The Lancet published a meta-analysis of 27 statin trials

Data, Drugs, and Deception: a True Story

 

Wednesday, May 23, 2012

      

Last week The Lancet published a meta-analysis of 27 statin trials, an attempt to determine whether patients with no history of heart problems benefit from the drugs—true story. The topic is controversial, and no less than six conflicting meta-analyses have been performed—also a true story. But last week’s study claims to show, once and for all, that for these very low risk patients, statins save lives—true story.

Actual true story: the conclusions of this study are neither novel nor valid.

The Lancet meta-analysis, authored by the Cholesterol Treatment Trialists group, examines individual patient data from 27 statin studies. Their findings disagree with an analysis published in 2010 in the Archives of Internal Medicine, and with analyses from two equally respected publications, the Therapeutics Letter and the Cochrane Collaboration.* Despite this history of dueling data the authors of last week’s meta-analysis, in a remarkable break from scientific decorum, conclude their report with a directive for the writers of statin guidelines: the drugs should be broadly recommended based on the new analysis.

As an editorialist points out, if implemented, the CTT group recommendations in the United States would lead to 64 million people, more than half of the population over the age of 35, being started on statin therapy—true story.

Where is the magic, you ask, in this latest effort? What is different? In some ways, nothing. Indeed just a year and a half earlier The Lancet published a meta-analysis of 26 of the same 27 studies, with the same results, by the same authors (true story, and an odd choice on the part of the journal). So the findings aren’t new. They are, however, at odds with other meta-analyses. Why? It is the way they calculated their numbers. This meta-analysis, like the earlier one from the same group, reports outcomes per-cholesterol-reduction. The unit they use is a “1 mmol/L reduction in low density lipoprotein (LDL)”, in common U.S. terms, a roughly 40-point drop in LDL.

That’s the magic: each of the benefits reported in the paper refers to patients with a 40-point cholesterol drop. Voilá. One can immediately see why these numbers would look different than numbers from reviews that asked a more basic question: did people who took statins die less often than people taking a placebo? (The only important question.) Instead, they shifted the data so that their numbers corresponded precisely to patients whose cholesterol responded perfectly.
Patients whose cholesterol drops 40 points are different than others, and not just because their body had an ideal response to the drug. They may also be taking the drug more regularly, and more motivated. Or they may be exercising more, or eating right, and more health conscious than other patients. So it should be no surprise that this analysis comes up with different numbers than a simple comparison of statins versus placebo pills. Ultimately, then, this new information tells us little or nothing about the benefits someone might expect if they take a statin. Instead it tells us the average benefits among those who had a 40-point drop in LDL.

But LDL drop cannot be predicted. Some won’t drop at all, some will drop just a bit, and some may drop more. Therefore the numbers here tell an interesting story about certain patients who took statins, but they have no relevance to patients and doctors considering statins. And yet, the latter group is the target of the study's concusions.

True story: in prior meta-analyses that found no mortality benefit the investigators simply looked at studies of patients without heart disease and compared mortality between the statin groups and the placebo groups. No machinations, no acrobatics, no per-unit-cholesterol. They took a Joe Friday approach (just the facts, ma’am), and found no mortality benefit.

Perhaps never has a statistical deception been so cleverly buried, in plain sight. The study answers this question: how much did the people who responded well to the drug benefit? This is, by definition, a circular and retrospective question: revisiting old data and re-tailoring the question to arrive at a conclusion. And to be fair they may have answered an interesting, and in some ways contributory, question. However the authors’ conclusions imply that they answered a different, much bigger question. And that is not a true story.

Guideline writers, doctors, patients, journalists, and policy makers will all have to pay close attention to avoid the trappings of deceptive data, dressed up as a true story.

*The Cochrane Collaboration analysis reports an overall mortality benefit with statins (RR=0.86), however their summary suggests that statins should be used for primary prevention “with caution.” In particular on p.12, after a discussion of the biases in many of the trials that led to their numerical finding, they clearly state that using statins for patients with anything less than a 2% per year risk of coronary events “is not supported by existing evidence.” This cutoff encompasses virtually all people that would be considered candidates for primary prevention.
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Read the complete article here.

Thyroid Pills & Heart Disease - Dach

Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD

Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD

The Low Thyroid Condition and Heart Disease

In 1976 Broda Barnes was the first to connect low thyroid function with heart attacks and heart disease.  His book is called, Hypothyroidism The Unsuspected Illness by Broda Barnes, Click Here to read my Book Review..

Above Left Image: Photo of WP Thyroid Pills Bottle courtesy of RLC labs Natural thyroid pills

Discovering the Connection
How did Broda Barnes discover the connection between low thyroid and heart disease?  Barnes took summer vacations in Graz Austria every year to study the autopsy files.  Graz had a high prevalence of thyroid disorders, and anyone in Graz who died over the past 100 years required an autopsy to determine cause of death, as mandated by the authorities.  This rather large amount of autopsy data showed that low thyroid patients survived the usual childhood infectious diseases thanks to the invention of antibiotics, and years later develop heart disease.  Barnes also found that thyroid treatment was protective in preventing heart attacks, based on his own clinical experience.  Likewise for diabetes, Dr. Barnes found that adding thyroid medication was beneficial at preventing the onset of vascular disease in diabetics.  Again, blood tests are usually normal.
New research like the Hunt Study confirms that Broda Barnes was right all along, creating a paradigm shift in thyroid treatment, and constituting a frontal assault on the Institution of Medicine’s thyroid dogma.

The Hunt Study - Thyroid Function and  Heart Disease
 
TSH is short for thyroid stimulating hormone, made by the pituitary gland.  TSH actually stimulates the thyroid gland to make more thyroid hormone, and can therefore be used as a barometer of thyroid function.  If thyroid function is low, the pituitary sends out more TSH to stimulate the thyroid to make more thyroid hormone.  
Mainstream Medicine regards the TSH as the single most important test for determining thyroid function. High TSH means low thyroid function, and a Low TSH means normal or high thyroid function.


What Did The Hunt Study Find?
The Hunt Study from the April 2008 Archives of Internal Medicine examined mortality from coronary heart disease (CHD) and TSH level.  The authors conclude,
“The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.”
Above Image: Thyroid Gland makes thyroid hormone.

The Hunt Study measured thyroid function with the TSH test in 17,000 women and 8,000 men with no known thyroid disease or heart disease. All patients had “normal TSH” levels meaning the TSH values were in the lab reference range of 0.5 to 3.5.   The women were stratified into three groups, lower TSH, intermediate and upper TSH levels, and mortality from heart disease was recorded over an 8 year observation period.

