The Link between Nerve Damage and Statin Drugs

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:

1. HDL/Total Cholesterol Ratio: Should ideally be above 24 percent. If below 10 percent, you have a significantly elevated risk for heart disease.
2. 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.
• Make sure you are getting enough high quality, animal-based omega 3 fats, such as krill oil.
• 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.
• Exercise daily.
• Avoid smoking or drinking alcohol excessively.
• Be sure to get plenty of good, restorative sleep.

The goal of the tips above is not to necessarily lower your cholesterol as low as it can go; the goal is to optimize your levels so they’re working in the proper balance with your body.
Read the Full Article Here: http://articles.mercola.com/sites/articles/archive/2012/01/25/nerve-damage-with-cholesterol-meds.aspx


http://healthimpactnews.com/2012/the-link-between-nerve-damage-and-statin-drugs/

Back to basics: Coronary calcium

Posted on January 30, 2012 by Dr. William Davis

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.

http://www.trackyourplaque.com/blog/2012/01/back-to-basics-coronary-calcium.html?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+blogspot%2Ftpzx+%28The+Heart+Scan+Blog%29&utm_content=Google+Reader

Statin Drugs - To prescribe or not to prescribe.

To prescribe or not to prescribe: That is the statin question, experts debate

January 23, 2012 Michael O'Riordan

inShare0

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."

Doctors Threaten Strike; Others want us all to be guinea pigs

Doctors Threaten Strike; Others want us all to be guinea pigs
.
.
.

A new medical threat proposed

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:

1. In 2008, 21 homeless individuals in Poland died during an avian flu vaccine experiment.[14]
2. 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.
.
.
.
=================================================================

Read the full article here. Emphasis added by bd.

Don’t believe everything you read (including in scientific journals)

Don’t believe everything you read (including in scientific journals)

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

 

.

.

.

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.                       
=================================================
Read the complete article HERE.

Statins and Diabetes

Statins and Diabetes

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.

http://hallofrecord.blogspot.com/2012/01/statins-and-diabetes.html

New Ways of Marketing Statins: Cholesterol Lowering Drugs for the Flu?

 

New Ways of Marketing Statins: Cholesterol Lowering Drugs for the Flu?

by Dr. Mercola
A new study has led to what is perhaps the most ludicrous recommendation for flu treatment ever — statin drugs!
The researchers reported that statin use may reduce death risk in people hospitalized with the flu, and the media is reporting sensational headlines like “Statins reduce flu death risk by half.”
This is particularly outrageous, because the study was seriously flawed and designed to make statin drugs useful for another condition while they do nothing to address the underlying cause.
To validly determine if statin drugs are effective for flu they need to compare it to placebo, not a poison.
So what did they do?
They compared statin drugs to other toxic drugs, this time antiviral medications. So what the study actually found was that, more than likely, antiviral drugs were killing people twice as quickly as the statins!

What did the Study Really Show?

In the observational study published in The Journal of Infectious Disease, researchers examined data from 3,000 patients hospitalized with the flu, 33 percent of whom were given statins while the rest received antiviral drugs. The results showed that people who did not receive statins were twice as likely to die.
Another way of saying this, of course, is that people who received antiviral drugs were twice as likely to die as those given statins. And what this really means is that the antiviral medications were exceptionally harmful, not that statins were beneficial.
Still, it is not surprising that the drug’s manufacturer and the media are reporting favorable results for statin drugs, even though the researchers themselves pointed out the many limitations to their study, noting, for example:
” … it was difficult to ascertain the underlying functional health status of these patients, which may potentially confound the relationship between statins and severity of influenza.”
Further, one of the study’s authors has been a consultant to numerous drug companies, including Sanofi Pasteur, Novartis, Pfizer, Dynavax, and GlaxoSmithKline, whereas the study itself was funded by the Emerging Infections Program Cooperative Agreement of the U.S. Centers for Disease Control and Prevention (CDC), which also has worrisome ties to the drug industry.

Statins are Not Wonder Drugs

The drug companies started pushing their statin drugs, which are ordinarily prescribed to lower cholesterol levels, for the flu back in 2009 during the swine flu scare, and they are working hard to get the accepted as “wonder drugs” for the treatment of everything from pneumonia to Alzheimer’s disease.
However, as Dr. Stephanie Seneff, a senior scientist at MIT, explains, statins are dangerous because they suppress the synthesis of a true biological wonder drug, namely cholesterol. And she believes it is actually cholesterol (in high amounts prior to patients’ starting statin therapy) that is responsible for many of the statins’ alleged benefits:
“Statin drugs are particularly problematic because they suppress the synthesis of a biological wonder drug, namely cholesterol. Repeatedly, retrospective studies have shown an alleged benefit for statins, which is actually a benefit derived from the many years of high cholesterol that preceded statin treatment. This game has been played out for sepsis, pneumonia, multiple sclerosis, diabetes, and Alzheimer’s, and these are just the ones I’m aware of. When the proper placebo-controlled study is done, the effect reverses — statins make the situation worse. But these negative results are kept well concealed from the public’s eyes. This is how the myth has been kept alive that statins, instead of cholesterol, are the wonder drug.”
There are, in fact, 304 adverse health effects that may be associated with statin drugs, and this may only be the tip of the iceberg.

