Why I won’t take statins for my high cholesterol - Julianne

Why I won’t take statins for my high cholesterol

In Summary, for those who took the statin for 5 years (with known heart disease):

Benefits in NNT

• 1 in 83 were helped (life saved)
• 1 in 39 were helped (preventing non-fatal heart attack)
• 1 in 125 were helped (preventing stroke)

Harms in NNH

• 1 in 100 were harmed (develop diabetes*)
• 1 in 10 were harmed (muscle damage)

If you have had a heart attack and change your diet to a Mediterranean diet – you will get far more benefit than Statin drugs:

In Summary, for those who adhered to the Mediterranean diet:

Benefits in NNT

• 1 in 18 were helped (preventing repeat heart attack)
• 1 in 30 were helped (preventing death)
• 1 in 30 were helped (preventing cancer)

Harms in NNH

• None were harmed

 

 

And if you want to prevent heart disease the Mediterranean diet is also far more effective than statin drugs:

 

In Summary, for those who ate the Mediterranean diet:

Benefits in NNT

• 1 in 61 were helped (avoiding a stroke, heart attack, or death)

Harms in NNH

• None were harmed (diet effects)

Read the full article here.

FDA Approves Dangerous and Worthless Cholesterol Drug - Brownstein

FDA Approves Dangerous and Worthless Cholesterol Drug

by Dr. David Brownstein

On May 3, 2013, the FDA approved a Big Pharma Cartel founding member Merck drug Liptruzet.  Liptruzet is a combination drug of Zetia and Lipitor.  I wrote to you about the failure of Zetia in three separate blog posts.  They can all be found by clicking here:  http://blog.drbrownstein.com/?s=zetia.
Zetia is a failed drug.  It should never be prescribed and should have been pulled from the market years ago.  There is no excuse for any doctor prescribing Zetia for any condition.  Zetia works by blocking cholesterol absorption in the gut.  Conventional doctors believe that drug therapies that lower cholesterol levels reduce the risk of heart disease.  However, Zetia, which has been around for over 10 years, has never been shown to lower the risk of developing a heart attack or stroke.  Furthermore, Zetia has never been shown to prolong life.

Why the FDA would approve this combination of Zetia and Lipitor is beyond belief.  The previous combination of Zetia and Zocor, known as Vytorin, was proven to be a colossal failure in multiple studies—see my previous blog posts.

FDA’s action is a perfect example of why we spend more money on health care than any other people on the planet.  Liptruzet will cost $5.50 per pill.  This means a patient prescribed Liptruzet will spend over $2,000.00 per year on a worthless drug that will be associated with side effects such as muscle aches and pains, memory loss, and neurological disorders.  We take too many ineffective drugs that are too expensive.  Do all of these drugs translate into better healthcare outcomes?  Heck no.  As compared to every other wealthy Western country, we finish last or near the bottom on every single health indicator.  In Liptruzet’s case, there is no justifiable reason for the FDA to approve it.  This is another example, amongst many, of why the FDA should be disbanded.  The FDA gives false credibility to Big Pharma.

If you are on Zetia, I suggest talking to your doctor about stopping it.  Ask him/her for any studies showing a clinical benefit such as a significantly lowered risk for heart disease, heart attack, stroke, or increased longevity.  I can assure you that you won’t be getting any articles from your doctor since they don’t exist.   More information about cholesterol-lowering medications can be found in my book, Drugs That Don’t Work and Natural Therapies That Do. 
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BMJ exposes ways we have been misled over the ‘benefits’ of statins - Briffa

BMJ articles exposes the ways we have been misled over the ‘benefits’ of statins

By Dr John Briffa on 1 November 2013   

 

The ‘Cochrane Collaboration’ is an international collective of researchers whose self-proclaimed role is to provide accurate and robust assessments of health interventions. The group specialises in ‘meta-analyses’: the grouping together of several similar studies on interventions including drug therapies.
In 2011, Cochrane researchers assessed the evidence relating to statin use in individuals at low risk of cardiovascular disease (defined as a less than 20 per cent risk over 10 years), and concluded that there was limited evidence of overall benefit [1]. I appeared on Channel 4 news to discuss this publication and the issues surrounding it, and you can see the discussion here.

Earlier this year, the same Cochrane group updated their data and concluded that overall risk of death and cardiovascular events (e.g. heart attack or stroke) were reduced by statins in low risk individuals, without increasing the risk of adverse events (including muscle, liver and kidney damage) [2]. It seems the Cochrane reviewers had had quite some change of heart. A paper published in the BMJ on 22 October questions the evidence on which this U-turn appears to have been made [3].

The authors of the BMJ piece note that although the 2013 meta-analysis included four additional trials, these trials did not substantially change the findings. The change in advice was actually based on another meta-analysis, published in 2012, conducted by a group known as the Cholesterol Treatment Trialists’ (CTT) collaboration [4].

Among other things, the CTT authors concluded that, in low risk individuals, for each 1.0 mmol/l (39 mg/dl) reduction in LDL-cholesterol, statins reduce overall risk of death and heart attack by about 9 per cent and 20 per cent respectively. The conclusion was that statins have significant benefits in low risk individuals that greatly exceeded known risks of treatment.

However, the CTT authors took the odd step of calculating the benefits of statins according to a theoretical reduction in LDL-cholesterol levels. A much more realistic appraisal would be simply to calculate if, compared to placebo, statins actually reduce the risk of health outcomes.
The BMJ authors use the data from the CTT meta-analysis and found that risk of death was not reduced by statins at all. So, the CTT authors had used had extrapolated the data in a way that showed a benefit that actually does not exist in reality.

