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

by Jason Fung

EXERCISE AND WEIGHT LOSS CONVENTIONALLY, DIET AND exercise have been prescribed as treatments for obesity as if they are equally important. But diet and exercise are not fifty-fifty partners like macaroni and cheese. Diet is Batman and exercise is Robin. Diet does 95 percent of the work and deserves all the attention; so, logically, it would be sensible to focus on diet. Exercise is still healthy and important—just not equally important. It has many benefits, but weight loss is not among...

Consider this baseball analogy. Bunting is an important technique, but accounts for only perhaps 5 percent of the game. The other 95 percent revolves around hitting, pitching and fielding. So it would be ridiculous to spend 50 percent of our time practicing the bunt. Or, what if we were facing a test that is 95 percent math and 5 percent spelling? Would we spend 50 percent of our time studying spelling? The fact that exercise always produces less weight loss than expected has been well documented in medic...

COMPENSATION: THE HIDDEN CULPRIT WHY DOES ACTUAL weight loss fall so far below projected? The culprit is a phenomenon known as “compensation”—and there are two major mechanisms. First, caloric intake increases in response to exercise—we just eat more following a vigorous workout. (They don’t call it “working up an appetite” for nothing.) A prospective cohort study of 538 students from the Harvard School of Public Health15 found that “although physical activity is thought of as an energy deficit activity, our estimates do not support this hypothesis.” For every extra hour of exercise, the kids ate an extra 292 calories. Caloric intake and expenditure are intimately related: increasing one will cause an increase in the other. This is the biological principle of homeostasis. The body tries to maintain a stable state. Reducing Calories In reduces Calories Out. Increasing Calories Out increases Calories In.

In addition, the benefit of exercise has a natural upper limit.

You cannot make up for dietary indiscretions by increasing exercise. You can’t outrun a poor diet.

Furthermore, more exercise is not always better. Exercise represents a stress on the body. Small amounts are beneficial, but ...

If we want to reduce obesity, we need to focus on what makes us obese. If we spend all our money, research, time and mental energy focused on exercise, we will have no resources left with which to actually fight obesity. We are writing a final examination called Obesity 101. Diet accounts for 95 percent of the grade and exercise for only 5 percent. Yet we spend 50 percent of our time and energy studying exercise. It is no wonder that our current grade is F—for Fat.

THE OVERFEEDING PARADOX SAM FELTHAM, A qualified master personal trainer, has worked in the U.K. health-and-fitness industry for more than a decade. Not accepting the caloric-reduction theory, he set out to prove it false, following the grand scientific tradition of self-experimentation. In a modern twist to the classic overeating experiments, Feltham decided that he would eat 5794 calories per day and document his weight gain. But the diet he chose was not a random 5794 calories. He followed a low-carbohydrate, high-fat diet of natural foods for twenty-one days.

Feltham believed, based on clinical experience, that refined carbohydrates, not total calories, caused weight gain.

The macronutrient breakdown of his diet was 10 percent carbohydrate, 53 percent fat and 37 percent protein. Standard calorie calculations predicted a weight gain of about 16 pounds (7.3 kilograms). Actual weight gain, however, was only about 2.8 pounds (1.3 kilograms). Even more interesting, he dropped more than 1 inch ...

Perhaps Feltham was simply one of those genetic-lottery people who are able to eat anything and not gain weight. So, in the next experiment, Feltham abandoned the low-carb, high-fat diet. Instead, for twenty-one days, he ate 5793 calories per day of a standard American diet with lots of highly processed “fake” foods. The macronutrient breakdown of his new diet was 64 percent carbs, 22 percent fat and 14 percent protein—remarkably similar to the U.S. Dietary Guidelines. This time, the weight gain almost exactly mirrors that predicted by the calorie formula—15.6 pounds...

In the same person and with an almost identical caloric intake, the two different diets produced strikingly different results. Clearly, something more than calories is at work here since diet composition apparently plays a large role. The overfeeding paradox is that excess calories alone are not sufficient for weight gain—in contradiction to the caloric-reduction theory. OVERFEEDING EXPERIMENTS: UNEXPECTED RESULTS THE HYPOTHESIS THAT eating too much causes obesity is easily testable. You simply take a group of volunteers, deliberately overfeed them and watch what happens. If the hypothesis is true, the result should be obesity. Luckily for us, such experiments have already been done. Dr. Ethan Sims performed the most famous of these studies in the late 1960s.1, 2 He tried to force mice to gain weight. Despite ample food, the mice ate only enough to be full. After that, no inducement could get them to eat. They would not become obese. Force-feeding the mice caused an increase in their metabolism, so once again, no weight was gained. Sims then asked a devastatingly brilliant question: Could he make humans deliberately gain weight? This question, so deceptively simple, had never be...

