To date, mutations in at least nine of these genes have been identified 1. As a result, primary coenzyme Q 10 deficiency is a clinically heterogeneous disorder that includes five major phenotypes: i severe infantile multi-systemic disease, ii encephalomyopathy, iii cerebellar ataxia , iv isolated myopathy , and v nephrotic syndrome.

Whereas most mitochondrial respiratory chain disorders are hardly amenable to treatments, oral coenzyme Q 10 supplementation has been shown to improve muscular symptoms in some yet not all patients with primary coenzyme Q 10 deficiency Neurological symptoms in patients with cerebellar ataxia are only partially relieved by coenzyme Q 10 CoQ 10 H 2 supplementation Secondary coenzyme Q 10 deficiency results from mutations or deletions in genes that are not directly related to coenzyme Q 10 biosynthetic pathway.

Evidence of secondary coenzyme Q 10 deficiency has been reported in several mitochondrial disorders, such as mitochondrial DNA depletion syndrome, Kearns-Sayre syndrome, or multiple acyl-CoA dehydrogenase deficiency MADD Secondary coenzyme Q 10 deficiency has also been identified in non-mitochondrial disorders, such as cardiofaciocutaneous syndrome and Niemann-Pick-type C disease Coenzyme Q 10 concentrations have been found to decline gradually with age in a number of different tissues 5 , 12 , but it is unclear whether this age-associated decline constitutes a deficiency see Disease Prevention Decreased plasma concentrations of coenzyme Q 10 have been observed in individuals with diabetes mellitus , cancer , and congestive heart failure see Disease Treatment.

Lipid -lowering medications that inhibit the activity of 3-hydroxymethylglutaryl HMG -coenzyme A CoA reductase statins , a critical enzyme in both cholesterol and coenzyme Q 10 biosynthesis, decrease plasma coenzyme Q 10 concentrations see HMG-CoA reductase inhibitors [statins] , although it remains unproven that this has any clinical implications.

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 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 Q 10 plays an important role in mitochondrial ATP synthesis and functions as an antioxidant in mitochondrial membranes see Biological Activities. One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle.

Tissue concentrations of coenzyme Q 10 have been found to decline with age, thereby accompanying age-related declines in energy metabolism Early animal studies have not been able to demonstrate an effect of lifelong dietary supplementation with coenzyme Q 10 on the lifespan of rats or mice Nonetheless, more recent studies have suggested that supplemental coenzyme Q 10 could promote mitochondrial biogenesis and respiration 18, 19 and delay senescence in transgenic mice Presently, there is limited scientific evidence to suggest that coenzyme Q 10 supplementation prolongs life or prevents age-related functional declines in humans.

Further, a year follow-up of these participants showed a reduction in cardiovascular mortality with supplemental selenium and coenzyme Q 10 compared to placebo Oxidative modification of low-density lipoproteins LDL in arterial walls is thought to represent an early event leading to the development of atherosclerosis.

Reduced coenzyme Q 10 CoQ 10 H 2 inhibits the oxidation of LDL in the test tube in vitro and works together with α-tocopherol α-TOH to inhibit LDL oxidation by regenerating α-TO· back to α-TOH. In the absence of a co- antioxidant , such as CoQ 10 H 2 or vitamin C, α-TO· can, under certain conditions, promote the oxidation of LDL in vitro 6.

Supplementation with coenzyme Q 10 increases the concentration of CoQ 10 H 2 in human LDL Studies in apolipoprotein E-deficient mice, an animal model of atherosclerosis, found that coenzyme Q 10 supplementation with supra- pharmacological amounts of coenzyme Q 10 inhibited lipoprotein oxidation in the blood vessel wall and the formation of atherosclerotic lesions Interestingly, co-supplementation of these mice with α-TOH and coenzyme Q 10 was more effective in inhibiting atherosclerosis than supplementation with either α-TOH or coenzyme Q 10 alone 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. Although coenzyme Q 10 supplementation shows promise as an inhibitor of LDL oxidation and atherosclerosis, more research is needed to determine whether coenzyme Q 10 supplementation can inhibit the development or progression of atherosclerosis in humans.

Inherited coenzyme Q 10 deficiencies are rare diseases that are clinically and genetically heterogeneous see Deficiency. Early treatment with pharmacological doses of coenzyme Q 10 is essential to limit irreversible organ damage in coenzyme Q 10 -responsive deficiencies 1.

