Good Calories, Bad Calories (110 page)

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*20 Browner’s analysis also assumed that restricting dietary fat would reduce cancer deaths, which was speculative then and is even more speculative now.

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*21 Wil iam Taylor, the Harvard physician who had done the first of the three analyses on the questionable benefits of eating less fat, was unimpressed with this argument. “Most patients don’t come into my office saying I real y want to contribute to the public health statistics in this country,” he said. “If they did, I’d know what to do for them.”

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*22 Melvin Konner has doubts about the conclusions. “Boyd and I probably did underestimate the amount of meat in the Paleolithic diet based on our extrapolations for hunter-gatherers,” he said. “I just don’t think it’s nearly as extreme as this paper claims.”

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*23 They did not, however, lose any weight because of this, which is paradoxical, and an issue we wil discuss later.

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*24 This paradox could also include Switzerland. In 1979, Swiss public-health authories reported that cardiovascular mortality had undergone a “suprising decline” in Switzerland between 1951 and 1976, during a period in which the Swiss increased their consumption of animal fats by 20 percent.

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*25“Among women high blood cholesterol is not associated with al -cause mortality nor even with cardiovascular mortality,” wrote UCSF epidemiologist Steve Hul ey and his col aborators in a 1992 Circulation editorial about these data, entitled “Health Policy on Blood Cholesterol: Time to Change Directions.”“We are coming to realize that the results of cardiovascular research in men, which represents the great majority of the effort thus far, may not apply to women.”

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*26 Conspicuously absent from the final analysis, because it was not a “randomized” trial and so the results could not be trusted, was the famous Helsinki Mental Hospital Study that had been cited by three generations of investigators, including The Surgeon General’s Report on Nutrition and Health and the National Academies of Science Diet and Health report, as providing the most compel ing evidence that cholesterol-lowering diets lowered mortality, not just heart disease.

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*27 In Across Australia, Baldwin Spencer and F. J. Gil en describe embarking on an expedition through central Australia in the late 1890s with eight thousand pounds of flour (forty bags, each weighing two hundred pounds) and seven hundred pounds of sugar.

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†28 A typical diet of one Australian Aborigine settlement, according to a joint American/Australian expedition in 1948, “consisted of white flour, rice, tea and sugar, buffalo and beef.”

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*29 In 1938, C. P. Donnison confirmed this observation in his book Civilization and Disease, using British Colonial Office yearly medical reports, which listed hospital inpatient diagnoses in al the British colonies. Many of the colonial physicians, wrote Donnison, reported that diabetes had never been seen in their local native populations. “Others say they have seen an odd case or two during many years experience.” In those populations that had been more influenced by civilization, he continued, “a greater incidence is recorded.”

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*30 Such as peas, beans, and lentils.

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*31 Joslin also cited a 1936 article by Himsworth in The Lancet, but this latter article, if anything, tended to implicate carbohydrates as a cause of diabetes.

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*32 Although, he noted in the 1946 edition of his textbook, “Dr. F. G. Brigham tel s me Mrs. K. with multiple sclerosis developed diabetes after starting in to eat candy to gain weight.”

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*33 This close relationship temporarily diverged at the end of World War I, when sugar rationing was relaxed. As Cleave noted, however, this coincided with the introduction of penicil in into clinical use to treat the infections that often kil adult diabetics. Diabetes management and control also improved dramatical y with the development of the standard insulin syringe in 1944, and long-acting insulin two years later.

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*34 Although, as we noted earlier (Chapter 1), the amount of animal fat Americans ate decreased during this period, and so the increased total fat consumption was entirely due to the increased consumption of vegetable fats.

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*35 There is even a plausible biological mechanism to explain how refined carbohydrates and sugars could cause or exacerbate cancer. See Chapter 13.

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*36 John Higginson, director of the World Health Organization’s International Agency on Cancer Research, later described Non-infective Diseases in Africa as a “bril iant review” that had been “regrettably ignored.”

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*37“The title Western diseases is preferred to that of the diseases of civilization,” they explained, “for it proved obnoxious to teach African and Asian medical students that their communities had a low incidence of these diseases because they were uncivilized.”

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*38 According to records from the local trading ships, this increase was nearly tenfold between 1961 and 1980: from seven pounds per person per year to sixty-nine pounds.

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*39 Although Reaven deserves much of the credit for identifying the syndrome and compel ing the diabetes and heart-disease research communities to take notice, I wil refer to it as metabolic syndrome, because that is now the preferred public-health terminology, rather than Syndrome X, except when discussing Reaven’s work in particular.

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†40 The first time the Washington Post mentioned metabolic syndrome or Reaven’s research was in 1999, in an article about popular weight-loss diets.

The second time was in 2001, in an article that actual y discussed metabolic syndrome as a risk factor for heart disease. By that time, the paper had published a couple of thousand articles that at least touched on the issue of cholesterol and heart disease.

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*41 A triglyceride molecule is composed of three fatty acids—hence, the “tri”—linked together by a glycerol molecule.

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*42 To be precise, Gofman’s Science paper identified IDL—i.e., intermediate-density lipoproteins—as the class associated with heart disease. He would later decide that LDL was more important than IDL. For the sake of simplicity, I’ve used LDL throughout.

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*43 One notable case was Theodore Cooper, who was assistant secretary for health in 1976, when he testified about “diet and kil er diseases” to the Senate Select Committee on Nutrition and Human Needs. Cooper said that his personal dietary concern was with carbohydrates rather than fats. “If I have a problem, it is a tendency to gain weight,” Cooper explained. “I am classified Type IV. As a Type IV, my lipid levels are much more subject to elevation if I consume large amounts of carbohydrates or alcohol.”

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*44 This was not because the NIH had any interest in testing the HDL/heart-disease relationship, according to Gordon, but only because Fredrickson, Levy, and Lees’s new measurement technique required that the amount of cholesterol in HDL be known so that the amount in LDL could be calculated.

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*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 smal , 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 mel itus, IDDM. The less severe form, which is characterized by insulin resistance rather than a lack of insulin, used to be cal ed adult-onset diabetes. It is now cal ed Type 2 or non-insulin-dependent diabetes mel itus or NIDDM. This is the terminology that I’l now use as wel .

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*52 Named after Frederick Banting, the co-discoverer of insulin, a distant relative of Wil iam 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., smal , 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 Rockefel er University and the researchers who trained with him get credit for much of the AGE work that fol owed.

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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 al 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 wil ful misinterpretation of the epidemiologic observations: “If they could possibly make people believe that cancer was going to result from pol ution, 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 al 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 actual y compared his chronical y 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 al calories.

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*64 Different IGFs have different effects. To keep the fol owing discussion reasonably simple, I’l 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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