Statin treatment associated with depleted levels of coenzyme Q10 and cytochrome oxidase

This study was published in Toxicology Mechanisms and Methods 2009 Jan;19(1):44-50

 

Study title and authors:

Decreased ubiquinone availability and impaired mitochondrial cytochrome oxidase activity associated with statin treatment.

Duncan AJ, Hargreaves IP, Damian MS, Land JM, Heales SJ.

Department of Molecular Neuroscience, UCL Institute of Neurology, London WC1N 1BG, UK.

 

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/19778232

This study investigated the involvement of statins in impaired cellular energy production. Mitochondria are the cells power plants, and coenzyme Q10 (ubiquinone) and cytochrome oxidase (complex IV) are vital enzymes needed in cellular energy production.

In a study published in the Journal of the American College of Cardiology, coenzyme Q10 (ubiquinone) was shown to lower cardiovascular deaths by 43% and lower the overall death rate by 42%.

Cytochrome oxidase (Complex 4) deficiency is a condition that can affect several parts of the body, including the muscles used for movement (skeletal muscles), the heart, the brain, or the liver. Cytochrome oxidase deficiency can lead to muscle weakness (myopathy), poor muscle tone (hypotonia), severe brain dysfunction (encephalomyopathy). Approximately one quarter of individuals with cytochrome oxidase deficiency have a type of heart disease that enlarges and weakens the heart muscle (hypertrophic cardiomyopathy). Another possible feature of this condition is an enlarged liver, which may lead to liver failure. Most individuals with cytochrome c oxidase deficiency have a buildup of a chemical called lactic acid in the body (lactic acidosis), which can cause nausea and an irregular heart rate, and can be life-threatening. Many people with cytochrome oxidase deficiency have a loss of mental function, movement problems, hypertrophic cardiomyopathy, eating difficulties, and brain abnormalities. Cytochrome oxidase deficiency is frequently fatal in childhood.

(i) Two patients experiencing muscle problems following treatment with simvastatin (40 mg per day) and cyclosporin (patient 1) and simvastatin (40 mg per day) and itraconazole (patient 2).
(ii) Analysis of the two patients skeletal muscle revealed a decreased ubiquinone status (77 and 132; reference range: 140-580 pmol/mg) and decreased complex IV activity (0.006 and 0.007 reference range: 0.014-0.034).
(iii) To assess statin treatment in the absence of possible pharmacological interference from cyclosporin or itraconazole, primary astrocytes (cells from the central nervous system) were cultured with lovastatin.
(iv) Lovastatin treatment resulted in a decrease in ubiquinone (statin treatment 97.9 versus control 202.9 pmol/mg), and a decrease in complex IV activity (statin treatment 0.008 versus control: 0.011).

Duncan concludes: "These data, coupled with the patient findings, indicate a possible association between statin treatment, decreased ubiquinone status, and loss of complex IV activity".

List of some drugs that may cause side effects when coadministered with statins

This paper was published in the Medical Journal of Australia 2001 Nov 5;175(9):486-9

Study title and author:
Statin-associated myopathy.

Hamilton-Craig I.
North Adelaide Cardiac Clinic, SA. admin@medped-aust.com

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/11758079

Dr Hamilton-Craig notes that myopathy (muscle disease) can be caused by all statins.