It is not clear to what extent coenzyme Q 10 supplementation might have therapeutic benefit in patients with inherited secondary Q 10 deficiencies. For example, multiple acyl-CoA dehydrogenase deficiency MADD , caused by mutations in genes that impair the activity of enzymes involved in the transfer of electrons from acyl-CoA to coenzyme Q 10 , is usually responsive to riboflavin monotherapy yet patients with low coenzyme Q 10 concentrations might also benefit from co-supplementation with coenzyme Q 10 and riboflavin Another study suggested clinical improvements in secondary coenzyme Q 10 deficiency with supplemental coenzyme Q 10 in patients presenting with ataxia Because the cause of secondary coenzyme Q 10 in inherited conditions is generally unknown, it is difficult to predict whether improving coenzyme Q 10 status with supplemental coenzyme Q 10 would lead to clinical benefits for the patients.

Finally, coenzyme Q 10 deficiency can be secondary to the inhibition of HMG-CoA reductase by statin drugs see Deficiency.

The trials failed to establish a diagnosis of relative coenzyme Q 10 deficiency before the intervention started, hence limiting the conclusion of the meta-analysis.

While statin therapy may not necessary lead to a reduction in circulating coenzyme Q 10 concentrations, further research needs to examine whether secondary coenzyme Q 10 deficiency might be predisposing patients to statin-induced myalgia 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 heart disease CHD , accumulation of atherosclerotic plaque in the coronary arteries may prevent parts of the cardiac muscle from getting adequate blood supply, ultimately resulting in heart damage and impaired pumping ability.

Heart failure can also be caused by myocardial infarction , hypertension , diseases of the heart valves, cardiomyopathy , and congenital heart diseases.

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 A study of 1, heart failure patients found that low plasma coenzyme Q 10 concentration was a good biomarker of advanced heart disease A number of small intervention trials that administered supplemental coenzyme Q 10 to congestive heart failure patients have been conducted.

Pooling data from some of the trials showed an increase in serum coenzyme Q 10 concentrations three studies but no effect on left ventricular ejection fraction two studies or exercise capacity two studies The heart muscle may become oxygen-deprived ischemic as the result of myocardial infarction or during cardiac surgery.

Increased generation of reactive oxygen species ROS when the heart muscle's oxygen supply is restored reperfusion might be an important contributor to myocardial damage occurring during ischemia-reperfusion Pretreatment of animals with coenzyme Q 10 has been found to preserve myocardial function following ischemia-reperfusion injury by increasing ATP concentration, enhancing antioxidant capacity and limiting oxidative damage , regulating autophagy , and reducing cardiomyocyte apoptosis Another potential source of ischemia-reperfusion injury is aortic clamping during some types of cardiac surgery, such as coronary artery bypass graft CABG surgery.

In a small randomized controlled trial in 30 patients, oral administration of coenzyme Q 10 for 7 to 10 days before CABG surgery reduced the need for mediastinal drainage, platelet transfusion, and positive inotropic drugs e. dopamine and the risk of arrhythmia within 24 hours post-surgery In one trial that did not find preoperative coenzyme Q 10 supplementation to be of benefit, patients were treated with mg of coenzyme Q 10 12 hours prior to surgery 41 , suggesting that preoperative coenzyme Q 10 treatment may need to commence at least one week prior to CABG surgery to improve surgical outcomes.

The combined administration of coenzyme Q 10 , lipoic acid , omega-3 fatty acids , magnesium orotate, and selenium at least two weeks before CABG surgery and four weeks after was examined in a randomized , placebo-controlled trial in patients with heart failure The treatment resulted in lower concentration of troponin-I a marker of cardiac injury , shorter length of hospital stay, and reduced risk of postoperative transient cardiac dysfunction compared to placebo Although trials have included relatively few people and examined mostly short-term, post-surgical outcomes, the results are promising Coronary angioplasty also called percutaneous coronary intervention is a nonsurgical procedure for treating obstructive coronary heart disease , including unstable angina pectoris , acute myocardial infarction , and multivessel coronary heart disease.

Angioplasty involves temporarily inserting and inflating a tiny balloon into the clogged artery to help restore the blood flow to the heart.

Periprocedural myocardial injury that occurs in up to one-third of patients undergoing otherwise uncomplicated angioplasty increases the risk of morbidity and mortality at follow-up.