The Truth About Antiviral Flu Drugs

Anti-viral flu drugs like Tamiflu and Relenza are conventional medicine’s go-to option for treating the flu, but you should know that they carry serious side effects — and may only shorten the time you are sick by one to two days. These drugs are part of a group of anti-influenza drugs called neuraminidase inhibitors, which work by blocking a viral enzyme that helps the influenza virus to invade cells in your respiratory tract.
The problem is that your nervous system also contains neuraminidase enzymes essential for proper brain functioning, and when blocked with these dangerous drugs, severe neurotoxicity may ensue (especially in the infants and children whose blood-brain barrier has not yet developed sufficiently).
Serious side effects include convulsions, delirium or delusions, suicidal behavior and 14 deaths in children and teens have been reported as a result of neuropsychiatric problems and brain infections. Japan actually banned Tamiflu for children in 2007 because of the steep risks.
It was also around this time that the U.S. Food and Drug Administration (FDA) began reviewing reports of abnormal behavior and other brain effects in more than 1,800 children who had taken Tamiflu. Further, the drug commonly causes a myriad of side effects that, ironically, resemble the flu symptoms the drug claims to treat. You can decide for yourself whether these risks are worth a measly one- or two-day reduction in your flu symptoms:

Nausea	Vomiting
Diarrhea	Headache
Dizziness	Fatigue
Cough	Behavioral side effects (such as reports of children jumping off roofs shortly after taking the drug)

Statin Study Highlights Flu Shot Ineffectiveness

Whenever I address the topic of influenza, I like to mention flu shots, simply because the propaganda supporting them is so widespread — and the truth deserves to be heard. Not only is there a shocking lack of evidence supporting the use of the flu vaccine, but a number of studies have actually confirmed the danger and ineffectiveness of the shots.
One major study determined that the best the flu vaccine could do during a season where, in the rare case, the vaccine actually matched the wild-type strains in circulation, was to reduce the risk of influenza infection by a paltry 1 percent relative to unvaccinated controls. This means that despite receiving the shot – riddled, as it is, with side effects such as the debilitating and potentially deadly nerve disease Guillain-Barre Syndrome — there is still an overwhelming likelihood that you will not be protected from the flu as a result of receiving the vaccine.
The reason for this has to do with how flu strains work. Along with the faulty science behind the creation of the vaccine, the act of determining which flu strains will affect your area is pretty much a guessing game. Mainstream medical officials urge you to receive the shot, but health officials are fully aware that it is truly impossible to know for sure which strain to vaccinate against.
With such a wide selection of strains (hundreds, if not thousands), it is very rare for officials to actually pick the correct strains – the best case scenario is that an appropriate match will occur 10 percent of the time, according to the study. Interestingly, as it was not the researchers’ intent, the statin-flu study also highlighted the striking lack of effectiveness of the flu vaccine in preventing flu deaths:
“Our finding that vaccine was not effective in preventing mortality from influenza is likely explained by the timing of our study. We evaluated the impact of statins on influenza mortality in 2007–2008, a year in which the vaccine was not well matched to the circulating viruses … In addition, vaccination status may not impact mortality in the event of vaccine failure regardless of match to circulating strains; 50% of our patients were over the age of 70, an age group in which influenza vaccine is known to be less effective.”

Why Doesn’t the CDC Fund a Study on Vitamin D for Flu Treatment?

Apparently the CDC would rather throw money at a potential cash cow for the drug makers than promote the real natural alternatives that can stop the flu in its tracks without any side effects. Where is the CDC-sponsored study on vitamin D and the flu, for instance? According to the findings from a 2010 study that didn’t get any widespread attention, vitamin D is a highly effective way to avoid influenza. In fact, children taking low doses of vitamin D3 were shown to be 42 percent less likely to come down with the flu.
Dr. John Cannell, founder of the Vitamin D Council, was one of the first to introduce the idea that vitamin D deficiency may actually be an underlying cause of influenza, which would help explain its apparent benefits as a flu-fighter. His hypothesis was published in the journal Epidemiology and Infection in 2006, which was followed up with another study published in the Virology Journal in 2008.
Dr. Cannell’s hypothesis received further support and confirmation when, in the following year, the largest and most nationally representative study of its kind to date discovered that people with the lowest blood vitamin D levels reported having significantly more recent colds or cases of the flu. You can find my full recommendations for how to optimize your vitamin D levels in this past article.

