to overeating. There is, instead, powerful built-in protection against it.
The thrifty-gene hypothesis assumes chronic food shortages prevented obesity. However, many traditional societies had plentiful food year round. For example, the Tokelau, a remote tribe in the South Pacific, lived on coconut, breadfruit and fish, which were available year round. Regardless, obesity was unknown among them until the onset of industrialization and the Westernization of their traditional diet. Even in modern-day North America, widespread famine has been uncommon since the Great Depression. Yet the growth of obesity has happened only since the 1970s.
In wild animals, morbid obesity is rare, even with an abundance of food, except when it is part of the normal life cycle, as with hibernating animals. Abundant food leads to a rise in the numbers of animals, not an enormous increase in their size. Think about rats or cockroaches. When food is scarce, rat populations are low. When food is plentiful, rat populations explode. There are many more normal-sized rats, not the same number of morbidly obese rats.
There is no survival advantage to carrying a very high body-fat percentage. A male marathon runner may have 5 percent to 11 percent body fat. This amount provides enough energy to survive for more than a month without eating. Certain animals fatten regularly. For instance, bears routinely gain weight before hibernation—and they do so without illness. Humans, though, do not hibernate. There is an important difference between being fat and being obese. Obesity is the state of being fat to the point of having detrimental health consequences. Bears, along with whales, walruses and other fat animals are fat, but not obese, since they suffer no health consequences. They are, in fact, genetically programmed to become fat. We aren’t. In humans, evolution did not favor obesity, but rather, leanness.
The thrifty-gene hypothesis doesn’t explain obesity, but what does? As we will see in Part 3, “A New Model of Obesity,” the root cause of obesity is a complex hormonal imbalance with high blood insulin as its central feature. The hormonal profile of a baby is influenced by the environment in the mother’s body before birth, setting up a tendency for high insulin levels and associated obesity later in life. The explanation of obesity as a caloric imbalance simply cannot account for this predominantly genetic effect, since eating and exercise are voluntary behaviors. Obesity as a hormonal imbalance more effectively explains this genetic effect.
But inherited factors account for only 70 percent of the tendency to obesity that we observe. The other 30 percent of factors are under our control, but what should we do to make the most of this? Are diet and exercise the answer?
The Calorie Deception
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THE CALORIE-REDUCTION ERROR
TRADITIONALLY, OBESITY HAS been seen as a result of how people process calories, that is, that a person’s weight could be predicted by a simple equation:
Calories In – Calories Out = Body Fat
This key equation perpetrates what I call the calorie deception. It is dangerous precisely because it appears so simple and intuitive. But what you need to understand is that many false assumptions are built in.
Assumption 1: Calories In and Calories Out are independent of each other
This assumption is a crucial mistake. As we’ll see later on in this chapter, experiments and experience have proven this assumption false. Caloric intake and expenditure are intimately dependent variables. Decreasing Calories In triggers a decrease in Calories Out. A 30 percent reduction in caloric intake results in a 30 percent decrease in caloric expenditure. The end result is minimal weight loss.
Assumption 2: Basal metabolic rate is stable
We obsess about caloric intake with barely a thought for caloric expenditure, except for exercise. Measuring caloric intake is simple, but measuring the body’s total energy expenditure is complicated. Therefore, the simple but completely erroneous assumption is made that energy expenditure remains constant except for exercise. Total energy expenditure is the sum of basal metabolic rate, thermogenic effect of food, nonexercise activity thermogenesis, excess post-exercise oxygen consumption and exercise. The total energy expenditure can go up or down by as much as 50 percent depending upon the caloric intake as well as other factors.
Assumption 3: We exert conscious control over Calories In
Eating is a deliberate act, so we assume that eating is a conscious decision and that hunger plays only a minor role in it. But numerous overlapping hormonal systems influence the decision of when to eat and when to stop. We consciously decide to eat in response to hunger signals that are largely hormonally mediated. We consciously stop eating when the body sends signals of satiety (fullness) that are largely hormonally mediated.
For example, the smell of frying food makes you hungry at lunchtime. However, if you have just finished a large buffet, those same smells may make you slightly queasy. The smells are the same. The decision to eat or not is principally hormonal.
Our bodies possess an intricate system guiding us to eat or not. Body-fat regulation is under automatic control, like breathing. We do not consciously remind ourselves to breathe, nor do we remind our hearts to beat. The only way to achieve such control is to have homeostatic mechanisms. Since hormones control both Calories In and Calories Out, obesity is a hormonal, not a caloric, disorder.
Assumption 4: Fat stores are essentially unregulated
Every single system in the body is regulated. Growth in height is regulated by growth hormone. Blood sugars are regulated by the hormones insulin and glucagon, among others. Sexual maturation is regulated by testosterone and estrogen. Body temperature is regulated by a thyroid-stimulating hormone and free thyroxine. The list is endless.
We are asked to believe, however, that growth of fat cells is essentially unregulated. The simple act of eating, without any interference from any hormones, will result in fat growth. Extra calories are dumped into fat cells like doorknobs into a sack.
This assumption has already been proven false. New hormonal pathways in the regulation of fat growth are being discovered all the time. Leptin is the best-known hormone regulating fat growth, but adiponectin, hormone-sensitive lipase, lipoprotein lipase and adipose triglyceride lipase may all play important roles. If hormones regulate fat growth, then obesity is a hormonal, not a caloric disorder.
Assumption 5: A calorie is a calorie
This assumption is the most dangerous of all. It’s obviously true. Just like a dog is a dog or a desk is a desk. There are many different kinds of dogs and desks, but the simple statement that a dog is a dog is true. However, the real issue is this: Are all calories equally likely to cause fat gain?
“A calorie is a calorie” implies that the only important variable in weight gain is the total caloric intake, and thus, all foods can be reduced to their caloric energy. But does a calorie of olive oil cause the same metabolic response as a calorie of sugar? The answer is, obviously, no. These two foods have many easily measurable differences.
