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immunize yourself against the pandemic of lifestyle diseases

Archive for the ‘atherosclerosis’ Category

Otherwise known as hardening of the arteries, the commonest cause of death in the world and 99.99% preventable.

Geneticist Cures His Own Type 2 Diabetes by Changing his Lifestyle not his Genes

Posted by Colin Rose on April 15, 2012

This story in Science Now, a vehicle published by the AAAS for vulgarization of  basic science, is a classic example of the hype surrounding gene sequencing and gene expression. To judge from this headline any reader would assume that the cure for Type 2 diabetes was simply to measure genes and gene expression. However when one reads the actual publication one discovers that the geneticist cured his diabetes by changing his lifestyle and didn’t even look at his “omics” while doing so. It`s a shame he didn`t report his omics during the lifestyle change because there would undoubtedly have been significant changes in gene expression only by changing the environment with no drugs. Such a demonstration might encourage other people to make those lifestyle changes before taking drugs knowing that there are signficant effects on the expression of genes. In a personal communication Dr. Snyder said that he has the data and will publish it later.

Before the days of genomics when I was reviewing grant applications, any application that proposed to blindly measure thousands of variables hoping to find something  related to a disease or a macroscopic process was immediately rejected as a “fishing expedition”. But genomics is now big business. $Billions are being spent on it in the futile hope that a genetic silver bullet will be found for those diseases of self-destructive lifestyles that account for most of our morbidity and premature mortality. As Dr. Snyder has elegantly demonstrated, we need to first change lifestyles and then maybe worry about the genetics of whatever rare diseases remain.


Classic hype by the promoters of “omics”, short for genomics, proteomics and metabolomics. The underlying myth is that by measuring enough genes and their products something will be found that can be targeted with a genetic silver bullet and save us from our self-destructive lifestyles.


Dr. Snyder measured various gene products from day 0 to day 420 when he inexplicably stopped. He developed type 2 diabetes during a respiratory virus infection probably due to increased insulin resistance. He then realized he had to change his lifestyle and cut his calorie intake and exercised. By day 550 his blood glucose was back to normal. The cure of his diabetes had nothing to do with measuring his gene expression and everything to do with changing his environment.


Dr. Snyder developed two viral infections while monitoring his “omics” but inexplicably stopped measuring them 20 days after he developed type 2 diabetes. The heavy black bar indicates when he changed his lifestyle by eating less calories and exercising more during which time he only measured his blood glucose.

The Future is your DNA?

“The future is your DNA.” Who was the PR type at McGill who came up with that slogan? As we see above, Dr. Snyder, geneticist extraordinaire, has clearly shown that his future is his lifestyle. Everyone is born with a fixed genome. There are very rare diseases that are purely genetic in cause but the diseases that maim and kill most of the world’s population are primarily environmental. Our genomes are optimized to permit reproductive success in an environment of scarcity and borderline starvation and are not and never will be optimized to an environment of unlimited addictive  highly processed food, alcohol and other drugs. Any amount of “omics” will not change that basic fact. In addition, the genomics promoters gloss over the profound problem in trying to make a connection between a linear code and the three-dimensional organism produced from the code. The phenotype is the result of unfathomably complex, self-referrential signalling and, so except for some relatively rare diseases that can be linked to genetic errors, there is no direct connection of the genome to predilection to common diseases. That is why huge amounts of data must be collected and huge amounts of money spent to glean even a borderline connection. This is why a recent study published in Science by the AAAS, the same organization that publishes ScienceNow, mentioned above, concluded that “for 23 of the 24 diseases, the majority of individuals will receive negative test results, … [so] these negative test results will, in general, not be very informative, as the risk of developing 19 of the 24 diseases in those who test negative will still be, at minimum, 50 – 80% of that in the general population”. In other words common diseases are caused by environmental factors regardless of the genome. Your future is your lifestyle choices.

In the more than ten years since the human genome was sequenced there is zero evidence that anyone has lived any longer because of that effort, as intellectually satisfying as it was. In Western societies, what has significantly prolonged life in the last decade is reduction in cigarette smoking. But other legal addictions to prescription drugs, junk food and alcohol threaten to wipe out these gains. Dr. Levin pleads for gene sequencing to solve the mysteries of chronic diseases like atherosclerosis that causes heart attacks and most stokes. “Via genomics medicine will become a more personalized, predictive and preventative science.” Such talk makes for good politics and attracts huge expenditures from governments, such as the likes of Génome Québec. Governments hate having to tell the electorate to change those self-destructive lifestyles that are the proven cause of atherosclerosis and most cancers but love to be seen as pursuing superficially attractive but futile high-tech cures that will obviate the need to control those legal addictions to which the electorate is very attached.

Posted in atherosclerosis, diabetes, Type 2, diet, environment, exercise, food, genomics, junk food | Tagged: , | 1 Comment »

“Low risk” nurse with normal cholesterol but self-destructive lifestyle ends up with heart transplant after CCTA

Posted by Colin Rose on December 20, 2010

Here in a nutshell is a demonstration of the problem with expecting technology to substitute for good clinical medicine and save us from our self-destructive addictions. If anyone is puzzled about the dichotomy between the exorbitant cost of the US medical system and its relative lack of effect on any measure of health here is the reason.

Below is a story from followed by the actual paper in the Archives of Internal Medicine minus the references.

In the absence of any symptoms attributable to coronary artery disease there was no reason to do any more testing but the temptation to use high tech tools without good indication is irresistible to many doctors. CCTA is the latest expensive test to detect coronary atherosclerosis. Patients think that they will never have a heart attack and live longer if the disease is detected and some surgical procedure, like an angioplasty or bypass is done and doctors making $millions from doing them are not about to discourage them and point out the total lack of evidence for any significant benefit from angiography or the surgical procedures in patients with chronic coronary disease.

The authors have labelled this patient “low risk” because her “cholesterol” was normal but clearly she was at high risk based on her obesity and hypertension, both indices generally of  junk food addiction, in spite of her being a nurse.  When she started new exercises she probably got muscle pain from weight lifting. With an obvious self-destructive lifestyle, she should not have been “simply reassured” as recommended by the editors. But instead of encouraging her to make meaningful lifestyle change her doctors ordered tests with no clinical indication.

Framingham scores, lipid profiles and CRPs can be very deceptive because they do not assess LDL modification in the arterial wall, essential to the formation of atherosclerotic plaque. In spite of having “normal” numbers for all the usual “risk factors” she had advanced atherosclerosis in her coronary arteries. Apparently no dietary history was taken and no attempt was made to encourage her to change her lifestyle, an example of gross diagnostic and therapeutic incompetence, all too common in an era of absolute faith in the power of technology to protect us from our self-destructive addictions. Doctors abdicate professionalism by ordering tests instead of dealing with the real problems, like junk food addiction, which take much time for which they are not compensated and risk alienating patients who demand a high-tech fix or reassurance so that they can continue their risky behaviour.


Case study shows how “just-in-case” CCTA in a low-risk patient may spectacularly backfire

DECEMBER 17, 2010 | Reed Miller

San Francisco, CA – Coronary computed tomographic angiography (CCTA) in patients with a low pretest risk of coronary disease wastes resources and can even lead to horrendous outcomes, a case study published December 13, 2010 in the Archives of Internal Medicine shows. The report tells the story of a 52-year-old white female who initially presented with chest pain and had a CCTA; this was followed by an unfortunate chain of events in which she suffered an aortic dissection during cardiac catheterization and that culminated in her having a heart transplant.

