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Archive for the ‘diet’ Category

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.

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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.

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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.

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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 »

The Cardiometabolic Risk Working Group: Another Coven Practising Drug-Induced Magical Thinking

Posted by Colin Rose on April 14, 2011

The latest issue of the Canadian Journal of Cardiology, published by the Canadian Cardiovascular Society (CCS), both of which are largely funded by the drug industry has shamelessly published a “Position Statement by the Cardiometabolic Risk Working Group” (see highlights below). We have previously blogged about the American “Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults” and the Canadian “Working Group on Hypercholesterolemia and Other Dyslipidemias”. Now that the ability of “cholesterol” to induce terror in doctors and patients has become a little worn and less profitable, drug dealers have invented a new disease, “cardiometabolic risk” with which to terrorize asymptomatic people into demanding even more drugs and doctors into prescribing them. Many of the members of the previous covens have migrated to the new one.

These medical covens take it upon themselves to dictate to the rest of the medical profession what drugs should be prescribed to prevent diseases of lifestyle in the otherwise “normal” population, so-called primary prevention. How are these covens assembled and what gives them the authority to establish norms for other doctors? This paper reveals in stunning clarity the answers to these questions. As we can see from the Acknowledgements and Disclosures sections, most of the authors of this Position Statement have many long-term financial relations with many drug dealers. Of the ten members of the executive committee of the Cardiometabolic Risk Working Group, nine have multiple financial relations with drug dealers and of the whole Working Group 19 out of 21 have similar relations. Clearly, drug dealers have distributed tens, if not hundreds, of millions of dollars to these doctors, justified under various guises, to facilitate a culture of drug dependency. Drug dealers choose members of  the Working Group, pay them to be “authors”, pay a medical writer to compose the Position Statement and get it published in a journal which would not exist without the financial support of the same drug dealers. Why am I not impressed and why would any other doctor follow the advice of this coven? But most family physicians and many cardiologists treat this sort of statement, endorsed by presumably unassailable organizations like the CCS, as revealed truth by a mysterious higher authority in possession of occult knowledge that must be accepted or suffer ostracism by one’s colleagues. Of course it doesn’t hurt that a 30-second drug prescription for numerical symptoms of junk food addiction is much easier that spending many unpaid hours reducing the addiction, the only real way to prevent its consequences.

Here is an example of the occult numerological incantations of the Working Group. Compare this with the occult number philosophy of Agrippa based on the pentacle below.

Optimize lipid levels. In patients with cardiometabolic risk with a moderate or high Framingham Risk Score, treatment should be initiated with a statin to reduce low-density lipoprotein cholesterol (LDL-C) by at least 50% and to 2.0 mmol/L. Apo B levels are a better measurement of lipid-related risk in these patients, and the target level for treatment is 0.8 g/L in high-risk and moderate-risk individuals. There is a large residual risk for patients at high risk for CVD, despite LDL-C reduction with high-dose statins. Many patients with cardio- metabolic risk may also have an acquired combined hyperlipidemia, associated with increased triglycerides (TGs), a modest increase in LDL-C, and low high-density lipoprotein cholesterol (HDL-C). LDL particle numbers are increased, as reflected by the increased levels of apo B100. Beyond LDL-C lowering, strategies that might reduce the residual risk include reducing the total cholesterol (TC) to HDL-C ratio, high-sensitivity C-reactive protein, and TG, although there are no clinical trial data to date to support such strategies. In the patient with diabetes, glycemic control optimization and health behaviour modification should be attempted prior to the addition of another agent, such as a fibrate. In the Action to Control Cardiovascular Risk in Diabetes trial the addition of fenofibrate to simvastatin in patients with type 2 diabetes failed to show any reduction of CV events, although there may have been benefit in the subset of individuals with high TG/low HDL-C.

