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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

One complicating factor in this research is that the underlying cause of dementia is exceedingly difficult to diagnose, even on autopsy. For this reason, it’s possible that the research linking diabetes to a higher incidence of Alzheimer’s does so because it confuses the consequences of a known complication of diabetes—vascular dementia—with an apparently increased incidence of Alzheimer’s dementia. These are the two most common causes of dementia, but the actual diagnoses are not clear-cut.

Alzheimer’s dementia is typically perceived as a slow, insidious process that can be identified on autopsy by the presence of neurofibrillary tangles, which are twisted protein fibers located within neurons, and amyloid plaques, which accumulate outside the neurons. Vascular dementia, a recognized complication of diabetes, is perceived as a more abrupt cognitive decline that is caused by small strokes in the blood vessels of the brain. Vascular dementia is usually diagnosed because the dementia appeared shortly after a stroke, or because an autopsy revealed the characteristic stroke-related signs of vascular damage. That vascular dementia is a complication of diabetes means that diabetics are far more likely to be diagnosed someday with vascular dementia than nondiabetics.

In cases of dementia, however, the determination of the actual cause is likely to be arbitrary. Most of us, if we live long enough, will accumulate both vascular damage and Alzheimer’s plaques and tangles in our brains, even if we don’t manifest any perceptible symptoms of dementia. (Similarly, most of us will have plaques in our arteries even if we don’t manifest clinical signs of heart disease.) Vascular dementia and Alzheimer’s dementia appear to coexist frequently, a condition known as mixed dementia. When dementia is present, the diagnosis of its ultimate cause is a matter of clinical judgment. This gray zone of mixed dementia was examined in a seminal study of nearly seven hundred elderly members of the Sisters of Notre Dame congregation, led by the University of Kentucky epidemiologist David Snowdon. The results suggest that, the less vascular damage we have in our brains, the more easily we can tolerate the lesions of Alzheimer’s without exhibiting signs of dementia. It’s the extent and location of the vascular damage in the brain, according to Snowdon, that appears to be the determining factor.

The implication is that the accumulation of damage to neurons and blood vessels is one unavoidable process of aging. There is a point when the slow accumulation of Alzheimer’s lesions and vascular damage passes some threshold and manifests itself as dementia, and diabetics are always likely to reach that threshold sooner than nondiabetics, if only because they accumulate vascular damage more rapidly, even if the diabetes bestows on them no special predisposition to develop Alzheimer’s plaques and tangles. So whatever dietary factors or lifestyle factors lead to Type 2 diabetes will always increase the likelihood of manifesting dementia.