In this review he finds:
(a)  The risk of myopathy is increased by: the use of high doses of statins, concurrent use of fibrates, concurrent use of hepatic cytochrome P450 inhibitors, acute viral infections, major trauma, surgery, hypothyroidism and other conditions.
(b) Cytochrome P450 are enzymes that give protection against potential toxicity from the foods and drugs (including statins) that we ingest by breaking down and eliminating the toxic substance. These enzymes are found primarily within liver cells as well as many other cell types. Cytochrome P450 inhibitors inhibit the effectiveness of cytochrome P450 enzymes and thereby increase the levels of statins in the body which leads to increased toxicity and more side effects. Cytochrome P450 inhibitors include: Amiodarone; (Cordarone), Azole Antifungals; Fluconazole (Diflucan), Itraconazole (Sporanox), Ketoconazole (Nizoral), Posaconazole (Noxafil, Posanol), Voriconazole (Vfend), Calcium Channel Blockers; (Amlodipine, Diltiazem, Verapamil), Cyclosporine; (Neoral), Danazol; (Cyclomen), Dronedarone (Multaq), Fibric Acid Derivatives; (Fenofibrate, Gemfibrozil), Glyburide; Grapefruit/Grapefruit Juice; Macrolide Antibiotics; Clarithromycin (Biaxin), Erythromycin, Nefazodone; Phenytoin; (Dilantin), Protease Inhibitors; Atazanavir (Reyataz), Boceprevir (Victrelis), Darunavir (Prezista), Fosamprenavir (Lexiva, Telzir), Indinavir (Crixivan), Lopinavir/Ritonavir (Kaletra), Nelfinavir (Viracept), Ritonavir (Norvir), Saquinavir (Invirase), Telaprevir (Incivek), Tipranavir (Aptivus), Ranolazine (Ranexa), Telithromycin (Ketek),
Ticagrelor (Brilinta).
(c) Statin-associated myopathy should be suspected when a statin-treated patient complains of unexplained muscle pain, tenderness or weakness.
(d) Statin therapy should be stopped in cases of suspected myopathy.

Statins cause flu-like symptoms

This paper was published in Medical Science Monitor 2002 May;8(5):CR384-8

Study title and author:
Flu-like response on statins.

Sinzinger H.
Wilhelm Auerswald Atherosclerosis Research Group (ASF), Vienna, Austria. helmut.sinzinger@univie.ac.at

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/12011782

This paper describes five patients who developed flu-like symptoms after starting statin therapy.

(i) The patients reported a flu-like response on statins with very severe symptoms of exhaustion, weakness, aching muscles and joints and raised body temperature.
(ii) These symptoms started within three weeks of starting statin therapy.
(iii) The symptoms appeared even in the lowest available dose of statins.
(iv) Only three of the patients had elevated creatine kinase levels.
(v) Four of the patients had elevated 8-epi-prostaglandin-F(2 alpha) levels, (an indication of muscle damage).
(vi) The patients discontinued the statins and within five weeks their symptoms completely disappeared.

Sinzinger concluded: "This set of data is absolutely new as it shows for the first time that flu-like symptoms may be due to statin use."

Statins are significantly associated with increased myositis risk.

This study was published in the Journal of Clinical Epidemiology 2007 Aug;60(8):812-8

Study title and authors:
Statin and statin-fibrate use was significantly associated with increased myositis risk in a managed care population.

McClure DL, Valuck RJ, Glanz M, Murphy JR, Hokanson JE.
Clinical Research Unit, Kaiser Permanente Colorado, Denver, CO 80237-8066, USA. david.1.mcclure@kp.org

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17606177

This four year study quantified the risk of myositis (myositis cases were defined as creatine kinase levels more than 10x upper limit of normal and a myopathy (muscle disease) diagnosis) associated with statin and fibrate drug use within a managed care organization population.

The study found:
(a) Statin users had a 180% increased risk of myositis compared to non-users.
(b) Statin-fibrate combination users had a 810% increased risk of myositis compared to non-users.

The results from this study show that statins, with or without fibrates, were significantly associated with increased myositis risk.

Statins increase the risk of muscle disease by 36% in diabetics

This study was published in Clinical Therapeutics 2008 Mar;30(3):535-42

Study title and authors
The risk of myopathy associated with thiazolidinediones and statins in patients with type 2 diabetes: a nested case-control analysis.

Koro CE, Sowell MO, Stender M, Qizilbash N.
Worldwide Epidemiology, GlaxoSmithKline, Collegeville, Pennsylvania 19426, USA. carol.e.koro@gsk.com

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/18405791

This study investigated the association of statins and various antidiabetic drugs with the risk of myopathy (muscle disease) in patients with type two diabetes. The study included 3,696 patients with myopathy who were matched with 21,871 controls.

The study found that compared with patients who did not use either statins nor antidiabetic drugs, those who used statins had a 36% increased risk of muscle disease.

How statins cause muscle damage

This study was published in the Journal of Clinical Investigation 2007 Dec;117(12):3940-51

Study title and authors:
The muscle-specific ubiquitin ligase atrogin-1/MAFbx mediates statin-induced muscle toxicity.

