Chapters (40)
- Cover Page
- Title Page
- Dedication
- Prologue A Brief History of Banting
- Part One
- Chapter 1
- Chapter 2
- Chapter 3
- Chapter 4
- Part Two
- Chapter 5
- Chapter 6
- Chapter 7
- Chapter 8
- Chapter 9
- Chapter 10
- Chapter 11
- Chapter 12
- Chapter 13
- Part Three
- Chapter 14
- Chapter 15
- Chapter 16
- Chapter 17
- Chapter 18
- Chapter 19
- Chapter 20
- Chapter 21
- Chapter 22
- Chapter 23
- Chapter 24
- Epilogue
- Notes
- Bibliography
- Acknowledgments
- Illustration Credits
- A Note About the Author
- Also by Gary Taubes
- Footnotes
- Copyright
*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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