Part of its ongoing “Less is More” series begun last April, the latest case, reviewed by Dr Matthew Becker (St Vincent’s Heart and Vascular Institute, Erie, PA), Dr John Galla (Providence Hospital, Mobile, AL), and Dr Steven Nissen (Cleveland Clinic, OH), describes how the well-meaning attempt to reassure a patient with a low risk of coronary disease backfired spectacularly.

“Perhaps the most important point to be learned from the case described by Becker and colleagues is that there are safer ways to reassure patients,” say journal editors Drs Rita RedbergMitchell Katz, and Deborah Grady (University of California, San Francisco) in an accompanying editorial. “Patients value our advice. Talking with our patients should be our first choice for reassurance.” They add that “applying the ‘less-is-more’ principles prospectively could have avoided this unfortunate case.”

From diagnostic uncertainty to disaster
The 52-year-old nurse had hypertension and mild obesity and had recently begun an exercise and diet regimen to control her weight and blood pressure. She presented to her primary physician with chest pain, but no other symptoms: she had a normal ECG with a normal lipid profile and normal C-reactive-protein level. Her doctor attributed the chest pain to a musculoskeletal cause but performed a CCTA to reassure her that she was not at risk for a coronary event.

The CCTA showed discrete, noncalcified, nonobstructive plaque in the mid and distal segments of the left circumflex and dominant right coronary arteries and diffuse, complex calcification in the proximal left anterior descending (LAD) coronary artery. Because that calcification was difficult to quantify, the physician recommended that she undergo cardiac catheterization to get a clearer look at the LAD.

This exam, performed at the local community hospital, revealed only a mild irregularity in the LAD, but during the procedure, the patient complained of chest pressure, which prompted an aortogram that revealed an aortic root dissection that was compromising the left main coronary artery.

So the patient underwent urgent coronary artery bypass graft (CABG) surgery and stayed in the hospital for two weeks with a residual left ventricular ejection fraction of 35%. The bypass graft soon failed and was treated with multiple drug-eluting stents, but despite her compliance with dual antiplatelet medical therapy, a stent in the vein graft supplying the circumflex artery developed a thrombosis, causing an ST-segment-elevation MI complicated by cardiogenic shock. The thrombosis was successfully treated, but the patient remained in refractory cardiogenic shock and ultimately underwent orthotopic heart transplantation.

Unnecessary testing happening every day
“With few cardiac risk factors and an atypical chest pain presentation, this patient had a low pretest probability for coronary artery disease and should have been reassured and not undergone any further risk stratification,” say the authors. “Lacking randomized data suggesting improvement in clinical outcomes and with clear risks, including contrast load, radiation exposure, and suboptimal diagnostic specificity, CCTA should have a very limited role in the evaluation of patients who present with chest pain.”

They acknowledge the risk of complications associated with cardiac catheterization is low, but catastrophic events are always a possibility. They believe the physicians in this case overestimated the stenosis in this patient’s coronaries because they did not fully appreciate the CCTA’s potential for false-positive findings. Complete visualization of all segments of the coronary tree with CCTA is often hindered by cardiac motion, which can lead to the appearance of “blooming artifacts” of coronary calcification that may cause the observer to overestimate the extent of stenosis.

Becker et al point out that previous studies comparing CCTA with conventional coronary angiography in diverse patient populations show CCTA’s sensitivity is between 79% and 100% for the detection of obstructive coronary disease, but its specificity is only 64% to 85%, corresponding to “an unacceptably high false-positive rate” of up to 81% in some populations.

As reported by heartwire, the recently released professional guidelines on Appropriate Use Criteria for Cardiac Computed Tomography list CCTA as “inappropriate” for detection of CAD patients with a low risk of heart disease, ability to exercise, nonacute symptoms that may be an “ischemic equivalent,” and an interpretable ECG.

Patient could have been simply reassured
“If a test is not sufficiently accurate to change clinical management in a particular setting, it should not be done,” but according to Redberg et al, often these tests are done anyway—sometimes even before the patient sees a physician—because nobody has assessed the patient’s pretest probability of the disease or properly considered how the test result will change the clinical management of the patient.

“There are cases where [the test presents] more risks than benefits, and you really need to consider the risks and benefits and not [assume that] just because you can do the test, you should do the test. And this case highlights that,” Redberg told heartwire.

Cases like this where an inappropriate test leads to many complications and near catastrophe are rare, “but to have a CT or another test that was just done for reassurance, when you could have just told the patient ‘You’re fine,’—I think that’s done every day lots of times.

“You don’t know which [tests] are going to lead to that kind of problem, but you do know which of those is not going to give you any benefit, so if there is no benefit, it’s better not to be taking any risk, even a small one.”


Left Main Trunk Coronary Artery Dissection as a Consequence of Inaccurate Coronary Computed Tomographic Angiography

Matthew C. Becker, MD; John M. Galla, MD; Steven E. Nissen, MD

Arch Intern Med. Published online December 13, 2010. doi:10.1001/archinternmed.2010.464


A 52-year-old woman presented to a community hospital with atypical chest pain. Her low-density lipoprotein cholesterol and high-sensitivity C-reactive protein levels were not elevated. She underwent cardiac computed tomography angiography, which showed both calcified and noncalcified coronary plaques in several locations. Her physicians subsequently performed coronary angiography, which was complicated by dissection of the left main coronary artery, requiring emergency coronary artery bypass graft surgery. Her subsequent clinical course was complicated, but eventually she required orthotropic heart transplantation for refractory heart failure. This case illustrates the hazards of the inappropriate use of cardiac computed tomography angiography in low-risk patients and emphasizes the need for restraint in applying this new technology to the evaluation of patients with atypical chest pain.


A 52-year-old white female nurse with a medical history that was notable for hypertension and mild obesity presented to her local primary care physician with the recent onset of chest pain. Further investigation revealed that in an effort to lose weight and assist in the control of her hypertension, she had adopted a new diet and exercise program several weeks earlier. At her initial presentation, she described 48 hours of nonexertional, sharp chest pain that was aggravated by elevation of her right arm and deep inspiration. She denied associated symptoms of shortness of breath, nausea, vomiting, or diaphoresis, and her office electrocardiogram showed no abnormalities.Other than mild hypertension (blood pressure, 142/85 mm Hg), the results of her physical examination were unremarkable except that elevation of her right arm and palpation of the right chest wall reproduced the symptoms with which she presented. With a normal lipid profile and an ultrasensitive C-reactive protein level, she was diagnosed as having atypical chest pain most likely of musculoskeletal origin. Hydrochlorothiazide was used to treat her hypertension, and cardiac computed tomography angiography (CCTA) was performed to exclude the possibility of coronary artery stenosis and to reassure her. Interpretation of the CCTA findings suggested that both the left circumflex and the dominant right coronary arteries had discrete areas of mild, noncalcified, nonobstructive plaque in their mid and distal segments. The large-caliber left anterior descending coronary artery (LAD) was reported to have diffuse and complex calcification of the proximal segment, which made accurate quantification of the luminal stenosis challenging.