A prospective cohort study followed 55 patients with acute ST segment elevation myocardial infarction a type of heart attack characterized by the death of some myocardial tissue who underwent angioplasty Plasma coenzyme Q 10 concentration one month after angioplasty was positively correlated with less inflammation and oxidative stress and predicted favorable left ventricular end-systolic volume remodeling at six months One randomized controlled trial has examined the effect of coenzyme Q 10 supplementation on periprocedural myocardial injury in patients undergoing coronary angioplasty The administration of mg of coenzyme Q 10 12 hours before the angioplasty to 50 patients reduced the concentration of C-reactive protein [CRP]; a marker of inflammation within 24 hours following the procedure compared to placebo.

However, there was no difference in concentrations of two markers of myocardial injury creatine kinase and troponin-I or in the incidence of major adverse cardiac events one month after angioplasty between active treatment and placebo Additional trials are needed to examine whether coenzyme Q 10 therapy can improve clinical outcomes in patients undergoing coronary angioplasty.

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.

In most of the studies, coenzyme Q 10 supplementation improved exercise tolerance and reduced or delayed electrocardiographic changes associated with myocardial ischemia compared to placebo. However, only two of the studies found significant decreases in symptom frequency and use of nitroglycerin with coenzyme Q 10 supplementation.

Presently, there is only limited evidence suggesting that coenzyme Q 10 supplementation would be a useful adjunct to conventional angina therapy. Very few high-quality trials have examined the potential therapeutic benefit of coenzyme Q 10 supplementation in the treatment of primary hypertension In contrast, a meta-analysis that used less stringent selection criteria included 17 small trials and found evidence of a blood pressure-lowering effect of coenzyme Q 10 in patients with cardiovascular disease or metabolic disorders The effect of coenzyme Q 10 on blood pressure needs to be examined in large, well-designed clinical trials.

Endothelial dysfunction: Normally functioning vascular endothelium promotes blood vessel relaxation vasodilation when needed for example, during exercise and inhibits the formation of blood clots. Atherosclerosis is associated with impairment of vascular endothelial function, thereby compromising vasodilation and normal blood flow.

Endothelium-dependent vasodilation is impaired in individuals with elevated serum cholesterol concentrations, as well as in patients with coronary heart disease or diabetes mellitus. Evidence from larger studies is needed to further establish the effect of coenzyme Q 10 on endothelium-dependent vasodilation.

Recently published pooled analyses of these trials have given mixed results Larger studies are needed to examine the effect of coenzyme Q 10 supplementation on low-grade inflammation. Blood lipids : Elevated plasma lipoprotein a concentration is an independent risk factor for cardiovascular disease.

Other effects of coenzyme Q 10 on blood lipids have not been reported 51, 53, A therapeutic approach combining coenzyme Q 10 with other antioxidants might prove to be more effective to target co-existing metabolic disorders in individuals at risk for cardiovascular disease Diabetes mellitus is a condition of increased oxidative stress and impaired energy metabolism.

Plasma concentrations of reduced coenzyme Q 10 CoQ 10 H 2 have been found to be lower in diabetic patients than healthy controls after normalization to plasma cholesterol concentrations 56, Randomized controlled trials that examined the effect of coenzyme Q 10 supplementation found little evidence of benefits on glycemic control in patients with diabetes mellitus.

Maternally inherited diabetes mellitus-deafness syndrome MIDD is caused by a mutation in mitochondrial DNA , which is inherited exclusively from one's mother.

Of note, the pathogenesis of type 2 diabetes mellitus involves the early onset of glucose intolerance and hyperinsulinemia associated with the progressive loss of tissue responsiveness to insulin. Recent experimental studies tied insulin resistance to a decrease in coenzyme Q 10 expression and showed that supplementation with coenzyme Q 10 could restore insulin sensitivity 7.

Coenzyme Q 10 supplementation might thus be a more useful tool for the primary prevention of type 2 diabetes rather than for its management.

Parkinson's disease is a degenerative neurological disorder characterized by tremors, muscular rigidity, and slow movements.

Mitochondrial dysfunction and oxidative damage in a part of the brain called the substantia nigra may play a role in the development of the disease Decreased ratios of reduced -to- oxidized coenzyme Q 10 have been found in platelets of individuals with Parkinson's disease 61, Two recent meta-analyses of randomized, placebo-controlled trials found no evidence that coenzyme Q 10 improved motor-related symptoms or delayed the progression of the disease when compared to placebo 68, 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 be involved in the pathology of Huntington's disease.

