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

by Jason Fung

“If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.” In

Even if we compare relatively recent activity rates to those of the 1980s, before the obesity epidemic came into full swing, rates have not decreased appreciably.7 In a Northern European population, physical-activity energy expenditure was calculated from the 1980s to the mid 2000s. The surprising finding was that if anything, physical activity has actually increased since the 1980s. But this study’s authors went one step further. They calculated the predicted energy expenditure for a wild mammal, which is predominantly determined by body mass and ambient temperature. Compared to its wild-mammal cousins such as the seemingly vigorous

cougar, fox and caribou, Homo obesus 2015 is not less physically active. Exercise has not decreased since hunter-gatherer times, or even since the 1980s, while obesity has galloped ahead full steam. It is highly improbable that decreased exercise played any role in causing obesity in the first place. If lack of exercise was not the cause of obesity epidemic, exercise is probably not going to reverse it.

Nonexercise activity thermogenesis is the energy used in activity other than sleeping, eating or exercise; for instance, in walking, gardening, cooking, cleaning and shopping. The thermogenic effect of food is the energy used in digestion and absorption of food energy. Certain foods, such as dietary fat, are easily absorbed and take very little energy to metabolize. Proteins are harder to process and use more energy. Thermogenic effect of food varies according to meal size, meal frequency and macronutrient composition. Excess post-exercise oxygen consumption (also called after-burn) is the energy used in cellular repair, replenishment of fuel stores and other recovery activities after exercise.

You can’t outrun a poor diet.

This situation, of course, partially explains the difficulty in losing accumulated fat. Before getting money from the bank, you spend what’s in your wallet first. But you don’t like having an empty wallet. In the same manner, before getting energy from the Fat Bank, you spend the energy in the Glycogen Wallet. But you also don’t like an empty Glycogen Wallet. So you keep the Glycogen Wallet filled, which prevents you from accessing the Fat Bank. In other words, before you can even begin to burn fat, you start feeling hungry and anxious because your glycogen is becoming depleted. If you continually refill your glycogen stores, you never need to use your fat stores for energy.

THE “INSULIN CAUSES obesity” hypothesis is easily tested. We can prove a causal relationship by experimentally giving insulin to a group of people and then measuring their weight gain. Therefore, for our experiment, here’s our fundamental question: If you take insulin, will you get fat? The short answer is an emphatic “Yes!” Patients who use insulin regularly and physicians who prescribe it already know the awful truth:4 the more insulin you give, the more obese you get. Insulin causes obesity. Numerous studies, conducted mostly on diabetic patients, have already demonstrated this fact. Insulin causes weight gain.

Type 1 diabetes is an autoimmune disease that destroys the insulin-producing beta cells of the pancreas. Insulin falls to extremely low levels. Blood sugar increases, but the hallmark of this condition is severe weight loss. Type 1 diabetes has been described since ancient times. Aretaeus of Cappadocia, a renowned ancient Greek physician, wrote the classic description: “Diabetes is . . . a melting down of flesh and limbs into urine.” No matter how many calories the patient ingests, he or she cannot gain any weight. Until the discovery of insulin, this disease was almost universally fatal. Insulin levels go waaayyy down. Patients lose a lot of weight.

Diabulimia is the deliberate under-dosing of insulin for the purpose of immediate and substantial weight loss. It is extremely dangerous and certainly not advisable. However, the practice persists because it is an extremely effective form of weight loss. Insulin levels go down. Weight is lost.

As the insightful Gary Taubes wrote in his book Why We Get Fat: And What to Do about It, “We do not get fat because we overeat. We overeat because we get fat.” And why do we get fat? We get fat because our body set weight thermostat is set too high. Why? Because our insulin levels are too high.

A critical physiological variable such as body fatness is not left up to the vagaries of daily caloric intake and exercise. Instead, hormones precisely and tightly regulate body fat. We don’t consciously control our body weight any more than we control our heart rates, our basal metabolic rates, our body temperatures or our breathing. These are all automatically regulated, and so is our weight. Hormones tell us we are hungry (ghrelin). Hormones tell us we are full (peptide YY, cholecystokinin). Hormones increase energy expenditure (adrenalin). Hormones shut down energy expenditure (thyroid hormone). Obesity is a hormonal dysregulation of fat accumulation. Calories are nothing more than the proximate cause of obesity. Obesity is a hormonal, not a caloric imbalance.

