Statin Related Muscle Pain and Coenzyme Q 10

Statins are used to lower cholesterol levels in an effort to reduce the risk of developing cardiovascular disease. They are used after a patient has exhausted lifestyle changes such as changing their diet to a low cholesterol diet, exercising regularly and losing weight without their cholesterol dropping to levels that are considered acceptable to reduce your risk of vascular events.

Patients starting on statins often complain of muscles aches, pains and slow recovery of muscle pain after exercising. In a few individuals the muscle pain, inflammation and damage becomes severe. One of the known, but little understood, negative side effects of statin medications are the lowering of your Coenzyme Q 10 level. CoQ10 works at the subcellular level in energy producing factories called mitochondria. Statin drugs, which inhibit the enzyme HMG-CoA Reductase lower cholesterol while also lowering CoQ10 levels by 16-54 % based on the study reporting these changes.

The November 16, 2018 edition of the Journal of the American Medical Association published a review article by David Rakel, MD and associates that suggested that supplementing your diet with CoQ 10 would reduce muscle aches and pains while on statin therapy. Twelve studies were reviewed and the use of CoQ10 was associated with less muscle pain, weakness, tiredness and cramps compared to placebo. The studies used daily doses of 100 to 600 mg with 200 mg being the most effective dosage. Finding the correct dosage is important because the product is expensive with forty 200 mg tablets selling for about $25.

Since CoQ10 is fat soluble, you are best purchasing formulations that are combined with fat in a gel to promote absorption. As with all supplements, which are considered foods not drugs , it is best if they are UPS Labs certified to insure the dosage in the product is the same as listed on the label and that it contains no unexpected impurities.

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Men’s Sexual Function Tied to Statin Use

Statins v2Statin medication has been used for years to lower cholesterol and reduce an individual’s risk and chances of having a heart attack, a stroke or symptoms of peripheral arterial vascular disease. The “off label” uses of statins have been noted by many practitioners and researchers as well. The Bale and Doneen research team have for years believed that statins stabilize soft lipid plaque in the wall of blood vessels and reduce sudden heart attacks and strokes by reducing inflammation. At the American College of Cardiology meetings recently a paper was presented and appeared in the online version of the Journal of Sexual Medicine hinting that statins improved erectile dysfunction. John Kostis, MD, of Rutgers Robert Wood Johnson Medical School in New Jersey said that statins improvement of erectile dysfunction was about 1/3 of what pills like Viagra, Levitra or Cialis can achieve but significantly better than placebo or life style improvements. He felt the improvement in erectile dysfunction was due to the medications lowering of lipid levels and to their improvement of the endothelial cells that line the inner walls of our blood vessels.

For many years erectile dysfunction was felt to be a marker for cardiovascular disease because it was felt that the ED reflected an inability to achieve adequate blood flow in the vascular tree of the genital organs. Testosterone, the male hormone, is a byproduct of cholesterol metabolism. It was originally felt that by lowering cholesterol you were indirectly lowering testosterone levels and this might affect your sexual performance. This study in 647 patients enrolled in 11 randomized studies with different statins would tend to reach a different conclusion that by lowering the lipids and maintaining the blood flow you can actually improve erectile function despite lowering the testosterone indirectly.

Dr. Kostis was quick to point out that statins should not be used as a sexual enhancing drug in men with normal or low cholesterol levels. He called for a larger study looking at multiple statins versus placebos and the current ED meds on the market.

HDL Cholesterol: The Good Cholesterol Can Go Bad

CholesterolWhen discussing lipids and cholesterol the public, in particular, has been educated to the fact that the cholesterol is divided into several different types based on where it settles in a test tube after being spun in a centrifuge. The good cholesterol or HDL (high density lipoprotein) is said to be healthy and protective while the LDL (low density lipoproteins) are felt to be detrimental to your health. For years now we have been striving to lower the LDL cholesterol by eating correctly, exercising and when necessary taking medications such as statins.  At the same time we are trying to raise our HDL, or protective cholesterol, by exercising.  The higher your HDL cholesterol is, and the lower your LDL cholesterol is, your risks of not having a cardiovascular event improve.

In reality we know that HDL cholesterol carries bad cholesterol away from the blood vessel walls and deposits it in the liver where it is broken down and removed.  HDL is like a convoy of trucks ferrying your cholesterol away from vital places. The LDL cholesterol does just the opposite, carrying unwanted lipids to the vessel walls and depositing them there. 

 Just when we were getting comfortable with this concept, researchers at many institutions were able to break the LDL or bad cholesterol down into even more discrete groups. Apparently the large fluffy type of LDL is now considered beneficial. At the same time they have broken the HDL or protective cholesterol down into smaller divisions with some types being “broken” and causing inflammation in the artery walls leading to heart attacks and strokes. 