Interestingly, co-administration of coenzyme Q 10 with remacemide an NMDA receptor antagonist , the antibiotic minocycline, or creatine led to greater improvements in most biochemical and behavioral parameters To date, only two clinical trials have examined whether coenzyme Q 10 might be efficacious in human patients with Huntington's disease.

All dosages were generally well tolerated, with gastrointestinal symptoms being the most frequently reported adverse effect. Blood concentrations of coenzyme Q 10 at the end of the study were maximized with the daily dose of 2, mg The trial was prematurely halted because it appeared unlikely to demonstrate any health benefit in supplemented patients — about one-third of participants completed the trial at the time of study termination Although coenzyme Q 10 is generally well tolerated, there is no evidence that supplementation can improve functional and cognitive symptoms in Huntington's disease patients.

Friedreich's ataxia FRDA : FRDA is an autosomal recessive neurodegenerative disease caused by mutations in the gene FXN that encodes for the mitochondrial protein , frataxin.

Frataxin is needed for the making of iron -sulfur clusters ISC. ISC-containing subunits are especially important for the mitochondrial respiratory chain and for the synthesis of heme -containing proteins Frataxin deficiency is associated with imbalances in iron-sulfur containing proteins, mitochondrial respiratory chain dysfunction and lower ATP production, and accumulation of iron in the mitochondria, which increases oxidative stress and oxidative damage to macromolecules of the respiratory chain Clinically, FRDA is a progressive disease characterized by ataxia , areflexia , speech disturbance dysarthria , sensory loss, motor dysfunction, cardiomyopathy , diabetes , and scoliosis Follow-up assessments at 47 months indicated that cardiac and skeletal muscle improvements were maintained and that FRDA patients showed significant increases in fractional shortening, a measure of cardiac function.

Moreover, the therapy was effective at preventing the progressive decline of neurological function Large-scale, randomized controlled trials are necessary to determine whether coenzyme Q 10 , in conjunction with vitamin E, has therapeutic benefit in FRDA.

At present, about one-half of patients use coenzyme Q 10 and vitamin E supplements despite the lack of proven therapeutic benefit Spinocerebellar ataxias SCAs : SCAs are a group of rare autosomal dominant neurodegenerative diseases characterized by gait difficulty, loss of hand dexterity, dysarthria, and cognitive decline.

SCA1, 2, 3, and 6 are the most common SCAs In vitro coenzyme Q 10 treatment of forearm skin fibroblasts isolated from patients with SCA2 was found to reduce oxidative stress and normalize complex I and II-III activity of the mitochondrial respiratory chain Early interest in coenzyme Q 10 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 Q 10 concentrations than healthy controls Two randomized controlled trials have explored the effect of coenzyme Q 10 as an adjunct to conventional therapy for breast cancer.

Supplementation with coenzyme Q 10 failed to improve measures of fatigue and quality of life in patients newly diagnosed with breast cancer 84 and in patients receiving chemotherapy There is little evidence that supplementation with coenzyme Q 10 improves athletic performance in healthy individuals.

Most did not find significant differences between the group taking coenzyme Q 10 and the group taking placebo with respect to measures of aerobic exercise performance, such as maximal oxygen consumption VO 2 max and exercise time to exhaustion Two studies actually found significantly greater improvement in measures of anaerobic 87 and aerobic 86 exercise performance with a placebo than with supplemental coenzyme Q More recent studies have suggested that coenzyme Q 10 could help reduce both muscle damage-associated oxidative stress and low-grade inflammation induced by strenuous exercise 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 Q 10 supplementation.

Coenzyme Q 10 is synthesized in most human tissues. The biosynthesis of coenzyme Q 10 involves three major steps: 1 synthesis of the benzoquinone structure from 4-hydroxybenzoate derived from either tyrosine or phenylalanine, two amino acids; 2 synthesis of the polyisoprenoid side chain from acetyl-coenzyme A CoA via the mevalonate pathway; and 3 the joining condensation of these two structures to form coenzyme Q In the mevalonate pathway, the enzyme 3-hydroxymethylglutaryl HMG -CoA reductase, which converts HMG-CoA into mevalonate, is common to the biosynthetic pathways of both coenzyme Q 10 and cholesterol and is inhibited by statins cholesterol-lowering drugs; see Drug interactions 1.