Total energy expenditure, comprising mostly basal metabolic rate, is not constant, but varies considerably in response to caloric intake. After the experiment ended, body weight quickly and effortlessly returned to normal. Most of the participants did not retain any of the weight they gained. Overeating did not, in fact, lead to ...

In another study, Dr. Sims compared two groups of patients. He overfed a group of thin patients until they became obese. The second group was made up of very obese patients who dieted until they were only obese—but the same weight as the first group.4 This resulted in two groups of patients who were equally heavy, but one group had originally been thin and one group originally very obese. What was the difference in total energy expenditure between the two groups? Those originally very obese subjects were burning only half as many calories as the originally thin subjects. The bodies of the originally very obese subjects were trying to return to their original hi...

Let’s return to our power plant analogy. Suppose that we receive 2000 tons of coal daily and burn 2000 tons. Now all of a sudden, we start receiving 4000 tons daily. What should we do? Say we continue to burn 2000 tons daily. The coal will pile up until all available room is used. Our boss yells, “Why are you storing your dirty coal in my office? Your ass is FIRED!” Instead, though, we’d do the smart thing: increase coal burning to 4000 tons daily. More power is generated and n...

Our body also responds in a similarly smart manner. Increased caloric intake is met with increased caloric expenditure. With the increase in total energy expenditure, we have more energy, more body heat and we feel great. After the period of forced overeating, the increased metabolism quickly sheds the excess pounds of fat. The increase in nonexercise ...

The theory of obesity that’s been dominant for the last half century—that excess calories inevitably lead to obesity—the theory that’s assumed to be unassailably true, was simply not true. None of it was true. And if excess calories don’t cause weight gain, then reducing calories won’t cause weight loss. THE BODY SET WEIGHT YOU CAN TEMPORARILY force your body weight higher than your body wants it to be by consuming excess calories. Over time, the resulting higher metabolism will reduce your weight back to normal. Similarly, you can temporarily force your body weight lower than your body wants it to be by reducing calories. Over time, the resulting lowered metabolism will raise your weight back to normal. Since losing weight reduces total energy expenditure, many obese people assume that they have a slow metabolism, but the opposite has proved to be true.8 Lean subjects had a mean total energy expenditure of 2404 calories, while the obese had a mean total energy expenditure of 3244 calories, despite spending less time exercising. The obese body was not trying to gain weight. It was trying to lose it by burning off the excess energy. So then, why are the obese . . . obese? The fundamental biological principle at work here is homeostasis. There appears to be a “set point” for body weight and fatness, as first proposed in 1984 by Keesey and Corbett.9 Homeostatic mechanisms defend this body set weight against changes, both up and down. If weight drops below body set weight, com...

Eating more is not the cause of weight gain but instead the consequence. Eating more does not make us fat. Getting fat makes us eat more. Overeating was not a personal choice. It is a hormonally driven behavior—a natural consequence of increased hunger hormones. The question, then, is what makes us fat in the first place. In other words, why is the body set weight so high?

The body set weight also works in the reverse. If we overeat, we will briefly gain weight—say to 220 pounds (approximately 100 kilograms). If the body set weight stays at 200 pounds, then the body activates mechanisms to lose weight. Appetite decreases. Metabolism incre...

Our body is not a simple scale balancing Calories In and Calories Out. Rather, our body is a thermostat. The set point for weight—the body set weight—is vigorously...

No wonder it is so hard to keep the weight off! Diets work well at the start, but as we lose weight, our metabolism slows. Compensatory mechanisms start almost immediately and persist almost indefinitely. We must then reduce our caloric intake further and further simply to maintain the weight loss. If we don’t, our weight plateaus and then starts to creep back up—just as every dieter already knows.

