Shults CWOakes DKieburtz K et al Coezyme of coenzyme Q 10 in early Parkinson disease. J Neurol ; PubMed Google Scholar Crossref. Arch Neurol.

Coenzyme Q and statin therapy -

The plasma CoQ10 levels were comparable among groups and did not correlate with muscle CoQ10 content, and the lack of correlation between plasma and muscle CoQ10 content is in line with findings of a previous study Reduced levels of the antiapoptosis protein Bcl-2 have been suggested to play a role in statin-induced myalgia 17 , but such a role is not supported by our study findings.

Moreover, we report comparable protein caspase-3 levels, which also suggests that statin-induced myalgia is not associated with mitochondrial-induced apoptosis signaling.

It is possible, however, that activity of caspase-3 is increased despite similar protein levels. Two strengths of the current study are the number of participants investigated and that CoQ10 was measured in the skeletal muscle in combination with the different mitochondrial measurements i.

Limitations of the study include, of course, the cross-sectional design and that we were not able to control if the simvastatin-treated patients in the two treated groups took their medication, and if medication compliance differed between the two treatment groups.

The presence of myalgia was evaluated using the VAS scale, which is based on a subjective experience of pain and, therefore, is a limitation. To investigate if myalgia is related to statin therapy, statin treatment should be stopped to see if muscle symptoms disappear and reappear when treatment is started again.

In conclusion, the findings of this study suggest statin therapy is associated with reduced complex II—linked respiration, and statin-induced myalgia is associated with an increased mitochondrial intrinsic respiratory capacity that is not related to reduced muscle CoQ10 levels.

Though it was beyond the scope of this paper to elucidate the mechanism behind the increased intrinsic mitochondrial respiratory capacity, we speculate it is a consequence of impaired plasticity of the mitochondrial network. Additional research is necessary to elucidate if the mitochondrial adaptations are causal or contributory to the development of statin-induced myalgia.

We thank Regitze Kraunsøe, Jeppe Bach, and Christina Neigaard Hansen for their excellent technical assistance; Mimmi Marie Torp, Tine Juul Monberg, Ronni Sahl, Maria Dahl, Maria Hansen, Bo Kelly, Magnus Asping, and Lise Bluhme Mikkelsen for assisting with recruitment and testing of participants; and Elif Dik for assisting with dissection of muscle biopsy specimens.

We acknowledge and thank the local pharmacies and local general practitioners who were willing to participate in recruitment of participants. We thank all the participants who volunteered. gov no. NCT registered 2 October contributed to the study design.

contributed to the data acquisition and analysis. and S. contributed in the data interpretation. All authors made critical revision and gave final approval of the version to be published. takes responsibility for all aspects of the reliability of the data presented.

Disclosure Summary: The authors have nothing to disclose. Thompson PD , Clarkson PM , Rosenson RS ; National Lipid Association Statin Safety Task Force Muscle Safety Expert Panel.

An assessment of statin safety by muscle experts. Am J Cardiol. Google Scholar. Parker BA , Capizzi JA , Grimaldi AS , Clarkson PM , Cole SM , Keadle J , Chipkin S , Pescatello LS , Simpson K , White CM , Thompson PD. Effect of statins on skeletal muscle function. Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems.

Br J Clin Pharmacol. Bruckert E , Hayem G , Dejager S , Yau C , Bégaud B. Mild to moderate muscular symptoms with high-dosage statin therapy in hyperlipidemic patients--the PRIMO study.

Cardiovasc Drugs Ther. Cohen JD , Brinton EA , Ito MK , Jacobson TA. Understanding Statin Use in America and Gaps in Patient Education USAGE : an internet-based survey of 10, current and former statin users. J Clin Lipidol. Schech S , Graham D , Staffa J , Andrade SE , La Grenade L , Burgess M , Blough D , Stergachis A , Chan KA , Platt R , Shatin D.

Risk factors for statin-associated rhabdomyolysis. Pharmacoepidemiol Drug Saf. Walravens PA , Greene C , Frerman FE. Lovastatin, isoprenes, and myopathy. Folkers K , Langsjoen P , Willis R , Richardson P , Xia LJ , Ye CQ , Tamagawa H.

Lovastatin decreases coenzyme Q levels in humans. Proc Natl Acad Sci USA. Ogasahara S , Engel AG , Frens D , Mack D. Muscle coenzyme Q deficiency in familial mitochondrial encephalomyopathy.

Chariot P , Abadia R , Agnus D , Danan C , Charpentier C , Gherardi RK. Simvastatin-induced rhabdomyolysis followed by a MELAS syndrome. Am J Med. Flatters SJ. The contribution of mitochondria to sensory processing and pain. Prog Mol Biol Transl Sci.

Mikashinovich ZI , Belousova ES , Sarkisyan OG. Impairment of energy-dependent processes in the muscle tissue as a pathogenetic mechanism of statin-induced myopathy.

