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

by Jason Fung

Dr. Fung’s novel contribution is his insight that treatment in type 2 diabetes focuses on the symptom of the disease—an elevated blood glucose concentration—rather than its root cause, insulin resistance. And the initial treatment for insulin resistance is to limit carbohydrate intake. Understanding this simple biology explains why this disease may be reversible in some cases—and, conversely, why the modern treatment of type 2 diabetes, which does not limit carbohydrate intake, worsens the outcome.

the best hope for treating and preventing obesity, a disease of insulin resistance and excessive insulin production, must surely be the same low-carbohydrate, high-fat diet used for the management of the ultimate disease of insulin resistance, type 2 diabetes. And so this book was born.

•You have type 2 diabetes? Here, let me give you a pill. •You have high blood pressure? Here, let me give you a pill. •You have high cholesterol? Here, let me give you a pill. •You have kidney disease? Here, let me give you a pill. But all along, we needed to treat obesity. We were trying to treat the problems caused by obesity rather than obesity itself. In trying to understand the underlying cause of obesity, I eventually established the Intensive Dietary Management Clinic in Toronto, Canada.

HERE’S THE QUESTION that has always bothered me: Why are there doctors who are fat? Accepted as authorities in human physiology, doctors should be true experts on the causes and treatments of obesity. Most doctors are also very hardworking and self-disciplined. Since nobody wants to be fat, doctors in particular should have both the knowledge and the dedication to stay thin and healthy. So why are there fat doctors? The standard prescription for weight loss is “Eat Less, Move More.” It sounds perfectly reasonable. But why doesn’t it work? Perhaps people wanting to lose weight are not following this advice. The mind is willing, but the flesh is weak. Yet consider the self-discipline and dedication needed to complete an undergraduate degree, medical school, internship, residency and fellowship. It is hardly conceivable that overweight doctors simply lack the willpower to follow their own advice. This leaves the possibility that the conventional advice is simply wrong. And if it is, then our entire understanding of obesity is fundamentally flawed. Given the current epidemic of obesity, I suspect that such is the most likely scenario. So we need to start at the very beginning, with a thorough understanding of the disease that is human obesity.

We must start with the single most important question regarding obesity or any disease: “What causes it?” We spend no time considering this crucial question because we think we already know the answer. It seems so obvious: it’s a matter of Calories In versus Calories Out.

PROXIMATE VERSUS ULTIMATE CAUSE EXCESS CALORIES MAY certainly be the proximate cause of weight gain, but not its ultimate cause. What’s the difference between proximate and ultimate? The proximate cause is immediately responsible, whereas the ultimate cause is what started the chain of events.

Consider alcoholism. What causes alcoholism? The proximate cause is “drinking too much alcohol”—which is undeniably true, but not particularly useful. The question and the cause here are one and the same, since alcoholism means “drinking too much alcohol.” Treatment advice directed against the proximate cause—“Stop drinking so much alcohol”—is not useful. The crucial question, the one that we are really interested in, is: What is the ultimate cause of why alcoholism occurs. The ultimate cause includes •the addictive nature of alcohol, •any family history of alcoholism, •excessive stress in the home situation and/or •an addictive personality. There we have the real disease, and treatment must be directed against the ultimate, rather than the proximate cause. Understanding the ultimate cause leads to effective treatments such as (in this case) rehabilitation and social support networks.

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.

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. Without evidence or historical precedent, it was arbitrarily decided that excess calories caused weight gain, not specific foods. Fat, as the dietary villain, was now deemed fattening—a previously unknown concept. The Calories-In/Calories-Out model began to displace the prevailing “fattening carbohydrates” model. But not everybody bought in. One of the most famous dissidents was the prominent British nutritionist John Yudkin (1910–1995). Studying diet and heart disease, he found no relationship between dietary fat and heart disease. He believed that the main culprit of both obesity and heart disease was sugar.9, 10 His 1972 book, Pure, White and Deadly: How Sugar Is Killing Us, is eerily prescient (and should certainly win the award for Best Book Title Ever). Scientific debate raged back and forth about whether the culprit was dietary fat or sugar.

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.