Hanai J, Cao P, Tanksale P, Imamura S, Koshimizu E, Zhao J, Kishi S, Yamashita M, Phillips PS, Sukhatme VP, Lecker SH.
Renal Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17992259

In 2001, scientists from the Harvard Medical School discovered the atrogin-1 gene, which plays a major role in muscle atrophy. (Muscle atrophy is the wasting or loss of muscle tissue).

Hanai notes that statins can lead to a number of side effects in muscle, including muscle fibre breakdown. This study sought to find the mechanisms of how statins may induce muscle injury. Since atrogin-1 plays a key role in the development of wasting in skeletal muscle, the study investigated if statins might “turn on” this gene.

They study comprised of three separate experiments to test this hypothesis.

(i) The first experiment examined the expression of the atrogin-1 gene in biopsies of 19 human patients (eight of the patients had muscle pain/damage while using statins). The results showed that atrogin-1 expression was significantly higher among the statin users.
(ii) The second experiment studied statins’ effects on cultured muscle cells treated with various concentrations of lovastatin. Compared with control samples, the lovastatin-treated cells became progressively thinner and more damaged. However, the cells lacking the atrogin-1 gene were resistant to statins’ deleterious effects.
(iii) Thirdly statins were tested on zebra fish. These tests also found that lovastatin led to muscle damage and as the lovastatin levels increased, so too was the damage. Again, (as in the cultured muscle cells) fish lacking the atrogin-1 gene were resistant to statin-induced damage.

Hanai concluded: "Collectively, our human, animal, and in vitro findings shed light on the molecular mechanism of statin-induced myopathy (muscle damage) and suggest that atrogin-1 may be a critical mediator of the muscle damage induced by statins.

Statin use linked to musculoskeletal diseases, joint pain and injuries

This study was published in the Journal of the American Medical Association Internal Medicine 2013:1-9

Study title and authors:
Statins and Musculoskeletal Conditions, Arthropathies, and Injuries
Ishak Mansi, MD; Christopher R. Frei, PharmD, MSc; Mary Jo Pugh, PhD; Una Makris, MD; Eric M. Mortensen, MD, MSc

This study can be accessed at: http://archinte.jamanetwork.com/article.aspx?articleid=1691918

The objective of the study was to determine whether statin use is associated with musculoskeletal disorders. ( Musculoskeletal disorders can affect the body's muscles, joints, tendons, ligaments and nerves). This analysis compared 6,967 statin users with 6,967 nonusers.

The study found:
(a) Statin users had a 19% increased risk of all musculoskeletal diseases compared to nonusers.
(b) Statin users had a 13% increased risk of injury-related diseases (dislocation, sprain, strain) compared to nonusers.
(c) Statin users had a 9% increased risk of drug-associated musculoskeletal pain compared to nonusers.
(d) Statin users had a 7% increased risk of joint pain compared to nonusers.

Mansi concludes: "Musculoskeletal conditions, arthropathies, injuries, and pain are more common among statin users than among similar nonusers".

Muscle disease is a dangerous side-effect of statin drugs

This paper was published in Ugeskrift for Laeger 2010 Feb 15;172(7):544-5

 

Study title and author:

Statin-induced dysphagia

Edholm B.

Øre-naese-halskirurgisk Afdeling, Slagelse Sygehus, DK-5000 Odense C, Denmark. bjarkeedholm@hotmail.com

 

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/20156405

Dysphagia is the medical term for swallowing difficulties.

The paper reports on a man who developed dysphagia and muscle fatigue after statin therapy.

(i) A 68-year-old man was referred to hospital with progressive dysphagia.
(ii) The patient further developed muscle fatigue (it was difficult for him to lift his arms above his head) and additional signs of myopathy (muscle disease) such as high levels of creatine kinase.
(iii) The dysphagia was diagnosed as a late-onset side-effect of statin therapy.
(iv) He stopped taking statins and 14 days later the power to his arms returned, his swallowing function was significantly better and his creatine kinase levels normalised.

The author of the paper, Bjarke Edholm from the Slagelse Hospital in Denmark, concluded: "As an increasing number of patients are being treated with lipid-lowering drugs (statins), it is important to recall that myopathy is a dangerous side-effect which may have either quick or delayed onset, and that dysphagia can be the initial symptom".

