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

by Jason Fung

Dr. David Ludwig from Harvard University9 found that the low-fat diet slowed body metabolism the most.

What was the best diet for maintaining metabolism? The very-low-carbohydrate diet. This diet also seemed to reduce appetite. Dr. G. Boden wrote in the Annals of Internal Medicine in 2005, “When we took away the carbohydrates, the patients spontaneously reduced their daily energy consumption by 1,000 calories a day.”10 Insulin levels dropped and insulin sensitivity was restored.

Perhaps eating refined carbohydrates leads to “food addictions.” Natural satiety signals are hormones that are extremely powerful deterrents to overeating. Hormones such as cholecystokinin and peptide YY respond to ingested proteins and fats to signal us to stop eating. ...

At some point, you simply cannot eat any more, and the idea of consuming two more pork chops is sickening. That feeling is your satiety hormo...

But what if you were offered a small slice of cake or apple pie? Doesn’t seem so hard to eat now, does it? As kids, we used to call this the second-stomach phenomenon: after the first stomach for regular food was full, we imagined that there was a second one for desserts. Somehow, despite being full, we still have room for highly refined carbohydrates like cake and pie—but not proteins or fats. Highly refined an...

Think about foods that people say they’re “addicted” to. Pasta, bread, cookies, chocolate, chips. Notice anything? All are highly refined carbohydrates. Does anybody ever say they are addicted to fish? Apples? Beef? Spinach? Not likely. Those are all delicious foods, but not addictive. Consider some typical comfort foods. Macaroni and cheese. Pasta. Ice cream. Apple pie. Mashed potatoes. Pancakes. Notice anything? 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 hor...

The Atkins diet severely restricted highly indulgent foods such as cakes, cookies, ice cream and other desserts. These foods are clearly fattening, no matter what diet you believe in. We continue to eat them simply because they are indulgent. Food is a celebration, and feasting has accompanied celebration throughout human history. This is as true in year 2015 AD as it was in year 2015 BC. Birthdays, weddings and holiday celebrations—what do we eat? Cake. Ice cream. Pie. Not whey powder shakes and lean pork. Why? Because we want to indulge. The Atkins diet does not allow for this simple fact, and that doomed it to failure. The first-hand experience of many people confirmed that the Atkins diet was not a lasting one. Millions of people abandoned the Atkins approach, and the New Diet Revolution faded into just another dietary fad. The company Atkins Nutritionals, founded in 1989 by Dr. Atkins, filed for bankruptcy, having sustained heavy losses as its customers fled. The weight-loss benefits could not be sustained.

THE CARBOHYDRATE-INSULIN HYPOTHESIS WAS INCOMPLETE THE CARBOHYDRATE-INSULIN HYPOTHESIS, the idea that carbohydrates cause weight gain because of insulin secretion, was not exactly wrong. Carbohydrate-rich foods certainly do increase insulin levels to a greater extent than the other macronutrients. High insulin certainly does lead to obesity.

However, the hypothesis stands incomplete. There are many problems, with the paradox of the Asian rice eater being the most obvious. Most Asians, for at least the last half-century, ate a diet based on white, polished rice, a highly refined carbohydrate. Yet until recently, obesity remained quite rare in these populations.

Total and percentage carbohydrate intake in China far exceeds the other nations. Sugar intake in China, however, is extremely low compared to the other nations. Japan’s carbohydrate intake is similar to that of the U.K. and the U.S., but its sugar consumption is far lower. Despite high carbohydrate intakes, obesity rates in China and Japan stayed very low until recently. So the carbohydrate-insulin hypothesis was not incorrect, but clearly something else was going on.

Total carbohydrate intake was not the entire story. Sugar seemed to be contributing much more to obesity than other refined carbohydrates.

Similarly, natives of the Japanese island of Okinawa eat a diet that is nearly 85 percent unrefined carbohydrates. The dietary staple is sweet potato. They eat three times as many green and yellow vegetables, but only 25 percent of the sugar consumed by residents of nearby Japan. Despite the high intake of carbohydrates, there is virtually no obesity, and the average body mass index is only 20.4. They are one of the longest-lived peoples in the world, with more than triple the rate (compared to nearby Japan) of people living past 100 years. Clearly, the carbohydrate-insulin hypothesis is an incomplete theory, leading many to abandon it rather than try to reconcile it with the known facts. One possibility is that there is an important difference in eating rice versus wheat. Asians tend to eat rice, whereas Western societies tend to take their carbohydrate as refined wheat and corn products. It is also possible that changes in Western obesity rates are related to changes in the variety of wheat we are eating. Dr. William Davis, author of Wheat Belly, a New York Times bestseller, suggests that the dwarf wheat that we eat today may be far different from the original wheat. The Einkorn variety of wheat has been cultivated since 3300 BC. By the 1960s, as the world’s population grew larger, agricultural techniques aimed at increasing the yield of the wheat led to new varieties of wheat called dwarf and semi-dwarf wheat. Currently, 99 percent of commercially grown wheat is dwarf a...