And what of the claim that statins reduce the risk of cardiovascular events such as heart attack or stroke? The data shows that about 150 low-risk individuals would need to be treated for five years to prevent one such event (i.e. only about one in 750 individuals will benefit per year).

They also draw our attention to the impact of statin treatment on ‘serious adverse events’. This outcome can be improved by statins as a result of, say, a reduced number of heart attacks, but worsened through side effects such as muscle or liver damage. The BMJ authors note that the CTT review did not consider serious adverse events (a major omission). Without knowing more about this, though, we simply cannot make a judgement regarding the overall effect of statins, and whether the net effect is beneficial or not. Interestingly, of three major trials that were included in the CTT review that assessed overall serious adverse effects, none found overall benefits from statin treatment.
So, while the CTT authors seem to have over-hyped the benefits of statins, they seem at the same time to have been quite keen to steer clear of talk of their very real risks and the absence of evidence foroverall benefit.

The BMJ authors draw our attention to the fact that every single trial included in the CTT was industry funded. Such trials are well known to report results more favourably and perhaps downplay risks than independently funded research. The BMJ authors cite specific ways in which the adverse effects of drugs seen in clinical trials can be ‘minimised’. These include:

• The exclusion of individuals from trials with known health issues likely to be exacerbated by statins or signal susceptibility to statin side effects (such as liver, kidney and muscle disease).
• The use of a ‘run-in’ period before the study starts which detects and then excludes individuals who do not tolerate statins.
• The possibility that individuals ‘drop out’ from the study because of side effects, meaning that the incidence of some side effects can be ‘lost’ from the data.
• Failure of the study investigators to assess and monitor adverse events such as muscle damage and changes in brain function.
• Failure to properly ascertain or report adverse events.

It is noted that the Cochrane authors admit the reporting of adverse effects in studies is generally poor, but also state that it’s unlikely statins have major life-threatening hazards. The authors of the BMJ piece are not convinced, though, writing: “[The] large discrepancies between the frequency of adverse events reported in commercially funded randomised controlled trials included in the CTT meta-analysesand non-commercially funded studies show that determination of harms cannot be left to industry alone.”

The BMJ piece is accompanied by an editorial from the journal’s editor, Fiona Godlee [5]. Her comment on this issue starts:

None of this does much to bolster confidence in the published literature.

Godlee goes on to write:

Nor am I reassured by discussions at two recent meetings co-hosted by the European Federation of Pharmaceutical Industry Associations (EFPIA). Drug company AbbVie is suing the European Medicines Agency to stop summary reports of its clinical trials becoming publicly available. AbbVie’s lawyer made clear that the company considers even the data on adverse events to be commercially confidential. Despite industry’s claims to be in favour of greater transparency, EFPIA and its American counterpart PhRMA are supporting Abbvie. The BMJ and BMA have joined forces to intervene on behalf of the EMA.

If I were to summarise, I’d say that, at best, there seems to be a degree of complacency regarding the veracity of statin data on the part of both the CTT and the Cochrane researchers. There is a sense that they are happy to present the ‘positive’ findings in the best possible light, and at the same time seem relaxed about the clear gaps we have in our knowledge about potential harms. The fact that statins appear to have no overall benefit in those at low risk of cardiovascular disease should not go unacknowledged, either.

Worse still, we have evidence that drug trials can be designed, conducted and reported in ways that obscure the truth. And sometimes, even when we have data that can help us make informed decisions about the appropriateness of a treatment, some drug companies will fight tooth and nail to prevent that data seeing the light of day.

This sort of subterfuge may be good for sales and share price, but it is almost certainly bad for our collective health. On this point, the BMJ authors state than instead of doctors following guidelines and prescribing statins for individuals at low risk of cardiovascular disease, they should explain the magnitude of benefits and uncertainties regarding harm. In addition, they might also discuss the fact that the vast majority of cardiovascular disease risk is linked with lifestyle factors such as smoking, diet and physical activity. Fiona Godlee backs this approach, but states that the benefits of lifestyle change are: “something that the dominance of industry sponsored clinical trials too often obscures.”
Personally, I am delighted that the misdeeds of drug companies and some researchers can now be exposed in this way, and in a high-profile medical journal at that. In the past, I think there was much more opportunity for the industry and its hired hands to mislead us. Greater transparency means that the industry as a whole is getting more of what I believe it deserves: our contempt.
References:
1. Taylor F, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev 2011;1:CD004816.
Medline
2. Taylor F, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev2013;1:CD004816.
3. Abramson JD, et al. Should people at low risk of cardiovascular disease take a statin?
BMJ 2013;347:f6123
4. Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. The Lancet 2012;380(9841):581–90.
5. Godlee F. Statins for all over 50? No BMJ 2013;347:f6412.
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Read the complete article here.

Large meta-analyses of statins

The following was posted on the Track Your Plaque forum on 9/14/2013

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  Here are some highlights from here: http://chriskresser.com/the-diet-heart-myth-statins-dont-save-lives-in-people-without-heart-disease backed up by studies. 

An analysis by Dr. David Newman in 2010 which drew on large meta-analyses of statins found that among those with pre-existing heart disease that took statins for 5 years (1):

96% saw no benefit at all

1.2% (1 in 83) had their lifespan extended (were saved from a fatal heart attack)

2.6% (1 in 39) were helped by preventing a repeat heart attack

0.8% (1 in 125) were helped by preventing a stroke

0.6% (1 in 167) were harmed by developing diabetes

10% (1 in 10) were harmed by muscle damage  A heart attack or stroke can have a significant negative impact on quality of life, so any intervention that can decrease the risk of such an event should be given serious consideration. But even in the population for which statins are most effective—those with pre-existing heart disease—83 people have to be treated to extend one life, and 39 people have to be treated to prevent a repeat heart attack.

