If your doctor is pushing you to take a statin drug to lower your LDL Cholesterol you might consider printing out this letter and presenting it to him to point out some of the concerns about this treatment and that you would be open to his response to those concerns.
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Patient’s Details:
Dear Doctor
____________________
I wish to
raise the following concerns with you regarding your advice that I should lower
my cholesterol with the use of statins or other medications.
Large scale
studies have shown that cholesterol levels follow a normal distribution having
a range of values from around 2.7 mmol/l (105 mg/dL) to 8.8 mmol/l (343
mg/dL). This same normal distribution is
seen in people who do have heart disease and people who do not have heart
disease [1].
I am concerned
about the definition of ‘high’ cholesterol, since most adults naturally have a
cholesterol level that is above the suggested target.Furthermore, records show that cholesterol
levels in industrialised countries are decreasing, not increasing [2].
What is being suggested as ‘high’ is in fact just normal in many cases.
I am also concerned by the fact
that most people who have a heart attack have an average cholesterol level, not
a high cholesterol level: this has been found during studies completed on
people in the UK,
Australia, New
Zealand and America[3][4][5].
Studies have also
raised questions about so called ‘bad’ cholesterol. A study published in the American Heart Journal looked at
cholesterol levels for people who have been admitted to hospital in America
with coronary artery disease (CAD). The study included 136,905 people.The
average LDL level for this group of people was 2.7 mmol/l (105 mg/dL)[6].Which was actually lower than the average level for the general
population: the average for the general population was 3.2 mmol/l (125
mg/dL)[7].
If people with
CAD have lower LDL levels than the general population, then where is the
evidence that higher LDL levels cause heart disease?
The conclusion of a BBC Radio 4 program in the UK
was that 99% of people who take statins for primary prevention do not benefit
from them. This was admitted by the UK
governments chief advisor on heart disease (Professor Boyle) [8].
Any benefit
associated with statins is routinely shown as a relative percentage reduction
and this is misleading for patients. To illustrate this point we could look at the Lipid Lowering Arm of
the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT-LLA) [9].
Within the group of people who were given the
statin, 1.9% of them had a heart attack or died of heart disease, versus 3% of
people in the placebo group. The statin reduced the risk by just 1.1%.
Unfortunately the authors of the report described the results as a 36% relative risk reduction.
There is evidence that high cholesterol in elderly people
is associated with a longer life. This was the conclusion of a study completed
by a team of researchers at Yale University School of Medicine [10].
Researchers in the Netherlands also found that in the case of the elderly, life
expectancy increases when cholesterol levels are higher. Those with higher
cholesterol levels appeared to be better protected from cancer and infection [11].
I am also
concerned that adverse effects from statins have been under-reported. The
procedures used during clinical trials, such as the run-in period, may mean
that the trial participants are not representative of the general population.
‘Stopped
Our Statins’ is a forum for people who have experienced significant adverse
effects from the use of statins. The most commonly reported adverse
effects on this forum include:
Gout,
Numbness / Tingling of the Hands/Feet, Muscle ~ Weakness, Cramps, Spasm,
Stiffness, Insomnia, Loss of
Libido, Impotence, Heart Palpitations, Heart Arrhythmias, Depression, Short Term Memory Loss, Long Term Memory Loss, Transient Global
Amnesia, Neck and Shoulder Pain, Fatigue, Migraine, Headaches, Chest Pain,
Digestive Disorders, Trouble Walking (Shuffling), Trouble Walking (Balance),
Hand Tremors, Speech - Trouble finding the right word, Slurred Speech,
Dizziness, Sciatica Pain.
Although
this data is not part of a clinical trial it does provide testament to the wide
range of adverse effects experienced in the real world with real people.
Before I
make the decision whether or not to lower my cholesterol through medication, I
would be very grateful if you could provide a response to the points raised
above.
Thank you
very much for your consideration.
Yours
sincerely,
References:
[1]Smith, J 2009 $29 Billion Reasons to Lie about Cholesterol: Making Profit by Turning
HealthyPeople into Patients
Troubador Publishing, Leicester
[2]Blood
Cholesterol Chapter 10 of the British Heart Foundation Coronary Heart
Disease Statistics. July 2007
[3]
Durrington, P Dyslipidaemia Lancet
2003; 362:717-731
[4]Tonkin,
AM et al. Effects of Pravastatin in 3260 Patients with Unstable Angina: Results
from the LIPID Study Lancet 2000;
355:1871-1875
[5]Rubins, HB et al.