Subsequently, the patient’s physician recommended cardiac catheterization to enable more precise assessment of the LAD luminal stenosis. Selective coronary angiography was performed at the local community hospital and revealed only a mild luminal irregularity of the LAD. Shortly after the second injection of contrast, the patient complained of intense chest pressure and was noted to be hypotensive and tachycardic (blood pressure, 78/45 mm Hg; heart rate, 110/min). Mild “staining” of contrast was noted in the left coronary cusp of the aorta, and an ascending aortogram revealed a dissection of the aortic root extending into, and resulting in compromise of, the left main coronary artery. An intra-aortic balloon pump was placed, and the patient underwent urgent coronary arterybypass with saphenous vein grafting of both the LAD and the left circumflex coronary artery.

Following a prolonged, 14-day hospital course and a residual left ventricular ejection fraction of 35%, the patient was discharged home with intensive cardiac rehabilitation. Unfortunately, within 6 months of the bypass, she presented again with escalating chest pain and was noted have premature graft failure that was treated with percutaneous coronary intervention with multiple drug-eluting coronary stents. Despite her compliance with dual antiplatelet medical therapy (aspirin and clopidogrel daily), she presented 8 weeks later with an ST-segment elevation myocardial infarction complicated by cardiogenic shock. Emergent catheterization revealed thrombosis of the stent in the vein graft supplying the circumflex artery that was successfully treated with a catheter-based intervention. However, the patient remained in refractory cardiogenic shock and ultimately required urgent orthotopic heart transplantation.


Emergency department visits for chest pain syndromes represent a large and growing health care burden. Because patients with chest pain require urgent triage and timely management, there are great incentives for developing a new generation of novel, complementary diagnostic strategies. A recent addition to the diagnostic armamentarium, multidetector CCTA, can noninvasively generate reconstructed images of the coronary circulation. However, the brisk expansion and rapid adoption of CCTA over the past decade has outpaced supportive clinical data and has led to the referral of a much larger, and often lower-risk, segment of the population for coronary artery catheterization. We believe that in this case the unwarranted use of advanced diagnostic imaging (false-positive CCTA findings) directly contributed to unnecessary cardiac catheterization that resulted in a tragic complication and significant morbidity.Advanced diagnostic imaging technologies or the latest biomarker cannot, and should not, replace a thorough history and physical examination with subsequent decision making guided by the bestevidence-based practice. The need for testing in patients with chest pain is based on the clinician’s estimation of the pretest probability of coronary disease. In a patient with a low pretest probability (<10%) of having significant coronary disease, the preferred course is to reassure the individual and to focus the treatment plan on primary or secondary prevention strategies. Additional diagnostic testing rarely garners useful information and exposes the patient to unnecessary risk—both from the diagnostic test itself and from subsequent invasive testing because of false-positive results. While the risk of complications associated with cardiac catheterization is low, catastrophic events can occur. As opposed to CCTA, in appropriately selected patients coronary angiography allows the presence, location, and, most importantly, the functional significance (eg, fractional flow reserve, intravascular ultrasonography) of lesions to be determined. Because there is often discordance between luminal stenosis and the physiologic significance of lesions, functional testing has assumed critical importance in the assessment of patients with a moderate pretest probability (10%-90%) of coronary disease.

Therefore, given the possible adverse consequences of the overuse of diagnostic imaging in a broad and uncensored population of patients with chest pain, recent joint professional guidelines emphasize that ” . . . an appropriate imaging study is one in which the expected incremental information, combined with clinical judgment, exceeds the expected negative consequences by a sufficiently wide margin for a specific indication that the procedure is generally considered acceptable care and a reasonable approach for the indication. . . . “Furthermore, because of differences in body habitus, coronary physiology, exercise physiology, symptom presentation, and disease prevalence, the diagnostic accuracy of stress testing may be affected by the female sex. In addition to having a markedly different ST-segment response to exercise from a young age, data suggest that ST-segment depression tends to be less sensitive and specific for coronary artery disease in women. With normal electrocardiographic findings, negative cardiac biomarkers, and a classically atypical presentation, our patient had an age-specific risk level that was below average. She had a low pretest probability of coronary disease (<10% risk of myocardial infarction or death per 10 year interval), making further testing inappropriate and the chance of false-positive study results unacceptably high. However, in an era of rapid advancement in diagnostic imaging strategies, the savvy clinician must not forget the basic tenets of data-driven medicine, patient selection, and risk tolerance and ultimately realize when less may be more. Such is precisely the case with CCTA.

Because CCTA is rapid and noninvasive and has wide availability, it has increasingly been used to detect coronary atherosclerosis in a broad array of patient populations. However, the lack of randomized data suggesting clinical benefit, as well as technical and anatomical limitations, restricts its application in many patients. Studies comparing CCTA with conventional coronary angiography in diverse patient populations suggest that CCTA is highly sensitive (79%-100%) for the detection of obstructive coronary disease, with a positive predictive value ranging from 86% to 91%. However, these same studies report suboptimal specificity (64%-85%) and negative predictive values of 83% to 90% that correspond to an unacceptably high false-positive rate of up to 81% in selected subpopulations. Further limiting the diagnostic accuracy of CCTA is the fact that complete visualization of all segments of the coronary tree is hindered by cardiac motion (heart rate, >70/min), smaller vessel caliber (<2 mm), and tortuousity that may result in portions of a vessel moving in and out of an imaging plane. Furthermore, given its high attenuation coefficient, the presence of coronary calcification commonly produces a “blooming artifact” that makes accurate assessment of adjacent arterial luminal challenging and may result in overestimation of the degree of luminal stenosis, which is likely the case in the patient described herein. Therefore, CCTA often overestimates the presence and severity of coronary atherosclerosis to a degree that is dependent on the study population, the equipment used, and the experience of the interpreting physician, which may lead to unnecessary, higher-risk, and costly invasive procedures.

Nevertheless, the use of CCTA has increased dramatically over the past decade, with some estimates suggesting up to 26% per year. In an era in which comparative efficacy of therapies has assumed critical importance, the unchecked growth of CCTA seems not only unfounded but also irresponsible and unsustainable. Aside from its cost implications, CCTA also exposes the patient to substantial amounts of ionizing radiation. It is estimated that the collective dose received from medical radiation increased by more than 700% between 1980 and 2006, with increases in computed tomography accounting for more than 50%. Furthermore, 64-slice CCTA (without tube current modulation) exposes the patient to an average effective dose of 15 mSv of radiation compared with only 7 mSv for diagnostic coronary angiography. With recent data suggesting that 1.5% to 2.0% of all reported cancers in the United States may be linked to ionizing radiation from computed tomography, there is reason for pause.

In conclusion, our patient suffered a rare but devastating complication from an cardiac catheterization that was the direct result of unnecessary CCTA and false-positive findings. With few cardiac risk factors and an atypical chest pain presentation, this patient had a low pretest probability for coronary artery disease and should have been reassured and not undergone any further risk stratification. Lacking randomized data suggesting improvement in clinical outcomes and with clear risks including contrast load, radiation exposure, and suboptimal diagnostic specificity, CCTA should have a very limited role in the evaluation of patients who present with chest pain.

Posted in atherosclerosis, cardiology, CCTA, cholesterol, coronary artery disease, coronary computed tomographic angiography, diet, ethics, heart transplant, junk food, lifestyle, obesity, professionalism, surgery, technology, waist circumference | 1 Comment »

“When diet doesn’t work”

Posted by Colin Rose on September 21, 2009

Here is a graphic illustration of the concept of moral hazard as applied to the drug treatment of lifestyle diseases.


Reprinted from AdWatch


Many studies confirm that doctors’ behaviour can be influenced by drug advertising, but many of them are unaware of this.
Not only the advertising text, but also the images play an important part.
For example, see the above image in the Lescol advertisement published in the April 2008 issue of Rivista SIMG (Journal of the Italian Society of General Practitioners).