Primary prevention (those without pre-existing heart disease)Statins do reduce the risk of cardiovascular events in people without pre-existing heart disease. However, this effect is more modest than most people assume. Dr. Newman also analyzed the effect of statins given to people with no known heart disease for 5 years (5):

98% saw no benefit at all

1.6% (1 in 60) were helped by preventing a heart attack

0.4% (1 in 268) were helped by preventing a stroke

1.5% (1 in 67) were harmed by developing diabetes

10% (1 in 10) were harmed by muscle damageThese statistics present a more sobering view on the efficacy of statins in people without pre-existing heart disease. They suggest that you’d need to treat 60 people for 5 years to prevent a single heart attack, or 268 people for 5 years to prevent a single stroke. These somewhat unimpressive benefits must also be weighed against the downsides of therapy, such as side effects and cost. During that hypothetical 5 year period, 1 in 67 patients would have developed diabetes and 1 in 10 patients would have developed muscle damage (which can be permanent in some cases, as we’ll see later in this section).

To summarize:

The only population that statins extend life in are men under 80 years of age with pre-existing heart disease.

In men under 80 without pre-existing heart disease, men over 80 with or without heart disease, and women of any age with or without heart disease, statins have not been shown to extend lifespan.

Statins do reduce the risk of cardiovascular events in all populations. A heart attack or stroke can have a significant, negative impact on quality of life—particularly in the elderly—so this benefit should not be discounted.

However, the reductions in cardiovascular events are often more modest than most assume; 60 people with high cholesterol but no heart disease would need to be treated for 5 years to prevent a single heart attack, and 268 people would need to be treated for 5 years to prevent a single stroke.

Statins have been shown to cause a number of side effects, such as muscle pain and cognitive problems, and they are probably more common than currently estimated due to under-reporting.

My intention here is not to suggest that statins have no place in the treatment of heart disease, but rather to give you the objective information you need to decide (along with your doctor) whether they are appropriate for you. The decision whether to take them should be based on whether you have pre-existing heart disease, what your overall risk of a heart attack is, how healthy your diet and lifestyle is, what other treatments you’ve already tried, and your own risk tolerance and worldview. It’s clear that statins reduce heart disease as well as the risk of death in those that have already had a heart attack, so if you’re in this group and you’ve already tried diet and lifestyle interventions without much impact on your lipid or inflammatory markers, you are more likely to benefit.
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Read the whole thing here if you are a member.

Will 2015 Dietary Guidelines Advisory Committee address Dr. Rimm’s legitimate concerns? - Watson

Why was a respected Harvard researcher afraid he would get “kicked off the stage”?

Alan Watson | May 10, 2012 

 

On October 31, 2008, during that first meeting of the 2010 Dietary Guidelines Advisory Committee (DGAC), Dr. Eric B. Rimm, Associate Professor of Medicine, Harvard Medical School, questioned what he called the “artificial limit” on dietary fat in the U.S. Dietary Guidelines.

 

From the transcripts:  www.cnpp.usda.gov/DGAs2010-Meeting1.htm

 

Dr. Rimm: “I wanted to make a radical point, one for which I’ll probably get kicked off the stage, but the whole issue of total fat and the 20 to 35 percent of calories from fat is one that has troubled me…”

Dr. Rimm:  “… But the high end, 35 percent of calories from fat, actually was not really based on much science; it’s based on the fact that we don’t have a lot of science beyond 35 percent, and there was a concern that higher fat diets would lead to obesity.”

Dr. Rimm:  I think if you look at the science, there is actually no good human data to suggest that higher fat diets lead to obesity. If anything, higher fat diets, at 35 to 40 percent, lead to lower triglycerides because it’s a lower carbohydrate intake.

Dr. Rimm:  “… I think there is the dogma that low-fat diets are beneficial, and you can go in the grocery store and see a lot of low-fat foods that are essentially just high in carbohydrate, highly processed sugars.”

Dr. Rimm did not get “kicked off the stage,” but the issue never came up again. He was simply ignored. The final report of the 2010 Dietary Guidelines ultimately contained even more stringent reductions in saturated fats – recommending that most Americans reduce saturated fat intake to just 7 percent of calories.

In an interview with Melissa Healy in the Los Angeles Times, June 28, 2010, Dr. Walter C. Willett, Chairman, Department of Nutrition, Harvard School of Public Health, agreed with his Harvard associate:

“The best available evidence demonstrates that percent of calories from fat in a diet has no bearing on weight loss – a point the dietary guidelines committee acknowledges.”

 

“It makes no sense to base the dietary guidelines on an outdated recommendation.”

 

Why did the Committee table Dr. Rimm’s concerns about artificial limits on dietary fat? Why was a respected Harvard researcher afraid he would get “kicked off the stage”? Are Committee members not allowed to question “low fat equals good health”? If so, why has USDA and HHS convened a 2015 Dietary Guidelines Advisory Committee?

New evidence exonerating saturated fats as a cause of heart disease continues to accumulate:

Dr. Ronald Krause – a highly respected American Diet Heart researcher – reviewed 21 studies involving 350,000 subjects to assess the correlation between saturated fat consumption and cardiovascular disease. The conclusion:

Intake of saturated fat was not associated with an increased risk of heart disease or stroke (American Journal of Clinical Nutrition, Jan. 13, 2010).

