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Statins side effects

comparison in high-risk group

Cognative impairment and other mental problems; very significant increase in the incidents of cancer, and over 30% serious side effects with high-dose statins.  The article at bottom of the page found a 52% increase in cancer deaths.



British Medical Journal, one of a couple on line sources that is free.


BMJ 2006;332(7553):1330 (3 June), doi:10.1136/bmj.332.7553.1330

Analysis and comment


Should we lower cholesterol as much as possible?

Uffe Ravnskov, independent researcher1, Paul J Rosch, clinical professor2, Morley C Sutter, professor emeritus3, Mark C Houston, clinical professor of medicine4

1 Magle Stora Kyrkogata 9, S 22350 Lund, Sweden, 2 Departments of Medicine and Psychiatry, New York Medical College, Valhalla, NY, USA, 3 Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver BC, Canada, 4 Vanderbilt University School of Medicine, St Thomas Hospital, Nashville, TN, USA

Correspondence to: U Ravnskov

Statins are portrayed as harmless drugs that almost everyone would benefit from, but little is known about the side effects at the high doses now being suggested


Are higher statin doses safe?

To achieve this new goal, people at high risk would have to take higher statin doses than currently suggested. This would increase the risk of adverse side effects. In the treating to new targets (TNT) trial, the only study comparing a low and high dose of the same statin, not even 80 mg atorvastatin was able to lower mean low density lipoprotein cholesterol below 1.81 mmol/l.3 Clinical experience has taught us that a dose increase of that size of any drug will inevitably increase both the number and the seriousness of side effects. This apparently did not concern the authors, who concluded, "Intensive lipid lowering therapy with 80 mg of atorvastatin per day in patients with stable CHD [coronary heart disease] provides significant clinical benefit."

However, overall mortality was not reduced because the smaller number of cardiovascular deaths in the 80 mg atorvastatin group was offset by increased deaths from other causes leaving a benefit of 250 (5%) fewer non-fatal cardiovascular events. Because many non-fatal events resolve with little residual damage or discomfort, meticulous recording of all possible adverse side effects is mandatory. However, the authors have not provided adequate information on adverse events.4 5

Deficient information about side effects

The authors failed to elaborate on their criteria for determining whether an adverse effect was considered related to treatment. Surprisingly, that decision was not made by the authors but by the investigator with direct responsibility for the patients. Specific information about the symptoms that were designated as side effects was also incomplete. For instance, only the number of patients with aminotransferase concentrations that were persistently over three times the upper limit of normal was listed (51 more cases in the high dose group). Why not give the number of participants showing any persistent rise as is customary in drug trials?

In the recent incremental decrease in end points through aggressive lipid lowering (IDEAL) trial,6 which compared usual dose simvastatin with 80 mg atorvastatin, no significant difference was seen on the major end points. However, the number of adverse effects were far higher than in any previous statin trial. Almost 90% of participants in both groups had side effects, and in almost half of them they were recorded as serious. The authors of the IDEAL trial did not comment on this alarming finding except by mentioning that "there was no difference between the groups in the frequency of adverse events that were rated as serious"; neither did they inform readers about the nature of these events.

Adverse effects of statins

Many adverse effects are first recognised in the post-marketing surveillance process, and their frequency is likely to be understated because few doctors report them. A request among general practitioners in Rhode Island found that the serious side effects that had been reported from any drug to the Food and Drug Administration included only 1% of those observed.7 Nevertheless, many hitherto unknown potential side effects from statins have already been reported.

Heart failure
All statins inhibit the synthesis of hydroxymethylglutaryl coenzyme A reductase, an enzyme involved in synthesis of the precursor of cholesterol and other important molecules such as coenzyme Q10, vital for mitochondrial energy production. Thus statins lower plasma Q10 concentrations and worsen cardiac function in patients with heart failure, and oral coenzyme Q10 can improve or prevent this serious complication.8-10 Heart failure has not been reported with statins, possibly because it has been seen to be the result of the primary disease rather than an adverse effect but also because patients with imminent or manifest congestive failure are routinely excluded from statin trials.