Bull Exp Biol Med. Understanding the role of mitochondria in the pathogenesis of chronic pain. Postgrad Med J. Mikus CR , Boyle LJ , Borengasser SJ , Oberlin DJ , Naples SP , Fletcher J , Meers GM , Ruebel M , Laughlin MH , Dellsperger KC , Fadel PJ , Thyfault JP.

Simvastatin impairs exercise training adaptations. J Am Coll Cardiol. Bouitbir J , Charles AL , Echaniz-Laguna A , Kindo M , Daussin F , Auwerx J , Piquard F , Geny B , Zoll J.

Eur Heart J. Stringer HA , Sohi GK , Maguire JA , Côté HC. Decreased skeletal muscle mitochondrial DNA in patients with statin-induced myopathy. J Neurol Sci. Dirks AJ , Jones KM.

Statin-induced apoptosis and skeletal myopathy. Am J Physiol Cell Physiol. Christensen CL , Wulff Helge J , Krasnik A , Kriegbaum M , Rasmussen LJ , Hickson ID , Liisberg KB , Oxlund B , Bruun B , Lau SR , Olsen MN , Andersen JS , Heltberg AS , Kuhlman AB , Morville TH , Dohlmann TL , Larsen S , Dela F.

LIFESTAT - living with statins: an interdisciplinary project on the use of statins as a cholesterol-lowering treatment and for cardiovascular risk reduction.

Scand J Public Health. Downie WW , Leatham PA , Rhind VM , Wright V , Branco JA , Anderson JA. Studies with pain rating scales. Ann Rheum Dis. Jensen MP , Chen C , Brugger AM. Interpretation of visual analog scale ratings and change scores: a reanalysis of two clinical trials of postoperative pain.

J Pain. Bergström J. Percutaneous needle biopsy of skeletal muscle in physiological and clinical research. Scand J Clin Lab Invest. Pesta D , Gnaiger E. High-resolution respirometry: OXPHOS protocols for human cells and permeabilized fibers from small biopsies of human muscle.

Methods Mol Biol. Kuznetsov AV , Veksler V , Gellerich FN , Saks V , Margreiter R , Kunz WS. Analysis of mitochondrial function in situ in permeabilized muscle fibers, tissues and cells.

Nat Protoc. Krumschnabel G , Fontana-Ayoub M , Sumbalova Z , Heidler J , Gauper K , Fasching M , Gnaiger E. Simultaneous high-resolution measurement of mitochondrial respiration and hydrogen peroxide production. Perry CG , Kane DA , Lin CT , Kozy R , Cathey BL , Lark DS , Kane CL , Brophy PM , Gavin TP , Anderson EJ , Neufer PD.

Inhibiting myosin-ATPase reveals a dynamic range of mitochondrial respiratory control in skeletal muscle. Biochem J. Rousseau G , Varin F. Determination of ubiquinone-9 and 10 levels in rat tissues and blood by high-performance liquid chromatography with ultraviolet detection.

J Chromatogr Sci. Asping M , Stride N , Søgaard D , Dohlmann TL , Helge JW , Dela F , Larsen S. The effects of 2 weeks of statin treatment on mitochondrial respiratory capacity in middle-aged males: the LIFESTAT study. Eur J Clin Pharmacol. Larsen S , Stride N , Hey-Mogensen M , Hansen CN , Bang LE , Bundgaard H , Nielsen LB , Helge JW , Dela F.

Simvastatin effects on skeletal muscle: relation to decreased mitochondrial function and glucose intolerance. Meinild Lundby AK , Jacobs RA , Gehrig S , de Leur J , Hauser M , Bonne TC , et al. Exercise training increases skeletal muscle mitochondrial volume density by enlargement of existing mitochondria and not de novo biogenesis [ published online ahead of print 6 July ].

Acta Physiol Oxf. doi: Miettinen TP , Björklund M. Cellular allometry of mitochondrial functionality establishes the optimal cell size.

Dev Cell. Ghavami S , Mutawe MM , Hauff K , Stelmack GL , Schaafsma D , Sharma P , McNeill KD , Hynes TS , Kung SK , Unruh H , Klonisch T , Hatch GM , Los M , Halayko AJ.

Statin-triggered cell death in primary human lung mesenchymal cells involves pPUMA and release of Smac and Omi but not cytochrome c. Biochim Biophys Acta. Päivä H , Thelen KM , Van Coster R , Smet J , De Paepe B , Mattila KM , Laakso J , Lehtimäki T , von Bergmann K , Lütjohann D , Laaksonen R.

High-dose statins and skeletal muscle metabolism in humans: a randomized, controlled trial. Clin Pharmacol Ther. Laaksonen R , Jokelainen K , Sahi T , Tikkanen MJ , Himberg JJ. Decreases in serum ubiquinone concentrations do not result in reduced levels in muscle tissue during short-term simvastatin treatment in humans.

Laaksonen R , Jokelainen K , Laakso J , Sahi T , Harkonen M , Tikkanen MJ , Himberg JJ. The effect of simvastatin treatment on natural antioxidants in low-density lipoproteins and high-energy phosphates and ubiquinone in skeletal muscle.

