Scientists sometimes shift the scientific goalposts

Dr. John Briffa

Scientists sometimes shift the scientific goalposts

Posted on 10 August 2011

It’s easy to believe that statins have dramatic life-saving properties. The reality is, however, that for the majority of people who take them, they don’t. In the biggest and best review published to date, statins were not found to reduce overall risk of death in individuals with no previous history of cardiovascular disease [1]. What this study shows is that for great majority of people who take statins, the chances of them saving their life are, essentially, nil (just so you know).

Of course, you wouldn’t expect everyone to take this finding lying down. A number of people responded to this study with letters to the journal in which it appeared, attempting to cast doubt on its findings. None of it amounted to much, but I thought I would focus on one response, which in my view demonstrates how some scientists and doctors attempt to shift the scientific goalposts to make their point and suit their ends.

The response came from Drs Gabriel Chodick and Varda Shalev [2]. The main thrust of their objections come in the form of three studies that were included in the review referred to above that they claim have ‘major limitations’. Here’s what they say about each of these studies:

“…their meta-analysis included 3 studies with major limitations: a significant decrement in low-density lipoprotein cholesterol levels over the study period in the placebo arm (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]), old age at therapy initiation (Pravastatin in Elderly Individuals at Risk of Vascular Disease [PROSPER] Study), and incomplete information on low-density lipoprotein cholesterol levels over the follow-up period (Air Force/Texas Coronary Atherosclerosis Prevention Study [AFCAPS/TexCAPS]). All these studies showed negative results; their inclusion would have biased against finding a benefit to statin treatment.”

With regard to the first study, what Drs Chodick and Shalev seem to be saying is that the control group (the group treated with placebo rather than statin) saw natural reductions in cholesterol, so the benefits of taking a statin did not to show up. However, the impact that statins had on cholesterol levels relative to a control group is not important – the only important thing is the impact statins had on health (and, in particular, overall risk of death). This is also true for the last study highlighted by Drs Chodick and Shalev.

As regard the second study, it’s not clear why the advanced years of participants would be a barrier to determining the effectiveness of statins. Actually, the elderly are known to be at particularly high risk of cardiovascular disease, meaning that if anything, this population would, theoretically, be generally most likely to benefit from statin therapy.

In summary: none of Drs Chodick and Shalev’s objections hold any water at all. But they don’t stop there. Here’s the final paragraph from their letter.

“Also, randomized controlled trials are often characterized by limited follow-up periods. Therefore, all-cause mortality benefits may not be apparent in randomized controlled trials among a primary prevention population. It would be informative in this regard to take into account the results of large observational studies with longer follow-up periods to better capture the benefits of statins in primary prevention patients.”

What they’re saying here is that clinical trials don’t go on long enough to detect benefits. It’s better, in their mind, to revert to longer studies that are observational (also known as ‘epidemiological’) in nature. However, such studies look at associations between things, but can never be used to prove the benefits of statins. Only intervention studies can do this.

So, what the authors of this letter are effectively saying is that we should ignore the best evidence we have in favour of quite-useless epidemiological evidence.

One of the authors of this letter is, in fact, an epidemiologist, and really should know better. But then again, both of the authors work for a company that assists drug companies in, among other things, ‘reducing the time to market’ and the writing and submission of scientific articles for publication.

See here for more details. It’s a clear conflict of interest, of course, and perhaps goes some way to explain why they make apparently spurious objections to existing evidence and appear to be calling for an approach that can never really get to the truth.

References:
1. Ray KK, et al. Statins and all-cause mortality in high-risk primary prevention: a meta-analysis of 11 randomized controlled trials involving 65 229 participants. Arch Intern Med. 2010;170(12):1024-1031
2. Chodick G, et al. Statins and all-cause mortality in high-risk primary prevention: a second look at the results. Arch Intern Med. 2010;170(22):2041-2
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Read the full article here.

