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

Pennington proposed that the same thing causes obesity in humans. The adipose tissue amasses fat calories in a normal manner after meals, but it doesn’t release those calories fast enough, for whatever reason, to satisfy the needs of the cells between meals. This was the metabolic defect that causes obesity, he said, and it could apparently be corrected or minimized by removing carbohydrates from the diet.

By hypothesizing the existence of such a defect, Pennington was able to explain the entire spectrum of observations about obesity in humans and animals simply by applying the same law of energy conservation that other obesity researchers had misinterpreted. The law applies to the fat tissue, Pennington noted, just as it does to the entire human body. If energy goes into the fat tissue faster than it comes out, the energy stored in the fat tissue has to increase. Any metabolic phenomenon that slows down the release of fat from the fat tissue—that retards the “energy out” variable of the equation—will have this effect, as long as the rate at which fat enters the adipose tissue (the energy in) remains unchanged, or at least does not decrease by an equal or a greater amount. Fat calories accumulating in the adipose tissue wouldn’t be available to the cells for fuel. We would have to eat more to compensate, or expend less energy, or both. We’d be hungrier or more lethargic than individuals without such a defect.

Pennington suggested that as the adipose tissue accumulates fat its expansion will increase the rate at which fat calories are released back into the bloodstream (just as inflating a balloon will increase the air pressure inside the balloon and the rate at which air is expelled out of the balloon if the air is allowed to escape), and this could eventually compensate for the initial defect itself. We will continue to accumulate fat—and so continue to be in positive energy balance—until we reach a new equilibrium and the flow of fat calories out of the adipose tissue once again matches the flow of calories in. At this point, Pennington said, “the size of the adipose deposits, though larger than formerly, remains constant: the weight curve strikes a plateau, and the food intake is, again, balanced to the caloric output.”

By Pennington’s logic obesity is simply the body’s way of compensating for a defect in the storage and metabolism of fat. The compensation, he said, occurs homeostatically, without any conscious intervention. It works by a negative feedback loop. By expanding with fat, the adipose tissue “provides for a more effective release of fat for the energy needs of the body.” Meanwhile, the conditions at the cellular level remain constant; the cells and tissues continue to function normally, and they do so even if we have to become obese to make this happen.