 Dr. Stanley Hazen, MD of the Cleveland Clinic’s Lemer Research Institution is one of the cardiologists promoting the concept of existing “broken” HDL which is damaging to our vessels and bodies.  Hazen’s research shows that in people with heart disease, about 1 in 5 HDL particles in the artery wall are dysfunctional.  People who have more of this dysfunctional HDL are at higher risk of heart disease, independent of the well-known risk factors such as age, diabetes, smoking and blood pressure.  This dysfunctional HDL is very hard for a lab to detect. 

 Dr. Hazen was part of a team that developed the MPO or myeloperoxidase blood level as a marker of plaque buildup in artery walls as a result of dysfunctional HDL and other risk elements.   High myeloperoxidase levels are associated with inflammation and damage to the vessel walls resulting in increased risks of heart attack and stroke.  The MPO test is licensed and copyrighted to the Cleveland Clinic and only available through the Cleveland Heart Labs program.

 We offer the Cleveland Heart Lab panel of tests as part of the cardiovascular risk assessment we present to individuals who do not have cardiovascular or cerebrovascular disease.  It is the only panel of tests that offers the Myeloperoxidase Level.  If interested please ask about this panel at your next visit.

A Large Review Proves Statins Are Safe

StatinsThe online version of Circulation: Cardiovascular Quality and Outcome published a review of the safety of statin drugs. The study looked at 135 randomized research trials including 246,955 participants. Medications examined included atorvastatin (Lipitor), fluvastatin (Lescol), simvastatin (Zocor), lovastatin (Mevacor), pravastatin (Pravachol), rosuvastatin (Crestor) and trials of pitavastatin.

They found there were no differences in the rates of discontinuation of the statins because of adverse events compared with discontinuation of placebo. The same applied to elevation of the muscle enzyme creatine kinase, muscle aches or myalgias and/or the development of cancer. As the doses of these medicines increased they found the participants reported more adverse effects.

Christie Ballantyne, MD of the Baylor College of Medicine reviewed the study for MedPage, the online journal of the University Of Pennsylvania School Of Medicine, and felt the study certainly confirmed the tolerability of the statins as a class of drugs to lower cholesterol and reduce cardiovascular events. He reaffirmed the very small increased risk of statin use and developing Type II Diabetes and the need to monitor liver function blood tests while taking the drugs. He concluded these risks were well worth taking in view of the benefits to your health statins provided.

Inflammation and Vascular Disease

Heart, stethescopeI was privileged to hear Bradley Bale, MD and Amy Doneen, MSN, ARNP talk about the development of coronary artery disease and cerebrovascular disease in patients with low or few cardiac risk factors.  They cited American Heart Association studies looking at groups of men and women between ages 45 and 65 who have their first heart attack or stroke despite being in compliance with suggested lipid and blood pressure guidelines. They pointed out that the first Myocardial Infarct or Stroke occurred in 88% of women who met lipid guidelines and 66 % of men.  These are people who do not smoke, do not have untreated or uncontrolled lipid levels, are not diabetics and who lead an active life style.  They asked “why”?

Dr. Bale and Ms. Doneen work with the well respected cardiovascular Center of Excellence at the Cleveland Clinic program in Ohio, and believe that inflammation is the root of the problem.  They believe that soft plaque composed of lipids and other cells lurks beneath the endothelial cells lining blood vessels. In the presence of inflammatory stimulants, this soft plaque ruptures suddenly through the endothelial level into the blood stream. When it comes in contact with the blood flowing through the vessels the body believes we are bleeding and cut and chemical mediators are released that initiate the formation of a clot. When this clot occurs in a small coronary artery we have a heart attack or myocardial infarction or precipitate a lethal irregular heartbeat. When this clot occurs in the blood vessels of the brain, we have an acute stroke or cerebrovascular accident.

The key to prevention in the so called low risk patient is to detect the inflammation in advance, and treat it. They are firm believers in performing B Mode Duplex ultrasounds of the carotid arteries in the neck to look for the presence of soft plaque beneath the endothelial cell lining. This soft plaque is distinctly different from the safe but calcified plaque we can see on CT scans used for cardiac scoring studies.  They couple this imaging study with a series of complex blood tests which identify inflammation. These include a myeloperoxidase level, the Lp-PLA2 level, the urine microalbumen to creatinine ratio, a F2-IsoPs level and the cardiac specific CRP level.

