Side effects of pravastatin

Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, more commonly known as statins, are recommended as first-line agents in the reduction of low-density lipoprotein cholesterol (LDL-C).(1) Although cholesterol is imperative for normal cellular function, excess LCL-C leads to atherogenesis. Plaque formation in the arteries results in coronary artery disease (CAD), heart attack, and/or stroke. There is known morbidity and mortality benefit associated with LDL-C reduction from statin therapy; therefore, it is vital that patients take the medication in a way that provides the greatest effect.(2)

Although some cholesterol comes from dietary intake, a significant amount is produced endogenously. It was previously hypothesized that human cholesterol production may be cyclical in nature mimicking the confirmed pattern of cholesterol synthesis in animals. Human trials then confirmed the fluctuation in cholesterol synthesis, noting the greatest cholesterol production from the liver during fasting states.

The apparent circadian rhythm of cholesterol production sparked the recommendation that statins be dosed at bedtime to provide the greatest medication concentration when endogenous cholesterol production is the highest.(3)

Investigation of pharmacokinetic properties of individual statins disproved the need for all agents to be dosed at bedtime.(1) Although all statins go through hepatic metabolism, the elimination half-lives vary in length. Simvastatin, fluvastatin, and lovastatin have a short elimination half-life compared to other drugs within the class. Agents with significantly shorter elimination half-lives require bedtime dosing to maximize efficacy – allowing the greatest statin concentration to be present while endogenous cholesterol synthesis is the highest. Alternatively, the longer half-lives of rosuvastatin, atorvastatin, pitavastatin, and pravastatin allow these agents to maintain a therapeutic drug concentration over a 24-hour period and allow alternate administration times.(2)

Even if properly counseled to take statins with a shorter half-life at bedtime, some patients do not comply which may result in decreased efficacy. Agents with longer half-lives allow for greater flexibility in administration time, which may improve compliance and ultimately result in greater LDL-C reduction and ability to achieve cholesterol goals.

  1. Expert panel on the detection, evaluation, and treatment of high blood cholesterol in adults: executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high cholesterol in adults (adult treatment panel III). JAMA. 2001:285:2486-2497.
  2. Plakogiannis R, Cohen H. Optimal low-density lipoprotein cholesterol lowering – morning versus evening statin administration. Ann Pharmacother. 2007;41:106-110.
  3. Jones PJ, Schoeller DA. Evidence for diurnal periodicity in human cholesterol synthesis. J Lipid Res. 1990;31:667-673.
  4. Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill;2011.
  5. Kalant H, Grant DM, Mitchell J. Principles of Medical Pharmacology. 7th ed. Toronto: Saunders Elsevier;2007


Before taking pravastatin,

  • tell your doctor and pharmacist if you are allergic to pravastatin, any other medications, or any of the ingredients in pravastatin tablets. Ask your pharmacist for a list of the ingredients.
  • tell your doctor and pharmacist what prescription and nonprescription medications, vitamins, nutritional supplements, and herbal products you are taking or plan to take. Be sure to mention any of the following: antacids; antifungals such as fluconazole (Diflucan) and ketoconazole (Nizoral); boceprevir (Victrelis); cimetidine (Tagamet); clarithromycin (Biaxin); colchicine (Colcrys); cyclosporine (Neoral, Sandimmune); digoxin (Lanoxin); diltiazem (Cardizem, Cartia, Taztia, Tiazac); erythromycin (E.E.S., E-Mycin, Erythrocin); other cholesterol-lowering medications such as fenofibrate (Tricor), gemfibrozil (Lopid), and niacin (nicotinic acid, Niacor, Niaspan); ritonavir (Norvir) taken with darunavir (Prezista); spironolactone (Aldactone); verapamil (Calan, Covera, Verelan); and warfarin (Coumadin). Your doctor may need to change the doses of your medications or monitor you carefully for side effects. Other medications may also interact with pravastatin, so be sure to tell your doctor about all the medications you are taking, even those that do not appear on this list.
  • if you are taking cholestyramine (Questran) or colestipol (Colestid), take them 4 hours before or 1 hour after pravastatin.
  • tell your doctor if you have liver disease. Your doctor will order laboratory tests to see how well your liver is working even if you do not think you have liver disease. Your doctor will probably tell you not to take pravastatin if you have liver disease or if the tests show that you may be developing liver disease.
  • tell your doctor if you drink more than two alcoholic beverages per day, if you are 65 years of age or older, if you have ever had liver disease or if you have or have ever had low blood pressure, muscle aches or weakness, seizures, or thyroid or kidney disease.
  • tell your doctor if you are pregnant or plan to become pregnant. You should not become pregnant while you are taking pravastatin. Talk to your doctor about birth control methods that you can use during your treatment. If you become pregnant while taking pravastatin, stop taking pravastatin and call your doctor immediately. Pravastatin may harm the fetus.
  • do not breastfeed while you are taking this medication.
  • if you are having surgery, including dental surgery, tell the doctor or dentist that you are taking pravastatin. If you are hospitalized due to serious injury or infection, tell the doctor who treats you that you are taking pravastatin.
  • ask your doctor about the safe use of alcoholic beverages while you are taking pravastatin. Alcohol can increase the risk of serious side effects.