Studying a sample of 540 Danish adult adoptees, Dr. Stunkard compared them to both their adoptive and biological parents. If environmental factors were most important, then adoptees should resemble their adoptive parents. If genetic factors were most important, the adoptees should resemble their biological parents. 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. Environmental cues such as dietary habits, fast food, junk food, candy intake, lack of exercise, number of cars, and lack of playgrounds and organized sports 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.

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

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.

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 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.

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-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 ...

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. Sugar will increase the blood glucose level and provoke an insulin response from the pancreas. Olive oil will not. When olive oil is absorbed by the small intestine and transported to the liver, there is no significant increase in blood glucose or insulin. The two different foods evoke vastly different metabolic and hormonal responses.

Reducing Calories In works only if Calories Out remains stable. What we find instead is that a sudden reduction of Calories In causes a similar reduction in Calories Out, and no weight is lost as the body balances its energy budget. Some historic experiments in calorie reduction have shown exactly this.

CALORIC REDUCTION: EXTREME EXPERIMENTS, UNEXPECTED RESULTS EXPERIMENTALLY, IT’S EASY to study caloric reduction. We take some people, give them less to eat, watch them lose weight and live happily ever after. Bam. Case closed. Call the Nobel committee: Eat Less, Move More is the cure for obesity, and caloric reduction truly is the best way to lose weight. Luckily for us, such studies have already been done.

Thirty-six young, healthy, normal men were selected with an average height of five foot ten inches (1.78 meters) and an average weight of 153 pounds (69.3 kilograms). For the first three months, subjects received a standard diet of 3200 calories per day. Over the next six months of semi-starvation, only 1570 calories were given to them. However, caloric intake was continually adjusted to reach a target total weight loss of 24 percent (compared to baseline), averaging 2.5 pounds (1.1 kilograms) per week. Some men eventually received less than 1000 calories per day. The foods given were high in carbohydrates, similar to those available in war-torn Europe at the time—potatoes, turnips, bread and macaroni. Meat and dairy products were rarely given. In addition, they walked 22 miles per week as exercise. Following this caloric-reduction phase, their calories were gradually increased over three months of rehabilitation. Expected caloric expenditure was 3009 calories per day.8 Even Dr. Keys himself was shocked by the difficulty of the experiment. The men experienced profound physical and psychological changes. Among the most consistent findings was the constant feeling of cold experienced by the participants. As one explained, “I’m cold. In July I walk downtown on a sunny day with a shirt and sweater to keep me warm. At night my well fed room mate, who isn’t in the experiment, sleeps on top of his sheets but I crawl under two blankets.”9 Resting metabolic rate dropped by 40 perce...

Let’s reflect on what was happening here. Prior to the study, the subjects ate and also burned approximately 3000 calories per day. Then, suddenly, their caloric intake was reduced to approximately 1500 per day. All body functions that require energy experienced an immediate, across-the-board 30 percent to 40 percent reduction, which wrought complete havoc.

Consider the following: •Calories are needed to heat the body. Fewer calories were available, so body heat was reduced. Result: constant feeling of cold. •Calories are needed for the heart to pump blood. Fewer calories were available, so the pump slowed down. Result: heart rate and stroke volume decreases. •Calories are needed to maintain blood pressure. Fewer calories were available, so the body turned the pressure down. Result: blood pressure decreased. •Calories are needed for brain function, as the brain is very metabolically active. Fewer calories were available, so cognition was reduced. Result: lethargy and inability to concentrate. •Calories are needed to move the body. Fewer calories were available, so movement was reduced. Resu...

The body reacts in this way—by reducing energy expenditure—because the body is smart and doesn’t want to die. What would happen if the body continued to expend 3000 calories daily while taking in only 1500? Soon fat stores would be burned, then protein stores would be burned, and then you would die. Nice. The smart course of action for the body is to immediately reduce caloric expenditure to 1500 calories per day to restore balance. Caloric expenditure may even be ...

In other words, the body shuts down. In order to preserve itself, it implements across-the-board reductions in energy output. The crucial point to remember is that doing so ensures survival of the individual in a time of extreme stress. Yeah, you might feel lousy, but you’ll live to tell the tale. Reducing output is the smart thing for the body to do. Bur...