Statins associated with inflammation of the muscles

This study was published in the Journal of Clinical Rheumatology 2001 Oct;7(5):340-5

 

Study title and author:

A case of atorvastatin combined toxic myopathy and inflammatory myositis.

Folzenlogen D.

Department of Internal Medicine, Division of Immunology and Rheumatology, University of Missouri, MA 425, One Hospital Drive, Columbia, MO 65212, USA.

 

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17039167

This paper reports the case of a 76-year-old male patient undergoing statin therapy.

(i) The patient had elevations of muscle enzymes and was diagnosed with inflammatory polymyositis (chronic inflammation of the muscles) combined with statin toxic myopathy (muscle disease).
(ii) His symptoms and enzyme abnormalities resolved with the removal of the statin medication.

This case highlights the association between statins and inflammation of the muscles.

Statins inflame and destroy blood vessels

This paper was published in Clinical Rheumatology 2008 Dec;27 Suppl 2:S75-7

Study title and authors:
A case of ANCA-associated systemic vasculitis induced by atorvastatin.

Haroon M, Devlin J.
Department of Rheumatology, Waterford Regional Hospital, Waterford, Republic of Ireland. mharoon301@hotmail.com

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/18839266

Vasculitis is a group of disorders that destroy blood vessels by inflammation. ANCA-associated vasculitides are diseases caused by vasculitis in which antineutrophil cytoplasmic antibodies (ANCAs) can be detected in the blood.

This paper reports a case of statin induced ANCA-associated vasculitides.

(i)  A 45-year-old male patient reported to an Accident and Emergency department with a six week history of pain and stiffness involving his legs. Both calves were markedly tender, and he was not able to bear weight.
(ii) He also complained of numbness involving his left big toe for a few days, which later spread to involve his arms, and tinnitus and hearing loss in his left ear.
(iii) He had been taking atorvastatin 10 mg for six months.
(iv) Investigations showed markedly increased inflammatory markers, markedly increased antineutrophil cytoplasmic antibody (ANCA) levels and muscle damage.
(v) A diagnosis of statin-induced ANCA-associated vasculitis and statin-induced distal myopathy (muscle disease) was made.
(vi) The patients symptoms and laboratory abnormalities resolved rapidly after cessation of the statin drug and implementation of treatment.

This case shows the association between statins and ANCA-associated vasculitis. 

Statin treatment associated with significant muscle mitochondrial DNA depletion

This study was published in Clinical Pharmacology and Therapeutics 2007 May;81(5):650-3

Study title and authors:
Decreased skeletal muscle mitochondrial DNA in patients treated with high-dose simvastatin.

Schick BA, Laaksonen R, Frohlich JJ, Päivä H, Lehtimäki T, Humphries KH, Côté HC.
Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, and Research Unit, Tampere University Hospital, Finland.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17329991

Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source.

Any depletion of muscle mitochondrial DNA may lead to muscle weakness and/or liver failure, and more rarely, brain abnormalities. “Floppiness,” feeding difficulties and developmental delays are common symptoms.

The aim of this study was to determine whether muscle mitochondrial DNA levels are altered during statin therapy. This clinical trial included 43 patients, aged 31 to 69 years, who had their levels of muscle mitochondrial DNA measured at the start of the study and again after eight weeks. The subjects were placed into three groups:
(i) Simvastatin 80 mg per day.
(ii) Atorvastatin 40 mg per day.
(iii) Placebo.

The study found:
(a) A significant decrease in muscle mitochondrial DNA levels was observed in the simvastatin group and a smaller decrease in levels in the atorvastatin group.
(b) Half the patients in the simvastatin group had a greater than 50% decrease in muscle mitochondrial DNA levels.
(c) 13% of the patients in the atorvastatin group had a greater than 50% decrease in muscle mitochondrial DNA levels.

The study shows that statin treatment may be associated with significant muscle mitochondrial DNA depletion.

The researchers conclude: "Given that statin therapy is often life-long, the large decrease (47%) observed raises concern about the potential longterm effect of statins on mitochondrial DNA and skeletal muscle mitochondria".

Statins exacerbate exercise-induced skeletal muscle injury

This study was published in Metabolism 1997 Oct;46(10):1206-10

 

Study title and authors:

Lovastatin increases exercise-induced skeletal muscle injury.

