ubiquinone and Myalgia

Statin associated muscle symptoms are common and affect adherence to statin treatment. The objective of this study was to assess whether patients with statin-associated myalgia can be successfully treated with Coenzyme Q10 (CoQ10) to improve symptoms and maintain them on statin therapy.. This systematic review was performed in line with the 2015 PRISMA statement. Relevant studies were identified via a search of MEDLINE, EMBASE and the Cochrane Library. Studies were screened to include randomised controlled trials of oral CoQ10 supplementation versus a placebo in adults with statin-associated myalgia. Continuation of statin therapy was a secondary outcome. Risk of bias was assessed using the Cochrane Risk of Bias tool. Pooled and sensitivity analyses were performed.. 413 records were identified by the search strategy. Eight studies were selected for review, and 7 of them (with 321 patients) were included in the meta-analysis. Selected studies were published between 2007 and 2016 with the number of participants ranging from 37 to 76. Only two of these studies demonstrated a positive effect of CoQ10 therapy in relieving muscle pain. The meta-analysis did not demonstrate any benefit of CoQ10 supplementation in improving myalgia symptoms compared to placebo (weighted mean difference -0.42; 95% Confidence Interval [CI] -1.47 to 0.62). Similarly, CoQ10 did not improve the proportion of patients remaining on the statin treatment (RR 0.99; 95%CI, 0.81 to 1.20).. This systematic review and meta-analysis did not demonstrate that CoQ10 supplementation was beneficial for patients with statin-associated muscle pain or improved adherence to statin therapy.

Topics: Adult; Aged; Dietary Supplements; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Medication Adherence; Middle Aged; Myalgia; Randomized Controlled Trials as Topic; Risk Assessment; Risk Factors; Treatment Outcome; Ubiquinone

Statin drugs markedly reduce low-density lipoprotein cholesterol and consequently the incidence of cardiac events. In approximately 5-10% of adults, these drugs are associated with a range of muscle side effects such as muscle pain, cramping and weakness. Reduction in mitochondrial coenzyme Q10 (CoQ10), or ubiquinone, has been proposed as a mechanism for these statin-associated muscle symptoms (SAMS), and thus various formulations of CoQ10 are marketed and consumed for the prevention and treatment of SAMS. However, data supporting the efficacy of CoQ10 are equivocal, with some studies showing that CoQ10 supplementation reduces the incidence and severity of SAMS and others finding no beneficial effects of supplementation. Methodological and pharmacological issues may confound interpretation of data on this topic. For example, many patients who report SAMS, such as those who have been enrolled in previous CoQ10 studies, may be experiencing non-specific (non-statin-associated) muscle pain. In addition, the effectiveness of oral CoQ10 supplementation to increase mitochondrial CoQ10 in human skeletal muscle is not well established. This manuscript will critically evaluate the published data on the efficacy of CoQ10 supplements in the prevention and treatment of SAMS.

Topics: Animals; Dietary Supplements; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Muscle, Skeletal; Myalgia; Ubiquinone

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are extremely well tolerated but are associated with a range of mild-to-moderate statin-associated muscle symptoms (SAMS). Estimates of SAMS incidence vary from <1% in industry-funded clinical trials to 10-25% in nonindustry-funded clinical trials and ∼60% in some observational studies. SAMS are important because they result in dose reduction or discontinuation of these life-saving medications, accompanied by higher healthcare costs and cardiac events. The mechanisms that produce SAMS are not clearly defined. Statins block the production of farnesyl pyrophosphate, an intermediate in the mevalonate pathway, which is responsible for the production of coenzyme Q10 (CoQ10). This knowledge has prompted the hypothesis that reductions in plasma CoQ10 concentrations contribute to SAMS. Consequently, CoQ10 is popular as a form of adjuvant therapy for the treatment of SAMS. However, the data evaluating the efficacy of CoQ10 supplementation has been equivocal, with some, but not all, studies suggesting that CoQ10 supplementation mitigates muscular complaints. This review discusses the rationale for using CoQ10 in SAMS, the results of CoQ10 clinical trials, the suggested management of SAMS, and the lessons learned about CoQ10 treatment of this problem.