Pravastatin is generally well tolerated; adverse reactions have usually been mild and transient. In 4-month-long placebo-controlled trials, 1.7% of pravastatin-treated patients and 1.2% of placebo-treated patients were discontinued from treatment because of adverse experiences attributed to study drug therapy; this difference was not statistically significant.

Adverse Clinical Events

Short-Term Controlled Trials

In the PRAVACHOL placebo-controlled clinical trials database of 1313 patients (age range 20-76 years, 32.4% women, 93.5% Caucasians, 5% Blacks, 0.9% Hispanics, 0.4% Asians, 0.2% Others) with a median treatment duration of 14 weeks, 3.3% of patients on PRAVACHOL and 1.2% patients on placebo discontinued due to adverse events regardless of causality. The most common adverse reactions that led to treatment discontinuation and occurred at an incidence greater than placebo were: liver function test increased, nausea, anxiety/depression, and dizziness.

All adverse clinical events (regardless of causality) reported in ≥ 2% of pravastatin-treated patients in placebo-controlled trials of up to 8 months duration are identified in Table 1:

Table 1: Adverse Events in ≥ 2% of Patients Treated with Pravastatin 5 to 40 mg and at an Incidence Greater Than Placebo in Short-Term Placebo-Controlled Trials (% of patients)

The safety and tolerability of PRAVACHOL at a dose of 80 mg in 2 controlled trials with a mean exposure of 8.6 months was similar to that of PRAVACHOL at lower doses except that 4 out of 464 patients taking 80 mg of pravastatin had a single elevation of CK > 10 times ULN compared to 0 out of 115 patients taking 40 mg of pravastatin.

Long-Term Controlled Morbidity And Mortality Trials

Adverse event data were pooled from 7 double-blind, placebo-controlled trials (West of Scotland Coronary Prevention Study ; Cholesterol and Recurrent Events study ; Long-term Intervention with Pravastatin in Ischemic Disease study ; Pravastatin Limitation of Atherosclerosis in the Coronary Arteries study ; Pravastatin, Lipids and Atherosclerosis in the Carotids study ; Regression Growth Evaluation Statin Study ; and Kuopio Atherosclerosis Prevention Study ) involving a total of 10,764 patients treated with pravastatin 40 mg and 10,719 patients treated with placebo. The safety and tolerability profile in the pravastatin group was comparable to that of the placebo group. Patients were exposed to pravastatin for a mean of 4.0 to 5.1 years in WOS, CARE, and LIPID and 1.9 to 2.9 years in PLAC I, PLAC II, KAPS, and REGRESS. In these long-term trials, the most common reasons for discontinuation were mild, non-specific gastrointestinal complaints. Collectively, these 7 trials represent 47,613 patient-years of exposure to pravastatin. All clinical adverse events (regardless of causality) occurring in ≥ 2% of patients treated with pravastatin in these studies are identified in Table 2.