Myalgia and rhabdomyolysis
Muscle complaints are claimed to occur in less than 1% of patients taking statins, but this is almost certainly an underestimate. In a study of 22 professional athletes with familial hypercholesterolaemia who were treated with various statins, sixteen discontinued the treatment because of muscle side effects.11 Competitive athletes may be more sensitive to muscle pain and weakness, but even mild symptoms may have a deleterious effect on elderly people and others who already have muscular weakness.

In rare cases, myopathy has led to rhabdomyolysis and death from renal failure. In the TNT trial,3 five non-fatal cases of rhabdomyolysis were reported, four of them during the treatment period. To consider them unrelated to the treatment because they were not dose-dependent, as did the authors, seems premature. In a recent review of statin side effects the authors had found 4.2 cases of rhabdomyolysis per 100 000 patient years after atorvastatin treatment.12 If true, and if the five cases observed in the TNT trial (50 000 patient years) were not due to treatment it means that rhabdomyolysis should be twice as common in untreated people than in those treated with statins.


Mental and neurological symptoms
Cholesterol is vital for the development and function of the brain.
It is therefore unsurprising that reduced concentrations may produce mental and neurological complaints such as severe irritability, aggressive behaviour, suicidal impulses, cognitive impairment, memory loss, global amnesia, polyneuropathy, and erectile dysfunction.13-19 In many cases the symptoms were reversible and re-occurred after re-challenge. None of these side effects are mentioned on the product labels or information inserts for statins.

At least five animal experiments have found that the statins are carcinogenic in amounts that produce blood concentrations similar to those achieved by doses commonly administered to patients.20 Nevertheless, the FDA approved them because cell experiments did not convincingly prove that statins were either mutagenic or genotoxic. But carcinogenicity may be due to the effects of statins on cholesterol because numerous cohort studies have found low cholesterol to be a risk factor for cancer. This may take a long time to surface. No increase of cancer was seen in a 10 year follow-up of participants in the Scandinavian simvastatin survival study, and the authors therefore concluded that 10 years of statin treatment does not induce cancer.21 Neither does 10 years' smoking tobacco.

A significant increase in breast cancer was seen in the cholesterol and recurrent events trial (CARE), with most cases being recurrences.22 Since then patients with a history of cancer have been excluded from statin trials. If statin treatment is carcinogenic it should be seen first in people at high risk such as smokers and old people. As far as we know, no trial has analysed cancer incidence separately for smokers and non-smokers. In the trial of pravastatin in elderly individuals at risk of vascular disease (PROSPER), the only statin trial exclusively in elderly people, the significant increase in cancer mortality neutralised the benefit from fewer cardiovascular deaths (figure).23 This finding was dismissed by referring to a meta-analysis of all statin trials that failed to find an association with cancer, but the authors ignored mentioning that the mean age of participants in these trials was about 25 years lower than in PROSPER.

Selection bias
The low frequency of side effects in the TNT trial compared with the IDEAL trial may be explained by the way patients were selected for treatment. In the TNT trial more than 3000 people were excluded because they did not fulfil the criteria, already had raised aminotransferase concentrations, cancer, or another disease associated with a limited lifespan, or for "other reasons." After one to eight weeks' treatment with low dose atorvastatin, an additional 5429 patients were rejected, including 197 with non-fatal clinical endpoints, 193 with adverse events, 69 who did not comply with the treatment, 195 who had ischaemic events, 15 with fatal clinical endpoints, and 373 for other reasons. No information was provided on the nature of the side effects or the causes of death. Similarly, it is not clear which side effects later caused 7.2% to stop the treatment.3 Finally, of the 18 468 patients originally screened for the TNT trial, only 10 003 (54%) were selected, whereas for the IDEAL trial the number was 91.7%, meaning that the patients studied in the TNT trial were much healthier than those included in the IDEAL trial and also than those seen in the doctor's office.

Summary points

US recommendations for low density lipoprotein cholesterol concentrations could put most of the Western world's adult population on statins

Doses of statins would have to be more than eight times higher than currently used

Increasing the dose of atorvastatin by eight times does not lower total mortality

Adverse side effects in clinical trials are under-reported

Any reduction in non-fatal events may be outweighed by more numerous and more severe adverse effects





 From Worst Pill, possible the best consumer advocate watchdog of the pharmaceutical industry—a part of Public Citizen and thus associated with Ralph Nader.