In Kitava, high carbohydrate intake did not lead to elevated insulin. The notion that carbohydrates are the only driver of insulin is incorrect. A critical piece of the puzzle had been neglected. Specifically, sugar plays a crucial role in obesity, but how does it fit in? The missing link was insulin resistance.

INSULIN RESISTANCE: THE MAJOR PLAYER OPRAH WINFREY HAS waged her weight loss battles publicly for several decades. At her heaviest, she weighed 237 pounds (107.5 kilograms). By 2005, she’d battled her way to a relatively svelte 160 pounds (72.6 kilograms). She was exultant. She’d cut her carbohydrates. She’d exercised. She had a personal chef and a personal trainer. She did everything “right.” She had every advantage not available to the rest of us. So why did she gain back 40 pounds (18 kilograms) by 2009? Why couldn’t she keep the weight off? Why is long-standing obesity so difficult to treat? Time dependence in obesity is almost universally understood but rarely acknowledged. Usually, obesity is a gradual process of gaining 1 to 2 pounds (0.5 to 1 kilogram) per year. Over a period of twenty-five years, though, that can add up to 50 extra pounds (23 kilograms).

Those who have been obese their entire lives find it extremely difficult to lose weight. In contrast, people with recent weight gain have a much, much easier time dropping the excess pounds.

Conventional caloric theories of obesity assume that losing 10 pounds (4.5 kilograms) is the same experience whether you’ve been overweight for one week or one decade. If you reduce the calories, the weight will be lost. But this is simply not true. Likewise, the carbohydrate-insulin hypothesis makes no allowance for duration of obesity: reducing carbohydrates shou...

But the time frame matt...

So we must acknowledge the phenomenon of time dependence. Obesity at age seventeen has consequences that reach decades into the future.1 Any comprehensive theory of obesity must be able to explain why its duration matters so much. High insulin levels cause weight gain. Food choices play a role in raising insulin levels. But we are missing yet another pathway that increases insulin, one that is both time dependent and independent of diet: insulin resistance. Insulin resistance is Lex Luthor. It is the hidden force behind most of modern medicine’s archenemies, including obesity, diabetes, fatty liver, Alzheimer’s disease, heart disease, cancer, high blood pressure and high cholesterol. But while Lex Luthor is fictional, the insulin resistance syndrome, also called the metabolic syndrome, is not.

HOW DO WE DEVELOP RESISTANCE? THE HUMAN BODY is characterized by the fundamental biological principle of homeostasis. If things change in one direction, the body reacts by changing in the opposite direction to return closer to its original state. For instance, if we become very cold, the body adapts by increasing body-heat generation. If we become very hot, the body sweats to try to cool itself. Adaptability is a prerequisite for survival and generally holds true for all biological systems. In other words, the body develops resistance. The body resists change out of its comfort range by adapting to it.

As we develop insulin resistance, our bodies increase our insulin levels to get the same result—glucose in the cell. However, we pay the price in constantly elevated insulin levels. Why do we care? Because insulin resistance leads to high insulin levels, and as we’ve seen, high insulin levels cause obesity.

ANTIBIOTIC RESISTANCE LET’S START WITH antibiotic resistance. When new antibiotics are introduced, they kill virtually all the bacteria they’re designed to kill. Over time, some bacteria develop the ability to survive high doses of these antibiotics. They’ve become drug-resistant “superbugs,” and infections from them are difficult to treat and can sometimes lead to death. Superbug infections are a large and growing problem in many urban hospitals worldwide. All antibiotics have begun to lose their effectiveness due to resistance.

Persistent, high-level use of antibiotics causes antibiotic resistance.

VIRAL RESISTANCE

If you became infected with measles virus as a child, you’d be protected from reinfection with measles for the rest of your life.

In other words, viruses cause viral resistance. Higher doses, usually in the form of repeated vaccinations, cause more resistance.

DRUG RESISTANCE WHEN COCAINE IS taken for the first time, there is an intense reaction—the “high.” With each subsequent use of the drug, the high becomes less intense. Sometimes users start to take larger and larger doses to achieve the same high. Through exposure to the drug, the body develops resistance to its effects—a condition called tolerance. People can build up tolerance to narcotics, marijuana, nicotine, caffeine, alcohol, benzodiazepines and nitroglycerin.