Table 2: Adverse Events in ≥ 2% of Patients Treated with Pravastatin 40 mg and at an Incidence Greater Than Placebo in Long-Term Placebo-Controlled Trials

Body System/Event Pravastatin
% of patients
% of patients
Rash (including dermatitis) 7.2 7.1
Edema 3.0 2.7
Fatigue 8.4 7.8
Chest Pain 10.0 9.8
Fever 2.1 1.9
Weight Gain 3.8 3.3
Weight Loss 3.3 2.8
Musculoskeletal Pain 24.9 24.4
Muscle Cramp 5.1 4.6
Musculoskeletal Traumatism 10.2 9.6
Nervous System
Dizziness 7.3 6.6
Sleep Disturbance 3.0 2.4
Anxiety/Nervousness 4.8 4.7
Paresthesia 3.2 3.0
Urinary Tract Infection 2.7 2.6
Upper Respiratory Tract Infection 21.2 20.2
Cough 8.2 7.4
Influenza 9.2 9.0
Pulmonary Infection 3.8 3.5
Sinus Abnormality 7.0 6.7
Tracheobronchitis 3.4 3.1
Special Senses
Vision Disturbance (includes blurred vision, diplopia) 3.4 3.3
Viral Infection 3.2 2.9

In addition to the events listed above in the long-term trials table, events of probable, possible, or uncertain relationship to study drug that occurred in < 2.0% of pravastatin-treated patients in the long-term trials included the following:

Dermatologic: scalp hair abnormality (including alopecia), urticaria.

Endocrine/Metabolic: sexual dysfunction, libido change.

General: flushing.

Immunologic: allergy, edema head/neck.

Musculoskeletal: muscle weakness.

Nervous System: vertigo, insomnia, memory impairment, neuropathy (including peripheral neuropathy).

Special Senses: taste disturbance.

Postmarketing Experience

In addition to the events reported above, as with other drugs in this class, the following events have been reported during postmarketing experience with PRAVACHOL, regardless of causality assessment:

Musculoskeletal: myopathy, rhabdomyolysis, tendon disorder, polymyositis.

There have been rare reports of immune-mediated necrotizing myopathy associated with statin use .

Nervous System: dysfunction of certain cranial nerves (including alteration of taste, impairment of extraocular movement, facial paresis), peripheral nerve palsy.

There have been rare postmarketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These cognitive issues have been reported for all statins. The reports are generally nonserious, and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks).

Hypersensitivity: anaphylaxis, angioedema, lupus erythematosus-like syndrome, polymyalgia rheumatica, dermatomyositis, vasculitis, purpura, hemolytic anemia, positive ANA, ESR increase, arthritis, arthralgia, asthenia, photosensitivity, chills, malaise, toxic epidermal necrolysis, erythema multiforme (including Stevens-Johnson syndrome).

Gastrointestinal: abdominal pain, constipation, pancreatitis, hepatitis (including chronic active hepatitis), cholestatic jaundice, fatty change in liver, cirrhosis, fulminant hepatic necrosis, hepatoma, fatal and non-fatal hepatic failure.

Dermatologic: a variety of skin changes (e.g., nodules, discoloration, dryness of mucous membranes, changes to hair/nails).

Renal: urinary abnormality (including dysuria, frequency, nocturia).

Respiratory: dyspnea, interstitial lung disease.

Psychiatric: nightmare.

Reproductive: gynecomastia.

Laboratory Abnormalities: liver function test abnormalities, thyroid function abnormalities.

Laboratory Test Abnormalities

Increases in ALT, AST values and CPK have been observed .

Transient, asymptomatic eosinophilia has been reported. Eosinophil counts usually returned to normal despite continued therapy. Anemia, thrombocytopenia, and leukopenia have been reported with statins.

Pediatric Patients

In a 2-year, double-blind, placebo-controlled study involving 100 boys and 114 girls with HeFH (n=214; age range 8-18.5 years, 53% female, 95% Caucasians, < 1% Blacks, 3% Asians, 1% Other), the safety and tolerability profile of pravastatin was generally similar to that of placebo.

Read the entire FDA prescribing information for Pravachol (Pravastatin Sodium)

Statins increase weight and blood sugar and raise diabetes risk, study finds

Scientists analysed genetic data from up to 220,000 people and results from almost 130,000 patients who took part in earlier statin trials.

They found patients taking statins experienced a modest 12% increased risk of developing type 2 diabetes over a four-year period, and gained around half a pound (240 grams) in weight on average.

Statins work by reducing the efficiency of a liver enzyme, causing liver cells to trap more low-density lipoprotein (LDL) – the harmful form of cholesterol – from the bloodstream.

The cholesterol is converted to bile salts and eliminated naturally from the body.