There are Effective Natural Options for Beating the Flu

I have not caught the flu in over two decades, and you can avoid it too, without using drugs or getting vaccinated. Following these guidelines will help to keep your immune system in optimal working order so that you’re far less likely to acquire the infection to begin with — and if you do, these strategies will help you to get better, faster.

• Optimize your vitamin D levels. As I’ve previously reported, optimizing your vitamin D levels is one of the absolute best strategies for avoiding infections of ALL kinds, and vitamin D deficiency is likely the TRUE culprit behind the seasonality of the flu — not the flu virus itself. This is probably the single most important and least expensive action you can take.If you are coming down with flu-like symptoms and have not optimized your levels, you can take doses of 50,000 units a day a vitamin D3 for three days to treat the acute infection.
• Avoid sugar and processed foods. Sugar decreases the function of your immune system almost immediately, and as you likely know, a strong immune system is key to fighting off viruses and other illness. Be aware that sugar is present in foods you may not suspect, like ketchup and fruit juice.In fact, the first thing you want to do when you feel yourself coming down with a cold or flu is to avoid ALL sugars, artificial sweeteners, and processed foods.
• Get enough rest. Just like it becomes harder for you to get your daily tasks done if you’re tired, if your body is overly fatigued it will be harder for it to fight the flu. Be sure to check out my article Guide to a Good Night’s Sleep for some great tips to help you get quality rest.
• Implement effective tools to address your stress. We all face some stress every day, but if stress becomes overwhelming then your body will be less able to fight off the flu and other illness.If you feel that stress is taking a toll on your health, consider using an effective energy psychology tool such as the Emotional Freedom Technique, which is remarkably effective in relieving stress associated with all kinds of events, from work to family to trauma.
• Exercise. When you exercise, you increase your circulation and your blood flow throughout your body. The components of your immune system are also better circulated, which means your immune system has a better chance of finding an illness before it spreads. You can review my exercise guidelines for some great tips on how to get started.
• Take a good source of animal-based omega-3 fats like krill oil. Increase your intake of healthy and essential fats like the omega-3 found in krill oil, which is crucial for maintaining health. It is also vitally important to avoid damaged omega-6 oils like trans fats found in most processed foods, as it will seriously damage your immune response.
• Wash your hands. Washing your hands will decrease your likelihood of spreading a virus to your nose, mouth or other people. Be sure you don’t use antibacterial soap for this — antibacterial soaps are completely unnecessary, and they cause far more harm than good. Instead, identify a simple chemical-free soap that you can switch your family to.
• Eat garlic regularly. Garlic works like a broad-spectrum antibiotic against bacteria, virus, and protozoa in your body. And unlike with antibiotics, no resistance can be built up so it is an absolutely safe product to use. However, if you are allergic or don’t enjoy garlic it would be best to avoid as it will likely cause more harm than good.
• Avoid hospitals whenever possible. I’d recommend you stay away from hospitals unless you have an emergency, as hospitals are prime breeding grounds for infections of all kinds, and could be one of the likeliest places you could be exposed to flu bugs.

For even more details on specific immune-boosting foods and supplements that can help boost your immune function to help you kick your cold or flu faster, without drugs, please see my article The First Thing to do When a Cold or Flu Strikes.
Read the Full Article Here: http://articles.mercola.com/sites/articles/archive/2012/01/12/statin-drugs-for-flu-treatment.aspx


http://healthimpactnews.com/2012/new-ways-of-marketing-statins-cholesterol-lowering-drugs-for-the-flu/

Wisdom from The British Medical Journal blogger

BMJ's Ten Commandments for the Ideal Physician

The British Medical Journal's great blogger Richard Lehman has published the following Ten Commandments for excellent clinical practice. These are great rules of thumb for any savvy health care practitioner--but they do require that wee bit of extra work to truly understand the statistics behind the medical literature.

 

The New Therapeutics: Ten Commandments

• Thou shalt treat according to level of risk rather than level of risk factor.
• Thou shalt exercise caution when adding drugs to existing polypharmacy.
• Thou shalt consider benefits of drugs as proven only by hard endpoint studies.
• Thou shalt not bow down to surrogate endpoints, for these are but graven images.
• Thou shalt not worship Treatment Targets, for these are but the creations of Committees.
• Thou shalt apply a pinch of salt to Relative Risk Reductions, regardless of P values, for the population of their provenance may bear little relationship to thy daily clientele.
• Thou shalt honour the Numbers Needed to Treat, for therein rest the clues to patient-relevant information and to treatment costs.
• Thou shalt not see detailmen, nor covet an Educational Symposium in a luxury setting.
• Thou shalt share decisions on treatment options with the patient in the light of estimates of the individual’s likely risks and benefits.
• Honour the elderly patient, for although this is where the greatest levels of risk reside, so do the greatest hazards of many treatments.