 (see chart below).
70% Increase in Heart Disease Mortality for TSH in Upper Normal Range
The Hunt study found that group with the higher TSH had a 70% increased mortality from heart disease compared to the lower TSH group.  Remember all these TSH vales were in the normal lab range. See chart below for results of the Hunt Study:

Left Image: Heart with Occluded Coronary Artery and Infarction at the apex, courtesy of wikimedia commons.

Results of the Hunt Study:

	TSH	Death from Heart Disease
Group 1	0.50-1.4	baseline risk
Group 2	1.5-2.4	40% higher than baseline
Group 3	2.5-3.5	70% higher than baseline

This Finding is Earthshaking !!

This means that merely by taking natural thyroid pills to reduce TSH to the low end of “normal” (0.5), one can reduce death from cardiovascular disease by 70 percent.  This mortality benefit is mind boggling and far exceeds any drug intervention available.

Thyroid Hormone Also Improves LDL Lipo-Proteins
Another report from the Hunt Study published in 2007 showed that LDL cholesterol was linearly associated with TSH level. (see chart below).
Below Chart showing LDL cholesterol (non-HDL) goes up as TSH goes up.  Note that TSH always remains within in the lab “normal range” (0.5-3.5).
Above chart shows linear increase in LDL cholesterol as TSH increases. Image Courtesy of Hunt Study European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007
The Conclusion is Clear:
The best way to normalize lipoprotein profile and reduce mortality from heart disease is to reduce TSH to the lower end of the normal range with thyroid medication.  A TSH in the upper end of the normal range is associated with increased cardiovascular mortality and elevations in LDL lipo-protein measurements.  A TSH at the lower end of the normal range is associated with protection from heart disease.

Statin Drugs or Thyroid to Prevent Heart Disease in Women?

My previous article discussed the issue of statin drugs for women.  Decades of published statin drug studies show that statin drugs simply don’t work for women, and don’t reduce mortality from heart disease in women.  But on the other hand, the HUNT study shows that TSH levels in the lower normal range provide a 70% reduction in heart disease mortality for women.  This can be accomplished safely with inexpensive thyroid medication under a physician’s supervision.  So for women concerned about preventing heart disease, this is good news, pointing out a natural alternative to statin drugs that works much better.

Natural Thyroid is Better
Rather than Synthroid, we prefer to use natural thyroid which is a dessicated porcine thyroid gland from RLC Labs.  The reason for this is that we have seen better clinical results with the natural thyroid preparations compared to synthroid.
Above image: thyroid hormone Courtesy Wikimedia .
Natural Thyroid is Safer, but can Cause Adverse Effects of Palpitations
Although natural thyroid is safe, there is always the possibility of adverse effects from thyroid excess, defined as too much thyroid medication.  The first sign of thyroid excess is usually a rapid heart rate at rest or perhaps palpitations (at rest).  We spend about five minutes at the office going over this adverse effect before starting patients on thyroid medication.  Usually patients will notice the heart rate going up or the heart beat sounding louder than usual as the first sign that can be easily recognized.  Once recognized, the patient is instructed to stop the thyroid medication, and symptoms usually resolve within 6 hours (for natural thyroid).  It is perfectly safe to stop the thyroid medication at any time, as there will be no acute changes, merely a gradual reversion to the original state that existed before starting the thyroid pills.

Some patients are very sensitive to thyroid medication and will have thyroid excess symptoms such as rapid heart rate and palpitations from small amounts of thyroid medication.  These are usually the elderly with underlying heart disease and/or magnesium deficiency, and we usually avoid giving thyroid medication to these patients.  We also liberally supplement everyone with magnesium if their RBC magnesium levels are low.

About 5 per cent of our patients initially started on thyroid will notice symptoms of thyroid excess with a rapid heart rate, and they will stop the medication for a day or two and restart at a lower dosage with no problem.  This is more common in Hashimoto’s patients whose own production of thyroid hormones may fluctuate from month to month.  Patients with magnesium deficiency or adrenal fatigue with low cortisol output on salivary testing will also tend to be more sensitive to small amounts of thyroid medication, so caution is advised in these groups as well.

Thyroid Excess Can Rarely Cause Atrial Fibrillation
Upper Image: EKG strip with Red Arrow shows atrial fibrillation, no recognizable P-wave.  Lower Image: EKG strip with normal rhythm with recognizable P wave (blue arrow). Courtesy of Wikimedia Commons.
So far, we have not had a patient go into atrial fibrillation from thyroid medication, probably because we spend so much time with each patient discussing the symptoms of thyroid excess, and the importance of stopping the thyroid medication if these symptoms are noted.

Mainstream Docs Don’t Have Time To Discuss Adverse Effects
One of the reasons the mainstream conventional docs will give only a minuscule amount of synthroid to the low thyroid patient is that they simply don’t have the time to discuss thyroid excess and can’t afford an adverse event which is more likely if the patient doesn’t have a clue about what to watch out for.  In addition, mainstream medical docs don’t recognize the syndrome of adrenal fatigue or magnesium deficiency , so they can run into problems with thyroid excess without understanding why, and this also makes them very cautious, tending to under treat.
Left Image: Doctor thinking about thyroid dosage.
In patients with underlying heart disease who are prone to cardiac arrhythmias, thyroid excess can cause atrial fibrillation with characteristic EKG appearance.  Atrial fibrillation can be a problem, because if it becomes chronic and doesn’t go away on its own, the cardiologist will try a maneuver called cardioversion, the application of an electrical shock to restart a normal cardiac rhythm.  Or, if that doesn’t work, prescribe blood thinners, all of which is not without risk.  So it is better to avoid atrial fibrillation altogether by simply stopping the thyroid pills whenever symptoms of rapid heart rate or palpitations are noted while at rest.  Exercise induced rapid heart rate, of course, doesn’t count since that is normal cardiovascular response to exercise.

How To Design A Better Hunt Study
How would I design an even better Hunt Study? That’s easy. Include another group of patients with TSH levels above and below the study group, namely, below 0.5, and above 3.5.  I would also include data on annual CAT coronary calcium scores.  I would predict that the lower TSH group (below 0.5) would have even less heart disease than the higher TSH group, and that coronary calcium score, indicating plaque burden, would go up as TSH went up.

Read More About the Hunt Study from William Davis MD and Jacob Teitelbaum MD:
Is normal TSH too high?   by William Davis MD
Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks by Jacob Teitelbaum, MD.

Credit and Thanks is given to William Davis MD and Jacob Teitelbaum MD for bringing the Hunt Study to my attention.

