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JAMA reports that very few Americans are gracious enough to comply with the CDC mandate to become Healthy People by 2020, just like we failed in 2010, failed in 2000, failed in 1990, and failed at all “10-year plans” ever conceived by our public health nannies…Yet the life expectancy continues to increase!  Well,  perhaps the goal is not really to make us healthy but to make us feel sick perpetually.

Positioning himself to become our national food czar, Robert Lustig reiterates for the journal Nature his argument condemning the simple carbohydrate as a toxin or poison.

The abuse of language is necessary to explain a complicated epidemic with a sound bite.  By common sense definition, a poison has a narrow therapeutic index and harms everyone equally.  Lustig’s idea of a poison reflects circular reasoning: a substance which is harmful when ingested in excess.  By that definition, no substance can escape the label.

So Lustig must restrict the proposition with dubious qualifiers: sugar is toxic because it is addictive–a loose concept of addiction; fructose is not metabolized if you don’t exercise–so why isn’t sloth the culprit?; only “added” sugars are harmful–but mothers have been adding sugar to pies for centuries.

I was disappointed that Gary Taubes, who did such a great job debunking the claims against dietary fats in the first few chapters of his well-researched book, fell subsequently in the same trap of fervently believing in a simplistic explanation for a most complicated problem.

Risk mongering

Cardiovascular disease and stroke account for roughly 50% of all deaths.

Public health luminaries have now poured over reams of data and super-meta-analyses to provide the following insight, according to theheart.org:

“This isn’t necessarily news, but this is a new way to look at it that I hope will grab people’s attention more,” he said. “If I can tell you that, sure your 10-year risk may be low, but based on your profile right now, your lifetime risk might be 50% or more of having a major heart attack or stroke before you die. . . . I hope that’s a little more of a motivating message.”

God forbid funding for the NIH be reduced!…What would we do without this kind of advice?


Dr. Paul Grayburn provides a brief review on CAC score interpretation in the NEJM.  He presents the case scenario of a patient whose score increased from 39 to 119 over a 5-year period.

Grayburn toes the party line on the subject:  “limited value.”

As usual, he presents risk assessment as if it is a totally objective variable.  This is at odds with his statement that CAC scoring “is useful in encouraging medical compliance.”  The patient in question, whom Grayburn considered to be at low risk, became anxious about the increased score despite being on rosuvastatin for the prior 3 years.  Someone then made the decision to do a treadmill test, quadruple the statin dose (his baseline LDL was 86), and add aspirin even though there are “no prospective randomized, controlled trials demonstrating that an abnormal CAC score influences treatment decisions.”

Another puzzle in this editorial is Grayburn’s comment about the MESA score, which combines CAC results and clinical variables:

Interestingly, had this patient’s total cholesterol level been only 10 mg per deciliter higher, his MESA risk score would have increased from 12% to 20% with a CAC score of 119 — a disparity that highlights the need to consider CAC scores only in the context of other clinical risk factors, particularly cholesterol levels and blood pressure.

By combining the CAC score with Framingham, the MESA score projects clinical risk as a function of “arterial age.”  When CAC scores are even mildly elevated (such as 119), the Framingham risk estimate jumps dramatically.

But as Rayburn mentions earlier in the editorial, “According to the guidelines, CAC scoring was not needed, because this man’s predicted coronary event rate was low.”  Yet his Framingham risk would also have been low if the total cholesterol was 10 points higher (the Framingham score is not nearly as sensitive as the MESA score to changes  total cholesterol levels).  The benefit of calcium scans is precisely to identify patients who would otherwise fall under the radar.

CAC score will and should influence behavior.  The decision to order a calcium scan should be left to the doctor and the patient.

For the whistleblowers to file, that is.  Since they get 30% of the 300% Medicare fine, they essentially get paid for a stent procedure done by somebody else at full Medicare rate.  Factor in that they don’t need malpractice coverage, that’s not a bad way to make a living…But will they protest the declining reimbursements?…

JACC has yet another report by database doctors on the relationship between obesity and STEMI outcomes.  As expected, we are treated to reems of data placed  in hypnotic tables.  The punch line comes with a graph showing a U-shaped relationship between BMI and in-hospital mortality as another example of the obesity paradox.  The relationship flattens out after multi-variable adjustment except for the super obese, who remain subject to increased mortality.