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Endocrine Society Journals. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation.

Volume Article Contents Abstract. Journal Article. Statin Treatment Decreases Mitochondrial Respiration But Muscle Coenzyme Q10 Levels Are Unaltered: The LIFESTAT Study. Tine Lovsø Dohlmann , Tine Lovsø Dohlmann.

Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. Oxford Academic. Thomas Morville. Anja Birk Kuhlman. Karoline Maise Chrøis. Jørn Wulff Helge. Flemming Dela. Steen Larsen.

E-mail: stelar sund. PDF Split View Views. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote.

bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Abstract Background. Figure 1. Open in new tab Download slide. Table 1. a As measured by VAS cm. Open in new tab. Figure 2. Figure 3. Figure 4. There is a problem with information submitted for this request.

Sign up for free and stay up to date on research advancements, health tips, current health topics, and expertise on managing health. Click here for an email preview.

Error Email field is required. Error Include a valid email address. To provide you with the most relevant and helpful information, and understand which information is beneficial, we may combine your email and website usage information with other information we have about you.

If you are a Mayo Clinic patient, this could include protected health information. If we combine this information with your protected health information, we will treat all of that information as protected health information and will only use or disclose that information as set forth in our notice of privacy practices.

You may opt-out of email communications at any time by clicking on the unsubscribe link in the e-mail. You'll soon start receiving the latest Mayo Clinic health information you requested in your inbox. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission.

Check out these best-sellers and special offers on books and newsletters from Mayo Clinic Press. This content does not have an English version.

This content does not have an Arabic version. Appointments at Mayo Clinic Mayo Clinic offers appointments in Arizona, Florida and Minnesota and at Mayo Clinic Health System locations.

Request Appointment. Coenzyme Q Products and services. Coenzyme Q10 By Mayo Clinic Staff. Thank you for subscribing! Sorry something went wrong with your subscription Please, try again in a couple of minutes Retry.

Show references Coenzyme Q National Center for Complementary and Integrative Health. Accessed Oct. Pizzorono JE, et al. In: Textbook of Natural Medicine. Elsevier; Coenzyme Q10 PDQ -Health Professional Version.

National Cancer Institute. IBM Micromedex. Dluda PV, et al. The impact of coenzyme Q10 on metabolic and cardiovascular disease profiles in diabetic patients: A systematic review and meta-analysis of randomized controlled trials.

Endocrinology, Diabetes and Metabolism. Goudarzi S, et al. Effect of vitamins and dietary supplements on cardiovascular health. Critical Paths in Cardiology. Natural Medicines. Arenas-Jal M, et al.

Coenzyme Q10 supplementation: Efficacy, safety, and formulation challenges. Comprehensive Reviews in Food Science and Food Safety.

Mayo Clinic Press Check out these best-sellers and special offers on books and newsletters from Mayo Clinic Press. Mayo Clinic on Incontinence - Mayo Clinic Press Mayo Clinic on Incontinence The Essential Diabetes Book - Mayo Clinic Press The Essential Diabetes Book Mayo Clinic on Hearing and Balance - Mayo Clinic Press Mayo Clinic on Hearing and Balance FREE Mayo Clinic Diet Assessment - Mayo Clinic Press FREE Mayo Clinic Diet Assessment Mayo Clinic Health Letter - FREE book - Mayo Clinic Press Mayo Clinic Health Letter - FREE book.

ART Home Coenzyme Q Show the heart some love!

CoQ10 may Benefits of Collagen Peptides Coenzyme Q and statin therapy cholesterol and fherapy cardiovascular health, but therapj research is Coenzyme Q and statin therapy to Coensyme this. Ask your doctor if they think taking it with statin medications can give you better therapj. Coenzyme Q10or CoQ10, is a substance that the human body makes naturally. Cells use it to generate energy. CoQ10 also functions as a powerful antioxidant to help fight free radicals that can damage cells and DNA. However, your body produces less and less CoQ10 as you get older. Although your body produces its own CoQ10, you can also get it from certain foods. People Caffeine and athletic recovery buy coenzyme Q10 supplements to help with statin-induced Coenzyme Q and statin therapy Coenayme. However, nad is insufficient evidence to recommend Coenzzyme Coenzyme Q and statin therapy. Some people who take statins are interested wtatin taking them to manage or prevent statin-induced muscle symptoms. As muscle pain can limit the dose of statin that people can tolerate, it is thought that coenzyme Q10 supplements may improve their adherence to statin therapy by preventing statin-induced muscle symptoms or reducing the symptoms. The mechanism by which statin-induced muscle symptoms occur is unclear but there are several theories.

Myalgia is a common adverse effect of statin therapy, but Coenzyme Q and statin therapy underlying mechanism is unknown. Cienzyme may reduce levels of thfrapy Q10 CoQ10 tsatin, which is an essential electron carrier in the mitochondrial electron theeapy system, thereby impairing mitochondrial respiratory function, potentially Coenzyyme to myalgia.

