CoQ10 is present in cell membranes at high concentrations, acting as a powerful antioxidant scavenger of free radicals and taking part in regeneration of other key antioxidants such as tocopherol (vitamin E) and ascorbate (vitamin C). 10
CoQ10 is an electron carrier in the lipid phase of the mitochondrial membrane, producing energy. CoQ10 is therefore essential for ATP production.
CoQ10 may prevent initiation and/or propagation of lipid peroxidation in plasma lipoprotein biological membranes. Thus, CoQ10 prevents LDL oxidation, indicating a potential role reducing risk of cardiovascular disease.
HMG-CoA reductase inhibitors such as lovastatin, pravastatin, and atorvastatin15 significantly decrease blood concentrations of CoQ10. Approximately 100 mg/day of CoQ10 is recommended to prevent a decrease in blood CoQ10.
Tricyclic antidepressants inhibit CoQ10-dependent enzyme activity. A 30 to 100 mg CoQ10 supplement is advised.
CoQ10 supplements have been found to increase risk of bleeding for people taking Warfarin, an anticoagulant. 13 Caution is warranted.
Proparanolol (Inderal), a beta-blocker to treat hypertension, can inhibit CoQ10-dependent enzymes.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Bioavailability and antioxidant activity of some food supplements in men and women using the D-Roms test as a marker of oxidative stress.
Supplementation with CoQ10 as part of a low-dose antioxidant combination (vitamins C and E, beta-carotene, selenium, zinc) was shown in humans to reduce oxidative potential. Eleven men and three women received either: 5 mg zinc, 48 mcg selenium, 400 mcg vitamin A, 50 mcg beta-carotene, 15 mg vitamin E and 10 mg cysteine (Formula 1); 30 mg citrus bioflavonoids, 30 mg vitamin C, 10 mg coenzyme Q(10) and 1 mg vitamin B-6 (Formula 2); or both Formula 1 and 2 (Formula 3). Each formula was administered for 1 week in a cross-over design. The derivatives of reactive oxygen metabolites (D-Roms) test was used to assess oxidative stress and potential in Carratelli units (U.CARR). Formulas 1 and 3 reduced mean U.CARR concentrations, which suggests that an antioxidant combination, including CoQ10, reduces oxidative stress in humans. 12
Antioxidative effect of dietary coenzyme Q10 in human blood plasma
Antioxidant activity of 90 mg/day CoQ10 supplementation in humans was determined before and after induction of oxidative stress by fish oil supplementation. CoQ10 concentrations increased significantly from 0.7 +/- 0.1 micromol/L to 1.7 +/- 0.3 micromol/L after one week of supplementation. CoQ10 decreased TBARS concentrations, an antioxidant marker, during the first two weeks. Alpha-tocopherol content was increased but ascorbate did not change. These results indicate an antioxidant role of CoQ10 in the blood. 4
Coenzyme Q (10) improves blood pressure and glycemic control: a controlled trial in subjects with type 2 diabetes.
A randomized, double-blind, placebo-controlled trial with seventy-four patients who had been diagnosed with type 2 diabetes and dyslipidemia received either 100 mg CoQ10 twice daily, 200 mg fenofibrate daily, both CoQ10 and fenofibrate, or neither for 12 weeks. Supplementation with CoQ10 resulted in a three-fold increase of plasma CoQ10 concentrations (3.4 +/- 0.3 micromol/L; P<0.001). CoQ10 supplementation significantly decreased systolic (-6.1 +/- 2.6 mmHg; P=0.021) and diastolic (-2.9 +/- 1.4 mmHg; P=0.048) blood pressure and HbA1C (-0.37 +/- 0.17%; P=0.032). Fenofibrate did not alter blood pressure, HbA1C, or plasma F(2)-isoprostanes (a marker of oxidative stress). Although plasma F(2)-isoprostane concentrations were not decreased, CoQ10 supplementation was shown to improve blood pressure and long-term glycemic control in patients with Type 2 diabetes. 14
Effect of hydrosoluble coenzyme Q10 on blood pressures and insulin resistance in hypertensive patients with coronary artery disease.
