Dr. Briffa on statins and cholesterol reduction

Recent review on statins ignores body of evidence that suggests these drugs don’t work through cholesterol-reduction



http://www.drbriffa.com/blog/   November 15, 2010

Recent review on statins ignores body of evidence that suggests these drugs don’t work through cholesterol-reduction

Big cholesterol news emerged last week on the publication (much publicised) of a massive meta-analysis of statin treatment in those at relatively high risk of cardiovascular disease. The idea of this meta-analysis was to assess whether aggressive lowering of cholesterol (specifically LDL-cholesterol) brings additional benefits in terms of cardiovascular disease protection. The meta-analysis included results from a total of 26 trials (involving a total of about 170,000 individuals) [1].

What this meta-analysis found was that more intensive lowering of cholesterol was associated with a reduced risk of ‘vascular events’ such as heart attacks, fatal heart attacks and the most common form of stroke (ischaemic stroke). The authors state that for each 1.0 mmol/L (39 mg/dl) reduction in LDL-cholesterol, risk of vascular events was reduced by about a fifth. They go on to say “reduction of LDL cholesterol by 2-3 mmol/L would reduce risk by about 40-50 per cent.”

Perhaps not surprisingly, this meta-analysis is being used to ram home the conventional view that cholesterol causes cardiovascular disease, and that lower levels of LDL-cholesterol are better. However, there are a number of reasons why this study fails to tell the whole story about statins and cholesterol reduction.

Statin drugs have a number of different mechanisms which might allow them to reduce cardiovascular disease risk in a way which has nothing to do with cholesterol reduction. For example, statins have anti-inflammatory effects, which we would expect to lead to reduced risk of cardiovascular disease. Now, when we intensively lower cholesterol with these drugs, non-cholesterol-related effects (e.g. anti-inflammatory action) will generally be increased too. So, we cannot assume that any additional benefits from more intensive statin therapy have come from more intensive lowering of cholesterol.

In this meta-analysis, the results of a large number of studies was pooled. The problem is, these studies used a range of different drugs at different doses. Sometimes, the drugs were being tested against placebos, and sometimes they were being tested against other drugs. Rarely, two doses of the same drug were tested. Basically, the studies represent a huge hotchpotch of ‘methodologies’ and ‘variables’.

If you really want to take a scientific approach to assessing the role of cholesterol reduction on health, you would ‘control your variables’. This basically means changing only one thing. So, for instance, you could give two groups of people differing doses of the same statin. You could then see if the group on the higher dose had additional benefits, and also see if this appeared to be related to cholesterol reduction or something else. You’d be surprised how rarely such studies are done.

One example of such a study is the so-called TNT study [2]. Here, individuals with heart disease (very high risk of future vascular events) were given either 10 or 80 mg of atorvastatin for an average of about 5 years. The higher dose did lead to lower LDL levels and lower risk of death due to heart-related disease. The absolute reduce in risk was 0.5 per cent, by the way, so nothing to get too excited about. Plus, this study did not report on the non-cholesterol-related effects of the two different dosages, and so it’s impossible to gauge if the relative benefit of the higher dosage was down to LDL reduction and/or something else.

It should also be borne in mind, by the way, that the higher dose of statin in this study (eight times the lower dose, remember) did not lead to a reduction in overall risk of death. In other words, taking 8 times the dose of this drug for five years did not, overall, extend life by a single day, even in individuals at high risk of heart attacks and stroke.

The idea that the anti-inflammatory effects of statins (and not their cholesterol-reducing effects) may be at the heart of their benefits has been bolstered by work focusing on an inflammatory marker known as C-reactive protein (CRP). Statins are known to have the capacity to reduce CRP levels.

In one study [3] assessing the relationship between statin therapy and cholesterol and CRP levels, it was discovered that “Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol.” (emphasis mine).

In another study [4] published in the same edition of the journal, statin therapy and cardiovascular disease risk assessed using ultrasound scanning of the inside of the coronary arteries. It was found that “atherosclerosis regressed in the patients with the greatest reduction in CRP levels, but not in those with the greatest reduction in LDL cholesterol levels.”