Calories In and Calories Out are highly dependent variables. With reflection, it should immediately be obvious that caloric expenditure must decrease. If we reduce daily calorie intake by 500 calories, we assume that 1 pound (0.45 kilograms) of fat per week is lost. Does that mean that in 200 weeks, we would lose 200 pounds (91 kilograms) and weigh zero pounds? Of course not. The body must, at some point, reduce its caloric expenditure to meet the lower caloric intake. It just so happens that this adaptation occurs almost immediately and persists long term. The men in the Minnesota Starvation Experiment should have lost 78 pounds (35.3 kilograms), but the actual weight ...

What happened to their weight after the semi-starvation period? During the semi-starvation phase, body fat dropped much quicker than overall body weight as fat stores are preferentially used to power the body. Once the participants started the recovery period, they regained the weight rather quickly, in about twelve weeks. But it didn’t stop there. Body w...

The body quickly responds to caloric reduction by reducing metabolism (total energy expenditure), but how long does this adaptation persist? Given enough time, does the body increase its energy expenditure back to its previous higher level if caloric reduction is maintained? The short answer is no.11 In a 2008 study, participants initially lost 10 percent of body weight, and their total energy expenditure decreased as expected. But how long did this situation last? It remained reduced over the course of the entire study—a full year. Even after one year at the new, lower body weight, their total energy expenditure was still reduced by an average of almost 500 calories per day. In response to caloric reduction, metabolism decreases almost immediately, and that decrease persists more or less indefinitely. The applicability of these findings to caloric-reduction diets is obvious. Assume that prior to dieting, a woman eats and burns 2000 calories per day. Following doctor’s orders, she adopts a calorie-restricted, portion-controlled, low-fat diet, reducing her intake by 500 calories per day. Quickly, her total energy expenditure also drops by 500 calories per day, if not a little mor...

The results were telling. The “Eat Less, Move More” group started out terrifically, averaging more than 4 pounds (1.8 kilograms) of weight loss over the first year. By the second year, the weight started to be regained, and by the end of the study, there was no significant difference between the two groups. 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 from 0.82 to 0.83 inches (2.1 centimeters), which indicates these women were actually fatter than before. Weight loss over 7.5 years of the Eat Less, Move More strategy was not even one single kilogram (2.2 pounds). This study was only the latest in an unbroken string of failed experiments. Caloric reduction as the primary means of weight loss has disappointed repeatedly. Reviews of the literature by the U.S. Department of Agriculture13 highlight this failure. All 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.

What is happening when we try to reduce calories and fail to lose weight? Part of the problem is the reduced metabolism that accompanies weight loss. But that’s only the beginning.

HUNGER GAMES 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. The body is pleading with us to eat in order for it to regain the lost weight.

This effect was demonstrated in 2011, in an elegant study of hormonal adaptation to weight loss.14 Subjects were given a diet of 500 calories per day, which produced an average weight loss of 29.7 pounds (13.5 kilograms). Next, they were prescribed a low-glycemic-index, low-fat diet for weight maintenance and were encouraged to exercise thirty minutes per day. Despite their best intentions, almost half of the weight was regained. Various hormonal levels, including ghrelin—a hormone that, essentially, makes us hungry—were analyzed. Weight loss significantly increased ghrelin levels in the study’s subjects, even after more than one year, compared to the subjects’ usual baseline. What does that mean? It means that the subjects felt hungrier and continued to feel so, right up to end of the study. The study also measured several satiety hormones, including peptide YY, amylin and cholecystokinin, all of which are released in response to proteins and fats in our diet and serve to make us feel full. This response, in turn, produces the desired effect of keeping us from overeating. More than a year after initial weight loss, the levels of all three satiety hormones were significantly lower than before.

What does that mean? It means that the subjects felt less full. With increased hunger and decreased satiety, the desire to eat rises. Moreover, these hormonal changes occur almost immediately and persist almost indefinitely. People on a diet tend to feel hungrier, and that effect isn’t some kind of psychological voodoo, nor is it a 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 n...

