The Elderly on Primary-Prevention Statins: No Survival Gains in ALLHAT - Medscape

The Elderly on Primary-Prevention Statins: No Survival Gains in ALLHAT

CHICAGO, IL — Statins for primary prevention do not lower the risk of death, whether cardiovascular or from any cause, when given to people aged 65 years or older with CV risk factors, suggests a secondary analysis of a major trial that caused a stir 15 years ago^[1].
The ALLHAT-LLT trial had randomized >10,000 people aged >55 with dyslipidemia and hypertension but no clinical heart disease to receive open-label pravastatin 40 mg/day or usual care. In its 2002 publication^[2], the trial famously saw no significant mortality reduction for the statin after 6 years, nor an improvement in fatal or nonfatal coronary heart disease events.

The results were similar in the new post hoc analysis of the trial focusing on the 2867 participants aged 65 years and older, as a whole and by the two age groups 65 to 74 years and >75 years, according to a report published May 22, 2017 in JAMA Internal Medicine with lead author Dr Benjamin H Han (New York University Langone School of Medicine, NY).
Although no significant outcomes differences were seen between the two randomized groups in any of the age categories, there was a trend (P=0.07) for increased all-cause mortality on the statin in the oldest age group.

As Han pointed out for heartwire from Medscape, the overall trial had well-recognized limitations. For example, the statin was given on an open-label basis. Also, it has been long noted that the ALLHAT-LLT usual-care group could receive statins at the physicians' discretion, which could potentially blur any differences in treatment outcomes.

Calls for Caution

"I would be very cautious in drawing any real conclusions from this study, as the study was not specifically designed to study statins in older adults, so all of the analyses are underpowered. None of their major conclusions were statistically significant," according to Dr Ann Marie Navar (Duke Clinical Research Institute, Durham, NC), who isn't connected with the ALLHAT-LLT report.
"Most statin trials have shown no difference in mortality, but [they showed] that statins do reduce the risk of coronary heart disease, a trend also seen in this secondary analysis," Navar told heartwire by email.

"The trend toward increasing mortality is certainly provocative but really needs to be explored in a trial specifically designed to test this issue."
The post hoc analysis included 1467 participants who had been randomized to pravastatin; their mean age was 71.3, and 48% were women. Their mean LDL-C level was 147.7 mg/dL at baseline and 109.1 mg/dL after 6 years.
The 1400 participants in the usual-care group had a mean age of 71.2 years, and 51% were female. Their mean LDL-C level was 147.6 mg/dL at baseline and 128.8 mg/dL after 6 years.
For all patients over the age of 65 who took pravastatin, the hazard ratio for all-cause mortality was 1.18 (95% CI 0.97–1.42, P=0.09) compared with the usual-care group. It was 1.08 (95% CI 0.85–1.37, P=0.55) for the 65–74 group and 1.34 (95% CI 0.98-1.84 P=0.07) for those aged 75 and older. Nor were there significant HRs for the secondary CHD end points.

In multivariate analysis, the corresponding HRs were 1.15 (95% CI 0.94–1.39) for 65 and older, 1.05 (95% CI 0.82–1.33) for those 65 to 74, and 1.36 (95% CI, 0.98-1.89) for 75 and older. The prospectively defined covariates included age, sex, race/ethnicity, primary-prevention aspirin use, smoking history, type 2 diabetes, body mass index, and systolic and diastolic blood pressures.

The Issues
"We are seeing a lot more older adults being put on statins for primary prevention, but the problem is, the evidence for doing so is limited," Han said.

"As geriatricians, we emphasize that treatment recommendations really need to be individualized with patients and need to also take into account not just what their cardiovascular risk is, but what their life expectancy is, what other competing risks they may have, and what their functional status and everyday activities are," Han observed.

Moreover, "for older adults, taking another medicine every day for the rest of your life isn't a small thing, especially if you have other chronic conditions, and right now we don't have any evidence that there's any benefit to doing so if you do not have any history of cardiovascular disease."

An editor's note accompanying the ALLHAT-LLC report points out the potential risks of extending statins to groups that may be unlikely to benefit clinically^[3]. For example, statin therapy may be associated with myopathy, myalgias, muscle weakness, and arthropathies, notes Dr Gregory Curfman (Harvard Medical School, Boston, MA).

"These disorders may be particularly problematic in older people and may contribute to physical deconditioning and frailty. Statins have also been associated with cognitive dysfunction, which may further contribute to reduced functional status, risk of falls, and disability," he writes.

"The combination of these multiple risks and the ALLHAT-LLT data showing that statin therapy in older adults may be associated with an increased mortality rate should be considered before prescribing or continuing statins for patients in this age category."

Is There a "Point of No Return"?

"It takes decades for the plaque to build up in the arteries that eventually causes strokes and heart attacks. Data from thousands of adults studied in clinical trials show us that statins, when started early, can interrupt or slow down that process," according to Navar.

But, "we don't know if there is a 'point of no return' where it's too late to start a statin, and ALLHAT was not designed to answer that question. We need a large randomized trial to really know how effective statins are when started in older adults without cardiovascular disease," she said.

"There is a lot of negative press about statins, and I really worry about the effect of studies like these on the public's perception. This study was a secondary analysis of a trial that was not designed to study the effect of statins in older adults," Navar observed.

"Data from thousands of adults in multiple randomized trials have shown that statins prevent heart disease and do not kill people. I hope that the media, in the never-ending search for clickbait, doesn't overemphasize the statistically nonsignificant mortality trend and lead people who are known to benefit to discontinue their statins."

The study was funded by the National Heart Lung & Blood Institute. Study medications were contributed by Pfizer, AstraZeneca, and Bristol-Myers Squibb, and financial support was provided by Pfizer. The study authors and Curfman report no relevant financial relationships. Navar reported research support from the National Institutes of Health, Amgen, and Sanofi & Regeneron Pharmaceuticals and serving as a consultant for Amgen and Sanofi.
Read the full article here.

Thousands of Women in Lipitor diabetes Lawsuit - Liebhard

Thousands of Women in Lipitor Lawsuit Claims to Join South Carolina Litigation, Status Report Shows

Published on June 16, 2014 by Sandy Liebhard 

More than a hundred cases filed by some 3,000 female Lipitor lawsuit plaintiffs will soon join the federal diabetes drug litigation in the U.S. District Court, District of South Carolina, according to court documents.