In yet another study [5] it was found that when treating with statins, those with the highest levels of inflammatory markers at the start of the study derived the most benefit, irrespective of initial cholesterol
levels.

Evidence that statins don’t work through their cholesterol-reducing effect comes from other evidence, including the findings that:

•Statins substantially reduce the risk of stroke, despite the fact that raised cholesterol levels are a weak or non-existent risk factor for stroke [6,7].

•Statins are claimed to reduce CVD risk in individuals who have ‘normal’ or even ‘low’ cholesterol levels [8].

•More intensive cholesterol reduction does not necessarily lead to improved outcomes [9].

Despite what the authors of the recent Lancet review would have us believe, there is considerable evidence that statins primarily work through mechanism that are independent of their cholesterol-reducing effects.

Stepping aside from the science for a moment, let’s also perhaps inject some common sense. Let us not forget that cholesterol is a natural constituent of the body that is a major component in cell membranes, the brain, steroid hormones (including sex hormones) and vitamin D (which appears to have major disease-protective properties). It simply does not make sense to me that driving levels of this key substance to lower and lower levels if, in and of itself, beneficial to health. We would not make the case for driving levels of, say, sodium to lower and lower levels, would we? Or blood sugar levels?

All rationality and common sense seems to fly out of the window when certain doctors and scientists start talking about cholesterol. And when it comes to the science, it’s clear that many are ignorant of or choose to ignore the stacks of evidence that clearly contradict their stance.

References:

1. Cholesterol Treatment Trialists’ Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet 9 November 2010 [epub ahead of print]

2. La Rosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-35

3. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med 2005;352(1):20-8

4. Nissen SE, et al. Statin therapy, LDL cholesterol, C-reactive protein and coronary artery disease. N Engl J Med. 2005;352(1):29-38

5. Ridker PM, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation. 1998;98(9):839-44

6. Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration. Lancet 1995;346(8991-8992):1647-53.

7. Imamura T, et al. LDL cholesterol and the development of stroke subtypes and coronary heart disease in a general Japanese population: the Hisayama study. Stroke 2009;40(2):382-8

8. Ridker PM, et al, JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-2207

9. Kastelein JJ, et al, ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358(14):1431-1443

More Misleading Information and Propaganda from the British Heart Foundation

Good new article by Justin Smith author of "$29 billion reasons to lie about cholesterol"
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More Misleading Information and Propaganda from the British Heart Foundation

Tuesday, November 9, 2010 at 11:30AM


Here is the latest headline from the British Heart Foundation (BHF):

“Research by BHF-funded scientists has shown that when it comes to cholesterol, ‘lower seems to be better’ for protecting us against heart attacks... The researchers looked at the effects of increasing the dosage of statins, a medicine that reduces cholesterol. They showed that a bigger drop in cholesterol – from more intensive treatment with statins – cut risks even more.”

This refers to a study just released in the Lancet. This study, and the media hype that the BHF have created about it, is nothing more than an attempt to confuse and mislead people.

If you read the headlines and the summary report you could certainly be forgiven for thinking that statins are wonder drugs and cholesterol really is humanity’s nemesis. This study did indeed find a reduction in heart attacks associated with more intensive use of statin drugs. However, there are at least four major reasons why the results are misleading.

The first reason is that the reduction in risk quoted in the interpretation of the study refers to a reduction in LDL cholesterol that is not normally seen in real life. This exaggerates the perceived benefits.

The interpretation refers to reductions in LDL levels of 2-3 mmol/l. The authors state that this reduction in LDL cholesterol would reduce the risk of a vascular event (such as a heart attack) by 40-50 percent.

Well, LDL cholesterol is typically around 2-3 mmol/l anyway, so the suggestion that it could be reduced by 2-3 mmol/l is nonsense – most people would have to be clinically dead to achieve this drastic reduction. So, the suggested risk reduction is completely academic and for most people could never happen.

The second reason is that, as usual, relative percentages are used instead of absolute percentages. This problem is ubiquitous in statin clinical trials and I have commented on it many times before. The risk reductions of 40-50 percent are relative percentages, which can only mislead people. In real terms, the percentages come down to single digits or less.