 

A prospective study from Australia looked at adults over a period of 15 years and found that people who ate the most full-fat dairy products had a 69 percent lower risk of cardiovascular death than those who ate the least (European Journal of Clinical Nutrition, April 7, 2010).
The Japan Collaborative Cohort Study for Evaluation of Cancer Risk found that saturated fat intake was inversely associated with mortality from stroke (American Journal of Clinical Nutrition, Aug. 4, 2010).

Researchers at Louisiana State University found that eating eggs for breakfast resulted in greater weight loss and better energy levels than eating two bagels even though the number of calories was about the same (The FASEB Journal 2007; 21:538.1).

Will the 2015 Dietary Guidelines Advisory Committee address Dr. Rimm’s legitimate concerns?
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Read the complete article here.

Preventing Glucose-Induced Cardiovascular Damage - Michaels

Preventing Glucose-Induced Cardiovascular Damage

Conditions Associated With Elevated Blood Glucose and Advanced Glycation End Products

Elevated cholesterol and atherosclerosis49,50 Symptoms of carotid artery atherosclerosis (major risk for stroke)51 Risk of developing high risk cardiac rhythm disturbances following heart attack52 Cataracts of the eye35 Overall risk of developing cancer53 Risk of developing fatal cancer54 Increased prostate size in benign prostatic hyperplasia (BPH)55 Abnormal elevation in liver enzymes, markers of liver damage56 Incidence and severity of obstructive sleep apnea57

Blood vessels are lined by a thin layer of cells called the endothelium which constantly regulates blood pressure and flow. Damage to the endothelium, which occurs in response to elevated glucose levels, is an important first step in producing heart attacks, heart failure, and stroke.

Studies now show that benfotiamine can prevent endothelial dysfunction and substantially improve blood vessel and heart muscle function, even in the face of glucose-induced tissue damage.

The process of healthy endothelial cell replication is vital to maintaining healthy arteries. Excess levels of glucose can reduce endothelial cell replication. The addition of benfotiamine to endothelial cells grown in a high-glucose environment corrects the defective replication. Benfotiamine accomplishes this through normalization of advanced glycation end product production.

High glucose levels also trigger early death of endothelial cells through the process called apoptosis; benfotiamine supplementation reverses increased apoptosis in cultures of endothelial cells by several mechanisms.

The body produces toxic alcohol-like compounds called polyols during periods of high blood sugar. Polyols disrupt endothelial and cardiovascular cell function. Benfotiamine reduces production of polyols, accelerates the rate of glucose breakdown, and reduces free glucose levels within cells. All of these effects further contribute to protection of endothelial cell function.

After a heart attack, or as a result of persistently high blood pressure, heart muscle cells beat more weakly than they should, resulting in heart failure. High glucose levels and advanced glycation end products substantially contribute to this diminished heart muscle function. Studies show that benfotiamine abolishes many of the abnormalities in heart muscle cell contractility, which may "rescue" impaired heart muscle and improve its ability to pump blood effectively. Benfotiamine activates important cell survival signaling pathways in heart muscle cells failing under the effects of elevated glucose.

Atherosclerosis

Not all advanced glycation end products (AGEs) are produced internally in the body. Consuming a meal rich in AGEs (such as one abundant in browned meats or caramelized sugars) can increase blood levels of AGEs and impair endothelial function. Supplementation with benfotiamine, 1,050 mg/day for 3 days, completely prevented the changes in endothelial function and blood flow produced by such a meal in a group of human subjects.

In addition to its effective control of AGE-related endothelial dysfunction, benfotiamine exerts powerful direct antioxidant effects. In rats with experimentally induced vascular endothelial dysfunction, benfotiamine reduced oxidative stress and enhanced favorable generation of nitric oxide, a compound that contributes to blood vessel relaxation.33,34 The result was an improvement in endothelial integrity and function.

All of these endothelium-protecting effects make benfotiamine an essential nutrient in your fight against the devastating effects of elevated blood glucose on your cardiovascular system.
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Read the complete article here.

Is salt really so bad for you? - Fenster

Is salt really so bad for you?

Decades of science show NO conclusive evidence that cutting back on dietary sodium reduces cardiovascular morbidity

By Michael S. Fenster                     
                        

Enlarge

(Credit: This piece originally appeared on Pacific Standard.

 

No salt, low salt, salt free, heart-healthy salt substitution–any added salt will hurt your constitution. It reads like some bizarre, Seussian tale. Excepting that we’ve heard it not from the good Dr. Geisel but from the medical community and public health advocates everywhere. We watch as celebrity chefs take the salt elimination cooking challenge to prepare an “improved healthy” cuisine. Self-anointed “experts” cadge, coax, and cajole us to decrease our salt, or, more specifically, sodium intake. If that doesn’t work then the specter of heart attacks and strokes is unleashed upon us, along with a dash of fire and brimstone for good measure. It is, after all, clearly in our best personal and the greater public interest.
The hypothesis is sound and the supporting data is impeccable, right?

The theory goes as follows: Salt acts to make us retain fluid. When we retain more fluid it increases our blood pressure (albeit temporarily). Increased blood pressure is hypertension. Hypertension is a risk factor for cardiovascular disease like heart attacks and stroke. Heart attacks and strokes are bad. Therefore, hypertension is bad. Thus, sodium must be bad; A causes B which causes C, therefore A causes C. Get rid of A and you get rid of C—simple basic arithmetic, no? Reduce sodium intake and you will reduce blood pressure and thus reduce the incidence of stroke and heart attack. Reducing sodium intake is good—simple, effective, and undeniably the prevailing conventional wisdom these days.