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

http://carlatpsychiatry.blogspot.com/2012/01/bmjs-ten-commandments-for-ideal.html

Why Doesn’t My Doctor Know All of This?

The following is not specifically about heart disease or cholesterol as is most of this blog content. But it does apply. Thyroid dysfunction can be tied in with heart disease if in no other way than making certain lipid abnormalities difficult or nearly impossible to normalize in the quest to reduce plaque growth. In short, I believe this is a valuable discussion of an important issue applicable to CAD.

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

Why Doesn’t My Endocrinologist Know All of This?

A question often raised by patients is: “Why doesn’t my physician know about the inaccuracies and limitations of standard thyroid tests?” The reason is that the overwhelming majority of physicians (endocrinologists, internists, family practitioners, rheumatologists, etc.) do not read medical journals. When asked, most doctors will claim that they routinely read medical journals, but this has been shown not to be the case. Many reasons exist, but it comes down to the fact that doctors do not have the time — they are too busy running their practices. The overwhelming majority of physicians rely on what they have learned in medical school and on consensus statements by medical societies, such as the Endocrine Society, the American Association of Clinical Endocrinologists or the American Thyroid Association, to direct treatment decisions.

Historically, relying on a consensus statement to treat or not to treat a particular patient has been shown to result in poor care and, as such, society consensus statements and practice guidelines are considered to be worst level of evidence in support of a particular therapy or treatment. A number of organizations, including the World Health Organization and others, have ranked the strength and accuracy of various types of evidence used in the medical decision process. In all scoring systems, the highest strength of evidence is randomized control trials and meta-analyses, with lower scores for other types of evidence. All grading systems place consensus statements and expert opinion by respected authorities (societies) as the poorest level of evidence, because historically they have failed to adopt new concepts and treatments based on new knowledge or new-found understanding demonstrated in the medical literature (1-6).

For instance, a recent study published in the 2009 Journal of American Medical Association studied the evidence supporting the practice guidelines and consensus statements published by the American College of Cardiology and the American Heart Association. It was found that only 11% of the recommendations, practice guidelines and consensus statements were based on quality evidence and over half were based on poor quality evidence that was little more than the panel’s opinion. The review also found that even the strongest (Class 1) recommendations, which are considered medical dogma, cited as a legal standards and often go unquestioned as medical fact, were only supported by high quality evidence 19% of the time and not revised based on new evidence (6).

Similarly, the Endocrine Society, the American Association of Clinical Endocrinologists and the American Thyroid Association also have a long history of guidelines and recommendations that are not supported by the medical literature and fail to adjust or abandon recommendations when new understanding and knowledge contradicts their recommendations. A case in point is the recommendation by these societies that a normal TSH adequately rules out thyroid dysfunction, despite massive amounts of literature that demonstrate this not to be the case (see Diagnosis of Hypothyroidism) or that T4 only replacement is adequate for most patients. A doctor who simply follows outdated society treatment guidelines that relies on a simple laboratory test and ignores the clinical aspects of a patient is not practicing evidence-based medicine. (1-7). Such doctors may be adequate as lab technicians, but as doctors and clinicians they fall short (1-7). This method of practice is consistently rebuked as improper and poor medicine, but has become the standard used by a large percentage of endocrinologists and physicians who feel medicine can be related to simply reading “normal” or “abnormal” in a laboratory column.

Discussing the lack of scientific basis of most medical society’s consensus statements and treatment guidelines in Internal Medicine News, Dr. Diana Petritti, states, “Expert opinion and consensus statements can be quite misleading when used as the basis for a practice. Expert opinions imply that there is something that the experts know that clinician doesn’t know. I don’t think it’s always appreciated that it’s only opinion. There is a tendency to make guidelines and recommendations seem authoritative. I believe that physicians think that there is a great deal more behind authoritative recommendations than there might be when you lift the lid of the box and see what’s underneath(8).”

There has been significant concern by health care organizations and medical experts that physicians are placing too much reliance on consensus statements and failing to learn of new information presented in medical journals. Thus, they lack the ability to translate this new information into treatments for their patients. The concern is that doctors fail to practice evidence-based medicine, erroneously relying on what they have previously been taught and on “expert” societies instead of changing treatment philosophies based on new information as it becomes available. This is especially true for endocrinological conditions, where physicians are very resistant to changing old concepts of diagnosis and treatment — despite overwhelming evidence to the contrary — because it is not what they were taught in medical school and endocrinology residency.