Lead researcher Dr Daniel Swerdlow, from University College London’s Institute of Cardiovascular Science, said: ”Commonly occurring variants in the gene encoding the same liver enzyme are associated with a lower LDL cholesterol.

”Incorporating information from up to 220 000 individuals, we found that these genetic variants were also associated with a higher weight and marginally higher type 2 diabetes risk.

”The effects were very much smaller than from statin treatment, but the genetic findings indicate that the weight gain and diabetes risk observed in the analysis from trials are related to the known mechanism of action of statins rather than some other unintended effect.”

The findings are published in the latest online edition of The Lancet medical journal.

Co-author Professor Aroon Hingorani, director of the UCL institute, stressed that the effects of the genetic variants were ”orders of magnitude” lower than those of statins.

”The genetic findings of our study help to explain the mechanism by which statins increase weight and diabetes risk,” he said.

He added there was ”no indication” that individuals’ genetic make-up meaningfully influenced the response to statin treatment.

Current clinical guidelines suggest that statins should be offered to people with a 10% or higher risk of developing heart disease in the next 10 years.

Statins are also recommended for patients who have had a heart attack or stroke to reduce the risk of future incidents.

Professor Naveed Sattar, another member of the research team from the University of Glasgow’s Institute of Cardiovascular and Medical Sciences, said: ”Previous analyses have indicated that the cardiovascular benefits of statin treatment greatly outweigh the risk of new-onset type 2 diabetes.

”Nevertheless, many patients eligible for statin treatment would also benefit from lifestyle changes including increased physical activity, eating more healthily and stopping smoking.

”The modest increases in weight and diabetes risk seen in this study could easily be mitigated by adopting healthier diets and lifestyles. Reinforcing the importance of lifestyle changes when discussing these issues with patients would further enhance the benefit of statin treatment in preventing heart attacks and strokes.”

Professor Jeremy Pearson, associate medical director of the British Heart Foundation, which co-funded the study, said: ”This study should reassure people that the benefits of taking statins far outweigh the small effect on diabetes risk. But the results also reinforce that, alongside prescribed medication, taking steps to maintain a healthy weight is essential to stay heart healthy.”

Professor Colin Baigent, deputy director of Oxford University’s Clinical Trial Service and Epidemiological Studies units, said: ”Although it is helpful to understand mechanisms, this research does not change our assessment of the safety of statins.

“The magnitude of the benefits of statins arising from the prevention of heart attacks and strokes greatly outweighs any small risks of diabetes, so the current recommendations for statin use remain appropriate.”

Why No Obesity Drug Will Ever Be The Next Lipitor

Former Xenical User via Wikipedia

“The next Lipitor.” That’s the prediction Christopher James of investment bank MLV & Co. made for Vivus’ new obesity drug in a Bloomberg story last week. He was quoted as saying it could be given to tens of millions of patients.

Not likely.

It’s not that Vivus’ drug, Qnexa, doesn’t have potential to become the best-selling weight loss pill ever. It’s that it could be many times bigger than any weight loss medicine ever and still not even come close to hitting Lipitor’s peak of $11 billion in global annual sales. (Until it went off patent last year, Lipitor, a Pfizer cholesterol medicine, was the best selling drug ever.)

It seems intuitively obvious that the market for an obesity drug would be vast. But the reality is that obesity drugs have never sold in Lipitor-like numbers, and they are not likely to unless someone comes up with one that is absolutely perfect in terms of efficacy and side effects.

In the late 1990s, there was a huge fad of combining the weight loss drugs Pondimin (fenfluramine), sold by American Home Products, and the stimulant phentermine. Doctors also started using Redux, a newer AHP weight loss drug. In 1996, its first year on the market, Redux had sales or $132 million, and Pondimin had sales of $48 million, according to a December 1997 Reuters story. In March 1997, both drugs were withdrawn because they appeared to increase the risk of heart valve defects.

Meridia, from Abbott Laboratories , was launched in 1997. The drug, a stimulant, helped patients lose weight (46% of people lost 10% or more of their body weight in clinical trials) but also affected heart rate. In 2005, sales in the U.S. were about $60 million, with another $240 million abroad. In 2010, the drug was withdrawn in the U.S. and elsewhere after clinical trial data indicated it raised the risk of heart attack and stroke.