The Cholesterol-Lowering Statin Drugs and Memory Loss

     Worst Pills Best Pills Newsletter article December, 2005

In the October 2005 issue of the Canadian Adverse Reaction Newsletter, 19 case reports of memory loss or impairment associated with the use of a cholesterol-lowering statin drug were analyzed. The statin drugs marketed in the U.S. are atorvastatin (LIPITOR), fluvastatin (LESCOL), lovastatin (MEVACOR), pravastatin (PRAVACHOL), rosuvastatin (CRESTOR), and simvastatin (ZOCOR).

In these 19 cases, the onset of memory impairment occurred within one month of starting a statin in five individuals, within one year in seven, and after one year in three cases. The date of onset was not reported in four cases. Eleven reports indicated that the memory problem resolved or improved when the statin was discontinued or the dose of the drug was reduced. One report said that memory problems returned after treatment with a statin was reinitiated.

The median age of statin-treated patients in whom memory problems were reported was 70 years and ranged from 50 to 78 years of age.

The professional product labeling for all statin drugs sold in the U.S. except for rosuvastatin mention memory impairment as a possible adverse effect. The professional labeling for atorvastatin indicates that in clinical trials conducted before the drug was approved, amnesia was reported in less than two percent of patients. Memory impairment is listed in the professional labeling for pravastatin as occurring in less than one percent of patients in clinical trials conducted before the drug was approved.

Pharmacists and physicians from the Duke University Medical Center reported in the July 2003 issue of the journal Pharmacotherapy that between November 1997 and February 2002, there were 60 adverse drug reaction reports involving a statin drug and memory loss made to the FDA.[1] In 36 of these cases, simvastatin was the statin involved, atorvastatin accounted for 23 reports, and in one report pravastatin was the statin in question.

In these 60 reports, the patients’ average age was 62 years and ranged from 30 to 84 years. In thirty of the 60 reports documented both the time that statin treatment was started and the appearance of memory impairment. The median time for a memory problem to appear was two months.  

In 33 of the 60 cases, the statin was stopped after the appearance of memory impairment. Of these 33 patients, memory impairment resolved or improved in 14 cases when the statin was stopped. Memory loss recurred in four patients when statin treatment was restarted.

Published studies have suggested that statin treatment can contribute to memory impairment. In theory, this may happen because of cholesterol’s essential role in the production of the material that forms a coating around nerves called myelin. The statin drugs may enter the brain and decrease the amount of central nervous system cholesterol available to produce myelin, leading to a loss of the myelin coat that may cause memory problems.

Potentially, statin-induced memory impairment could be mistaken for other conditions such as early Alzheimer’s disease. This could result in the prescribing of a drug to treat Alzheimer’s when it is not needed.


[1]  See [Pharmacotherapy 23(7):871-880, 2003. 2003 Pharmacotherapy Publications]



In this study of 50 consecutive patients in a cardiology clinic a very gross underestimation of side effects of statin was uncovered.   All were taken off statins following an evaluation for side effects.  They were given CoQ10, an enzyme essential in the production of ATP, the body’s source for energy that drives muscle contractions, cellular transport, and much more.  Based on the change from being on statins to taken off statins and given Q10, for a period averaging 22 months, there was reported a reduction of fatigue from 84% of cohort to 16% (this meant that 84% of the 50 patients reported fatigue), “myalgia [muscle pain] from 64% to 6%, dyspnea [difficulty breathing or painful breath] from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy [deranged function and structure of peripheral motor, sensory & autonomic neurons] from 10% to 2%.”  As to why these findings are superior to PhARMA generated research, go to for an account of PhARMA’s control over the production of information—jk.

BioFactors Issue Volume 25, Number 1-4 / 2005 Pages147-152. 

Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation


Fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ10 at an average of 240 mg/day upon initial visit. Patients have been followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients. We conclude that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ10. We saw no adverse consequences from statin discontinuation.


BioFactors Volume 18, Issue 1-4, pages 101–111, 2003  16 DEC 2008 DOI: 10.1002/biof.5520180212

The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications


The depletion of the essential nutrient CoQ10 by the increasingly popular cholesterol lowering drugs, HMG CoA reductase inhibitors (statins), has grown from a level of concern to one of alarm. With ever higher statin potencies and dosages, and with a steadily shrinking target LDL cholesterol, the prevalence and severity of CoQ10 deficiency is increasing noticeably. An estimated 36 million Americans are now candidates for statin drug therapy. Statin-induced CoQ10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials. This drug-induced nutrient deficiency is dose related and more notable in settings of pre-existing CoQ10 deficiency such as in the elderly and in heart failure. Statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs. We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear. As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function.



