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Niacin prevents MI 25%

Atherosclerosis, Volume 210, Issue 2 , Pages 353-361, June 2010

Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis



High-density lipoprotein cholesterol (HDL-C) concentration is a strong predictor of cardiovascular events in both nave and statin-treated patients. Nicotinic acid is an attractive option for decreasing residual risk in statin-treated or statin-intolerant patients since it increases HDL-C by up to 20% and decreases low-density lipoprotein cholesterol and lipoprotein(a) plasma concentrations.


We performed a computerized PubMed literature search that focused on clinical trials evaluating niacin, alone or in combination with other lipid-lowering drugs, published between January 1966 and August 2008.


Among 587 citations, 29 full articles were read and 14 were eligible for inclusion. Overall 11 randomized controlled trials enrolled 2682 patients in the active group and 3934 in the control group. In primary analysis, niacin significantly reduced major coronary events (relative odds reduction, 95% CI 13, 35), stroke (26%, 95% CI, 41) and any cardiovascular events (27%, 95% CI, 37). Except for stroke, the pooled between-group difference remained significant in sensitivity analysis excluding the largest trial. In comparison with the non-niacin group, more patients in the niacin group had regression of coronary atherosclerosis (relative increase, 95% CI, 67) whereas the rate of patients with progression decreased by 41%, 95% CI, 53. Similar effects of niacin were found on carotid intima thickness with a weighted mean difference in annual change of −17μm/year (95% CI−22, −12).


Although the studies were conducted before statin therapy become standard care, and mostly in patients in secondary prevention, with various dosages of nicotinic acid 1–3, this meta-analysis found positive effects of niacin alone or in combination on all cardiovascular events and on atherosclerosis evolution.


There has been a message circulating in the medical community to avoid Inisotol and Nicotinamide proportedly because though a source of niacin, they don’t lower cholesterol.  Given the influence of PhARMA, and their attack upon aspirin and hormone replacement therapy for women, I suspect that the same has been done with niacin.  Flushing is an unpleasant side effect from a large dose of niacin.  Because of this very few people would take the 1.5 grams a day claimed needed.  I need to review the literature to sort out this issue.  Below is the accepted explanation as to why it doesn’t work; however, I suspect that in the studies used for the article above, the participants weren’t taking 1.5 grams of niacin per day. 


Nicotinamide, also known as niacinamide and nicotinic acid amide, is the amide of nicotinic acid (vitamin B3 / niacin). Nicotinamide is a water-soluble vitamin and is part of the vitamin B group. Nicotinic acid, also known as niacin, is converted to nicotinamide in vivo, and, though the two are identical in their vitamin functions, nicotinamide does not have the same pharmacologic and toxic effects of niacin, which occur incidental to niacin's conversion. Thus nicotinamide does not reduce cholesterol or cause flushing,[1] although nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.[



JK has included this study not reliable because it reveals what big PhARMA is doing to limit the use of Niacin, which is an off-patent competition of the statins.  JK has uncovered a pattern of attacking off-patent drugs when doing so improves the sales of block buster classes of drugs.  A pattern of new studies designed to show the existing therapy inferior to the new patented therapy.  In this website are sections which set the record straight in 3 off-patent drugs:  a) aspirin which competes with Warfarin and Plavix, b) estrogen which competes with bisphonates for osteoporosis; c) Niacin which competes with Statins. Both aspirin & estrogen also greatly lower the risk for Alzheimer’s. Thus they reduce the sales of  acetylcholinesterase inhibitors (Tacrine, Rivastigmine, Galantamine and Donepezil) and the other (memantine) is an NMDA receptor antagonist, and other drugs used to suppress various behavior issues.  Aspirin and to a lesser extent estrogen (estradiol) lower the risk of cancer.  (It should be noted that the bisphonates and drugs used to treat Alzheimer’s are minimally effective at best, and that statins which lover LDL have not been consistently shown to prolong life or reduce MI.  All these minimal-at-best results are obtained by marketing departments of Big PhARMA and published in journal articles that lack proper peer review; viz., the raw data on which the articles are based upon is not submitted for peer review, and average positive bias runs 32% according to one study which obtained the raw for comparison). 