The deliberations of the Cardiometabolic Risk Working Group have much in common with pagan covens with occult rituals and symbols like the pentacle which when worn will drive out evil numbers such as “cholesterol”. Expensive statins for “cholesterol” and ARBs for high blood pressure are the new pentacle. The significance of the pentacle, as described by Heinrich Cornelius Agrippa in his Three Books of Occult Philosophy, makes as much sense as the Position Statement of the Working Group.  “A Pentangle also, as with the vertue of the number five hath a very great command over evil spirits, so by its lineature, by which it hath within five obtuse angles, and without five acutes, five double triangles by which it is surrounded. The interior pentangle containes in it great mysteries, which also is so to be enquired after, and understood; of the other figures, viz. triangle, quadrangle, sexangle, septangle, octangle, and the rest, of which many, as they are made of many and divers intersections…

When one manages to decode the occult numerology of the Statement one can see that the goal of the Working Group is to have every overweight junk-food addict in Canada, the typical “high-risk” patient, on some combination of pills for “high” blood pressure and “high” cholesterol. The “targets” for blood pressure and cholesterol are set low and arbitrarily to guarantee that most of the Canadian population would be on some drug. The drug dealers can be assured that doctors will prescribe the newest, most expensive patented drug rather than a cheaper generic alternative because they have already spend hundreds of millions of dollars in advertising the advantages of the patented drugs. This is called clever marketing but it has nothing to do with the health of the population. The consequences of self-destructive lifestyles will not be lessened by any number of drugs which will have the unintended consequence of worsening those lifestyles when people are convinced they can continue those lifestyles with impunity under the “protection” of drugs that make the numerical symptoms of those lifestyles look better. While the Position Statement gives lip service to the necessity of “health behaviour interventions” it insists also on the necessity of “vascular protective measures”, code for expensive drug prescription.

Canada is currently in the middle of a federal election campaign in which the most important issue for voters is “health care”. All parties are promising to increase “health care” spending by 6% a year indefinitely. With an inflation rate of only 2%, a PhD in mathematics is not required to see that in the not too distant future “health care” will consume the entire tax revenue of federal and provincial governments. The increase in “health care” spending is driven by the sort of activities represented by this Position Statement but no candidate dares to mention drug-induced magical thinking in their campaign speeches or platforms. The electorate loves its addictions and demands infinite “health care” to provide the mirage of protection from the consequences of those addictions and any candidate who points out the obvious absurdity of this belief is dead electoral meat.

How can we exorcise the myths promoted by these venal covens? There at two excellent drug review publications written by authors with absolutely no connection to drug dealers that should be required reading for every doctor: Prescrire, a French publication available in English, which is expensive but is the gold standard in independent thinking about drugs and the Drug and Therapeutics Bulletin of Navarre, a Spanish publication, available in English, which is free but covers a limited range of drugs. A recent excellent article from the latter, “Magical numbers in pharmacological prevention of cardiovascular disease and fractures: a critical appraisal“, analyzed in detail the occult numerology of the drug-funded covens’ pontifications on “primary prevention” and concludes,

A considerable part of the pharmacological recommendations to prevent cardiovascular events and fractures in healthy persons lack any solid justification. No clear efficacy, nor the size of the effect of these agents or a clear balance between risk and benefit make the intervention clinically and socially worthwhile. The “therapeutic targets” and the “operative definition” of disease or risk factor that include instruments or tables to calculate risk are new gateways to unnecessary medicalization. In the context of modern medicine, immersed in conflicts of interest, the physician is obliged to interpret the results of trials and the recommendations from guidelines and consensus at a critical distance, and to place emphasis on the development of clinical prudence as a desired skill.

In other words a truly professional doctor will ignore any advice from the drug dealer funded covens and use his or her own best judgement.

Lawrence A. Leiter, David H. Fitchett, Richard E. Gilbert, Milan Gupta, G. B. John Mancini, Philip A. McFarlane, Robert Ross, Hwee Teoh, Subodh Verma,  Sonia Anand, Kathryn Camelon, Chi-Ming Chow, Jafna L. Cox, Jean-Pierre Després, Jacques Genest, Stewart B. Harris, David C. W. Lau, Richard Lewanczuk, Peter P. Liu, Eva M. Lonn, MD, Ruth McPherson, Paul Poirier, Shafiq Qaadri, Rémi Rabasa-Lhoret, Simon W. Rabkin, Arya M. Sharma, Andrew W. Steele, James A. Stone, Jean-Claude Tardif, Sheldon Tobe, Ehud Ur

Posted in Canada, cardiology, cholesterol, cme, continuing medical education, diabetes, diabetes, Type 2, diet, drug marketing, drugs, election, ethics, health care, junk food, medical terrorism, obesity, professionalism, statins | 5 Comments »

“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 theheart.org 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.