VICIOUS CYCLES THE AUTOMATIC RESPONSE to the development of resistance is to increase the dosage. For example, in the case of antibiotic resistance, we respond by using more antibiotics. We use higher doses or newer drugs. The automatic response to drug resistance is to use more drugs. An alcoholic takes higher and higher doses of alcohol to beat the resistance, which temporarily “overcomes” the resistance. However, this behavior is clearly self-defeating. Since resistance develops in response to high, persistent levels, raising the dose in fact raises resistance. If a person uses larger amounts of cocaine, he or she develops greater resistance. As more antibiotics are used, more antibiotic resistance develops. This cycle continues until we simply can’t go any higher. And it’s a self-reinforcing cycle—a vicious cycle.

Insulin causes insulin resistance.

I can make you insulin resistant. I can make anybody insulin resistant. All I need to do is give insulin.

With normal but persistent amounts of insulin alone, these healthy, young, lean men can be made insulin resistant. I can start these men on the road to diabetes and obesity simply by administering insulin—which causes insulin resistance.

The longer the cycle continues, the worse it becomes—that’s why obesity is so time dependent.

People who are stuck in this vicious cycle for decades develop significant insulin resistance. That resistance leads to high insulin levels that are independent of that person’s diet. Even if you were to change your diet, the resistance would still keep your insulin levels high. If your insulin levels stay high, then your body set weight stays high. The thermostat is set high, and your weight will be drawn irresistibly upward.

The fat get fatter. The longer you are obese, the harder ...

But you already knew that. Oprah knew it. Everybody already knew it. Most current theories of obesity cannot explain this effect, so they instead ignore it. But obesity is time-dependent. Like rust, it takes time to develop. You can study moisture conditions and metal composition. But ...

A diet high in foods that provoke an insulin response may initiate obesity, but over time, insulin resistance becomes a larger and larger part of the problem and can become, in fact, a major driver of high insulin levels. Obesity drives itself. A long-standing obesity cycle is ext...

When we ingest excess carbohydrates, we develop hepatic insulin resistance. Significant dietary intervention will reverse the hepatic insulin resistance, but will have no effect on insulin resistance in the muscles or the brain. Lack of exercise may lead to insulin resistance in the muscles. Exercise will increase insulin sensitivity there, but has little effect on insulin resistance in the liver or brain.

In response to hepatic or muscle insulin resistance, overall insulin levels increase. However, at the appetite centers in the hypothalamus, insulin’s effect is unchanged. The brain is not resistant to insulin. When high insulin levels reach the brain, the insulin retains its full effect to raise body set weight.

Whenever the body is exposed to a constant stimulus, it acclimates to it (once again, homeostasis at work). Have you ever watched a baby sleep in a crowded, noisy airport? The ambient noise is very loud, but constant. The baby adapts by developing resistance to the noise. It basically just ignores it. Now imagine the same baby sleeping in a quiet house. A slight creak of the floorboards may be enough to wake him up. Even though it is not loud, it is very noticeable. The baby isn’t used to the noise. High persistent levels create resistance. Hormones work in exactly the same way.

How does this apply to insulin and obesity? Consider the experiment described earlier that used constant infusions of insulin. Even healthy young men quickly developed insulin resistance. But the levels of insulin administered were normal. What changed? The periodic release. Normally, insulin is released in bursts, which prevents the development of insulin resistance. In the experimental condition, the constant bombardment of insulin led the body to down regulate its receptors and develop insulin resistance. Over time, insulin resistance induces the body to produce even more insulin to “overcome” the resistance.

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.

Should we eat candy or olive oil? This is the question of macronutrient composition, or “what to eat.” However, the persistence of insulin plays a key role in the development of insulin resistance, so there is also the question of meal timing, or “when to eat.” Both components are equally important. Unfortunately, we spend obsessive amounts of time and energy trying to understand what we should ...

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

Figure 10.3. The balance of time spent each day in the insulin-dominant versus the insulin-deficient state has changed greatly since the 1970s. Crazier still—we have been brainwashed to believe that constant eating is somehow good for us! Not just acceptable, but healthy.

Millions of dollars are spent to give children snacks all day long. Then millions more are spent to combat childhood obesity. These same kids are berated for getting fat. Millions more are spent to fight obesity as adults.

FUELING THE INCREASE in eating opportunities was the desire of big food companies to make more money. They created an entirely new category of food, called “snack food,” and promoted it relentlessly. They advertised on TV, print, radio and Internet. But there is an even more insidious form of advertising called sponsorship and research. Big Food sponsors many large nutritional organizations. And then there are the medical associations. In 1988, the American 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.

Consider the ingredient list of a popular meal-replacement shake. The first five ingredients are water, corn maltodextrin, sugar, milk protein concentrate and canola oil. This nauseating blend of water, sugar and canola oil does not really meet my definition of healthy.

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!

The fox, it seemed, was now guarding the hen house. Shills for Big Food had been allowed to infiltrate the hallowed halls of medicine. Push fructose? No problem. Push obesity drugs? No problem. Push artificial meal replacement shakes? No problem.

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.