved glycemic (blood glucose) control nor decreased insulin requirements in Type 1 (insulin-dependent) diabetics compared to placebo (45). Similarly, 200 mg/d of coenzyme Q10 supplementation for 6 months did not improve glycemic control or serum lipid profiles in Type 2 (non-insulin dependent) diabetics (46). Since coenzyme Q10 supplementation did not interfere with glycemic control in either study, the authors of both studies concluded that coenzyme Q10 supplements could be used safely in diabetic patients as adjunct therapy for cardiovascular diseases. 
Maternally inherited diabetes mellitus and deafness (MIDD) is the result of a mutation in mitochondrial DNA, which is inherited exclusively from one's mother. Although mitochondrial diabetes accounts for less than 1% of all diabetes, there is some evidence that long-term coenzyme Q10 supplementation (150 mg/d) may improve insulin secretion and prevent progressive hearing loss in these patients (47, 48). 
Neurodegenerative diseases 
Parkinson's disease: Parkinson's disease is a degenerative neurological disorder characterized by tremors, muscular rigidity, and slow movements. It is estimated to affect approximately 1% of Americans over the age of 65. Although the causes of Parkinson's disease are not all known, decreased activity of complex I of the mitochondrial electron transport chain and increased oxidative stress in a part of the brain called the substantia nigra are thought to play a role. Coenzyme Q10 is the electron acceptor for complex I as well as an antioxidant, and decreased ratios of reduced to oxidized coenzyme Q10 have been found in platelets of individuals with Parkinson's disease (49, 50). A 16-month randomized placebo-controlled trial evaluated the safety and efficacy of 300, 600, or 1200 mg/d of coenzyme Q10 in 80 people with early Parkinson's disease (12). Coenzyme Q10 supplementation was well tolerated at all doses and associated with slower deterioration of function in Parkinson's disease patients compared to placebo. However, the difference was statistically significant only in the group taking 1200 mg/d. Although these preliminary findings are promising, they need to be confirmed in larger clinical trials before recommending the use of coenzyme Q10 in early Parkinson's disease. 
Huntington's disease: Huntington's disease is an inherited neurodegenerative disorder characterized by selective degeneration of nerve cells known as striatal spiny neurons. Symptoms, such as movement disorders and impaired cognitive function, typically develop in the fourth decade of life and progressively deteriorate over time. Animal models indicate that impaired mitochondrial function and glutamate-mediated neurotoxicity may play roles in the pathology of Huntington's disease. Coenzyme Q10 supplementation has been found to decrease brain lesion size in animal models of Huntington's disease and to decrease brain lactate levels in Huntington's disease patients (51, 52). However, feeding transgenic mice that express the Huntington's disease protein a combination of coenzyme Q10 and remacemide resulted in only transiently improved motor performance and did not prolong survival (53). Remacemide is an antagonist of the neuronal receptor that is activated by glutamate. A 30-month randomized placebo-controlled trial of coenzyme Q10 (600 mg/d), remacemide, or both in 347 patients with early Huntington's disease found that neither coenzyme Q10 nor remacemide significantly altered the decline in total functional capacity, although coenzyme Q10 supplementation (with or without remacemide) resulted in a nonsignificant 13% decrease in the decline (54). Currently, there is insufficient evidence to support a recommendation for coenzyme Q10 supplementation in early Huntington's disease.
Cancer
Interest in coenzyme Q10 as a potential therapeutic agent in cancer was stimulated by an observational study that found that individuals with lung, pancreas, and especially breast cancer were more likely to have low plasma coenzyme Q10 levels than healthy controls (55). Although a few case reports and an uncontrolled trial suggest that coenzyme Q10 supplementation may be beneficial as an adjunct to conventional therapy for breast cancer (56), the lack of controlled clinical trials makes it impossible to determine the effects, if any, of coenzyme Q10 supplementation in cancer patients.
PERFORMANCE
Athletic performance
Although coenzyme Q10 supplementation has improved exercise tolerance in some individuals with mitochondrial encephalomyopathies (see Deficiency) (26), there is little evidence that it improves athletic performance in healthy individuals. At least 7 placebo-controlled trials have examined the effects of 100-150 mg/d of coenzyme Q10 supplementation for 3-8 weeks on physical performance in trained and untrained men. Most found no significant differences between groups taking coenzyme Q10 and groups taking placebos with respect to measures of aerobic exercise performance, such as maximal oxygen consumption (VO2 max) and exercise time to exhaustion (57-61). One study found the maximal cycling workload to be slightly (4%) increased after 8 weeks of coenzyme Q10 supplementation compared to placebo, although measures of aerobic power were not increased (62). Two studies actually found significantly greater improvement in measures of anaerobic (60) and aerobic (61) exercise performance after supplementation with a placebo compared to coenzyme Q10. Studies on the effect of supplementation on physical performance in women are lacking, but there is little reason to suspect a gender difference in the response to coenzyme Q10 supplementation.