Topics: Dietary Supplements; Energy Metabolism; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Muscle, Skeletal; Muscular Diseases; Myalgia; Polyisoprenyl Phosphates; Polymorphism, Single Nucleotide; Sesquiterpenes; Ubiquinone

Topics: Dietary Supplements; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Ubiquinone

To evaluate the efficacy of coenzyme Q10 (CoQ10) supplementation on statin-induced myopathy.. We searched the MEDLINE, Cochrane Library, Scopus, and EMBASE databases (November 1, 1987, to May 1, 2014) to identify randomized controlled trials investigating the impact of CoQ10 on muscle pain and plasma creatine kinase (CK) activity as 2 measures of statin-induced myalgia. Two independent reviewers extracted data on study characteristics, methods, and outcomes.. We included 6 studies with 302 patients receiving statin therapy: 5 studies with 226 participants evaluated the effect of CoQ10 supplementation on plasma CK activity, and 5 studies (4 used in the CK analysis and 1 other study) with 253 participants were included to assess the effect of CoQ10 supplementation on muscle pain. Compared with the control group, plasma CK activity was increased after CoQ10 supplementation, but this change was not significant (mean difference, 11.69 U/L [to convert to μkat/L, multiply by 0.0167]; 95% CI, -14.25 to 37.63 U/L; P=.38). Likewise, CoQ10 supplementation had no significant effect on muscle pain despite a trend toward a decrease (standardized mean difference, -0.53; 95% CI, -1.33 to 0.28; P=.20). No dose-effect association between changes in plasma CK activity (slope, -0.001; 95% CI, -0.004 to 0.001; P=.33) or in the indices of muscle pain (slope, 0.002; 95% CI, -0.005 to 0.010; P=.67) and administered doses of CoQ10 were observed.. The results of this meta-analysis of available randomized controlled trials do not suggest any significant benefit of CoQ10 supplementation in improving statin-induced myopathy. Larger, well-designed trials are necessary to confirm the findings from this meta-analysis.

Topics: Creatine Kinase, MM Form; Dietary Supplements; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Outcome Assessment, Health Care; Pain Measurement; Randomized Controlled Trials as Topic; Ubiquinone; Vitamins

Statins represent the most widely prescribed drugs. Accordingly, in daily practice statin-related muscle pain and other myopathic sensations are frequently seen. In this practice review the clinical approach to statin myopathy is discussed.

Topics: Aged; Aged, 80 and over; Atorvastatin; Diagnosis, Differential; Drug Substitution; Drug Therapy, Combination; Female; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Myalgia; Patient Education as Topic; Pyrroles; Quinolines; Risk Factors; Ubiquinone

Statins are the first-line pharmacotherapy for cholesterol reduction. Use of these drugs in large randomized clinical trials has consistently shown significant reductions in major vascular events, including death, myocardial infarction, stroke, and coronary revascularization. The updated guidelines for the treatment of high blood cholesterol from the American College of Cardiology/American Heart Association (ACC/AHA), will lead to an increase in the number of patients taking statins. Hence, the number of cases of statin intolerance may subsequently increase, emphasizing the need to understand and treat this important problem.

Topics: Cholesterol; Creatine Kinase; Drug Interactions; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Liver; Liver-Specific Organic Anion Transporter 1; Myalgia; Myositis; Organic Anion Transporters; Polymorphism, Genetic; Rhabdomyolysis; Risk Factors; Ubiquinone