A status report recently submitted by parties involved in the federal litigation indicates that 134 cases alleging new-onset Type 2 diabetes will be transferred to the multidistrict litigation in the coming weeks, on behalf of 3,000 plaintiffs.

According to Lipitor lawsuits included in the soon-to-be transferred claims, use of the cholesterol medication, may increase a woman’s likelihood of developing Type 2 diabetes, which its manufacturer allegedly knew about but concealed from the public. Lipitor diabetes lawsuits included in the federal proceeding, which was created by the U.S. Judicial Panel on Multidistrict Litigation (JPML) less than six months ago, include similar actions against Pfizer Inc. that accuse the company of marketing a product that was designed defectively.

A Case List updated June 16th by the JPML also shows a continued increase in the number of Lipitor lawsuits filed in South Carolina federal court. An update posted that day reflects 846 cases now pending in the federal litigation, which held its most recent status conference on June 13th. A month earlier, a total of 703 claims had been filed in South Carolina.

More than 840 Claims Now Filed in Lipitor Diabetes Litigation

Lipitor is a medication approved by the U.S. Food and Drug Administration (FDA) to help lower cholesterol levels in individuals who may be at an increased risk for strokes and heart attacks.
Since entering the market in 1996, the FDA issued a mandate in February 2012 that required Pfizer to adjust Lipitor’s labeling to include its possible association with Type 2 diabetes.  This action was prompted by research published a month earlier in JAMA: Internal Medicine that found post-menopausal women at an increased risk for developing the disease. In May 2013, results of a study published in the British Medical Journal showed a 22 percent increased risk for Type 2 diabetes in patients taking atorvastatin, the generic version of Lipitor.
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Read the complete article here.

UPDATE:

Pfizer confronts surge of lawsuits over Lipitor

By Jessica Dye

Fri Aug 8, 2014 1:22am EDT

Merck Uses Legal Threats To Stifle Negative Advice About Zetia And Vytorin

Merck Uses Legal Threats To Stifle Negative Advice About Zetia And Vytorin In Italy

   

 

In response to repeated legal threats, a public health doctor in Italy has withdrawn advice to curtail use of a controversial drug. The drug, ezetimibe, is a key ingredient in Zetia and Vytorin, which is manufactured by Merck Merck. The cholesterol-lowering drug has been the subject of fierce controversy because it has never been shown to improve clinical outcomes. Despite the controversy, in 2013 the drugs had combined sales of more than $2.6 billion.
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Read the complete article here.

Statins linked to lower physical activity - Clinical Endocrinology

Statins linked to lower physical activity

By: MARY ANN MOON, Clinical Endocrinology News Digital Network - Jun 9, 2014

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FROM JAMA INTERNAL MEDICINE

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Vitals

 

Key clinical point: Statin use in older men may have the consequence of reducing their physical activity.

 

Major finding: Statin users engaged in 9.6% fewer minutes of moderate physical activity and 9.0% fewer minutes of vigorous activity per day than did nonusers, as well as 1% more minutes per day of sedentary behavior, than men who didn’t use statins. This equates to a mean decrease of approximately 151 minutes/week of walking and 37.8 minutes/week of more vigorous exercise, and an increase of 21.8 hours/week in sedentariness, for the statin users.

 

Data source: An observational study with both cross-sectional and longitudinal components, involving 4,137 U.S. men aged 65 years and older, of whom about one-fourth used statins throughout the 7-year study period.

 

Disclosures: This study was funded by the Medical Research Foundation of Oregon; the MrOS study was supported by the National Institutes of Health. Dr. Lee and his associates reported no potential financial conflicts of interest.

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View on the News
 Weighing harms and benefits
 

Initiating statin therapy in older men was associated with a modest but significant drop in physical activity, according findings from a large, observational study published online June 9 in JAMA Internal Medicine.

 

In addition, older men who used statins showed lower activity levels and higher levels of sedentariness than did nonusers, for as long as they took the drugs. Although results of an observational study such as theirs cannot prove causality, it is likely that the statins’ well-known adverse effects of inducing muscle pain, myopathy, and muscular fatigue account for these differences, said David S.H. Lee, Pharm.D., Ph.D., of Oregon State University/Oregon Health and Science University, Portland, and his associates.

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Read the complete article here.

CTT the house of statin secrets - Burne

SOS: Sanity over Statins – CTT the house of statin secrets

by Jerome Burne

Should a professional body, however eminent, be allowed to keep information about the safety of products they are supplying to public hidden so no one else can run tests on them?

That is the question raised by HealthInsightUK’s finding that a large and respected organisation whose job it is to analyses the findings of statin trials – The Cholesterol Treatment Trialists’ (CTT) Collaboration in Oxford – has an agreement to keep secret much of the information contained in its huge database which holds results from 27 trials of these drugs, nearly each of which was run by a drug company.

Questions about the secrecy of the CTT have been put in the spotlight following the recent recommendation by NICE to change the guidelines on statins. If the proposals are accepted, millions more healthy people in the UK who have no sign of heart disease will be prescribed these drugs. A key part of the evidence supporting this proposal was a study by CTT published in the Lancet in 2012.

HealthInsightUK has also established that the CTT do not hold data on the side-effects of statins. A spokesman confirmed that they base their estimate of risk on the published results of trials conducted by the drug companies. He dismissed claims that side-effects such as muscle pain and depression were wide spread, saying they were only “hypotheses”.

Denied access to data

This could explain why the CTT has regularly reported a much lower rate of side-effects than trials run by independent researchers. Knowing the true rate of side-effects is particularly important with statins because many patients have to take them for one to benefit. If the estimate of side effects is too low the benefits may not outweigh the risks.

Concern about the secrecy surrounding CTT’s data is not new. Dr Jim Wright editor of the highly respected and independent journal Canadian Therapeutics Initiative which analyses drug studies has described how several years ago he had tried and failed to get access to statin data held by CTT.
“They had agreed someone from my team could have access to their data, although the researcher would have to go to Oxford to see it. However after travelling 6000 miles, they were told that the data was not available.”

This is just an anecdote but many others have since reported the same thing. The latest concern about access to CTT data was triggered last year when the Cochrane Collaboration – famed for its rigorous assessment of the benefit of drugs and other treatments – produced a report saying that statins should be more widely used on people without heart disease. The report was heavily based on the CTT Lancet study. Was it actually possible to check their findings?