"I would never subject a patient to the potentially severe side effects of statins..."

"While inflammation may be involved in either one or both I would not recommend statins as therapy. The supposed benefit provided by statins in reduction of non-fatal heart attacks by a few percentage points is no greater than that achieved with other anti-platelet and/or anti-inflammatory drugs. Therefore I would never subject a patient to the potentially severe side effects of statins in order to achieve a questionable benefit that can be provided by drugs of much lower risk."
Dr. Ernest N. Curtis, M.D.
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From: The Cholesterol Delusion Part 2

"A delusion is a false belief held with conviction despite incontrovertible evidence to the contrary."

The Cholesterol Delusion

by Ernest N. Curtis M.D. ( Internal Medicine and Cardiology ) A delusion is a false belief held with conviction despite incontrovertible evidence to the contrary. In the medical field no delusion has had wider acceptance and a longer run than the belief that cholesterol levels in the blood are a major factor in the causation of atherosclerosis and its two chief complications - heart attack and stroke. The supposed benefit provided by statins in reduction of non-fatal heart attacks by a few percentage points is no greater than that achieved with other anti-platelet and/or anti-inflammatory drugs. Therefore I would never subject a patient to the potentially severe side effects of statins in order to achieve a questionable benefit that can be provided by drugs of much lower risk. Read the full 'The Cholesterol Delusion' two part article here: The Cholesterol Delusion - part 1 of 2 The Cholesterol Delusion - part 2 of 2 Dr. Ernest N. Curtis received his B.A. In Biological Sciences from the University of California, Berkeley and his M.D. From the University of California, Irvine. After a Residency in Internal Medicine and a Fellowship in Cardiology, he entered private practice in Long Beach, California where he has practiced for the last 32 years.

The switch from an $11-billion/year drug juggernaut to an OTC medication won't be easy for Pfizer

New York, NY - Pfizer is hoping to sell atorvastatin (Lipitor) to consumers over the counter (OTC) as a way to offset the expected plunge in revenue as the world's best-selling prescription drug goes off patent in November, according to the Wall Street Journal.

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Read full article here.

Low Salt Diet Increases Cardiovascular Mortality

Read the full article with links and references here.

 

Another article here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203
 

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Low Salt Diet Increases Cardiovascular Mortality by Jeffrey Dach MD