Xenical from Roche, was launched in 1999. In 2001, sales peaked at about $600 million. Then they started to drop, and never regained momentum. The drug’s main side effect, oily stools and flatulence, were described in nauseating (and hysterical) detail by movie director Kevin Smith in his book, “Silent Bob Speaks.” Xenical was safe enough that it was introduced as an over-the-counter medicine by GlaxoSmithKline under the name Alli, with a huge marketing push, in 1997. AdAge reported that sales topped $260 million – and then dropped 50% the next year.

The same pattern emerges with each of these drugs. First, a large number of people do try the new medicine, leading to early success. But then the drugs get abandoned, and sales crater. In order for a new obesity medicine to even make the $1 billion mark, it has to do almost least twice as well as any preceding obesity drug ever has. Then it has to sustain that performance.

Why wouldn’t this happen? A 2007 study in the International Journal of Obesity gives a good picture of these past launches. Researchers used administrative data from British Columbia, Canada, to find 17,000 users of Xenical and 3,500 users of Meridia. They found that after two years, only 2% of patients were still taking their medicines. Even in obesity clinical trials, the drop-out rates are very high.

The way that Sanofi , the French drug giant, planned to market its obesity pill, Acomplia, is telling. The drug was an anti-appetite medicine that worked by blocking the same receptors that marijuana stimulates to cause the munchies. Experts were predicting it would be one of the best-selling drug in the world. But Sanofi was careful not just to pitch it as a weight loss drug, but also as one that might lower cardiovascular risk. The company even conducted cardiac imaging studies to try and show that Acomplia prevented plaque build up in the arteries. The reason was obvious: heart medicines get taken for a long time, and people tend to stay on them. The 200 million prescriptions each year for drugs like Lipitor dwarf any weight-loss drug ever.

Of course, that was all for naught. Acomplia raised the risk of neurological side effects, including suicidality, and was never approved in the U.S. and has been withdrawn worldwide.

In order to believe that Qnexa, or, for that matter, other obesity drugs under development such as Orexigen’s Contrave or lorcaserin from Arena Pharmaceuticals, is going to become a mega-seller, one has to believe that it is going to be accepted by patients with obesity in a way no medicine ever has.

Qnexa does help patients lose weight. In clinical trials, the top dose of the pill, which combines the stimulant phentermine with the Johnson & Johnson epilepsy drug topiramate (also called Topamax), helped patients lose an average 10.6% of their body weight. Sixty-nine percent of people on the highest dose of the drug lost more than 5% of their body weight, compared to 20% of those on placebo. All doses of the Qnexa met the FDA’s standards for efficacy. But the drug also causes birth defects, psychiatric issues, and cognitive problems like memory loss. The jury is out on whether it is good or bad for the heart.

There was a time in the 1980s when cholesterol drugs were not very big products, because they didn’t lower cholesterol much, had lots of side effects, and hadn’t been proven to prevent heart attacks or save lives. Then came Mevacor, the first statin, from Merck, which reduced cholesterol dramatically with few side effects. Sales started to rise. Then a large trial in heart patients proved that Merck’s next cholesterol-lowering statin, Zocor, prevented heart attacks and deaths in people who had already had a heart attack. Lipitor became the best-selling drug in the world because it was even more potent, safe, and was tested in even more large clinical trials. Does Qnexa really seem like it might follow that kind of path to broad use?

Some, or even all, of these obesity drugs could become $1 billion sellers. But investors should be careful of forecasts that rise much higher than that. It’s easy to come up with math that shows truly staggering numbers for some future obesity market. History tells another story.

Are Statins Good Or Bad?