Is Less More? New Study Challenges Conventional Thought on Desirable Cholesterol Levels, Links Very Low Cholesterol to Cancer

     Worst Pills Best Pills Newsletter article February, 2008

In the U.S., current thinking about cholesterol is generally that “lower is better.” But there is a growing body of evidence, most recently a study published in the July 2007 Journal of the American College of Cardiology, that suggests very low cholesterol levels are linked to cancer.

This leaves two fundamental questions unanswered: How low is low enough? And might there be dangers from going too low?

The issue is not so cut-and-dry. High cholesterol, especially if accompanied by other risk factors, can lead to very serious cardiovascular problems such as hardened arteries, strokes and heart attacks. And because heart disease is the leading cause of death in the U.S. – claiming over 650,000 lives in 2004 alone, according the Centers for Disease Control and Prevention – there has been a major push from the public health community to fight heart disease head on.

To this end, the Department of Health and Human Services, through the National Cholesterol Education Program (NCEP), has worked since 1985 to “reduc[e] the percentage of Americans with high blood cholesterol” through education programs aimed both at the public and health professionals. The project has been successful in achieving its goals, dramatically increasing blood cholesterol screening and lowering average total cholesterol levels among U.S. adults from 213 mg/dL to 203 mg/dL since 1978. In its most recent guidelines, the NCEP pushed harder for still lower cholesterol levels, suggesting drug therapy for almost all high-risk patients with an LDL-C (“bad” cholesterol) of 100 and over.

But how the new study fits into this traditional treatment of high cholesterol is unclear at this point.

Study causes controversy among editors

The Journal of the American College of Cardiology study was a metaanalysis examining the relationship between lowering LDL-C using statins and the development of cancer.

A meta-analysis, such as the one done for this study, involves combining data from studies already published or completed to see trends that might be missed in any one individual study. In this case, the authors limited their data to the 13 large, randomized, controlled (with a comparison group) trials on statins published up to November 2005 that included data on newly diagnosed cancer. Although in all these studies there was a comparison group that did not receive the statins, those study participants were not included in the meta-analysis. The four statins that met the criteria were lovastatin (MEVACOR), simvastatin (ZOCOR)fluvastatin (LESCOL) and pravastatin (PRAVACHOL) .

In their analysis, researchers found a “highly significant inverse relationship between achieved LDL-C levels and rates of newly diagnosed cancer.” In other words, researchers saw more new cases of cancer in patients with the lowest cholesterol levels. However, cancer rates were not related to the degree of LDL-C lowering – that is to say, cancer rates were not linked to how much the cholesterol levels decreased, but how low cholesterol levels became. While it is true that the cholesterol lowering in the meta-analysis was obtained by treatment with statins, similar cholesterol lowering by other methods (diet, exercise or other cholesterol- lowering drugs) might, or might not, have the same effects.

There was some disagreement among the editors of the Journal as to whether to publish the study, which challenges the standard school of thought in U.S. cholesterol management that lower is better. Ideally, a study would give clearer insight as to how doctors and patients should proceed. However, as the editors pointed out, the findings, though provocative, did not provide clear answers and much more research must be done to provide doctors and their patients with a recommendation for the appropriate management of cholesterol levels. The editors chose to publish the article although its practical impact would be unclear, saying: “In the five years that we have been stewards of the Journal, no other manuscript has stimulated such intense scrutiny and discussion.”

New study builds on existing experience

The authors and editors were very concerned by the study’s finding, especially because similar evidence has existed for decades.

An increased incidence in side effects has been associated with low cholesterol since as early as 1971. That year a Japanese report showed a correlation between bleeding in the brain and very low cholesterol levels. This study was followed in the 1970s and 1980s with a number of other studies showing a surprising increase in mortality from noncardiovascular causes (cancer, respiratory, digestive, trauma) as cholesterol levels fell. Those findings caused enough worry at the National Institutes of Health’s National Heart, Lung and Blood Institute (NHLBI) that the agency called a conference to discuss the matter.

