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

by Jason Fung

Prior to puberty, boys and girls average the same body-fat percentage. After puberty, women on average carry close to 50 percent more body fat than men. This change occurs despite the fact that men consume more calories on average than women.

First, he tried to eat less, but that only left him hungry. Worse, he failed to lose weight.

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.

The three macronutrients are fat, protein and carbohydrates: lowering dietary fat meant replacing it with either protein or carbohydrates. Since many high-protein foods like meat and dairy are also high in fat, it is difficult to lower fat in the diet without lowering protein as well. So, if one were to restrict dietary fats, then one must increase dietary carbohydrates and vice versa.

For example, the American Heart Association’s 1995 pamphlet, The American Heart Association Diet: An Eating Plan for Healthy Americans, declared we should eat six or more servings of “breads, cereals, pasta and starchy vegetables (that) are low in fat and cholesterol.” To drink, “Choose . . . fruit punches, carbonated soft drinks.”

Data about biological parents is often incomplete, confidential and not easily accessible by researchers. Fortunately, Denmark has maintained a relatively complete registry of adoptions, with information on both sets of parents.

The results sent a shockwave through the obesity-research community. Approximately 70 percent of the variance in obesity is familial. Seventy percent. Seventy percent of your tendency to gain weight is determined by your parentage.

Abundant food leads to a rise in the numbers of animals, not an enormous increase in their size. Think about rats or cockroaches. When food is scarce, rat populations are low. When food is plentiful, rat populations explode. There are many more normal-sized rats, not the same number of morbidly obese rats.

For example, the smell of frying food makes you hungry at lunchtime. However, if you have just finished a large buffet, those same smells may make you slightly queasy. The smells are the same. The decision to eat or not is principally hormonal.

“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.

The British obesity epidemic largely ran parallel to North America’s. But once again, the association of weight gain with increased calorie consumption does not hold true.3 In the British experience, neither increased caloric intake nor dietary fat correlated to obesity—which argues against a causal relationship.

The First Law of Thermodynamics states that energy can neither be created nor destroyed in an isolated system. This law is often invoked to support the Calories In/Calories Out model.

If we eat an extra 200 calories today, nothing prevents the body from burning that excess for heat. Or perhaps that extra 200 calories is excreted as stool. Or perhaps the liver uses the extra 200. We obsess about caloric input into the system, but output is far more important.

Her dietary compliance is good, but one year later, things have not improved. Her weight slowly creeps back up, even though she eats the same number of calories. Tired of feeling so lousy, she abandons the failed diet and resumes eating 2000 calories per day. Since her metabolism has slowed to an output of only 1500 calories per day, all her weight comes rushing back—as fat. Those around her silently accuse her of lacking willpower.

The failing isn’t ours. The portion-control caloric-reduction diet is virtually guaranteed to fail. Eating less does not result in lasting weight loss.

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.

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 normal.

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’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.

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.

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.

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.

Giving leptin doesn’t make people thin. Human obesity is a disease of leptin resistance, not leptin deficiency. This leaves us with much the same question that we began with. What causes leptin resistance? What causes obesity?

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 this mistake is made in human obesity studies all the time. Obesity develops over decades. Yet hundreds of published studies consider only what happens in less than a year. Thousands more studies last less than a week. Still, they all claim to shed light on human obesity.

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 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 body conserves calories needed for fat growth by shutting down other functions, and metabolism slows. Increased Calories In and decreased Calories Out (eating more and moving less) does not cause obesity, but is instead the result of obesity.

If insulin causes obesity, it must do so predominantly through its effect in the brain. Obesity is controlled in the central nervous system through the body set weight, not in the periphery. In this hypothesis, high insulin levels increase the body set weight.

ACTUALLY, I CAN make anybody fat. How? By prescribing insulin. It won’t matter that you have willpower, or that you exercise. It won’t matter what you choose to eat. You will get fat. It’s simply a matter of enough insulin and enough time.

In the San Antonio Heart Study,3 high fasting insulin was tightly correlated to weight gain over eight years of follow up. As we shall see in chapter 10, an insulin-resistant state leads also to high fasting insulin. This relationship is not coincidental, as insulin resistance itself plays a key role in causing obesity.

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.

Insulin is commonly used to treat both types of diabetes. In type 1 diabetes, there is destruction of the insulin-producing cells of the pancreas, resulting in very low levels of insulin. Patients require insulin injections to survive. In type 2 diabetes, cells are resistant to insulin and insulin levels are high. Patients do not always require insulin and are often treated first with oral medications.

The patients’ blood sugar levels were great. But what happened to their weight? It increased by an average of 19 pounds (8.7 kilograms)! Despite eating less than ever, patients gained weight like crazy. It wasn’t calories that drove their weight gain. It was insulin.

The drug olanzapine, used to treat psychiatric disorders, is commonly associated with weight gain—5.2 pounds (2.4 kilograms) on average. Does olanzapine raise insulin levels? Absolutely—prospective studies confirm that it does.25 As insulin rises, so does weight.

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.

A recent study29 suggests that 75 percent of the weight-loss response in obesity is predicted by insulin levels. Not willpower. Not caloric intake. Not peer support or peer pressure. Not exercise. Just insulin.

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.

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.

Dr. Robert Lustig, a pediatric obesity specialist, believes that high insulin levels act as an inhibitor of leptin, the hormone that signals satiety. Leptin levels increase with body fat. This response acts on the hypothalamus in a negative feedback loop to decrease food intake and return the body to its ideal weight. However, because the brain becomes leptin resistant due to constant exposure, it does not reduce its signal to gain fat.

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.

In our modern-day lives, we have many chronic, nonphysical stressors that increase our cortisol levels. For example, marital issues, problems at work, arguments with children and sleep deprivation are all serious stressors, but they do not result in the vigorous physical exertion needed to burn off the blood glucose. Under conditions of chronic stress, glucose levels remain high and there is no resolution to the stressor.

Any disease that causes excess cortisol secretion results in weight gain. Cortisol causes weight gain.

SLEEP DEPRIVATION IS a potent psychological stressor and thus stimulates cortisol. This, in turn, results in both high insulin levels and insulin resistance. A single night of sleep deprivation increases cortisol levels by more than 100 percent.

Dr. Atkins argued in his 1972 bestseller that severely restricting carbohydrates would keep insulin levels low, thus reducing hunger and eventually leading to weight loss. It didn’t take long for the nutritional authorities to respond. In 1973, the American Medical Association’s Council on Foods and Nutrition published a blistering attack on Atkins’s ideas.

The low-carb diet’s popularity, rekindled in the 1990s, ignited into a full-scale inferno in 2002 when award-winning journalist Gary Taubes wrote a controversial lead article in the New York Times entitled “What If It’s All Been a Big Fat Lie?”

In 2007, the Journal of the American Medical Association published a more detailed study.6 Four different popular weight plans were compared in a head-to-head trial. One clear winner emerged—the Atkins diet. The other three diets (Ornish, which has very low fat; the Zone, which balances protein, carbohydrates and fat in a 30:40:30 ratio; and a standard low-fat diet) were fairly similar with regard to weight loss.

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 hormones for refined carbs.