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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.”

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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

ABSTRACT


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.

REPORT OF A CASE

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.

COMMENT


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 »

Junk food addiction causes obesity

Posted by Colin Rose on March 28, 2010

http://www.nationalpost.com/story.html?id=2737117.

BK Combo with Poutine

Bacon and cheesecake can alter the brain in ways similar to heroin and cocaine, according to scientists who say they have found the most compelling proof yet that high-fat foods rewire the brain and drive the development of compulsive eating.

When rats raised on regular chow were suddenly given unrestricted access to a high-fat diet, they lost complete control over their eating. Not even mild foot shocks kept them from compulsively feasting on chocolate bars, cream-stuffed cakes, sausage, frosting and other highly palatable human foods. Within 40 days, their body weight had increased 25%.

The rats not only got fat, they also showed addiction-like changes in brain reward circuits — the same changes that have been reported in humans addicted to drugs.

Specifically, the obese rats showed lower levels of a receptor in the brain called the dopamine D2 receptor. The D2 receptor responds to dopamine, the chemical associated with feelings of reward. The brain releases bursts of dopamine when we eat food that tastes good.

The more junk food the rats ate, the more they overloaded the brain’s reward circuitries until they essentially crashed. As the pleasure centres in the brain became more and more blase, and less responsive, the rats quickly turned into compulsive overeaters. They were motivated to keep eating to get their fix.

“They’re in a state of reward deficit, so that they’re now even more motivated to obtain rewarding food, perpetuating this vicious cycle even further,” said study co-author Paul Kenny, an associate professor at Scripps Research Institute in Florida.

The lowered D2 receptor levels — a side effect of overeating high-fat food — also seemed to drive the animals to develop “habitual” feeding behaviours that made them “less able to shift their dietary preferences,” Dr. Kenny says.

When the researchers took the high-fat foods away, leaving only the healthy, but boring chow — what the scientists dubbed the “salad bar option” — the rodents essentially voluntarily starved themselves.

“They liked the junk food so much they would rather starve than shift onto the regular chow,” Dr. Kenny said. Even after two weeks of having no junk food, “they still hadn’t returned to the level of intake that you see in the control animals for the standard chow. That goes to show just how powerful this food was.”

When they artificially knocked down the dopamine receptor using a special virus, nothing happened when rats were given regular chow. They didn’t become compulsive in any way, Dr. Kenny said. “Their brain reward systems looked fine.

“But the second you gave it palatable food, it showed very rapidly these addiction-like changes.”

Some people may be born with a predisposition to have lower D2 levels.

“That may be why they’re more likely to gain weight. They’re already halfway down that road, if you will,” Dr. Kenny said.

The findings, published on Sunday in an advance online edition of the journal Nature Neuroscience, could have profound implications for the millions of Canadians struggling to control their eating.

“What this is telling you is that, if you persist in eating food that you know is bad for you, there is a chance that you will develop a habit, and you will keep on going back to that food unless you make a really strong, conscious effort to stop it,” Dr. Kenny said.

“It’s incumbent upon people to make sure that they’re more respectful and aware of what they’re eating. Just be aware that there are dangers and risks associated. Enjoy (high-fat) food but make sure it’s occasionally and very-well controlled. Don’t overindulge repeatedly, because there could be repercussions.”

Dr. Valerie Taylor, an assistant professor in psychiatry and behavioural neuroscience at McMaster University in Hamilton, said the study is a validation “that some people are simply more vulnerable to the whole concept of being addicted to food.”

“The fact that we’re now in this high-temptation environment further serves to exacerbate that.”

Dr. Taylor said the study provides “very strong evidence supporting what a lot of us who work in the field have seen clinically — that, for some people, it’s more than just simply willpower. There’s something else going on.”

According to the latest estimates from Statistics Canada, 37% of the adult population age 20 to 69 — 7.9 million people — are overweight. Another 24% — 5.3 million — are obese.

The new study is part of a growing body of research into the “hedonic mechanisms” contributing to obesity. The preliminary findings captured headlines in October when an abstract presented at a neuroscience meeting in Chicago reported that junk food binge eating is hard to stop.