For more information on thyroid and heart disease, read my previous articles:
Saving Time Russert and George Carlin
Healthy Men Should Not Take Statin Drugs
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
How to Reverse Heart Disease with the Coronary Calcium Score (part one)
Reversing Heart Disease Part Three
Cholesterol Lowering Drugs for the Elderly, Bad Idea
Cholesterol Lowering Statin Drugs for Women Just Say No

Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie Florida 33314
954-792-4663
www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com
(c) 20013 Jeffrey Dach MD All Rights Reserved, This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.
Link to this article:http://wp.me/P3gFbV-LU
http://jeffreydach.com/2008/10/12/hunt-study-shows-thyroid-prevents-heart-attacks-by-jeffrey-dach-md.aspx
Links and References:
http://archinte.ama-assn.org/cgi/content/abstract/168/8/855
Arch Intern Med. 2008;168(8):855-860. Thyrotropin Levels and Risk of Fatal Coronary Heart Disease,
The HUNT Study
Arch Intern Med. 2008;168(8):855-860. Background  Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.
Methods  In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.
Results  During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.
Conclusions  Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.
Author Affiliations: Department of Public Health, Faculty of Medicine (Drs Åsvold and Vatten), and Human Movement Science Programme (Dr Nilsen), Norwegian University of Science and Technology, Trondheim, Norway; St Olavs Hospital, Trondheim University Hospital, Trondheim (Dr Åsvold); Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Dr Bjøro); and Department of Social Medicine, University of Bristol, Bristol, England (Dr Gunnell).
http://www.eje-online.org/cgi/content/full/156/2/181
European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007  CLINICAL STUDY  The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study
Bjørn O Åsvold1,2, Lars J Vatten1, Tom I L Nilsen1 and Trine Bjøro3  1 Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N-7489 Trondheim, Norway, 2 St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway and 3 Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Correspondence should be addressed to L J Vatten
Jacob Teitelbaum MD
http://www.endfatigue.com/health_articles_f-n/Heart-low_thyroid_major_cause_heart_attacks.html
Jacob Teitelbaum, MD. Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks,
William Davis MD
http://heartscanblog.blogspot.com/2008/06/is-normal-tsh-too-high.html
William Davis MD, begin quote:”Is normal TSH too high? There’s no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.  But how do we distinguish “normal” thryoid function from “low” thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.  Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called “negative feedback loop:” If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.  An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)  The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid “rules.” endquote WIlliam Davis MD
International Hormone Societyhttp://www.intlhormonesociety.org/ref_cons/
Ref_cons_9_thryoid_treatment_of_clinically_hypothyroid_biochemically_hypothyroid_patients.pdf
International Hormone Society, references, clinically hypothyroid , lab euthyrroid
Other Blogs:
http://thyroid.blogspot.com/
Thyroid Blog by Dr. Richard B. Guttler M.D., F.A.C.E.
Location: Santa Monica, California, United States
http://www.stopthethyroidmadness.com/
Stop the Thyroid Madness Blog – a patient tries in vain to convince soctors to switch from Synthroid to Armour
http://thyroid.about.com/
MAry Shomon thyroid blog
Disclaimer click here: http://www.drdach.com/wst_page20.html
The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship.  Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.  Finally, the material produced by myself may be reproduced for personal use, provided that appropriate credit is given
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(c) 2007-2013 Jeffrey Dach MD All Rights reserved. This article may be copied or reproduced on the internet provided a link and credit is given.

 

Statins Do Not Save Lives - Smith

New Study Confirms Statins Do Not Save Lives

Thursday, August 29, 2013

 

A 'new' study of statin medications has just been published in the Journal of the American College of Cardiology. I say new, but actually its a new manipulation of old data.

The researchers looked at eight previously conducted clinical trials done on statins. The population studied was elderly people without existing cardiovascular disease. After doing their calculations, it was concluded that statins did slightly reduce the risk of heart attack and stroke, but the use of statins did not reduce the risk of death from cardiovascular disease. There was also no reduction in the risk of death from all causes.

The bottom line is that it has once again been established that statins do not extend life expectancy for people without cardiovascular disease.

This is one of the key points that STATIN NATION exposes.  The video excerpt below provides a summary of this issue:



A Bit More Detail
Around 75% of all the people who take a statin, are taking it for  primary prevention. This means they do not have a heart problem but are taking the medication in the hope of preventing a heart problem in the future.  When it comes to primary prevention none of the largest clinical trials have been able to conclusively show any net benefit.

The AFCAPS (1), ASCOT (2), CARDS (3), PROSPER (4) and WOSCOPS (5) clinical trials all failed to show a statistically significant reduction in all cause mortality (deaths from all causes, not just heart disease related deaths).

All cause mortality data, of course, is the only true measure one can use to determine if a statin is going to extend life expectancy or not. Whilst some clinical trials of statins have shown a very slight reduction in heart disease, in primary prevention, this has always been countered by deaths from other causes. The net result is that people do not live any longer after taking a statin.

In 2010, a meta-analysis of 11statin trials was published in the Archives of Internal Medicine. Professor Kausik Ray and colleagues concluded that statins provided no benefit in terms of deaths from all causes, when used for primary prevention (6). This analysis had the “cleanest” dataset of any analysis completed to date - the researchers were able to exclude patients with existing heart disease (known as secondary prevention) and only include data associated with primary prevention.
When we look at the use of statins for people who already have a diagnosed heart problem (the 25% of people, in secondary prevention) the picture becomes less clear cut. Some trials have found significant increases in life expectancy for these people, however, the trials have always been too short for us to assess the long-term impact of being on a statin.

Even if statins do provide a short-term benefit for those with a heart problem, it is debatable that this has anything to do with the cholesterol-lowering effect of statins. Quite simply, the amount of benefit does not match up with the degree of cholesterol-lowering. The potential beneficial affects of statins for people with heart disease is now widely recognised to be associated with a reduction in inflammation. And recent evidence suggests that this is mediated through an improvement in iron metabolism (7).

“Benefits Outweigh Risks” 
Any decision to take a medication should of course involve a clear understanding of the benefits balanced against the risks. Many authorities have repeatedly stated that the benefits of statins far outweigh the risks. Clearly, this is not correct.

First of all, as we have seen above, there is no net benefit for the 75% of people who take a statin in primary prevention. So, for these people, the choice should be abundantly clear, since they will only expose themselves to the significant adverse effects associated with statins.

Statins have been linked with more than 300 different adverse effects. The most common adverse effects include: depression, suicide, sleep disturbances, memory loss, sexual dysfunction, lung disease, muscle-related problems, cognitive loss, neuropathy, pancreatic dysfunction and liver dysfunction. More recent studies have also shown that statins cause type 2 diabetes and acute kidney injury.

In addition, many doctors are concerned about statins and a potential increase in the risk for cancer and heart failure. A recent study found that the long term use of statins doubles the risk of breast cancer in women.

