The essence of the study results is that those following a low-carbohydrate diet had greater weight-loss and improvements in blood lipids. The Mediterranean diet did well also. Both of these results are predictable from what we know about metabolic regulation, but for the mainstream, this result clearly induces significant dissonance. I particularly enjoyed Dean Ornish's attempt at reconciling this dissonance. Here's a choice quote:
I'm also very skeptical of the quality of data in this study. For example, the investigators reported that those on the "low-fat" diet consumed 200 fewer calories per day—or 10,000 fewer calories per year—than those on the Mediterranean diet, yet people lost more weight on the Mediterranean diet. That's physiologically impossible.
I think Dr. Ornish needs to bone up on his biochem. We'll hit this point later in the series on Energy Regulation, but the body very definitely has a mechanism to dump excess fat calories in the form of heat. And of course Ornish's calorie-centric focus completely ignores other regulatory effects, such as insulin's effect on fat storage. Ornish does spend plenty of time telling you all about himself, what he believes, why his particular diet flavor is superior, etc. The article reads more like an infomercial than scientific exposition. Comparison of different scientific hypotheses requires inclusion of ALL relevant evidence. Ornish heavily weighs evidence of his own creation, which (not surprisingly) supports his own preconceived notions. If you selectively weigh evidence in this way, you can come to any conclusion you want.
Here's another fun quote from Ornish: "Most people associate an Atkins diet with bacon, butter and brie, not a plant-based diet like the one I recommend." There's that "I" again. Shouldn't the diet be recommended by the evidence, not one individual? I guess Dr. Ornish is smarter than the rest of us. Maybe he would grace us with a more detailed explanation of why he's "right" given our knowledge of metabolic regulation at the molecular and cellular level?
I'm not holding my breath.
Ornish's comment also highlights one of the major origins of dissonance surrounding these recent results: the seemingly unshakable belief that saturated fat ("bacon, butter, and brie") plays a role in a wide range of disease processes. We saw in the original post on cognitive dissonance that there actually exists essentially no evidence of causality (I just confirmed this with an ex-official of the American Heart Association). For example, there may be some statistical association between saturated fat consumption and development of heart disease (particularly if you limit the observational data set), but there's no evidence at all of causality at the molecular and cellular level. Let's look at a some ways in which this association might arise:
- Fast food is often high in saturated fat. It's also often high in total refined carbohydrates, particularly fructose. The damage wrought by increase carbohydrates (fructose is particularly good at this) and the hormonal derangement from repeated insulin spikes (and probably fructose as well) quite logically predicts an increase in heart disease. The likely high consumption of oxidized fats from deep-fried foods is the cherry on top of this sundae. Lipoprotein molecules are composed of a water soluble membrane including both proteins and fatty acids. White blood cells have a specific receptor for oxidized LDL (but not unoxidized LDL), so if your LDL includes some oxidized fat from your French fries, you should expect an increased immune response, which is known to be important in the development of atherosclerosis. So if a population has a high consumption of fast food, not only is their saturated fat consumption higher, so is the consumption of refined carbohydrates and oxidized fats. Which of these actually causes the observed increase in heart disease?
- Grain-fed beef is known to have some nutritional issues. Grains are not the natural food of cattle, who prefer to eat leafy material, which tends to be rich in the omega-3 alpha-linolenic acid. When compared with grass-fed beef, grain-fed has a significantly higher ratio of omega-6/omega-3 fatty acids. There is a biochemical reason to believe this could increase heart disease, due to the pro-inflammatory effect of omega-6 fats. Grain-fed beef is also much higher in saturated fat, so there would be an association between saturated fat intake and increased omega-6/omega-3 ratio.
- Grain-fed beef is also higher in total fat. Guess what - carbohydrates make cows fat too! But this fat is essentially "empty calories" in that the increased fat intake does not bring significant additional micronutrients, probably displacing calories from foods that are nutrient dense. Again, at the molecular/cellular level, there are good reasons to believe these micronutrients (like magnesium) are protective against the development of heart disease.
- Eating a crappy diet like fast food makes people sick. Sick people tend to stay inside. If you don't go outside, in all likelihood you are deficient in Vitamin D. Vitamin D deficiency is implicated in a whole host of diseases, including heart disease. I'll bet saturated fat consumption is correlated with Vitamin D deficiency as well.
I'm sure with a little thought we could come up with several more. The point is this: associating causality with an individual statistical correlation is a very slippery slope. If you have no evidence for causality, making such an association implies that you are ignoring other possible causes WITHOUT EVIDENCE. Attempting to treat sick people based on this association could be expected to be ineffective at best, harmful at worst. And of course you wind up with the precise situation we observe today, which is that some bogus dogmatic belief blocks the advancement of science due to cognitive dissonance.