Distribution of Lipids in 8,500 Men with Coronary Artery Disease American Journal of Cardiology1995; 75:1202-1205
[6]Sachdeva, A et al Lipid Levels in Patients
Hospitalized with Coronary Artery Disease: An analysis of 136,905 Hospitalizations
in Get with the Guidelines American Heart
Journal 2009; 157:111-117
[7]Carroll, MD et al Trends in Serum Lipids
and Lipoproteins of Adults, 1960-2002 Journal
of the American Medical Association 2005; 294:1773-1781
[8]BBC Radio 4 Program “The Investigator” April 3, 2008 20:00hrs GMT
[9] Sever,
PS et al. Prevention of Coronary and Stroke Events with Atorvastatin in
Hypertensive Patients who have Average or Lower-Than-Average Cholesterol Concentrations,
in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm
(ASCOT-LLA): A Multicentre Randomised Controlled Trial Lancet 2003; 361:1149-1158
[10] Krumholz, H et al. “Lack of Association Between
Cholesterol and Coronary Heart Disease Mortality and Morbidity and All-Cause
Mortality in Persons Older Than 70 Years” Journal of the American Medical
Association 1994; 272:1335-1340
[11] Weverling-Rijnsburger, AW et al. “Total Cholesterol and
Risk of Mortality in the Oldest Old” Lancet 1997; 350:1119-1123
"So it's not really about cholesterol. It's about the particles that cause atherosclerosis. Today you and I are able to directly quantify and characterize lipoproteins, relagating cholesterol to join frontal lobotomies in the outdated medical practice garbage dump in the sky."
Never saw a headline like this? Neither have I. That’s because it doesn’t happen.
Cholesterol doesn’t harm, maim, or kill. It is simply used as a crude–very crude–marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a “dipstick,” for lipoproteins in the blood to those who don’t understand how to identify, characterize, and quantify actual lipoproteins in the blood.
Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.
What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It’s not about cholesterol; it’s about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.
So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL’s relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.
A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.
But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It’s bound to topple sooner or later, and the bigger it gets, the less stable it becomes.
If you are concerned about future potential for heart disease and heart attack, don’t get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.
by Dr. Mercola Spending on cholesterol-lowering drugs like statins increased by $160 million in 2010, for a total spending of nearly $19 billion in the U.S., the IMS Institute for Healthcare Informatics reported in their Use of Medicines in the United States: Review of 2010.
In all, more than 255 million prescriptions were dispensed for these drugs in 2010, making them the most commonly prescribed type of medication in the United States.
Unfortunately, this excessive use is an artifact of a medical system that regards prescribing pills to lower cholesterol as a valid way to protect one’s heart health — even though the low “target” cholesterol levels have not been proven to be healthy … and cholesterol is actually NOT the underlying culprit in heart disease.
Worse still, these drugs, which are clearly not necessary for the vast majority of people who take them, are proven to cause serious and significant side effects, including, as new research shows, definite nerve damage.
Are You Taking Drugs You Don’t Need … and Getting Nerve Damage as a Result?
It must be understood that any time you take a drug there is a risk of side effects.
Oftentimes, these risks are not fully understood, especially when multiple drugs enter the equation, and appear only after a drug has already been taken by millions of people.
Even once a drug has been FDA-approved, you are depending on a limited number of clinical trials to dictate a drug’s safety … but it’s impossible to predict how a drug will react when introduced into your system, in a real-world setting.
Not to mention, the accuracy of medical research is dubious at best.
In many ways, any time you take a drug YOU are the guinea pig, and unforeseen side effects are the rule, rather than the exception. In terms of statin drugs, side effects are already clearly apparent; at GreenMedInfo.com you can see 304 conditions that may be associated with the use of these drugs, and this is likely only the tip of the iceberg. Among one of the more well-known risks is harm to your muscles and peripheral nervous system with long-term use. Indeed, new research on 42 patients confirmed that: ” … long-term treatment with statins caused a clinically silent but still definite damage to peripheral nerves when the treatment lasts longer than 2 years.”