Lescol (fluvastatin sodium) is one of the statin class of drugs used to treat of high cholesterol when diet and other lifestyle changes don’t work.
The Summary of Product Characteristics states “for best results in lowering cholesterol, it is important that you closely follow the diet suggested by your doctor”.

What kind of advice could the doctor have given the two people on the beach?

They seem to be really happy and relaxed. The pastel colours, the calm sea and the blue sky in the background convey the impression that all is going well and no changes are needed.

The designer must have been influenced by the Colombian painter Fernando Botero, famous for his fat men and women, who generally emanate a sense of calmness and satisfaction.

What I can understand, as a doctor, after looking at this image?
“It doesn’t matter what I advise my patients to eat; it isn’t worth them trying to change their lifestyle behaviours.
Only the pill can make the difference!”

Posted in atherosclerosis, cardiology, cholesterol, diet, drug marketing, drugs, food, junk food, moral hazard, statins | Tagged: , , | Leave a Comment »


Posted by Colin Rose on August 16, 2009

Those chiropractors certainly look like willfully ignorant charlatans but some medical doctors are also guilty of the same unwillingness to perform or abide by the results of randomized trials. For example angioplasty of coronary arteries for “treating” stable angina (chest pain caused by inadequate blood flow to the heart during exercise) has been shown in multiple randomized trials to cause more heart attacks than treating with drugs only. But these procedures are still done at great expense to our medical system. As an example of unwillingness to perform randomized trials, consider “bariatric” surgery. Even our Minister of Health and Social Services, Yves Bolduc, a neurosurgeon, believes various forms of gastric surgery is a cure for obesity but there has never been a single randomized, sham-operated controlled study showing surgery is any better than treatment for junk-food addiction alone without the operation. Bariatric surgeons refuse to do a randomized trial and are not compelled to. And yet $billions are being spent on these operations. Like the chiropractors, if you ask these doctors why they are ignoring or not doing randomized trials they will answer that they know what is right for the patient, no need to do trials.

The Gazette
16 Aug 2009

“Awhite crystalline substance is known to be either glucose or fructose. How would you identify it?” That’s been a standard question asked on organic chemistry exams for over a hundred years. Glucose and fructose are both simple sugars with exactly…read more…

Posted in bariatric surgery, coronary artery disease, ethics, obesity, professionalism, randomized trial, surgery | Tagged: , | Leave a Comment »

Eat less, live long

Posted by Colin Rose on March 16, 2009

On the average North Americans are eating at least 30% too many calories. Calorie restriction is relative. If we cut our calories by 30% we wouldn`t be restricting calories, just eating enough without gaining weight and we could cut medical costs by $many billions. But you will never hear a office-holding politician say “Eat less”; he/she would never be elected again.

Eat less, live long
National Post
16 Mar 2009

As the world faces an ageing population with a rapidly growing segment that will require nursing home care for Alzheimer’s disease, more and more scientific energy is being directed at stemming the “Silver Tsunami.” One intriguing possibility is that a…read more…

Posted in atherosclerosis, diabetes, Type 2, diet, obesity | Tagged: , , | Leave a Comment »

‘The Heart Truth’ for both men and women

Posted by Colin Rose on February 26, 2009

Unilever, the maker of Becel margarine, would like us to believe that Becel is a health food; the more you eat the better. To that end Unilever contributes $millions to various cardiovascular and dietetic organization who reciprocate by putting the Becel logo on their literature and web sites.

There is no such thing as a healthy refined fat. Both margarine and butter are junk food, naked calories. Besides, pure fat is tasteless. The taste in butter and margarine comes only from their salt content. Obesity is the major nutritional problem and refined fats (butter, margarine or oil)are the most concentrated form of calories and should have no place in a healthy diet.

The Heart Truth’ for both men and women
Margaret McKellar, brand manager, Becel.
National Post
26 Feb 2009

Re: Barbara Kay, Apparently Men No Longer Have Heart Disease Or Strokes: That’s The Message From Becel Margarine And The Heart And Stroke Foundation, Feb. 16. I have had personal experience in dealing with loss due to heart disease and stroke. My…read more…



Posted in atherosclerosis, cholesterol, diet, junk food, lifestyle, obesity | Tagged: , , , | Leave a Comment »

The Atherogenic Football Diet

Posted by Colin Rose on February 1, 2009

Who are the coaches and “nutritionists” that advise football players to eat atherogenic, obesogenic , diabetogenic, hypertensogenic diets just so they can trample the opposing team? They should be banned from the game.
By Madison Park

(CNN) — Football players guzzle protein shakes, down steaks and lift weights. They train and gain weight, hoping to build mass under the careful eye of the team’s coaches, nutritionists and gurus.

“It was a scripted lifestyle where they tell you how to eat, how to take care of yourself, how much body fat you should have,” said Chuck Smith, a former defensive end for the Atlanta Falcons and the Carolina Panthers.

But once their glory days are over, they have the same problem as millions of other Americans: They’re fat.


Football Team

“When I trained, they told us to eat all you can eat,” said Smith, who played in Super Bowl XXXIII with the Falcons. “Drink beer, eat peanut butter to gain weight. All those eating habits were great for football. But when I got done, no question I had to make adjustments.”

Without scheduled practices, meals, and games on Sunday, it became tougher to keep in shape.

When players were younger, they had the opposite problem.

Many tried to gain weight, believing that bigger is better. But as they age and retire from football, many are seeing that “big” is causing problems.

Smith, who weighed 274 pounds during his professional days, often had four plates of food in one sitting “to keep my weight up.” After retirement, Smith had to unlearn those habits.

“I had to retrain my thinking,” he said. “I don’t need to be full. I don’t have to stuff myself to feel comfortable. That took a long time. You stuff yourself to gain weight, then you get out of shape.”

Smith learned he had high cholesterol (he had to take Lipitor), and his blood pressure was climbing, too.

“I had to take the bon-bons out of my mouth,” said Smith, 39. “I had to empower myself. Strength coaches, nutritionists aren’t going to take care of me. Guys have to empower themselves to take care of themselves.”

Smith is now a fitness trainer at Defensive Line Incorporated, where he works with football players. Through healthy foods and workouts, he trimmed his body fat, lowered his cholesterol and shed 50 pounds.

Some players understand the risks, said Dr. Archie Roberts, a former National Football League quarterback and retired cardiac surgeon.

“They understand that if they stay 250, 300, 350 pounds as they age, that’s going to shorten their life span and cause them more health problems,” he said. “Others don’t get it and they’re unable — for whatever reason — to lose the weight, and they will suffer the consequences, just like anybody else in the general population carrying too much weight.”

Diabetes, hypertension and high cholesterol are all cardiovascular risks associated with obesity.

Roberts heads the Living Heart Foundation, a nonprofit promoting health for former football players. For five years, he has conducted research to determine whether former football players are at added risk for heart problems (they’re not).

After left tackle Bob Whitfield retired from the New York Giants in 2007, he gained 20 pounds. The 37-year-old Pro-Bowler is trying to lose 40 pounds, which would bring him to 290 pounds, the lowest he has weighed since ninth grade.

“You don’t want to be the person at the buffet and people look at you crazy,” Whitfield said. “Overall, you want to have a healthier lifestyle. It doesn’t mean you want to be muscled up. … I don’t want to be the biggest man in the room anymore.”