Judging from the author’s connection to pharmaceutical industry is very likely another hatchet job on the non-prescription drug.  Among signs are the fact that MI & strokes are reduced by Niacin by 26% & 24%, yet this was considered insignificant.  Also indicative of the hatchet job is the use of the flushing form of niacin and a high dosage (1500-3000 mgs).  Standard literature recommends a treatment likely to have very poor compliance.  JK needs to research the use of non-flush forms of niacin and lower doses.   JK would have to go to early studies, before big PhARMA was pushing statins. 

As with aspirin and estrogen, it is not the earlier studies that are flawed, so JK hopes to find the same for niacin. 

The New England Journal of Medicine

Niacin at 56 Years of Age — Time for an Early Retirement?

Editorial:  Robert P. Giugliano, M.D., S.M. November 15, 2011 (10.1056/NEJMe1112346)

A reduction in serum cholesterol with niacin therapy in humans was first described in 1955, when Altschul and colleagues reported, in a letter to the editor, the findings in 11 healthy medical students and 57 patients.1 Subsequent clinical studies showed multiple favorable effects of niacin therapy on lipid particles, including decreases in levels of low-density lipoprotein (LDL) cholesterol, triglycerides, small dense LDL cholesterol, very-low-density lipoprotein, lipoprotein(a), and apolipoprotein Β and increases in levels of high-density lipoprotein (HDL) cholesterol and selective lipoprotein A-1 particles.2 The mechanism of action of niacin is complex, involves several biochemical pathways, and is still not well defined.3

The current indications for niacin — reducing the risk of reinfarction, favorably altering lipid levels, and slowing the progression of atherosclerosis — are derived from three lines of evidence: the Coronary Drug Project (CDP),4 studies of combination therapy consisting of niacin and a second lipid-lowering agent, and evaluation of surrogate markers.

From 1966 through 1969, the CDP enrolled 8341 men, 40 to 64 years of age, with a prior myocardial infarction to one of five lipid-modifying therapies. There was no significant difference between the men who were treated with niacin (1119 subjects) and those who received placebo (2789 subjects) in the primary end point of the rate of death from any cause (24.4% and 25.4%, respectively) over a minimum follow-up period of 5 years. However, the rates of myocardial infarction and of cerebrovascular events were significantly reduced with niacin — by 26% and 24%, respectively. It is worth noting, however, that 40 or more years ago, many therapies that have since been proved to reduce mortality or morbidity after myocardial infarction either were not routinely administered (e.g., aspirin and beta-blockers) or were not yet available (e.g., statins, inhibitors of the renin–angiotensin–aldosterone system, P2Y12 inhibitors, and implantable defibrillators). The second line of evidence, derived from studies of combined therapy consisting of niacin and a second lipid-lowering drug, do not inform us about the benefit of adding niacin alone to background therapy; for example, in the HDL-Atherosclerosis Treatment Study ( number, NCT00000553), was it simvastatin, simvastatin plus niacin, or niacin alone that was responsible for the observed clinical benefit?5 Finally, studies using surrogate markers (e.g., carotid intima–media thickness) remain controversial,6 since they have shown inconsistent results, even when proven lipid-modifying therapies that clearly reduce clinical end points have been evaluated by these means.7,8 Thus, a critical appraisal of the prior studies of niacin reveals three shaky pillars supporting its clinical efficacy and identifies a need for large, modern trials of clinical end points. The first of these is reported in this issue of the Journal.9

The Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes trial (AIM-HIGH, NCT00120289)9 was designed with 85% power to show a 25% reduction in the primary end point (a composite of the first event of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, hospitalization for an acute coronary syndrome, or symptom-driven coronary or cerebral revascularization), with the addition of 1500 to 2000 mg of niacin per day in patients 45 years of age or older with established cardiovascular disease and an atherogenic dyslipidemia. The trial was cast as a test of the HDL-raising effects of niacin, but as shown in the causal diagram10 in Figure 1Figure 1Description: Diagram of the Relationships among Niacin, Major Lipid Levels, and Clinical Outcomes., any clinical benefit observed with niacin would be difficult to attribute solely to the effect on HDL. The strengths of the trial design include the efforts made to maintain the double-blinding (blinding of lipid values other than LDL and administration of very low doses of niacin in the placebo group), the well-controlled LDL cholesterol level achieved (a median of <70 mg per deciliter [1.81 mmol per liter]), the event-driven design, and the low rates of loss to follow-up (0.7%) and withdrawal of consent (0.8%). Despite achievement of the expected favorable changes in the levels of HDL cholesterol (an increase of 25%), LDL cholesterol (a decrease of 12%), and triglycerides (a decrease of 29%) with niacin, the clinical results were chillingly null; niacin did not reduce the incidence of the primary composite end point, nor did it show any clinical benefit overall or in a major subgroup. The trial was stopped early by the independent data and safety monitoring board because the boundary for futility had been crossed, and an unexpected higher number of ischemic strokes was observed in patients assigned to niacin.

What are the potential explanations for these findings? It is important to understand that although the event rate was lower than initially projected, it would be incorrect to conclude that the study was designed with insufficient power, since by definition, an event-driven trial is adequately powered for the number of events and the treatment effect specified. Rather, the assumption of a 25% treatment effect appears to have been too generous given the modest absolute difference between the treatment groups in the HDL cholesterol levels achieved (a difference of 4 to 5 mg per deciliter [0.10 to 0.13 mmol per liter]), the low LDL cholesterol levels achieved owing to potent background lipid therapy (with approximately 75% of the patients in the placebo group receiving simvastatin at doses ≥40 mg, and approximately 20% receiving combination therapy consisting of ezetimibe plus simvastatin), and a 25% rate of premature discontinuation in the niacin group. Although the numeric excess in ischemic strokes (which, after inclusion of three upgraded events identified during a post hoc re-review of investigator-reported transient ischemic attacks, yielded a borderline significant result) is of concern, there are several reasons, internal and external to the study, that raise doubts regarding a causal relationship. No prior study or meta-analysis with niacin had observed a similar imbalance in ischemic stroke (in fact, the rate of total stroke was reduced by approximately 20% in the CDP), and no plausible biologic mechanism has been advanced. Furthermore, eight patients (all in the niacin group) had a stroke 2 months or more after discontinuation of the drug. Finally, the specter of a spurious association between a therapy and a low-frequency unexpected event in a moderate-sized trial, when multiple end points are evaluated without statistical adjustment for multiplicity of testing, is not new to the lipid field.11

Nonetheless, the disappointing results of AIM-HIGH do not provide support for the use of niacin as an add-on therapy to statins in patients with preexisting stable cardiovascular disease who have well-controlled LDL cholesterol levels. Given the lack of efficacy shown in this trial, the frequent occurrence of flushing with niacin therapy that some patients find intolerable, and the unresolved question of an increased risk of ischemic stroke, one can hardly justify the continued expenditure of nearly $800 million per year in the United States for branded extended-release niacin.12 However, before holding a final retirement party for niacin, it would appear to be more prudent to assign it to occasional part-time work, such as in statin-intolerant patients (see the Perspective article by Maningat and Breslow13), while we await the results from the much larger Heart Protection Study 2: Treatment of HDL to Reduce the Incidence of Vascular Events trial (HPS2-THRIVE; NCT00461630),14 which is targeted to be completed in 2013. Regardless of whether niacin is ultimately retired or not, one should not abandon the HDL-raising hypothesis altogether. Several ongoing studies15,16 with other promising drugs that raise HDL cholesterol levels substantially (by as much as 150%) by means of different mechanisms, and that in some cases can lower LDL cholesterol levels by as much as 40%, are well under way.

