Coenzyme Q10
Research into the effects and possible clinical application of coenzyme q10 (CoQ10) has continued unabated in recent years, building a considerable body of literature. In addition to its possible use in neurodegenerative disease (see Alternative Medicine Alert December 2003:133-136), recent investigations have explored many diverse areas of research, including atherosclerosis and asthma.
CoQ10 and atherosclerosis
In a randomized, double-blind, controlled trial, the effects of oral treatment with CoQ10 (120 mg/d) on the risk factors of atherosclerosis were compared in 73 (CoQ, group A) and 71 (B vitamin, group B) patients after acute myocardial infarction (AMI).1
After one year, total cardiac events (24.6% vs. 45.0%, P < 0.02) including non-fatal infarction (13.7% vs. 25.3%, P < 0.05) and cardiac deaths were significantly lower in the intervention group compared to control group. The extent of cardiac disease, elevation in cardiac enzymes, left ventricular enlargement, previous coronary artery disease, and elapsed time from symptom onset to infarction at entry to study showed no significant differences between the two groups. Plasma levels of vitamin E (32.4 ± 4.3 vs. 22.1 ± 3.6 umol/L) and high-density lipoprotein cholesterol (1.26 ± 0.43 vs. 1.12 ± 0.32 mmol/L) showed significant (P < 0.05) increases, whereas thiobarbituric acid reactive substances, malondialdehyde (MDA, 1.9 + 0.31 vs. 3.1 + 0.32 pmol/L), and diene conjugates showed significant reduction respectively, in the CoQ10 group compared to the control group. Approximately one-half of the patients in each group (36 vs. 31) were receiving lovastatin (10 mg/d) and both groups had a significant reduction in total and low-density lipoprotein cholesterol compared to baseline levels.
It is possible that treatment with CoQ10 in patients with recent AMI may be beneficial in patients with high risk of atherothrombosis, despite optimal lipid-lowering therapy during a follow-up of one year. Adverse effect of treatments showed that fatigue (40.8% vs. 6.8%, P < 0.01) was more common in the control group than the CoQ10 group.
CoQ10, Ginkgo biloba, and warfarin
Twenty-four outpatients on stable, long-term warfarin treatment were included in a randomized, double-blind, placebo-controlled crossover trial to determine the clinical effect of CoQ10 and Ginkgo biloba on warfarin therapy.2 CoQ10 100 mg daily, G. biloba 100 mg daily, and placebo were given in random order over treatment periods of four weeks, each followed by a two-week wash-out period. The international normalized ratio (INR) was kept between 2.0-4.0 by appropriate adjustment of the warfarin dosage.
Fourteen women and 10 men, median age 64.5 years (range 33-79 years) were included. Three patients withdrew from the study for personal reasons. The INR was stable during all treatment periods. The geometric mean dosage of warfarin did not change during the treatment periods: G. biloba, 36.7 mg/week (95% confidence interval [CI] 29.2-46.0); CoQ10, 36.5 mg/week (95% CI 29.1-45.8); placebo, 36.0 mg/week (95% CI 28.6-45.1).
The study indicated that CoQ10 and G. biloba do not influence the clinical effect of warfarin.
CoQ10 and Prader-Willi syndrome
To determine if CoQ10 levels are decreased in Prader-Willi syndrome (PWS), plasma CoQ10 levels were studied in 16 subjects with PWS—13 with obesity of unknown cause, and 15 subjects without obesity, but of similar age and compared with body composition.3
CoQ10 is an essential component of the mitochondrial respiratory chain and an important scavenger of reactive oxygen species. Low levels are found in individuals with reduced energy expenditure, cardiac and skeletal muscle dysfunction, and mitochondrial disorders; many of these same manifestations are seen in individuals with PWS. In addition, CoQ10 supplementation frequently is given to individuals with this syndrome.