Except… one thing is missing.

The conclusive data—or any data-that definitively shows that cutting back on dietary sodium reduces mortality or significantly reduces cardiovascular morbidity. For over half a century, starting in the 1960s, there has been a vehement and salty exchange just out of public earshot involving respected scientists on both sides of this line. But with the advent of an aggressive public policy to reduce dietary sodium intake for presumed public health benefit and studies emerging suggesting negative consequences of a low-sodium diet, the clamor of dissension is heating up.
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JAMA on salt HERE.
Read the complete article here.

Here is an article from The Kennebec Journal on the division regarding the salt controversy. Here are a couple of quotes:

"Four months after an Institute of Medicine report said reducing salt to the lowest recommended level doesn't improve health and may harm it, the U.S. Centers for Disease Control and Prevention said they disagree. In an article published Monday in the American Journal of Hypertension, the CDC and New York City health officials said getting Americans to eat less salt remains a key objective with the potential to save thousands of lives."

and

"Lowering sodium to the extent required to lower blood pressure has a variety of other effects," including some that boost heart attacks, strokes and death, he said. "It's just not that simple. The message from the evidence is we don't know."

Here is another article from Food Politics by Marion Nestle.
Another article on salt here.

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

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/
 

The Dark Side of Statins - Colpo

The Dark Side of Statins: Stroke, Muscle Breakdown, Kidney Failure & More

from AnthonyColpo by Anthony Colpo

If you’ve read The Great Cholesterol Con, the name Brian Barker should ring a bell. Brian was featured in Chapter 9 of the book, where I described the life-changing events that took place after his doctor prescribed him a statin drug. Brian remains very ill to this day, and his experiences both sadden and infuriate me. I met Brian and his lovely wife Heather in Sydney in 2005, and it was dispiriting to see such truly nice folks have to suffer what they’ve been through, and it’s infuriating to realize they’re victims of a patently stupid medical mindset that often views toxic statin drugs as wonder pills that should be prescribed freely to everyone over fifty. Ironically, Brian had no personal history of heart disease whatsoever, but his doctor at the time – faithful believer of drug company and medical authority propaganda that he was – figured he’d throw Brian on simvastatin anyhow, “just as an extra precaution”. This flippantly prescribed and utterly unnecessary “extra precaution” transformed Brian from a healthy, active man into a chronically and seriously ill patient who now needs others to help him with the most basic of daily tasks.

In this article, Heather Barker describes their ordeal in full, from that fateful day in May 2002 when Brian was first prescribed a statin drug, to the present, where he continues to struggle not only with ill health but a callous New Zealand health bureaucracy that seems hellbent on denying Brian the financial compensation he is legally entitled to.

A statin is a lipid-lowering agent and although the mechanism is not fully understood or agreed upon by the medical professionals – statins do appear to lower cholesterol. However is the lowering of cholesterol beneficial in reducing heart mortality and what are some of the consequences of lowering cholesterol? This is my personal experience and I do not wish to contradict or undermine those people who tirelessly work towards lowering cardiovascular disease.

My husband Brian and I live in Auckland, New Zealand. Brian was an active person who enjoyed walking, swimming, writing and watching sport. He had solid computer skills in his job with a major airline and was responsible for paying about 700 staff. Brian was a good communicator and was extremely thorough and analytical in his work. He was able to do complex equations in his head and prided himself on accuracy. Honesty and confidentially were key to this job. He also contributed short stories to books held in the National Library and enjoyed looking forward to planned holidays.

That was until a weekend in June 2002 when our lives changed forever. On May 1st 2002 Brian started taking a statin prescribed by a cardiologist based on Brian’s family history and not his health. The cardiologist agreed he was physically fit and did not otherwise meet the criteria for a statin. No blood tests were taken.

Several weeks later Brian became seriously ill with a life threatening event we now know is called rhabdomyolysis which means his muscle tissue melted. This caused acute renal failure. Our GP did not recognize the symptoms which included severe pain in the right flank, frequent vomiting, nausea, no urine output, confusion and weakness.

The GP did not feel it was necessary to do blood tests until pressured by me to do so. When the test results showed Brian had renal failure the doctor’s response was to get Brian to drink a further 4 litres of water. This exacerbated the already dangerous situation. It was 5 days after the initial onset of these symptoms before Brian was hospitalized.

Caused by Simvastatin

Once hospitalised at North Shore Hospital the doctors examined Brian and confirmed the renal failure due to the statin. Neither of us understood most of what was said but were grateful for their help. Brian was transferred to the renal unit at Auckland Hospital and started dialysis. This was now 7 days after the onset of symptoms.

During the course of his treatment both in the hospital and as an outpatient, Brian and I mentioned his weakness, pain, nausea, tingling sensations in many of his muscles, fatigue and frequency in urinating once his kidneys started working again. The list also included urinary incontinence, impotence, confusion, tiredness, widespread discomfort, nightmares, anxiety, thumping headaches and an inability to seize and understand facts.

While he was on dialysis Brian had what we were told 3 years later was a stroke. Neurologists have told us this was due to the extreme stress his body was under in addition to the toxicity from the statin.

Reporting the Problem

Mandatory reporting of adverse reactions is not required in NZ, so I gave the information to the Centre for Adverse Reactions in Dunedin and it was also recorded at the WHO database by Merck Sharp and Dome.

Brian remained on dialysis for some time and eventually his kidney function returned but he remained very ill and was unable to do much without assistance.