Cortisol, part of a class of steroid hormones called glucocorticoids (glucose + cortex + steroid), is produced in the adrenal cortex. In Paleolithic times, the stress that led to a release of cortisol was often physical: for instance, being chased by a predator. Cortisol is essential in preparing our bodies for action—to fight or flee. Once released, cortisol substantially enhances glucose availability,1 which provides energy for muscles—very necessary in helping us to run and avoid being eaten. All available energy is directed toward surviving the stressful event. Growth, digestion and other long-term metabolic activities are temporarily restricted. Proteins are broken down and converted to glucose (gluconeogenesis).

Insulin is a storage hormone. Under high insulin levels (mealtimes), the body stores energy in the form of glycogen and fat. Cortisol, however, prepares the body for action, moving energy out of stores and into readily available forms, such as glucose. That cortisol and insulin would have similar weight-gain effects seems remarkable—but they do. With short-term physical stress, insulin and cortisol play opposite roles. Something quite different happens, though, when we’re under longterm psychological stress.

Cortisol raises blood sugar, while insulin lowers it. Insulin resistance (discussed in depth in chapter 10) is crucial to the development of obesity. Insulin resistance leads directly to higher insulin levels, and increased insulin levels are a major driver of obesity. Multiple studies confirm that increasing cortisol increases insulin resistance.9, 10, 11 If increasing cortisol raises insulin, then reducing cortisol should lower it.

Stress contains neither calories nor carbohydrates, but can still lead to obesity. Long-term stress leads to long-term elevated cortisol levels, which leads to extra pounds.

Somehow, despite being full, we still have room for highly refined carbohydrates like cake and pie—but not proteins or fats. Highly refined and processed foods somehow do not trigger the release of satiety hormones, and we go ahead and eat that cake.

All are highly refined carbohydrates. There is evidence that these foods activate the reward

systems in our brains, which gives us “comfort.” Refined carbohydrates are easy to become addicted to and overeat precisely because there are no natural satiety hormones for refined carbs. The reason, of course, is that refined carbohydrates are not natural foods but are instead highly processed.

A 1993 study measured this effect.8 Patients were started on intensive insulin treatment. In six months, they went from no insulin to 100 units a day on average. Their blood sugars were very, very well controlled. But the more insulin they took, the more insulin resistance they got—a direct causal relationship, as inseparable as a shadow is from a body. Even as their sugars got better, their diabetes was getting worse! These patients also gained an average of approximately 19 pounds (8.7 kilograms), despite reducing their calorie intake by 300 calories per day. It didn’t matter. Not only does insulin cause insulin resistance, it also causes weight gain.

We know that the hypothalamic area of the brain controls the body set weight and that insulin plays a key role in resetting the body set weight up or down.

In the case of insulin resistance, it comes down to both meal composition and meal timing—the two critical components of insulin resistance. The types of food eaten influence the insulin levels.

Let’s assume breakfast is taken at 8 a.m. and dinner at 6 p.m. That means that they have balanced ten hours of eating with fourteen hours of fasting. The periods of increased insulin (feeding) are balanced by periods of decreased insulin (fasting). Eating large amounts of refined carbohydrates like sugar and white bread makes for higher insulin peaks. So why was obesity slow to progress? The decisive difference is that there was a daily period of low insulin levels. Insulin resistance requires persistently high levels. The nightly fasting caused periods of very low insulin, so resistance could not develop. One of the key factors in obesity’s development was removed.

Many obesity specialists and physicians suggest eating even more frequently, every 2.5 hours.

By 2003, most people were eating five to six times a day. That is, three meals a day plus two to three snacks in between. The average time between meals has dropped 30 percent, from 271 minutes to 208 minutes. The balance between the fed state (insulin dominant) and the fasted state (insulin deficient) has been completely destroyed. (See Figure 10.2.) We now spend most of our time in the fed state. Is it any great mystery that we’re gaining weight?

