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

by Jason Fung

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.

Proximate vs Ultimate Cause

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. Result: weakness during physical activity. •Calories are needed to replace hair and nails. Fewer calories were available, so hair and nails were not replaced. Result: brittle nails and hair loss.

Calorie-deficit impact

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.

Calory-deficit doesn't work

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 delicious, or because of salt, sugar and fat. We eat too much because our own brain compels us to.

Why we eat so much

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.

Exercise doesn't really solve obesity problem

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 (2.5 centimeters) from his waist measurement. He gained weight, but it was lean mass.

High fat low carb experiment

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 (7.1 kilograms). His waist size positively ballooned by 3.6 inches (9.14 centimeters). After only three weeks, Feltham was developing love handles.

High carbs and processed food experiment

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 increases, trying to burn off the excess calories. The result is weight loss.

Why we gain weight

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 message to most human cells to take glucose out of the blood to use for energy. 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 door opens and glucose enters. All hormones work in roughly the same fashion.

What is hormone

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 without being absorbed. All cells in the body can use blood sugar (glucose). 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 hand, tend to raise both blood sugars and insulin levels minimally. Insulin is then broken down and rapidly cleared from the blood with a half-life of only two to three minutes.

What happened when we eat

Several hours after a meal, blood sugars and insulin levels start to drop. Less glucose is available for use by the muscles, the brain and other organs. The liver starts to break down glycogen into glucose to release it into general circulation for energy—the glycogen-storage process in reverse. This happens most nights, assuming you don’t eat at night. Glycogen is easily available, but in limited supply. During a short-term fast (“fast” meaning that you do not eat), your body has enough glycogen available to function. During a prolonged fast, your body can make new glucose from its fat stores—a process called gluconeogenesis (the “making of new sugar”). Fat is burned to release energy, which is then sent out to the body—the fat-storage process in reverse. Insulin is a storage hormone. Ample intake of food leads to insulin release. Insulin then turns on storage of sugar and fat. When there is no intake of food, insulin levels fall, and burning of sugar and fat is turned on. This process happens every day. Normally, this well-designed, balanced system keeps itself in check. We eat, insulin goes up, and we store energy as glycogen and fat. We fast, insulin goes down and we use our stored energy. As long as our feeding and fasting periods are balanced, this system also remains balanced. If we eat breakfast at 7 a.m. and finish eating dinner at 7 p.m., the twelve hours of feeding balances the twelve hours of fasting. Glycogen is like your wallet. Money goes in and out constant...

What happened after you eat

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.

Inject insulin cause weight-gain

Once we understand that obesity is a hormonal imbalance, we can begin to treat it. If we believe that excess calories cause obesity, then the treatment is to reduce calories. But this method has been a complete failure. However, if too much insulin causes obesity, then it becomes clear we need to lower insulin levels. The question is not how to balance calories; the question is how to balance our hormones. The most crucial question in obesity is how to reduce insulin.

The key to weight-loss is to balance our hormone

And so, by extension, stress causes weight gain—something that many people have intuitively understood, despite the lack of rigorous evidence. 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. Reducing stress is difficult, but vitally important. Contrary to popular belief, sitting in front of the television or computer is a poor way to relieve stress. Instead, stress relief is an active process. There are many time-tested methods of stress relief, including mindfulness meditation, yoga, massage therapy and exercise. Studies on mindfulness intervention found that participants were able to use yoga, guided meditations and group discussion to successfully reduce cortisol and abdominal fat.20

High Cortisol (stressed hormone) cause weight-gain

Restriction of sleep to four hours in healthy volunteers resulted in a 40 percent decrease in insulin sensitivity,29 even after a single sleep-deprived night.30 After five days of sleep restriction, insulin secretion increased 20 percent and insulin sensitivity decreased by 25 percent. Cortisol increased by 20 percent.31 In another study, shortened sleep duration increased the risk of type 2 diabetes.32

Lack of sleep can cause type-2 diabetes

THREE MEALS A DAY. NO SNACKS. LET’S TURN BACK the clock to the U.S. in the 1960s. Food shortages from the war are a thing of the past. Obesity is not yet a major issue. Why not? After all, they ate Oreo cookies, KitKats, white bread and pasta. They ate sugar, although not quite as much. They also ate three meals per day, with no snacks in between. 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.

Why America people is ok eating 3 times a day in 1960

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.