Losing weight triggers two important responses. First, total energy expenditure is immediately and indefinitely reduced in order to conserve the available energy. Second, hormonal hunger signaling is immediately and indefinitely amplified in an effort to acquire more food. Weight loss results in increased hunger and decreased metabolism. Th...

Functional magnetic resonance imaging studies show that areas of the brain controlling emotion and cognition light up in response to food stimuli. Areas of the prefrontal cortex involved with restraint show decreased activity. In other words, it is harder for people who have lost weight to resist food.15 This has nothing whatsoever to do with a lack of willpower or any kind of moral failure. It’s a normal hormonal fact of life. We feel hungry, cold, tired and depressed. These are all real, measurable phy...

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. We do not eat too much because we choose to, or because food is too delici...

THE VICIOUS CYCLE OF UNDER-EATING AND SO WE have the vicious cycle of under-eating. We start by eating less and lose some weight. As a result, our metabolism slows and hunger increases. We start to regain weight. We double our efforts by eating even less. A bit more weight comes off, but again, total energy expenditure decreases and hunger increases. We start regaining weight. So we redouble our efforts by eating even less. This cycle continues until it is intolerable. We are cold, tired, hungry and obsessing about calories. Worst of all, the weight always comes back on. At some point, we go back to our old way of eating. Since metabolism has slowed so much, even resuming the old way of eating causes quick weight gain, up to and even a little past the original point. We are doing exactly what our hormones are influencing us to do. But friends, family and medical professionals silently blame the victim, thinking that it is “our fault.” And we ourselves feel that we are a failure. Sound familiar? All dieters share this same sad story of weight loss and regain. It’s a virt...

The low-fat, low-calorie diet has already been proven to fail. This is the cruel hoax. Eating less does not result in lasting weight loss. It. Just. Does. Not. Work.

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

But here’s the dismal truth: whether physical activity increases or decreases, it has virtually no relationship to the prevalence of obesity. Increasing exercise did not reduce obesity. It was irrelevant. Certain states exercised more. Other states exercised less. Obesity increased by the same amount regardless. Is exercise important in reducing childhood obesity? The short answer is no. A 2013 paper5 compared the physical activity (measured using accelerometry) of children aged three to five years to their weight. The authors concluded there is no association between activity and obesity.

Total energy expenditure = Basal metabolic rate + Thermogenic effect of food + Nonexercise activity thermogenesis + Excess post-exercise oxygen consumption + Exercise. The key point here is that total energy expenditure is not the same as exercise. The overwhelming majority of total energy expenditure is not exercise but the basal metabolic rate: metabolic housekeeping tasks such as breathing, maintaining body temperature, keeping the heart pumping, maintaining the vital organs, brain function, liver function, kidney function, etc.

Let’s take an example. Basal metabolic rate for a lightly active average male is roughly 2500 calories per day. Walking at a moderate pace (2 miles per hour) for forty-five minutes every day, would burn roughly 104 calories. In other words, that will not even consume 5 percent of the total energy expenditure.

The vast majority (95 percent) of calories are used for basal metabolism. Basal metabolic rate depends on many factors, including •genetics, •gender (basal metabolic rate is generally higher in men), •age (basal metabolic rate generally drops with age), •weight (basal metabolic rate generally increases with muscle mass), •height (basal metabolic rate generally increases with height), •diet (overfeeding or underfeeding), •body temperature, •external temperature (heating or cooling the body) and •organ function. Nonexercise activity thermogenesis is the energy used in activity other than sleeping, eating or exercise; fo...

Certain foods, such as dietary fat, are easily absorbed and take very little energy to metabolize. Proteins are harde...

Because of the complexity of measuring basal metabolic rate, non-exercise activity thermogenesis, thermogenic effect of food and excess post-exercise oxygen consumption, we make a simple but erroneous assumption that these factors are all constant over time. This assumption leads to the crucially flawed conclusion that exercise is the only variable in total energy expenditure. Thus, increasing Calories Out becomes equated with Exercise More.

One major problem is that the basal metabolic rate does not stay stable. Decreased caloric intake can decrease basal metabolic rate by up to 40 percent. We shall see that increased caloric intake can increase it by 50 percent.