Statin-associated myalgia occurs in about 1-3% of patients in the medical literature. Plasma CoQ10 levels are reduced in patients undergoing statin.. The primary outcome was the detection of clinical symptoms and the perception of pain evaluated throughout specific questionnaires. The secondary outcome was the variation in lipid profile and the variation in safety parameters.. We enrolled 60 Caucasian patients, intolerant to statins. During the run-in period, patients underwent a 1-month wash-out period during which statins were stopped. At the end of the wash-out period, if CPK and/or transaminases returned within an acceptable range, statins were re-introduced at half of the previously taken dose. After one month, patients were randomized to take either a liquid CoQ10 supplement or a placebo for three months at 100 mg/day.. The Clinical Index Score for myalgia assessment was lower after 3 months with CoQ10, while it did not change with the placebo. The VAS score was lower after 3 months of CoQ10 supplementation, while no variation was recorded with the placebo. In the group treated with the dietary supplement, CoQ10 plasma concentrations were inversely correlated with CPK levels, Clinical Index Score absolute values, and VAS.. The addition of CoQ10 with half dosage statin in patients with previous intolerance to statins improves the perception of clinical symptoms such as asthenia, myalgia or pain.

Topics: Aged; Dose-Response Relationship, Drug; Double-Blind Method; Dyslipidemias; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Myalgia; Pain Measurement; Surveys and Questionnaires; Ubiquinone

Myalgia is a common adverse effect of statin therapy, but the underlying mechanism is unknown. Statins may reduce levels of coenzyme Q10 (CoQ10), which is an essential electron carrier in the mitochondrial electron transport system, thereby impairing mitochondrial respiratory function, potentially leading to myalgia.. To investigate whether statin-induced myalgia is coupled to reduced intramuscular CoQ10 concentration and impaired mitochondrial respiratory function.. Patients receiving simvastatin (i.e., statin) therapy (n = 64) were recruited, of whom 25 experienced myalgia (myalgic group) and 39 had no symptoms of myalgia (NS group). Another 20 had untreated high blood cholesterol levels (control group). Blood and muscle samples were obtained. Intramuscular CoQ10 concentration was measured, and mitochondrial respiratory function and reactive oxygen species (ROS) production were measured. Citrate synthase (CS) activity was used as a biomarker of mitochondrial content in skeletal muscle.. Intramuscular CoQ10 concentration was comparable among groups. Mitochondrial complex II-linked respiration was reduced in the statin-myalgic and -NS groups compared with the control group. When mitochondrial respiration was normalized to CS activity, respiration rate was higher in the myalgic group compared with the NS and control groups. Maximal ROS production was similar among groups.. Statin therapy appeared to impair mitochondrial complex-II-linked respiration, but the mitochondrial capacity for complex I+II-linked respiration remained intact. Myalgia was not coupled to reduced intramuscular CoQ10 levels. Intrinsic mitochondrial respiratory capacity was increased with statin-induced myalgia but not accompanied by increased ROS production.

Topics: Adult; Aged; Cardiovascular Diseases; Cross-Sectional Studies; Electron Transport; Electron Transport Complex I; Electron Transport Complex II; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Mitochondria; Muscle, Skeletal; Myalgia; Reactive Oxygen Species; Simvastatin; Ubiquinone

Coenzyme Q10 (CoQ10) supplementation is the most popular therapy for statin myalgia among both physicians and patients despite limited and conflicting evidence of its efficacy.. This study examined the effect of coenzyme Q10 (CoQ10) supplementation on simvastatin-associated muscle pain, muscle strength and aerobic performance in patients with confirmed statin myalgia.. Statin myalgia was confirmed in 120 patients with prior symptoms of statin myalgia using an 8-week randomized, double-blind crossover trial of simvastatin 20 mg/d and placebo. Forty-one subjects developed muscle pain with simvastatin but not with placebo and were randomized to simvastatin 20 mg/d combined with CoQ10 (600 mg/d ubiquinol) or placebo for 8 weeks. Muscle pain (Brief Pain Inventory [BPI]), time to pain onset, arm and leg muscle strength, and maximal oxygen uptake (VO2max) were measured before and after each treatment.. Serum CoQ10 increased from 1.3 ± 0.4 to 5.2 ± 2.3 mcg/mL with simvastatin and CoQ10, but did not increase with simvastatin and placebo (1.3 ± 0.3 to 0.8 ± 0.2) (p < 0.05). BPI pain severity and interference scores increased with simvastatin therapy (both p < 0.01), irrespective of CoQ10 assignment (p = 0.53 and 0.56). There were no changes in muscle strength or VO2max with simvastatin with or without CoQ10 (all p > 0.10). Marginally more subjects reported pain with CoQ10 (14 of 20 vs 7 of 18; p = 0.05). There was no difference in time to pain onset in the CoQ10 (3.0 ± 2.0 weeks) vs. placebo (2.4 ± 2.1 wks) groups (p = 0.55). A similar lack of CoQ10 effect was observed in 24 subjects who were then crossed over to the alternative treatment.. Only 36% of patients complaining of statin myalgia develop symptoms during a randomized, double-blind crossover of statin vs placebo. CoQ10 supplementation does not reduce muscle pain in patients with statin myalgia. Trial RegistrationNCT01140308; www.clinicaltrials.gov.