A randomized, double-blind clinical trial investigated the effects of CoQ10 in people with coronary artery disease who were taking antihypertensive medication. Subjects were given 120 mg/day of CoQ10 (30 subjects) or a B vitamin supplement (29 subjects) for 8 weeks. Blood pressure, 2-hour plasma insulin, lipids and oxidized lipids concentrations were measured. Researchers found that CoQ10 decreased systolic and diastolic blood pressure, fasting and two-hour plasma insulin, glucose, triglycerides, lipid peroxides, malondialdehyde and diene conjugates. CoQ10 supplements increased HDL cholesterol and vitamins A, C, E, and beta carotene (P<0.05). These results indicate that CoQ10 supplements have beneficial effects for people with hypertension and coronary artery disease. 5
Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension.
A randomized, double-blind, placebo-controlled trial investigated the antihypertensive effects of CoQ10. The study enrolled 46 men and 37 women with isolated systolic hypertension. Participants consumed 60 mg of CoQ10 twice daily or a placebo for twelve weeks. Blood pressure was monitored before and at the end of twelve weeks of supplementation. The results indicated a mean reduction in systolic blood pressure of 17.8 +/- 7.3 mmHg (mean + SEM) in subjects treated with CoQ10 at the end of 12 weeks. CoQ10 was found in this study to be beneficial for systolic hypertension. 6
Usefulness of coenzyme Q10 in clinical cardiology: a long-term study.
Over an eight year period, 424 people with cardiovascular disease were treated with CoQ10 in addition to standard treatments. Subjects had ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), primary diastolic dysfunction (PDD), hypertension (HTN), mitral valve prolapse (MVP) or valvular heart disease (VHD). Subjects consumed 75 to 600 mg/day of CoQ10; the amount of CoQ10 varied based on baseline CoQ10 levels with the goal of increasing the whole blood level to greater than or equal to 2.10 micrograms/mL. Some participants took CoQ10 for less than 1 year and a third of the participants took it for more than 3 years. Participants were followed for a mean of 17.8 months. Clinical response was assessed according to the New York Heart Association (NYHA) functional scale. Fifty-eight percent of the participants improved by one NYHA class, 28% improved by two classes, and 1.2% improved by three classes. CoQ10 supplementation significantly improved echocardiographic parameters such as left ventricular wall thickness, mitral valve inflow slope and fractional shortening. Treatment with CoQ10 was also found to reduce medication requirements. This study indicated that CoQ10 can be beneficial for people with cardiovascular disease. 7
Effect of coenzyme Q10 administration on endothelial function and extracellular superoxide dismutase in patients with ischaemic heart disease: a double-blind, randomized controlled study.
A randomized, placebo-controlled clinical trial investigated the impact of CoQ10 in patients with coronary artery disease. Thirty-three participants completed the study. Participants consumed 100 mg of CoQ10 three times daily for one month. To assess impact, all participants underwent a brachial artery ED assessment, a cardiopulmonary exercise test, and a measurement of endothelium-bound ecSOD activity at baseline and after one month of supplementation. In the CoQ10 treated group, increases in ecSOD, ED relaxation, and peak VO(2) and O(2) pulse were statistically greater than in the placebo group. These results indicate that CoQ10 supplements may be beneficial for people with coronary artery disease. 17
Effect of coenzyme Q10 on myopathic symptoms in patients treated with statins.