SAFETY
Toxicity
There have been no reports of significant adverse side effects with oral coenzyme Q10 supplementation at doses as high as 1200 mg/d for up to 16 months (12) and up to 600 mg/d for 30 months (54). Some people have experienced gastrointestinal symptoms, such as nausea, diarrhea, appetite suppression, heartburn, and abdominal discomfort. These adverse effects may be minimized if daily doses higher than 100 mg are divided into two or three daily doses. Because controlled safety studies in pregnant and lactating women are not available, the use of coenzyme Q10 supplements by pregnant or breastfeeding women should be avoided (13, 63).
Drug Interactions
Warfarin: Concomitant use of warfarin (Coumadin) and coenzyme Q10 supplements has been reported to decrease the anticoagulant effect of warfarin in at least 4 cases (64). An individual on warfarin should not begin taking coenzyme Q10 supplements without consulting the health care provider that is managing his or her anticoagulant therapy. If warfarin and coenzyme Q10 are to be used concomitantly, blood tests to assess clotting time (prothrombin time; PT/INR) should be monitored frequently, especially in the first two weeks. 
HMG-CoA reductase inhibitors (statins): HMG-CoA reductase is an enzyme that plays a critical role in the regulation of cholesterol synthesis as well as coenzyme Q10 synthesis, although it is now recognized that there are additional rate-limiting steps in the biosynthesis of cholesterol and coenzyme Q10. HMG-CoA reductase inhibitors, also known as statins, are widely used cholesterol-lowering medications that may also decrease the endogenous synthesis of coenzyme Q10. A number of studies have observed decreases in plasma or serum coenzyme Q10 levels in people on HMG-CoA reductase inhibitor therapy, especially those taking simvastatin (Zocor) (65-67). In contrast to most earlier studies, a randomized cross-over trial in healthy individuals found no significant changes in serum coenzyme Q10 levels after 4 weeks of pravastatin (Pravachol) and atorvastatin (Lipitor) therapy despite significant decreases in total and LDL-cholesterol levels on both medications. In rats, high doses of lovastatin for 4 weeks decreased blood, liver, and heart concentrations of coenzyme Q (68). However, it is not clear whether HMG-CoA reductase inhibitor therapy decreases tissue coenzyme Q10 concentrations in humans. Although simvastatin treatment for 6 months lowered serum coenzyme Q10 levels in patients with high serum cholesterol, skeletal muscle concentrations of coenzyme Q10 were not decreased compared to baseline or healthy controls (69). At present, more controlled research is needed to determine whether coenzyme Q10 supplementation is beneficial for those taking HMG-CoA reductase inhibitors.
SUMMARY
Coenzyme Q10 is a fat-soluble compound primarily synthesized by the body and also consumed in the diet.
Coenzyme Q10 is required for mitochondrial ATP synthesis and functions as an antioxidant in cell membranes and lipoproteins. More information
Endogenous synthesis and dietary intake appear to provide sufficient coenzyme Q10 to prevent deficiency in healthy people. More information
Oral supplementation of coenzyme Q10 increases plasma, lipoprotein, and blood vessel levels, but it is unclear whether tissue coenzyme Q10 levels are increased, especially in healthy individuals. More information
Coenzyme Q10 supplementation has resulted in clinical and metabolic improvement in some patients with hereditary mitochondrial disorders. More information
Although coenzyme Q10 supplementation may be a useful adjunct to conventional medical therapy for congestive heart failure, additional research is needed. More information
Roles for coenzyme Q10 supplementation in other cardiovascular diseases, neurodegenerative diseases, cancer, and diabetes require further research. More information
Coenzyme Q10 supplementation does not appear to improve athletic performance. More information
Although coenzyme Q10 supplements are relatively safe, they may decrease the anticoagulant efficacy of warfarin (Coumadin). More information
Presently, it is unclear whether individuals taking cholesterol-lowering medications, known as HMG-CoA reductase inhibitors (statins), would benefit from coenzyme Q10 supplementation. More information

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