Health & Nutrition by Michael R. Eades, M.D.

During my Monday morning troll of the medical literature I came across a paper in Nutrition Research showing that a semi-sort-of low-carb diet improves lipid profiles significantly better than does a low-fat diet.

The researchers who performed this study are a tad more enlightened that the normal run-of-the-mill lot we typically find doing this sort of work in that these folks looked at the lipid parameters most likely to be valid, if the lipid hypothesis is ever proven: triglycerides, HDL-cholesterol (HDL), and the number of small, dense LDL-cholesterol (LDL) particles.

Before we get into the study results, I want to take a bit to go over the problems that bedevil anyone trying to study diet. Macronutrients - fat, protein and carbohydrate - exert numerous effects on metabolism. And so do calories. The problem is in determining which of these variables causes the effect in question. If we place two groups of subjects on differing diets, one on a low-carb, high-fat diet and the other on a low-fat, high-carb diet, and we keep the calories the same in both groups, and we find that those subjects on the low-carb diet reduce their triglycerides, what does that tell us. Most of us will conclude that the reduction in carbs brought about the effect. But did it? It could just as easily have been the increase in fat.

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John Tierney, science blogger for the New York Times, was as taken aback by the abject stupidity hostility of the comments to his recent post on fat in the diet that included a response from Gary Taubes about the Israeli low-carb study as I was in my recent post about his post. He decided to post on the subject again, specifically addressing the comments quibbling with the findings on saturated fat. And he included more feedback from Gary.

What we have to keep in mind here is that nutrition is a science (or at least should be) and science is about generating hypotheses, making predictions from our hypotheses, and then seeing if they hold true. The relevant hypothesis here — i.e., what we’ve believed for the past 30-odd years — is that saturated fat causes heart disease by elevating either total cholesterol or LDL cholesterol, specifically. So our prediction is that the diet with the higher saturated fat content will have a relatively deleterious effect on cholesterol. We do the test; we repeat it a half dozen times in different populations. Each time it fails to confirm our prediction. So maybe the hypothesis is wrong. That seems like a reasonable conclusion. No one is proving anything here — as some of your respondents like to decry — we’re just looking at the evidence and trying to decide which hypotheses it supports and which it tends to refute.

The knee-jerk response — as exemplified by quite a few respondents — is to assume that sometime in the not-too-distant past, maybe the 1960s or 1970s, before this low-fat dogma set in, such trials, or far better trials, were done and found the opposite — that the higher the saturated fat in the diet, the lower the cholesterol and the better the cholesterol profile. Or the higher the saturated fat, the greater the mortality. But that’s simply not the case, as I point out in my book. In fact, I’ve been criticized (by Gina Kolata, among others) for going on and on in the book about all the different studies. But I did so precisely because I didn’t want to be accused of cherry picking the data. (I was anyway, but that’s just the nature of this business.) When Ancel Keys, for instance, reported in the 1950s reported that saturated fats raised total cholesterol, which they did in his studies, he based it on comparisons of butter fat to polyunsaturated oils in studies that lasted only two to nine weeks. (He also reported, curiously enough, that the saturated fats had no significant effect on LDL.)

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The day before yesterday a group of doctors from the nutrition committee of the American Academy of Pediatrics came out with a couple of the most absurd recommendations imaginable. Not only were these recommendations silly beyond belief, one was downright dangerous to boot. I’m talking, of course, about the recommendations that children as young as 8 years old who have LDL concentrations ≥ 190 mg/dL be prescribed statins. (The other one marinated in idiocy is the recommendation that low-fat dairy products be be used in overweight children between the ages of 12 months and 2 years. These two are among 7 recommendations published in the July issue of the journal Pediatrics. All 7 recommendations are listed below*)

Drs. Stephen R. Daniels, Frank R. Greer and the rest of those on the nutrition committee are nominees for the Reckless Award. In fact, their recommendations are so egregious that had they come before the eponymous Dr. John Reckless’s suggestion that statins be put in the drinking water the award would be named after them instead.

Why is the recommendation to give statins to children aged 8 and greater so dangerous? Because no drug therapy is without risk. When as a physician you give drugs to patients, you know there are risks involved, but you balance these risks with the rewards to the patient from taking the drug. In the case of statins, there is absolutely no evidence whatsoever that statins will reduce the incidence of early heart disease and/or death in these children as they reach adulthood. And there is no evidence whatsoever that years of statin therapy in these kids as they age won’t cause disastrous problems later on.

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Last week a host of reports about a study showing that eating a big breakfast brings about a much greater weight loss than eating a smaller breakfast saturated the media. Predictably, the press was all over this report with varying flavors or reporting depending upon the reporters biases. Some, obviously carb biased, reported from a high-carb perspective; others - more well-balanced, no doubt - reported from that bias. Others simply focused on the ‘big.’ Let’s see what’s going on here.

The first thing one must realize is that this is not a paper published in a peer-reviewed journal, this is a poster presentation at a medical meeting, in this case the annual meeting of the Endocrine Society held in San Francisco last week. A while back I wrote at length on the difference between this type of presentation and a paper that has gone through the peer-review process. Poster presentations such as this one go through a sort of peer review process when they are presented in the sense that attendees ask questions and point out weaknesses. But the public never sees this. The public sees the press reports about these presentations without the peer review. Papers that are published run through the peer-review gauntlet before they see the light of day and are ever reported on.

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