from Jeffrey Dach MD Bio-Identical Hormone Blog by Jeffrey Dach MD

Low Salt Diet Found to Increase Mortality by Jeffrey Dach MD The Low Salt Diet Revisited A recent study on the effect of a low salt diet made headlines, finding that a low salt diet increases mortality for patients with congestive heart failure.(1-6) The study concluded there was not enough evidence to advise a low-salt diet for the rest of us. They doubted a low salt diet would benefit the population.(6) In this article we will re-examine the low salt diet, clear away the confusion, and make recommendations about salt intake, hypertension, and health. Above left image, harvesting sea salt courtesy of wikimedia commons. (Salt Farmers - Pak Thale.jpg) Health Benefits of Salt We know from many years of published studies that increasing salt intake increases blood volume and also blood pressure. Salt is essential for maintaining blood volume, blood pressure, and overall health. The salt content of blood is similar to ocean water. Both have sodium chloride, also known as salt. Importance of Salt One example of the importance of salt is the common practice of starting an intravenous solution of salt and water as the first line treatment for the trauma patient upon arrival to the hospital Emergency Room. Low Salt Diet to Reduce Blood Pressure One of the central dogmas of mainstream medicine is the "low salt diet" as a treatment for reducing blood pressure in the hypertensive patient. Indeed, popular wisdom says that the "low salt diet" is also healthy for the rest of us "normal" people who don't have hypertension.(25) Along with the rest of my medical school class, I was indoctrinated to believe this. Is this really true? Many studies have looked at this question. They show the "low salt diet" will in fact reduce blood pressure slightly. However, this effect is minimal, and is counteracted by compensatory mechanisms that release harmful substances into the bloodstream, hormones and chemical mediators that counteract the "low salt diet". The released chemical mediators include insulin, epinephrine, norepinephrine, renin, aldosterone, etc. These are harmful and damaging to the vascular system. (7-11) Low Salt Diet Increases Cardiovascular Mortality In addition, a number of studies have found that a "low salt diet" increases cardiovascular mortality. (5) A study published in the 1995 Hypertension found 4.3 times greater mortality in hypertensive men on a low salt diet.(12) They also found higher plasma renin in these men, a hormone produced by the body which causes salt and water retention by the kidney to compensate for the low salt diet.(12-15) A 2011 JAMA provides the reasons for this increased mortality and says ... (16) The underlying mechanisms explaining the inverse association between cardiovascular mortality and 24-hour urinary sodium excretion might be that a salt intake low enough to decrease blood pressure also increases sympathetic nerve activity, decreases insulin sensitivity, activates the renin-angiotensin system, and stimulates aldosterone secretion. (16) A 1998 JAMA report found that a low salt diet increased plasma renin 3.6-fold and aldosterone by 3.2-fold, increases that were proportional to the degree of sodium restriction. (17) The authors also reported the "low salt diet" increased other harmful substances such as noradrenaline, cholesterol, and low-density lipoprotein cholesterol (LDL). (17) A 1999 report in American Journal of Hypertension found that "moderate salt restriction aggravates both systemic and vascular insulin resistance." (18) The Difference Between Refined Salt and Natural Sea Salt In his book, Salt Your Way to Health, Dr. David Brownstein points out the difference between Refined Salt, commonly used in all processed foods, and Natural Sea Salt.(21) White refined salt is processed so that all the trace minerals are removed, and instead has chemicals added (up to 2% of weight). The added chemicals are ferrocyanide, aluminum, ammonium citrate, etc and are used for anti-caking, free-flowing, and to prolong shelf life. The final result is a lifeless, unnatural salt product which tends to acidify the body also called refined salt. Natural Sea Salt, on the other hand, retains all the trace minerals naturally found in the ocean. In addition it alkalinizes the body and has many health benefits. Natural Sea Salt is made by evaporating ocean water, and then collecting or harvesting the salt. Popular brands of natural sea salt include: 1) Celtic Sea Salt®, Light Grey, By The Grain & Salt Society, Coarse Ground, 1 lb 2) Roland Fine Sea Salt, 27.8-Pound Package (See all Sea Salt) Case reports from Dr Brownstein's Natural Ocean Sea Salt Book Case Number One- Food Allergies (from the Salt book) 61 year old female with numerous allergies. The patient switched from refined salt to natural sea salt, measured urine and saliva pH, which went up (alkaline) and noted allergies resolved. Case Number Two-Male Hypertension on Meds, Jack 63 year old hypertensive on two BP meds, Dyazide and Lopressor causing fatigue and erectile dysfunction. He switched from a low salt diet to natural sea salt and two months later blood pressure was lower. Pt reduced BP meds to dyazide at half dose. Case three, Barbara -Hypertension, 53 y/o went to primary care doctor for check up and was shocked to find her BP was 165/100. She had been on a low salt diet for years. Blood tests showed a low sodium level (137). She was then placed on natural sea salt, half tsp per day, and vitamin-mineral regimen, and eliminated refined foods. Two months later her blood pressure was 110/70, and she felt better. Case Four Sandra, similar story to Barbara. Case Five, Seizure Disorder. Jerry 12 years old with recurrent seizures on meds.Sodium was 138 on low salt diet. Switched to natural sea salt. Seizures decreased by 50%. Case Six Migraines. Lisa 31 , three migraines per month, clinically dehydrated, low sodium 139. Instructed to take half tsp Celtic Sea Salt per day, and 2 liters of water per day. Migraine headaches disappeared. Case Seven- Fibromyalgia . Judy 35 y/o , five years with fibromyalgia. BP drops upon standing. Adrenal Fatigue. RX adrenal hormones (DHEA, cortisol, pregnenolone, testosterone, progesterone ) , and natural sea salt., whole foods, plentiful water. Immediate improvement. Clinical Uses of Natural Sea Salt Adrenal Exhaustion: Sea Salt is essential for treatment of adrenal fatigue. Diabetes, Elevated Blood Sugar- It is impossible to control blood sugar on a "low salt diet". These do well on sea salt. Muscle Cramps - often relieved by minerals in Sea Salt. Osteoporosis Treatment requires minerals found in Sea Salt Hypertension-Low salt diet causes increased mortality. Use natural sea salt, with reduction in blood pressure noted in any cases. How to Reduce Blood Pressure Naturally -Salt Substitutes The low sodium, high potassium, high magnesium salt substitute (26) A number of studies have looked at substituting table salt with a variant with reduced sodium, and increased potassium, and magnesium, which has shown to reduce blood pressure. (26) Magnesium alone is an excellent mineral supplement which may be effective for blood pressure control in hypertensive patients.(27) Salt Substitute From Finland Jonathan Wright's clinic offers a salt substitute which contains potassium, magnesium, and lysine which was found beneficial in a Finland.(28)(29) WrightSalt is available through the Tahoma Clinic Dispensary (www.tahomadispensary.com 888-893-6878 ), or Ayush Herbs (800-925-1371), L-Arginine and the ADMA Connection In 1998 the Nobel Prize in Medicine was awarded to Furchgott and colleagues for the discovery of the role of Nitric Oxide in blood pressure regulation (among other things). (29-31) Recently, a new test has been devised called the ADMA from Metametrix Labs which is useful in hypertensive patients, showing the ability (or inability) to manufacture Nitric Oxide. If ADMA is found to be high, indicating low Nitric Oxide production, then increases can be achieved with a simple amino acid supplement called L-Arginine. (29-31) The increased Nitric Oxide brings down and controls blood pressure.(32) The references for the ADMA test can be found here. No Iodine Added to Natural Sea Salt Remember, Natural Sea Salt does not contain added iodine, so it is important to test for iodine levels, and supplement with iodine if found low. Iodine supplementation is our most important means for breast cancer prevention. Credit and thanks goes to the book, Salt Your Way to Health, by David Brownstein MD for much of the information in this article. Jeffrey Dach MD 7450 Griffin Suite 190 Davie Florida 954 792-4663