Consider our thermostat analogy. Normal room temperature is 70°F (21°C). If the house thermostat were set instead to 32°F (0°C), we’d find it too cold. Using the First Law of Thermodynamics, we decide that the temperature of the house depends upon Heat In versus Heat Out. As fundamental law of physics, it is inviolable. Since we need more Heat In, we buy a portable heater and plug it in. But Heat In is only the proximate cause of the high temperature. The temperature at first goes up in response to the heater. But then, the thermostat, sensing the higher temperature, turns on the air conditioner. The air conditioner and the heater constantly fight against each other until the heater finally breaks. The temperature returns to 32°F.

The mistake here is to focus on the proximate and not the ultimate cause. The ultimate cause of the cold was the low setting of the thermostat. Our failure was that we did not recognize that the house contained a homeostatic mechanism (the thermostat) to return the temperature to 32°F.

The smarter solution would have been for us to identify the thermostat’s control and simply set it to a more comfortable 70°F and so avoid the fight b...

The reason diets are so hard and often unsuccessful is that we are constantly fighting our own body. As we lose weight, our body tries to bring it back up. The smarter solution is to identify the body’s homeostatic mec...

Since obesity results from a high body set weight, the treatment for obesity is to lower it. But how do we lower our thermostat? The search for answe...

LEPTIN: THE SEARCH FOR A HORMONAL REGULATOR DR. ALFRED FROHLICH from the University of Vienna first began to unravel the neuro-hormonal basis of obesity in 1890; he described a young boy with the sudden onset of obesity who was eventually diagnosed with a lesion in the hypothalamus area of the brain. It would be later...

This established the hypothalamic region as a key regulator of energy balance, and was also a vital clue that obesity is a hormonal imbalance. Neurons in these hypothalamic areas were somehow respons...

Brain tumors, traumatic injuries and radiation in or to this critical area cause massive obesity that is often resistant to treatment,...

The hypothalamus integrates incoming signals regarding energy intake and expenditure. However, the control mechanism was still unknown. Romaine Hervey proposed in 1959 that the fat cells produced a circulating “satiety factor.”12 As fat stores increased, the level of this factor would also increase. This factor circulated through the blood to the hypothalamus, causing the brain to send out signals to reduce appetite or increase metabolism, thereby reducing fat stores ...

Discovered in 1994, this factor was leptin, a protein produced by the fat cells. The name leptin was derived from “lepto,” the Greek word for thin. The mechanism was very similar to that proposed decades earlier by Hervey. Higher levels of fat tissue produce higher levels of leptin. T...

Rare human cases of leptin deficiency were soon found. Treatment with exogenous leptin (that is, leptin manufactured outside the body) produced dramatic reversals of the associated massive obesity. The discovery of leptin provoked tremendous excitement within the pharmaceutical and scientific communities. There was a sense that the obesity gene had, at long last, been found. However, while it played a crucial role in these rare cases of massive obesity, it was still to be determined whether it played any role in common human obesity. Exogenous leptin was administered to patients in escalating do...

The vast majority of obese people are not deficient in leptin. Their leptin levels are high, not low. But these high levels did not produce the desired effect of lowering body f...

Leptin is one of the primary hormones involved in weight regulation in the normal state. However, in obesity, it is a secondary hormone because it fails the causality test. Giving leptin doesn’t make people thin. Human obesi...

This leaves us with much the same question that we began with. What causes leptin resist...

Health-care professionals could not abandon the calorie model, so what was left to do? Blame the patient, of course! Doctors and dieticians berated, ridiculed, belittled and reprimanded. They were drawn irresistibly to caloric reduction because it transformed obesity from their failure to understand it into our lack of willpower and/or laziness. But the truth cannot be suppressed indefinitely.

The caloric-reduction model was just wrong. It didn’t work. Excess calories did not cause obesity, so reduced calories could not cure it. Lack of exercise did not cause obesity, so increased exercise could not cure it.

The false gods of the caloric religion had been exposed as charlatans. From those ashes, we can now begin to build a newer, more robust theory of obesity. And with greater understanding of weight gain, we have a new hope...