The best estimates suggest that at around 20% of the people who take a statin will experience significant adverse effects. This needs to be considered when thinking about both primary and secondary prevention, since this 20% is a much greater number than the number of people who might benefit, even in secondary prevention.

References: 
1. Downs JR, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study. JAMA 1998; 279:1615-22.
2. Sever PS, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003; 361:1149-1158.
3. Clhoun HM, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atovastatin Diabetes Study (CARDS). Lancet 2004; 364:685-696.
4. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet 2002; 360:1623-1630.
5. Shepherd J, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia (WOSCOPS). N Engl J Med 1995; 333:1301-1307.
6. 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; 170:1024-31.
7. Zacharski, LR et al. The Statin–Iron Nexus: Anti-Inflammatory Intervention for Arterial Disease Prevention. American Journal of Public Health. Published online ahead of print February 14, 2013.
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Read the complete article here.

Why Women Should Stop Their Cholesterol Lowering Medication - Hyman

Why Women Should Stop Their Cholesterol Lowering Medication

by Dr Mark Hyman   January 19th, 2012

If you are a post-menopausal women with high cholesterol, your doctor will almost certainly recommend cholesterol lowering medication or statins. And it just might kill you. A new study in the Archives of Internal Medicine found that statins increase the risk of getting diabetes by 71 percent in post-menopausal women.

Since diabetes is a major cause of heart disease, this study calls into question current recommendations and guidelines from most professional medical associations and physicians. The recommendation for women to take statins to prevent heart attacks (called primary prevention) may do more harm than good.

Statins have been proven to prevent second heart attacks, but not first heart attacks.

Take it if you already have had one, but beware if your doctor recommends it for you if have never had a heart attack.

This current study adds to an increasing body of literature questioning the benefits of statins, while highlighting their potential risks.

New Study Shows 48 Percent Risk of Diabetes in Women Who Take Statins

This study examined the data from the large government sponsored study called the Women’s Health Initiative, the same study that disabused us of the idea that Premarin prevented heart attacks in postmenopausal women.

In fact, based on this randomized controlled trial, estrogen replacement therapy, once considered the gold standard of medical care for the prevention of heart disease, was relegated to the trash bin of history joining medicine’s many other fallen heroes including DES, Thalidomide, Vioxx, Avandia, and more.

In this new study researchers reviewed the effect of statin prescriptions in a group of 153,840 women without diabetes and with an average age of 63.2 years. About 7 percent of women reported taking statin medication between 1993 and 1996. Today there are many, many more women taking statin medications, thus many more are at risk from harm from statins.

During the 3-year period of the study, 10,242 new cases were reported – a whopping 71 percent increase in risk from women who didn’t take statins. This association stayed strong at a 48 percent increased risk of getting diabetes, even after taking into account age, race/ethnicity, and weight or body mass index. These increases in disease risk were consistent for all statins on the market.
This effect also occurred in those with and without heart disease. Surprisingly disease risk was worse in thin women. Minority women were also disproportionately affected. The risk of diabetes was 49 percent for white women, 57 percent for Hispanic women, and 78 percent for Asian women.
But in a typical “my mind’s made up, don’t confuse me with the facts” statement by the medical establishment, the researchers said we should not change our guidelines for statin use for the primary prevention of heart disease.

In a large meta-analysis published in the Lancet last year, scientists found that statins increased the risk of diabetes by 9 percent. If current guidelines were followed for those who should take statins, and people actually took them (thank God only 50 percent of prescriptions are ever filled by patients), there would be 3 million more diabetics in America. Oops.

Other studies have recently called into question the belief that high cholesterol levels increase your risk of heart disease as you get older. For those over 85 it turns out having high cholesterol will protect you from dying from a heart attack, and, in fact, from death from any cause.

Low Cholesterol May Kill You

A recent study showed that in healthy older persons, high cholesterol levels were associated with lower non-cardiovascular-related mortality. This is extremely concerning because millions of prescriptions are written every day to lower cholesterol in the older population, yet no association has been found between higher cholesterol and heart disease deaths for those aged 55 to 84; and for those over 85, the association seems to be inverse — higher cholesterol predicts lower risk of death from heart disease.

The pharmaceutical industry, medical associations, and academic researchers whose budgets are provided by grants from the pharmaceutical industry continue to preach the wonders of statins, but studies like these should have us look good and hard at our current practices. Are we doing more harm than good?

Cardiologists recommend putting statins in the water and giving them out at fast food restaurants and having them available over the counter. They believe in driving cholesterol as low as possible. Statin prescriptions are handed out with religious fervor, but do they work to prevent heart attacks and death if you haven’t had a heart attack already?

Bottom line: NO! If you want to learn why this is true, read on.

Statins Don’t Work to Prevent First Heart Attacks

Recently, the Cochrane Group did a review of all the major statin studies by an international group of independent scientists. The review failed to show benefit in using statins to prevent heart attacks and death. In addition, many other studies support this and point out the frequent and significant side effects that come with taking these drugs. (i) If scientists found that drinking two glasses of water in the morning prevented heart attacks, even if the evidence was weak, we would jump on board. Big up side, no down side.

But this is not the case with statins. These drugs frequently cause muscle damage, muscle cramps, muscle weakness, muscle aches, exercise intolerance (ii) (even in the absence of pain and elevated CPK – a muscle enzyme), sexual dysfunction, liver and nerve damage and other problems in 10-15 percent of patients who take them. (iii) They can also cause significant cellular, muscle, and nerve injury as well as cell death in the ABSENCE of symptoms. (iv)

There is no lack of research calling into question the benefits of statins. Unfortunately, that research doesn’t get the benefit of billions of dollars of marketing and advertising that statins do. One big trial was touted as proving statins work to prevent heart attacks, but the devil is in the details.

It was the JUPITER (v) trial that showed that lowering LDL (or bad cholesterol) without a reduction in inflammation (measured by C-reactive protein) didn’t prevent heart attacks or death. (vi) Statins happen to reduce inflammation so the study has been touted as proof of the effectiveness of these medications.

Mind you it wasn’t lowering the cholesterol that helped (which is the intended purpose of statins), but the fact that they lower inflammation. What is ignored by people who use this study to “prove” that statins work is the fact that there are so many better ways to lower inflammation than taking these drugs.

Yet other studies have shown no proven benefit for statins in healthy women (vii) with high cholesterol or in anyone over 69 years old. (viii) Some studies even show that aggressive lowering of cholesterol can cause MORE heart disease. The ENHANCE trial showed that aggressive cholesterol treatment with two medications (Zocor and Zetia) lowered cholesterol much more than one drug alone, but led to more arterial plaque and no fewer heart attacks. (ix)

Other research calls into question our focus on LDL or the bad cholesterol. We focus on it because we have good drugs to lower it, but it may not be the real problem. The real problem is low HDL that is caused by insulin resistance (diabesity).