Getting Compensated

In New Zealand we have a compulsory accident cover. It is called the Accident Compensation Corporation. ACC is the sole and compulsory provider of accident insurance for all work and non-work injuries. The ACC Scheme is administered on a no-fault basis, so that anyone, regardless of the way in which they incurred an injury, is eligible for coverage under the Scheme. Due to the Scheme’s no-fault basis, people who have suffered personal injury do not have the right to sue an at-fault party, except for exemplary damages.

ACC  accepted our claim that Brian had a medical misadventure and he was assured by his case manager at ACC that any future treatment relating to his injury – for the duration of his life would be covered by ACC. This was in 2002.

ACC provided support with speech language therapists, physiotherapists, psychologists and ongoing treatment from muscular skeletal specialists.

When Brian did not make a full recovery he was retired from his employment and I left my full time job to assisted Brian with day to day tasks like showering and getting dressed. Making decisions were now often difficult for him, he was easily confused about what was required of him and exhausted much of the day. Logging in to a computer was much too hard for him and driving was initially impossible. Brian had become very vulnerable and emotional often weeping with fear and frustration at his inability to move on with his life.

I read as much as I could about rhabdomyolysis and muscle damage. We changed our diet to include far more vegetables, eliminated processed foods and reduced carbohydrates and under medical advice from overseas doctors I included – CoQ10, Omega 3, and magnesium.

I was also really concerned to find thousands of others world wide had been damaged by statins. I had information from the Centre of Adverse Reactions in Dunedin in 2010 which said 11 people in NZ have died fromsimvastatin and there are over 30 reports of rhabdomyolysis  in their database. I didn’t ask about other statins. It is my belief that ACC and in general, the medical profession and pharmaceutical companies would prefer these statistics were not made public.

Compensation Quicksands

The first eight years after the adverse reaction were really hard for Brian and he has shown courage and determination to be the best he can. Many of the original symptoms from 2002 became more manageable but he still suffers from ongoing pain and is limited in his capacity to function fully in society. Until 2009 ACC was very supportive so we could concentrate on Brian’s rehabilitation.

However since 2009, ACC has continued to strive to ‘prove’ he didn’t have an adverse reaction to the statin or the symptoms from the statin injury are spent or most frustratingly that the symptoms are all age related or pre-existed 2002.

Over the next two years he was sent for assessment after assessment, in total around 15. Each assessment leaves him exhausted and traumatised. He was compelled to attend each appointment in order to preserve his entitlements with the ACC. Brian battled on and almost every specialist agreed with the original diagnosis. However it took just one report challenging the original diagnosis to determine that the effects of the injury were now spent. As a consequence Brian has now had his entitlements suspended.

This has directly impacted on our relationship and health. At times, both of us have felt we could not face one more day of this additional pressure. Brian’s nightmares and anxiety have become more regular and his speech and confidence in communicating with people has deteriorated as he has to endure the retelling of details of the original injury and subsequent illness to medical assessors contracted by ACC.

In 2012 we opted for Brian to have a muscle biopsy to ‘show’ he had long standing damage from the statin. The results did not show any mitochondrial damage but did show cell hypertrophy. The muscular skeletal specialist has explained that essentially the muscle cells which survived the rhabdomyolysis became super big and have contributed to the body wide discomfort.

Brian has also had a blood test to see if he had any genes that could predispose him to statin-induced myotoxicity. But he was negative for these tests.

Was it Needed?

To our knowledge Brian had no pre-existing health disorders, he didn’t have diabetes or any cardiovascular disease. But his father, mother and brother had all had heart attacks. So it is reasonable to assume that taking a statin to lower cholesterol would be just the thing for Brian. This is what the advertisements say. This is what the doctors say – at least the ones who haven’t read the impartial reports about cardiovascular disease and mortality.

It is strange then to think that Brian’s mother was on a statin but still had a heart attack.

His younger brother was on a statin for years and developed a heart problem and later had a heart attack and triple bypass and he is still on high doses of a statin. He has also developed diabetes.

Does Cholesterol Need to be Lowered?

Maybe lowering cholesterol isn’t the answer. Many well known doctors and researchers are bold enough to query the statistics provided by the pharmaceutical companies. And to their credit many doctors we have dealt with over the last 11 years have been very supportive and for that we would like to thank them.

Could it be that inflammation or other factors cause atherosclerosis? Is animal fat relevant? Does a diet full of processed foods affect our heart? Would we be better with a diet rich in olive oil and fish? Physicians, scientists and science writers are debating these issues. Having a debate about it is good. It’s a start. Our goal should be to reduce disease but not at the risk of damaging other parts of the body. Nobody should have to go through what we go through every day.

Persisting and unresolved damage from the statin injury has remained a problem for Brian, but we must also endure ongoing legal battles with ACC to ensure his Claimant Rights are being met.

There are still too many doctors and health professionals who are not willing to look at drug side effects, overall risk versus benefit and most importantly the need to remember the Hippocratic Oath: ‘I will prescribe regimens for the good of my patients according to my ability and my judgment and never do harm to anyone.’

–

Heather’s article originally appeared at RxISK.org. Clicking here will not only link to the original article but also comments by others who suffered serious health issues after being prescribed statin drugs.

You can also report a drug side effect and get a free RxISK Report here.

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bibleand The Great Cholesterol Con. For more information, visit TheFatLossBible.net orTheGreatCholesterolCon.com
Copyright © Anthony Colpo.
Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.
=============================================================================================
Read the complete article here.

Potassium, your invisible friend - Kendrick

Poatassium, your invisible friend Dr. Malcolm Kendrick

 

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.’

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you. If you consume more of it you will, most likely, live both longer and in better health.

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality.