1. Altschul R, Hoffer A, Stephen JD. Inf luence of nicotinic acid on serum cholesterol in man. Arch Biochem Biophys 1955;54: 558-9.

2. Kamanna VS, Kashyap ML. Mechanism of action of niacin on lipoprotein metabolism. Curr Atheroscler Rep 2000;2:36-46.

3. Hochholzer W, Berg DD, Giugliano RP. The facts behind niacin. Ther Adv Cardiovasc Dis 2011;5:227-40.

4. Clofibrate and niacin in coronary heart disease. JAMA 1975;231:360-81.

5. Brown BG, Zhao X-Q, Chait A, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med 2001;345:1583-92.

6. Polak JF, Pencina MJ, Pencina KM, O’Donnell CJ, Wolf PA,

D’Agostino RB. Carotid-wall intima–media thickness and cardiovascular events. N Engl J Med 2011;365:213-21.

7. Carotid Atorvastatin Study in Hyperlipidemic Post-Menopausal Women. a Randomised Evaluation of Atorvastatin versus Placebo (CASHMERE) (NCT#00163163). Pfizer PhRMA Web synopsis protocol A2581051. Final report. October 29, 2007 ( ).

8. Smilde TJ, van Wissen S, Wollersheim H, Trip MD, Kastelein JJ, Stalenhoef AF. Effect of aggressive versus conventional lipid lowering on atherosclerosis progression in familial hypercholesterolaemia (ASAP): a prospective, randomised, double-blind trial. Lancet 2001;357:577-81.

9. The AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011. DOI: 10.1056/NEJMoa1107579.

10. Greenland S, Pearl J, Robins JM. Causal diagrams for epidemiologic research. Epidemiology 1999;10:37-48.

11. Peto R, Emberson J, Landray M, et al. Analyses of cancer data from three ezetimibe trials. N Engl J Med 2008;359:1357-66.

12. DrugPatentWatch. Niaspan patent expiration dates, annual sales, and drug therapeutic class (

13. Maningat P, Breslow JL. Needed: pragmatic clinical trials for statin-intolerant patients. N Engl J Med 2011. DOI: 10.1056/NEJMp1112023.

14. Heart Protection Study 2: treatment of HDL to reduce the incidence of vascular events. (NCT #00461630). HPS2 THRIVE home page (

15. Cannon CP, Shah S, Dansky HM, et al. Safety of anacetrapib in patients with or at high risk for coronary heart disease.

N Engl J Med 2010;363:2406-15.

16. Schwartz GG, Olsson AG, Ballantyne CM, et al. Rationale and design of the dal-OUTCOMES trial: efficacy and safety of

dalcetrapib in patients with recent acute coronary syndrome.  Am Heart J 2009;158(6):896.e3-901.e3. Copyright 2011






Combination of Statin and extended, high dose, niacin has no benefit.  Better to take Niacin alone.

NIH stops clinical trial on combination cholesterol treatment  Posted May 26, 2011

IH stops clinical trial on combination cholesterol treatment
Lack of efficacy in reducing cardiovascular events prompts decision
The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health has stopped a clinical trial studying a blood lipid treatment 18 months earlier than planned. The trial found that adding high dose, extended-release niacin to statin treatment in people with heart and vascular disease, did not reduce the risk of cardiovascular events, including heart attacks and stroke.

Participants were selected for AIM-HIGH because they were at risk for cardiovascular events despite well-controlled low-density lipoprotein (LDL or bad cholesterol). Their increased risk was due to a history of cardiovascular disease and a combination of low high-density lipoprotein (HDL or good cholesterol) and high triglycerides, another form of fat in the blood. Low HDL and elevated triglycerides are associated with an increased risk of cardiovascular events. While lowering LDL decreases the risk of cardiovascular events, it has not been shown that raising HDL similarly reduces the risk of cardiovascular events.

