Atorvastatin Decreases the Coenzyme Q10 Level in the Blood of Patients

Atorvastatin Decreases the Coenzyme Q10 Level in the Blood of Patients at Risk for Cardiovascular Disease and Stroke

Background: Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are widely used for the treatment of hypercholesterolemia and coronary heart disease and for the prevention of stroke. There have been various adverse effects, most commonly affecting muscle and ranging from myalgia to rhabdomyolysis. These adverse effects may be due to a coenzyme Q10 (CoQ10) deficiency because inhibition of cholesterol biosynthesis also inhibits the synthesis of CoQ10.

Conclusions: Even brief exposure to atorvastatin causes a marked decrease in blood CoQ10 concentration. Widespread inhibition of CoQ10 synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.

Source: Arch Neurol. 2004;61:889-892

 

Effects of Coenzyme Q10 in Early Parkinson

Effects of Coenzyme Q10 in Early Parkinson Disease
Evidence of Slowing of the Functional Decline

Conclusions: Coenzyme Q10 was safe and well tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects assigned to coenzymeQ10 than in those assigned to placebo, and the benefit was greatest in subjects receiving the highest dosage. Coenzyme Q10 appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.

Source: Arch Neurol. 2002;59:1541-1550

 

Coenzyme Q10 in the treatment of hypertension

Coenzyme Q10 in the treatment of hypertension:
a meta-analysis of the clinical trials

Our objective was to review all published trials of coenzyme Q10 for hypertension, assess overall efficacy and consistency of therapeutic action and side effect incidence. Meta-analysis was performed in 12 clinical trials (362 patients) comprising three randomized controlled trials, one crossover study and eight open label studies. In the randomized controlled trials (n¼120), systolic blood pressure in the treatment group was 167.7 (95% confidence interval, CI: 163.7–171.1) mmHg before, and 151.1 (147.1–155.1) mmHg after treatment, a decrease of 16.6 (12.6–20.6, Po0.001) mmHg, with no significant change in the placebo group. Diastolic blood pressure in the treatment group was 103 (101–105) mmHg before, and 94.8 (92.8–96.8) mmHg after treatment, a decrease of 8.2 (6.2–10.2, Po0.001) mmHg, with no significant change in the placebo group. In the crossover study (n¼18), systolic blood pressure decreased by 11 mmHg and diastolic blood pressure by 8 mmHg (Po0.001) with no significant change with placebo. In the open label studies (n¼214), mean systolic blood pressure was 162 (158.4–165) mmHg before, and 148.6 (145–152.2) mmHg after treatment, a decrease of 13.5 (9.8–17.1, Po0.001) mmHg. Mean diastolic blood pressure was 97.1 (95.2–99.1) mmHg before, and 86.8 (84.9–88.8) mmHg after treatment, a decrease of 10.3 (8.4–12.3, Po0.001) mmHg. We conclude that coenzyme Q10 has the potential in hypertensive patients to lower systolic blood pressure by up to 17 mmHg and diastolic blood pressure by up to 10 mmHg without significant side effects.

Source: Journal of Human Hypertension (2007) 21, 297–306. doi:10.1038/sj.jhh.1002138;

 

Coenzyme Q10:An Independent Predictor of Mortality in Chronic Heart Failure

Coenzyme Q10 An Independent Predictor of Mortality
in Chronic Heart Failure

Objectives The aim of this study was to investigate the relationship between plasma coenzyme Q10 (CoQ10) and survival in patients with chronic heart failure (CHF).

Background Patients with CHF have low plasma concentrations of CoQ10, an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ10 is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. Therefore we tested the hypothesis that plasma CoQ10 is a predictor of total mortality in CHF and could explain this association.

Methods Plasma samples from 236 patients admitted to the hospital with CHF, with a median (range) duration of follow-up of 2.69 (0.12 to 5.75) years, were assayed for LDL-C, TC, and total CoQ10.

Results Median age at admission was 77 years. Median (range) CoQ10 concentration was 0.68 (0.18 to 1.75) mol/l. The optimal CoQ10 concentration for prediction of mortality (established with receiver-operator characteristic [ROC] curves) was 0.73 mol/l. Multivariable analysis allowing for effects of standard predictors of survival—including age at admission, gender, previous myocardial infarction, N-terminal peptide of B-type natriuretic peptide, and estimated glomerular filtration rate (modification of diet in renal disease)—indicated CoQ10 was an independent predictor of survival, whether dichotomized at the ROC curve cut-point (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.2 to 3.3) or the median (HR: 1.6; 95% CI: 1.0 to 2.6).

Conclusions Plasma CoQ10 concentration was an independent predictor of mortality in this cohort. The CoQ10 deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ10.

Source: Molyneux et al.JACC Vol.52, No. 18, 2008:1435–41 

 

The level of CoQ 10 decrease with age

Age-related Changes in the Lipid Compositions of Rat and Human Tissues

In human pancreas and adrenal the ubiquinone content was highest at one year of age, whereas in other organs the corresponding peak value was at 20 years of age, and was followed by a continuous decrease upon further aging. A similar pattern was observed in the rats, with the highest concentration of ubiquinone being observed at 30 days of age.

Source: LIPIDS, Vol. 24, No. 7 (1989)