If You Take Statins for Two Years or More, Nerve Damage Appears to be the Rule
What does it mean when you sustain damage to peripheral nerves? As reported by the National Institute of Neurological Disorders and Stroke (NINDS): “Symptoms are related to the type of affected nerve and may be seen over a period of days, weeks, or years. Muscle weakness is the most common symptom of motor nerve damage. Other symptoms may include painful cramps and fasciculations (uncontrolled muscle twitching visible under the skin), muscle loss, bone degeneration, and changes in the skin, hair, and nails.”
At GreenMedInfo.com you can see 88 studies on statin-induced neurotoxicity (nerve damage), with12 studies further statin drugs directly to neuropathy, including chronic peripheral neuropathy. As explained by NINDS: “Peripheral neuropathy describes damage to the peripheral nervous system, the vast communications network that transmits information from the brain and spinal cord (the central nervous system) to every other part of the body. Peripheral nerves also send sensory information back to the brain and spinal cord, such as a message that the feet are cold or a finger is burned. Damage to the peripheral nervous system interferes with these vital connections. Like static on a telephone line, peripheral neuropathy distorts and sometimes interrupts messages between the brain and the rest of the body. Because every peripheral nerve has a highly specialized function in a specific part of the body, a wide array of symptoms can occur when nerves are damaged. Some people may experience temporary numbness, tingling, and pricking sensations (paresthesia), sensitivity to touch, or muscle weakness. Others may suffer more extreme symptoms, including burning pain (especially at night), muscle wasting, paralysis, or organ or gland dysfunction. People may become unable to digest food easily, maintain safe levels of blood pressure, sweat normally, or experience normal sexual function. In the most extreme cases, breathing may become difficult or organ failure may occur. Some forms of neuropathy involve damage to only one nerve and are called mononeuropathies. More often though, multiple nerves affecting all limbs are affected-called polyneuropathy.”
One of the more disturbing implications of this finding is that since statins damage the peripheral nerves, it is also highly likely that they damage the central nervous system (which includes the brain), as well. One study published in the journal Pharmacology in 2009, found statin-induced cognitive impairment to be a common occurrence, with 90% reporting improvement after drug discontinuation. There are, in fact, at least 12 studies linking memory problems with statin drug use in the biomedical literature, indicating just how widespread and serious a side effect statin-induced neurological damage really is.
Lower Your Cholesterol and Increase Your Diabetes Risk by Nearly 50%
As mentioned, neurological damage is only one potential risk of statins. They are also being increasingly associated with increased risk of developing diabetes.
Most recently, a study published in the Archives of Internal Medicine revealed statins increase the risk of diabetes for postmenopausal women by 48 percent! Statins appear to provoke diabetes through a few different mechanisms, the primary one being by increasing your insulin levels, which can be extremely harmful to your health. Chronically elevated insulin levels cause inflammation in your body, which is the hallmark of most chronic disease. In fact, elevated insulin levels lead to heart disease, which, ironically, prevention of is the primary reason for taking a statin drug in the first place!
As written on GreenMedInfo: “The profound irony here is that most of the morbidity and mortality associated with diabetes is due to cardiovascular complications. High blood sugar and its oxidation (glycation) contribute to damage to the blood vessels, particularly the arteries, resulting in endothelial dysfunction and associated neuropathies due to lack of blood flow to the nerves. Statin drugs, which are purported to reduce cardiovascular disease risk through lipid suppression, insofar as they contribute to insulin resistance, elevated blood sugar, and full-blown diabetes, are not only diabetogenic but cardiotoxic, as well.”
A separate meta-analysis has also confirmed that statin drugs are indeed associated with increased risk of developing diabetes. The researchers evaluated five different clinical trials that together examined more than 32,000 people. They found that the higher the dosage of statin drugs being taken, the greater the diabetes risk. The “number needed to harm” for intensive-dose statin therapy was 498 for new-onset diabetes — that’s the number of people who need to take the drug in order for one person to develop diabetes.