Statins, also known as HMG-CoA reductase inhibitors, are drugs that are prescribed for people with high levels of cholesterol. They block the action of an enzyme (HMG-CoA reductase) made in the liver that is required to produce cholesterol, hence their name, HMG-CoA reductase inhibitors.
The human body needs cholesterol in order to function. However, high levels can lead to atherosclerosis – when cholesterol-containing plaques accumulate in the arteries and undermine blood flow. Statins reduce blood cholesterol levels, and in doing so reduce the risk of developing stroke, heart attack and angina.
Statins have been linked to various adverse events (undesirable side effects), and many lay people wonder whether they are good or bad. The aim of this article is to show some studies which looked at the harms and benefits of statins.
Diabetes risk – scientists from St. George’s University, London, England, and the University of Glasgow, Scotland examined five statin trials that had been published from 2005 to 2010. They found there was a link between high statin doses and diabetes risk – patients on high doses of statins had a 12% higher risk of developing diabetes. However, they emphasized that the benefits – reducing serious heart problems – far outweigh any risks. ()
Low heart-risk patients – researchers from the Cochrane Heart Group at the London School of Hygiene and Tropical Medicine in London, UK, stated that there is not enough evidence that statins benefit low-risk heart disease patients. Team leader, Fiona Taylor said doctors should be cautious about prescribing them to low-risk patients, especially in light of evidence on how statins affect people with no history of cardiovascular disease. ()
Hemorrhage history – a study carried out at Massachusetts General Hospital and Harvard Medical School, Boston suggested that patients with a history of hemorrhage may find that statins increase their risk of recurrence to the point that this outweighs any benefits (). They wrote:
“A particular subgroup of patients for whom the advisability of statin use is unclear are those at high risk for intracerebral hemorrhage (or a stroke caused by bleeding within the brain). The reason for added concern is the increased incidence of intracerebral hemorrhage observed among subjects randomized to statin therapy in a clinical trial of secondary stroke prevention.”
Childhood lupus – children with lupus should not be given statins, even though their condition raises the risk of developing coronary artery disease later on in life, researchers from Duke University Medical Center revealed in a study. They said that even though statins have a positive effect on lipid levels and CRP (C-reactive protein), their effect on atherosclerosis is not considerable enough to warrant their routine use for children with lupus. They said the rare long-term risks associated with statins outweigh the benefits. ()

Statins and liver damage

Liver damage – statins can cause levels of liver enzymes to increase. If this is slight, most patients can continue taking the medication. However, if the increase is severe, the patient will have to stop, otherwise there is a risk of eventual permanent liver damage.
Patients on some medications, such as gemfibrozil (Lopid) and niacin have a higher risk of developing liver problems if they are also on statins.
Patients on statins should have a blood test six weeks after starting on them in order to check liver function. Then, there should be annual blood tests if no liver problems were detected.

Statins and muscle problems

Statins may cause statin myopathy – there is inflammation of the muscles. The patient feels muscle pain and tenderness. The higher the statin dose, the more likely a patient will experience these pains.
In severe cases rhabdomyolysis can develop – the muscles break down and release the protein myoglobin into the bloodstream. Myoglobin can damage the kidneys.
Patients on certain medications have a higher risk of rhabdomyolysis. These include niacin, cyclosporine, nefazodone, gemfibrozil, antifungal medications, and erythromycin (Erythrocin).
Any patient on statins who starts having muscle pains should tell their doctor.
According to the American Heart Association:
“For the person who experiences myopathy with a statin, other alternatives should be discussed with their physician. Patients who are taking statins and not experiencing any side effects should continue to take their medication unless advised for other reasons to stop by their healthcare provider. Only the very rare side effect of rhabdomyolysis (muscle injury), signaled by dark urine, should lead a patient to stop their statin immediately but then talk promptly with their healthcare provider.” ()

Effect of statins on brain cells

A 2009 study published in the Journal of Lipid Research reported that statins can have profoundly varying effects on brain cells, both good and bad effects. The authors said that doctors should take great care when determining what dosage patients should be prescribed, especially the elderly.
John Albers and team compared simvastatin and pravastatin on neurons and astrocytes (two types of brain cells). Astrocytes support cells that help repair damage. They applied the drugs directly to cells thus eliminating the drugs’ differences in crossing the blood-brain barrier. They found differences in both types of cells and between the drugs. Simvastatin reduced the astrocytes’ expression of cholesterol transporter ABCA1 by about 80%, while pravastatin did the same by 50%. Both statins increased expression of the Tau protein in astrocytes and neurons – Tau protein is linked to Alzheimer’s disease. Pravastatin also increased the expression of amyloid precursor protein (APP), another Alzheimer’s hallmark.
Brain cholesterol levels tend to be reduced during old age. The researchers wondered whether among elderly individuals, the effects of stain therapy might have the potential to transient or permanent cognitive impairment. ()