Calorie is not a calorie

It is noteworthy that, in the 1920s, sugar was relatively expensive. A 1930 study9 showed that type 2 diabetes was far more common among the wealthier northern states compared to the poorer southern states. As sugar became extremely cheap, however, this relationship inverted. Now, poverty is associated with type 2 diabetes, rather than the other way around.

Sugar price affect obesity

The sad but inescapable conclusion is that we are now passing on our obesity to our children. Why? Because we are now marinating our children in insulin starting in the womb, they develop more severe obesity sooner than ever before. Because obesity is time dependent and gets worse, fat babies become fat children. Fat children become fat adults. And fat adults have fat babies in turn, passing obesity on to the next generation.

How obesity got transfer to our child

She writes, “These findings raise the question whether [artificial sweetener] use might be fueling—rather than fighting—our escalating obesity epidemic.” The bad news for diet soda kept rolling in. Over the ten years of the Northern Manhattan Study,9 Dr. Hannah Gardener from the University of Miami found in 2012 that drinking diet soda was associated with a 43 percent increase in risk of vascular events (strokes and heart attacks). The 2008 Atherosclerosis Risk in Communities Study (ARIC)10 found a 34 percent increased incidence of metabolic syndrome in diet soda users, which is consistent with data from the 2007 Framingham Heart Study,11 which showed a 50 percent higher incidence of metabolic syndrome.

The danger of sweetener

The study found a 30 percent increase risk of cardiovascular events (heart attacks and strokes) in those drinking two or more diet drinks daily. The benefits for heart attack, stroke, diabetes and metabolic syndrome were similarly elusive. Artificial sweeteners are not good. They are bad. Very bad. Despite reducing sugar, diet sodas do not reduce the risk of obesity, metabolic syndrome, strokes or heart attacks. But why? Because it is insulin, not calories, that ultimately drives obesity and metabolic syndrome. The important question is this: Do artificial sweeteners increase insulin levels? Sucralose13 raises insulin by 20 percent, despite the fact that it contains no calories and no sugar. This insulin-raising effect has also been shown for other artificial sweeteners, including the “natural” sweetener stevia.

Sweetener triggers insulin too

Dr. David Ludwig from Harvard randomly divided two groups of overweight adolescents.18 One group was given water and diet drinks to consume while the control group continued with their usual drinks. At the end of two years, the diet soda group was consuming far less sugar than the control group. That’s good—but that is not our question. Does drinking diet soda make any difference to adolescent obesity? The short answer is no. There was no significant weight difference between the two groups.

Experiment between sugar and sweetener consumption

Caloric reduction is the main advantage of artificial sweeteners. But it is not calories that drives obesity; it’s insulin. Since artificial sweeteners also raise insulin levels, there is no benefit to using them. Eating chemicals that are not foods (such as aspartame, sucralose or acesulfame potassium) is not a good idea. They are synthesized in large chemical vats and added to foods because they happen to be sweet and not kill you. Small amounts of glue won’t kill you either. That doesn’t mean we should be eating it. The bottom line is that these chemicals do not help you lose weight and may actually cause you to gain it.

Why sweetener is popular but useless

All foods stimulate insulin, thus all foods could be fattening—and that’s where the calorie confusion emerges. Since all foods could be fattening, we imagined that all foods could be measured in a common unit: the calorie. But the calorie was the wrong unit. Calories do not cause obesity. Instead, insulin is responsible. Without a framework for understanding insulin, it was impossible to understand the inconsistencies of the epidemiologic evidence.

Everything is about insulin

The year 1990 marked the beginning of the end for trans fat when Dutch researchers noted that consuming trans fats increased LDL (low-density lipoprotein or “bad” cholesterol) and lowered HDL (high-density lipoprotein or “good” cholesterol) in subjects.15 Closer scrutiny of the health effects led to an estimate that a 2 percent increase in trans-fat consumption would increase risk of heart disease by a whopping 23 percent.16 By 2000, the tide had turned decisively. Most consumers were actively avoiding trans fats, and Denmark, Switzerland and Iceland banned trans fats for human consumption.

Trans-fat

THERE ARE FIVE basic steps in weight loss: 1. Reduce your consumption of added sugars. 2. Reduce your consumption of refined grains. 3. Moderate your protein intake. 4. Increase your consumption of natural fats. 5. Increase your consumption of fiber and vinegar.

Basic step in weight-loss