Everyone wanted the data

A number of senior researchers approached by HealthInsight have supported Dr Wright’s claim that the data held by CTT hasn’t been available. Professor Rita Redberg cardiologist and editor of the journal JAMA Internal Medicine, has stated in an email that: “CTT will not make their data available to any colleagues and other researchers who wish to study risks and benefits of statins. The CTT data is not accessible publicly.”

“I have not requested access to the CTT data,’ says Dr David H. Newman, Director of Clinical Research, Mount Sinai School of Medicine, New York.

‘However, I’m not aware of anyone who has gained access to these data, which speaks volumes since everyone has wanted it. For the science to be considered even potentially credible, another independent group will have to replicate their analysis.”

Professor Harriet Rosenberg of the Health and Society Program at York University in Toronto commented that: “many scholars have asked the CTT for data without success” in a formal reply to the Cochrane review last year.

The response by the CTT when such individual claims are made is to say that anyone with a well formulated proposal can get access to their data. But emails seen byHeathinsightUK throw doubt on that. They were exchanged between one of CTT’s top researchers Professor Colin Baigent and an Australian TV journalist researching a story about statins.
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Read the complete article here.

Ezetimibe Prescribing Fails to Keep Up With Evidence - JAMA

Ezetimibe Prescribing Fails to Keep Up With Evidence     

Mike Mitka, MSJ 

             

JAMA. Published online March 19, 2014. doi:10.1001/jama.2014.2896

          

 

Although physicians like to think they practice evidence-based medicine, that appears to not be the case with prescribing the cardiovascular drug ezetimibe. And some critics say that use of surrogate markers to guide practice rather than clinical outcomes such as occurrence of myocardial infarction, stroke, or death has likely played a role.

 

Ezetimibe is an intestinal cholesterol absorption inhibitor found to reduce low-density lipoprotein cholesterol (LDL-C) levels by about 20% when given alone. It also further reduces LDL-C levels when added to statin therapy, which blocks cholesterol synthesis in the liver by inhibiting HMG-CoA reductase.

 

The Food and Drug Administration approved ezetimibe in 2002 for use in the United States primarily because it lowered LDL-C levels, a surrogate marker for prevention of cardiovascular disease. Whether ezetimibe improved clinically meaningful outcomes remained a question.

 

That question was somewhat answered in January 2008, with the announcement that the Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression (ENHANCE) trial, sponsored and conducted by industry, found that the addition of ezetimibe failed to reduce atherosclerosis progression compared with simvastatin alone, despite lowering LDL-C levels. Atherosclerosis progression was determined by a change in the intima-media thickness of the walls of the carotid and femoral arteries—yet another surrogate end point (Kastelein JJP et al. N Engl J Med. 2008;358[14]:1431-1443).

Place holder to copy figure label and caption

Graphic Jump Location

US and Canadian physicians continue to prescribe ezetimibe even after a study found giving the drug with a statin failed to reduce atherosclerosis progression compared with the statin alone.

 

 

The ENHANCE result prompted some leaders in the cardiology community to question ezetimibe’s place in cardiovascular disease treatment. Harlan Krumholz, MD, professor of medicine and epidemiology and public health at Yale University in New Haven, Connecticut, said the study should change practice. “Although not definitive, [ENHANCE] increases our uncertainty about the clinical value of this novel drug. Without some evidence of improved outcomes associated with its use, ezetimibe should be relegated to a last option for patients who need medication for hypercholesterolemia, and even in these cases, it is reasonable for clinicians and their patients to wait for further information before considering it,” he wrote in NEJM Journal Watch (http://tinyurl.com/pk9xr29).

 

So did the ENHANCE results change practice? In the United States, the answer is “somewhat,” while in Canada, the answer appears to be “no.”

 

In a study published in the American Heart Journal, researchers looked at ezetimibe prescription trends before and after ENHANCE, using data collected from CompuScript in Canada and IMS Health in the United States from January 1, 2002, to December 31, 2009. The researchers found the monthly number of ezetimibe prescriptions per 100 000 population rose from 6 to 1082 in the United States from November 2002 to January 2008 and then declined to 572 per 100 000 population by December 2009, a decrease of 47.1%. In Canada, however, use continuously increased from 2 to 495 per 100 000 from June 2003 (when the drug was approved in Canada) to December 2009 (Lu L et al. Am Heart J. doi:10.1016/j.ahj.2014.01.014 [published online February 27, 2014]).

 

Coauthor Cynthia A. Jackevicius, PharmD, MSc, a professor of pharmacy practice and administration at Western University of Health Sciences in Pomona, California, and an adjunct scientist, Institute for Clinical Evaluative Sciences, in Toronto, said her team was initially surprised by the Canadian results.

 

“Previous findings showed ezetimibe use in Canada experienced a more conservative uptake, so we expected to see a decrease in use in response to the ENHANCE study,” Jackevicius said. “So we looked for different factors, and one is the Canadian lipid guidelines, which specifically said ezetimibe could be added to statins, and that didn’t change after ENHANCE came out.”

A study of ezetimibe use in Saskatchewan, the only Canadian province that lists the drug for open formulary access, even though guidelines say it’s a second-line agent for lowering cholesterol, reflects Jackevicius’s team’s findings. Using data from provincial health administrative databases, the Saskatchewan researchers found that ezetimibe prescriptions were 2.5% of cholesterol-lowering dispensations in 2004 and 8.8% of such dispensations in 2011 (Alsabbagh WM et al. Can J Cardiol. 2014;30[2]:237-243). The authors concluded that allowing unrestricted use of ezetimibe in Saskatchewan may have led to a large number of inappropriate prescriptions, at odds with Canadian clinical guidelines.

 

And although ezetimibe use declined in the United States, its use per 100 000 population is still greater than Canada’s, generating US expenditures of more than $2.2 billion in 2009.

 

Krumholz, one of the coauthors on the study with Jackevicius, remains perplexed as to the continuing popularity of ezetimibe. “The drug continues to defy gravity, and that’s probably a result of really strong marketing and the singular focus on cholesterol numbers,” he said.

 

Krumholz said heart health campaigns urging patients to “know your numbers” and treatment goals based on cholesterol measurements, such as getting asymptomatic individuals’ LDL-C levels below 130 mg/dL, have worked in ezetimibe’s favor at the expense of evidence-based medicine. “Is this the drug that lowers your LDL-C and helps you? We don’t know that,” he said. “The comfort of hitting a target offers little benefit if you don’t know that it is really protecting you.”