In fact studies show that if you lower the bad (LDL) cholesterol in people with low HDL (good cholesterol) that is a marker of diabesity – the continuum of obesity, prediabetes and diabetes – there’s no benefit. (x)

Most people simply ignore the fact that 50-75 percent of people who have heart attacks have normal cholesterol. (xi) The Honolulu Heart Study showed older patients with lower cholesterol have higher risks of death than those with higher cholesterol. (xii)

Some patients with multiple risk factors, or who have had previous heart attacks do benefit, but when you look closely the results are underwhelming. It’s all in how you spin the numbers. For high-risk males (those who are overweight and have high blood pressure, diabetes, and/or a family history of heart attacks) and are younger than 69 there is some evidence of benefit, but one hundred men would need to be treated to prevent just one heart attack.

That means that 99/100 men who take the drug receive no benefit. Drug ads say the risk is reduced by 33 percent. Sounds good, but that just means the risk of getting a heart attack goes down from 3 percent to 2 percent.

Despite the extensive data showing that statins are a questionable therapy at best, they are still the number one selling drug in the US. What isn’t so well known is that 75 percent of statin prescriptions are written for people who will receive no proven benefit. The cost of these prescriptions? Over $20 billion a year.

Yet somehow the 2004 National Cholesterol Education Program guidelines expanded the previous guidelines to recommend that even more people without heart disease take statins (from 13 million to 40 million) (xiii) What are we thinking?

Why would respected scientists go against the overwhelming research that statins don’t prevent heart disease in people who haven’t already had a heart attack?

You can find the answer if you follow the money. Eight of the nine experts on the panel who developed these guidelines had financial ties to the drug industry. Thirty-four other non-industry affiliated experts sent a petition to protest the recommendations to the National Institutes of Health saying the evidence was weak.

What Should Women Do?
It is time to push the sacred cow of statins overboard.
But first let me say this. If you have had a heart attack, or have heart disease, the evidence shows they do in fact help protect against a second heart attack, so keep taking them. However, you should be aware that most prescriptions for statins are given to healthy people whose cholesterol is a little high. For these folks the risk clearly outweighs the benefit.

The editorial that accompanies the recent study on women taking cholesterol-lowering medication that I opened this article with was quite clear. Dr. Kirsten Johansen from the University of California, San Francisco said that the increased risk of diabetes in women without heart disease has “important implications for the balance of risk and benefit of statins in the setting of primary prevention in which previous meta-analyses show no benefit on all-cause mortality.”

In plain English, she said that we shouldn’t be using statin drugs for women without heart disease because:

1. The evidence shows they don’t work to prevent heart attacks if you never had one.
2. They significantly increase the risk of diabetes.

Treating risk factors like high cholesterol is misguided. We must treat causes – what we eat, how much we exercise, how we handle stress, our social connections and environmental toxins are all more powerfully linked to creating health and preventing disease than any drug on the market.
Remember what you put at the end of your fork is more powerful than anything you will ever find at the bottom of a pill bottle.

My new book The Blood Sugar Solution, which comes out at the end of February, gives exact details on what you should put at the end of your fork to prevent and reverse diabesity. It provides a comprehensive solution to the health problems facing our nation today.

Now I’d like to hear from you …

What do you think of statins?

Have you taken statins? What has your experience been?

Why do you think the medical establishment prescribes drugs that research shows don’t work?
Please leave your thoughts by adding a comment below – but remember, we can’t offer personal medical advice online, so be sure to limit your comments to those about taking back our health!

To your good health,
Mark Hyman, MD

References:

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(i) Abramson J, Wright JM. Are lipid-lowering guidelines evidence-based? Lancet. 2007 Jan 20;369(9557):168-9

(ii) Sirvent P, Mercier J, Lacampagne A. New insights into mechanisms of statin-associated myotoxicity. Curr Opin Pharmacol. 2008 Jun;8(3):333-8.

(iii) Kuncl RW. Agents and mechanisms of toxic myopathy. Curr Opin Neurol. 2009 Oct;22(5):506-15. PubMed PMID: 19680127.

(iv) Tsivgoulis G, et. al, Presymptomatic Neuromuscular Disorders Disclosed Following Statin Treatment, Arch Intern Med. 2006;166:1519-1524

(v) Mora S, Ridker PM. Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)–can C-reactive protein be used to target statin therapy in primary prevention? Am J Cardiol. 2006 Jan 16;97(2A):33A-41A.

(vi) Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ; JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207.

(vii)Abramson J, Wright JM. Are lipid-lowering guidelines evidence-based? Lancet. 2007 Jan 20;369(9557):168-9

(viii) IBID

(ix) Brown BG, Taylor AJ Does ENHANCE Diminish Confidence in Lowering LDL or in Ezetimibe? Engl J Med 358:1504, April 3, 2008 Editorial

(x) Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, Kastelein JJ, Bittner V, Fruchart JC; Treating to New Targets Investigators. HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. N Engl J Med. 2007 Sep 27;357(13):1301-10.

(xi) Hansson GK Inflammation, Atherosclerosis, and Coronary Artery Disease N Engl J Med 352:1685, April 21, 2005

(xii) Schatz IJ, Masaki K, Yano K, Chen R, Rodriguez BL, Curb JD. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet. 2001 Aug 4;358(9279):351-5.

(xiii) http://www.nhlbi.nih.gov/about/ncep/index.htm

About Dr Mark Hyman

MARK HYMAN, MD is dedicated to identifying and addressing the root causes of chronic illness through a groundbreaking whole-systems medicine approach called Functional Medicine. He is a family physician, a four-time New York Times bestselling author, and an international leader in his field. Through his private practice, education efforts, writing, research, and advocacy, he empowers others to stop managing symptoms and start treating the underlying causes of illness, thereby tackling our chronic-disease epidemic. More about Dr. Hyman or on Functional Medicine. Click here to view all Press and Media Releases

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Statin Anti-Cholesterol Drugs Revisited - DACH

Statin Anti-Cholesterol Drugs Revisited By Jeffrey Dach (about the author)     (Page 1 of 7 pages) Life Arts 11/4/2012

This article takes a critical look at statin anti-cholesterol drugs, and asks the hard questions. Do statin drugs work? Who do they work for? Who do they harm? Who should be taking them, and who should not be taking them? Examples of Statin Drugs are Lipitor, Zocor, Simvastatin, Pravachol, Crestor, Mevacor, etc. These drugs reduce the production of cholesterol by the liver by inhibiting an enzyme called HMG-CoA. Due to a belief that cholesterol causes coronary artery disease, statin drug reduction of cholesterol is a mainstream medical treatment intended to prevent heart disease. Do statin drugs prevent coronary artery disease, heart attacks and mortality from heart disease? This article will answer that question.