This concern is particularly clear in an article published in the New England Journal of Medicine entitled “Clinical Research to Clinical Practice: Lost in Translation” (9). The article was written by Claude Lenfant, M.D., Director of National Heart, Lung and Blood Institute, and it is well supported. He states that there is great concern that doctors continue to rely on what they learned 20 years before and are uninformed about scientific findings. According to Dr. Lenfant, medical researchers, along with public officials and political leaders, are increasingly concerned about physicians’ inability to translate research findings in their medical practice to benefit their patients. He says that very few physicians learn about new discoveries from reading medical journals or by attending scientific conferences; thus, they lack the ability to translate new knowledge in the field into enhanced treatments for their patients. He states that a review of past medical discoveries reveals how excruciatingly slow the medical establishment is to adopt novel concepts, noting that even simple methods to improve medical quality are often met with fierce resistance. “Given the ever-growing sophistication of our scientific knowledge and the additional new discoveries that are likely in the future, many of us harbor an uneasy, but quite realistic suspicion that this gap between what we know about disease and what we do to prevent and treat them will become even wider. And it is not just recent research results that are not finding their way into clinical practice; there is plenty of evidence that ‘old’ research outcome have been lost in translation as well (1).”

Dr. Lenfant discusses the fact that the proper practice of medicine involves the combination of medical knowledge, intuition and judgment and that physicians’ knowledge is lacking because they don’t keep up with the medical literature. He states that there is often a difference of opinion among physicians and reviewing entities, but that judgment and knowledge of the research pertaining to the patient’s condition is central to the responsible practice of medicine. “Enormous amounts of new knowledge are barreling down the information highway, but they are not arriving at the doorsteps of our patients. (9).”

These thoughts are echoed by physicians who have researched this issue as well, such as William Shankle, M.D., Professor, University of California, Irvine. He states, “Most doctors are practicing 10 to 20 years behind the available medical literature and continue to practice what they learned in medical school….There is a breakdown in the transfer of information from the research to the overwhelming majority of practicing physicians. Doctors do not seek to implement new treatments that are supported in the literature or change treatments that are not (10).”

This view is echoed by the Dean of Stanford University School of Medicine who states that in the absence of translational medicine the delivery of medical care would remain stagnant and uninformed by the tremendous progress taking place in science and medicine (11).

This concern has also received significant publicity in the mainstream media. An example is an article by Sidney Smith, M.D., former president of the American Heart Association, published in 2003 in the Wall Street Journal entitled Too Many Patients Never Reap the Benefits of Great Research. Dr. Smith is very critical of physicians for not seeking out available information and applying that information to their patients, arguing that doctors feel the best medicine is what they’ve been doing and thinking for years. They discount new research, Dr. Smith says, because it is not what they have been taught or practiced, and they refuse to admit that what they have been doing or thinking for many years is not the best medicine. He states, “A large part of the problem is the real resistance of physicians…; many of these independent-minded souls don’t like being told that science knows best, and the way they’ve always done things is second-rate (12).” The National Center for Policy Analysis also expresses concern for the lack of ability of physicians to translate medical therapies into practice (13).

A review published in The Annals of Internal Medicine found that there is clearly a problem of physicians not seeking to advance their knowledge by reviewing the current literature, believing proper care is what they learned in medical school or residency and not basing their treatments on the most current research. The review found that the longer a physician is in practice, the more inappropriate and substandard the care (14). Thus, it is not a surprise that the scientific evidence as expressed in the literature is often opposite to what is continually repeated as dogma by most physicians and those considered to be “experts.”

Another example is a study published in the Journal of the American Medical Informatics Association (15). In reviewing the study, the National Institute of Medicine reports that there is an unacceptable lag between the discovery of new treatment modalities and their acceptance into routine care: “The lag between the discovery of more effective forms of treatment and their incorporation into routine patient care averages 17 years.” (16) In response to this unacceptable lag, the Business and Professions Code passed an amendment relating to the healing arts. This amendment — CA Assembly Bill 592; An Act to Amend Section 2234.1 of the Business and Professions Code — states: Since the National Institute of Medicine has reported that it can take up to 17 years for a new best practice to reach the average physician and surgeon, it is prudent to give attention to new developments not only in general medical care but in the actual treatment of specific diseases, particularly those that are not yet broadly recognized [such as the concept of tissue hypothyroidism, chronic fatigue syndrome and fibromyalgia] (17).