 

Although ENHANCE has not derailed ezetimibe prescribing, the newest cholesterol management guidelines just might. The guidelines, issued late last year by the American College of Cardiology and the American Heart Association, abandon the idea of reaching a target level for LDL-C, instead recommending the use of statins to reduce LDL-C levels only for certain types of patients.

Will this change in the guidelines affect ezetimibe prescribing? “It will be interesting to see what the guidelines will do,” Krumholz said.

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Read the complete article here.

Testosterone and the Heart Part Two - Dach

Testosterone and the Heart Part Two by Jeffrey Dach MD

Posted on November 12, 2013 by Jeffrey Dach

In Part One, we discussed a 2010 study from Boston University in which testosterone was given to immobilized, elderly, obese male smokers.  The study was halted early because of poor outcome with increased heart attacks and “cardiac events”  in the testosterone treated group.

Second Study Shows  Poor Outcome in Testosterone Group

A second study from the University of Texas was just published in JAMA .(2)  This study was done on Veterans undergoing coronary angiography with documented coronary artery disease.  Some of these Veterans had low testosterone levels (below 300) .  These veterans were given testosterone treatment and followed.  At the end of three years of follow up, the untreated men had a  20%  incidence of stroke,  heart attack or death, while the testosterone treated group had a higher 26% incidence.  This is 20% untreated, vs. 26% treated.  Clearly, the testosterone did not miraculously reverse the atherosclerosis disease in this group of veterans.(2-6)

Benefits of Testosterone Clearly Documented in Medical Literature

As discussed in part one, decades of research studies have shown that low testosterone in men is a risk factor for early mortality from cardiovascular disease, and testosterone treatment reduces mortality, especially in the diabetic males. (7-10)

Testosterone Treatment Does Not Reverse Heart Disease

However, it is clear from these two studies that testosterone by itself is insufficient as a therapy to reverse coronary artery plaque in men who have diets and lifestyles which promote heart disease, and who already have significant underlying coronary artery disease.

Left Image logo courtesy of Track Your Plaque Blog.

Track Your Plaque Program

For our office patients who are interested in reversing coronary artery plaque, we use the William Davis MD Track Your Plaque Program. This is an excellent program which is well thought out.  See my article on this: Reversing Heart Disease.


I wonder what the outcome of these two studies would have been if the testosterone treated group had been started on the Track Your Plaque Program which monitors lipo-protein profile and the Calcium Score, and uses diet and lifestyle modification and supplements to reduce Calcium Score and increase LDL particle size.

There are many unanswered questions.  I also  wonder what the Vitamin D levels were, and what the thyroid levels were on these men,   How much trans fats were they consuming?  How much were they smoking and how much alcohol did they consume?  How much overweight were they?

Conclusion

One conclusion seems clear and that is testosterone by itself does not replace the Track Your Plaque Program of Diet, Lifestyle modification and Supplements to reverse heart disease.  As these two studies show, clinical outcomes for Testosterone Treatment may actually be worse for subgroups of men with severe coronary artery disease, especially when no changes are made to the diet and lifestyles that promote heart disease.

Jeffrey Dach MD
7450 Griffin Road, Suite 180/190
Davie, Florida 33314
954-792-4663www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com

Articles With Related Content:

Low Testosterone Diagnosis and Treatment
HCG in Males with Low Testosterone
Testosterone Benefits, PSA and Prostate Part One
Testosterone and PSA Part Two
Clomid for Men with Low Testosterone Part One
Low Testosterone From Pain Pills
Low Testosterone Associated with Increased Mortality
Testosterone Reduces Mortality
Testosterone Blockade Increases Mortality
Testosterone Found Beneficial For Diabetes

Links and References:
(1)http://www.ncbi.nlm.nih.gov/pubmed/20592293
N Engl J Med. 2010 Jul 8;363(2):109-22. Epub 2010 Jun 30.
Adverse events associated with testosterone administration.
Basaria S, Coviello AD, Travison TG, Storer TW, Farwell WR, Jette AM, Eder R, Tennstedt S, Ulloor J, Zhang A, Choong K, Lakshman KM, Mazer NA, Miciek R, Krasnoff J, Elmi A, Knapp PE, Brooks B, Appleman E, Aggarwal S, Bhasin G, Hede-Brierley L, Bhatia A, Collins L, LeBrasseur N, Fiore LD, Bhasin S. Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts 02118, USA.
2) http://jama.jamanetwork.com/article.aspx?articleID=1764051  Association of Testosterone Therapy With Mortality, Myocardial Infarction, and Stroke in Men With Low Testosterone Levels  by Rebecca Vigen, MD, MSCS1; Colin I. O’Donnell, MS2,3; Anna E. Barón, PhD2,3; Gary K. Grunwald, PhD2,3; Thomas M. Maddox, MD, MSc2,3,4; Steven M. Bradley, MD, MPH2,3,4; Al Barqawi, MD3; Glenn Woning, MD3; Margaret E. Wierman, MD2,3; Mary E. Plomondon, PhD2,3,4; John S. Rumsfeld, MD, PhD2,3,4; P. Michael Ho, MD, PhD2,3,4  The University of Texas at Southwestern Medical Center, Dallas 2VA Eastern Colorado Health Care
JAMA. 2013;310(17):1829-1836.
3) http://health.clevelandclinic.org/2013/11/concerns-raised-about-testosterone-therapy/  Concerns Raised about Testosterone Therapy Study: testosterone replacement linked to heart risks By Steven Nissen, MD | 11/8/13 2:26 p.m.
4) Testosterone treatments linked with heart riskshttp://www.thetowntalk.com/viewart/20131112/LIFESTYLE/311130006/Testosterone-treatments-linked-heart-risks
5) http://online.wsj.com/news/articles/SB10001424052702303661404579180294201174958  Testosterone Therapy Tied to Heart Risks
Veterans With History of Heart Disease Had Higher Risk of Death, Heart Attack and Stroke, According
6) http://www.latimes.com/science/sciencenow/la-sci-heart-disease-testosterone-replacement-20131105,0,3592717.story  Testosterone medication may boost risk of heart attack, stroke, death
7) http://www.ncbi.nlm.nih.gov/pubmed/22496507  J Clin Endocrinol Metab. 2012 Jun;97(6):2050-8. doi: 10.1210/jc.2011-2591. Epub 2012 Apr 11.  Testosterone treatment and mortality in men with low testosterone levels. Shores MM, Smith NL, Forsberg CW, Anawalt BD, Matsumoto AM.
Source  Veterans Affairs Puget Sound Health Care System, 1660 South Columbian Way, S-116PES, Seattle, Washington 98108, USA.
8) http://www.endocrine-abstracts.org/ea/0025/ea0025p163.htm
Endocrine Abstracts (2011) 25 P163
Low testosterone predicts increased mortality and testosterone replacement therapy improves survival in men with type 2 diabetes
Vakkat Muraleedharan1,2, Hazel Marsh1 & Hugh Jones1,2
9) http://www.ncbi.nlm.nih.gov/pubmed/23999642
Eur J Endocrinol. 2013 Oct 21;169(6):725-33. doi: 10.1530/EJE-13-0321. Print 2013.
Testosterone deficiency is associated with increased risk of mortality and testosterone replacement improves survival in men with type 2 diabetes.
Muraleedharan V, Marsh H, Kapoor D, Channer KS, Jones TH.
Source  Robert Hague Centre for Diabetes and Endocrinology, Barnsley Hospital NHSFT, Gawber Road, Barnsley S75 2EP, UK.
Jeffrey Dach MD
7450 Griffin Road, Suite 180/190
Davie, Florida 33314
954-792-4663
www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com
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Read the complete article here.

