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Research Newsletter-Fall/Winter 2012

Victoria J. Drake, Ph.D.


Victoria J. Drake, Ph.D.
Micronutrient Information Center

Coenzyme Q10 is a member of the ubiquinone family of compounds. Humans can endogenously synthesize ubiquinones; therefore, coenzyme Q10 is not an essential nutrient. Coenzyme Q10 is a fat-soluble compound that is located in cell membranes and lipoproteins. The chemical structure of coenzyme Q10 allows it to accept and donate electrons. Coenzyme Q10 is part of the mitochondrial electron transport chain, which is a group of electron carriers in mitochondria that transport electrons to and from each other in a sequence in order to generate adenosine triphosphate (ATP)—the energy currency of cells. Coenzyme Q10 is also important to help maintain an acid pH in lysosomes, allowing for normal function of enzymes within that organelle that digest cellular debris and waste. Along with vitamin E, coenzyme Q10 is an effective antioxidant in cell membranes and lipoproteins.

Although coenzyme Q10 is synthesized by the body, it can also be obtained from the diet, with the richest sources being meat, poultry, fish, soybean and canola oils, and nuts. However, the contribution of dietary coenzyme Q10 to tissue levels is not clear. Deficiency symptoms have not been reported among healthy individuals, and primary coenzyme Q10 deficiency is a rare, autosomal recessive genetic disorder caused by defects in the compoundís biosynthetic pathway. This condition is characterized by low tissue levels of coenzyme Q10 and, consequently, compromised neuronal and muscular function. Clinical symptoms in some patients with primary coenzyme Q10 deficiency improve upon oral supplementation with coenzyme Q10.

Some studies have shown that tissue levels of coenzyme Q10 decline with age. Decreased plasma levels of coenzyme Q10 have also been observed in patients with diabetes, congestive heart failure, and some cancers. Thus, there is considerable interest in whether oral supplementation with coenzyme Q10 can help prevent or treat these and other conditions. Oral supplements have been shown to increase coenzyme Q10 levels in plasma and lipoproteins, but it is not yet clear whether oral supplementation in humans increases coenzyme Q10 concentrations in other tissues of individuals with normal endogenous coenzyme Q10 biosynthesis.

There is little evidence on the effect of coenzyme Q10 supplementation on slowing the aging process or preventing chronic diseases. In rodents, lifelong dietary supplementation with coenzyme Q10 increased tissue concentrations of the compound and decreased age-related DNA damage; however, lifespan was not extended. To date, research has mainly focused on whether oral coenzyme Q10 supplementation could treat various conditions, including genetic mitochondrial disorders, cardiovascular diseases, and neurological diseases.

Mitochondrial encephalomyopathies result from genetic defects in the mitochondrial electron transport chain. Symptoms are improved in some patients with mitochondrial encephalomyopathies after coenzyme Q10 supplementation, although patients with genetic defects in coenzyme Q10 biosynthesis experience the most dramatic improvement. A phase III clinical trial is presently under way to investigate whether coenzyme Q10 might be therapeutic in patients with other mitochondrial disorders.

Because coenzyme Q10 levels are decreased in the heart muscle of patients with severe heart failure, several small intervention trials have examined whether coenzyme Q10 supplementation improves cardiac function in such patients. A 2006 meta-analysis of ten randomized, controlled trials in heart failure patients found that coenzyme Q10 supplementation (99-200 mg/day for one to six months) resulted in a significant, 3.7% improvement in left ventricular ejection fraction, a measure of the heartís pumping ability. Overall, studies to date are mixed, and large-scale, clinical trials are needed to determine whether coenzyme Q10 supplementation has utility as an adjunct to conventional therapy in the treatment of congestive heart failure. One such large trial is currently being conducted.

Other studies have looked at whether coenzyme Q10 supplementation prevents the free radical-induced heart damage that occurs following a heart attack or during some types of heart surgery, such as coronary artery bypass graft (CABG) surgery. Small, placebo-controlled trials have found that pretreatment with coenzyme Q10 (100-300 mg/day for 7-14 days before surgery) improves various shortterm outcomes following surgery, such as left ventricular ejection fraction, cardiac output, and postoperative recovery. However, such trials have included relatively few people and have been limited to CABG surgical patients. Studies have also investigated whether coenzyme Q10 supplementation (60-600 mg/day) in addition to conventional therapy might help patients with angina pectoris, a condition characterized by chest pain, especially during exercise, due to inadequate oxygen supply to the heart muscle. Most trials have reported improvements in exercise tolerance and electrocardiograms (recordings of the electrical activity of the heart, used to diagnose cardiac arrhythmias, myocardial ischemia, and heart attack) compared to a placebo. Yet, only two studies to date have found coenzyme Q10 supplementation to reduce symptom frequency and nitroglycerin consumption.

