The Obesity Code: Unlocking the Secrets of Weight Loss (Why Intermittent Fasting Is the Key to Controlling Your Weight)

by Jason Fung

Finally, on the advice of his surgeon, Banting tried a new approach. With the idea that sugary and starchy foods were fattening, he strenuously avoided all breads, milk, beer, sweets and potatoes that had previously made up a large portion of his diet. (Today we would call this diet low in refined carbohydrates.) William Banting not only lost the weight and kept it off, but he also felt so well that he was compelled to write his famous pamphlet. Weight gain, he believed, resulted from eating too many “fattening carbohydrates.” For most of the next century, diets low in refined carbohydrates were accepted as the standard treatment for obesity. By the 1950s, it was fairly standard advice. If you were to ask your grandparents what caused obesity, they would not talk about calories. Instead, they would tell you to stop eating sugary and starchy foods. Common sense and empiric observation served to confirm the truth. Nutritional “experts” and government opinion were not needed. Calorie counting had begun in the early 1900s with the book Eat Your Way to Health, written by Dr. Robert Hugh Rose as a “scientific system of weight control.” That book was followed up in 1918 with the bestseller Diet and Health, with Key to the Calories, written by Dr. Lulu Hunt Peters, an American doctor and newspaper columnist. Herbert Hoover, then the head of the U.S. Food Administration, converted to calorie counting. Dr. Peters advised patients to start with a fast, one to two days abstaining from...

The discovery of vaccines and antibiotics, combined with increased public sanitation, had reshaped the medical landscape. Formerly lethal infections, such as pneumonia, tuberculosis and gastrointestinal infections, became curable. Heart disease and cancer now caused a relatively greater percentage of deaths, giving rise to some of the public misperception of an epidemic. (See Figure 1.1.6)

The increase in life expectancy from 1900 to 1950 reinforced the perception of a coronary-disease epidemic.

Currently, the average age at first heart attack is sixty-six years.8 The risk of a heart attack in a fifty-year-old man is substantially lower than in a sixty-eight-year-old man. So the natural consequence of a longer life expectancy is an increased rate of coronary disease.

Since many high-protein foods like meat and dairy are also high in fat, it is difficult to lower fat in the diet without lowering protein as well. So, if one were to restrict dietary fats, then one must increase dietary carbohydrates and vice versa. In the developed world, these carbohydrates all tend to be highly refined. Low Fat = High Carbohydrate This dilemma created significant cognitive dissonance. Refined carbohydrates could not simultaneously be both good (because they are low in fat) and bad (because they are fattening). The solution adopted by most nutrition experts was to suggest that carbohydrates were no longer fattening. Instead, calories were fattening.

But not everybody bought in. One of the most famous dissidents was the prominent British nutritionist John Yudkin (1910–1995).

THE ISSUE WAS finally settled in 1977, not by scientific debate and discovery, but by governmental decree.

Not only was dietary fat guilty of causing heart disease, but it also caused obesity, since fat is calorically dense. The resulting declaration became the Dietary Goals for the United States. An

should and should not eat. But from now on, Big Brother would be telling us. And he said, “Eat less fat and more carbohydrates.” Several specific dietary goals were set forth. These included •raise consumption of carbohydrates until they constituted 55 percent to 60 percent of calories, and •decrease fat consumption from approximately 40 percent of calories to 30 percent, of which no more than one-third should come from saturated fat. With no scientific evidence, the formerly “fattening” carbohydrate made a stunning

The Dietary Guidelines for Americans, now updated every five years, spawned the infamous food pyramid in all its counterfactual glory. The foods that formed the base of the pyramid—the foods we should eat every single day—were breads, pastas and potatoes. These were the precise foods that we had previously avoided to stay thin.

To drink, “Choose . . . fruit punches, carbonated soft drinks.” Ahhh. White bread and carbonated soft drinks—the dinner of champions. Thank you, American Heart Association (AHA).

Inevitably, sugar consumption increased. From 1820 to 1920, new sugar plantations in the Caribbean and American South increased the availability of sugar in the U.S. Sugar intake plateaued from 1920 to 1977. Even though “avoid too much sugar” was an explicit goal of the 1977 Dietary Guidelines for Americans, consumption increased anyway until the year 2000.

Refined grain consumption increased by almost 45 percent. Since carbohydrates in North America tended to be refined, we ate more and more low-fat bread and pasta, not cauliflower and kale.11

Ironically, the American Heart Association, even as late as the year 2000, felt that low-carbohydrate diets were dangerous fads, despite the fact that these diets had been in use almost continuously since 1863.