Getting Off Statin Drug Stories - Dach

Getting Off Statin Drug Stories by Jeffrey Dach MD

Left Image: courtesy of Uffe Ravnskov, MD Fat and Cholesterol are Good for You.Book Cover

Just Ask Judith Walsh MD in JAMA

 

 

Getting Off Statin Drug Stories
by Jeffrey Dach MD
Case Number One, Martha
Martha is 55 years old, healthy and no history of heart disease.  Nonetheless, Martha has been taking a statin drug for “high cholesterol” under the care of “the top cardiologist” in South Florida for the past five years.  Martha has also been under my care taking a bioidentical hormone program for menopausal symptoms, and doing very well.  Every six months, we run a lab panel which always shows  low cholesterol of 170, courtesy of her statin anti-cholesterol drug.


 And, every time Martha comes into the office to review her lab results, I print out a 2004 JAMA article by Judith Walsh, MD who reviewed thirteen statin drug clinical trials from 1966 to 2003.(1)  Dr. Judth Walsh concludes that cholesterol lowering drugs provide no health benefit for women.  I give her this article and, at the same time, explain to her that no woman should be on a statin drug.  Lowering cholesterol with a statin drug has no health benefit for women, that’s a fact, and public information readily available.

Playing Games With Statins

Every six months I recommend to Martha stopping the statin drug, and every six month, her cardiologist puts her back on the statin drug.  This has been going on for three years now.

Finally Success At Convincing Martha to Stop the Statin Drug

Finally this last time, Martha seems more receptive to idea that the statin drug is harming her and not helping her.  She is sitting in my office recounting multiple health problems for which she sees numerous doctors: back pain, asthma, sinus infections, skin problems, and allergies.  I suggested to Martha the possibility that many of her health problems are  caused by the low cholesterol from the statin drug.  Martha finally sees the light, goes home and tosses the bottle of pills into the garbage can.

Feeling Better

About a week later, Martha called me and reported, “I feel so much better off that statin drug, thank you so much! “.  Apparently, the statin drug was causing adverse health effects, and Martha was now feeling much better.

Believing in the Propaganda
This case illustrates the difficulty in convincing patients to stop their statin drug.  It is difficult to counter the drug company propaganda, and convince these patients they are harming their health with the statin drugs. Many continue to believe in the myth that cholesterol causes heart disease, and they go on to become statin drug medical victims.  I see them every day.  When we have a success like Martha who finally gets off her statin drug, this is a cause for celebration.


Left Image: Ignore the Awkward.: How the Cholesterol Myths Are Kept Aliveby Uffe Ravnskov MD

Case Number Two – Roger
Roger is a seventy one year old retired executive, and an avid tennis player.  He has no history of coronary artery disease and has always been healthy. Two years ago, his cardiologist said his cholesterol of 210 was “too high”, and prescribed a statin anti-cholesterol drug.  A year later, Roger’s tennis game deteriorated, he found his timing and balance was off, and he lost every game to players who could never beat him before.

Adverse Effects of the Statin Drug

I suggested to Roger that the decline in his tennis game was most likely an adverse effect of the statin drug on his muscle and nerve function.  He was losing his balance and coordination. 

I recommended stopping the statin anti-cholesterol drug.  At first, Roger resisted and said his wife wanted him to take the statin drug because she thought it was ”good medical care”, and she (mistakenly) believed that a lower cholesterol was somehow preventive of heart disease.

How to Counter the Propaganda: A Book For You
In order to counter the drug company cholesterol propaganda, I gave Roger a copy of the book, Fat and Cholesterol are Good for You, by Uffe Ravnskov MD PhD. This book reviews the medical studies which supposedly show that cholesterol is the cause of heart disease, and reveals that they do no such thing. This is a medical myth.  Neither cholesterol consumption nor cholesterol blood levels cause heart disease.  Similarly, many medical studies demonstrate that anti-cholesterol drugs work very well to reduce blood cholesterol levels, however, this treatment does not prolong life and makes most people sick with adverse side effects.

Roger was amazed and his eyes practically popped out out of his head when he “saw the light”.  The statin drugs were turning him another medical victim.  Once Roger learned the truth about the ”cholesterol causes heart disease” myth,  he took his statin drug bottle and threw it into the garbage can.  Two weeks later, off the statin drug,  Roger was back to his old self, prancing about the tennis court like a gazelle, and winning every game with ease.


Left Image : The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease by Uffe Ravnskov MD
 Are You Still a Believer in Anti-Cholesterol Drugs?

If you are still a believer in Statin Drugs, take a look at this primary prevention study published July 2010 in the Archives of Internal Medicine by Dr. Ray.(3)  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 ! (3)  There was no benefit from the statin drugs !!!  This article was published in the mainstream medical literature !!