The third reason is that, as usual, the issue of deaths from all causes is not addressed. Statins can reduce the risk of suffering a heart attack or other cardiovascular event, but at the same time, these drugs can also increase the risk of dying from other causes, and overall, there is usually no net benefit.

There is not much point in taking an expensive medication if the risk for one disease is reduced at the cost of increasing the risk for another disease within the same time period.

I called the BHF today and asked them for the data concerning deaths from all causes. The press office said they didn't know, but they did kindly send me the full report for the study.

In this trial, the risk of dying from any cause was reduced from 2.3 percent to 2.1 percent. So, in real terms, the benefit of more intensive statin use equates to a risk reduction of just 0.2 percent.

But even this meagre 0.2 percent risk reduction may not be experienced by real people who take statins. This issue relates to the fourth problem with this study.

The forth reason why the results are misleading is that the analysis did not distinguish between people at a lower risk for a heart attack and people at a higher risk.

Around 7 million people are taking statins in England alone, and in America it is estimated that more than 20 million people may be taking them. The vast majority of these people are taking statins for primary prevention. This means that they do not have cardiovascular disease but are given the medications in the hope of preventing future disease.

To date, there is no convincing evidence that statins provide any net benefit to people when they are taken for primary prevention - they do not reduce the overall death rate. This was the conclusion of the latest analysis in the Archives of Internal Medicine.

The analysis that the BHF are supporting includes data from higher risk groups - the results do not represent the majority of people who currently take a statin.

Low cholesterol levels associated with depression and other mental health issues

Dr John Briffa has a good article which states in the introductory paragraph...


"I know that some doctors and scientists would have us believe that, where cholesterol is concerned, "lower is better", but I have real difficulty mustering any entheusiasm for this stance. And one major reason for this is the fact that low levels of cholesterol are associated with enhanced risk of death, perhaps most notably from increased risk of cancer."

Please read the complete article here.

The True Cause of Heart Disease – Part Two

"Dr. Dwight Lundell is on the front line fighting a health war. His mission is to find a cure for heart disease. And he believes he has done just that."

Read the full article at Total Health Breakthroughs

It's Those Statins Again !

Good article from

"View from the hill"

Ten Commandments for Avoiding CHD

Not a particularly new article but one I just re-read by Sally Fallon and Mary G. Enig, PhD. It appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2001.

The following excerpt appears well into the article and is a good 'cut-to-the-chase' list to summarize what to do about this scourge. I encourage all who are interested to read the full article found here.

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Ten Commandments for Avoiding CHD

1. Don't smoke. If you find it impossible to quit, at least try to cut back and smoke only additive-free cigarettes. Smokers should avoid polyunsaturated oils at all costs. Saturated fats and vitamins A and D are particularly protective of the lungs.
2. Exercise regularly but you needn't overdo. A brisk daily walk, 10 minutes on the trampoline, swimming, and sports are all appropriate.
3. Avoid overweight by eating nutrient-dense foods and keeping sweets to a minimum, but avoid crash dieting.
4. Don't work too hard. Counteract stress by doing something that you love to do everyday. During periods of unavoidable hardship or loss, increase consumption of foods rich in protective nutrients.
5. As much as possible, avoid exposure to fumes, chemicals, pollutants and pesticides.
6. Avoid all processed foods labeled "lowfat" or that contain polyunsaturated vegetable oils, hydrogenated fats, white flour, refined sugar and additives.
7. Consume high-quality animal products including a variety of seafood and milk, butter, cheese, eggs, meat, fats and organ meats from animals raised on green pasture.
8. Consume a variety of fresh vegetables and fruits, preferably organically grown.
9. Ensure sufficient mineral intake by using whole dairy products; bone broths; and whole grains, legumes and nuts that have been properly prepared to reduce phytic acid and other factors that block mineral absorption.⁴¹
10. Supplement the diet with foods rich in protective factors including small amounts of cod liver oil (vitamins A and D); wheat germ oil (vitamin E); flax oil (omega-3 fatty acids); kelp (iodine); brewers yeast (B vitamins); desiccated liver (vitamin B12); rose hip or acerola powder (vitamin C); and coconut oil (antimicrobial fatty acids).

