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

This fact was absolutely critical to the dietary prevention of heart disease, Gofman said. If a physician put a patient with high cholesterol on a low-fat diet, that might lower the patient’s LDL, but it would raise VLDL. If LDL was abnormally elevated, then this low-fat diet might help, but what Gofman called the “carbohydrate factor” in these low-fat diets might raise VLDL so much that the diet would do more harm than good. Indeed, in Gofman’s experience, when LDL decreased, VLDL tended to rise disproportionately. And if VLDL was abnormally elevated to begin with, then prescribing a low-fat, high-carbohydrate diet would certainly increase the patient’s risk of heart disease.

This was why Gofman described the measurement of total cholesterol as a “false and highly dangerous guide” to the effect of diet on heart disease. Total-cholesterol measurements tell us nothing about the status of VLDL and LDL. Prescribing low-fat diets indiscriminately to anyone whose cholesterol appears to be elevated, or bombarding us with “generalizations such as ‘we all eat too much fat,’ or ‘we all eat too much animal fat,’” would increase heart-disease risk for a large proportion of the population. “Neglect of [the carbohydrate] factor can lead to rather serious consequences,” wrote Gofman in 1958, “first, in the failure to correct the diet in some individuals who are very sensitive to the carbohydrate action; and second, by allowing certain individuals sensitive to the carbohydrate action to take too much carbohydrate as a replacement for some of their animal fats.”

By 1955, Pete Ahrens at Rockefeller University had come to this same conclusion, although Ahrens was specifically studying triglycerides, rather than the VLDL particles that carry the triglycerides. Ahrens was considered by many investigators to be the single best scientist in the field of lipid metabolism. He had observed how the triglycerides of some patients shoot up on low-fat diets and fall on high-fat diets. This led Ahrens to describe a phenomenon that he called carbohydrate-induced lipemia (an excessive concentration of fat in the blood). When he gave lectures, Ahrens would show photos of two test tubes of blood serum obtained from the same patient—one when the patient was eating a high-carbohydrate diet and one on a high-fat diet. One test tube would be milky white, indicating the lipemia. The other would be absolutely clear. The surprising thing, Ahrens would explain, was “that the lipemic plasma was obtained during the high-carbohydrate period, and the clear plasma during the high-fat regimen.” (Joslin had reported the same phenomenon in diabetics thirty years earlier. “The percent of fat” in the blood, he wrote, “rises with the severity of the disease…and is especially related to the quantity of carbohydrate, which is being oxidized, rather than with the fat administered.”)