Anthony Colpo answers a question on Lipitor etc.

My story about Lipitor’s Danger


Hi Anthony

I want to share with you my first-hand experience of the dangerous side effects of taking Lipitor to lower cholesterol.



I’m in my late 40s and was on Lipitor at 20mg daily for four years until nearly two years ago when my doctor decided to put me onto Lipitor at 40mgs as he was not happy with my blood test results.

In January the pain in my elbows became much worse and as I am journalist the cause was put down to overuse syndrome. My bloods also registered heightened fatty deposits in my liver, which were confirmed by an ultrasound.



I began a course of physiotherapy but after four sessions and no improvement I talked to a friend who recommended I look into the side effects of Lipitor. What I found horrified me as my doctor had never mentioned a co-relation between Lipitor and liver damage or muscular joint issues. I took the brave step of not taking any further Lipitor and within a week the effects were drastic. To the amazement of my physio the elbow pain has gone completely and I have no lingering problems there at all.

I changed doctors and my recent blood test shows my liver results to be back to normal.

My cholesterol check shows the LDL levels had gone up (2.7 to 3) but my HDL levels improved (1.74 to 1.67) or good cholesterol, and the Chol/HDL ratio was 2.9.



I’m sticking to drug free and taking supplements of Solgar Phystosterol Comples 1000mg (plant sterols) and a vitamin B-complex. I also take the magical MAQUI berry superfood but I know you are a sceptic on benefits. All I know is my energy levels are back to 10-15 years ago.