During the study's 32 months of follow-up, participants who took high dose, extended-release niacin and statin treatment had increased HDL cholesterol and lowered triglyceride levels compared to participants who took a statin alone. However, the combination treatment did not reduce fatal or non-fatal heart attacks, strokes, hospitalizations for acute coronary syndrome, or revascularization procedures to improve blood flow in the arteries of the heart and brain.

"Seeking new and improved ways to manage cholesterol levels is vital in the battle against cardiovascular disease," said Susan B. Shurin, M.D., acting director of the NHLBI. ""This study sought to confirm earlier and smaller studies. Although we did not see the expected clinical benefit, we have answered an important scientific question about treatment for cardiovascular disease. We thank the research volunteers whose participation is key in advancing our knowledge in this critical public health area, and the dedicated investigators who conducted the study."

The AIM-HIGH trial, which stands for Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health, enrolled 3,414 participants in the United States and Canada with a history of cardiovascular disease who were taking a statin drug to keep their LDL cholesterol low. Study participants also had low HDL cholesterol and high triglycerides, which meant that they were at significant risk of experiencing future cardiovascular events. Niacin, also known as Vitamin B3, has long been known to raise HDL and lower triglycerides. Eligible participants were randomly assigned to either high dose, extended-release niacin (Niaspan) in gradually increasing doses up to 2,000 mg per day (1,718 people) or a placebo treatment (1,696 people). All participants were prescribed simvastatin (Zocor), and 515 participants were given a second LDL cholesterol-lowering drug, ezetimibe (Zetia), in order to maintain LDL cholesterol levels at the target range between 40-80 mg/dL.

The NHLBI funded the AIM-HIGH study with additional support from Abbott Laboratories, a pharmaceutical company based in Abbott Park, Ill. Abbott also provided Niaspan and Merck Pharmaceuticals, based in Whitehouse Station, N.J., provided Zocor. All drugs used in the study were approved for marketing in the United States and Canada and have been on the market for many years.

Researchers began recruiting participants in early 2006. The study was scheduled to finish in 2012. The average age of the participants was 64 years. Pre-existing medical conditions included coronary artery disease (92 percent); metabolic syndrome, which is a cluster of risk factors for heart disease (81 percent); high blood pressure (71 percent); and diabetes (34 percent). More than half of participants reported having a heart attack prior to entering the study.

The rationale for the AIM-HIGH study was based in part on a large number of observational studies that consistently showed that low HDL cholesterol increases the risk of cardiovascular events in men and women, independent of high LDL cholesterol. In addition, previous small clinical studies showed that relatively high residual cardiovascular risk exists among patients with cardiovascular disease, low HDL cholesterol, and high triglycerides despite intensive management of LDL cholesterol.

However, efforts to find HDL-raising treatments that actually reduce this residual risk have thus far proved disappointing. Fenofibrate, an HDL-raising drug, failed to reduce the rate of cardiovascular events in patients with diabetes in the Action to Control Cardiovascular Risk in Diabetes (ACCORD trial) despite favorable effects on HDL and triglycerides. Another HDL-raising drug, torcetrapib, actually increased the rate of cardiovascular events in the Investigation of Lipid Level Management to Understand its Impact in Atherosclerotic Events (ILLUMINATE) trial despite lowering LDL and triglycerides and raising HDL levels, as intended.

Earlier studies of niacin had shown more favorable results. Unlike AIM-HIGH, the earlier studies were not designed specifically to evaluate the impact of raising HDL on the risk of cardiovascular events while maintaining excellent LDL control. Several other trials testing this hypothesis, including a large international trial of high dose, extended-release niacin, are still ongoing.