Looking back at his career, Whitfield doesn’t think his size made him a better player.

“When that mass gets too heavy, you decline, you can’t accelerate, you don’t have as much force,” he said. “I never felt that being bigger gives you a competitive advantage. I put it on flexibility, the explosive nature of your movements.”

Several decades ago, 300-pound players were a rarity; now, the league has more than 500, Roberts said.

Decades ago, the Washington Redskins’ offensive line was known for its size and dominance.

“They had the largest line in the NFL, called the Hogs, 20 years ago,” said Dr. Ben Levine, director of the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital in Dallas, and professor of medicine. “If you go back and look at their size, they’re about the size of the running backs today. The impression was these guys were massive, huge. They couldn’t play in the NFL today. They’re too small.”

Smith said he wasn’t forced to gain weight, but perceptions exist on how a player should look based on his position. That “needs to change in the NFL,” he said.

Being faster, stronger and more aggressive is more important than size, Smith said. He drew an analogy to airline stewardesses: “We want her to be tall and slim so she can walk down the aisles. Now is there really a difference between a 135-pound woman and a 150? Well, maybe a little bit different in the hips, but the same effectiveness happens when she does her job.”

He added, “I’m a classic example that size doesn’t matter.”

But that’s not what young, aspiring players think.

Jackie Buell, director of sports nutrition at Ohio State University, said she encounters players who seek to gain as much as 30 pounds by next season and seldom care whether it’s fat or muscle.

Buell’s research examined 70 college linemen and found that nearly half have metabolic syndrome, meaning that the players have at least three of the five risk factors of developing diabetes and heart disease. Her next project is to explore whether junior high and high school football players are developing metabolic syndrome.

“My fear is, these young men have this metabolic profile, what happens when they stop working out intensively?” Buell said. 

Posted in atherosclerosis, athlete, cholesterol, diabetes, Type 2, diet, drugs, football, junk food, lifestyle, obesity, statins, waist circumference | Tagged: , , , | Leave a Comment »

Every disease is “genetic”. So what?

Posted by Colin Rose on December 29, 2008

Every disease is caused by some combination of nature and nurture, genetic susceptibility and the environment, especially nutrition. Fortunately, most of the common fatal diseases and those costing the most to the disease care system are mostly environmentally caused. Attempts to find a simple genetic cause for atherosclerosis, hypertension, obesity and Type 2 diabetes were and are unscientific fishing expeditions driven by the analogy that we could immunize the population against these chronic diseases of lifestyle, as we can immunize against acute infectious diseases like polio or smallpox. As this paper makes clear the four-billion year old genetic code is a highly refined, self-referential system that is unlikely ever to be completely understood.

Unfortunately, changing the environment, aka lifestyle, necessitates conquering legal addictions to junk food, tobacco and alcohol. We would much rather spend $many billions on a futile attempt to find a magic genetic bullet to obviate the destructive consequences of addiction than face the painful necessity of eliminating them. 


Genetic diseases may be tougher to crack, new research suggests 

Last Updated: Friday, December 26, 2008 | 4:07 PM ET 

Finding a cure for many genetic diseases — including some cancers and neurodegenerative ailments — may be much more complicated than previously thought, new research indicates.

An international team’s work on alternative splicing, the process that produces 75,000 of the proteins in human cells, found that small changes in the environment near an alternative splice could produce a large change in the proteins produced.

That’s important, because mutations in DNA sequences in alternative splicing cause more than half of all genetic diseases.

If the materials used in splicing are seen as forming a long sentence, then the individual parts can be considered words, said Tim Nilsen, director of the Case Western Reserve University School of Medicine’s Center for RNA Molecular Biology in Cleveland.

“Adding or deleting one word,” he said “can radically change the meaning of the sentence.”

Biologists believe that rules hidden in the DNA code control alternative splicing, so once the code is broken, cures can be found for genetic diseases.

But the finding by Nilsen’s team on the importance of the environment means the code is much more complicated than thought. That will likely delay that progress of scientists who hope to amend the code to cure genetic diseases, said Joseph Nadeau, chair of the medical school’s genetics department.

“It’s context, not [genetic] code, that’s important,” he said.

The study, Dynamic regulation of alternative splicing by silencers that modulate 5′ splice site competition, was published in the Dec. 24 issue of Cell.

Nilsen led a team from three U.S. institutions — Case Western, Columbia University and the Memorial Sloan-Kettering Cancer Institute — and the Max Planck Institute for Biophysical Chemistry in Germany.

Posted in addiction, atherosclerosis, diabetes, Type 2, diet, environment, genetics, junk food, lifestyle | Leave a Comment »

Drug Marketing by “Study”

Posted by Colin Rose on December 13, 2008



Posted in atherosclerosis, cardiology, cholesterol, drug marketing, professionalism, statins | Tagged: , , , , , , , , , , | Leave a Comment »

Cardiac disease threatens diabetics

Posted by Colin Rose on November 26, 2008

Dr. Terrence Ruddy, chief of cardiology at the University of Ottawa Heart Institute, says the increasing number of people with diabetes is a major concern across the medical profession.

“The increasing number with diabetes is directly related to the increasing number with obesity,” he says. “We have an epidemic of obesity in young and older people. In older people, that is giving them diabetes now. In younger people, it will give them diabetes in the next 20 to 40 years.” It’s vital to reduce obesity, “not just for 40- to 50-year-olds but in 10 to 20-year-olds,” he says. “We need more money flowing into educational programs focused on lifestyle changes — increased activity, appropriate diet and weight loss in young people. Decrease obesity to decrease diabetes.”

Yet at least 500 cardiologists around the world were paid by AstraZeneca to take part in JUPITER, a clinical “trial” of Crestor in which most subjects were overweight or obese and NO attempt was made to reduce their weights. 1.5% per year became diabetic due to their inflamed excess visceral fat. Probably at least US$500 million flowed into this “trial” with NO “educational programs focused on lifestyle changes”.

Doctors pay lip service to the need to fight obesity but money talks. Those cardiologists probably received at least $1000 per subject to enroll them in the JUPITER “trial”. Why would they dare to insist upon lifestyle change first before enrolling the subject and forgo this income? Members of the “JUPITER Study Group” presumably overseeing the “trial” for AstraZeneca were probably paid $100,000 each for their “consultation”. Why would they insist on lifestyle change first before agreeing to participate?


Cardiac disease threatens diabetics
The Gazette
26 Nov 2008

Just one year after Dale Frayling was diagnosed with type 2 diabetes, he suffered his first heart attack. Four months later, he had a second, more severe attack followed by bypass surgery. That was 11 years ago. The Saskatoon resident, now 57, has…read more…


Also blogged here: 1, 2


Here is the list of the cardiologists paid to participate in the JUPITER study who care more about money than advising patients on the best way to prevent atherosclerosis and diabetes.