I hope all your readers can reconsider just why they are taking such poisons as the statin drugs. British Medical research I saw showed 75% of heart attacks happen to adults with average to low cholesterol levels. So why are so many people taking the poison?



Keep up the great work Anthony.



Yours,

Peter.



Anthony replies:


Hi Peter,


British Medical research I saw showed 75% of heart attacks happen to adults with average to low cholesterol levels. So why are so many people taking the poison?
M-O-N-E-Y.

That’s the main reason.

With a little creative statistical manipulation and “friendly” influence on those who set lipid guidelines, cholesterol-lowering drugs have a potential market that encompasses most of the adult population. That, combined with existing sales already in the tens of billions of dollars a year, means you can rest assured drug companies will do whatever they can to downplay any adverse effects of statins, and to aggressively promote their ‘benefits’ to the medical profession and public alike.

When you combine that with widespread religious-like reverence for the nonsensical cholesterol theory of heart disease, it’s hard to get doctors to accept these drugs should not be administered to the majority of their target population.

Defenders of these over-hyped and largely ineffective drugs counter that the side effect rate of statins is very low.
Rubbish.

One of the problems is that most clinical trials include a screening process that carefully weeds out participants with any pre-existing health issues (including liver, kidney or muscular disorders). Adverse event rates in carefully screened clinical trials are simply not a reliable reflection of real-life side effect rates.

As for the allegedly low rate of adverse effects in clinical practice, I’ve lost count of the number of people who have complained to their doctor about debilitating weakness, joint and muscle pain after being placed on statins, only to be told by their doctors that it couldn’t possibly be the drug. Nope, the patient is simply “getting old”, “imagining things”, or “believing too much of what they read on the Internet”.

After all, their wonderful ever-smiling knicknack-bearing pharmaceutical salesman/woman never said anything about side effects, and everyone in the medical world simply knows statins are wonder-drugs! They know this because (drug company-sponsored) researchers and the media (quoting from drug company press releases) told them so. No need to check the facts for yourself when so many other clearly impartial and detached (cough, cough) commentators are more than happy to do it for you!

A study published in the October-November-December 2009 issue of Primary Care Cardiovascular Journal, showed statin-induced myopathy is far more common than previously claimed by drug companies and health officials. Researchers analysed the patient records of one 8,000 patient practice and found only one recorded case of muscle symptoms in a patient taking statins. But after questioning 96 randomly selected statin-using patients from the practice, they identified 19 cases of potential muscle damage[2]. Grab a calculator and check the percentage difference between 1:8000 and 19:96, and you’ll have some idea of just how massively underreported statin side effects are.

In effect, the wonderfully low official adverse rates cited for statins appear are nothing but an artefact of practitioner ignorance and incompetence.

And even when doctors do possess enough wherewithal to connect statins with their patients’ side effects, that’s still no guarantee they’ll file an official report. Lodging an adverse events report in countries like Australia, UK, and USA is typically a time-consuming affair with no financial compensation and the possibility of being questioned by officials. A lot of doctors no doubt figure they can do without the hassle.

Of course, the poor bugger who suffers amidst this mess is the patient, who often has to unnecessarily endure months or years of side effects. That so many doctors remain blind to the cause of their statin-using patients’ complaints, when the source can easily be identified within minutes of Internet searching by any layperson, is a terribly sad indictment of our drug company-owned medical system.

Thanks for sharing your experiences and best of luck, cheers,

Anthony.
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Read his complete post here

What about salt?

Salt consumption is discouraged these days and it seems to be zeroed in on the effects of blood pressure on heart disease and stroke. But wait a minute. Read this from Health Impact News Daily
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To Salt or Not to Salt, That is the Question

Newswise — A new eight year long European study concludes that salt consumption is not dangerous and may in fact be beneficial. This is certainly contrary to advice from American Medical Association, American Heart Association and the Center for Disease Control and Prevention, which says higher sodium consumption can increase the risk of heart disease. It’s not unusual to see differing opinions, but what are we ordinary folks to make of the controversy?