As is customary in clinical trials, the NHLBI established an independent data and safety monitoring board (DSMB) to monitor trial progress and participant safety. At a regularly scheduled meeting on April 25, 2011, the study's DSMB concluded that high dose, extended-release niacin offered no benefits beyond statin therapy alone in reducing cardiovascular-related complications in this trial. The rate of clinical events was the same in both treatment groups, and there was no evidence that this would change by continuing the trial. For this reason, the DSMB recommended that the NHLBI end the study.
The DSMB also noted a small and unexplained increase in ischemic stroke rates in the high dose, extended-release niacin group. This contributed to the NHLBI acting director's decision to stop the trial before its planned conclusion. During the 32-month follow-up period, there were 28 strokes (1.6 percent) reported during the trial among participants taking high dose, extended-release niacin versus 12 strokes (0.7 percent) reported in the control group. Nine of the 28 strokes in the niacin group occurred in participants who had discontinued the drug at least two months and up to four years before their stroke. Previous studies do not suggest that stroke is a potential complication of niacin, and it remains unclear whether this trend in AIM-HIGH arose by chance, was related to niacin administration or some other issue.

All AIM-HIGH study participants have been informed of the results and will be scheduled for clinic visits within the next 2.5 months. Participants will be followed for an additional 12 to 18 months.

"Patients who were not in the AIM-HIGH trial should not stop taking high dose, extended-release niacin without talking to their doctor first," said Shurin.

"The lack of effect on cardiovascular events is unexpected and a striking contrast to the results of previous trials and observational studies," said Jeffrey Probstfield, M.D., AIM-HIGH co-principal investigator and professor of medicine and epidemiology at the University of Washington, Seattle. "The AIM-HIGH findings do not support the trial's hypothesis that, in the population studied, adding extended-release niacin to simvastatin in participants with well-controlled LDL cholesterol can provide additional clinical benefit."

"The results from AIM-HIGH should not be extrapolated to apply to potentially higher-risk patients such as those with acute heart attack or acute coronary syndromes, or in patients whose LDL cholesterol is not as well-controlled as those in AIM-HIGH," said William E. Boden, M.D., AIM-HIGH co-principal investigator and professor of medicine and preventive medicine at the University at Buffalo, N.Y.

The niacin tested in the study is a proprietary formulation used in doses of 500-2,000 milligrams (mg), manufactured by Abbott Laboratories and approved and regulated by the U.S. Food and Drug Administration. Low doses of niacin, typically 20 to 100 mg, can be found in multivitamin formulations available without a prescription. The FDA regulates the use of high doses of niacin (over 500 mg), which is approved by prescription for helping treat low HDL cholesterol and/or high triglycerides. At prescription-level doses, some people experience flushing. The extended-release formulation of niacin tested in AIM-HIGH was intended to help reduce the likelihood of flushing.

An estimated 1 in 7 Americans has high blood cholesterol. It is a major risk factor for cardiovascular disease, which kills 800,000 Americans a year. Cholesterol can build up in the walls of arteries and cause them to narrow, a condition known as atherosclerosis.

"As we continue to search for new approaches to treating cholesterol problems, it is important to remember the value of existing treatments. The key to treating high cholesterol so patients can reduce their risk of cardiovascular disease is to lower the level of LDL cholesterol, through well-established drug treatments such as statins and lifestyle changes," said Patrice Desvigne-Nickens, M.D., NHLBI project officer for the AIM-HIGH trial.

The AIM-HIGH investigators will now focus on completing data collection and analysis. The preliminary outcomes of the study are expected to be reported at scientific meetings in the fall of 2011.

Find more information about this clinical trial (NCT00120289) at

To arrange an interview with an NHLBI spokesperson, please contact the NHLBI Communications Office at (301) 496-4236 or To arrange an interview with Jeffrey Probstfield, M.D., contact University of Washington School of Medicine, Office of Communications at 206-616-6730. To arrange an interview with William E. Boden, M.D., contact Ellen Goldbaum-Kolin in the Public Relations Department at 716-645-4605, or Dr. Boden at 716-859-1784.

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit

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.