Plasma CoQ10 levels were significantly decreased (P < 0.05), using several statistical approaches in subjects with PWS (0.45 ± 0.16 microg/mL), compared to subjects without obesity (0.93 ± 0.56 microg/mL), but not different from subjects with obesity (0.73 ± 0.53 microg/mL). When plasma CoQ10 was normalized relative to cholesterol, triglyceride, and creatinine levels, and fat and lean mass (determined by dual energy X-ray absorptiometry) in the subjects with either PWS or obesity, no significant differences were observed. However, a lower muscle mass was found in the PWS subjects.
CoQ10 and asthma
The aim of this study was to assess the levels of CoQ10, alpha-tocopherol, beta-carotene, and malondialdehyde in asthmatics.4 Fifty-six asthmatics (15 males and 41 females) age 19-72 years (mean age 46 years) were enrolled in the study. The control group included 25 healthy volunteers (16 males, 9 females) age 25-50 years.
Concentrations of CoQ10 and alpha-tocopherol decreased significantly both in plasma and whole blood compared with healthy volunteers (P < 0.009, P < 0.004; P < 0.035, P < 0.001, respectively). The level of MDA was elevated, but not statistically significantly. No changes were seen in beta-carotene levels. Positive correlation was found between concentrations of CoQ10 and alpha-tocopherol.
These results suggest possible contribution of suboptimal concentrations of CoQ10 on antioxidative imbalance in asthmatics and provide rationale for its supplementation with clinical evaluation.
CoQ10, blood pressure, and glycemic control
The objective of this study was to assess effects of dietary supplementation with CoQ10 on blood pressure and glycemic control in subjects with Type 2 diabetes, and to consider oxidative stress as a potential mechanism for any effects.5 The study was performed at the University of Western Australia, Department of Medicine at Royal Perth Hospital, Australia.
Seventy-four subjects with uncomplicated Type 2 diabetes and dyslipidemia were involved in a randomized, double-blind, placebo-controlled 2 ´ 2 factorial intervention. Subjects were randomly assigned to receive an oral dose of 100 mg CoQ10 twice daily (200 mg/d), 200 mg fenofibrate each morning, both, or neither for 12 weeks.
Fenofibrate did not alter blood pressure, HbA(1c), or plasma F2-isoprostanes. There was a three-fold increase in plasma CoQ10 concentration (3.4 ± 0.3 micro mol/L, P < 0.001) as a result of CoQ10 supplementation. The main effect of CoQ10 was to significantly decrease systolic (-6.1 ± 2.6 mmHg, P = 0.021) and diastolic (-2.9 ± 1.4 mmHg, P = 0.048) blood pressure and HbA(1c) (-0.37 ± 0.17%, P = 0.032). Plasma F2-isoprostane concentrations were not altered by CoQ10 (0.14 ± 0.15 nmol/L, P = 0.345).
These results show that CoQ10 supplementation may improve blood pressure and long-term glycemic control in subjects with Type 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F2-isoprostanes.
References
1. Singh RB, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction. Mol Cell Biochem 2003;246:75-82.
2. Engelsen J, et al. Effect of Coenzyme Q10 and Ginkgo biloba on warfarin dosage in patients on long-term warfarin treatment. A randomized, double-blind, placebo-controlled cross-over trial. Ugeskr Laeger 2003;165:1868-1871.
3. Butler MG, et al. Coenzyme Q10 levels in Prader-Willi syndrome: Comparison with obese and non-obese subjects. Am J Med Genet 2003;119:168-171.
4. Gazdik F, et al. Levels of coenzyme Q10 in asthmatics. Bratisl Lek Listy 2002;103:353-356.
5. Hodgson JM, et al. Coenzyme Q10 improves blood pressure and glycaemic control: A controlled trial in subjects with type 2 diabetes. Eur J Clin Nutr 2002;56: 1137-1142.
Coenzyme Q10. Altern Med Alert 2003;6(suppl 12):S1-S2.
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