The study followed 3,681 middle-aged Europeans who did not have high blood pressure or heart disease at the start of the study. They were divided into three groups: low salt; moderate salt; and high salt consumption. There were 50 deaths in the low salt group, 24 in the moderate consumption group and only 10 in the high consumption group. In fact, the heart disease risk in the low consumption group was 56% higher in the low salt group. What they concluded was that the less salt the participants ate, the more likely they would die from heart disease.

“The optimal level of salt in our diets has been a controversial subject for at least 20 years,” say co-authors Dian Griesel, Ph.D. and Tom Griesel of the new book, TurboCharged: Accelerate Your Fat Burning Metabolism, Get Lean Fast and Leave Diet and Exercise Rules in the Dust (BSH, 2011). The problem they say generally boils down to the effect (or lack thereof) salt has on blood pressure.

“There is no disagreement that high blood pressure (even moderately high) is a risk factor for heart disease and stroke,” say the Griesels. “However, salt consumption does not seem to have the same effect on everyone. In addition, there is usually no distinction on the type of salt used. There are many naturally harvested salts that also contain many trace minerals, which undoubtedly have an effect. Medical literature on salt consumption (like many other things) is inconsistent.”

The main take away from all this is the importance of knowing what your blood pressure is and making an effort to do whatever is necessary to have consistent readings in the healthy range of 120/70 or less. If you are a person who is sensitive to salt consumption, a reduction is definitely needed or perhaps even a switch to a natural alternative like sea salt might help. But beware of hidden salt. The biggest source of salt in our diet is the refined and processed foods purchased at the grocery store along with food served in restaurants, particularly fast-food which amounts to about 75% of salt consumption for the average person.

Read the Full Article Here: http://www.newswise.com/articles/to-salt-or-not-to-salt-that-is-the-question
See also:  Change in season: Why salt doesn’t deserve its bad rap and here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

Statin drugs are associated with decreased myocardial function

Two recent articles highlight the fact that statin drugs are associated with decreased myocardial function.

Statin use is known to be associated with myopathy, muscle weakness and rhabdomyolysis, a breakdown of muscle fibers resulting in the release of muscle fiber contents into the bloodstream. For the study, myocardial function was evaluated in 28 patients.

According to Green Med Info:

“There was significantly better function noted … in the control group vs the statin group”.

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From: http://www.greenmedinfo.com/toxic-article/statin-therapy-decreases-myocardial-heart-function
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Statin therapy decreases myocardial (heart) function.

Abstract Title:

Statin therapy decreases myocardial function as evaluated via strain imaging.

Article Link:

Clin Cardiol. 2009 Dec ;32(12):684-9.

Article Source:

Pubmed

Abstract Author(s):

Feras Aloka, George S Abela, Jack Rubinstein

Article Affiliation:

Cardiology Division, Department of Medicine, Michigan State University, East Lansing, MI 48824, USA.

Abstract:

OBJECTIVES: The purpose of this study was to evaluate the effects of statin therapy on myocardial function as measured with echocardiography with tissue Doppler imaging (TDI) and strain imaging (SI) independent of its lipid-lowering effect. BACKGROUND: Statin use is known to improve outcomes in the primary and secondary prevention of ischemic heart disease, but their use is also associated with myopathy, muscle weakness and in rare cases, rhabdomyolysis. We sought to evaluate whether TDI and SI is able to identify changes in myocardial function associated with statin use. METHODS: Myocardial function was evaluated in 28 patients via echocardiography with TDI and SI. We identified 12 patients (5 females) without overt cardiovascular disease (including hypertension, smoking, and diabetes) that were on statin therapy and compared their echocardiographic findings with 16 (12 females) age, sex, and cholesterol-profile-matched controls. Tissue Doppler imaging parameters of diastolic (E(')/A(') and E/E(')) and systolic (S') function were measured. Regional systolic function was obtained by SI in 4-chamber, 2-chamber, long axis, and average global views. RESULTS: There was no significant difference in myocardial function as measured by Doppler and minor differences as measured via TDI among the 2 groups. There was significantly better function noted with SI in the control group vs the statin group in the 4-chamber (-19.05% +/- 2.45% vs -16.47% +/- 2.37% P = 0.009), 2-chamber (-20.30% +/- 2.66% vs -17.45% +/- 4.29% P = 0.03), long axis (-17.63% +/- 3.79% vs -13.83% +/- 3.74% P = 0.01), and average global (-19.0% +/- 2.07% vs -15.91% +/- 2.81% P = 0.004) views. CONCLUSION: Statin therapy is associated with decreased myocardial function as evaluated with SI.

Study Type : Human Study

Additional Links:

Diseases : Cardiovascular Diseases, Statin-Induced Pathologies

Toxic Ingredients : Statin Drugs
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From: http://www.ncbi.nlm.nih.gov/pubmed/20027659
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Clin Cardiol. 2009 Dec;32(12):684-9.

Statin therapy decreases myocardial function as evaluated via strain imaging.

Rubinstein J, Aloka F, Abela GS.

Source

Cardiology Division, Department of Medicine, Michigan State University, East Lansing, MI 48824, USA.

Abstract

OBJECTIVES:

The purpose of this study was to evaluate the effects of statin therapy on myocardial function as measured with echocardiography with tissue Doppler imaging (TDI) and strain imaging (SI) independent of its lipid-lowering effect.

BACKGROUND:

Statin use is known to improve outcomes in the primary and secondary prevention of ischemic heart disease, but their use is also associated with myopathy, muscle weakness and in rare cases, rhabdomyolysis. We sought to evaluate whether TDI and SI is able to identify changes in myocardial function associated with statin use.

METHODS:

Myocardial function was evaluated in 28 patients via echocardiography with TDI and SI. We identified 12 patients (5 females) without overt cardiovascular disease (including hypertension, smoking, and diabetes) that were on statin therapy and compared their echocardiographic findings with 16 (12 females) age, sex, and cholesterol-profile-matched controls. Tissue Doppler imaging parameters of diastolic (E(')/A(') and E/E(')) and systolic (S') function were measured. Regional systolic function was obtained by SI in 4-chamber, 2-chamber, long axis, and average global views.

RESULTS:

There was no significant difference in myocardial function as measured by Doppler and minor differences as measured via TDI among the 2 groups. There was significantly better function noted with SI in the control group vs the statin group in the 4-chamber (-19.05% +/- 2.45% vs -16.47% +/- 2.37% P = 0.009), 2-chamber (-20.30% +/- 2.66% vs -17.45% +/- 4.29% P = 0.03), long axis (-17.63% +/- 3.79% vs -13.83% +/- 3.74% P = 0.01), and average global (-19.0% +/- 2.07% vs -15.91% +/- 2.81% P = 0.004) views.

CONCLUSION:

Statin therapy is associated with decreased myocardial function as evaluated with SI.

Comment in

• Clin Cardiol. 2010 Mar;33(3):179; author reply 179.