Paul M Ridker, M.D., Eleanor Danielson, M.I.A., Francisco A.H. Fonseca, M.D., Jacques Genest, M.D., Antonio M. Gotto, Jr., M.D., John J.P. Kastelein, M.D., Wolfgang Koenig, M.D., Peter Libby, M.D., Alberto J. Lorenzatti, M.D., Jean G. MacFadyen, B.A., Børge G. Nordestgaard, M.D., James Shepherd, M.D., James T. Willerson, M.D., Robert J. Glynn, Sc.D., for the JUPITER Study Group

Appendix. JUPITER Clinical Sites

Argentina 253: Altamirano J, Berrizbeitia M, Boskis P, Colombo H, Cuadrado J, Cuneo
C, Diaz M, Esper R, Fernandez A, Foye R, Hershson A, Kuschnir E, La Greca R,
Lorenzatti A, Lozada A, Luciardi H, Luquez H, Maffei L, Majul C, Marin M, Muntaner
J, Nul D, Paolasso E, Rey R, Rodenas P, Rodriguez P, Rojas C, Telsolin P, Vita N,
Belgium 487: Adrianes G, Argento O, Bacart P, Baeck L, Baguet J, Balthazar Y, Battello
G, Behets J, Beke P, Bemden S, Berwouts P, Boermans P, Bolly F, Borms J, Boulad M,
Boulanger L, Bous J, Boxstael R, Brands Y, Buyse L, Calozet Y, Camps K, Capiau L,
Celis H, Coucke F, D’Argent F, De Beeck G, De Meulemeester M, De Praeter K, De
Rouck S, Delcourt A, Delvaux J, Demanet E, Derijcke M, Deruyck C, Devaux J, Dupont
C, Duyse J, Erpicum L, Gilio C, Gillet A, Grosjean J, Heeren J, Henry G, Heyvaert F,
Hollanders G, Hutsebaut A, Janssens P, Lannoy H, Ledoux C, Legros P, Leliaert R,
Martens R, Maury O, Mehuys G, Michaux J, Migeotte A, Mortelmans J, Mulders N,
Parijs P, Peer W, Pieters E, Reynders P, Riet D, Robert P, Stee J, Teheux J, Teuwen J,
Timmermans B, Tshinkulu M, Vantroyen D, Veevaete M, Vercruysse K, Vereecken G,
Vermeersch L, Vernijns J, Verspecht E, Vinck G, Vrancken F, Watte G, Weymans J,
Windmolders S, Ziekenhuis J, Ziekenhuis P, Brazil 327: Albuquerque D, Barbosa E,
Bertolami M, Blacher C, Brasileiro A, Eliaschewitz F, Esteves J, Feitosa G, Filho H,
Filho R, Fonseca F, Forti A, Francischetti E, Franco R, Gomes M, Gross J, Jardim P,
Kohlmann O, Loures-Vale A, Magalhaes M, Maia L, Moriguchi E, Nogueira P, Oigman W,
Repetto G, Saraiva J, Xavier H, Bulgaria 197: Balanescu S, Benov H, Chompalova B,
Donova T, Gocheva N, Goudev A, Grigorov M, Gruev T, Hergeldjieva V, Marchev S,
Mihov A, Pasheva V, Penev A, Popov A, Raev D, Sirakova V, Slavcheva A, Stoikov A,
Stoilov R, Tisheva S, Todorov G, Torbova S, Uzunangelov J, Canada 2020: Achyutna G,
Akhras R, Arun N, Barriere G, Bartlett J, Behiels S, Bell A, Bergeron J, Berlingieri J,
Bhamjee H, Bodok-Nutzati R, Booth W, Boyd C, Brault S, Bruckswaiger D, Bukovy B,
Campbell G, Carlson B, Cha J, Chehayeb R, Cheng W, Chilvers M, Chouinard G,
Chow W, Conter H, Conway J, Craig D, Dattani I, Del Grande R, Dharamshi S,
Dickson M, Dion D, Dowell A, Drexler J, Dube S, Dupont A, Dworkin B, Fields L,
Filteau P, Gardiner E, Gervais B, Gillis G, Girard R, Goldman H, Gorfinkel I, Goulet S,
Greenspoon A, Gritter R, Gupta A, Gupta M, Habib R, Harding R, Hart R, Henein S,
Henry D, Hirsch A, Ho K, Hoag G, Houde D, Howlett E, Ing G, Jadd J, Janes J, Jardine F,
Johnston T, Kanani S, Kazimirski M, Kelly A, Klajner F, Kooy J, Lalani A, Lam S,
Laranjeiro J, Larose D, Leiter L, Leung W, Li J, Lowe D, Luces K, Ma P, MacKinnon R,
Martinho V, Matangi M, McCrossin M, McIsaac J, McMullen W, Mehta P, Meunier M,
Misik K, Ng A, Nigro F, Noronha L, O’Mahony W, Pandey S, Papp E, Patel V , Patrick L,
Peddle C, Pinsky N, Poirier P, Powell C, Price J, Rolfe A, Saliba N, Sawkiw R, Senior R,
Shu D, Smith R, Somani R, Soowamber M, Stakiw K, Talbot P, Taliano J, Tan K,
Teitelbaum I, Threoux P, Tremblay G, Turcotte C, Tytus R, Walsh P, Webb G,
Willoughby P, Woo V, Woodland R, Yee G, Chile 83: Blanco M, Cardenas N,
Dominguez J, Gutierrez M, Jalaf M, Olivares P, Rodriguez B, Saelezer C, Stockins B,
Colombia 345: Ardila W, Aschner P, Botero J, Botero R, Calderon C, Casas L,
Castellanos R, Chaves A, Cure C, Escobar I, Fortich A, Garcia L, Hernandez E, Isaza D,
Jaramillo N, Kattah W, Marin M, Matiz C, Quintero A, Rizcala A, Rodriguez N, Ruiz A,
Urina M, Valenzuela A, Costa Rica 270: Cob-Sanchez A, Gutreiman-Golberg M,
Lainez-Ventosilla A, Ramirez-Zamoraa L, Slon-Hitti C, Vinocour-Fornieri M, Denmark
336: Hansen H, Nordestgaard B, Steffensen R, Stender S, El Salvador 162: Abrego H,
Renderos J, Rivera-Ochoa L, Estonia 85: Eha J, Jaanson E, Kaasik U, Keba E, Maetos E,
Petersen M, Reinmets S, Roostalu U, Vahula V, Veidrik K, Germany 222: Bellmann R,
Hanefeld M, Horacek T, Klein C, Knels R, Koenig W, Laus S, Meibner G, Mondorf C,
Schell E, Schuster H, Sehnert W, Stahl H, Szelazek G, Winkelmann B, Witczak E, Israel
143: Avishay E, Gavish A, Grossman E, Haratz D, Hussein O, Keider S, Levy Y, Shapiro
I, Shveydel E, Wolfovitz E, Yogev R, Zeltser D, Mexico 741: Escarcega J, Galvez G,
Gonzalez J, Guajardo S, Gutierrez-Fajardo P, Ibara M, Leon J, Lozano F, Munoz E, Pina
J, Romero-Zazueta A, Sanchez R, Takahashi H, Villalpando C, Villegas E, Netherlands
987: Agous I, Bak A, Bartels G, Basart D, Cornel J, De Schipper L, Holwerda N, Kose
V, Koster Y, Lok D, Lokhorst B, Mosterd A, Nierop P, Oude Ophuis A, Somer S, Tiebesl
J, Trip M, Van Hessen M, Van Kempen W, Wassenaar M, Norway 204: Andresen M,