  The authors noted that:
“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

The paper showed that:

• Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)

• Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)

• Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)

• Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758
I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed. It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

• lowers blood pressure
• lowers the risk of arrhythmias
• lowers the risk of cardiovascular disease
• lowers the risk of stroke
• lowers the risk of heart attacks
• lowers the risk of cancer, and
• lowers the risk of death

These benefits have been confirmed in a number of different studies. However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).
With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug¹. And with no side-effects at all.

When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke².

Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people. However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.

I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition that needs immediate treatment, or else it will cause arrhythmias and death.

It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.

My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.


1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)
2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.’

 

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you. If you consume more of it you will, most likely, live both longer and in better health.

 

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

 

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

 

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality.

 

 The authors noted that:

“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

 

The paper showed that:

• Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)

• Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)

• Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)

• Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758

I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed. It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

 

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

 

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

• lowers blood pressure
• lowers the risk of arrhythmias
• lowers the risk of cardiovascular disease
• lowers the risk of stroke
• lowers the risk of heart attacks
• lowers the risk of cancer, and
• lowers the risk of death

These benefits have been confirmed in a number of different studies. However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).
With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug¹. And with no side-effects at all.

When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke².

Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people. However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.

I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition that needs immediate treatment, or else it will cause arrhythmias and death.

It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.

My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.

1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)
2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

Poatassium, your invisible friend

March 4, 2013Dr. Malcolm KendrickLeave a commentGo to comments

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.’

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you. If you consume more of it you will, most likely, live both longer and in better health.

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality. The authors noted that:

“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

The paper showed that:

• Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)

• Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)

• Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)

• Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758

I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed. It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

• lowers blood pressure
• lowers the risk of arrhythmias
• lowers the risk of cardiovascular disease
• lowers the risk of stroke
• lowers the risk of heart attacks
• lowers the risk of cancer, and
• lowers the risk of death

These benefits have been confirmed in a number of different studies. However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).
With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug¹. And with no side-effects at all.
When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke².
Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people. However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.
I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition that needs immediate treatment, or else it will cause arrhythmias and death.
It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.
My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.
1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)
2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

Dr Blanchet podcast 20121219

Listen to an excellent podcast to learn about stroke and heart disease prevention by having tests to measure presence of disease before a catastrophic event happens. Wish I had known this before 1994!

http://tuesdaytalkshow.podomatic.com/entry/2012-12-19T08_01_16-08_00

Drug company kills off another cholesterol-modifying drug - Briffa

Drug company kills of another cholesterol-modifying drug

Dec, Fri 14th, 2012

 

I rarely meet someone who has not heard of cholesterol and does not believe it to be a largely dangerous substance. And increasing number of people seem to be aware of the conventional wisdom regarding the different forms of cholesterol, specifically low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C). Actually, these names are a bit misleading, as these particles are not cholesterol (though they do contain cholesterol). But, anyway, the conventional wisdom is that LDL-C dumps cholesterol on the inside of our arteries while HDL-C clears cholesterol. As a result, LDL-C and HDL-C are often dubbed ‘bad-’ and ‘good-’ cholesterol.

The most commonly prescribed cholesterol drugs are known as statins, and their main mechanism of action is to lower LDL-C levels. However, other types of cholesterol-modifying drugs exist, including a relatively new class known as cholesterylester transfer protein inhibitors (CEPT inhibitors), which the conversion of supposedly healthy HDL-C into supposedly unhealthy LDL-C. If you believe the conventional wisdom on cholesterol (I don’t), then this should translate into benefits for health with regard cardiovascular disease (e.g. heart disease and stroke).

All this theory is meaningless, however. The only important thing is not the effect drugs (or anything else) have on cholesterol levels, it’s the impact they have on health. Some years back the drug company Pfizer spent in the region of $800 million developing a CEPT inhibitor by the name of torcetrapib. It had ‘positive’ effects on LDL-C and HDL-C levels, but also turned out to kill people. Pfizer promptly and quite rightly ceased development of the drug.

The crashing failure of torcetrapib has not stopped other drug companies seeking to find a commercially viable CEPT inhibitor of their own. More recently, drug company Roche invested in the development of a drug known as dalcetrapib. However, in the middle of this year Roche abandoned plans for further development, and a recently-published study shows us why [1].

In this study, published in the New England Journal of Medicine, almost 16,000 patients who had suffered from ‘acute coronary syndrome’ (e.g. angina or heart attack) were treated with dalcetrapib or placebo for an average of about two and a half years.

These are just the sort of patients one would expect to benefit most from an intervention because, as a group, they would generally be at high risk of future problems. Also, the number of subjects here is huge, and therefore more than big enough to detect any real benefit the drug may have.

The researchers assessed the effects of dalcetrapib using a ‘composite endpoint’ – which essentially means lumping several outcomes together. The composite outcome included death from heart disease, non-fatal heart attack, ischemic stroke (strokes due to blockage of blood vessels rather than bleeding), unstable angina (angina that can come on at rest), and cardiac arrest with resuscitation. The use of composite endpoints ups the odds that a ‘statistically significant’ benefit for a drug will be found (compared to when only one single outcome is chosen).

Biochemical analysis revealed that dalcetrapib did, as expected, have considerable HDL-boosting effect. But the study showed that this drug had no benefits for health at all.

Another interesting thing about the study was that dalcetrapib was found to increase markers of inflammation – a process which is believed to play a key part on the development of heart disease and stroke.

This study was originally designed to run for longer but was terminated early once these results were in. Early termination of studies is known to generally inflate the benefits of drugs and downplay their risks. Who knows what may have happened if they’d continued.