PMID:

 

20027659

 

[PubMed - indexed for MEDLINE]

Death blow for Zetia? (ezetimibe) Dr. William Davis

Posted: 11/25/2009 11:14:54 AM
The recent results of the ARBITER6-HALTS trial, I believe, should cause us to eliminate Zetia (ezetimibe) from our list of agents regarded as safe. In all honesty, despite some of the negative press on Zetia, especially in regards to the data suggesting no effect on carotid plaque in people with heterozygous familial hypercholesterolemia, I had maintained hope that a subset of people who are "hyperabsorbers" of sterol-backbone substances, such as the various forms of sterols, would benefit from Zetia's capacity to block their absorption. But the ARBITER trial, I believe, essentially closes the lid on Zetia, regardless of any potential effect on sterol absorption. The study demonstrates that niacin in combination with a statin (mostly Lipitor or Crestor) reduces carotid intimal-medial thickness (CIMT) modestly; while Zetia does not when added to statin. Most concerningly, greater LDL-reducing efficacy with Zetia was associated with an increase in CIMT.  The authors raise the question, suggested in prior studies, that Zetia, despite being billed as only a cholesterol absorption inhibitor, exerts other effects when systemically absorbed, including impairment of reverse cholesterol transport. I believe that enough doubt has been cast on the efficacy and safety of Zetia that we should avoid its inclusion. Of course, speak to your doctor before making any changes.  =============================================================

Cholesterol-reducing drug ezetimibe appears to do more harm than good

Dr Briffa's article discusses cholesterol reducing drug ezetimibe and its harm.

"

Posted on 10 June 2011 

Cholesterol is said to cause heart disease (I’m not so sure, myself), and a mainstay of treatment here is a class of drugs known as ‘statins’ that reduce the rate at which cholesterol is manufactured in the liver. Statins have been used in medicine for over 20 years, but more recently has seen the development and licensing of a cholesterol-reducing drug known as ezetimibe, which works in different way to statins. Instead of acting on the liver, it reduces cholesterol absorption from the gut.

There’s no doubt that ezetimibe reduces cholesterol levels effectively, and it is licensed on this basis. However, the impact that a drug (or food or anything) has on cholesterol is irrelevant – it’s its impact on health that matters. While we have been brainwashed into believing that whatever reduces cholesterol is good for health, this simply isn’t true. Actually, there is abundant evidence that reducing cholesterol per se is not broadly beneficial to health. And some evidence suggests that it might even be damaging to health.


As it happens, ezetimibe use has been linked with an increased risk of cancer, and enhanced narrowing of arteries (though not statistically significant) [1], as well as an increased risk of cancer in one study [2].

Ezetimibe is a drug that reduces cholesterol levels in the bloodstream. It does this in a different way to statins (the most commonly-prescribed cholesterol drugs). Statins work by inhibiting the rate at which cholesterol is manufactured in the liver, while ezetimibe impairs the absorption of cholesterol from the gut.

Ezetimibe was originally licensed on the basis of its cholesterol-reducing abilities. Yet, to date, no study has ever been published which demonstrates that it has the power to reduce the risk of actual disease or death. In fact, in one study, coupling ezetimibe with a statin (simvastatin) resulted in increased (though not statistically significant) narrowing of the arteries compared to the statin alone [1].

I was interested to read a recent study in which ezetimibe was again tested for its affects on narrowing in the arteries (atherosclerosis) [3]. In this study, individuals with ‘peripheral vascular disease’ (atherosclerosis in the arteries in the legs) had the extent of their disease measured using MRI. Here’s how the individuals in the study were treated:

1. those not previously on a statin were given simvastatin (40 mg a day) or simvastatin (40 mg a day) plus ezetimibe (10 mg a day).

2. those already taking a statin had ezetimibe (10 mg a day) added to their regime.
MRI was repeated after 1 and 2 years. Here’s what the results showed:

Overall, ezetimibe resulted in lower ‘unhealthy’ LDL-cholesterol levels when used in conjunction with the statin than the statin alone. However, individuals in group 2 saw a progression of their disease (by 8 per cent over two years), compared with no progression in group 1.

In other words, in those taking a statin, the addition of ezetimibe actually worsened their disease.

This study, on the back of previous evidence, strongly suggests that ezetimibe poses hazards for health. Yet, it remains on the market. This is what can happen when our attention is diverted away from the truly important thing (health), towards cholesterol or some other supposed marker of disease."
For references listed in the above article go here