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Researchers examined medical records of over 2 million statin users in England and Wales in order to quantify side effects during the first 5 years of statin use.

In that 2010 study that analyzed the medical records of 2 million statin users, increases in the risk of liver dysfunction, muscle-related side effects, acute kidney injury and cataracts associated with statin use were reported. Larger doses of statin drugs are associated with greater likelihood of side effects, and additional risk factors such as other drugs, older age, diabetes and high triglycerides also increase the likelihood of adverse effects. In addition to these known adverse effects, there is debate over whether statins may have detrimental effects on brain function. Approximately 17 percent of patients who take a statin experience an adverse effect. Even if this seems like a low level of risk, statins treat a condition that is preventable and reversible via dietary and lifestyle modification.

It's well established that there is an increased risk of type 2 diabetes in statin users, one meta-analysis reporting a 9 percent increase in risk, another reporting a 13 percent increase in risk.
Statin use appears to promote diabetes by impairing insulin secretion by the beta cells of the pancreas and also by reducing insulin sensitivity.

A study examining Canadian healthcare records for 2 million patients who had been newly prescribed a statin, and found an increase in the incidence of hospitalization for acute kidney injury during the first six months of statin use, high potency statins in particular.

The most common side effects of statins are impaired muscle function, which may be due to impaired energy production in the mitochondria of the muscle cells. These side effects include muscle pain and a severe breakdown of muscle called rhabdomyolysis. Rhabdomyolysis can also lead to kidney and liver dysfunction. Because of the negative effects of statins on skeletal muscle, there is evidence that statins may also blunt the fitness-building response to aerobic exercise training. The likelihood of muscular side effects depends on the dose of the statin, and they are more prevalent in physically active patients.

The question now is do statins have effects that actually promote atherosclerosis and heart failure, That being said then what is the potential benefits? A team of researchers from Japan and the U.S. has compiled and described possible molecular mechanisms by which statins could actually accelerate heart disease. The researches say that the abnormalities caused to the energy production machinery in skeletal muscle imply that heart muscle could be similarly damaged. They propose that statins are toxic to the mitochondria because they promote the depletion of CoQ10, an important component of mitochondrial energy production. Cardiac muscle tissue would be especially vulnerable to CoQ10 depletion because of its high energy demands. CoQ10 supplementation is often used as a therapy for statin-associated muscle pain, although its efficacy is debated. The authors make the case that statin-induced CoQ10 depletion in cardiac muscle promotes serious damage and inflammation in the heart, and may lead to atherosclerosis or heart failure. Accordingly, they point out certain trials in which cholesterol reduction with statins was associated with a greater mortality risk or worsening of cardiac function. They also note that statins may cause coronary calcification by inhibiting the production of vitamin K2. More research must be done to confirm these heart disease-promoting effects of statins.

Try these alternatives to statin drugs, Exercise, Dietary and lifestyle changes should be the number 1 course of action. Medication is unnecessary in most people who make the changes. A high-nutrients of foods like cruciferous vegetables, nuts, beans and berries work to bring LDL down and restore the arteries.

A high-fiber, high-nutrient diet like vegetables, fruit and nuts was found to reduce cholesterol by 33 percent within two weeks.


1. U.S. Centers for Disease Control and Prevention: Statin drug use in the past 30 days among adults 45 years of age and over, by sex and age: United States, 1988–1994, 1999–2002, and 2005–2008 [http://www.cdc.gov/nchs/data/hus/2010/fig17.pdf]

2. Taylor F, Huffman MD, Macedo AF, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev 2013, 1:CD004816.

3. Okuyama H, Langsjoen PH, Hamazaki T, et al. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms. Expert Rev Clin Pharmacol 2015, 8:189-199.

4. Hippisley-Cox J, Coupland C. Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database. BMJ 2010, 340:c2197.

5. Golomb BA, Evans MA. Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism. Am J Cardiovasc Drugs 2008, 8:373-418.

6. Kelley **, Glasser S. Cognitive effects of statin medications. CNS Drugs 2014, 28:411-419.

7. Zhang H, Plutzky J, Turchin A. Discontinuation of statins in routine care settings. Ann Intern Med 2013, 159:75-76.

8. Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet 2010, 375:735-742.

9. Rajpathak SN, Kumbhani DJ, Crandall J, et al. Statin therapy and risk of developing type 2 diabetes: a meta-analysis. Diabetes Care 2009, 32:1924-1929.

10. Koh KK, Quon MJ, Han SH, et al. Atorvastatin causes insulin resistance and increases ambient glycemia in hypercholesterolemic patients. J Am Coll Cardiol 2010, 55:1209-1216.

11. Dormuth CR, Hemmelgarn BR, Paterson JM, et al. Use of high potency statins and rates of admission for acute kidney injury: multicenter, retrospective observational analysis of administrative databases. BMJ 2013, 346:f880.

12. Larsen S, Stride N, Hey-Mogensen M, et al. Simvastatin effects on skeletal muscle: relation to decreased mitochondrial function and glucose intolerance. J Am Coll Cardiol 2013, 61:44-53.

13. Mikus CR, Boyle LJ, Borengasser SJ, et al. Simvastatin impairs exercise training adaptations. J Am Coll Cardiol 2013, 62:709-714.

14. Gillett RC, Jr., Norrell A. Considerations for safe use of statins: liver enzyme abnormalities and muscle toxicity. Am Fam Physician 2011, 83:711-716.

15. Zhou Q, Liao JK. Pleiotropic effects of statins. - Basic research and clinical perspectives. Circ J 2010, 74:818-826.

16. Folkers K, Langsjoen P, Willis R, et al. Lovastatin decreases coenzyme Q levels in humans. Proc Natl Acad Sci U S A 1990, 87:8931-8934.

17. 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 2015, 90:24-34.

18. Jenkins DJ, Kendall CW, Popovich DG, et al. Effect of a very-high-fiber vegetable, fruit, and nut diet on serum lipids and colonic function. Metabolism 2001, 50:494-503.
1 Responses
159619 tn?1538184537
A couple thoughts, first off the statement;

"It's well established that there is an increased risk of type 2 diabetes in statin users, one meta-analysis reporting a 9 percent increase in risk, another reporting a 13 percent increase in risk. "

is very misleading. Most people read this and think there is a 13% risk of developing type II which is not correct. The normal risk of 2% of the population is increased by up to 13% meaning the true risk is up to 5%. That is the number that needs to be used to measure the benefits verses risk.

Also, no one can prove that number is even correct as there is no way of knowing how many of the control group that developed type II would have done so without the statin. Many patients on statins have the same risk factors for type II as they do for CAD so the numbers are really just speculation. A lot of scaremongering in that statement.
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