The Principals of Medical Ethics adopted by the American Medical Association in 1980 states that a physician shall continue to study, apply, and advance scientific knowledge, make relevant information available to patients, colleagues, and the public (18). This has, unfortunately, been replaced with a goal of providing merely “adequate” care. The current insurance reimbursement system in the United States fosters this thinking, as the worst physicians are financially rewarded by insurance companies. While it is true that the best physicians are continually fighting to provide cutting edge treatments and superior care that the insurance companies deem not medically necessary, even these physicians eventually get worn down and are forced to capitulate to the current system that promotes substandard care.

This was clearly demonstrated in a study published in the March 2006 edition of The New England Journal of Medicine entitled “Who is at Greater Risk for Receiving Poor-Quality Health Care.” The study found that the majority of individuals received substandard, poor-quality care, and that there was no significant difference among different income levels or whether or not the individual was covered by insurance. It used to be the case that only those in low socioeconomic classes without insurance received poor-quality care. But insurance company restrictions on treatments and diagnostic procedures have made the same poor care afforded to those of low socioeconomic status the new standard-of-care for society at large (19). An example of this is a physician’s failing to spend the time to adequately assess a potential hypothyroid patient and instead simply does a TSH test.

Most physicians will satisfy their required amount of continuing medical education (CME) by going to a conference a year, usually at a highly desirable location that has skiing, golf, boating, etc. Physicians are rarely monitored as to whether or not they actually showed up for the lectures or went skiing instead. One must also understand that the majority of conferences organized by medical societies are in fact sponsored by pharmaceutical companies. These payments by pharmaceutical companies are called unrestricted grants, so that the society has free reign to do what they want with the money and thus can claim there is no influence of lecture content by the companies. The problem, however, is that if the society wants to continue getting these “unrestricted” grants, they must think twice about providing content that the sponsoring pharmaceutical company might disapprove of. Consequently, ground breaking research that goes against the status quo and does not support the drug industry receives little attention.

Evidence-based medicine involves the synthesis of all available data when comparing therapeutic options for patients. Evidence-based medicine does not mean that data should be ignored until a randomized control trial of a particular size and duration is completed. A physician who tries to avoid the need of being a physician and is fine with just being a technician or health care provider will adamantly defend the “one-size fits all” method of diagnosis and treatment. But the best doctors who truly practice evidence-based medicine and not merely the perception of such will not rely on consensus statements to best provide their patients. Instead of relying on old dogma, the best physicians will seek out and translate both basic science results and clinical outcomes to decide on the safest, most efficacious treatment for their patients. Further, the best physicians will continually assess the current available data to decide which therapies are likely to carry the greatest benefits for patients and involve the lowest risks.

http://nahypothyroidism.org/why-doesn%E2%80%99t-my-doctor-know-all-of-this/

From: Oxford University Press Quarterly Journal of Medicine.
http://qjmed.oxfordjournals.org/content/early/2010/11/29/qjmed.hcq230.full

Statin-induced diabetes: perhaps, it’s the tip of the iceberg

The meta-analysis by Mills et al.¹ involving 170 255 patients randomized in 76 trials reported on the efficacy and safety of statin therapy for the prevention of cardiovascular disease (CVD) and found a relative 9% increased risk in the development of incident diabetes (P = 0.001) among subjects randomized to statins compared with placebo in the 17 trials reporting on diabetes development. It is noteworthy that the average age of the subjects in the meta-analysis was 59.6 years, average follow-up was 2.7 years and more than half of the subjects were randomized for the primary prevention of CVD. We feel that the implications of statin-induced diabetes are not trivial, but of major concern, particularly in the primary prevention of CVD when statin therapy might be used for decades in individuals at relatively low risk²; many questions need answering before statin therapy can be safely recommended across broad populations.

Interestingly, a recently published meta-analysis involving 91 140 patients randomized in 13 trials³ specifically looking at the risk of incident diabetes from statin therapy also revealed a significant 9% increased relative risk of the development of diabetes over a mean overall trial period of 4 years. Disturbingly, 2 of the 13 trials demonstrated very high incidence of the development of diabetes among the statin-treated subjects. The Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER),⁴ a primary prevention trial of 1.9-year duration in subjects with a mean age of 66 years, demonstrated a significant relative increase in diabetes incidence of 26% among subjects randomized to rosuvastatin; the absolute rate of incident diabetes expressed in events per 1000 patient-years was 13 and 16 among the placebo and rosuvastatin subjects, respectively. Low-density lipoprotein (LDL) cholesterol was decreased robustly by 50% in the rosuvastatin subjects and the median LDL cholesterol at the end of follow-up was 55 mg/dl. The PROspective Study of Pravastatin in the Elderly at Risk (PROSPER),⁵ a combined primary and secondary prevention trial of 3.2-year duration in subjects with a mean age of 76 years, demonstrated a significant relative increase in diabetes incidence of 32% among subjects randomized to pravastatin; the absolute rate of incident diabetes expressed in events per 1000 patient-years was 16 and 21 among the placebo and pravastatin subjects, respectively. LDL cholesterol was decreased by 31% in the pravastatin subjects. Therefore, it appears that the risk of statin-induced diabetes is more prominent with aggressive LDL cholesterol lowering and among the elderly subjects. It is of concern that thought leaders in the cardiovascular arena strongly suggest that statin use should be increased from 16 to 100 million people in the USA and LDL cholesterol should be aggressively lowered.⁶ This issue takes even more relevance given that the prevalence of diabetes is rapidly increasing in the USA⁷ and worldwide⁸; alarmingly, three-quarters of the elderly in the USA have diabetes or pre-diabetes.⁷