The final report goes further, and explains just what’s happening in the brain.

Three groups of rats were studied. In addition to unlimited access to their regular chow, one group was given one hour of access a day to the junk food, while another group had 18 to 23 hours of access each day, for 40 consecutive days.

Rats that had one hour access to the junk food binge-ate, gorging on the food during those one-hour sessions, so much so that they consumed almost two-thirds of their daily calories in that one-hour session. “But they didn’t gain weight, and they didn’t show those addiction-like changes,” Dr. Kenny said.

Rats given unlimited access to the sausages, frostings and cakes didn’t binge or gorge, but they snacked all day. They kept eating, consuming twice as many calories as the “control” rats, even when the flashing cue light came on that was paired with a foot shock.

“Many drug addicts know that what they’re doing is bad — they’re damaging their health, their finances, their family. But they find it very difficult to stop — the behaviour is almost beyond their control,” Dr. Kenny said.

“The same thing happened here: The animals kept on eating, even when there was something in the environment that said something bad was going to happen. They simply ignored it, and they just kept on eating.”

Dr. Kenny said treatments known to work for drug addictions may be effective for people who overeat junk food.

skirkey@canwest.com

Posted in addiction, diet, food, junk food, obesity | 3 Comments »

Junk food addiction

Posted by Colin Rose on October 28, 2009

The type of reactions Kessler describes when some people are presented with junk food is classical addictive behaviour. Why doesn’t Kessler like to call junk food obsession an addiction? My guess is that as a former FDA Commissioner he would like to think that the problem can be solved just by banning junk food. If he admits the existence of  junk food addiction he has to face the reality that all attempts to ban addictive substances of any sort have been disastrous; people will satisfy their addictions at any cost to themselves and their society. Whether we like it or not, we are all affected by the consequences of addiction; if you have any kind of disease insurance, public or private, you are paying much more than you would if there were no alcohol, tobacco or junk food addictions, all legal. Illegal cocaine and heroin addictions only increase your share of police and military costs. So, collectively, we have to put a  major effort into preventing and treating addiction, a medical problem so intractable that we pay police rather than doctors to deal with it.


Slaves to sugar
BY DAV ID KE SSLER
National Post
28 Oct 2009

For years, I wondered why I was fat. Science seemed to suggest it was my destiny. “Set-point theory” says that adult weight is destined to remain at a predetermined level and that we will adjust our energy intake and output to keep it there. According…read more…

Posted in addiction, diet, junk food | Tagged: | Leave a Comment »

You can say no

Posted by Colin Rose on October 27, 2009

A great book, but Kessler calls everything that can be digested “food”. Artificial concoctions formulated to appeal to addictions to sugar, fat and salt are junk food and have no more reason for existence than cocaine or tobacco. It is impossible to eat too much of unrefined cereals, vegetables, fruit, legumes, low-fat dairy products or lean meat with no added butter, margarine or oil.

WE CAN’T SAY NO
DAVID KESSLER
National Post
27 Oct 2009

To understand how eating promotes more eating, we must first understand the concept of “palatability” as the term is used scientifically. In everyday language, we call food palatable if it has an agreeable taste. But when scientists say a food is…read more…

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Weight gain destroys body and mind

Posted by Colin Rose on September 30, 2009

Being obese in middle age lowers a woman’s chance of being alive and free of chronic diseases after age 70 by nearly 80 per cent, according to new data from the landmark U.S. Nurses’ Health Study. The findings suggest every bit of weight gain between ages 18 and 50 lowers a woman’s odds of being a “healthy survivor” – living to age 70 or older, free from 11 major chronic diseases as well as physical, cognitive and mental impairment. For every one kilogram of weight gain since age 18, the odds of healthy survival decreased by five per cent, the study found. The worst odds for a long and healthy life were among women who were overweight at 18 – with a body mass index greater than 25 – and who gained 10 kilograms or more by mid-life. But even a higher BMI at 18 alone was associated with “moderately, albeit significantly” reduced odds of healthy survival at much older ages.

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“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

LescolItaly2008-04

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 »

Low fat diet trumps junk food gene

Posted by Colin Rose on September 19, 2009

ScienceDaily (Sep. 14, 2009) — The risk of becoming obese is 2.5 times higher for those who have double copies of the best known risk gene for overweight and obesity. However, this is only true if the fat consumption is high. A low fat diet neutralizes the harmful effects of the gene.