In even simpler terms, one out of every 498 people who are on a high-dose statin regimen will develop diabetes. (The lower the “number needed to harm,” the greater the risk factor is. As a side note, the “number needed to treat” per year for intensive-dose statins was 155 for cardiovascular events. This means that 155 people have to take the drug in order to prevent one person from having a cardiovascular event.)
The following scientific reviews also reached the conclusion that statin use is associated with increased incidence of new-onset diabetes:
A 2010 meta-analysis of 13 statin trials, consisting of 91,140 participants, found that statin therapy was associated with a 9 percent increased risk for incident diabetes. Here, the number needed to harm was 255 over four years, meaning for every 255 people on the drug, one developed diabetes as a result of the drug in that period of time.
In a 2009 study, statin use was associated with a rise of fasting plasma glucose in patients with and without diabetes, independently of other factors such as age, and use of aspirin or angiotensin-converting enzyme inhibitors. The study included data from more than 345,400 patients over a period of two years. On average, statins increased fasting plasma glucose in non-diabetic statin users by 7 mg/dL, and in diabetics, statins increased glucose levels by 39 mg/dL.
Side Effects Often Don’t Show Up Immediately …
Oftentimes statins do not have any immediate side effects, and they are quite effective at lowering cholesterol levels by 50 points or more. This makes it appear as though they’re benefiting your health, and health problems that develop later on are frequently misinterpreted as brand new, separate health problems.
Again, the vast majority of people do not need statin drugs, and if you are one of them, taking them is only going to expose you to serious, unnecessary risks!
If your physician is urging you to check your total cholesterol, please be aware that this test will tell you virtually nothing about your risk of heart disease, unless it is 330 or higher. HDL percentage is a far more potent indicator for heart disease risk. Here are the two ratios you should pay attention to:
HDL/Total Cholesterol Ratio: Should ideally be above 24 percent. If below 10 percent, you have a significantly elevated risk for heart disease.
Triglyceride/HDL Ratio: Should be below 2.
To understand why most people don’t need a statin drug, you first need to realize that cholesterol is NOT the cause of heart disease. Your body NEEDS cholesterol — it is important in the production of cell membranes, hormones, vitamin D and bile acids that help you to digest fat. Cholesterol also helps your brain form memories and is vital to your neurological function. For more information about cholesterol, and why conventional advice to reduce your cholesterol to ridiculously low levels is foolhardy, please listen to this interview with Dr. Stephanie Seneff.
Urgent Information: If You Take Statins You Need CoQ10
It’s extremely important to understand that taking a statin drug without also taking CoQ10 puts your health in serious jeopardy. Unfortunately, this describes the majority of people who take them in the United States.
CoQ10 is a cofactor (co-enzyme) that is essential for the creation of ATP molecules, primarily in your mitochondria, which you need for cellular energy production. Organs such as your heart have higher energy requirements, and therefore require more CoQ10 to function properly (cardiac muscle cells have up to 200 times more mitochondria, and hence 200 times higher CoQ10 requirements, than skeletal muscle). Statins deplete your body of CoQ10, which can have devastating results.
As your body gets more and more depleted of CoQ10, you may suffer from fatigue, muscle weakness and soreness, and eventually heart failure. Interestingly, heart failure, not heart attacks, is now the leading cause of death due to cardiovascular diseases. Coenzyme Q10 is also very important in the process of neutralizing free radicals. So when your CoQ10 is depleted, you enter a vicious cycle of increased free radicals, loss of cellular energy, and damaged mitochondrial DNA.
If you decide to take a CoQ10 supplement and are over the age of 40, it’s important to choose the “reduced” version, called ubiquinol. The reduced form is electron-rich and therefore can donate electrons to quench free radicals, i.e. function as an antioxidant, and is much more absorbable, as nutrients must donate electrons in order to pass through membrane of cells. In other words, ubiquinol is a FAR more effective form — I personally take 200 mg a day since it has such far-ranging benefits, including compelling studies suggesting improvement in lifespan.
How to Optimize (Not Necessarily Lower) Your Cholesterol Without Drugs
Seventy-five percent of your cholesterol is produced by your liver, which is influenced by your insulin levels. Therefore, if you optimize your insulin level, you will automatically optimize your cholesterol! By modifying your diet and lifestyle in the following ways, you can safely modify your cholesterol without risking your health by taking statin drugs:
Reduce, with the plan of eliminating, grains and sugars in your diet, replacing them with mostly whole, fresh vegetable carbs. Also try to consume a good portion of your food raw.
