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

By the late 1970s, researchers had also reported that malignant breast tumors had more receptors for insulin than did healthy tissue. The more insulin receptors on the surface of a cell, the more sensitive it will be to the insulin in its environment. Having a greater number of insulin receptors than healthy cells, as one report noted, might confer “a selective growth advantage to tumor cells.”

“Selective growth advantage” speaks directly to the process of Darwinian evolution that is considered the controlling force in tumor development. We can think of human cells as existing in a microscopic ecosystem, living in harmony with their environment, and balanced, as are all species, between the opportunities for growth and proliferation and the processes that lead to aging and death. In such an environment, the billions of cells that eventually constitute a tumor will be the descendants of a single cell that has accumulated a series of genetic mutations, each adding to its proclivity to proliferate unfettered by any of the normal inhibitions to growth. The process in which a healthy cell eventually results in malignancy is a gradual evolution driven by a series of mutations in the DNA of the genes, each bestowing on the cell either the inclination to multiply or a breakdown in the control and repair mechanisms that have evolved to counter precisely such potentially deleterious mutations. The descendants of such a mutant cell would inherit this fitness advantage over other cells in the tissue, and so, within a few years, a single such mutant cell will leave millions of descendants. As one of those descendants in turn gains, purely by chance, yet another advantageous error or mutation, its descendants will now come to dominate.

Each new mutation-bearing cell constitutes a new species, in effect, that is better suited to prevail in its local cellular environment. Eventually, with this continued accumulation of what to the body as a whole is simply bad luck, a single cell will come to possess precisely that set of mutant genes that drive it and allow it to grow and proliferate without limit. Because each single hit of genetic damage alone is not sufficient to produce a cancer cell, the accumulation of just the right half-dozen hits (actually, the wrong half-dozen hits) takes years or decades, which is why virtually all cancers become more common as we age.