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Again, please read and learn from the full article.

Dr. Dwight Lundell on omega-3s and CLA

Thursday, September 06, 2007

Dr. Dwight Lundell on omega-3s and CLA

An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."

Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.

In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.

When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.

You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?

In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.

In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.

I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.

Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?

Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.

The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.

Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.

Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.

In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?

My enthusiasm for CLA is based on:

1) Safety―this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.

2) Effectiveness―also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.

Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.

Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.

I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.

From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.

I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?

The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.

Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.

The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.


Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!


More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.

The True Cause of Heart Disease

The True Cause of Heart Disease - Part One of Two

via Total Health Breakthroughs by Ian Robinson on 7/14/10

Conventional wisdom tells us that high cholesterol is the cause of heart disease. But Dr. Dwight Lundell is fighting to expose this dangerous mainstream myth.

Dr. Lundell is a pioneer and leading expert in this field. He has enjoyed a long and a distinguished career, leading his peers to new breakthroughs.. He spent 25 years as a cardiovascular surgeon and performed over 5,000 heart surgeries.

His experience in cardiovascular and thoracic surgery includes certification by the American Board of Surgery, the American Board of Thoracic Surgery, and the Society of Thoracic Surgeons. He was a pioneer in “Off-Pump” heart surgery, reducing surgical complications and recovery times. He’s in the “Beating Heart Hall of Fame” and has been listed in Phoenix Magazine’s “Top Doctors” for 10 years.

He has been recognized by his peers as a leader and has served as Chief resident at the University of Arizona and Yale University Hospitals. He later served as Chief of Staff and Chief of Surgery.

He was also one of the founding partners of the Lutheran Heart Hospital which became the second largest heart hospital in the U.S.

Dr. Lundell recently agreed to grant us an in-depth and revealing interview about the pioneering work he is currently conducting. It’s our privilege and pleasure to share part one of that exclusive interview with you today.

THB: You are the author of a controversial heart-health book called The Great Cholesterol Lie. The book challenges conventional wisdom and accepted medical theories. What’s been the response to this book?

Dr. Lundell: The response to the book has been overwhelming. I regularly correspond with people from around the world who are enjoying better health from the new understandings they gained from learning about inflammation and heart disease.

THB: That’s good to hear. It’s a seminal book that charts your professional journey as a cardiac surgeon. And, more importantly, reveals your gradual discovery of the true cause of heart disease.

If you could go back in time to when you were a young cardiac surgeon… what would you tell yourself and would you take a different path?

Dr. Lundell: I was dedicated to treating heart disease and passionate about saving lives. It was my responsibility to provide patients with a second chance.

As a young cardiac surgeon in the 1980s coronary bypass operation was the only effective treatment for people afflicted with severe coronary artery disease. So, as you can imagine, this was a very exciting time. Our ability to help people increased and the risks of surgery decreased as techniques and technology improved.

The scientific consensus at that time was elevated cholesterol levels in the blood cause a gradual deposition of cholesterol in the lumen of the blood vessel so two treatment forces were obvious: lower the levels of cholesterol in the blood or do an operation to detour the blood around the accumulated plaque thus restoring flow and heart function.

Rather than looking at more effective ways to lower blood cholesterol, there was relatively little research going on as to what was causing plaque. Everyone settled on the idea that it was as simple as controlling fat and cholesterol.

Then new research was in part driven by industry and not basic science. As balloon angioplasty emerged as an alternative to open heart surgery, the companies that produce the balloons became concerned by high rates of re-stenosis. They began funding studies to understand exactly what was happening biologically to cause the re-stenosis. (Re-stenosis means a re-narrowing of the artery after angioplasty or a stent has been inserted.)

This stimulated a lot of research and culminated in the seminal article published in 1999 in the New England Journal of Medicine announcing that “atherosclerosis [is] an inflammatory disease.”