In vivo studies have demonstrated that despite lowering LDL cholesterol levels, some^9–11 but not all statins¹¹ significantly increase fasting plasma insulin levels and significantly decrease insulin sensitivity in hypercholesterolemic patients in a dose-dependent manner. Statins can significantly increase fasting plasma insulin levels and glycated hemoglobin levels in the absence of significant changes in fasting glucose.^9–11 Additionally, some statins have been shown to significantly decrease plasma adiponectin levels.^10,11

In vitro and animal studies^12,13 have shown that statins can significantly decrease the expression of the insulin-responsive glucose transporter 4 (GLUT4) in adipocytes. GLUT4 is distributed in the intracellular compartment in the basal state and relocates to the cell membrane in response to insulin signaling. Moreover, statins increase the expression of GLUT1¹² in adipocytes; GLUT1 is localized in the cell membrane. It is unclear how statins change the expression of GLUT1 and GLUT4; perhaps, it is related to an inhibition of isoprenoid biosynthesis by statins¹² or cholesterol lowering, leading to a change in membrane lipid raft structure resulting in decreased insulin signaling.¹⁴ Since GLUT4 concentrations are not reduced in skeletal muscle in obese subjects and subjects with diabetes, and skeletal muscle is the primary source of insulin-stimulated glucose disposal, it has been argued that whole-body insulin sensitivity cannot be explained by a decrease in the production of GLUT4¹⁵; however, it has been shown that the downregulation of GLUT4 and resulting glucose transport in adipose tissue can cause insulin resistance.¹⁶ It is notable that GLUT4 concentrations are decreased in skeletal muscle in elderly compared with younger subjects,¹⁵ which might explain why the elderly are more sensitive to the diabetes promoting effects of statin therapy. Furthermore, dysregulation of cellular cholesterol may attenuate pancreatic β-cell function, since cholesterol maintains normal function of voltage gated calcium channels and is vital in the mobilization and fusion of insulin granules with the cell membrane.¹⁷ In summation, there are many ways by which statin therapy might lead to hyperinsulinemia, insulin resistance, prediabetes and diabetes.

In addition to the classic complications of diabetes such as CVD, renal failure, blindness and neuropathy, epidemiological studies demonstrate that diabetes is related to the increased risk of many cancers.¹⁸ These include liver, pancreas, kidney, endometrial, colorectal, bladder and breast cancer and non-Hodgkin’s lymphoma. A large European population study with a median follow-up of 15.8 years has shown that compared with individuals with normal glucose tolerance, men and women with prediabetes or diabetes had a significant increase in cancer mortality, irrespective of the body mass index.¹⁹ There is epidemiological evidence that insulin resistance is associated with cancer in Eastern populations.²⁰ Interestingly visceral fat mass, assessed by computed tomography, but not subcutaneous fat mass, correlates positively with cancer²¹; indeed, visceral fat is a strong determinant of insulin resistance and hyperinsulinemia.

There are many ways by which hyperinsulinemia can promote cancer.^18,22 Hyperinsulinemia results in an increase in the biologically active free circulating insulin-like growth factor-1 (IGF-1) by increasing hepatic IGF-1 production²² and decreasing IGF-1 binding proteins.¹⁸ Tumor cells are replete with IGF-1 receptors and two isoforms of insulin receptors (IR-A and IR-B).²³ IGF-1 primarily signals through the IGF-1 receptor resulting in mitogenic effects and, not surprisingly, higher IGF-1 blood levels have been associated with an increased risk of several cancers.^24,25 Insulin signaling through the IR-A and IR-B results in mitogenic and metabolic effects, respectively.²² Hyperinsulinemia can persist for decades in prediabetic states and it is certainly conceivable that this prolonged mitogenic stimulus increases cancer promotion as has been seen in epidemiological studies.

