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*27 In Across Australia, Baldwin Spencer and F. J. Gillen 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 all 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 tells 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 II, when sugar rationing was relaxed. As Cleave noted, however, this coincided with the introduction of penicillin into clinical use to treat the infections that often kill adult diabetics. Diabetes management and control also improved dramatically 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 “brilliant 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 compelling the diabetes and heart-disease research communities to take notice, I will 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 actually 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 killer 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 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.