THB: How did you discover that the true cause of heart disease was inflammation?

Dr. Lundell: I was excited to understand this new research because in the operating room I had observed the classic signs of inflammation around the coronary artery and was very disappointed that surgery, although effective at relieving symptoms and extending life, was not a cure for heart disease.

Many brilliant scientists and university centers continued to do more research that confirmed the basis for coronary disease was chronic inflammation. Sadly the attention was all directed at finding a therapy rather than looking at the cause of chronic inflammation.

Research is hugely expensive and was largely funded by drug companies who were making billions of dollars from the prescriptions for statin drugs.

One of the many side effects of statin drugs is that they seem to have a mild anti- inflammatory effect. Because of the size of the industry and how entrenched the cholesterol theory had become, the focus continues to be on treating everyone with statin drugs rather than understanding the cause and the ability to control chronic inflammation.

The makers of statin drugs have been so skillful at influencing science and controlling public policy that prescribing statins is the standard of care. Anyone questioning or disagreeing with these policies is labeled as a heretic and disregarded.

THB: Why were you so convinced inflammation was the culprit? You were so convinced that you made a major life – and career – change based on that conviction.

Dr. Lundell: I knew that I did not have enough influence to change any of the policies or practices from inside mainstream medicine. Taking a lesson from the drug makers with their direct to consumer advertising I decided to write the book and hopefully people would learn and make the changes needed to truly prevent and cure heart disease.

THB: You describe inflammation very powerfully in your book as a battleground. Can you give our readers an overview of what inflammation is?

Dr. Lundell: Inflammation truly is a battleground. For most of human history we died because of infection and trauma. Our immune system and our inflammatory systems are designed to aggressively respond to these two challenges.

If we get invaded by bacteria or injured in some way, our immune system recognizes the challenge and marshals all of the body’s resources to respond to defeat the invader and heal the wound.

We all have experienced the classic signs of inflammation: warmth, swelling, redness, and pain. Acute inflammation is the response to acute injuries. Chronic inflammation is the response to chronic smaller injuries and so we do not always get the four classic signs.

THB: You’ve taken the bold step to speak out against statin medications. But playing devil’s advocate for a moment… surely there are some situations when statin medications are effective?

Dr. Lundell: Statin medications have proven to be somewhat beneficial to a small group of people; that is a middle aged man with a previous heart attack. They have never been documented to benefit any woman of any age with any condition. They have not been documented to help people who have not had a previous heart attack of any age or gender.

There may be some people who would take great offense at the previous paragraph – especially the makers of Crestor and cardiologists who support treating almost everyone with statin drugs.

They might quote the Jupiter study which was touted as proving Crestor would reduce heart attack rates by almost 50% in otherwise healthy people. Happily, this month in The Archives of Internal Medicine, four peer reviewed articles gave a scathing rebuke to the Jupiter study – the methodology, the conflict of interest by most of the authors, the early termination of the study which almost always provides false results, and the conclusion that statin drugs were beneficial in this population of patients. At last I am getting reinforcements!

THB: That’s a good point to make - and you make it well. So, if statin meds aren’t effective, why are they so dangerous?

Dr. Lundell: Statin drugs are dangerous not necessarily because of the side effects which can be disabling or fatal, but because they divert our attention from understanding and preventing heart disease and merely treat it with statins, allowing us to think that this is beneficial.

Even some of the foremost cardiologists in the country who have written extensively about inflammation as the true cause of heart disease offer no solutions except taking statin drugs. $30,000,000,000 in worldwide sales of statin drugs has a lot to do with it.

In part two of our revealing interview, Dr. Lundell tells us why inflammation is the true cause of heart disease and offers critical solutions to prevent it. We also discover the four most common lifestyle factors that injure heart health and get expert guidance on how to improve it. All this and more in next Wednesday’s edition of Undercover.