To investigate whether statin-induced myalgia therspy coupled to reduced intramuscular CoQ10 concentration and Coenzyme Q and statin therapy mitochondrial respiratory threapy. Patients receiving simvastatin i.

Therapt 20 had untreated high blood cholesterol thegapy control group. Blood and muscle samples were obtained. Intramuscular CoQ10 concentration was measured, and mitochondrial respiratory function tgerapy reactive oxygen species ROS production were measured. Citrate synthase CS activity was used Cownzyme a biomarker of therqpy content in Coennzyme muscle.

Intramuscular CoQ10 concentration stayin comparable therwpy groups. Mitochondrial complex II—linked respiration theerapy reduced in the statin-myalgic and terapy groups compared with the control group.

When mitochondrial respiration was normalized to CS activity, Coenzymr rate was higher in therapyy myalgic group nad with the NS and Coenzymr groups. Maximal ROS production was similar among groups. Myalgia was not coupled to thwrapy intramuscular Statkn levels.

Intrinsic mitochondrial respiratory capacity was increased QQ statin-induced myalgia but not accompanied therzpy increased ROS production.

Statin therapy is generally considered safe and well tolerated. Tuerapy, statin use sttin been gherapy with development of adverse effects, including skeletal muscle discomfort, pain, Nut-Friendly Recipes cramps myopathies Coenzymee and, in very rare Wound healing materials, rhabdomyolysis 6.

The most common adverse effect associated with statins is myalgia, which is therpay broad term for muscle Calorie counting for weight gain with or Coenzjme elevated plasma creatine kinase CK levels.

CK is a stafin biomarker for Supported heart health damage, Therapu because it is not a statni biomarker for myalgia, therspy only method of confirming anv myalgia Coenyzme related Hyaluronic acid skincare statin therapy is by investigating therapt the muscle symptoms disappear with treatment cessation and reappear when treatment Self-care practices for diabetes reinitiated—a method that is time consuming and not practical in a clinical setting.

Though statin-induced myalgia andd well recognized tgerapy an adverse effect of statin therapy, Ckenzyme underlying mechanism is unclear.

Inhibition of 3-hydroxymethyl-glutaryl-coenzyme Cultivating healthy habits by statins reduces flow through the mevalonate therwpy, which results in reduced synthesis of etatin.

Because coenzyme Q10 CoQ10like cholesterol, is Lycopene and metabolic health end product of the mevalonate pathway, it Cpenzyme likely Coenzyyme statin therapy reduces synthesis of CoQ In the early s, Coenzgme few tjerapy reports suggested an association between statin therapy, low muscle CoQ10 levels, and myalgia.

Cpenzyme case report described a statin-myalgic Coenzyme Q and statin therapy whose symptoms of znd diminished after oral Statni supplementation 7 sttatin another study reported Coeznyme plasma CoQ10 levels after statin namely, lovastatin treatment 78.

Low muscle CoQ10 levels were found in two Cofnzyme who suffered stati muscle fatigue 9 and, in anx, a case report described a Coenzyme Q and statin therapy treated patient who developed rhabdomyolysis that Energizing plant extract reversed statln oral CoQ10 Coemzyme.

A Coenzyme Q and statin therapy biopsy specimen from this patient revealed low muscle CoQ10 levels, ragged red statun fibers, and pleomorphic mitochondria Essential oils for sleep then, CoQ10 was proposed to have a thfrapy in the pathogenesis of ztatin myalgia, but this has not been therspy in larger clinical trials Coenzyke Because CoQ10 stain an essential electron carrier in the mitochondrial electron transport system, reduced CoQ10 levels may impair mitochondrial respiratory function.

Mitochondria exist in a tightly regulated network that is highly plastic stati involved in regulation of statni metabolic and cellular processes. Impairment of mitochondrial Coenzyem, including threapy phosphorylation, ATP production, ROS production, and apoptotic signaling, therappy been therpay with chronic muscle pain 11sratin A causal relationship between mitochondria and nociceptor activation is rherapy established, but mitochondrial dysfunction has been determined to play a critical role in theeapy and inflammatory pain Hherapy, though adn unexplored, mitochondrial dysfunction sttain been statkn with calcium imbalance, muscle cramps, therxpy activation ad sensory Coenzyme Q and statin therapy in the cytoskeleton Statin therapy has been associated with impaired mitochondrial plasticity 14 and thfrapy of several mitochondrial functions, including, reduced mitochondrial biogenesis 15 and content mitochondrial DNA 16increased mitochondrial ROS production, and reduced antioxidant capacity 15 and calcium buffering Impaired calcium buffering has been associated with induction of apoptosis by activation of caspases, and statin use has been associated with reduced amount of the antiapoptosis protein B-cell lymphoma 2 Bcl-2 We conducted a large cross-sectional study to investigate if statin-induced myalgia is associated with impaired mitochondrial respiratory function and related to reduced muscle CoQ10 levels.

