The Obesity Code. Jason Fung

are believed crucial in the development of obesity. But they play virtually no role. In fact, the fattest adoptees had the thinnest adoptive parents.

      Comparing adoptees to their biological parents yielded a considerably different result. Here there was a strong, consistent correlation between their weights. The biological parents had very little or nothing to do with raising these children, or teaching them nutritional values or attitudes toward exercise. Yet the tendency toward obesity followed them like ducklings. When you took a child away from obese parents and placed them into a “thin” household, the child still became obese.

      What was going on?

      Studying identical twins raised apart is another classic strategy to distinguish environmental and genetic factors. Identical twins share identical genetic material, and fraternal twins share 25 percent of their genes. In 1991, Dr. Stunkard examined sets of fraternal and identical twins in both conditions of being reared apart and reared together.⁴ Comparison of their weights would determine the effect of the different environments. The results sent a shockwave through the obesity-research community. Approximately 70 percent of the variance in obesity is familial.

       Seventy percent.

      Seventy percent of your tendency to gain weight is determined by your parentage. Obesity is overwhelmingly inherited.

      However, it is immediately clear that inheritance cannot be the sole factor leading to the obesity epidemic. The incidence of obesity has been relatively stable through the decades. Most of the obesity epidemic materialized within a single generation. Our genes have not changed in that time span. How can we explain this seeming contradiction?

       THE THRIFTY-GENE HYPOTHESIS

      THE FIRST ATTEMPT to explain the genetic basis of obesity was the thrifty-gene hypothesis, which became popular in the 1970s. This hypothesis assumes that all humans are evolutionarily predisposed to gain weight as a survival mechanism.

      The argument goes something like this: In Paleolithic times, food was scarce and difficult to obtain. Hunger is one of the most powerful and basic of human instincts. The thrifty gene compels us to eat as much as possible, and this genetic predisposition to gain weight had a survival advantage. Increasing the body’s food stores (fat) permitted longer survival during times of scarce or no food. Those who tended to burn the calories instead of storing them were selectively wiped out. However, the thrifty gene is ill adapted to the modern all-you-can-eat world, as it causes weight gain and obesity. But we are simply following our genetic urge to gain fat.

      Like a decomposing watermelon, this hypothesis seems quite reasonable on the surface. Cut a little deeper, and you find the rotten core. This theory has long ceased to be taken seriously. However, it is still mentioned in the media, and so its flaws bear some examination. The most obvious problem is that survival in the wild depends on not being either underweight or overweight. A fat animal is slower and less agile than its leaner brethren. Predators would preferentially eat the fatter prey over the harder-to-catch, lean prey. By the same token, fat predators would find it much more difficult to catch lean and swift prey. Body fatness does not always provide a survival advantage, but instead can be a significant disadvantage. How many times have you seen a fat zebra or gazelle on the National Geographic channel? What about fat lions and tigers?

      The assumption that humans are genetically predisposed to overeat is incorrect. Just as there are hormonal signals of hunger, there are multiple hormones that tell us when we’re full and stop us from overeating. Consider the all-you-can-eat buffet. It is impossible to simply eat and eat without stopping because we get “full.” Continuing to eat may make us become sick and throw up. There is no genetic predisposition 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?

PART TWO

       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.