Scientists in The Netherlands, however, found that statins can protect nerve cells against damage known to occur in the brains of patients with Alzheimer’s disease. We know that nerve cells eventually die as a result of overstimulation, a process known as excitotoxicity. The Dutch scientists overstimulated nerve cells in animal experiments and found that when treated with a statin (Lovastatin) the death of those overstimulated nerve cells could be prevented. The statins also prevented loss of memory capacity that typically occurs after the death of such cells. Statins stimulate the protective capacity of tumor necrosis factor, which is closely involved in the brain’s immune response.
In animal experiments they demonstrated that this tumor necrosis factor has a very beneficial effect on nerve cells and can protect them against death. ()

Statins and tendon complications

In 2008, researchers at Rouen University Hospital in Rouen Cedex, France identified 96 cases of tendon complications between 1990 and 2005 which were attributed to statins. Conditions included tendon rupture and tendonitis (majority of cases).
Their study showed that of 4,597 side-effects linked to statins, approximately 2% were attributed to tendon complications, with symptoms generally occurring within 8 months of starting statin therapy. The Achilles heel was the most common tendon affected, with swelling, warmth, stiffness and pain as the most common symptoms. Seventeen of the patients had such severe symptoms that they had to be hospitalized. The symptoms started after the patients began taking statins, and improved after statins were stopped, and then came back when therapy was restarted.
A considerable number of tendon complications may go unreported, they added. Although the prevalence of tendon complications with statins is low, all statins have the potential to cause such problems, even at recommended dosages. ()

Are statins good or bad

The answer to that question cannot be a simple one. If a person has a severe liver reaction when on statins, then they are obviously bad. However, a good doctor will find that out. Most studies agree that the benefits of statins, if prescribed properly and to suitable patients, far outweigh the risks.
Written by Christian Nordqvist
Original article date: 30 April 2004
Article re-written: 08 September 2011

Your body makes a waxy substance called cholesterol. You also get it from food. Your body needs it, but too much cholesterol in your blood can clog your arteries. This increases your risk of heart disease, heart attack, and death.

Statins are drugs that lower your cholesterol. But if you are age 75 or older and you haven’t had symptoms of heart disease, statins may be a bad idea. Here’s why:

Adults age 75 and older may not need statins.

Many older adults have high cholesterol. Their doctors usually prescribe statins to prevent heart disease.

But for older people, there is no clear evidence that high cholesterol leads to heart disease or death. In fact, some studies show the opposite—that older people with the lowest cholesterol levels actually have the highest risk of death.

Statins have risks.

Compared to younger adults, older adults are more likely to suffer serious side effects from using statins.

Statins can cause muscle problems, such as aches, pains, or weakness. Rarely, there can be a severe form of muscle breakdown.

In older adults, statins can also cause:

  • Falls
  • Memory loss and confusion
  • Nausea, constipation, or diarrhea.

Often, older adults take many drugs. These can interact with statins and lead to serious problems. Side effects, like muscle pain, may increase. Statins can also cause a fatal reaction when taken with heart-rhythm drugs.

Statins may increase the risk of type-2 diabetes and cataracts, as well as damage to the liver, kidneys, and nerves.

Weigh the risks and benefits.

You and your doctor should look carefully at the risks and benefits of statins, especially if you are older and do not have heart disease.

Older people may not live long enough to get the important benefits from statins. You and your family should speak with your doctor about your health concerns. Are you more concerned about preventing a heart attack that might never happen? Or do you want to avoid side effects that can lead to frailty, injury, and memory problems?

Statins can cost a lot.

A one-month supply of statins can cost as little as $4, or as much as several hundred dollars, depending on the statin prescribed. You may also have to pay for extra tests to check for side effects.

When should older adults take statins?

You should take statins if you have had a heart attack, stroke, or mini-stroke (transient ischemic attack, or TIA). Statins can help prevent a second heart attack or stroke.

This report is for you to use when talking with your health-care provider. It is not a substitute for medical advice and treatment. Use of this report is at your own risk.

© 2017 Consumer Consumer Developed in cooperation with AMDA—The Society for Post-Acute and Long-Term Care Medicine.

Managing statin muscle pain

There are several things you can do to prevent or minimize the aches and pains that might accompany statin use.