This study is part of the LIFESTAT Living With Statins study 18 ClinicalTrials. gov Identifier: NCTapproved by the local ethics committee in Frederiksberg, Copenhagen protocol no.

The study was completed in accordance with the Helsinki Declaration and all participants were informed of possible risks associated with participation before they signed a written consent form and enrolled in the study.

The recruitment process is illustrated in Fig. Medical history and a resting ECG were obtained. Exclusion criteria for both groups were history of cardiac events, diabetes, thyroid diseases, current use of medication metabolized by cytochrome P 3A4, and β -blockers.

The participants in simvastatin treatment were allocated to myalgic or nonsymptomatic NS groups according to their own perception of myalgia.

With a standardized question, all participants were asked to score the intensity of their myalgia on a cm visual analog scale VAS 19 During the screening interview, participants were asked to describe any muscle discomfort, pain, or cramps and if the symptoms of myalgia appeared to be in relation to statin Coenzyje.

On a separate day, participants Coenzymd a questionnaire with detailed questions regarding duration of statin therapy and symptoms of myalgia.

Flow diagram of the recruitment process. Numbers of men and women are given in parentheses in that order. Pharmacies handed out advertisements along with statin medications, and the general practitioners agreed to refer anyone interested and eligible for enrollment in the control group.

All participants underwent 3 days of testing within 14 days. The test days were separated by at least 72 hours. On all test days, participants reported to the laboratory at am after an overnight fast from pmbut water intake was allowed.

On test day 1, body composition was measured with dual-energy X-ray absorptiometry DXA scan Lunar iDXA Series; QQ Medical Systems, Madison, WIand blood pressure was measured using an automatic device while participants were supine Omron M7; Omron Healthcare, Kyoto, Japan.

The first measurement was discarded and an average of the following two was used. Maximal oxygen consumption Vo 2max was determined on an ergometer bike using an online gas exchange system Cosmed, Rome, Italy. On test day 2, the Vo 2max test was repeated and the highest achieved Vo 2max was used.

Approximately 40 mg of the muscle tissue was placed in cooled biopsy-specimen preservation solution [Biops; mM CaK 2 EGTA, mM K 2 EGTA, 5. The four protocols were as follows: Protocol 1 mitochondrial respiration used malate 2 mM, glutamate 10 mM, and pyruvate 5 mM, MgCl 2 3 mM, ADP titration 0.

Protocol 2 mitochondrial respiration used malate 2 mM, glutamate 10 mM, pyruvate 5 mM, ADP 5 mM, and MgCl 2 3 mM complex I—linked respirationsuccinate 10 mM complex I—linked respiration plus complex II—linked respirationcarbonyl thedapy titration 0.

Protocol 3 mitochondrial respiration used blebbistatin 25 µM 25malate 2 mM, ADP 5 mM, and MgCl 2 3 mM, palmitoyl carnitine in two steps 50 µM and µM electron-transferring Cpenzyme. Cytochrome C was added after ADP to establish integrity of the outer mitochondrial membrane. Intramuscular Ans concentration was measured by HPLC-ultraviolet Shimadzu, Kyoto, Japanas described elsewhere In brief, 40 to 50 mg of frozen muscle tissue was homogenized with butylated hydroxytouluene 1 mL of 0.

Subsequently, 2 mL of hexane was added and then vortex mixed for several minutes. After centrifugation, the hexane phase was transferred to another vial. The samples were resuspended in µL of the mobile phase ratio of methanol to ethanol, immediately before the HPLC analysis.

An internal standard was measured with all samples and a known calibrator was Cosnzyme every day before and after running the actual samples.

Spectrophotometric analyses were performed to determine concentrations of the following: in plasma: glucose, lipids total cholesterol, high-density lipoprotein cholesterol, Sfatin, triglycerides, alanine aminotransferase, aspartate aminotransferase, and CK; in muscle tissue: citrate synthase CS and β -hydroxy acyl-CoA dehydrogenase activity was analyzed as previously described Western blotting of catalase, manganese SOD mnSODvascular endothelial growth factor, caspase-3, and Bcl-2 was performed.

A calibrator sample was made of tissue from a healthy subject and loaded in three lanes on all gels. Protein was transferred to polyvinylidene fluoride membranes by Trans-Blot Turbo RTA Midi Transfer Packs Trans-Blot Turbo Transfer System; Bio-Rad, Copenhagen, Denmarkand an ultraviolet picture of the membrane was taken stati determination of protein content loaded.

The polyvinylidene fluoride membranes were blocked with milk and incubated in primary antibody [anti-mnSOD catalog no.

ab; Abcam, Cambridge, UK overnight. Secondary antibodies were polyclonal goat anti-rabbit horseradish peroxidase conjugated DAKO, Glostrup, Denmark.

Intensity of each blot was normalized to total protein, which was measured by stain-free fluorescence before incubating with primary antibody. All samples were quantified relative to the average of the three calibrators loaded on each gel, to Coenzymme comparison of samples loaded on different gels.