If cholesterol was truly the cause of heart attacks, then one would expect heart attack victims to reveal the high cholesterol causing their heart attack.   They found the opposite.  Heart attack victims have low cholesterol.  A study  analyzed 137,000 heart attack patients from 541 US hospitals and found mean cholesterol was only 174.  This is low, not high. (4)

In addition, if high cholesterol was truely the cause of heart attacks, one would expect heart attack victims with the highest cholesterol to have the worst prognosis, and lowest cholesterol to have the best prognosis.  They don’t.  A study from Henry Ford Hospital in Detroit showed that three years after a heart attack, the patients with lowest cholesterol had the highest mortality (14% vs. 7 %) (5).

Conclusion:

The cholesterol theory of heart disease is a myth maintained by drug company propaganda to support massive profits from cholesterol lowering drugs.  These drugs provide no health benefit in terms of prolonging life, and at the same time produce harm from adverse side effects.  Avoid becoming a victim of the statin drug propaganda machine.

Articles with related interest:
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
How to Reverse Heart Disease with the Coronary Calcium Score
Cholesterol Lowering Drugs for the Elderly, Bad Idea
Cholesterol Lowering Statin Drugs for Women Just Say No
…………………………………………………………………………………………………….

Heart Disease Part Two – Atherosclerosis: How Does it Happen?Preventing and Reversing Heart Disease Part Three by Jeffrey Dach MDHeart Disease, Ascorbate, Lysine and Linus Pauling by Jeffrey Dach MDA Choirboy for Cholesterol Turns Disbeliever by Jeffrey Dach MD
Links and References
(1) http://jama.ama-assn.org/content/291/18/2243
JAMA. 2004;291(18):2243-2252. Drug Treatment of Hyperlipidemia in Women
Judith M. E. Walsh, MD, MPH; Michael Pignone, MD, MPH
(2) Fat and Cholesterol are Good for You, Uffe Ravnskov GB Publishing (January 26, 2009)
(3) http://archinte.ama-assn.org/cgi/content/abstract/170/12/1024
Statins and All-Cause Mortality in High-Risk Primary Prevention A Meta-analysis of 11 Randomized Controlled Trials Involving 65 229 Participants. Kausik K. Ray, MD, MPhil, FACC, FESC; Sreenivasa Rao Kondapally Seshasai, MD, MPhil; Sebhat Erqou, MD, MPhil, PhD; Peter Sever, PhD, FRCP, FESC; J. Wouter Jukema, MD, PhD; Ian Ford, PhD; Naveed Sattar, FRCPath. Arch Intern Med. 2010;170(12):1024-1031.
Background  Statins have been shown to reduce the risk of all-cause mortality among individuals with clinical history of coronary heart disease. However, it remains uncertain whether statins have similar mortality benefit in a high-risk primary prevention setting. Notably, all systematic reviews to date included trials that in part incorporated participants with prior cardiovascular disease (CVD) at baseline. Our objective was to reliably determine if statin therapy reduces all-cause mortality among intermediate to high-risk individuals without a history of CVD.
Data Sources  Trials were identified through computerized literature searches of MEDLINE and Cochrane databases (January 1970-May 2009) using terms related to statins, clinical trials, and cardiovascular end points and through bibliographies of retrieved studies.
Study Selection  Prospective, randomized controlled trials of statin therapy performed in individuals free from CVD at baseline and that reported details, or could supply data, on all-cause mortality.
Data Extraction  Relevant data including the number of patients randomized, mean duration of follow-up, and the number of incident deaths were obtained from the principal publication or by correspondence with the investigators.
Data Synthesis  Data were combined from 11 studies and effect estimates were pooled using a random-effects model meta-analysis, with heterogeneity assessed with the I2 statistic. Data were available on 65 229 participants followed for approximately 244 000 person-years, during which 2793 deaths occurred.
The use of statins in this high-risk primary prevention setting was not associated with a statistically significant reduction (risk ratio, 0.91; 95% confidence interval, 0.83-1.01) in the risk of all-cause mortality. There was no statistical evidence of heterogeneity among studies (I2 = 23%; 95% confidence interval, 0%-61% [P = .23]).
Conclusion  This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up.
(4) http://www.ahjonline.com/article/S0002-8703(08)00717-5/abstract
AHJ Volume 157, Issue 1, Pages 111-117.e2 (January 2009)
Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines. Amit Sachdeva, MDa, Christopher P. Cannon, MDb, Prakash C. Deedwania, MDc, Kenneth A. LaBresh, MDd, Sidney C. Smith Jr, MDe, David Dai, MSf, Adrian Hernandez, MDf, Gregg C. Fonarow, MDa, on behalf of the GWTG Steering Committee and Hospitals
(5) http://www.ncbi.nlm.nih.gov/pubmed/19437396
Cardiol J. 2009;16(3):227-33. Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction. Al-Mallah MH, Hatahet H, Cavalcante JL, Khanal S.
Abstract
BACKGROUND: The relationship between admission low-density lipoprotein (LDL) levels and long-term outcomes has not been established in patients with acute coronary syndrome. We tested the hypothesis that patients who develop non-ST segment elevation myocardial infarction (NSTEMI) despite low LDL have a worse cardiovascular outcome in the long term.
METHODS: Patients admitted with NSTEMI between 1 January 1997 and 31 December 2000 and with fasting lipid profiles measured within 24 hours of admission were selected for analysis. Baseline characteristics and 3-year all-cause mortality were compared between the patients with LDL above and below the median. Multivariate analysis was used to determine the predictors of all-cause mortality, and adjusted survival was analyzed using the Cox proportional hazard model.
RESULTS: Of the total of 517 patients, 264 had LDL dL and 253 had LDL > 105 mg/dL. There was no difference in age, gender, severity of coronary artery disease, and left ventricular ejection fraction between the 2 groups. Thirty-six percent of patients with LDL 105 mg/dL were on lipid-lowering therapy on admission.
After 3 years, patients with admission LDL dL had higher all-cause mortality rate compared to patients with LDL > 105 mg/dL (14.8% vs. 7.1%, p = 0.005). The higher all-cause mortality persisted (OR 1.8, 95% CI 1.0-3.5, p = 0.05) even after adjustment for confounding variables.

CONCLUSIONS: In our cohort, lower LDL-cholesterol at admission was associated with decreased 3-year survival in patients with NSTEMI.