Topics: Aged; Connecticut; Cross-Over Studies; Double-Blind Method; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Muscle Strength; Muscle, Skeletal; Myalgia; Oxygen Consumption; Pain Measurement; Severity of Illness Index; Simvastatin; Surveys and Questionnaires; Time Factors; Treatment Outcome; Ubiquinone

Statin use is frequently associated with muscle-related symptoms. Coenzyme Q10 supplementation has yielded conflicting results in decreasing statin myopathy. Herein, we tested whether coenzyme Q10 supplementation could decrease statin-associated muscular pain in a specific group of patients with mild-to-moderate muscle symptoms.. Fifty patients treated with statins and reporting muscle pain were recruited. The Q10 group (n=25) received coenzyme Q10 supplementation over a period of 30 days (50 mg twice daily), and the control group (n=25) received placebo. The Brief Pain Inventory (BPI) questionnaire was used and blood testing was performed at inclusion in the study and after 30 days of supplementation.. The intensity of muscle pain, measured as the Pain Severity Score (PSS), in the Q10 group was reduced from 3.9±0.4 to 2.9±0.4 (P<0.001). The Pain Interference Score (PIS) after Q10 supplementation was reduced from 4.0±0.4 to 2.6±0.4 (P<0.001). In the placebo group, PSS and PIS did not change. Coenzyme Q10 supplementation decreased statin-related muscle symptoms in 75% of patients. The relative values of PSS and PIS significantly decreased (-33.1% and -40.3%, respectively) in the Q10 group compared to placebo group (both P<0.05). From baseline, no differences in liver and muscle enzymes or cholesterol values were found.. The present results show that coenzyme Q10 supplementation (50 mg twice daily) effectively reduced statin-related mild-to-moderate muscular symptoms, causing lower interference of statin-related muscular symptoms with daily activities.

Topics: Activities of Daily Living; Adult; Aged; Dietary Supplements; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Muscles; Myalgia; Pain Measurement; Placebos; Ubiquinone

Topics: Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Ubiquinone

Topics: Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Ubiquinone

Statin-induced myopathy (SIM) has been partially attributed to deficiency of dolichol and coenzyme Q10 (CoQ10). We aimed to test the safety and efficacy of plant polyprenols in combination with CoQ10 for alleviation of SIM.. In an open-label, one-center prospective pilot study patients with SIM received conifer-tree needle polyprenols (4mg/day) and CoQ10 (100mg/day) for 8 weeks. Symptoms and safety were evaluated according to symptom severity score (0-10), creatine kinase (CK) levels, exercise test, dynamometry, complete blood count, clinical biochemistry and electrocardiography.. Of the 14 patients, 11 completed the study per protocol. Two patients withdrew consent due to travels abroad, and it was discontinued for one patient with stage 3 chronic kidney disease due to asymptomatic elevations of liver enzymes at week 4. No safety parameters changed significantly in per protocol group. Non-significant increase of CK levels was observed (P=0.231). Muscle pain (n=10) and weakness (n=7) scores improved significantly (P<0.001 and P=0.018, respectively). Muscle pain completely disappeared in 2 patients, weakness resolved in 3 patients and cramps disappeared in two patients. Four patients assessed improvement strong enough to consider increase of statin dose. No changes were observed in exercise test or dynamometry.. Conifer-tree polyprenols in combination with CoQ10 may be generally safe in patients with SIM, but caution should be exercised in patients with glomerular filtration rate <60mL/min and routine monitoring of the liver enzymes and CK is advocated in all patients. The observed efficacy provides the rationale for a larger, double-blind controlled study with polyprenols.