A double blind clinical trial investigated the affect of CoQ10 on statin-associated pain symptoms in people with cardiovascular disease. Thirty-two people with cardiovascular disease experiencing pain associated with statin therapy were enrolled in the study. Subjects were randomly assigned to receive either 100 mg CoQ10 daily (n=18) or 400 IU vitamin E daily (n=14) for thirty days. An earlier study indicated statin associated myopathy was associated with reduced CoQ10 levels in muscle tissues.21 CoQ10 supplementation reduced pain severity by 40% (p<0.001) compared with baseline. CoQ10 also decreased the interference of pain symptoms on daily activities by 38% (p<0.02) compared with baseline. No changes were noted for vitamin E supplementation. The results of this study indicate that CoQ10 supplements may be beneficial for those taking statins. 20
Influence of coenzyme Q(10) and cerivastatin on the flow-mediated vasodilation of the brachial artery: results of the ENDOTACT study.
This randomized, prospective, cross-over design study investigated the efficacy of CoQ10, alone or with Cerivastatin, on flow-mediated vasodilation of the brachial artery. Twenty-five male volunteers with manifest endothelial dysfunction participated in the study. Manifest endothelial dysfunction was defined as flow mediated dilation (FMD) percent less than 4.5%. The study consisted of three six-week phases, separated by two-week wash-out periods. Subjects were randomly assigned to consume 0.3 mg Cerivastatin daily (1), 50 mg CoQ10 three times daily (2), or both (3). All three treatments significantly improved FMD% (beginning vs. end: (1) 3.50+/-4.05% vs. 8.80+/-6.39%, p=0.009; (2) -0.25+/-4.0% vs. 7.06%+/-4.39%, p=0.004; (3) 3.14+/-3.54% vs. 8.82+/-5.78%, p=0.011). As expected, treatment with Cerivastatin led to a significant decrease of plasma levels of CoQ10 (1.23+/-0.34 vs. 0.87+/-0.39 micrograms/mL, p=0.004). These results indicate a positive effect of CoQ10 on endothelial dysfunction. 23
Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction.
In a randomized, double-blind, controlled trial, the efficacy of CoQ10 after myocardial infarction was investigated. One-hundred-forty-four people with acute myocardial infarction enrolled in the study; 73 were assigned to consume 120 mg/day CoQ10 while 71 were assigned to a B vitamin control group. After one year, CoQ10 supplements reduced total cardiac events (24.6 vs 45.0%, p<0.02), non-fatal myocardial infarction (13.7 vs. 25.3%, p<0.05), and cardiac death. This study found that CoQ10 may be beneficial for people with acute myocardial infarction. 24
The effect of coenzyme Q10 on the exercise tolerance of middle-aged, untrained men.
CoQ10 supplementation can increase exercise tolerance. Fifteen middle-aged men were given 150 mg/day CoQ10 for 2 months. Blood CoQ10 concentrations were increased with CoQ10 supplements (p<0.05). Subjective perception of vigor was significantly increased from 5.73 +/- 0.35 before to 6.64 +/- 0.45 after the two month supplementation period (p<0.05). The forearm-hand grip test and the Lactate Threshold test were evaluated. VO2 max and the Lactate Threshold were not modified by antioxidant treatment. In addition, CoQ10 did not improve the forearm-handgrip test. Thus, CoQ10 supplementation improved CoQ10 levels and subjective perception of vigor but did not enhance aerobic capacity and forearm exercise metabolism. 9
Muscle and plasma coenzyme Q10 concentration, aerobic power and exercise economy of healthy men in response to four weeks of supplementation.
A small, single-blind trial investigated the affect of CoQ10 supplementation on CoQ10 concentration in skeletal muscle, VO2 max, and oxygen consumption during submaximal exercise in healthy, physically active men. Six men volunteered for the trial. The trial was divided into four two week phases: a placebo run-in period, the CoQ10 supplementation period (150 mg/day), the CoQ10 (150 mg/day) plus vitamin E (1000 IU/day) period, and a placebo wash-out period. While CoQ10 concentrations were significantly increased by supplementation (p<0.05), no other changes were noted. Thus, this study confirmed that CoQ10 is bioavailable but did not find any affect on exercise economy. 22
Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus.
