Home | 2-PAGE SUMMATION ON STATINS | Understanding Atherosclerosis & its MI Link--jk | understanding heart attack | lipids, lipoproteins, the basics | ABOUT Cholesterol | Tables of Risk Factors plus STATS | Niacin prevents MI 25% | Statins, inflammation & atherogenesis--their failure | inflammation, obesity and atherosclerosis | Risk Factors Athereosclerosis | High Cholesterol and treatments | STATINS, lowering cholesterol doesn't prolong life | MMP role in atherogenesis and statins | COX-2 Suppression and statins | High HDL not Prophylactic | Other Markers for Cardiovascular Disease | $70,000 standard heart treatment per year following a MI | Why improving cholesterol profile with statins has little effect | Statins side effects | Statins over prescribed | Recommendation for your heart | New Major Study Pans Statins | STATIN COMBO STUDY, NO BENEFITS | C-Reactive Protein and Statins | Ozone & cholesterol combine to cause heart disease | Calcium score and coronary disease--a review | Serious cognitive impairment from bypass operation, Scientific American | ARRHYTHMIA, sudden early death and prevention for relatives | STEM CELLS GROW HEART MUSCLE | BYPASS & STENTS over sold

STATINS, lowering cholesterol doesn't prolong life

Statins health benefit is the lowering of thrombi the same way aspirin does.  Lowering cholesterol doesn’t get at the root cause—oxidative damage of VLDL, unstable plaque (fresh), and atherosclerosis.  We recommend if you wish to lower your cholesterol profile, to use extended release niacin, 1,500 mgs. Niacin has been used for over 50 years with proven result, and extended release avoid the unpleasant flush which occurs short after taking a 500 mgs or more.  Current literature is of course less than supportive given the financial benefits of pushing statins.  


Big PhARMA has been pushing the stick lower as to when statins ought to be taken. The pitch of big PhARMA has been that improving the cholesterol profile slows the development of atherosclerosis—ignoring the oxidative evidence.  The role of oxidative damage and reactive chemicals has been known for over 30 years.   The reduction in mortality found is based not on their sales pitch of an improved cholesterol profile, but on the aspirin-like mechanism where by the statins effect clotting and thereby lower the risk of an MI.   


WHAT I WOULD RECOMMEND FOR THOSE WHOSE CHOLESTROL PROFILE IS TO TAKE 325 MGS OF ASPIRIN DAILY, AND THEREBY REDUCE BOTH THE RISK OF THROMBI AND CANCER.  Statins cause cognitive impairment, impotency, cancer, and fatigue—see for British review.



FiercePharma at

In what may become the most far-reaching effects of the failed Vytorin trial, experts are questioning the sacred link between cholesterol and heart disease. After all, Vytorin did do a better job of lowering LDL in the Enhance trial. So why did it utterly fail at holding off atherosclerosis? Why did Pfizer's experimental torcetrapib lower "bad" cholesterol and raise "good" cholesterol--and yet cause heart attacks and strokes, rather than prevent them? Why did AstraZeneca's Crestor fail to beat placebo at preventing heart attacks in the Corona study released last fall?

The ramifications of these questions are huge. The "lower LDL is good" is such a core belief in cardiology that drug makers have only had to prove that their meds lower the offending substance--not that the products actually prevented heart attack or stroke--to get FDA approval. And pharma sells billions of dollars worth of cholesterol-lowering drugs every year. If the link between LDL and disease were to be severed, or even weakened, companies would suffer.1

Now, a couple of statins--namely Lipitor and Zocor--have proven to reduce heart attacks and strokes in post-marketing trials. But is it the LDL-lowering itself that cut the risk? Or some other unknown action of those drugs?

Outcomes trials of Zetia, the med added to Zocor to make Vytorin, and Vytorin itself are ongoing. Tuesday, the American Heart Association called for the Zetia events trial to be finished as quickly as possible. But in another bit of Enhance fallout, patients in at least one of the outcomes trials have panicking, calling up clinical investigators to ask whether they should stay in the study.

   1 The answer is that LDL and VDL are missing one ingredient, oxidative damage.  Oxidative damage to especially VDL is necessary for plaque formation within an artery wall. The second part of the process is the trigger mechanism whereby the damaged VDL is deposited.  Plaque formation is a controlled by a feedback mechanism (only partially understood) whereby the muscle cells which make up the artery walls respond to reactive chemical or possible a blood born signal which is corolleated to certain reactive chemicals (one such is carbon monoxide).  When conditions improve, a certain type of white blood cell can release a polypeptide which shuts down the plaque-formation process.  Thus taking a drug which lowers LDL and VDL doesn’t stop the process.  However, have lots of VDL entails that this process proceeds for most people at a higher rate than those with lower VDL.  Even those with very low VDL, triglycerides, LDL, and cholesterol still can develop hardening of the arteries.    Various causative factors, among them certain types of chronic infections, can nevertheless bring about atherosclerosis—jk.   

AZ's Crestor flubs key heart failure trial

November 5, 2007


AstraZeneca didn't get its coveted results from the long-awaited CORONA trial. Crestor failed to show any statistically significant benefit in heart failure patients. So Crestor lacks a competitive edge enjoyed by rival Lipitor and generic statins: Trials that show a clear reduction in deaths and heart disease.

It was a long shot, really; heart failure isn't generally considered to be relieved by statins like Crestor. But AZ wanted something different from the old, tried-and-true data that shows the drugs stave off complications from heart disease. A head-to-head trial against Lipitor would have cost beaucoups, and it would have been risky to boot. What if Lipitor had come out ahead?