Updated: August 9, 2019Published: June, 2017

If you’re not taking a statin now, you may well be soon. These medications are commonly prescribed to lower “bad” LDL cholesterol and have been shown to reduce the risk of heart attack, stroke, and death. They are routinely recommended for people who have cardiovascular disease and for many people ages 40 to 75 who don’t have cardiovascular disease but have at least one risk factor (high blood pressure, high cholesterol, diabetes, or smoking) and a 7.5% or greater risk of a stroke or heart attack in the next decade. Moreover, recent research indicates that they may benefit high risk individuals over age 75 as well.

Muscle pain and other statin side effects

Taking a statin may give you some assurance that you’re doing all you can to avoid heart attack and stroke, but you may also experience side effects. Reported side effects include an increased chance of developing diabetes — which is largely restricted to people who are already at risk for diabetes, and who can be monitored with glucose or hemoglobin A1c tests. Statin use has also been associated with difficulties with memory and reasoning, although there is no clear evidence that the drugs were responsible. In very rare cases, statins may cause liver problems or a potentially life-threatening breakdown in muscle cells.

However, the most common side effect is muscle pain and cramping. “In the real world about 15% to 20% of patients report myalgias, or muscle-related symptoms, with women reporting such symptoms more than men do,” says Dr. Samia Mora, a cardiologist at Harvard-affiliated Brigham and Women’s Hospital. It is unclear why these symptoms may be more common in women, but it could be because they tend to be older, have smaller bodies, and more additional health issues than men do when they begin to take the medications. Women are also more likely than men to have undiagnosed low levels of thyroid hormone, which increases the risk of statin-related side effects.

What you can do about muscle pain from statins

Keep track of any new symptoms that develop when you begin taking a statin, and report them to your doctor. Some symptoms may go away as you continue to take the medication. If you’re taking the statin preventively, your doctor may try to determine if your muscle pain symptoms are actually due to the statin by suggesting a brief holiday from the drug to see if they disappear when you’re not taking it. However, don’t stop taking a statin without telling your doctor. Although there are no proven remedies for statin-related muscle pain, the following may help.

Exercise. There is some evidence that people who have exercised regularly before taking statins are less likely to experience muscle pain and cramping. Although gentle stretching may relieve muscle cramps, beginning a new vigorous exercise regimen while taking a statin may increase the risk of muscle pain.

Ramp up your lifestyle changes. Commit to an exercise routine, lose weight if you need to, and adopt a heart- healthy eating plan such as the Mediterranean diet. Doing so may enable you to reduce your statin dosage, or possibly even lower your cholesterol enough to enable you to stop the statin. Even if a healthier lifestyle does not lower your lipid levels, it may still lower your long-term risk of heart disease and stroke.

Have a thyroid blood test. If you have a low thyroid hormone level, taking replacement thyroid hormone pills may alleviate muscle pain and can also improve your lipid profile.

Take supplements. If you have a low blood level of vitamin D, restoring it to normal with a supplement may help reduce muscle pain and cramping. Some people find symptom relief with coenzyme Q10. However, small clinical trials haven’t substantiated the positive effects. Get your doctor’s advice about taking either of these.

Change your prescription. If, after a few weeks of statin use, you’re still experiencing muscle pain or cramping, you and your doctor might consider going to a lower statin dose or switching to a different statin, possibly one that is designed to be taken less frequently. Adding another type of cholesterol-lowering drug called ezetimibe (Zetia), which hasn’t been associated with muscle pain, may also allow your doctor to lower your statin dosage.

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Some months ago, my Dr put me on Zocor for high Cholesterol. A month or so later, I had acute joint pain(not muscle) that got to unbearable. Went off med. I also have arthritis(osteo). She put me back on Lescol 5 days ago, but arthritis in my thumb joints is getting noticable, and also now having pain(grabbing) at the base of my neck. I think I remember, in a general conversation with a pharmacist, was told Cholesterol meds negate the good any arthritis meds might do(I only take MSM for arthritis, so far, but have prescription for Arthrotec 50mg). I wondered if is is possible the Statin drugs do inhibit the work of arthritis meds?


As you correctly imply, statins are indeed associated with muscle pain and inflammation. However, they are not known to be associated with worsening joint pain. The pain from osteoarthritis comes and goes unpredictably. Since osteoarthritis and high cholesterol (and therefore statin use) are both very common, it is not surprising that sometimes the pain from OA will get worse (or better !) while someone is taking statins.

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