These tests and studies in combination with a traditional history and exam, sugar and lipid levels and EKG can help us identify those “low risk” patients who actually are high risk for a heart attack or stroke. The cause of the inflammation is often difficult to spot and may be in your mouth with dental or periodontal disease or in your joints with inflammatory arthritis.  Patients with excellent dental hygiene and normal appearing gums may harbor specific inflammatory bacteria that put them at risk. While this seems a bit forward thinking, remember we once questioned the research that showed that bacteria (H Pylori) caused gastric ulcers and intestinal bleeding.

I have begun instituting the inflammatory blood marker panels in my practice. Labs are sent to the Cleveland HeartLab for this purpose. I will be initiating periodic carotid ultrasound studies for the appropriate patients in the coming year.

It is often difficult for clinicians to distinguish snake oil sold for profit from cutting edge science. I have tried to spare my patients from worthless but profit driven products. I am convinced the Cleveland Clinic is just ahead of the rest of us in offering these services and I will make them available to the appropriate patients and will do it in a financially structured manner that does not add out of pocket cost to the patient. It’s not about adding another profitable income stream to the practice. It’s about identifying individuals who shouldn’t have a heart attack or stroke before they do.

Statins May Reduce Your Energy Level

Beatrice A. Golomb, MD, PhD. of the University of California San Diego and colleagues discussed the results of their ongoing studies in the Archives of Internal Medicine online edition regarding cholesterol lowering drugs Simvastatin and Pravastatin and recipients’ perception of their energy level. Their research suggested that Simvastatin might leave its users, especially women, feeling tired and drained after exertion.  The scores hinted that almost 40% of women felt more tired and fatigued during physical activity on Simvastatin than without the lipid-lowering drug.

The trial included 1,016 men and women with low-density lipoprotein (LDL) cholesterol screened at 115- 19- mg/dL who were randomized to receive 20 mg Simvastatin, 40 mg Pravastatin, or placebo each day for 6 months. These patients did not have documented heart disease, cardiovascular disease or diabetes.

There was a worsening of perceived energy level and exertion related fatigue in 4 of 10 women on Simvastatin. The effect was much less, and not significant, with Pravastatin or placebo.   In a recent review of statins and adverse effects in the Cleveland Clinic Journal of Medicine, the authors pointed out that muscles performing work required  fats and lipids as a source of fuel and energy to work successfully. They hypothesized the possibility that the goals of cardiology to reduce lipid levels to prevent cardiovascular disease to extremely low levels may create an environment in working muscles where the lipid levels are too low to generate the fuel or energy needed to perform the exercise and work needed to be done.

Clearly, further research needs to be done.  We must remember all these participants DID NOT have vascular disease and this is a primary prevention study to prevent them from developing cardiovascular disease.  Might there be other methods to achieve this?  Is Simvastatin the only statin to cause this type of problem or will the other statins do the same?  Is this a problem of the particular generic brand of Simvastatin used or is it an across the board effect of Simvastatin?  All these questions require additional research to obtain the answers that we need.

Statins Reduce Risks, Even in the Lowest Risk Groups

Current guidelines for the use of statins in the USA (Lipitor, Zocor, Crestor, Atoravastatin, Simvastatin, Pravastatin, etc.) call for only treating individuals who have a ten-year risk of major vascular event of at least 20%.

European researchers including Borislava Mihaylova, MSc DPhil, and colleagues on the Cholesterol Treatment and Trialists Collaborators team writing in the Lancet question whether the guidelines should be changed to treat individuals with even lower risks. Their large Meta analysis suggests that statins provide substantial benefits for primary prevention – especially in patients with a 5-10% ten year risk of a major vascular event. They looked at data from 27 trials including over 175,000 participants. When they took into account cost and side effects of statins, such as muscle pain and inflammation, rhabdomyolysis, diabetes and hemorrhagic stroke, they concluded that the benefits still far outweighed the risks. They think that the clear-cut affect on lower risk individuals coupled with the fact that almost 50% of vascular events occur in patients without previous cardiovascular disease necessitates the broadening of USA guidelines for treatment of patients. The researchers go on to hypothesize that as more generic statins enter the market, cost concerns will become far less of a factor in the decision to treat or not treat.

They noted that for each 1 mmol/L reduction in LDL cholesterol, there was a 21% reduction in the relative risk of major vascular events, and all cause death, irrespective of age, baseline LDL or previous cardiovascular disease.

This research makes it clear that there is great value in assessing the statistical cardiovascular risk of each individual and being more aggressive in the use of statins than current national guidelines call for.  Incorporating risk tools such as the Framingham Risk assessment plus looking at newer techniques such as the measurement of carotid artery intimal thickness may be appropriate in the decision to choose a statin or not.