Jeffrey Dach MD
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The controversial study that started the War on Cholesterol - Watson

The controversial study that started the War on Cholesterol…

      

Alan Watson | June 14, 2012   

Revisiting the Coronary Primary Prevention Trial (CPPT) – 1973 to 1984

Using "relative risk statistics" and changing the study's design, the CPPT researchers declared success and the War on Cholesterol began in earnest

 

Launched in 1973 by the National Institutes of Health, the Coronary Primary Prevention Trial (CPPT) set out to prove that lowering blood cholesterol with a drug and a low cholesterol, low saturated fat diet would reduce the risk of coronary heart disease and extend the lives of the study participants.

(As part of the study, twelve new Lipid Research Clinics were set up by the Heart Institute at large universities throughout the country including Baylor, Stanford, Johns Hopkins and the University of Washington in Seattle.)

The researchers were looking for middle-aged men with total cholesterol levels exceeding those of 95 percent of Americans. (Only men with the highest 0.8 percent total cholesterol qualified.) The CPPT researchers screened 480,000 applicants in order to select 3,806 high risk men between the ages of 35 and 59.

This meant that many of the participants had familial hypercholesterolemia, a rare genetic defect in cholesterol metabolism present in about 1 percent of the population. The trials chance of success was therefore greatly increased by focusing on this particular group of presumably vulnerable men.
In their preliminary report, CPPT researchers announced that they would study two separate outcomes:  (1) Nonfatal heart attacks and (2) fatal heart attacks or deaths from coronary heart disease. The CPPT directors emphasized that they would be satisfied with nothing less than the strongest statistical proof of their findings; they had to be “99 percent certain that the results were not due to chance.”

The researchers also announced their goal of reducing blood cholesterol in the treatment group by 25 percent and reducing the risk of heart disease in the treatment group by at least 50 percent.
Approximately half of the 3,806 men were provided low cholesterol, low saturated fat dietary advice and were treated with cholestyramine, a cholesterol-lowering bile acid resin (Questran).

(Cholestyramine lowers cholesterol by interfering with digestion. Statins such as Lipitor, Mevacor and Zocor were not available yet.)

The control group was provided the same dietary advice and an unpleasant tasting placebo – an indigestible mixture of sand, sugar and food coloring. Both trial groups suffered with moderate to severe gastrointestinal distress. There were eight gastrointestinal cancer deaths in the treatment group (out of 21 cases) and one in the placebo group (out of 11 cases).

(There were more deaths from cancer, intestinal disease, stroke, violence and suicide in the group taking the cholesterol-lowering drug, and overall mortality was essentially the same for both groups.)

Disappointing Results

In 1984, the disappointing results were tabulated. Cholesterol levels in the treatment group had decreased by no more than 7 percent. Cholestyramine and the low cholesterol, low saturated fat diet had failed to lower cholesterol enough to prove that lowering cholesterol would reduce the risk of heart disease and extend the lives in the treatment group.

The difference in nonfatal heart attacks was not statistically significant. In the treatment group, 130 participants (6.8 percent) had a heart attack versus 158 in the placebo group (8.3 percent). After 7 years, the fraction of the treatment group that had benefited was less than 2 percent.

                                       Nonfatal heart attacks               Fatal heart attacks/coronary deaths
1,900 Control Group:         158 or 8.3 percent                               38 or 2.0 percent
1,906 Treatment Group:     130 or 6.8 percent                              30 or 1.6 percent

The difference in fatal heart attacks was not significant either. In the treatment group, 30 participants (1.6 percent) suffered a fatal heart attack compared to 38 in the placebo group (2.0 percent) Again – after 7 years of taking an unpleasant drug (and following a low fat diet), the fraction of the treatment group that benefited was less than 1 percent.

However, by applying relative risk statistics (a percentage of a percentage), the CPPT researchers improved their results. They took the number of people who presumably didn’t have a heart attack because of taking the drug (28) and looked at it as a percentage of the people who did have heart attacks (158) but didn’t take the drug:

The less than 2 percent absolute difference in nonfatal heart attacks rose to a reported 19 percent reduction in risk of a heart attack!

 

In similar statistical fashion, the researchers announced a 24 percent reduction in the risk of dying from a heart attack. The 8 men or 1.6 percent out of 1,900 who presumably did not have a fatal heart attack because they took the drug became the same 24 percent who reduced their risk of mortality compared to those in the control group who did die (38) but did not take the drug.

Additional study design changes

To prop up their victory, the CPPT researchers decided to exclude  “uncertain” nonfatal heart attacks from the treatment group while including  “uncertain” fatal heart attacks in the placebo group. Also, using the original 99 percent standard, the small favorable trend in either group could only be explained by chance (as defined by the researchers themselves at the start of the trial.)
By applying the less stringent 95 percent standard and by combining the two groups into one (nonfatal and fatal heart attacks), the CPPT researchers improved their results – declared victory – while the press responded with unbridled enthusiasm.

In 1984, the press and medical journals portrayed CPPT as the long sought proof that animal fats were the cause of heart disease. It was widely reported that for the first time:

“It had been proven that lowering cholesterol would reduce the mortality from heart disease and lower the risk of having a heart attack.”

 

Much of what we hear today about diet and heart disease can be traced back to this notorious failed study. When other scientists voiced their objections to the trial’s design changes, the CPPT directors simply denied that they had ever embraced the original more stringent standards.

In January 1984, the Journal of the American Medical Association (JAMA) dutifully reported:

“The trial’s implications…could and should be extended to other age groups and women, and to others with more modest elevations of cholesterol levels. The benefits that could be expected from cholestyramine treatment are considerable.”

 

George Mann, M.D., professor in medicine and biochemistry at Vanderbilt University, severely criticized the CPPT directors and the trial’s unsupportable results:

“The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant…”

 

 Giving cholestyramine for over seven years to 1,906 middle age men – many with a genetic predisposition to atherosclerosis – had only saved the lives of eight but the Heart Institute was now recommending that cholesterol-lowering drug treatment be extended to patient groups that had not been part of the trial.

Even without the solid evidence they sought, the medical elite in the American Heart Association and the National Institute of Health decided to push ahead with cholesterol-lowering drugs and the still unproven low cholesterol, low saturated fat diet:

 “Now we have proved that it is worthwhile to lower blood cholesterol; no more trials are necessary. Now is the time for treatment.”