The authors claim to be “surprised” that there were few meaningful differences in “process of care” according to BMI.  In other words, obese patients are treated by doctors and hospital staff like other human beings.

This is unlike the attitude of academic and public health experts who are determined to make obese people the subject of the most intense scrutiny and intervention (at the risk of causing body image and eating disorders), despite the fact that obesity is not an independent risk factor for anything.

Unless it causes a functional abnormality that bothers the person, obesity may be best characterized as a “proto-”risk factor, ie. a risk factor for risk factors. Singling out the obese seems to be a perfect example of “profiling.”  But where is the outrage?

On the contrary, instead of finding comfort in the meager benefit that obese people can expect once they develop heart disease, the accompanying editorial states that the obesity paradox itself must be “combated.”

Truth is the first casualty of war.  This applies to public heath wars as much as it does to military ones.

A safe way to save?

In the department of pointless research…

Canadian researchers are studying the effects of extending the INR testing cycle from 1 to 3 months.  They followed ~ 125 patients in each group and determined that the percentage of time in the therapeutic range was similar.  Thankfully, there is no question of widespread adoption of this monitoring schedule (at least for now).

Schulman and colleagues recommend further study before widespread adoption of extended monitoring intervals in clinical practice, adding that this single-center study was “not a true evaluation” of INR monitoring and dosing assessment every 12 weeks because patients assigned to 12-week assessment had their blood drawn every four weeks and telephone contact with anticoagulation staff to remind them of important factors for INR instability. (italics mine)


At the end of a somewhat insipid roundtable discussion on PCI and the treatment of stable coronary heart disease, WC Roberts concludes by saying:

The progress in treating patients with myocardial ischemia in the last 40 years is remarkable.  However, it can never be good enough as long as average body weight continues to increase (…)  Atherosclerosis is due to abnormalities of serum cholesterol, mostly from eating calories high in cholesterol and saturated fats.  If we all existed on plant-based diets, we would not have needed this discussion.

But given what we know about the dietary fat/cholesterol/heart disease connections, about the anecdotal effect of the “primal-paleo” diet on an individual’s detailed metabolic profile, about the exceedingly high prevalence of CHD in India (where 40% of the population abstains from eating meat and another 30% eats it rarely), and about the specific health benefits of vegetarianism, perhaps Dr. Roberts should have more accurately limited himself to saying “if we all were more health conscious, we would be more healthy.”

Happy Thanksgiving.

Hard to know what to make of this report, given that the denominator is “estimated” by the manufacturer.  The database to which the fatal bleeds were reported is the EudraVigilance, managed by the European Medicines Agency (the EC’s regulatory body).  Unlike the FDA database, EudraVigilance cannot be queried by the public.  Their report states that out of the 256 fatal bleeds, 21 occurred in Europe.  I doubt that much of the others were from the US.  Presumably a bulk comes from Japan, which was the first country to issue a modification to the package insert.

There has always been (to my knowledge), a higher rate of hemorrhagic strokes in Japan.  The pharmacodynamics of the drug may also be different and less favorable  in this population.  These bleeding concerns may not apply to the US.  However, the absence of a reversing agent for Pradaxa remains a handicap.

UPDATE:  Indeed.

Inane hyperbolae are characteristic of current medical journalism.  Examples from Cardiology News:

A new era in the management of patients with a recent episode of acute coronary syndrome arrived with the report that adding a low dose of the oral anticoagulant drug rivaroxaban…


Cardiologists who heard these findings hailed the 2.5-mg twice daily dosage of rivaroxaban as an important addition to standard management of most patients with a recent ACS…

With what unit of time do they measure an “era?”  And how does an era “arrive?” By news wire, presumably.

A what utterance came out from the cardiologists who “hailed” the dosage?  And did they also bow in front of the pill?

Who writes this stuff?  (Who reads it?!..)

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