The NHLBI conference, held in 1990, examined data from 20 studies, including those from the U.S., Europe, Japan and Scandinavia. Data were pooled to examine outcomes in men and women as a function of their total cholesterol levels. Some studies were observational (no drugs involved); others were tests of cholesterol-lowering drugs. One analysis showed that the chance of death due to cancer, trauma, respiratory and digestive causes was actually increased at low total cholesterol levels. In fact, the only cause of death that decreased as cholesterol levels fell was cardiovascular (45 percent of deaths).

Medical community should recognize potential relationship

With the present study being larger than previous ones and therefore more convincing, there needs to be a more honest acceptance of this “disturbing” potential relationship so that physicians and patients can make more realistic choices between drug risks and benefits.

What You Can Do

Patients undergoing treatment for cholesterol levels should discuss with their physicians how low they are aiming to get their cholesterol levels, bringing to the doctor’s attention concerns about the dangers of very low cholesterols and discussing the differences between the goals for lowering cholesterol for primary and secondary prevention (see box below). 


If cholesterol remains high despite diet, add 10 grams of psyllium (METAMUCIL, PERDIEM) a day. Numerous studies have shown that psyllium, for example five grams twice a day, can significantly lower total cholesterol and LDL cholesterol.1 Psyllium, a naturally occurring vegetable fiber, is clearly safer than any of the cholesterol-lowering drugs.


Levin EG, Miller VT, Muesing RA, Stoy DB, Balm TK, LaRosa JC. Comparison of psyllium hydrophilic mucilloid and cellulose as adjuncts to a prudent diet in the treatment of mild to moderate hypercholesterolemia. Archives of Internal Medicine Sep 1990; 150: 1822 - 1827.



Cholesterol-Lowering2 Drugs for People 70 and Older

It is clear that the relationship between moderately elevated cholesterol levels and increased risk of heart disease is not as clear as people get older.2 As geriatricians Fran Kaiser and John Morely have written:

Given the uncertainty of the effects of cholesterol manipulation in older individuals, what should be the approach of the prudent geriatrician to hypercholesterolemia (elevated blood cholesterol levels)? In persons over 70 years of age, life-long dietary habits are often difficult to change and overzealous dietary manipulation may lead to failure to eat and subsequent malnutrition. Thus in this group minor dietary manipulations such as the addition of some oatmeal (or other sources of oat bran or soluble fiber) and beans and modest increases in the amount of fish eaten, may represent a rational approach. Recommending a modest increase in exercise would also seem appropriate. Beyond this, it would seem best to remember that the geriatrician’s dictum is to use no drug for which there is not a clear indication.3

The use of cholesterol-lowering drugs in people 70 or older should be limited to patients with very high cholesterol levels (greater than 300 milligrams) and those who manifest cardiovascular disease (previous history of heart attack or angina).4

The only large clinical trial looking exclusively at the effect of statins on people over the age of 70 provides clear evidence for avoiding these drugs for use in primary prevention of cardiovascular disease in older people who have not had a previous heart attack, stroke, angina, or other cardiovascular diseases or family history. Five thousand eight hundred and four people aged 70 through 82 were randomized to get a statin or a placebo and were followed for an average of 3.2 years. For the more than 3,200 people in this study without prior cardiovascular disease, the statin had no beneficial effect in preventing subsequent cardiovascular disease. There was, however, a significant 25% increased amount of cancer in those getting the statin, particularly gastrointestinal cancers, the cancer predicted in the animal studies of these drugs (see below). The increase was larger the greater the number of years the drug was being used. No other study analyzing cancer exclusively in large numbers of older patients getting statins has refuted this finding of increased gastrointestinal cancer.5

In summary, people over 70 using statins for primary prevention of cardiovascular disease have no benefit, compared to a placebo, but an increased risk of muscle damage (rhabdomyolysis), liver damage, and, as found in the study described above, an increased risk of cancer. It needs to be emphasized, however, that for those over 70 who have had previous cardiovascular disease, the use of statins may be beneficial.