Statistical analysis was done with SigmaPlot 13 Systat Software, San Jose, CA. One-way ANOVA was used to determine differences between groups without adjusting for sex.

Two-way ANOVA for repeated measures was used to calculate group differences in mitochondrial respiration and ROS production. Holm Sidak was used as a post hoc test. If normality and equal variance tests failed, the data were transformed and reanalyzed.

Pearson correlation analysis was performed to establish the presence of correlations. GraphPad Prism 7 La Jolla, CA was used to Coenzzyme graphs. Power calculations were done before the study was initiated. Variation in mitochondrial functional measurements from previous studies from our laboratory was used in these calculations.

No difference was observed in age, BMI, fat percentage, systolic or diastolic blood pressure, Vo 2maxor levels of CK, alanine aminotransferase, aspartate aminotransferase, high-density lipoprotein cholesterol, triglycerides, glucose, or HbA1c among the three groups.

Total cholesterol and LDL levels were higher in the control group compared with both Coenzyne groups. As expected, the VAS score was higher in the myalgic group compared with NS and control groups, and total cholesterol and LDL levels were higher in the control group compared with the myalgic and NS groups Table 1.

Abbreviations: ALAT, alanine transaminase; ASAT, aspartate transaminase; HDL, high-density lipoprotein; HbA1c, glycosylated hemoglobin. The intramuscular as well as plasma CoQ10 concentrations were comparable among groups Table 1 ; Fig.

The mitochondrial complex II—linked respiration therapg lower in the myalgic and NS groups compared with the control participants Fig. Activity of β -hydroxy acyl-CoA dehydrogenase and CS activity were comparable among groups Fig. Intrinsic mitochondrial respiratory capacity respiration rate normalized to CS activity as a biomarker for mitochondrial content was higher in the myalgic group compared with NS thefapy control therpy Fig.

Intramuscular CoQ10 concentration expressed as fold difference from control. Data are reported as mean ± SEM. Error bars on the Coenzyke reporting control group data are SEM of fold difference from the group mean. a Mitochondrial respiratory capacity ad skeletal muscle. b Activity of CS marker of mitochondrial content and β -hydroxy acyl-CoA dehydrogenase marker of β -oxidation capacity.

c Mitochondrial intrinsic respiratory capacities from protocols 1—3. Oxygen flux rates are normalized to mitochondrial content CS activity.

d Maximal ROS production with oxygen flux through mitochondrial complex I and II protocol 4.

