Good Calories, Bad Calories

^*45 In 2003, for instance, the National Cholesterol Education Program described the shift in emphasis from total cholesterol to LDL cholesterol this way: “Many earlier studies measured only serum total cholesterol, although most of total cholesterol is contained in LDL. Thus, the robust relationship between total cholesterol and [coronary heart disease] found in epidemiological studies strongly implies that an elevated LDL is a powerful risk factor [my italics].”

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^†46 In the technique described by Fredrickson, Levy, and Lees, LDL cholesterol is not measured directly but calculated from the measurements of triglycerides, HDL cholesterol, and total cholesterol.

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^*47 Those that did mention the effect of carbohydrates on HDL cholesterol rejected the relevance to heart disease, on the basis, as the American Heart Association explained, “that epidemiological studies have demonstrated an inverse relation between carbohydrate consumption and risk for CHD.”

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^*48 The nutritional constituents of such a piece of relatively fatty meat can be found in the Nutrient Database for Standard Reference at the USDA Web site, along with those of thousands of other foods.

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^*49 To be precise, Krauss says, he rediscovered this heterogeneity of LDL: Waldo Fisher of the University of Florida, and Verne Schumaker of the University of California, Los Angeles, had discovered it independently a decade earlier, but had not pursued it further.

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^*50 This suggests that saturated fat elevates LDL-cholesterol levels in part by increasing the amount of cholesterol in the LDL, and so making larger and fluffier LDL to begin with, rather than by increasing the number of LDL particles or by increasing the number of small, dense LDL particles.

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^*51 What used to be known as juvenile-onset diabetes, which is characterized by an insulin deficit, is referred to as Type 1 or insulin-dependent diabetes mellitus, IDDM. The less severe form, which is characterized by insulin resistance rather than a lack of insulin, used to be called adult-onset diabetes. It is now called Type 2 or non-insulin-dependent diabetes mellitus or NIDDM. This is the terminology that I’ll now use as well.

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^*52 Named after Frederick Banting, the co-discoverer of insulin, a distant relative of William Banting, of corpulence notoriety.

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^*53 The reports do acknowledge, as the AHA-NIH-ADA conference report put it, that “very high-carbohydrate diets may accentuate atherogenic dyslipidemia”—i.e., small, dense LDL, high triglycerides, and low HDL—but then it recommends a high-carbohydrate, low-saturated-fat diet as the treatment.

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^*54 Ralph DeFronzo, on the other hand, believes that sufficient studies have confirmed Stout’s observations and that insulin itself should thus be considered an “atherogenic hormone.”

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^*55 This hypothesis cannot, however, explain why atherosclerosis among diabetics has remained relatively impervious to the otherwise beneficial effects of insulin therapy to control blood sugar.

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^*56 Those in Cerami’s laboratory at Rockefeller University and the researchers who trained with him get credit for much of the AGE work that followed.

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^*57 There’s also evidence that HDL molecules can become glycated, inhibiting their function and “rendering the HDL more pro-atherogenic.”

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^*58 For this reason, fructose is referred to as the most lipogenic carbohydrate. Credit for this observation dates to 1916, to Harold Higgins of the Nutrition Laboratory of the Carnegie Institution.

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^*59 Individuals with a single copy of this apo E4 gene are nearly three times as likely to have both heart disease and Alzheimer’s than those with none. Apo E4 is a cousin of apo B, the protein component of LDL and VLDL, and it is also found in the lipoproteins that transport triglycerides and cholesterol. Because heart- disease researchers have focused on cholesterol as the cause of heart disease, Alzheimer’s researchers tend also to refer to apo E4 as involved in cholesterol transport as though that were all it did, thus “point[ing] to a link between cholesterol and Alzheimer’s.” But this took the overly simplistic 1960s view of heart disease and used it to misdirect the Alzheimer’s research.

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^*60 Harvard neurologist Dennis Selkoe and others have been working to track down a gene that seems to predispose individuals to age-related Alzheimer’s, rather than the inherited early-onset form. By February 2007, they had not found it, but they had localized it, in the lingo, to a chunk of a single chromosome that was known to include the gene for insulin-degrading enzyme. This made IDE the obvious candidate and suggested that anyone who inherited a particularly unlucky variant of the IDE gene would have an increased likelihood of getting Alzheimer’s.

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^*61 Higginson held the environmental movement responsible for what he considered a willful misinterpretation of the epidemiologic observations: “If they could possibly make people believe that cancer was going to result from pollution, this would enable them to facilitate the clean-up of water, of the air, or whatever it is,” he told Science in 1979. He was all for cleaning up the environment, he added, but “to make cancer the whipping boy for every environmental evil may prevent effective action when it does matter.”

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^*62 Those clinical trials that tested the dietary-fat-and-fiber hypotheses of cancer, as we discussed earlier, replaced red meat in the experimental diets with fruits, vegetables, and whole grains. When these trials failed to confirm that fat causes breast cancer, or that fiber prevents colon cancer, they also failed to confirm the hypothesis that red-meat consumption plays a role in either.

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^*63 Tannenbaum actually compared his chronically underfed mice with control mice fed the identical diet but supplemented with cornstarch. The inhibition of cancer, as Tannenbaum noted, could have been due to “carbohydrate-restriction” rather than restriction of all calories.

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^*64 Different IGFs have different effects. To keep the following discussion reasonably simple, I’ll refer to IGF and IGF receptors as though there were only one species of each, although I’m oversimplifying the science by doing so.

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^*65 The apparent severity of this epidemic is inflated by the way in which obesity is defined. The