Statin therapy might affect tumor metabolism by insulin independent means. As previously mentioned, some statins decrease adiponectin levels.^10,11 This is potentially problematic over the long-term since adiponectin is anti-proliferative and anti-angiogenic and has other oncostatic properties.²⁶ Furthermore, obesity is associated with lower circulating adiponectin levels and this might partially explain the association of obesity and various cancers. Additionally, the fact that statin therapy might increase GLUT1 expression¹² is of concern since GLUT1 is already overexpressed and is the main glucose transporter in cancer cells.²⁷ Glucose uptake by cancer cells is extremely avid and up to 30 times that of normal cells and utilized by glycolysis for energy and supplying important metabolites for rapid cellular proliferation.²⁸ Indeed, in human studies, increased expression of GLUT1 in cancer cells has been associated with poor prognosis of many cancers.^27,29

The Western diet is permissive to the diabetogenic effects of statin therapy. The prevalence of obesity has been steadily increasing in the USA and more than two-thirds of adults are overweight or obese.³⁰ As mentioned, the prevalence of diabetes has been increasing in the USA and a majority of the elderly subjects in the USA now have pre-diabetes or diabetes.⁷ Interestingly, total cholesterol and LDL cholesterol have been decreasing in the USA likely due to cholesterol awareness and the increased use of lipid-lowering medication, and more than half of the elderly subjects in the USA have reported using lipid-lowering medications.³¹ However, blood triglyceride levels have been steadily increasing despite the increasing use of lipid-lowering therapy.³¹ Intriguingly, it is now believed that abnormalities in fatty acid metabolism are at the root of diabetes, and ectopic lipid accumulation in muscle, liver and pancreatic β-cells leads to the development of insulin resistance by interfering with insulin signaling.^32,33 The increase in blood triglyceride levels is driven by a high carbohydrate diet and partially fueled by the increase in dietary sweetener consumption.³⁴ Unfortunately, fructose consumption, largely from sweetened beverages, has escalated drastically in North America over the past three decades³⁵ and excessive fructose intake leads to increased hepatic de novo lipogenesis resulting in hepatic steatosis, visceral fat accumulation and ectopic lipid deposition in skeletal muscle, thereby all leading to insulin resistance.

We are living in times when there seems to be a much stronger emphasis on the use of drugs over lifestyle change to prevent disease. The food industry has been uncooperative and blames personal responsibility as a cause of the obesity problem.³⁶ There is a belief among many patients that they can eat whatever they want as long as they are on statin therapy.³⁷ This has been amplified by a proposal to offer powdered statin in packets to be sprinkled on hamburgers at fast-food restaurants in order to neutralize the detrimental effect of the food choice.³⁸ Plant-based diets have been shown to decrease both CVD and cancer risk and even result in a rapid change in gene expression in neoplastic tissue, and they are not diabetogenic.^39–41 Moreover, a Mediterranean diet has been shown to counter the insulin raising effects of simvastatin therapy.⁴² It is extremely troubling that a goal has been proposed for decreasing the LDL cholesterol levels of all subjects worldwide to below 100 mg/dl and ideally below 60 mg/dl by statin therapy.⁴³

In conclusion, many important questions need answering before expanding the use of statin therapy, particularly for the primary prevention of CVD. In what proportion of subjects do statins increase plasma insulin levels, even if there is no progression to diabetes? Are some statins more likely than others to cause hyperinsulinemia because of physiochemical differences? Will prolonged statin therapy result in chronic hyperinsulinemia and potentially increase prediabetes, diabetes and/or cancer? Will this risk outweigh any perceived benefits, particularly in the elderly or in aggressively treated patients? Will the Western diet and lifestyle encourage the use of more statin therapy and provide a metabolic substrate to further perpetuate hyperinsulinemia and its subsequent complications? Is the increase in diabetes prevalence in the elderly subjects fueled partially by the increasing use of statins in this age group? What statins decrease blood adiponectin levels, and is it continuous, and, if so, what are the long-term clinical implications? How should physicians monitor patients for the adverse metabolic effects of statin therapy? Should subjects have a plasma insulin level measured prior to initiating and during statin therapy? What diet or diets will mitigate the hyperinsulinemic effects of statin therapy? Will statin therapy used by subjects with a history of cancer increase the chance of hyperinsulinemia increasing the promotion of occult micrometastatic disease? Finally, physicians should realize that statin-induced diabetes, as seen in the relatively short-term clinical trials, might be just the tip of the iceberg, and properly designed clinical trials must be done to determine what else lurks beneath the water in order to ensure the safety of patients on long-term treatment with these drugs.

• © The Author 2010. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oup.com