"all the relevant diet trials done in the last decade — randomized controlled trials comparing Atkins-like low-carb diets to AHA low-fat, calorie-restricted diets — of which there are now more than half a dozen, have observed the same result., In each one, LDL on the two diets was a virtual wash and cholesterol profiles (total/HDL) showed greater improvement on the Atkins diet. When the trial looked at blood pressure, that improved significantly on the higher fat, lower carb diet. In this Israeli study, they looked at markers of inflammation — same story.
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.)
These latest trials just happen to be the best data we have on the long-term effects of saturated fat in the diet, and the best data we have says that more saturated fat is better than less. It may be true that if we lowered saturated fat further — say to 7 % of all calories as the American Heart Association is now recommending — or total fat down to 10 percent, as Dean Ornish argues, or raised saturated fat to 20 percent of calories, as Keys did, that we’d see a different result, but that’s just another hypothesis. The trials haven’t been done to test it. It’s also hard to imagine why a small decrease in saturated fat would be deleterious, but a larger decrease would be beneficial.
It’s also true that I don’t think that LDL is a particularly meaningful predictor of heart disease risk, and I think total cholesterol is meaningless (based on the evidence that I recount in the book). But the point is that the AHA and the National Cholesterol Education Program and the authorities at the National Heart, Lung and Blood Institute do think LDL is meaningful, and that’s the basis by which they have always recommended low-saturated-fat diets. They also think that total cholesterol/HDL is the single best predictor of heart disease risk, so by their assessment, more saturated fat is better than less. I think the best predictors of risk regarding cholesterol profiles are HDL and the size and density of the LDL particles themselves, and maybe measurements of a protein known as ApoB (the protein component of the LDL particle itself) — and the existing diet trials in those cases also suggest that saturated fats are at worst harmless and perhaps even beneficial.
Last point, the funding. It’s true that the study was financed by the Atkins Foundation, but to assume that the researchers went out and falsified their findings or twisted their observations to satisfy the source of funding is naive. Regrettably, the only institutions that will finance clinical trials, for the most part, are those that stand to gain from the results. That’s why the pharmaceutical industry finances drug trials. It would be nice if the government financed all these trials, but they don’t. So it’s up to the Atkins Foundation and any other organizations that might hold similar beliefs. In this case, the Atkins-funded diet trial observed the exact same results as similar NIH-funded diet trials.
Worth noting here is that the NIH has also spent $5 million recently for a large (300+ subjects, two-year-long) Atkins vs. AHA low-fat diet trial. This is a larger and longer version of a pilot trial that observed results similar to the Israeli trial. To my knowledge, it’s the largest diet/weight trial the NIH has ever funded. The principal investigator was Gary Foster of Temple University, currently the president of the Obesity Society, which is to obesity these days what the American Heart Association is to heart disease. In February of 2007, Dr. Foster told me the researchers had “completed the final 2 year assessments on most but not all” of their subjects. This week he told me that a paper on the results is “in the peer review process” and that “journal policies prevent me from saying more than that.” It would be nice to see those results, and we can only hope they’ll be published soon."
http://tierneylab.blogs.nytimes.com/2008/07/24/the-fat-fight-goes-on/
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