Back Good Calories, Bad Calories
Chapters (40)
  1. Cover Page
  2. Title Page
  3. Dedication
  4. Prologue A Brief History of Banting
  5. Part One
  6. Chapter 1
  7. Chapter 2
  8. Chapter 3
  9. Chapter 4
  10. Part Two
  11. Chapter 5
  12. Chapter 6
  13. Chapter 7
  14. Chapter 8
  15. Chapter 9
  16. Chapter 10
  17. Chapter 11
  18. Chapter 12
  19. Chapter 13
  20. Part Three
  21. Chapter 14
  22. Chapter 15
  23. Chapter 16
  24. Chapter 17
  25. Chapter 18
  26. Chapter 19
  27. Chapter 20
  28. Chapter 21
  29. Chapter 22
  30. Chapter 23
  31. Chapter 24
  32. Epilogue
  33. Notes
  34. Bibliography
  35. Acknowledgments
  36. Illustration Credits
  37. A Note About the Author
  38. Also by Gary Taubes
  39. Footnotes
  40. Copyright

*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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