What was the result? The incidence of heart disease certainly did not decrease as expected. But there was definitely a consequence to this dietary manipulation—an unintentional one.

IT IS FAIRLY obvious that obesity runs in families.1 Obese children often have obese siblings. Obese children become obese adults.

The controversy revolves around whether this trend is a genetic or an environmental problem—the classic nature versus nurture debate.

Genetics can explain much of the inter-individual risk of obesity, but not why entire populations become obese. Nonetheless, families live in the same environment, eat similar foods at similar times and have similar attitudes.

Dietary and lifestyle habits have changed considerably since the 1970s including •adoption of a low-fat, high-carbohydrate diet, •increased number of eating opportunities per day, •more meals eating out, •more fast-food restaurants, •more time spent in cars and vehicles, •increased popularity of videos games, •increased use of computers,

•increase in dietary sugar, •increased use of high-fructose corn syrup and •increased portion sizes.

behaviors, after all, with little genetic input. So—exactly how much of a role does genetics play in human obesity?

THE CLASSIC METHOD for determining the relative impact of genetic versus environmental factors is to study adoptive families, thereby removing genetics from the equation.

No relationship whatsoever was discovered between the weight of the adoptive parents and the adoptees. Whether adoptive parents were thin or fat made no difference to the eventual weight of the adopted child. The environment provided by the adoptive parents was largely irrelevant.

This finding was a considerable shock. Standard calorie-based theories blame environmental factors and human behaviors for obesity.

Comparing adoptees to their biological parents yielded a considerably different result. Here there was a strong, consistent correlation between their weights.

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.

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 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.

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.

Body fatness does not always provide a survival advantage, but instead can be a significant disadvantage.

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.

There is no genetic predisposition to overeating. There is, instead, powerful built-in protection against it.

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.

Obesity is the state of being fat to the point of having detrimental health consequences.

humans, evolution did not favor obesity, but rather, leanness.

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.

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 trial aimed to confirm the cardiovascular health and weight-reduction benefits of the low-fat diet. The average weight of participants at the beginning of the study was 169 pounds (76.8 kilograms). The starting average body mass index was 29.1, putting participants in the overweight category

The group that received dietary counseling succeeded. Daily calories dropped from 1788 to 1446 a day—a reduction of 342 calories per day for over seven years. Fat as a percentage of calories decreased from 38.8 percent to 29.8 percent, and carbohydrates increased from 44.5 percent to 52.7 percent. The women increased their daily physical activity by 14 percent.

Did these women perhaps replace some of their fat with muscle? Unfortunately, the average waist circumference increased approximately 0.39 inches (0.6 centimeters), and the average waist-to-hip ratio increased

these studies, of course, serve only to confirm what we already knew. Caloric reduction doesn’t cause lasting weight loss. Anybody who has ever tried it can tell you. Many people tell me, “I don’t understand. I eat less. I exercise more. But I can’t seem to lose any weight.” I understand perfectly—because this advice has been proven to fail. Do caloric-reduction diets work? No. The Women’s Health Initiative Dietary Modification Trial was the biggest, baddest, most kick-ass study of the Eat Less, Move More strategy that has ever been or ever will be done—and it was a resounding repudiation of that strategy.

THE CALORIES IN, Calories Out plan for weight loss assumes that we have conscious control over what we eat. But this belief ignores the extremely powerful effect of the body’s hormonal state.

There are two major adaptations to caloric reduction. The first change, as we have seen, is a dramatic reduction in total energy expenditure. The second key change is that the hormonal signals that stimulate hunger increase.

With increased hunger and decreased satiety, the desire to eat rises. Moreover, these hormonal changes occur almost immediately and persist almost indefinitely.

expected hormonal response to weight loss. Dr. Keys’s Minnesota Starvation Experiment first documented the effect of “semi-starvation neurosis.” People who lose weight dream about food. They obsess about food. All they can think about is food. Interest in all else diminishes. This behavior is not some strange affliction of the obese. In fact, it’s entirely hormonally driven and normal. The body, through hunger and satiety signaling, is compelling us to get more food.

Reduced metabolism and the increased hunger are not the cause of obesity—they are the result. Losing weight causes the reduced metabolism and increased hunger, not the other way around. We do not simply make a personal choice to eat more. One of the great pillars of the caloric-reduction theory of obesity—that we eat too much because we choose to—is simply not true.

Let me state it as plainly as I can: “Eat Less” does not work. That’s a fact. Accept it.

DR. PETER ATTIA is the cofounder of Nutrition Science Initiative (NuSi), an organization dedicated to improving the quality of science in nutrition and obesity research. A

CERTAINLY, EXERCISE HAS great health benefits.