What causes weight gain? Contending theories abound: •Calories •Sugar •Refined carbohydrates •Wheat •All carbohydrates •Dietary fat •Red meat •All meat •Dairy products •Snacking •Food reward •Food addiction •Sleep deprivation •Stress •Low fiber intake •Genetics •Poverty •Wealth •Gut microbiome •Childhood obesity The various theories fight among themselves, as if they are all mutually exclusive and there is only one true cause of obesity. For example, recent trials that compare a low-calorie to a low-carbohydrate diet assume that if one is correct, the other is not. Most obesity research is conducted in this manner. This approach is wrong, since these theories all contain some element of truth. Let’s look at an analogy. What causes heart attacks? Consider this partial list of contributing factors: •Family history •Age •Sex •Diabetes •Hypertension •Hypercholesterolemia •Smoking •Stress •Lack of physical activity These factors, some modifiable and some not, all contribute to heart-attack risk. Smoking is a risk factor, but that doesn’t mean that diabetes is not. All are correct since they all contribute to some degree. Nonetheless, all are also incorrect, because they are not the s...

Obesity is a hormonal dysregulation of fat mass. The body maintains a body set weight, much like a thermostat in a house. When the body set weight is set too high, obesity results. If our current weight is below our body set weight, our body, by stimulating hunger and/or decreasing metabolism, will try to gain weight to reach that body set weight. Thus, excessive eating and slowed metabolism are the result rather than the cause of obesity. But what caused our body set weight to be so high in the first place? This is, in essence, the same question as “What causes obesity?” To find the answer, we need to know how the body set weight is regulated. How do we raise or lower our “fat thermostat”?

THE HORMONAL THEORY OF OBESITY OBESITY IS NOT caused by an excess of calories, but instead by a body set weight that is too high because of a hormonal imbalance in the body.

Hormones are chemical messengers that regulate many body systems and processes such as appetite, fat storage and blood sugar levels. But which hormones are responsible for obesity? Leptin, a key regulator of body fat, did not turn out to be the main hormone involved in setting the body weight. Ghrelin (the hormone that regulates hunger) and hormones such as peptide YY and cholecystokinin that regulate satiety (feeling full or satisfied), all pl...

A hormone suspected of causing weight gain must pass the causality test. If we inject this hormone into people, they must gain weight. These hunger and satiety hormones do not pass the causality test, bu...

In chapter 3, we saw the caloric-reduction view of obesity relies on five assumptions that have been proved to be wrong. This hormonal theory of obesity avoids making these false assumptions. Consider the following: Assumption 1: Calories In and Calories Out are independent of each other. The hormonal theory explains why Calories In and Calories Out are tightly synchronized with each other. Assumption 2: Basal metabolic rate is stable. The hormonal theory explains how hormonal signals adjust basal metabolic rate to either gain or lose weight. Assumption 3: We exert conscious control over Calories In. The hormonal theory explains that hunger and satiety hormones play a key role in determining whether we eat. Assumption 4: Fat stores are essentially unregulated. The hormonal theory explains that fat stores, like all body systems, are tightly regulated and respond to changes in food intake and activ...

THE MECHANICS OF DIGESTION BEFORE DISCUSSING INSULIN, we must understand hormones in general. Hormones are molecules that deliver messages to a target cell. For example, thyroid hormone delivers a message to cells in the thyroid gland to increase its activity. Insulin delivers the mes...

To deliver this message, hormones must attach to the target cell by binding to receptors on the cell surface, much like a lock and key. Insulin acts on the insulin receptor to bring glucose into the cell. Insulin is the key and fits snugly into the lock (the receptor). The doo...

When we eat, foods are broken down in the stomach and small intestine. Proteins are broken into amino acids. Fats are broken into fatty acids. Carbohydrates, which are chains of sugars, are broken into smaller sugars. Dietary fiber is not broken down; it moves through us wit...

Certain foods, particularly refined carbohydrates, raise blood sugar more than other foods. The rise in blood sugar stimulates insulin release. Protein raises insulin levels as well, although its effect on blood sugars is minimal. Dietary fats, on the other...

Insulin is then broken down and rapidly cleared from the blood with a half-life of o...

Insulin is a key regulator of energy metabolism, and it is one of the fundamental hormones that promote fat accumulation and storage. Insulin facilitates the uptake of glucose into cells for energy. Without sufficient insulin, glucose builds up in the bloodstream. Type 1 diabetes results from the autoimmune destruction of the insulin-producing cells in the pancreas, which results in extremely low levels of insulin. The discovery of insulin (for which Frederick Banting ...