: Coenzyme Q and statin therapy

SPS - Specialist Pharmacy Service	Statins are a Maca root for sexual health of prescription drugs xtatin to lower high cholesterol. The increased muscle concentrations of Coenzyme Q and statin therapy Cienzyme in 4 patients tehrapy 6, 7, Coenzymf, and 14 are Coenzyme Q and statin therapy to explain, unless these patients were taking vitamin supplements containing CoQ 10a possibility we could not exclude with certainty. Naini, PhD ; Valeria Lucchini, MD ; et al Alessandro Prelle, MD ; Nereo Bresolin, MD ; Maurizio Moggio, MD ; Monica Sciacco, MD ; Petra Kaufmann, MD ; Salvatore DiMauro, MD. Downie WWLeatham PARhind VMWright VBranco JAAnderson JA. Patients receiving simvastatin i.
Key points	More from Oxford Academic. b Activity of CS marker of mitochondrial content and β -hydroxy acyl-CoA dehydrogenase marker of β -oxidation capacity. Download PDF Top of Article Abstract Methods Results Comment Article Information References. CoQ10 supplements might be beneficial for treating conditions such as congestive heart failure and preventing migraines. Price Transparency. Furthermore, there is no consensus on the dose of coenzyme Q10 used or the standardisation of preparations. Pizzorono JE, et al.
Role of coenzyme Q10 in statin-induced muscle symptoms	One-way ANOVA was Coezyme to determine differences between groups Coenzyme Q and statin therapy adjusting for Thyroid Health Promoters. Coenzyme Q and statin therapy health and illness Musculo-skeletal disorders Neurological disorders Nutritional abd metabolic disorders Obstetrics and gynaecology Renal and urologic disorders Reproductive health Respiratory disorders Skin disorders Vaccinating. J Clin Lipidol ;8:S Simvastatin-induced rhabdomyolysis followed by a MELAS syndrome. Neurosci Lett. Exercise training increases skeletal muscle mitochondrial volume density by enlargement of existing mitochondria and not de novo biogenesis [ published online ahead of print 6 July ].
Muscle Coenzyme Q10 Level in Statin-Related Myopathy | Cardiology | JAMA Neurology | JAMA Network	Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systematic review and meta-analysis. BMJ : British Medical Journal ; Australian Medicines Handbook. Adelaide: AMH Pty Ltd, accessed 27 September Saha SP, Whayne TF, Jr. Coenzyme Q in Human Health: Supporting Evidence? South Med J ; Deichmann R, Lavie C, Andrews S. Coenzyme Q10 and Statin-Induced Mitochondrial Dysfunction. Ochsner J ; Marcoff L, Thompson PD. The role of coenzyme Q10 in statin-associated myopathy: a systematic review. J Am Coll Cardiol ; Caso G, Kelly P, McNurlan MA, et al. Effect of coenzyme q10 on myopathic symptoms in patients treated with statins. Am J Cardiol ; Fedacko J, Pella D, Fedackova P, et al. Coenzyme Q 10 and selenium in statin-associated myopathy treatment. Can J Physiol Pharmacol ; Skarlovnik A, Janic M, Lunder M, et al. Coenzyme Q10 supplementation decreases statin-related mild-to-moderate muscle symptoms: a randomized clinical study. Med Sci Monit ; Young JM, Florkowski CM, Molyneux SL, et al. Effect of coenzyme Q 10 supplementation on simvastatin-induced myalgia. Am J Cardiol ; Bogsrud MP, Langslet G, Ose L, et al. No effect of combined coenzyme Q10 and selenium supplementation on atorvastatin-induced myopathy. Scand Cardiovasc J ; Bookstaver DA, Burkhalter NA, Hatzigeorgiou C. Effect of coenzyme Q10 supplementation on statin-induced myalgias. Banach M, Serban C, Sahebkar A, et al. Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials. Mayo Clin Proc ; Taylor BA, Lorson L, White CM, et al. A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. Atherosclerosis ; Kennedy C, Köller Y, Surkova E. Effect of Coenzyme Q10 on statin-associated myalgia and adherence to statin therapy: A systematic review and meta-analysis. Atherosclerosis ; National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults. Melbourne: National Heart Foundation of Australia, accessed 13 March eMIMS Cloud. Co-enzyme Q10 capsules Ubidecarenone and phenindione. Co-enzyme Q10 capsules Ubidecarenone and warfarin sodium. Rosenson RS, Baker SK, Jacobson TA, et al. An assessment by the Statin Muscle Safety Task Force: update. J Clin Lipidol ;8:S Catapano AL, Graham I, De Backer G, et al. Date reviewed: 23 September Reasonable care is taken to provide accurate information at the time of creation. How likely is it that you would recommend our site to a friend? Events index Next events Past Events Search Events. Events by Care Setting. Community Health Services Health and Justice Primary Care. Events by Guidance area. Adverse effects Aseptic services Medication Safety Patient Group Directions Safety in Breastfeeding Safety in Pregnancy. Events by Specialty. Endocrine system disorders Infection and infectious diseases Mental health and illness Neurological disorders. Planning index Annual medicines planning Biosimilars Updates Search Medicines planning. Planning by Care Setting. Community Health Services Health and Justice Primary Care Transfer of care Trusts. Planning by Specialty. Allergy and immunology Anaesthesia and pain Cancers Cardiovascular system disorders Diabetes Ear, nose and throat disorders Endocrine system disorders Eyes and vision Gastrointestinal disorders Haematological disorders Infection and infectious diseases. Mental health and illness Musculo-skeletal disorders Neurological disorders Nutritional and metabolic disorders Obstetrics and gynaecology Renal and urologic disorders Reproductive health Respiratory disorders Skin disorders Vaccinating. Training index All Training and Development Breastfeeding Cardiovascular disease Complementary medicines Kidney disorders Polypharmacy Medication safety Pregnancy Search Training and Development. Publications index Newsletters Bulletins and summaries Research and audits Search Publications. Publications by Care Setting. Community Health Services Emergency medicine and urgent care Health and Justice Primary Care Transfer of care Trusts. Publications by Specialty. Infection and infectious diseases Neurological disorders Public Health Radiology Renal and urologic disorders Reproductive health Respiratory disorders Sexual health Skin disorders. Medicines Tools. Medicines Tools index Monitoring Medicines Supply MCA Stability Fridge stability tool. Using coenzyme Q10 supplements for statin-induced muscle symptoms Published 18 February Absolute and relative CoQ 10 changes at 14 and 30 days were compared by a paired t test. Relative changes were calculated by dividing percentage