Following a low-fat diet led to the inadvertent increase in refined-carbohydrate consumption, which stimulates high levels of insulin, which contributes to weight gain.

But in the development of obesity, the increase in meals is almost twice as important as the change in diet.11 We obsess about what we should eat. We eat foods that practically didn’t exist ten years ago. Quinoa. Chia seeds. Acai berries. All in the hopes of making us slim. But we spare not even a single thought as to when we should be eating.

Several myths are often perpetuated to convince people that snacking is beneficial. The first myth is that eating frequently will increase your metabolic rate. Your metabolic rate does increase slightly after meals to digest your food—the thermogenic effect of food. However, the overall difference is extremely small.12 Eating six small meals per day causes the metabolic rate to go up six times a day, but only a little. Eating three la...

The third myth is that eating frequently keeps blood glucose from becoming too low. But unless you have diabetes, your blood sugars are stable whether you eat six times a day or six times a month. People have fasted for prolonged periods without low blood sugar, the world record being 382 days.15 The human body has evolved mechanisms to deal with prolonged periods without food. The body instead burns fat for energy, and blood sugar levels remain in the normal range, even during prolonged fasting, due to gluconeogenesis.

In order to accommodate all those eating opportunities, societal norms have also changed. Previously, all eating was done at mealtimes at a table. Now, it is acceptable to eat anywhere. We can eat in the car. We can eat in the movie theatre. We can eat in front of the TV. We can eat in front of the computer. We can eat while walking. We can eat while talking. We can eat in a box. We can eat with a fox. We can eat in a house. We can eat with a mouse. You get the picture.

Snacks, which tend to be high in refined carbohydrates, also tend to cause high levels of insulin. Under these conditions, we should expect the development of insulin resistance.

Heart Association decided that it would be a good idea to start accepting cash to put its Heart Check symbol on foods of otherwise dubious nutritional quality. The Center for Science in the Public Interest1 estimates that in 2002, the AHA received over $2 million from this program alone.

In 2009, nutritional standouts such as Cocoa Puffs and Frosted Mini Wheats were still on the Heart Check list. The 2013 Dallas Heart Walk organized by the AHA featured Frito-Lay as a prominent sponsor. The Heart and Stroke Foundation in Canada was no better. As noted on Dr. Yoni Freedhoff’s blog,2 a bottle of grape juice proudly bearing the Health Check contained ten teaspoons of sugar. The fact that these foods were pure sugar seemed not to bother anybody.

In addition, impartiality—or the lack thereof—can be a serious issue when it comes to publishing medical and health information. The financial-disclosures section of some papers published in journals and on the web can run for more than half a page. Funding sources have enormous influence on study results.3

In a 2007 study that looked specifically at soft drinks, Dr. David Ludwig from Harvard University found that accepting funds from companies whose products are reviewed increased the likelihood of a favorable result by approximately 700 percent! This finding is echoed in the work of Marion Nestle, professor of nutrition and food studies at New York University. In 2001, she concluded that it is “difficult to find studies that did not come to conclusions favoring the sponsor’s commercial interest.”4

But the obesity epidemic couldn’t very well be ignored, and a culprit had to be found. “Calories” was the perfect scapegoat. Eat fewer calories, they said. But eat more of everything else. There is no company that sells

“Calories,” nor is there a brand called “Calories.” There is no food called “Calories.” Nameless and faceless, calories were the ideal stooge. “Calories” could now take all the blame. They say candy doesn’t make you fat. Calories make you fat. They say that 100 calories of cola is just as likely as 100 calories of broccoli to make you fat. They say that a calorie is a calorie. Don’t you know? But show me a single person that grew fat by eating too much steamed broccoli. I know it. You know it.