The average American consumes 50% of their diet as carbs. Most would benefit by lowering their carb intake to 25% and replacing those carbs with high quality fats.
Other heart-healthy foods include olive oil, palm and coconut oil, organic raw dairy products and eggs, avocados, raw nuts and seeds, and organic grass-fed meats, as described in my nutrition plan.
After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I’ve decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.
I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.
Imagine you’ve got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer’s lot. 50,000 miles pass, however, and you realize you’ve forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can’t let that happen with heart health.
If we propose to reverse coronary atherosclerotic plaque, we’ve got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you’ve gotten to your destination.
Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant “risk factor” for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat–”healthy whole grains”–slashes measured LDL values like NMR LDL particle number and apoprotein B.)
But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart’s arteries.
Measuring the amount of atherosclerotic plaque in your heart’s arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.
There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.
So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium “score.” No, it is not perfect. It does not reflect that moment’s blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.
But it’s the best we’ve got.
If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we’ve got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.
San Francisco, CA and Baltimore, MD - Are statins one of the greatest advances since the introduction of antibiotics, capable of preventing cardiovascular disease in a wide range of patients, even healthy ones, or are clinicians relying too heavily on the lipid-lowering medications, using the drugs too frequently in individuals who would be better treated with an overhaul of their diet and exercise habits?
The two very different sides of the statin argument are debated today in the Wall Street Journal [1], with Dr Roger Blumenthal (Johns Hopkins University Medical Center, Baltimore, MD) arguing the drugs prevent heart disease in patients with cardiovascular risk factors as well as in those who have already had a cardiovascular event. Good diet and exercise are the foundations of good health, says Blumenthal, but they're simply not enough sometimes, especially in patients with increased LDL-cholesterol levels or other cardiovascular risk factors.
"Every major medical guideline calls for doctors to prescribe a statin to certain seemingly healthy people with high levels of 'bad' cholesterol, which signals elevated risk for a heart attack," according to Blumenthal. "Doing so is one of the certainties of life, like the Cubs falling out of the pennant race by Labor Day."
Dr Rita Redberg (University of California, San Francisco), on the other hand, argues against the current practice of prescribing statins to patients with cardiovascular risk factors, including individuals with elevated cholesterol levels. To heartwire, she said that there are too many low-risk individuals taking statins, and they simply don't get a benefit. In these low-risk/low-benefit patients, given the residual risk of statins, benefit is exceeded by harm.
"Despite research that has included tens of thousands of people, there is no evidence that taking statins prolongs life, although cholesterol levels do decrease," she writes in the Journal. "Using the most optimistic projections, for every 100 healthy people who take statins for five years, one or two will avoid a heart attack. One will develop diabetes. But, on average, there is no evidence that the group taking statins will live any longer than those who don't."
Aggressive treatment of risk factors
Just last January, a controversial Cochrane review concluded that there was not enough evidence to recommend the widespread use of statins in the primary prevention of heart disease, a conclusion that was challenged by other researchers and clinicians.
To heartwire, Blumenthal said that it is extremely rare to "find a cardiologist, in this day and age, who thinks you shouldn't treat elevated cholesterol levels." Noting that Redberg is a close, personal friend, he said that she is simply not looking at the totality of the evidence, noting that the data support the use of statins in primary and secondary prevention. Waiting until the patient has had a clinical event is too late, argues Blumenthal, especially when the first manifestation of cardiovascular disease can often be sudden cardiac death.
"I agree that that less invasive testing and [fewer] interventions can be just as good or better in some settings, but to adopt a real conservative strategy you also need to have not only aggressive lifestyle changes, which Dr Redberg and I agree on, but an aggressive treatment of risk factors like high cholesterol and blood pressure," said Blumenthal. "We don't really have mortality data supporting the treatment of blood pressure to less than 160 [mm Hg], yet every authority would say that if you stopped treating these patients the rates of heart failure, stroke, and renal disease would go up."