Topics: Aged; Aged, 80 and over; Biomarkers; Double-Blind Method; Drug Therapy, Combination; Electrocardiography; Exercise Test; Female; Glomerular Filtration Rate; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Muscle Weakness; Myalgia; Pain Measurement; Pilot Projects; Prospective Studies; Terpenes; Tracheophyta; Treatment Outcome; Ubiquinone

Exercise and treating hyperlipidaemia with statins are two integral components of the American Heart Association guidelines to reduce cardiovascular risk in adults. Since statins can cause myalgias and myopathies, they could affect the duration or intensity of an exercise regimen. To determine the impact of statin use in adult masters swimmers, a survey was distributed to examine the association between swimming performance and statin usage in adult swimmers (≥35 years). After excluding those with chronic diseases or taking drugs that reduce physical capacity, 749 swimmers (118 taking statins, 73 not taking statins to control elevated cholesterol and 558 controls) were included in a regression model to determine the factors significantly affecting the duration and intensity of swimming workouts. Age and gender were significantly (P ≤ 0.001) associated with the distance swam per 60 min. Younger, male swimmers completed more yards per 60-min workout. Use of statins was not significantly associated with yards swam per 60-min workout. Nor did statin usage affect the number of swim sessions per month or the length of swim session. Evidently, statins do not cause enough fatigue or pain in masters swimmers to require a decrease in the duration or intensity of workouts.

Topics: Adult; Age Factors; Aged; Athletic Performance; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Linear Models; Male; Middle Aged; Muscle Fatigue; Myalgia; Self Report; Sex Factors; Swimming; Time Factors; Ubiquinone; United States

Although statins remain the cornerstone of lipid-lowering therapy for reducing the burden of atherosclerotic vascular disease, their administration has been associated with muscle-related adverse effects, including myalgia and rhabdomyolysis. Such adverse events are probably due to reduced antioxidant defenses associated with fewer intermediate metabolites in the cholesterol synthesis pathway. We hypothesize that the concomitant inhibition of xanthine oxidase via coadministration of allopurinol with statins could diminish reactive oxygen species (ROS)-related muscle damage, which would have in turn have positive effects on both the incidence of muscle-related adverse events and cardiovascular outcomes. Accordingly, inhibition of xanthine oxidase has been previously shown to be effective for reducing biomarkers of muscle damage following exercise in professional athletes. Because of the widespread statin utilization and increasing trends in their therapeutic use in atherosclerotic vascular diseases, the proposed strategy could have important clinical implications for reducing statin-induced myalgia and rhabdomyolysis.

Topics: Allopurinol; Animals; Biomarkers; Cardiovascular Diseases; Enzyme Inhibitors; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Myalgia; Reactive Oxygen Species; Rhabdomyolysis; Ubiquinone; Xanthine Oxidase

Topics: Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Muscle, Skeletal; Myalgia; Simvastatin; Ubiquinone

Topics: Creatine Kinase, MM Form; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Ubiquinone

Topics: Creatine Kinase, MM Form; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Ubiquinone

Topics: Creatine Kinase, MM Form; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myalgia; Ubiquinone

Topics: Cholesterol; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Myalgia; Simvastatin; Ubiquinone

Topics: Aged; Amino Acid Substitution; AMP Deaminase; Atorvastatin; Biopsy; Causality; Creatine Kinase, MM Form; Exercise Tolerance; Female; Heptanoic Acids; Homozygote; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Liver-Specific Organic Anion Transporter 1; Mitochondria, Muscle; Models, Genetic; Muscle, Skeletal; Mutation, Missense; Myalgia; Organic Anion Transporters; Parkinsonian Disorders; Point Mutation; Polymorphism, Single Nucleotide; Purine-Pyrimidine Metabolism, Inborn Errors; Pyrroles; Ubiquinone