Why would anybody give such completely asinine advice? Because nobody makes any money when you eat less. If you take more supplements, the supplement companies make money. If you drink more milk, the dairy farmers make money. If you eat more breakfast, the breakfast-food companies make money. If you eat more snacks, the snack companies make money. The list goes on and on. One of the worst myths is that eating more frequently causes weight loss. Eat snacks to lose weight? It sounds pretty stupid. And it is.

enough to offset the extra calories of the snack itself. This finding held true for both fatty and sugary snacks. Increasing meal frequency does not result in weight loss.6

Diet quality also suffers substantially because snacks tend to be very highly processed. This fact mainly benefits Big Food, since selling processed instead of real foods yields a much larger profit. The need for convenience and shelf life lends itself to refined carbohydrates. After all, cookies and crackers are mostly sugar and flour—and they don’t spoil.

Many people in France (a famously skinny nation) drink coffee in the morning and skip breakfast. The French term for breakfast, petit déjeuner (little lunch) implicitly acknowledges that this meal should be kept small.

Every morning, just before we wake up, a natural circadian rhythm jolts our bodies with a heady mix of growth hormone, cortisol, epinephrine and norepinephrine (adrenalin). This cocktail stimulates the liver to make new glucose, essentially giving us a shot of the good stuff to wake us up. This effect is called the dawn phenomenon, and it has been well described for decades.

Many people are not hungry in the morning. The natural cortisol and adrenalin released stimulates a mild flight-or-fight response, which activates the sympathetic nervous system. Our bodies are gearing up for action in the morning, not for eating. All these hormones release glucose into the blood for quick energy. We’re already gassed up and ready to go. There is simply no need to refuel with sugary cereals and bagels. Morning hunger is often a behavior learned over decades, starting in childhood.

Worse, taking breakfast increases the number of eating opportunities in a day. Breakfast eaters therefore tend to eat more and eat more often—a deadly combination.11

Socioeconomic status has long been known to play a role in the development of obesity in that poverty correlates very closely with obesity. States with the most poverty tend to also have the most obesity. The southern states are relatively less affluent than those in the west and north east. With a 2013 median income of $39,031,2 Mississippi is the poorest state in the U.S. It also has the highest level of obesity, at 35.4 percent.3 But why is poverty linked to obesity?

The food-reward hypothesis would predict that obesity should be more prevalent among the rich, since they can afford to buy more of the highly rewarding foods. But the exact opposite is true. Lower-income groups suffer more obesity. To be blunt, the rich can afford to buy food that is both rewarding and expensive, whereas the poor can afford only rewarding food that is cheaper.

Neither food reward nor physical exertion can explain the association between obesity and poverty. So what drives obesity in the poor? It is the same thing that drives obesity everywhere else: refined carbohydrates.

This leaves carbohydrates. If refined carbohydrates are significantly cheaper than other sources of food, then those living in poverty will eat refined carbohydrates. Indeed, processed carbohydrates are entire orders of magnitude less expensive. An entire loaf of bread might cost $1.99. An entire package of pasta might cost $0.99. Compare that to cheese or steak, which might cost $10 or $20. Unrefined carbohydrates, such as fresh fruits and vegetables, cannot compare to the low, low prices of processed foods. A single pound of cherries, for instance, may cost $6.99. Why are highly refined carbohydrates so cheap? Why are unprocessed carbohydrates so much more expensive? The government lowers the cost of production with hefty agricultural subsidies. But not all foods get equal treatment. Figure 12.26 indicates which foods (and programs) receive the most in subsidies.

Figure 12.2. U.S. agricultural subsidies, 1995–2012. In 2011, the United States Public Interest Research Groups noted that “corn receives an astounding 29 percent of all U.S. agricultural subsidies, and wheat receives a further 12 percent.”7 Corn is processed into highly refined carbohydrates for consumption, including corn syrup, high-fructose corn syrup and cornstarch. Wheat is almost never consumed as a whole berry but further processed into flour and consumed in a wide variety of foods. Unprocessed carbohydrates, on the other hand, receive virtually no financial aid. While mass production of corn and wheat receives generous support, the same cannot be said for cabbage, broccoli, apples, strawberries, spinach, lettuce and blueberries.

Food additives are subsidized far more heavily than whole foods.