In her essay, as well as to heartwire, Redberg states that there is not a significant mortality reduction with statins when used in primary prevention and that the use of lipid-lowering medications might lead some patients to not change their lifestyle since they are now being treated with medication. Moreover, the blood-pressure analogy is not accurate as there are more data on the prevention of cardiovascular events with treatment of hypertension.
"If we were to spend a small fraction of the annual cost of statins on making fruits and vegetables and physical activity more accessible, the effect on heart disease, as well as high blood pressure, diabetes, cancer, and overall life span, would be far greater than any benefit statins can produce," she writes.
WOSCOPS, JUPITER
Blumenthal, however, disagrees with Redberg's interpretation of the data, noting that the West of Scotland Prevention Study (WOSCOPS) showed that there was a strong trend toward reduced mortality after five years of treatment with statin therapy. The more recent Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) study was stopped early given significant reductions in cardiovascular morbidity and mortality in individuals with cardiovascular risk factors but without cardiovascular disease. Recently, long-term results from the Anglo-Scandinavian Cardiac Outcomes—Lipid-Lowering Arm (ASCOT-LLA) study showed that treatment with atorvastatin reduced all-cause mortality compared with placebo, mainly through a reduction in noncardiovascular death.
"The selective use of cholesterol-lowering medications is what every clinical guideline recommends, from Europe to Canada to the United States," said Blumenthal.
In contrast, Redberg noted that WOSCOPS studied men only and that 80% of patients in the study were current or former smokers with a body-mass index in the obese/overweight range. In addition, some of the patients had cardiac or peripheral vascular disease. "This was an extremely high-risk population and it's not who we're talking about when we're talking about people taking statins," Redberg told heartwire. Regarding JUPITER, Redberg noted the trial was stopped prematurely after just 1.9 years of follow-up and that the use of C-reactive protein (CRP) levels to guide treatment remains controversial.
Regarding the potential for a large-scale, long-term, randomized, clinical trial to definitively answer the questions about statins' benefit in primary prevention, Blumenthal said it would be impossible given how large, time-consuming, and expensive such a trial would be. Moreover, such a trial would also be stopped early because of the significant reductions in MIs, strokes, and revascularizations that would be observed in the statin-treated patients, he said.
"I don't think we should treat everybody who's 50 years of age, but I take the attitude that people with risk factors should be, especially those with dyslipidemia, hypertension, or a family history of heart disease," he said. "We're extremely aggressive in lifestyle changes, and I'm sure Dr Redberg is too, but she's taken the attitude of 'do no harm'—but she's also unfortunately taken the attitude of 'do no good,' especially if she's doesn't think we should be using medication."
Blumenthal said that given the emergence of cheap and potent statins, including simvastatin and atorvastatin, makes the drugs an affordable, low-risk option to reduce the risk of heart disease.
What about the side effects of statins?
To Redberg, the availability of generic statins does not change the equation, given the risk of potential side effects, such as muscle pain and weakness. Regarding the attitude of statin proponents that large-scale trials would be prohibitively expensive and very long, Redberg calls this a "disappointing stance," citing the billions of dollars that have already been spent on statin prescriptions and advertising.
"Every week in clinic I see patients who are suffering severe adverse effects of statins, and most of them are incredibly low-risk patients," Redberg told heartwire. "Most of them are women, who I think, unfortunately, suffer more adverse effects from statins, which is ironic because women are at a much lower risk than men from coronary disease anyway. None of the trials in primary prevention have shown a reduction in heart disease and none of them in women. None of them have shown a reduction in mortality in men or women. What this means for women is that they are much more likely to be getting adverse events and not likely to get any benefit at all from treatment."
Primary prevention, according to Redberg, should be based on proper diet and exercise, and these efforts should begin in the school system through physical education and improved nutritional content of lunches and snacks.
"Too often people feel that because lifestyle interventions are not always going to be successful they don't even try, and we can just write a prescription," said Redberg. "I don't think we're doing our best service to our patients with that type of approach. I think there is a lot to be gained from physician counseling on lifestyle changes as well as public-health measures."
Blumenthal agrees about the importance of making healthy food choices available and promoting better dietary habits and physical activity, but these habits are best learned when patients are young. Moreover, physician counseling on physical activity and lifestyle changes does not negate the value of statins in middle-aged and older adults with cardiovascular risk factors, such as elevated LDL-cholesterol levels.