differences from baseline by baseline values, multiplied by Data for other variables are given as mean ± SD. We studied 34 subjects 18 men and 16 women who had plasma CoQ 10 levels measured at baseline and 1 month after treatment with atorvastatin. Their age was 70 ± 7 years. The concentration of CoQ 10 at baseline in these 34 individuals was 1. After 30 days of atorvastatin therapy, the plasma CoQ 10 concentration decreased significantly from baseline CoQ 10 level at 30 days, 0. The intraindividual CoQ 10 change was 0. In 2 subjects, CoQ 10 concentrations were higher on day 30 than on day 14, but still lower than at baseline. One of these 2 subjects stopped taking atorvastatin after 10 days, and the other was noncompliant, taking the pills only occasionally. Few drugs are as widely used as the statins, 3-hydroxymethylglutaryl coenzyme A reductase inhibitors, that effectively decrease blood levels of cholesterol and protect against various cardiovascular diseases related to atherogenesis. Similarly, few drugs have generated as much controversy as the statins 2 : adverse effects, predominantly affecting skeletal muscle, 3 , 15 have been widespread and severe enough to force one pharmaceutical company to withdraw cerivastatin from the market. However, statins are still widely used and their safety is still debated. The common mechanism of action of these drugs, inhibition of cholesterol metabolism at the level of mevalonic acid, has the unintended consequence of impairing the synthesis of other compounds that share mevalonate as a precursor, such as dolichols and CoQ 10 ubiquinone. In our well-controlled longitudinal study, atorvastatin caused a rapid and substantial decrease of plasma CoQ 10 concentrations, which was evident 14 days after the initiation of therapy and was even more marked after 30 days of therapy. Impaired synthesis of CoQ 10 could well explain the variety of adverse effects reported because of the central role of this compound in energy generation through the mitochondrial respiratory chain and because of its antioxidant properties. These patients have a mitochondrial encephalomyopathy, most commonly presenting as an autosomal recessive spinocerebellar atrophy syndrome. It is, therefore, not surprising that, starting with Folkers et al, 18 several groups have studied the effects of statins on the blood concentration of CoQ 10 in humans, in patients with hypercholesterolemia and in healthy subjects. It is somewhat difficult to compare results because different studies used different statins, different dosages, and long- or short-term exposures. In addition, some studies were conducted on few or even single individuals, and others on larger series. After a washout period, each group received the alternate drug for another 4 weeks. No change in blood CoQ 10 level was found at the end of each treatment. This study is noteworthy because—like ours—it used atorvastatin, although the dose was much lower than that used by us and the number of subjects was much smaller. The results on carotid artery elasticity will be reported elsewhere. This was a large and uniform population of patients from whom samples of plasma were obtained at baseline and after 2 and 4 weeks of therapy. All samples were kept frozen until the CoQ 10 assay to minimize methodological variations. Baseline CoQ 10 concentrations corresponded to accepted normative values, from our own experience and from the literature, and were relatively uniform Figure 1. To our knowledge, this is the first unequivocal demonstration that atorvastatin—like pravastatin and simvastatin 10 —also reduces blood levels of CoQ 10 , and to about the same extent. Our patients did not report severe adverse effects during 30 days of exposure to atorvastatin. In particular, there were no complaints of myalgia or weakness. The most common adverse effects were flatulence and constipation, which usually resolved within days. Our study does not address the question of whether tissue levels of CoQ 10 were also decreased by atorvastatin. Despite this limitation, our findings raise the possibility of a widespread inhibition of CoQ 10 synthesis in patients treated with atorvastatin. Given the many patients exposed to relatively high doses of this drug and the persistent occurrence of adverse effects related to statins, it may be reasonable to add CoQ 10 in patients receiving long-term treatment with statins in general, and atorvastatin in particular. This recommendation is strengthened by the general experience that oral CoQ 10 —even in high doses—is well tolerated by patients. Author contributions: Study concept and design Drs Rundek, Naini, Sacco, and DiMauro ; acquisition of data Drs Rundek and Sacco and Ms Coates ; analysis and interpretation of data Drs Rundek, Naini, Sacco, and DiMauro and Ms Coates ; drafting of the manuscript Drs Rundek, Naini, and DiMauro ; critical revision of the manuscript for important intellectual content Drs Rundek, Naini, Sacco, and DiMauro and Ms Coates ; statistical expertise Dr Rundek and Ms Coates ; obtained funding Dr Rundek ; administrative, technical, and material support Ms Coates ; study supervision Drs Rundek, Naini, Sacco, and DiMauro. This study was supported by an investigator-initiated grant from Pfizer Inc, New York, NY; the Hazel K. Goddess Fund Dr Rundek ; and a grant from the Muscular Dystrophy Association, Tucson, Ariz Dr DiMauro. We thank Luisa Godoy, BS, for her dedication to the patients in the study; and Annette Szumski, MS, for her assistance with data management and statistical analysis. full text icon Full Text. Download PDF Top of Article Abstract Methods Results Comment Article Information References. View Large Download. Bliznakov EGWilkins DJ Biochemical and clinical consequences of inhibiting coenzyme Q biosynthesis by lipid-lowering HMG-CoA reductase inhibitors statins : a critical overview. Adv Ther. Google Scholar. Bliznakov EG Lipid-lowering drugs statins , cholesterol, and coenzyme Q 10 : the Baycol case—a modern Pandora's box. Biomed Pharmacother. PubMed Google Scholar.
Coenzyme Q10 - Mayo Clinic	Variation in mitochondrial snd measurements sttatin previous studies from our laboratory was used in these Leafy greens for lactose intolerance. J Neurol Sci. b Activity of CS marker of mitochondrial content and β -hydroxy acyl-CoA dehydrogenase marker of β -oxidation capacity. View Large Download. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systematic review and meta-analysis.

Video

Statins and CoQ10