“This means that the critical factor is what you eat. At least in the case of the FTO gene, the most important obesity gene identified so far,” says Emily Sonestedt, member of Marju Orho-Melanders research group at Lund University Diabetes Centre.

She is the main author of a study that is currently being published in the American Journal of Clinical Nutrition. Several studies have found that exercise diminishes the effect of the risk gene but this is the first study where the effect of the gene has been studied in relation to food habits. The risk variant of the FTO gene (fat mass and obesity associated) is common in the general population. 17 percent have double copies, meaning they have inherited it from both parents. Another 40 percent have a single copy.

“It is difficult to calculate how much people eat with any certainty, which is one of the reasons why no one has done this before. But we have good data” says Emily Sonestedt.

The information comes from the large Malmö Diet and Cancer study where food habits were carefully documented using, among other things, an extensive questionnaire, a long interview and a food diaries kept by the participants themselves. When the eating habits of the carriers of the double risk variant for obesity was analyzed the pattern was clear. The risk of obesity was dramatically increased only in the case of high fat consumption.

“Yes, for those who had a diet where less than 41 percent of the energy consumed came from fat, obesity was not more common, in spite of the inherited risk” says Emily Sonestedt.

The FTO genes acts in the hypothalamus, the part of the brain that regulates appetite and satiety, and the risk variant has been connected to an increased energy intake, especially in the form of fat.

“It could be that the carriers of the risk gene don’t feel as full from eating fat and therefore consume more and gain weight” says Emily Sonestedt.

The finding that the harmful effects of the gene can be cancelled by changing eating habits could, combined with mapping of the effects of other obesity genes, lead to better and more individualized nutritional counseling for those that want to avoid gaining weight.

“This shows that we are not slaves to our genes. Even if we are born with an inherited predisposition to obesity, life style is important” says Emily Sonestedt.


Journal reference:

  1. Sonestedt, Emily, Roos, Charlotta, Gullberg, Bo, Ericson, Ulrika, Wirfalt, Elisabet, Orho-Melander, Marju. Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity.American Journal of Clinical Nutrition, 2009; DOI:10.3945/ajcn.2009.27958

Posted in diet, obesity | Tagged: | 1 Comment »

WHAT YOU EAT MAKES YOU FAT

Posted by Colin Rose on September 13, 2009

Great article, Joe. We appreciate there are those that are confused. But there are also large numbers who know what is healthy to eat, but easily blind themselves to reality; they are junk food addicts. That “food”  that the cruise passengers are piling on their plates is specifically formulated to appeal to addictions to sugar, salt and the mouth feel of fat. Unfortunately, treating junk food addiction is just as hard as treating addictions to tobacco, cocaine or heroin. Doctors are not trained to and not paid to treat addictions. They are paid to “treat” the symptoms of junk food addiction, like hypertension, Type 2 diabetes and “cholesterol” and do futile gastric bypasses. “Treatment” of these symptoms deceives the addict into believing that s/he can avoid the consequences of the addiction and makes the addiction worse. Americans are inundated with direct-to-consumer (DTC) drug advertising, claimed to be a First Amendment right by corporations with $billion ad budgets, promoting this deception and doctors are paid to prescribe those drugs.  Canada is catching up fast. Obesity rates are rising and there is pressure from the media to allow DTC in Canada, presumably guaranteed by the Bill of Rights.

The solution? Each individual has to balance the transient pleasure of addiction against the long term disastrous consequences of the addiction. In our society this is the hardest thing most people have to do 24/7/52 for a lifetime and doctors must avoid aggravating addictive behaviour.


WHAT YOU EAT MAKES YOU FAT
JOE SCHWARCZ
The Gazette
13 Sep 2009

Occasionally, I like to spy on people. Only for the sake of science, of course. And what better opportunity to do that than on a cruise ship? I like cruising. Besides outstanding entertainment, impeccable service, interesting ports, activities galore…read more…

 

Posted in addiction, diet, drugs, ethics, food, junk food, lifestyle, moral hazard, obesity, professionalism, statins | Tagged: | 2 Comments »