Statins show in major study a 20-25% reduction in MI, however, aspirin does as well.  Moreover those on statins are more likely to have earlier intervention if experience a heart attack.  This is a confounding variable when comparing mortality rates—jk.

Association of Statin Therapy with Outcomes of Acute Coronary Syndromes: The GRACE Study

Frederick A. Spencer, MD; Jeanna Allegrone, BA; Robert J. Goldberg, PhD; Joel M. Gore, MD; Keith A.A. Fox, MB, ChB, FRCP; Christopher B. Granger, MD; Rajendra H. Mehta, MD; David Brieger, MD, the GRACE Investigators*

1 June 2004 | Volume 140 Issue 11 | Pages 857-866

Background: Statins administered early in patients with acute coronary syndromes may lead to modest reductions in recurrent ischemic events.

Objective: To examine the association between previous and early in-hospital statin therapy and the presentation and outcomes of an acute coronary syndrome.

Design: Cohort study.

Setting: 94 hospitals in 14 countries participating in the Global Registry of Acute Coronary Events (GRACE).

Patients: 19 537 patients with an acute coronary syndrome who were enrolled from April 1999 to September 2002.

Measurements: Statin use before and after presentation with an acute coronary syndrome and associated rates of myocardial infarction, hospital complications, and hospital mortality. The composite end point included death, in-hospital myocardial infarction, and stroke.

Results: Patients who were already taking statins when they presented to the hospital were less likely to have ST-segment elevation (odds ratio [OR], 0.79 [95% CI, 0.71 to 0.88]) or myocardial infarction (OR, 0.78 [CI, 0.70 to 0.86]). Patients who continued to take statins in the hospital were less likely to experience complications or die than patients who never received statins (OR, 0.66 [CI, 0.56 to 0.77]). Patients not previously taking statins who began statin therapy in the hospital were less likely to die than patients who never received statin therapy (OR, 0.38 [CI, 0.30 to 0.48]). However, adjustment for the hospital of admission attenuated the association between initiation of statin therapy and the composite end point (OR, 0.84 [CI, 0.65 to 1.10]).

Limitations: This observational study cannot exclude confounding by clinical and hospital factors.

Conclusions: These data support the hypothesis that statin therapy can modulate early pathophysiologic processes in patients with acute coronary syndromes. A randomized trial of statin therapy in acute myocardial infarction is warranted.


American Heart Association at

Another major study shows statins are at best no better than aspirin. 

After Myocardial Infarction: The IDEAL Study: A Randomized Controlled Trial

Date: November 16, 2005

Summary: Aggressively reducing the levels of “bad cholesterol” or low density lipoprotein (LDL) in patients who had already had a heart attack did not reduce the percentage of deaths from heart disease, the occurrence of heart attacks or sudden heart stoppages in patients who had had to be resuscitated.

This is particularly telling, for if as big PhARMA maintains the more you lower LDL the slower is the development of atherosclerosis.  However when comparing high dose statins to low dose usage, there was a negative result.  This conclusion supports the conclusion which I—and others maintain—that statins benefits is rather through the same mechanism as aspirin, that of reducing thrombus; and like aspirin, there is little if any reduction in the rate of  thrombus with a higher does of either aspirin or statins, nor is their combination superior--jk.

The Grace Study Results

The very choice of two different statins rather than two doses of the same statin is suspect, since for to test the benefits of a higher does, normally it is compared directly to a lower does, rather than a lower dose of a another drug of the same family of drugs.  Given the big PhARMA bias, the reasonable conclusion is that they have stacked the test protocol so as to favor the high dose treatment.  However, the results showed a very minor benefit. There were 8,888 subject followed for approximately 2 years.  The low dose group had 4% coronary deaths and the high dose a 3.9%.  For nonfatal myocardial infractions the difference was 6% versus 7.2%.  Given the greater expense and side effects there is scant reason for taking the higher does statin.  Moreover is one factors in the difference in deaths from cancer (a know risk of statins), it turns out that the higher dose had a higher death rate.  There were 112 death from cancer in the high does and 99 in the low does group, or a difference of 13.  Subtract the coronary deaths difference of 3 (178 versus 175 for the high does) and there is a net loss of life of 10 for the higher dose group.        

The entire study is available on the internet at  or in the JAMA at Vol. 294 No. 18, November 16, 2005

There are a number of troubling gaps in statin studies.  In particular (1) the failure to do a proper follow-up on the animal studies which confirm that they are carcinogens (a twenty year follow-up would be required, which is about the time it takes for cigarettes to significantly increase the incidence of cancer),  They could gather this information from the records of insurance companies.  (2) The fact that those with normal levels of LDL and LDL:HDL does not show significant benefit from statins.  (3) The failure to elucidate how statins reduce the incidence (like aspirin) of thrombi.  Possible the positive results for the high-risk group are because of this mechanism rather than an improved LDL:HDL ratio.  If it reduced the rate of plaque formation it should benefit everyone.  For example aspirin reduces the risk of colon cancer nearly 50%.  This benefit is for all people who take an aspirin per day—higher dose produces greater protection and the longer the better.  Why doesn’t this pattern of benefits apply to statins?  If lowering the LDL:HDL ratio by statins worked then we all should be taking them along with our vitamins, and start by the age of 30 for men.  (4) A good ratio without statins indicates a lower risk of MI, but a good ratio with statins confers little benefit (once the thrombi effect is adjusted for). This is glossed over in studies.  All too often there are various conditions for enrollment, testing, tracking of events, etc. in a study which are manipulated in a way so as to produce positive results.  (4) Failure to examine other serious side effects such as cognitive impairment & fatigue (effect up muscles and Q-10).  To quote Shakespeare, there is something rotten in Denmark--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.