Quotes from The Obesity Code - Part 1

From The Obesity Code, by Jason Fung, MD

Part 2: The Calorie Deception
Chapter 3: The Calorie-Reduction Error
Page 44: “The study also measured several satiety hormones, including peptide YY, amylin[,] and cholecystokinin, all of which are released in response to proteins and fats in our diet and serve to make us feel full. This response, in turn, produces the desired effect of keeping us from overeating. More than a year after initial weight loss, the levels of all three satiety hormones were significantly lower than before.”

Page 45: “Losing weight triggers two important responses. First total energy expenditure is immediately and indefinitely reduced in order to conserve the available energy. Second, hormonal hunger signaling is immediately and indefinitely amplified in an effort to acquire more food. Weight loss results in increased hunger and decreased metabolism. This evolutionary survival strategy has a single purpose: to make us regain the lost weight.”

“This has nothing whatsoever to do with a lack of willpower or any kind of moral failure. It’s a normal hormonal fact of life. We feel hungry, cold, tired[,] and depressed. These are all real, measurable physical effects of calorie restriction. Reduced metabolism and the increased hunger are not the cause of obesity—they are the result. Losing weight causes the reduced metabolism and increased hunger, not the other way around.”

Chapter 4: The Exercise Myth

Page 52: “ Total energy expenditure = Basal metabolic rate + Thermogenic effect of food + Nonexercise activity thermogenesis + Excess post-exercise oxygen consumption + Exercise.

Page 53: “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.”

Page 55: “The second mechanism of compensation relates to a reduction in non-exercise activity. If you exert yourself all day, you are less likely to exercise in your free time. The Hadza, who were walking all day, reduced their physical activity when they could. In contrast, those North Americans who were sitting all day probably increased their activity when given the chance.”

Chapter 5: The Overfeeding Paradox

Page 61: “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.”

Chapter 6: A New Hope

Page 71: “There is no clear, focused, unified theory of obesity. There is no framework for understanding weight gain and weight loss. This lack impedes progress in research—and so we come to our challenge: to build the hormonal obesity theory.”

Page 75: “What happens to the excess fat that is produced through de novo lipogenesis? This newly synthesized fat can be stored as visceral fat (around organs), as subcutaneous fat (underneath the skin) or in the liver.”

Page 76: “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.”

Chapter 7: Insulin

Page 79: “Patients who use insulin regularly and physicians who prescribe it already know the awful truth: 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.”

Page 81: “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.”

Page 86: “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.”

Chapter 8: Cortisol

Page 94: “Population studies consistently link short sleep duration and excess weight, generally with seven hours being the point where weight gain starts. Sleep five to six hours was associated with a more than 50 percent increased risk of weight gain. The more sleep deprivation, the more weight gained.”

Chapter 10: Insulin Resistance: The Major Player

Page 108: “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.”

Page: 115: “A diet high in foods the 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 extremely difficult to break, and dietary changes alone may not be sufficient.”

Page 116: “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.”

Page 119: “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.”

Page 121: “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. Eating six small meals per day causes the metabolic rate to go up six times a day, but only a little. Eating three larger meals per day causes metabolic rate to go up three times a day, but a lot each time. In the end, it’s a wash. The total thermogenic effect of food over twenty-four hours for both the grazing and gorging strategies is the same: neither yields a metabolic advantage. Eating more frequent meals does not aid in weight loss.”