"It's sort of silly to have this conversation in 2012 about not giving a cholesterol-lowering medication to a person who has dyslipidemia and other risk factors," Blumenthal told heartwire. "I'm not sure why she and some of the others have taken an extreme point of view that would be considered malpractice in the 48 continental states, and probably in Alaska and Hawaii, too."
But there are now other threats to our welfare. We justifiably do not trust doctors, and as a consequence, people are loath to allow themselves to be experimented on. Which is proving to be a problem for the doctors. As is clearly stated in their paper, Drs Susanne Sheehy and Joel Meyer believe that we should be forced, by law if necessary, to allow them to inject us with any material they like. Mandatory participation in vaccine trials, they suggest, is no different from requiring individuals to serve on jury duty, for instance, or to serve in the military.
They also believe that forcing people to take experimental vaccines, even when such vaccines come with obvious "inherent risks," is an individual's required duty to give back to society.
Perhaps the most disturbing element of the paper, though, is its suggestion that "increas[ing] the severity" of diseases will help to facilitate 'compulsory recruitment' into experimental vaccine trials. Deliberately creating more deadly strains of disease in order to scare people into vaccine programs, in other words, is apparently considered to be a valid approach by Sheehy and Meyer, whose passionate worship of vaccines have led them to such a preposterous notion.
Just how dangerous their ideas are is evidenced in what has happened in vaccine trials in the past. I'll just list a couple:
In 2008, 21 homeless individuals in Poland died during an avian flu vaccine experiment.[14]
And in the same year at least 14 Argentinean children died as part of an experimental vaccine trial conducted by British pharmaceutical giant GlaxoSmithKline [15]
With that track record it is no wonder that Drs Susanne Sheehy and Joel Meyer are having difficulty finding volunteers on which they can test dubious procedures. And have they forgotten that we have a perfectly adequate immune system – if only it is allowed to do its job. And vaccines damage that capability.
Let me make it quite clear. I am very wary of going anywhere near the sharp end of a hospital. And there is certainly no way I would agree to allow myself to participate in any medical trial.
The medical profession today all seem to think we 'patients' exist to provide them with a comfortable standard of life which we can never aspire to. Well, we don't! They are our servants; we pay their salaries. And there is a limit to how much we can afford. If they cannot live with that, so be it.
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News broke last week (see here for an example) that a University of Connecticut researcher had be found to have falsified data concerning his research into the antioxidant resveratrol (found in, among other things, red wine and red grapes). This week the British Medical Journal reports on the fact that a doctor and flu vaccine researcher based at Leicester University in the UK has been suspended for a range of misdemeanours including forging colleagues signatures and recruiting himself into a study under a disguised name.
It would be comforting to think of these events as isolated incidences in the scientific community. However, according to a recent piece in the British Medical Journal, scientific misconduct is ‘worryingly prevalent’, at least in the UK [1].
The BMJ sent out a questionnaire to more than 9,000 researchers and reviewers asking if they has knowledge of colleagues “inappropriately adjusting, excluding, altering, or fabricating data” for the purpose of publication. Of those who responded, 13 per cent admitted they had such knowledge. 6 per cent admitted they were aware of misconduct within their own institutions which remained insufficiently investigated.
On January 12, the Committee on Publication Ethics (COPE) held a summit to address the problem of research misconduct in the UK. Referring to the BMJ survey, the Chair of COPE Dr Elizabeth Wagner is quoted as saying “This survey chimes with our experience from COPE where we see many cases of institutions not cooperating with journals and failing to investigate research misconduct properly.”
In a recent editorial in the BMJ [2], Dr Wagner and the BMJ’s editor Fiona Godlee wrote: “There are enough known or emerging cases to suggest that the UK’s apparent shortage of publicly investigated examples has more to do with a closed, competitive, and fearful academic culture than with Britain’s researchers being uniquely honest.”
My feeling is if the culture wasn’t so ‘closed, competitive, and fearful’ we’d probably see that misconduct is even more prevalent than the recent BMJ survey suggests. And that’s a problem because we really do need to rely on the integrity of research findings in making truly informed decisions about health and the management of disease.