CoQ10 supplementation has been shown to improve endothelial dysfunction of the brachial artery in patients with type II diabetes and dyslipidemia. Forty patients with type II diabetes and dyslipidemia were randomized to receive either 200 mg supplemental CoQ10 or placebo for 12 weeks; results were also compared to 18 healthy controls. Flow-mediated dilation of the brachial artery increased by 1.6% (SEM 0.3) with CoQ10 supplementation and decreased by 0.4% (SEM 0.5) with placebo, p=0.05. CoQ10 supplements resulted in a three-fold increase in plasma CoQ10 (p<0.001). No changes in F2-isoprostanes, oxygen radical absorption capacity, concentration of lipids, glycemic control, or blood pressure. Supplementing with CoQ10 improved endothelial function of the peripheral circulation in dyslipidemic patients with Type II diabetes. It was suggested that these results may be due to increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress. 16
Combined effect of coenzyme Q10 and fenofibrate on forearm microcirculatory function in type 2 diabetes.
In a blinded, randomized, placebo-controlled, factorial trial, the affect of fenofibrate with or without CoQ10 on endothelial function. Eighty people diagnosed with type 2 diabetes mellitus and dyslipidemia enrolled in the study. Subjects were randomly assigned to receive fenofibrate (200 mg/day), CoQ10 (200 mg/day), both, or a placebo for twelve weeks. Forearm microcirculatory function was assessed with venous occlusion plethysmography during the infusion of acetylcholine (ACh), bradykinin (BK), sodium nitroprusside (SNP) and N(G)-monomethyl-L-arginine (L-NMMA) into the brachial artery; blood flow responses were calculated as area under the curve (AUC). Fenofibrate alone significantly reduced plasma cholesterol, triglyceride, and fibrinogen levels (P<0.001). In addition, fenofibrate alone significantly increased both HDL cholesterol and homocysteine. CoQ10 alone significantly decreased systolic blood pressure and HbA(1c) (P<0.05). The combination of fenofibrate and CoQ10 significantly increased the area under the curve for Ach, BK, and SNP. The combination of fenofibrate and CoQ10 were found to improve endothelial and non-endothelial forearm endothelial vasodilator function. CoQ10 supplements along with other therapies may be beneficial for people with type 2 diabetes. 25
Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and nonparkinsonian subjects.
Oxidative stress is characteristic of neurodegenerative disorders, such as Parkinson¡¯s disease. Complex I and Complex II/III activity in platelet mitochondria have been shown to be reduced in patients with early stage untreated Parkinson¡¯s disease. CoQ10 is the electron acceptor for Complex I and Complex II. Mitochondrial CoQ10 concentrations have been found to be low in patients with Parkinson's disease, which directly correlates with decreases in Complex I and Complex II/III activity. A pilot study using oral supplementation of 200 mg of CoQ10 either twice, three times or four times daily for one month in Parkinsonian patients, resulted in dose-dependent increases in plasma CoQ10 concentrations as well as an increase in Complex I activity. However, there was no change in motor functions in these patients. Although CoQ10 was well-tolerated at these high doses, mild changes in urine were noted for the highest dose (800 mg/day). 18
Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline.
A randomized, controlled, multi-center study was conducted in 80 patients with early Parkinson’s disease to determine whether CoQ10 supplementation could slow functional decline for people with Parkinson’s disease. Functional decline was assessed with the Unified Parkinson’s Disease Rating Scale at screening, baseline, and at 1-, 4-, 8-, 12- and 16-month visits. CoQ10 supplementation was found to be safe and well-tolerated at dosages up to 1200 mg/day over the 16-month period. Less disability developed in subjects assigned to CoQ10 than placebo, and benefit was greatest in patients receiving the highest dose (1200 mg/day). CoQ10 supplementation at 1200 mg/day appears to slow the progressive deterioration of function in patients with Parkinson’s disease. 19
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