Hypertension (systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg) affects about one-third of Americans, and nearly as many have prehypertension, defined as a systolic blood pressure of 120-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg. A 2007 meta-analysis of 12 clinical trials in hypertensive patients found that coenzyme Q10 reduced systolic and diastolic blood pressure by 11-17 mm Hg and 8-10 mm Hg, respectively. The randomized controlled trials included in this analysis used doses of 100-120 mg/day. In addition, several small, randomized, controlled trials have investigated whether coenzyme Q10 might improve vascular endothelial function (blood vessel dilation); the ability of blood vessels to relax or dilate is compromised in individuals with atherosclerosis, coronary artery disease, or diabetes. A 2011 meta-analysis examined the results of five such trials in those with type 2 diabetes mellitus, coronary artery disease, or endothelial dysfunction. Supplementation with coenzyme Q10 (150-300 mg/day for four to 12 weeks) was associated with a 1.7% increase in flow-dependent endothelial-mediated dilation, which may be clinically significant in terms of reducing risk for heart attack and stroke.

Because impaired mitochondrial function and oxidative stress contribute to the pathogenesis of neurodegenerative diseases, coenzyme Q10 has been studied as a potential therapy for Parkinsonís disease, Huntingtonís disease, and Friedreichís ataxia. Compared to control subjects, studies have documented decreased ratios of reduced to oxidized coenzyme Q10 in platelets (irregularly shaped cell fragments that assist in blood clotting) and higher concentrations of oxidized coenzyme Q10 in cerebrospinal fluid of patients with Parkinsonís disease. Additionally, one postmortem study found lower levels of total coenzyme Q10 in the cortex region of the brain compared to age- and sex-matched controls; however, no differences were observed in the other brain regions examined, including the substantia nigra—the site of neuron cell death in the brain stem of Parkinsonís patients. While results of an early clinical trial of high-dose coenzyme Q10 (1,200 mg/day) were promising, more recent trials have generally not reported beneficial effects in patients with Parkinsonís disease. In fact, a phase III trial of coenzyme Q10 supplementation (1,200-2,400 mg/day), in combination with vitamin E, was recently halted because it was deemed unlikely to be effective in treating Parkinsonís disease.

Coenzyme Q10 has also been investigated as a potential treatment for inherited neurodegenerative diseases like Huntingtonís disease and Friedreichís ataxia. Huntingtonís disease is characterized by selective degeneration of striatal spiny neurons. Disease symptoms, which include movement disorders and impaired cognition, typically develop in the fourth decade of life and progressively deteriorate over time. Research in animal models of Huntingtonís disease implicates impaired mitochondrial function and glutamatemediated neurotoxicity in disease pathogenesis. Some studies in mouse models of the disease have found that dietary coenzyme Q10 supplementation improves motor performance, reduces various hallmarks of Huntingtonís disease (i.e., brain atrophy, ventricular enlargement, striatal neuronal atrophy), and extends survival. Several studies in mice have also found that co-administration of coenzyme Q10 with remacemide (a drug that antagonizes the neuronal receptor activated by glutamate) results in greater improvements in most measured parameters. However, a 30-month randomized, placebo-controlled trial in 347 patients with early Huntingtonís disease found that coenzyme Q10 (600 mg/day)-racemide co-supplementation did not slow the functional decline associated with the disease. A phase III clinical trial administering a much higher dose of coenzyme Q10 (2,400 mg/day) or placebo to Huntingtonís disease patients is currently under way.

Coenzyme Q10 has also been investigated as a potential therapy for Friedreichís ataxia, an inherited neurodegenerative disease that causes iron accumulation within the mitochondria, resulting in increased oxidative stress and a decline in mitochondrial function. A pilot study in ten patients with the condition found that co-supplementation with coenzyme Q10 (200 mg/day) and vitamin E (2,100 IU/ day) led to improvements in cardiac and skeletal muscle function and also helped to prevent the progressive declines in neurological function. Another study found decreased serum levels of coenzyme Q10 and vitamin E in patients with Friedreichís ataxia, suggesting that supplementation with both compounds may provide therapeutic benefit. Large-scale randomized clinical trials are needed to determine their efficacy in Friedreichís ataxia.

Although the utility of coenzyme Q10 supplementation for prevention or treatment of various diseases requires further study, even high doses of the compound appear to be relatively safe. There have been no reports of significant adverse side effects of oral coenzyme Q10 supplementation at doses as high as 1,200 mg/day for up to 16 months and 600 mg/day for up to 30 months. Recently, 1,200 mg/day was proposed as the observed safe level for coenzyme Q10 supplementation. Gastrointestinal symptoms, such as nausea, diarrhea, appetite suppression, heartburn, and abdominal discomfort, have been reported, but taking divided doses throughout the day might minimize these symptoms. The safety of high doses of coenzyme Q10 in pregnancy has not been established. However, use of coenzyme Q10 supplements may interfere with certain drugs. For example, concomitant use of warfarin (Coumadin) and coenzyme Q10 may decrease the anticoagulatory effect of warfarin. Additionally, HMG-CoA reductase inhibitors (statins) used to reduce cholesterol levels may also decrease biosynthesis of coenzyme Q10, but it is not clear whether these drugs decrease coenzyme Q10 levels independent of a reduction in circulating lipids or decrease coenzyme Q10 concentrations in the bodyís tissues. For more information, please see the article on coenzyme Q10 in LPIís Micronutrient Information Center.

Last updated November 2012