Personally, I’m delighted that institutions such as the BMJ and COPE are shining a light onto this issue and thinking about how we might curb research misconduct. References: 1. Tavare A. Scientific misconduct is worryingly prevalent in the UK, shows BMJ survey. BMJ 2012;344:e377 2. Godlee F, et al. Research misconduct in the UK. BMJ 2012;344:d8357
There Is No Scientific Basis to Support Treating to LDL Targets
First, no major randomized clinical trial (RCT) has tested the benefits of treating patients according to LDL targets.5 The clinical trials tested fixed doses of drugs that lower lipid levels in specific patient populations. In some of these trials, drugs were shown to reduce risk (eg, statins), but in others, this reduction in risk was not demonstrated (eg, clofibrate and torcetrapib). Other drugs, such as ezetimibe, remain to be tested. The trials do not demonstrate that all drugs that reduce lipid levels reduce patient risk. Thus, the dogma that treating to target is based on clinical trial evidence belies the fact that no clinical trial has yet tested this strategy.
As noted above, trials show that not all drugs that improve lipid profiles reduce patient risk. In fact, almost all the trial evidence for patient benefit is for a single medication class—statins—that is known to have multiple biological activities that are often referred to as “pleiotropic” effects. Standard doses of the first generation of statins, such as simvastatin, dramatically reduce cardiovascular events and mortality. High-potency statins, such as atorvastatin, reduce nonfatal events by an additional 15–20%. Thus, the trial evidence indicates that the use of statins, and not treatment to target, can reduce risk. Although the mechanism(s) by which statins exert their benefit is controversial, one does not need to impugn the cholesterol hypothesis to recognize that different lipid-lowering drugs could possibly have deleterious effects that offset their potential benefit. Further, it is quite possible that a surrogate measure, such as LDL, may appear to be a single entity even though clinically important subcomponents (such as heterogeneity in particle size) or interactions (such as total cholesterol/high-density lipoprotein [HDL] ratio) may exist. Thus, we cannot assume that lowering LDL, by any means, will improve patient outcomes.
A closer look at the evidence demonstrates further reasons against basing treatment decisions on LDL levels. In considering recommendations, it is useful to recognize that there are only 2 factors that determine the benefit of a treatment for an individual patient: (1) the risks of morbidity or mortality in the absence of treatment and (2) the degree to which the treatment reduces or increases these risks.6 LDL levels are not useful in either of these areas. The LDL level contributes little to estimating cardiovascular risk overall and especially compared with non-HDL9 or total cholesterol/HDL ratio.10–12 Moreover, clinical trials demonstrate that the relative effects of statin therapy are not substantially related to a patient's pretreatment LDL.13,14 It should be noted that although C-reactive protein has been demonstrated to be an independent predictor of cardiovascular risk, it is not strongly related to the relative risk reduction of statins, although the evidence is not entirely consistent.13,15,16 Thus, there is strong scientific evidence that LDL is not a very useful factor in determining who is at risk for cardiovascular disease or how much that risk will be reduced by a statin.
The conclusion that the evidence does not support a target-based approach may seem counterintuitive to those whose work has been focused on the biology of cardiovascular disease mechanisms, but the science of clinical decision-making requires a different approach. The critical component of good clinical decision-making is not the scientific evidence regarding disease pathogenesis or treatment mechanisms but rather the best empirical predictors of patient risk and factors that reduce risk, the 2 elements that help determine the risks and benefits of a treatment in individual patients.6,7 As has been demonstrated conclusively, it does not matter whether LDL is the sole biological mechanism mediating the treatment benefits of statins. What matters is that LDL does not appreciably help predict a patient's cardiovascular risk or a statin's relative risk reduction and therefore provides a poor premise on which to base treatment recommendations. Beyond statins, we must extend our concern to the question of whether treatments might be harmful and not just whether they may or may not be effective.
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Read the complete article HERE.
If you are taking statins [Crestor,
Lipitor, etc] and you are not a male under 65 with a previously existing heart
condition, you may want to reconsider.
Dr
Michael Eades discusses the remarks of Dr. JoAnn Manson, who is describing the
analysis of data from the Women's Health Initiative study showing an association
between statin drugs and the development of diabetes.