Berz A, Bjurstrom M, Bo P, Brunstad O, Daae-Johansen T, Elle S, Fauske J, Fossdal B,
Gjefsen O, Hallaraker A, Haugen J, Helberg S, Holm-Johnsen S, Istad H, Jacobsen T,
Johansen R, Jorstad T, Jorum I, Kjorlaug K, Kontny F, Langaker K, Larsen B, Lonning
S, Loraas A, Mansilla-Tinoco R, Medhus R, Meyer I, Nasrala S, Ofjord E, Ose L, Palmas
J, Risberg K, Sandberg A, Sirnes P, Skjegstad E, Skjelvan G, Solnor L, Storm-Larsen A,
Tandberg A, Tomala T, Torkelsen A, Ursin A, Valnes K, Walaas K, Panama 202: Binns
R, Delgado A, Lombana B, Noriega L, Trujillo R, Poland 804: Artemiuk E, Asankowicz-
Bargiel B, Banas I, Baranska E, Baranski M, Bijata-Bronisz R, Sikorska A, Blasszczyk B,
Bolanowski J, Brokl-Stolarczyk B, Brzecki K, Buczkowski K, Chmielewski T, Chojnowska-
Jezierska J, Chwist-Nowak A, Cygan W, Czajkowska-Kaczmarek E, Dargiewicz A,
Dluzniewski M, Dudka C, Fares I, Flasinska J, Gadzinski W, Gaszczyk G, Golebiowski G,
Gozdur W, Grudzien K, Kalamarz J, Kalinowska A, Kornacewicz-Jach Z, Korol M,
Korycka W, Kostka T, Kostrzewska A, Kot A, Kowalczyk-Kram M, Kowalska-Werbowy B,
Krupinska G, Lotocka E, Luberda-Heynar Z, Lukas W, Lysek R, Machyna-Dybala A,
Mlynarczyk-Jeremicz K, Mocarska-Gorna B, Niedbal-Yahfouf I, Pasternak D, Potakowska I,
Ramian U, Roleder M, Rosinska-Migda J, Sidorowicz-Bialynicka A, Skierkowska J,
Skorinko I, Slaboszewska J, Sleziak-Barglik K, Sobieska E, Stachlewski P, Superson-Byra E,
Tissler-Nahorska G, Turbak R, Uzunow A, Wasowicz D, Wodniecki J, Wojnowski L,
Wrzol A, Zdrojewska J, Zurakowska-Krzywonos A, Zurowska-Gebala M, Romania 32:
Ablachim T, Abobului M, Bobescu E, Bojinca M, Cristea M, Gaita D, Stoicovici R, Tataru R,
Tudose A, Russia 273: Ardashev V, Arutyunov G, Azarin O, Barbarash O, Bondarev S,
Borisov M, Boyarkin M, Burova N, Chazova I, Dovgalevsky P, Duplyakov D, Egorova L,
Goloshchekin B, Gratsianskiy N, Ivleva A, Karpov R, Karpov Y, Khokhlov A, Khokhlov R,
Khrustalev O, Konyakhin A, Kostenko V, Libov I, Lukyanov Y, Mezentseva N, Panov A,
Repin M, Shabalin A, Shalaev S, Shilkina N, Shulman V, Sidorenko B, Smolenskaya O,
Starodubtsev A, Talibov O, Titkov Y, Tsyba L, Uspenskil Y, Vishnevsky A, Yarokhno N,
South Africa 2497: Ahmed S, Ashtiker H, Bester A, Bhorat Q, Biermann E, Boyd W, Burgess L,
Dindar F, Dulabh R, Engelbrecht I, Erasmus E, Fouche L, Furman S, Govind U, Herbst
L, Jacovides A, Kahanovitz C, Kruger C, Lakha D, Lombaard J, MacLeod A, Makan H,
Manuel E, McDonald M, Mitha E, Mitha I, Moola S, Nell H, Nieuwoudt G, Olivier P,
Padayachee T, Pillai P, Pillay S, Ranjith N, Reyneke S, Routier R, Sandell P, Sebastian P,
Skriker M, Smit J, van Rensburg D, van Zyl L, Vawda Z, Wellman H, Switzerland 15:
Stahl M, United Kindom 2873: Adbulhakim E, Angus M, Balmer F, Balmer J, Barrat R,
Blair D, Blyth A, Brodie R, Brydie D, Campbell C, Campbell I, Church M, Clark C,
Clements R, Donnachie H, Fitpatrick P, Godley C, Hill J, Jarvie F, Kieran W, Langridge S,
Leslie R, Liddell A, MacKenzie J, MacKintosh C, Mair R, Marshall G, Martin R,
McCann C, McKibbin C, McLachlan B, McLean F, Murray S, Norris A, Pawa R, Pexton
N, Ramage A, Reid S, Robertson A, Rourke E, Sarmiento R, Shaw H, Shaw R, Sheil L,
Spence G, Stewart E, Thomas H, Thomson J, Thomson W, Travers J, Ward R, Williams
L, Wooff D, Young W, Uruguay 14: Belzarena C, Huarte A, Kuster F, Lluberas R,
Speranza-Sanchez M, United States 4021: Abarikwu C, Abate L, Abbott R, Ackley C,
Adams G, Adkins S, Albakri E, Albarracin C, Allison J, Alvarado O, Alwine L, Amin K,
Amin M, Anderson J, Anderson M, Anderson W, Andrawis N, Andrews C, Angles L,
Aquino N, Ariani M, Armstrong C, Aronoff S, Arora N, Atri P, Baker J, Baker K, Balli
E, Banish D, Bardenheier J, Barnett G, Bartkowiak A, Basista M, Beliveau W, Bell G,
Benchimol G, Bennett B, Bennett N, Bermudez Y, Bernstein J, Berroya A, Bhargava M,
Biaggioni I, Bimson S, Bittar N, Bleser S, Blumberg M, Bobson C, Boeren J, Bogan R,
Boling E, Booras C, Borge A, Brady J, Brandon D, Bredlau C, Brideau D, Brobyn T,
Brodowski M, Broker R, Broussard C, Brown C, Browning D, Brusco O, Bryant J,
Buchanan P, Bueso G, Burgess G, Burke B, Buynak R, Byrd L, Camilo-Vazquez E,
Campbell J, Cannon L, Capo J, Carmouche D, Castaldo R, Castilleja J, Caudill T, Caulin-
Glaser T, Champlin J, Chardon-Feliciano D, Cheng T, Cherlin R, Cheung D, Chodock A,
Christensen J, Christian D, Christiansen L, Ciemiega R, Clark J, Coble S, Cohen K,
Colan D, Cole F, Cole R, Colleran K, Collins G, Conard S, Cook J, Cooperman M,
Cooze D, Copeland T, Corder C, Courtney D, Cox W, Crump W, Cruz L, Cuellar J,
Cunningham T, Daboul N, Dailey R, Dallas A, Dansinger M, Dao L, Darwin C, Dauber
I, Davidson M, Davis P, Degarmo R, Degoma R, Dempsey M, Denny D, Denyer G,
Desai V, Despot J, Dewan M, Dickert J, Diederich C, Doben S, Dobratz D, Douglas B,
Drehobl M, Dresner J, Dreyfus J, Drummond W, Dunbar W, Dunlap J, Dunmyer S,
Eaton C, Ecker A, Edris M, Egbujiobi L, Elkind A, Ellis J, Ellison H, Engeron E, Erdy G,
Ervin W, Eshowsky S, Estock D, Fang C, Fanning J, Feinberg B, Feld L, Fenton I,
Fernandez E, Ferrera R, Fiacco P, Fierer R, Finneran M, Fintel D, Fischer M, Flippo G,