Anti-Inflammatory Effect

After many decades of study and clinical trials, it has become clear that the benefit of statin drugs (if there is any) is probably not due to reduction in cholesterol, rather it is due to an anti-inflammatory effect of the drug.(link)

Reducing CoQ-10

Coincidentally, statin drugs inhibit the production of an important mitochondrial cofactor called Co-Q10, accounting for adverse effects as mitochondrial toxins. In addition, a low serum cholesterol level is a health risk for many reasons. Cholesterol is an important molecule in the body, and reducing cholesterol to low levels is associated with increased mortality and adverse effects on health. (27)

Asking A Few Questions

In this article we will revisit anti-cholesterol statin drugs while asking the following questions:

1) What is the efficacy for statin drugs in primary prevention of heart disease (in normal healthy people)?

2) What is the efficacy of statin drugs in secondary prevention (patients with known underlying heart disease)?

3) Which subgroups benefit from statin drugs, and which subgroups of the population are harmed by statin drugs?

The Elderly - Low Serum Cholesterol Predicts Increased Mortality

First, let's take a look at the medical practice of prescribing statin anti-cholesterol drugs for the elderly. Contrary to current dogma, higher cholesterol levels in the elderly are not a heath risk. Studies show that higher cholesterol in the elderly is associated with increased survival, while lower total serum cholesterol values in the elderly are a robust predictor of increased mortality. (1, 4,5)

The Prosper Study - Statins for the Elderly

When statin drugs are given to the elderly to reduce cholesterol values as was done in the PROSPER study, there was no mortality benefit for either primary or secondary prevention of heart disease. (1,6,7) True, there was a reduction in cardiac mortality of about 20% in the secondary prevention group in the Prosper study, however, this was counterbalanced by an increase in cancer mortality, yielding no over-all mortality benefit in the final analysis.

Women- No Mortality Benefit from Statins

Perhaps the best summary of the results of three decades of statin drug studies in women can be found in the Judith Walsh MD report in JAMA May 2004. (8) Again, Dr Walsh found that statin drug treatment to reduce cholesterol in women provided no mortality benefit in both primary and secondary prevention of heart disease. As we found in the PROSPER study for the elderly, statin drug use in women (with known heart disease) resulted in a reduction in mortality from heart disease, and a reduction in heart attacks in this secondary prevention group, however, this was offset by additional deaths from cancer and other mortality which yielded no over-all mortality benefit in the final analysis. (8)

MEN and Women- Primary Prevention- Dr Ray Archives of Internal Medicine

1 | 2 | 3 | 4 | 5 | 6 | 7

Jeffrey Dach MD is a physician and author of two books, Natural Medicine 101, and Bioidentical Hormones 101, both available on Amazon, or as a free e-book on his web sites. Dr. Dach is founder and chief medical officer of TrueMedMD, a clinic in (more...)

 

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Statins can drain the life out of us - Briffa

Statins can drain the life out of us



Statin drugs reduce cholesterol by inhibiting the an enzyme in the liver (HMG-CoA reductase) which plays a role in the production of cholesterol in the liver. Unfortunately, this enzyme also plays a part in the production of a substance known as Coenzyme Q10, which itself is important for energy production within the body’s cells. Statins therefore have the ability to drain the life out of people. Any doctor who sees patients and actually listens to them will know this from experience, and now someone’s actually gone and shown it with a scientific study [1].

The study was published on-line in the Archives of Internal Medicine. A group of individuals were randomised to take one of two statins (simvastatin at 20 mg per day or pravastatin at 40 mg per day) or placebo for six months. Participants were rated at regular intervals through the study for their perceived fatigue on exertion, general fatigue and energy levels.

One thing worth highlighting here is that the study was only 6 months in duration. This is relevant because it’s not uncommon for the adverse side-effects of statins to come on many months or even years after the treatment is started.

Overall, statins did indeed appear to cause a significant change in energy and worsen fatigue on exertion. Women were more affected than men.

Four out of 10 women reported either reduction in energy or worsening of fatigue on exertion.

Two out of 10 women reported problems with both these things.

One out of 10 women reported that both of these things were ‘much worse’.

The authors remark:

Effects were seen in a generally healthy sample given modest statin doses, and both simvastatin and pravastatin contributed to the significant adverse effect of statins on energy and fatigue with exertion. Particularly for women, these unfavorable effects were not uncommon… These findings are important, given the central relevance of energy and functional status to well-being.

If you or someone you know appears to have statin-related fatigue or other symptoms (such as muscle pain), please see this blog post about how this might be reversed using supplements of Coenzyme Q10.

References:
1. Golomb BA, et al. Effects of Statins on Energy and Fatigue With Exertion: Results From a Randomized Controlled Trial. Arch Int Med epub 11 June 2012
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Read the full article here.

Why Asians Should Ignore the Cholesterol Sham, and Why Healthy People Should Not Take Statins- Colpo

Why Asians Should Ignore the Cholesterol Sham, and Why Healthy People Should Not Take Statins

Anthony Colpo  Saturday, April 28th, 2012

Folks, before I get rolling, I would just like to dedicate this first instalment of many more cholesterol updates to come to my good buddies Pee Pee and Don Matesz and all those other dopey buggers who make a pastime of accusing me of being a cherry-picker. Today, I’m going to share with you studies you’ve probably never heard of, because they just happen to flatly contradict the mainstream assertion that low cholesterol is healthy and hence are quietly shoved aside by purveyors of this belief due to their embarrassing nature. As we know, one of the favourite strategies humans have for dealing with evidence that contradicts their cherished dogmas is to simply ignore it.

In the twisted worldview of Don, Pee Pee and their ilk, by presenting the studies that you likely never would have heard of due to their embarrassing nature, it is people like me – not them – that are cherry-picking.

Yeah, no worries.

Come and Get ‘Em!
Folks, who wants some cherries? I’ve got a basket full here, and you’re all welcome to grab a handful. They might not be highly-hyped, front page, AHA- or Big Pharma-press-release cherries, but they are definitely sweet, tasty, and certified peer-reviewed delicacies. Enjoy!

Low Cholesterol is Accompanied by Increased Mortality from Stroke, Heart Disease, and Cancer: The Jichi Study
The Asians we are told, are shining examples of the cholesterol theory. They eat a low-fat diet, which gives them wonderfully low cholesterol levels, which in turn not only protects them from heart disease but endows them with the longest average life expectancy on Earth.
Sounds great, doesn’t it?

Too bad it’s complete nonsense.