Thompson PD, Zmuda JM, Domalik LJ, Zimet RJ, Staggers J, Guyton JR.

Division of Cardiology, University of Pittsburgh, PA, USA.

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/9322808

This study investigated the association between statins, exercise and creatine kinase levels (high levels of creatine kinase are a marker for muscle damage) using a double-blind, placebo-controlled design. The study include 59 healthy men aged 18 to 65 years who were assigned to receive lovastatin (40 mg per day) or placebo for 5 weeks. The men completed 45 minutes of treadmill walking after 4 weeks of treatment.

The study found that the creatine kinase levels of the men who received lovastatin were 62% and 77% higher 24 and 48 hours after the treadmill exercise compared to the men who received placebo.

The researchers concluded that statins exacerbate exercise-induced skeletal muscle injury.

Statins increase the risk of chronic muscle diseases by 286%

This study was published in the Annals of the Rheumatic Diseases 2008 May;67(5):614-9

 

Study title and authors:

Increased exposure to statins in patients developing chronic muscle diseases: a 2-year retrospective study.

Sailler L, Pereira C, Bagheri A, Uro-Coste E, Roussel B, Adoue D, Fournie B, Laroche M, Zabraniecki L, Cintas P, Arlet P, Lapeyre-Mestre M, Montastruc JL.

Unit of Pharmacoepidemiology, EA 3696, Clinical Pharmacology Department, Paul Sabatier University, 37 Allées Jules Guesdes, 31000 Toulouse, France. sailler.l@chu-toulouse.fr

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17768174

This study evaluated the association between chronic muscle diseases and prior exposure to cholesterol lowering drugs. The study, which lasted for two years, included 37 patients with chronic muscle diseases such as dermatomyositis and polymyositis who were compared to 185 control subjects.

The study found that those who were exposured to statins had a 286% increased risk of dermatomyositis and polymyositis.

Statins increase the risk of muscle adverse reactions

This study was published in Muscle and Nerve 2011 Dec;44(6):877-81

Study title and authors:
Prevalence and risk factors of muscle complications secondary to statins.

El-Salem K, Ababneh B, Rudnicki S, Malkawi A, Alrefai A, Khader Y, Saadeh R, Saydam M.
Department of Neurosciences, Faculty of Medicine, Jordan University of Science and Technology, Irbid 22110, Jordan. khalidelsalem@hotmail.com

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/22102457

The aim of the study was to investigate the prevalence of muscle complications among patients using statins. The study included 345 patients receiving statins who were compared with an age- and gender-matched control group of 85 nonusers.

The study found that statin users had a 256% increased risk of muscle adverse reactions compared to nonusers.

Analysis of 119 statin randomized controlled trials find that statins increase the risk of muscle problems

This study was published in Pharmacoepidemiology and Drug Safety 2007 Feb;16(2):132-43

 

Study title and authors:

Systematic review and meta-analysis of clinically relevant adverse events from HMG CoA reductase inhibitor trials worldwide from 1982 to present.

McClure DL, Valuck RJ, Glanz M, Hokanson JE.

Kaiser Foundation Health Plan of Colorado, Clinical Research Unit, Denver, CO 80237-8066, USA. david.l.mcclure@kp.org

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17072896

The objective of the study was to determine the association of adverse events from a systematic review and meta-analysis of statin randomized controlled trials. The study included over 86,000 participants from 119 studies.

The study found:
(a) Statin users had a 59% increased risk of rhabdomyolysis (the breakdown of muscle fibers that leads to the release of muscle fiber contents into the bloodstream and often causes kidney damage) compared to nonusers.
(b) Statin users had a 156% increased risk of myositis (inflammation of the muscles) compared to nonusers.
(c) Statin users had a 9% increased risk of myalgia (muscle pain) compared to nonusers.

This analysis of 119 statin randomized controlled trials found that statins increased the risk of muscle problems.

Statins are associated with an approximate doubling of the risk of muscle disease

This study was published in Clinical Therapeutics 2007 Aug;29(8):1761-70

Study title and authors:
Does statin therapy initiation increase the risk for myopathy? An observational study of 32,225 diabetic and nondiabetic patients.