Flores A, Folkerth S, Forbes R, Fowler R, Francis P, Franco M, Frank A, Fraser N,
Fuchs R, Gabriel J, Gaddam S, Gaffney M, Gamponia M, Gandhi D, Ganzman H, Gaona
R, Gaona R Jr, Garibian G, Garofalo J,, Gatewood R, Gazda S, Geiger R, Geller M,
Germino W, Gibbs R, Gifford C, Gilhooley N, Gill S, Gillespie E, Godwin D, Goldberg
M, Goldberg R, Goldstein M, Gonzalez-Ortiz E, Goodman D, Gordon G, Gordon M,
Goswami A, Gottlieb D, Gottschlich G, Graham D, Gray J, Gray W, Green S, Greenberg
R, Greenspan M, Greenwald M, Grover D, Gupta, R, Gupta-Bala S, Guthrie R, Gutmann
J, Gvora T, Habib G, Hack T, Haidar A, Hamdy O, Hansen M, Hanshaw C, Hargrove J,
Harris H, Harris H, Harrison B, Hart T, Heacock J, Head D, Headley D, Henderson D,
Herman L, Herrera C, Hershberger V, Hershon K, Heym H, Hill G, Hippert R, Hirsch A,
Hnatiuk G, Hoekstra J, Holt W, Homan J, Honsinger R, Howard J, Howard V, Howard
W, Huling R, Imburgia M, Isajiw G, Ison R, Iverson W, Jacks R, Jackson B, Jackson K,
Jacobs J, Jacobson E, James A, Jayanty V, Johary A, Johnson G, Jones P, Jones T, Joseph
J, Julien C, Kahn Z, Kalvaria I, Kang J, Kaplan I, Karns R, Kashi K, Kaster S, Kaufman
A, Kawley F, Keller R, Kenton D, Kerlin J, Kern J, Kerwin E, Kerzner B, Ketchum J,
Khan J, Khan S, Khawar M, Khera A, Kinstrey T, Klein B, Klein E, Klein S, Klein T,
Kleinsteuber K, Klementowicz P, Knopp R, Knutson T, Koch S, Kramer M, Krause R,
Krisciunas V, Krueger C, Kruszewski D, Kumar R, Kunst E, Kuo D, Kuritsky L,
Kushner P, Kutner M, Kwiterovich P, Kwong S, Lanese J, Lang B, Lary J, Lasalle J,
Lasater S, Lasser N, Laughlin D, Lawless J, Lawlor D, Ledbetter J, Ledesma G, Lee D,
Lemanski P, Levinson G, Levinson L, Lewis D, Lewis L, Lewis S, Linden D, Loh I,
Look M, Lopez D, Loskovitz L, Lubin B, Lucas M, MacAdams M, Madden B, Magee P,
Maggiacomo F, Magier D, Magnuson S, Mahaffey R, Makowski D, Maletz L, Mally A,
Maloney R, Mancha V, Manolukas P, Marple R, Martin R, Masri A, Masri B, Mattingly
G, Mayer N, McCain A, McCall Bundy J, Mccartney M, Mcclain D, McConn M,
Mccullum K, Mcdavid R, Mcgettigan J, McIvor M, Mcneff J, Mendolla M, Mercado A,
Mersey J, Milam J, Milko T, Miller M, Miller R, Miller S, Mobley D, Modi T, Modiano
M, Mollen M, Montgomery R, Moran J, Morelli J, Morin D, Moskow H, Moursi M,
Mueller N, Mullins M, Myers E, Nadar V, Naiser J, Nash S, Natarajan S, Neft M,
Neuman D, Nevins B, Newman J, Newman R, Newman S, Nolen T, Nwasuruba C,
Oberoi M, Odom A, Ong Y, Oppy J, Owen S, Pampe E, Pangtay D, Parker R, Patel B,
Patel J, Patel M, Patel R, Paul A, Pearlstein R, Penepent P, Peniston J, Perlman M,
Persson D, Peters P, Peterson G, Peterson J, Pettyjohn F, Phillips A, Phillips D, Piel M,
Pillai T, Pi-Sunyer F, Pollack A, Pond M, Pongonis J, Porras C, Portnoy E, Potos W,
Powers J, Prasad J, Pritchett K, Pudi K, Pullman J, Purdy A, Quinones Y, Raad G,
Radbill M, Radin D, Rai K, Raikhel M, Raine C, Ramanujan R, Ramirez G, Ramos-
Santana Z, Rapo S, Ravin S, Rawtani P, Reeves R, Reeves W, Reiter W, Rendell M,
Resnick H, Reynolds W, Rhudy J, Rice L, Rictor K, Ringrose R, Riser J, Rizvi M, Rizzo
W, Robinson J, Robison W, Rogers W, Rohlf J, Rosen R, Ross, E, Roth E, Rovner S,
Rucki P, Runde M, Ryan W, Rybicki J, Saleem T, Salvato P, Santram D, Scharf B,
Schear M, Schectman G, Schmidt J, Schneider A, Schneider P, Schneider R,
Schoenfelder S, Schussheim A, Schwartz R, Schwartz S, Schwarze M, Scott C, Segal S,
Settipane R, Shah M, Shamim T, Shanes J, Shapero P, Shapiro J, Shealy N, Shepard M,
Shepherd A, Sheta M, Shrivastava R, Shusman R, Siddiqi M, Sidney A, Silvers D,
Simek C, Simpson C, Sinatra L, Singh S, Singson D, Slabic S, Smith D, Smith K, Smith
S, Smith T, Snell P, Specter J, Speer J, Spees R, Sperling M, Spuhler W, Staab P,
Stafford J, Stanton D, Stein E, Stern S, Stocks T, Stone A, Strader W, Strout C, Strzinek
R, Subich D, Suen J, Sugimoto D, Sulman S, Suresh D, Sweeney G, Szatkowski A, Szeto
J, Szewczak S, Szulawski I, Taber L, Taghizadeh B, Tague R, Tambunan D, Tannoury G,
Tavarez Valle J, Thieneman A, Thigpen D, Thompson P, Tidman R, Tilton G, Tokatlian
E, Topkis R, Torelli M, Tortorice F, Toth P, Touger M, Treat S, Trevino M, Trupin S,
Turner A, Turner M, Tweel C, Ugarte J, Ulmer E, Urbach D, Vacker M, Vallecillo J, van
de Beek M, Vargas L, Vazquez Tanus J, Verma, A, Vijayaraghavan K, Wade P, Wade T,
Wagner S, Wahle J, Walker J, Walker M, Weinstein R, Weisbrot A, Weiss R, West P,
White A, Wickemeyer W, Wieskopf B, Wiggins M, Williams H, Wilson M, Wiseman J,
Yataco A, Yates S, Zamarra J, Zamora B, Zawada E, Zemel L, Zigrang W, Zusman R,
Venezuela 209: Aguiton M, Arroyo-Parejo M, Beaujon Sierralta J, Carrizales de Marlin
Y, Colan Parraga J, Fernandez C, Fuenmayor N, Giesen G, Gonzalez Gomez C, Guaipo
A, Herrera Rivera C, Lopez de Montoreano N, Lopez Nouel R, Marturet L, Marulanda
M, Mata L, Morr I, Nass A, Palmucci G, Ponte C, Rivas I, de Roa E, Figarella Salazar G,
Sanchez F, Sirit U, Viloria A.

Posted in atherosclerosis, cardiology, cholesterol, coronary artery disease, diabetes, diabetes, Type 2, diet, drugs, junk food, obesity, professionalism, statins | Tagged: , , , , , , , , , , , , | 2 Comments »