Being the cherry-picker I am, I discussed the evidence, so often ignored by others, in The Great Cholesterol Con that low cholesterol is strongly associated with increased mortality in Japan.
Yeah, shame on me for pointing out to our Japanese brethren that this whole cholesterol-lowering thing is just another overhyped Western wank, one with the potential to harm instead of hurt their health.

Funnily enough, I don’t feel any shame at all. Au contraire, I believe reporting the facts is a noble thing to do, even if it upsets every last dogmatic sod who can’t get his head around the fact he has fallen hook, line and sinker for a load of unscientific rot.

Which is why, dear readers, I bring you the results from The Jichi Medical School Cohort Study, which involved 12,334 healthy Japanese adults aged 40 to 69 years who underwent a mass screening examination (1992-2005), including total cholesterol measurement. Information regarding cause of death was obtained from death certificates, and the average follow-up period was 11.9 years. In total, 635 men and 423 women died during the study period.

The subjects were divided into 4 groups according to total cholesterol level (<4.14mmol/L; 4.14mmol/L to <5.17 mmol/L; 5.17 mmol/L to <6.20 mmol/L, and; >6.21 mmol/L).
Before I report the results, it should be pointed out that the lowest quartile of cholesterol (<4.14mmol/L) , in both male and female participants, was marked by a higher number of current cigarette smokers.

So did multivariate analyses, which many misguided Western researchers seem to think grants epidemiology the same accuracy as RCT data, and which in this instance included adjustment for smoking, age, systolic blood pressure, HDL, drinking, and body mass index confirm the wonderful life-saving benefits of having low cholesterol?

Nope.

The safest cholesterol range in the study was 4.14–6.20 mmol/L in men, and 4.14mmol/L – >6.21 mmol/L in women. As the researchers stated:

“We noted a clear relationship between low cholesterol and increased mortality. Okamura et al reported that occult liver diseases are associated with mortality; however, in the present study, the relationship between low cholesterol and increased mortality was unchanged in analyses that excluded deaths due to liver disease. Our results suggest that hemorrhagic stroke and heart failure excluding myocardial infarction,contribute to the relationship between low cholesterol and high mortality.”

You can check out the full text of the study here:

Nago N, et al. Low Cholesterol is Associated With Mortality From Stroke, Heart Disease, and Cancer: The Jichi Medical School Cohort Study. Journal of Epidemiology, 2011; 21 (1): 67-74.
Yeah, I know, shame on me for allowing you to view the paper yourself…I need to do what folks like Don and Pee Pee do and make sweeping claims and libelous accusations, then refuse to back them up with even a single paper!

Must be the cherry-picker in me…

Low Cholesterol is Associated with Increased Mortality from CVD in Korean adults.
Maybe the Koreans can save the cholesterol cartel’s Asian thesis, no?
No.

A total of 12,740 Korean adults aged 40 to 69 who underwent a mass screening examination were followed up from 1993 to 2008. Groups with the lowest cholesterol (< 160 mg/dL) as well as the highest (>= 240 mg/dL) were associated with higher CVD mortality in analysis adjusting for age, sex, smoking and drinking status, body mass index, level of blood pressure, triglyceride and HDL.

The researchers noted:

“Based on the results of this study, caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk in Korean adults.”

Aw c’mon guys, the nice folks from Big Pharma won’t like that, will they? Don’t you know that the Asian market, especially China, represents a huge and largely untapped reservoir of profit, but by showing the kind of independent and critical thinking sadly lacking in most of your Western colleagues you’re ruining the party?

Tsk tsk.

Again, dear readers, if you’d like to read the paper yourself, feel free to do so here:

Bae JM, et al. Low cholesterol is associated with mortality from cardiovascular diseases: a dynamic cohort study in Korean adults. J Korean Med Sci. 2012 Jan; 27 (1): 58-63.

Statins are Largely a Waste of Time
As for statins, they’re not just a wank for Asians, they’re a load of cobblers for Westerners too.
The Journal of the American Medical Association recently published a “for” and “against” installment posing the following hypothetical question:

“Should a 55-year-old man who is otherwise well, with systolic blood pressure of 110 mm Hg, total cholesterol of 250 mg/dL, and no family history of premature CHD be treated with a statin?”

To answer this question, JAMA enlisted Blaha, Nasir and Blumenthal from The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease for the “yes” case, and Redberg and Katz from the Division of Cardiology, Department of Medicine, University of California, San Francisco (Dr Redberg) and Department of Health Services, County of Los Angeles (Dr Katz) for the “no” case (Drs Redberg and Katz are also Editor and Deputy Editor, respectively, over at the Archives of Internal Medicine).

To support their “yes” case, the Hopkins crew begin by citing a bunch of cholesterol guidelines that were formulated by panel members sponsored by manufacturers of statins. Yep, I’m sure we can rely on those for accurate, unbiased guidance when tooling around with someone’s health!

They then cite the WOSCOPS and AFCAPS/TexCAPS trials and report the former lowered heart attack and CHD mortality by 31%, while the latter reduced heart attacks by 40%.
Um, fellas … isn’t there something you’re forgetting to tell us about those studies?

Like the fact that the 27% reduction in CHD mortality in AFCAPS/TexCAPS did not reach statistical significance? And that there was no reduction whatsoever in overall mortality?

And the fact that the 27% reduction in CHD mortality in WOSCOPS also did not reach statistical significance?

Instead of reporting these facts about actual death rates, the researchers only reported (read: cherry-picked) outcomes that managed to reach statistical significance and ignored those that didn’t.
Recommending a toxic drug to healthy individuals free of CHD using such dubious interpretation of these largely unsuccessful studies is, to my way of thinking, BoLLOCKS.

The Hopkins team then trot out the absolute farce that was JUPITER, this time including a total mortality reduction of 20% reported in that trial. For me to outline all the discrepancies in this trial – that was conveniently cut short as the mortality trajectories of the treatment and control groups began to menacingly converge – would be a whole other article. Luckily, someone else has already saved me the time and posted a pearler of a critique right here:

http://junkfoodscience.blogspot.com.au/2008/11/when-news-sounds-too-good-statins-new.html

After reading that, I’m sure most everyone apart from Pee Pee, Matesz and the JUPITER researchers themselves will agree that citing JUPITER in support of anything other than the all-too-frequent shadiness of Big Pharma-sponsored research is POPPYCoCK and HogWASH.

The Hopkins team then go onto cite some more theoretical figures, then argue that statins are safe, claiming only 5% of patients experience muscle pains.

Incorrect. The reality is that such complaints are dramatically underreported, thanks to doctors’ refusal to believe the ‘wonder drug’ statin they prescribed could ever do anything negative to their patient. And in those who do acknowledge the cause of the muscle pain, filing an official complaint is a time-consuming affair for which they receive no compensation and may even be subject to interrogation about the circumstances that led to the filing of the report.