 

 The long War on Cholesterol had begun
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Statins do not help you live longer – or do anything much else for that matter - Kendrick

Statins do not help you live longer – or do anything much else for that matter

  

Sometimes you read a thing quickly, and then you have to read it again to make sure you read it right. Yesterday I was sent a copy of a ‘Patient page’ from the Journal of the American Medical Association (JAMA).  The page was from the April 3^rd 2013 edition, pp 1419. It is stamped ‘JAMA – copy for your patients’. JAMA is one of the highest impact medical journals in the world.

This patient page states that:

‘One question involves disagreement about whether the statin side effects are merely uncomfortable or actually pose significant health risks. The other question is whether reducing bad cholesterol will actually help you live longer than you otherwise would. Some of this disagreement involves how physicians interpret the results of studies. However, a 2010 analysis combined the results of 11 studies and found that taking statins did not lower the death rate for people who did not have heart disease. If your physician recommends taking a statin, talk to him or her about the risks and benefits for your individual situation.’

 

For many years I have been ridiculed by colleagues for saying that, if you do not already have established heart disease, statins do not increase your life expectancy. By which I mean that they don’t’ actually work. ‘Don’t be ridiculous.’ Is what they exclaim to me. I usually reply that the evidence is pretty clear, and always has been. But I know that they don’t believe me.

Recently, without warning, one of the most influential medical journals in the world turned round and confirmed it. JAMA has stated in black and white that if you do not have established heart disease e.g. angina, previous heart attack, you will not live any longer if you take a statin.

Frankly, I think JAMA will now come under ever increasing bombardment from the ‘experts’ and will end up retracting this statement. In fact, I am willing to bet that they will – having now seen some of the outraged letters sent in. However from time to time the truth – like a small grass shoot growing through a concrete pavement – will emerge. As it did in April.

(I should add, at this point, that around 95% of people who take statins do not have established heart disease.)

However, wrapped up in this issue, is an inevitable argument. I know this argument well, for I have heard it a thousand times. ‘Ah, but it is not just death we are talking about here…. statins prevent non-fatal heart attacks and non-fatal strokes and suchlike. These are terrible things that damage the quality of your life. Medicine is not only about getting people to live longer, it is also about quality of life. Preventing a non-fatal stroke is extremely important, and statins do this.’ In other words, statins don’t make you live longer, but they do provide other, very significant benefits, by preventing Serious Adverse Events (SEAs).

This is a good argument. At least it would be if it were true. However, we have no idea about whether it is true or not. For the simple reasons that the data on SEAs is almost entirely hidden from view. Data on SEAs are considered so commercially sensitive that, in most jurisdictions, pharmaceutical companies won’t release them (and don’t have to release them), even if you ask nicely*.

Before moving onto that issue, I know that I need to explain I am talking about here in a little more detail, and clear up a bit of confusion with the nomenclature. For in the area of adverse events/effects, we have two terms that sound very similar, but mean very different things.

Firstly, there are drug related adverse effects. These are often called ‘side-effects’. But side effects can be good, or bad. For example Viagra was developed as an angina drug but it was found to create enhanced erections, as a side-effect. [You can decide if this is a beneficial side-effect or not]. Viagra also causes headaches. This is also a side-effect, but it would be more accurate to call it a drug related adverse effect.

Drug related adverse effects = negative/unpleasant ‘side-effects’ of a drug
A Serious Adverse Event (SEA) may sound similar to a drug related adverse effect, but it means something completely different. An SEA is a significantly bad thing that a drug might prevent e.g. non-fatal heart attack. Or, it could be something that the drug causes e.g. rhabodmyolysis (muscle breakdown), followed by kidney failure. Which is something that is known to be caused by statins.
SEAs can therefore be good, or bad. Depending on whether they are caused by, or prevented by, the drug. This means that there is absolutely no point in presenting figures on SEAs prevented by statins, without knowing if they caused an equal number of SEAs at the same time.

Completely unsurprisingly, whilst we are bombarded with statistics about how many SEAs are prevented by statins, we have very little idea about how many SEAs are caused by statins. Because in most countries, these data are not released. Its’ commercially sensitive dontcha know. [Damned right it’s commercially sensitive. If the public saw these data they would stop taking half their meds overnight.]

There have, however, been glimpses of SEAs with statins – when the data escaped from the clutches of the pharmaceutical companies. When the Cochrane collaboration fist looked at primary prevention studies, two of the five major studies did report ‘negative’ SEAs (although they did not say what the SEAs were, and still won’t). In these two trials AFCPAS and PROSPER, the SEAs were:

Statin arm:      44.2%Placebo arm:  43.9%

‘In the 2 trials where serious adverse events are reported, the 1.8% absolute reduction in myocardial infarction and stroke should be reflected by a similar absolute reduction in total serious adverse events; myocardial infarction and stroke are, by definition, serious adverse events. However, this is not the case; serious adverse events are similar in the statin group, 44.2%, and the control group, 43.9% This is consistent with the possibility that unrecognized serious adverse events are increased by statin therapy and that the magnitude of the increase is similar to the magnitude of the reduction in cardiovascular serious adverse events in these populations.’  (read more…)

In short there were slightly more SEAs in those taking statins than in those taking placebo. Slightly more harm than good.

So what do we now know? We know that if you do not have established heart disease, and you take a statin, you will:

• not live any longer
• not avoid major Serious Adverse Events

Which means that there is no possible improvement in either the quality, or the quantity, of life. On the other hand there is a good chance that you will suffer from significant adverse effects e.g. muscle pain, joint pain, impotence, stomach upset, rashes etc. etc. On balance therefore we can state that, if you do not have established heart disease, statins provide no benefits on any important outcome. All they can do is to give you adverse effects. ‘Oh boy, that sounds like a great deal doc. Can’t wait, can’t wait, can I get them now?’

*Please see petition that I just put up on my blog. This petition arrived coincidentally as I was writing this article. At present the European Medicines Agency (EMA), will provide SEA data if requested (with huge persistence). The UK authorities will not release these data, nor will the FDA in the states. A recent move by the pharmaceutical industry is now threatening that the EMA will be forced to hide SEAs. ‘Six months ago two US pharmaceutical companies AbbVie and InterMune took a legal action against EMA that has closed down access to all trial data for all drugs for all doctors and researchers anywhere in the world.’

Closed down all access to all trial data for all drugs for all doctors and researchers anywhere in the world.

That statement is worth repeating. Be afraid, be very afraid indeed. And sign the petition please. Oh, and write to your MEP, as I am now doing.
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