Of note, pantothenic acid formerly vitamin B 5 is the precursor of coenzyme A, and pyridoxine vitamin B 6 , in the form of pyridoxal-5'-phosphate, is required for the conversion of tyrosine to 4-hydroxyphenylpyruvic acid that constitutes the first step in the biosynthesis of the benzoquinone structure of coenzyme Q The extent to which dietary consumption contributes to tissue coenzyme Q 10 concentrations is not clear.

Rich sources of dietary coenzyme Q 10 include mainly meat, poultry, and fish. Other good sources include soybean, corn, olive, and canola oils; nuts; and seeds. Fruit, vegetables, eggs, and dairy products are moderate sources of coenzyme Q 10 Some dietary sources are listed in Table 1.

Coenzyme Q 10 is available without a prescription as a dietary supplement in the US. Coenzyme Q 10 is fat-soluble and is best absorbed with fat in a meal. Oral supplementation with coenzyme Q 10 is known to increase blood and lipoprotein concentrations of coenzyme Q 10 in humans 2 , 15 , Nonetheless, under certain physiological circumstances e.

During pregnancy, the use of coenzyme Q 10 supplements mg twice daily from 20 weeks' gestation was found to be safe Because reliable data in lactating women are not available, supplementation should be avoided during breast-feeding Concomitant use of warfarin Coumadin and coenzyme Q 10 supplements has been reported to decrease the anticoagulant effect of warfarin in a few cases An individual on warfarin should not begin taking coenzyme Q 10 supplements without consulting the health care provider who is managing his or her anticoagulant therapy.

HMG-CoA reductase is an enzyme that catalyzes a biochemical reaction that is common to both cholesterol and coenzyme Q 10 biosynthetic pathways see Biosynthesis.

Statins are HMG-CoA reductase inhibitors that are widely used as cholesterol-lowering medications. Statins can thus also reduce the endogenous synthesis of coenzyme Q Therapeutic use of statins, including simvastatin Zocor , pravastatin Pravachol , lovastatin Mevacor, Altocor, Altoprev , rosuvastatin Crestor , and atorvastatin Lipitor , has been shown to decrease circulating coenzyme Q 10 concentrations However, because coenzyme Q 10 circulates with lipoproteins , plasma coenzyme Q 10 concentration is influenced by the concentration of circulating lipids , It is likely that circulating coenzyme Q 10 concentrations are decreased because statins reduce circulating lipids rather than because they inhibit coenzyme Q 10 synthesis In addition, very few studies have examined coenzyme Q 10 concentrations in tissues other than blood such that the extent to which statin therapy affects coenzyme Q 10 concentrations in the body's tissues is unknown , , Finally, there is currently little evidence to suggest that secondary coenzyme Q 10 deficiency is responsible for statin-associated muscle symptoms in treated patients.

In addition, supplementation with coenzyme Q 10 failed to relieve myalgia in statin-treated patients see Disease Treatment , Originally written in by: Jane Higdon, Ph.

Linus Pauling Institute Oregon State University. Updated in February by: Victoria J. Drake, Ph. Updated in March by: Victoria J. Updated in April by: Barbara Delage, Ph.

Reviewed in May by: Roland Stocker, Ph. Centre for Vascular Research School of Medical Sciences Pathology and Bosch Institute Sydney Medical School The University of Sydney Sydney, New South Wales, Australia. Acosta MJ, Vazquez Fonseca L, Desbats MA, et al.

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Leong JY, van der Merwe J, Pepe S, et al. Coenzyme Q10 CoQ 10 is an effective natural antioxidant with a fundamental role in cellular bioenergetics and numerous known health benefits. Reports of its natural occurrence in various food items are comprehensively reviewed and critically evaluated.

Meat, fish, nuts, and some oils are the richest nutritional sources of CoQ 10 , while much lower levels can be found in most dairy products, vegetables, fruits, and cereals. Large variations of CoQ 10 content in some foods and food products of different geographical origin have been found.

The average dietary intake of CoQ 10 is only mg, with about half of it being in the reduced form. The intake can be significantly increased by the fortification of food products but, due to its lipophilicity, until recently this goal was not easily achievable particularly with low-fat, water-based products.