Antioxidant Activity: CoQ10 is present in cell membranes in high amounts, 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~]
Coenzyme Q10 (CoQ10) supplementation has shown to decrease oxidative stress/damage in vivo. Supplementing with CoQ10 alone for 13 weeks, resulted in elevated CoQ homologues in tissue and mitochondria, as well as decreased oxidative damage and increased oxidative potential in rodents. Supplementation with CoQ10 as part of a low-dose antioxidant combination (vitamins C and E, beta-carotene, selenium, zinc) was also shown in humans, to reduce oxidative potential. Eleven men and three women received either: 5mg 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 a combination of Formula 1 and 2 (Formula 3). Each formula was administered for 1 week in a cross-over design. D-Roms test was used to detect oxygen metabolite derivatives as 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.[~11~][~12~]Antioxidant activity of 90 mg/day supplementation in humans was determined before and after induction of an oxidative stress by fish oil supplementation. CoQ10 decreased TBARS concentrations, an antioxidant marker, and increased a-tocopherol content. This indicated an antioxidant role of CoQ10 in blood.4
Blood Pressure: CoQ10 supplementation has shown to improve blood pressure and glycemic control in patients with type II diabetes. A randomized double-blind placebo controlled trial on seventy-four patients with type II diabetes and dyslipidemia received either 100mg CoQ10 twice daily, 200 mg fenofibrate, both CoQ10 and fenofibrate, or placebo for 12 weeks. CoQ10 supplementation significantly decreased systolic and diastolic blood pressure and HbA1C, whereas 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, supplementation with CoQ10 can help improve blood pressure and long-term glycemic control in patients with Type II diabetes.[~14~]
Hypertensive subjects with coronary artery disease were given 120 mg/day of CoQ10 for 8 weeks. Blood pressure, 2-hour plasma insulin, lipids and oxidized lipids concentrations were measured. Researchers found that CoQ10 decreased blood pressure, which was accompanied with lowered oxidative stress. Insulin response was also significantly improved.5 Burke et al6 reported a mean reduction in systolic blood pressure of 17 + 7.3 mmHg (mean + SEM) in subjects treated with CoQ10 (60 mg oral) for 12 weeks.
Cardiovascular Disease (CVD): Vitamin E has shown to be beneficial for the heart by reducing oxidation of LDL cholesterol, which over time can cause plaque to build up in arteries. One study examined vitamin E and CoQ10 supplementation in combination (0.2% + 0.5% wt/wt, respectively) in apolipotprotein E knockout mice fed a high-fat diet, to determine whether it is more anti-atherogenic than either vitamin E (0.2%) or CoQ10 (0.5%) supplementation alone. CoQ10 + vitamin E supplementation significantly decreased tissue lipid peroxidation after 24 weeks. This supports other data on CoQ10 and vitamin E working together as a powerful antioxidant team. In addition, HPLC determined that CoQ10 significantly inhibited atherosclerosis at the aortic arch and root. Vitamin E and CoQ10 supplementation taken together are more anti-atherogenic in apoE-/- mice than either CoQ10 or vitamin E alone. Further studies need to establish whether the anti-atherogenic activity of vitamin E + CoQ10 reflects the ability of antioxidants to inhibit the oxidation of lipoproteins in the vessel wall.[~13~]
Over 400 patients with various forms of CVD were treated with 75 - 600 mg/day of CoQ10. Some patients took CoQ10 for less than 1 year and a third of the patients took it for more than 3 years. CoQ10 supplementation significantly improved echocardiographic parameters such as left ventricular wall thickness, mitral valve inflow slope and fractional shortening. Treatment with CoQ10 also reduced medication requirements.7
Congestive Heart Failure: CoQ10 has been studied quite extensively in congestive heart failure (CHF). CoQ10 has been determined to be an important part of myocardium and myocardial energy function, along with L-carnitine, creatine, thiamine, taurine, and antioxidants: vitamins C and E and selenium. A randomized study comparing supplementation with taurine, CoQ10, carnitine, thiamine, creatine, and vitamins C and E and selenium against a placebo diet in hamsters with late-stage cardiomyopathy, found improvement in myocyte sarcomeric structure, developed pressure, and +dp/dt and –dp/dt after 3 months. In addition, biopsies have indicated a correlation between CoQ10 and ventricular function in human failing hearts. Supplementation with carnitine, taurine and CoQ10 (via MayoviveÒ) for 30 days resulted in restored myocardial levels and a significant decrease in left ventricular end-diastolic volume. CoQ10 supplementation should be considered as part of a therapeutic strategy to manage patients suffering from CHF.[~15~]
A meta-analysis with 8 studies reported the effect of supplemental CoQ10 on congestive heart failure. More than 350 patients were included in the meta-analysis. CoQ10 varied from 60 to 200 mg. Treatment with CoQ10 improved stroke volume, cardiac output, ejection fraction, cardiac index and end diastolic volume index, which suggested that CoQ10 may be an adjuvant treatment of congestive heart failure.8
Exercise: Since CoQ10 is essential for energy production, researchers have hypothesized that CoQ10 supplementation can increase exercise tolerance. Fifteen middle-aged men were given 150 mg/day CoQ10 for 2 months. 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, suggesting that short-term dosing with CoQ10 does not enhance aerobic capacity and forearm exercise metabolism.9
Diabetes - Type II: 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. Flow-mediated dilation of the brachial artery increased with CoQ10 supplementation and decreased with placebo. Supplementing with CoQ10 improved endothelial function of the peripheral circulation in dyslipidemic patients with Type II diabetes. This finding may be the result of increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress.[~16~]
The glycerol-3-phosphate shuttle is important for single transduction of plasma glucose and insulin release from pancreatic beta cells. Glycerol-3-phophate dehydrogenase (G3PD), the rate-limiting enzyme in the shuttle, is underexpressed in pancreatic beta cells of humans with type II diabetes, as well as rodents that are models for this disorder. It is thought that sub-optimal tissue concentrations of CoQ10 may further impair GSPD activity. Correcting a deficiency of tissue CoQ10 may improve glucose-stimulated insulin secretion from pancreatic beta cells of patients with diabetes. CoQ10 supplementation may play an important role with glycemic control in patients with diabetes.[~17~]
Neurodegenerative disorders: Oxidative stress is characteristic of neurodegenerative disorders, such as Parkinson’s disease. Complex I and complex II/III activity in platelet mitochondria have shown to be reduced in patients with untreated Parkinson’s disease in its early stage. 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, 3 times or 4 times daily for 1 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~]
A randomized controlled multi-center study was conducted in 80 patients with early Parkinson’s disease to determine if CoQ10 supplementation could slow the functional decline. Functional decline was assessed in patients undergoing evaluation with the Unified Parkinson’s Disease Rating Scale at screening, baseline, and at 1-,4-,8-,12- and 16-month visits. CoQ10 supplementation was suggested 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~]
|
Print this page
Contact an Expert