Nichols GA, Koro CE.
Kaiser Permanente, Center for Health Research, Portland, Oregon 97227-1098, USA. greg.nichols@kpchr.org

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17919557

The objective of this study was to determine the prevalence of myopathy (muscle disease) among subjects with or without diabetes, some of whom received statin treatment. the study included 32,225 subjects who were followed for nine years.

The study found:
(a) Statins users with diabetes had a 43% increased risk of myopathy compared to non-users with diabetes.
(b) Statin users without diabetes had a 143% increased risk of myopathy compared to non-users without diabetes.

The study reveals that statins are associated with an approximate doubling of the risk of muscle disease.

Statins increase the risk of muscle pain by 90%

This study was published in Circulation 2012 Nov 26

 

Study title and authors:

The Effect of Statins on Skeletal Muscle Function.

Parker BA, Capizzi JA, Grimaldi AS, Clarkson PM, Cole SM, Keadle J, Chipkin S, Pescatello LS, Simpson K, White CM, Thompson PD.

1 Hartford Hospital, Hartford, CT;

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/23183941

This study assessed the effects of statins on muscle function. The study included 420 healthy subjects, who had never previously taken statins, who received either 80 mg of atorvastatin or placebo for six months.

The study found:
(a) The creatine kinase levels of those who received statins increased by 20.8 U/L. (The appearance of creatine kinase in blood has been generally considered to be an indirect marker of muscle damage).
(b) Those who received statins had a 90% increased risk of muscle pain compared to those who received placebo.

The results of this trial show that statins increase the risk of muscle injury.

Statins impair energy production and promote muscle damage

This study was published in Muscle and Nerve 2011 Jan;43(1):76-81

Study title and authors:
Evaluation of skeletal muscle during calf exercise by 31-phosphorus magnetic resonance spectroscopy in patients on statin medications.

Wu JS, Buettner C, Smithline H, Ngo LH, Greenman RL.
Department of Radiology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215, USA. jswu@bidmc.harvard.edu

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/21171098

Phosphocreatine is a substance that is fundamental to the ability of the body to produce muscular energy.

Elevated blood levels of creatine kinase are indicative of muscle damage.

The study investigated the association of statin treatment on recovery from exercise. The study included ten patients, (who were subject to a four-week regimen of statin therapy), who had their phosphocreatine and creatine kinase levels measured pre- and post-statin therapy.

The study found:
(a) Phosphocreatine levels took 97% longer to recover from exercise after statin therapy.
(b) Creatine kinase levels rose by 17.7% after statin therapy.

The results of the study suggest that statin therapy may impair energy production and promote muscle damage.

Statins increase the risk of musculoskeletal pain

This study was published in the American Journal of Medicine 2012 Feb;125(2):176-82

Study title and authors:
Statin use and musculoskeletal pain among adults with and without arthritis.

Buettner C, Rippberger MJ, Smith JK, Leveille SG, Davis RB, Mittleman MA.
Harvard Medical School, Boston, MA, USA. cbuettne@bidmc.harvard.edu

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/22269621

This study investigated the relationship between statin use and musculoskeletal pain. (The musculoskeletal system is made up of the body's bones (the skeleton), muscles, cartilage, tendons, ligaments, joints, and other connective tissue that supports and binds tissues and organs together). The study included 8,228 adults aged 40 years or more.

The study found those taking statins had a 15% increased risk of musculoskeletal pain compared to non-users.

After only six months of therapy with a statin (Zocor), nearly a quarter of the patients suffered from side effects

This study was published in the New Zealand Medical Journal 1991 Nov 27;104(924):493-5

Study title and authors:

Simvastatin and side effects.

Scott RS, Lintott CJ, Wilson MJ.

Princess Margaret Hospital, Christchurch.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/1745460

The object of the study was to investigate the side effects of simvastatin (Zocor). The study included 110 patients newly commenced on simvastatin who completed a side effects questionnaire after six months of therapy.

The study found:
(a) 23.6% of patients suffered side effects.
(b) 13.6% of patients suffered muscle aches.
(c) 4.5% of patients suffered gastrointestinal symptoms.

After only six months of therapy with a statin (Zocor), nearly a quarter of the patients suffered from side effects.