There are even questions as to whether elderly people who are hypertensive should have their cholesterol lowered by drugs. One review concluded, “Further trials are required before routinely suggesting that it is advantageous to lower cholesterol in an elderly hypertensive who does not have pre-existing evidence of coronary heart disease.”6

Animal studies consistently show a cancer-causing effect for the two most popular classes of cholesterol-lowering drugs, the fibrates or fibric acid derivatives, which include clofibrate (ATROMID-S) and gemfibrozil (LOPID), and the widely used statin drugs, fluvastatin (LESCOL), lovastatin (MEVACOR), pravastatin (PRAVACHOL), and simvastatin (ZOCOR). Evidence of a cancer-causing effect from these drugs based on clinical trials in humans is inconclusive because of inconsistent results and a follow-up period that, to date, is too short to detect some cancers that can take years to develop. The ultimate effect of cholesterol-lowering drugs in humans may not be known for decades.

Researchers have taken the rodent cancer data from the 1992 and 1994 editions of the Physicians’ Desk Reference (PDR, a compilation of package inserts available in many public libraries). The package inserts for cholesterol-lowering drugs show that all the fibrates and statins cause cancer in rats and mice. Rats and mice are used because almost all known agents that cause cancer in humans have been found to cause it in these animals. In most instances, cancer-causing dose levels corresponded to maximums recommended for humans.  In a six year study it was found that for those over 70 without previous cardiovascular disease, there was no benefit but there was an increased risk of cancer, especially gastrointestinal cancer.

Although there is clear evidence that certain of the statin drugs not only lower total cholesterol and LDL cholesterol (the “bad” cholesterol) but also decrease the risk of heart attacks and strokes, this evidence is strongest for people who are at much higher risk of these diseases because they have already had a heart attack, angina, bypass surgery or angioplasty, or a stroke.

The evidence for treatment, especially with cholesterol-lowering drugs, is much weaker for people who have not yet had the cardiovascular disease described above, known as primary prevention. This is especially so for those people who do not have more than one of the following risk factors: hypertension, diabetes, smoking, obesity, or a close family history of premature heart attacks or strokes.


I believe that the lowering of event in the high-risk group is due to the aspirin like ability to lower thrombi, and not because of the lowering of LDL—jk.






Those who have a financial interest in the outcome manipulate the results, Major study finds that all 37 journal articles positive effects over stated; the average was 32%. Statins cause erectile dysfunction, cognitive imparement, and cancer.  

Lipitor (2011) lifetime sales $131 billion, tops all drugs.  Plavix at $60 billion is second.



52% short term


LA Times, Health section, July 21, 2008  --  excerpts

Vytorin, the combination drug (simvastatin (better known by its commercial name Zocor) and ezetimibe--known as Zetia) prescribed to lower cholesterol, sustained another blow today, when the author of a major clinical trial announced that the medication had failed to drive down hospitalization and death due to heart failure in patients with narrowing of the aortic valve. In the process, researchers in Norway detected a significant blip in cancers in the 1,800 subjects they followed

Today's findings suggested something more ominous: the incidence of cancer -- and of dying of cancer -- was significantly higher in the patients taking Vytorin. Altogether, 67 patients on placebo developed cancer during the trial. Among subjects on Vytorin, 102 developed cancers of various kinds.*  This is the second adverse press—the first being in March 08, when the ENHANCE trial found that Vytorin fared no better than a placebo at reducing plaque buildup on the walls of patients' arteries.* *

Comments by jk

Simvastatin (Zocor) is off patent.  Thus in a scramble for profits a combination drug (on patent) was introduced.  Direct to consumer market cost $155 in 07—mainly TV ads. 

*  The pressing issue is that since the development  of Statins, the very first animal studies in the 60s it has been known that Statins increase the incidents of cancer.  However, nearly all studies done thereafter have not included cancer. 

*  Several studies have failed to find a reduction in the build of plaque, even thought the statins including Zocor, reduce LDL and cholesterol.  Few studies include the principle reason for taking a statin, namely a reduction in the death rate.  Claims for such reduction probably entail a failure to control the contravening variable, aspirin usage.  Given a pile of evidence, including the very mechanism of plaque formation, which involves inflammation process, I must conclude that the use of statins is highly suspect.  Given the harm done including cognitive impairment, weakness, and cancer, if my skepticism is born out, the harm done by statins as a course of treatment will far surpass that of VIOXX which killed over 200,000 people world wide by accelerating atherosclerosis.