About Dr. Lundell: Dr. Dwight Lundell is the past Chief of Staff and Chief of Surgery at Banner Heart Hospital, Mesa, AZ. He is the founder of Healthy Humans Foundation and Chief Medical Advisor for Asantae. In 2003, Dr. Lundell made the most difficult decision of his 25 year surgical career. As traditional medicine continued to chase the cholesterol theory of heart disease, Dr. Lundell closed his surgical practice. He then devoted the rest of his life to speaking the truth that inflammation causes heart disease. By lowering inflammation, heart disease has a cure.

Dr. Lundell is the author of the world-wide bestselling book, The Great Cholesterol Lie. This book is a revealing look at heart disease and the faulty theories of low-fat diets and cholesterol. He also reveals his clinically-tested recommendations for lowering inflammation that can prevent and reverse heart disease.

To your health,

Ian Robinson,
Managing Editor, Total Health Breakthroughs

News regarding statins.

Clare McHarris posted the following on the Stopped Out Statins Yahoo group which I pasted in its entirety here. Thank You Clare!

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News regarding statins. The latest studies in the Archives of Internal Medicine are not supportive of statins. This was released today. Please read the two abstracts below.


Statins and All-Cause Mortality in High-Risk Primary Prevention
A Meta-analysis of 11 Randomized Controlled Trials Involving 65 229 Participants (click here)

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]).

________________

Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER Controversy
A Critical Reappraisal (click here)

Michel de Lorgeril, MD; Patricia Salen, BSc; John Abramson, MD; Sylvie Dodin, MD; Tomohito Hamazaki, PhD; Willy Kostucki, MD; Harumi Okuyama, PhD; Bruno Pavy, MD; Mikael Rabaeus, MD


Arch Intern Med. 2010;170(12):1032-1036.

Background Among the recently reported cholesterol-lowering drug trials, the JUPITER (Justification for the Use of Statins in Primary Prevention) trial is unique: it reports a substantial decrease in the risk of cardiovascular diseases among patients without coronary heart disease and with normal or low cholesterol levels.

Methods Careful review of both results and methods used in the trial and comparison with expected data.

Results The trial was flawed. It was discontinued (according to prespecified rules) after fewer than 2 years of follow-up, with no differences between the 2 groups on the most objective criteria. Clinical data showed a major discrepancy between significant reduction of nonfatal stroke and myocardial infarction but no effect on mortality from stroke and myocardial infarction. Cardiovascular mortality was surprisingly low compared with total mortality—between 5% and 18%—whereas the expected rate would have been close to 40%. Finally, there was a very low case-fatality rate of myocardial infarction, far from the expected number of close to 50%. The possibility that bias entered the trial is particularly concerning because of the strong commercial interest in the study.

Conclusion The results of the trial do not support the use of statin treatment for primary prevention of cardiovascular diseases and raise troubling questions concerning the role of commercial sponsors.

Statins, Pregnancy, Sepsis, Cancer, Heart Failure: a Critical Analysis:

Over the last few decades, the American pharmaceutical industry (henceforth, "Big Pharma") has applied a very successful formula to market fear and convert it into a multi-billion dollar industry. The algorithm goes like this:

1. find a substance whose concentration can be measured cheaply
2. find a prevalent disease whose presence correlates with a high concentration of that substance
3. find a drug that reduces the concentration of that substance
4. advertise aggressively to the general public and medical professionals, claiming a miracle cure.

In a substitution of variables, the substance is cholesterol, the disease is heart disease, and the drug is Lipitor, and, voila! Through aggressive advertising campaigns, Big Pharma has managed to convince the American public and the American doctors that statin drugs are the best thing since sliced bread.

But are they right? I think the evidence shows that very few people currently taking statin drugs are actually benefiting from them. Furthermore, many of them are actually worse off than they would have been had they never been on statins. Below, I will argue that any benefits incurred in combating heart disease are more than offset by increased susceptibility to fetal damage, toxic infection, and cancer.

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Essentially, by taking a statin, you are shifting the odds on what you die of. Pay the money, suffer the side effects, and as a result you may end up dying of cancer or a runaway infection before you would have died of heart disease if you had never taken the drug in the first place.
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Read the full article by Dr.Stephanie Seneff, a Principal Research Scientist at the Massachusetts Institute of Technology here.