Chapters (40)
- Cover Page
- Title Page
- Dedication
- Prologue A Brief History of Banting
- Part One
- Chapter 1
- Chapter 2
- Chapter 3
- Chapter 4
- Part Two
- Chapter 5
- Chapter 6
- Chapter 7
- Chapter 8
- Chapter 9
- Chapter 10
- Chapter 11
- Chapter 12
- Chapter 13
- Part Three
- Chapter 14
- Chapter 15
- Chapter 16
- Chapter 17
- Chapter 18
- Chapter 19
- Chapter 20
- Chapter 21
- Chapter 22
- Chapter 23
- Chapter 24
- Epilogue
- Notes
- Bibliography
- Acknowledgments
- Illustration Credits
- A Note About the Author
- Also by Gary Taubes
- Footnotes
- Copyright
But the sand-rat experiments themselves, carried out in the early 1960s at Duke University by the comparative physiologist Knut Schmidt-Nielsen, suggested that the abundance of food was not the relevant factor. Schmidt-Nielsen was trying to establish what aspect of the laboratory diet might be responsible for the obesity and diabetes that appeared in his sand rats. He had taken two groups of rats freshly trapped in Egypt and raised one on Purina Laboratory Chow—“49.4% digestible carbohydrates, 23.4% protein and 3.8% fat”—supplemented with “fresh mixed vegetables,” and the other on the fresh vegetables alone. Both had access to as much food as they desired, but only the chow-eating rats got diabetic and obese. This suggested that something about Purina Chow was the determining factor. Perhaps the rats liked it better than vegetables, and so they ate more, although that, too, could be a physiological effect related to the nutrient composition of the chow. It might have been the density of calories in the rat chow, which have less water content than vegetables and so more calories per gram. It was also possible that the cause of the diabetes and obesity in these rats, as Schmidt-Nielsen suggested, was “a carbohydrate intake that is greater than that occuring in the natural diet.”*73
Depending on the researchers’ preconceptions, the Israeli sand rats could have been considered an animal model of the carbohydrate hypothesis, rather than the thrifty-gene hypothesis. Monkeys in captivity, by the way, will also get obese and diabetic on high-carbohydrate chow diets. One of the first reports of this phenomenon was in 1965, by John Brobeck of Yale, whose rhesus monkeys got fat and mildly diabetic on Purina Monkey Chow—15 percent protein, 6 percent fat, and 59 percent digestible carbohydrates. According to Barbara Hansen, who studies diabetes and obesity and runs a primate-research laboratory at the University of Maryland, perhaps 60 percent of middle-aged monkeys in captivity are obese by monkey standards. “This is on the kind of diet recommended by the American Heart Association,” she says, “high-fiber, low-fat, no-cholesterol chow.”
The world is full of species that do fatten regularly, always to serve a purpose—long-distance migrations, reproduction, or survival during periods when food is either unavailable or too risky to procure. Hibernators seem to be an obvious choice to shed light on the assumptions underlying the thrifty-gene hypothesis. These animals accumulate enormous fat deposits in response to an environment that offers up periods of feast—spring, summer, and fall—and famine in the winter. Yet this accumulation goes unaccompanied by the chronic ills, such as diabetes, that appear in obese humans. Hibernating ground squirrels, for instance, will double their weight and body fat in a few weeks of late summer. Dissecting such squirrels at their peak weight is akin to “opening a can of Crisco oil,” as the University of California biologist Irving Zucker, a pioneer of this research, has described it, “enormous gobs of fat, all over the place.”