But what happens when, instead of brushing people off and telling them their symptoms are just due to “getting old”, researchers carefully inspect patient data and make further enquiries? A study published in the October-November-December 2009 issue of Primary Care Cardiovascular Journal, indicates that statin-induced myopathy is far more common than previously claimed by drug companies and health officials. Researchers analyzed 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:

Sciberras D, et al. Is general practice the optimal setting for the recognition of statin-induced myotoxicity? Primary Care cardiovascular Journal, Oct-Nov-Dec, 2009; 2: 195-200.

As for the question of whether statins should be prescribed to women, Blaha et al cite a review by Kostis et al that claims statins also work in women – but ignore two other reviews that concluded statins do not:

1. Walsh JM, Pignone M. Drug Treatment of Hyperlipidemia in Women. JAMA. 2004; 291 (18): 2243-2252.
2. Petretta M, et al. Impact of gender in primary prevention of coronary heart disease with statin therapy: A meta-analysis. International Journal of Cardiology, 2010; 138 (1): 25-31.

So what do Redberg and Katz, who argue the “No” case, have to say in response to the selectively cited arguments of Blaha and co?

Instead of citing a small handful of incompletely reported trials, they report that:

“Data from a meta-analysis of 11 trials including 65 229 persons with 244 000 person years of follow-up in healthy but high-risk men and women showed no reduction in mortality associated with treatment with statins. A 2011 Cochrane review of treatment with statins among persons without documented coronary disease came to similar conclusions. The Cochrane review also observed that all but one of the clinical trials providing evidence on this issue were sponsored by the pharmaceutical industry. It is well established that industry-sponsored trials are more likely than non–industry-sponsored trials to report favorable results for drug treatment because of biased reporting, biased interpretation, or both of trial results.”

As for the commonly claimed low rate of side effects in statin users, they note:

“This underestimation of adverse events occurs because the trials excluded up to 30% of patients with many common comorbidities, such as those with a history of muscular pains, as well as renal or hepatic insufficiency. Many randomized trials also excluded patients who had adverse effects of treatment during an open label run-in period. For example, in the Treat to New Targets trial, after initial exclusions based on comorbidities, an additional 35% of eligible patients, or 16% of patients, were excluded during an 8-week, open-label, run-in phase because of adverse events, ischemic events, or participants’ lipid levels while taking the drug not meeting entry criteria. Additionally, the results of randomized trials of statin treatment likely underestimate common symptoms such as myalgia, fatigue, and other minor muscle complaints because these studies often only collect data on more quantifiable adverse effects such as rhabdomyolysis.

Numerous anecdotal reports as well as a small trial have suggested that statin therapy causes cognitive impairment, but this adverse outcome would not have been captured in randomized trials. The true extent of cognitive impairment associated with statins remains understudied. It is disappointing that more data are not available on important adverse events associated with statin treatment, despite millions of prescriptions and many years of use. This information could be easily collected in observational studies and from registries. One population-based cohort study in Great Britain of more than 2 million statin users found that statin use was associated with increased risks of moderate or serious liver dysfunction, acute renal failure, moderate or serious myopathy, and cataract. The risk of diabetes with statin use has been seen in randomized clinical trials such as JUPITER, which found a 3% risk of developing diabetes in the rosuvastatin group, significantly higher than in the placebo group. In observational data from the Women’s Health Initiative, there was an unadjusted 71% increased risk and 48% adjusted increased risk of diabetes in healthy women taking statins.”

Their conclusion?

“Based on all current evidence, a healthy man with elevated cholesterol will not live any longer if he takes statins. For every 100 patients with elevated cholesterol levels who take statins for 5 years, a myocardial infarction will be prevented in 1 or 2 patients. Preventing a heart attack is a meaningful outcome. However, by taking statins, 1 or more patients will develop diabetes and 20% or more will experience disabling symptoms, including muscle weakness, fatigue, and memory loss.”

Statins. They still suck.
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Read the complete article here.

Slicing The Salami (and calling it steak).

Not about heart disease, cholesterol or statins but excellent excoriation of the ?study? published in Archives of Internal Medicine. Thanks blackdog!
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Slicing The Salami (and calling it steak).

I am taking a brief respite from the 'Loss of Innocence' saga, to excoriate about the publicity for the study about the intake of meats causing Cancer. Much was made of this in the print and broadcast media with precious little criticism or adverse comment from, well anyone. But in truth it was like most of these proselytising studies, that attempt to steer us from the path of our demise by feeding us the results from 'scientific' research that is not really scientific at all.

The study, published in the Archives of Internal Medicine is an observational study, which means it is not presenting any evidence, merely drawing conclusions from data provided by food frequency questionnaire's filled in by the cohort every four years! I can't even remember what I had for dinner last Tuesday, except to know it would have had meat in it, probably lots of it. These epidemiological type studies are really the starting point of a hypothesis to test it's credibility. They are not the end point, merely the beginning of a journey that should encompass all of the checks and balances that science should pursue to ensure that any statement made about anything should at least be founded in proven fact. So, is it likely that the cohort from whom the data was drawn, reported the facts of their diet without telling a few little lies? I really think not, but that's a side issue really.

Let us then look a little deeper. Firstly we see that all meat, processed or otherwise so long as it's red, is alarmingly 'lumped' together, although they

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 So eating preserved meats does have a mechanism that could be causative of some cancers, because it does actually exist, but frankly you would have to eat really large amounts, on a regular basis. And, the bun surrounding the 'unprocessed' burger meat (sic) is likely to be more harmful. And what country is renowned for it's consumption of burgers and barbecued meats? Might that be the country of origin of the cohort of this study, the USA? Always remember, long suffering reader, that observation (and correlation) does not prove causation.
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Read the full article by BLACKDOG here.

 

And I learned a new word - excoriate: to denounce vehemently; censure severely.

Getting Off Statin Drug Stories by Jeffrey Dach MD

Dr Dach's article, "Getting Off Statin Drug Stories" concludes with this:
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Are You Still a Believer in Anti-Cholesterol Drugs?
If you are still a believer in Statin Drugs, take a look at this study published July 2010 in the Archives of Internal Medicine by Dr. Ray.  He reviewed 11 statin drug clinical trials with 65,229
participants followed for approximately 244,000 person-years.  The astounding results showed the statin drug group all-cause mortality was THE SAME as the placebo group!  There was no benefit from the statin drugs !!!  This article was published in the mainstream medical literature !!

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Read the full article here http://jeffreydach.com/2011/03/04/getting-off-statin-drug-stories-jeffrey-dach.aspx?ref=rss