Of course you’re unlikely to hear about the dalcetrapib study because it wasn’t announced with the blaze of publicity usually afforded to more ‘positive’ studies about cholesterol-reducing drugs. But this is often the way with cholesterol-related research in particular: positive results are spun in a way which gives medication seeming miraculous properties, while negative results and inconvenient truths are swept under the carpet.

References:
1. Schwartz GG, et al. Effects of Dalcetrapib in Patients with a Recent Acute Coronary Syndrome. N Engl J Med 29 November 2012 (epub)
===============================================================
Read the complete article here.

Look AHEAD halted: Lifestyle management fails to reduce hard CV outcomes in diabetics - O'Riordan

Look AHEAD halted: Lifestyle management fails to reduce hard CV outcomes in diabetics

October 19, 2012 Michael O'Riordan

 

Los Angeles, CA - The Action for Health Diabetes (Look AHEAD) study, a trial comparing an intensive lifestyle-intervention program aimed at achieving and maintaining weight loss and fitness in patients with type 2 diabetes, has been stopped for futility.

 

A large cardiovascular-outcomes study funded by the National Institutes of Health that included 5145 adults with diabetes and a body mass index >25 kg/m², Look AHEAD failed to show a difference in the rate of nonfatal MI, nonfatal stroke, death, or hospitalization for angina among patients randomized to an intensive lifestyle intervention and those randomized to a control arm consisting of education alone.

 

Despite significant reductions in weight and improvements in physical-fitness levels among patients with diabetes, investigators concluded that the intervention arm, which included individual sessions with a nutritionist and/or personal trainer, as well as group sessions and refresher courses, failed to provide any benefit in terms of cardiovascular outcomes.

 

Dr Anne Peters (University of Southern California, Los Angeles), one of the study investigators, said in an interview that the trial was successful on one level—namely, that patients lost weight and improved their fitness. Data published at four years showed that the intensive intervention led to weight loss of up to 10% in the first year and that patients maintained a 6.5% reduction in body weight in the following three years. Over an 11-year follow-up period, the patients reported a 5% reduction in body weight from baseline, said Peters.

 

In addition, early data showed that treadmill fitness levels, hemoglobin A_1c levels, systolic and diastolic blood pressure, HDL-cholesterol levels, and triglyceride levels were all significantly improved among patients in the lifestyle-intervention arm when compared with the control group. The only cardiovascular risk factor that remained unchanged with treatment was LDL-cholesterol levels.

 

Despite the lack of cardiovascular benefit observed in Look AHEAD, Peters stressed that diabetic patients should not stop exercising or begin eating anything they wish.

 

"We do know that weight loss and exercise can prevent diabetes," said Peters. "I am a big advocate of prevention, both early prevention of obesity altogether, as well as prevention of diabetes in individuals who have become overweight. Lifestyle changes can help prevent diabetes. Once you have diabetes, I think weight loss and exercise can have benefits, but they are not going to reduce the risk for the primary outcome that we set for Look AHEAD, which was a risk for macrovascular events or death."

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Read the full article here.

.

.

.

Here is the official stated purpose of the Look AHEAD trial.

The primary objective of Look AHEAD is to examine, in overweight volunteers with type 2 diabetes, the long-term effects of an intensive lifestyle intervention program designed to achieve and maintain weight loss by decreased caloric intake and increased physical activity. This program will be compared to a control condition involving a program of diabetes support and education.

The primary hypothesis is that the incidence rate of the first post-randomization occurrence of a composite outcome, which includes

• cardiovascular death (including fatal myocardial infarction and stroke),
• non-fatal myocardial infarction,
• hospitalized angina, and
• non-fatal stroke,

over a planned follow-up period of up to 13.5 years will be reduced among participants assigned to the Lifestyle Intervention compared to those assigned to the control condition, Diabetes Support and Education.

 

Look AHEAD will also test for reductions in the incidence of three secondary composite outcomes and examine the effect of the intervention on cardiovascular disease risk factors, diabetes control and complications, general health, and quality of life, and psychological outcomes. The cost and cost-effectiveness of the Lifestyle Intervention relative to Diabetes Support and Education will be assessed.

=================================================

from https://www.lookaheadtrial.org/public/home.cfm

A comment by Dr. Jack Kruse had this to say about the trial...

Jack Kruse said...

You said, you could not find all cause mortality data for the stop. Not surprising to some of us. The trial was stopped because their hypothesis was being demolished. You and I both know it. But this post further supports my concerns with RCT and so called evidence based medicine. The modern health care complex trump this brand of medicine. I loathe it. There is nothing more dangerous to modern humans than evidence based medicine and we all remain unaware of those pitfalls. Peter has touched on just that here.

I wrote very recently in my Brain Gut 14 blog this: The manner in which we ask questions is deeply flawed in medicine. Here is where the major causative factor lies in medicine that too few are talking about in research literature. You need to know it. Positive findings, whether they are good or bad for our biology, are twice as likely to be published as negative findings.

This dramatically skews the meaning of what the evidence is really showing us in medicine. It is at the core why people do not get better with evidence based practices and remain a medical annuity for the system. This is a cancer at the core evidence-based medicine today. When you become aware of what you do not know, it becomes easier to get to optimal. They key is for you to avoid those pitfalls before you access the healthcare system. Unfortunately, physicians are paid on this data and that is why it appears to many people that doctors just don’t get it. Many of us do get it, but if we step out of line we get punished by the system. That is how I feel about this Look Ahead nonsense. I am more cynical than Peter. I think the trial was ended because a current growth industry in healthcare might have been placed in peril if the trial continued.

=================================================

from HyperLipid.