The Obesity Code: Unlocking the Secrets of Weight Loss

Chapter 7 posits a causal relationship between high insulin levels and obesity. Obese people secrete high levels of insulin compared to lean people. Their insulin levels also remain elevated for longer periods of time. Patients injected with insulin to treat diabetes tend to gain weight. The more insulin they take, the more obese they become. Fung cites the 1993 Diabetes Control and Complications Trial to support this claim. The study found that patients taking high doses of insulin gained about 9.8 pounds more than patients taking low doses of insulin over the course of six years. Over 30% of patients reported major weight gain (80). Later studies yielded similar results. A 2007 survey of three different insulin protocols, for instance, determined that “patients generally gained weight on all regimens” (81), but that those taking the highest doses of insulin gained the most weight. Oral medications that stimulate the pancreas to produce more insulin, such as sulfonylureas, also lead to weight gain, though less so than insulin injections. Drugs that magnify the impact of insulin on the body, such as thiazolidinediones, have comparable effects. By contrast, taking alpha glucosidase inhibitors, which block enzymes that aid carbohydrate digestion, hinder glucose absorption and decrease insulin levels, leading to significant weight loss. SGLT-2 inhibitors, which block the kidney’s reabsorption of glucose and lower blood sugar (resulting in less insulin production) also lead to weight loss. The research consistently shows that drugs that lower insulin levels cause weight loss while drugs that raise insulin levels cause weight gain. Thus, Fung concludes that insulin is a prime factor in the obesity epidemic, and that obesity results from a hormonal and not a caloric imbalance.

Chapter 8 focuses on the hormone cortisol and its synthetic version, prednisone. Used to treat a variety of diseases, including asthma, lupus, rheumatoid arthritis, and certain cancers, prednisone causes obesity due to its effect on cortisol.

Like insulin, cortisol is central to metabolizing carbohydrates. Often called the stress hormone, cortisol is produced in the adrenal cortex and mediates the body’s fight-or-flight response. Cortisol enhances the availability of glucose, providing energy to respond to danger. Although the body is well suited for short-term increases in cortisol (during exercise, for instance), it responds badly to long-term exposure from chronic stress. Studies reveal that cortisol raises both glucose and insulin levels, which drives weight gain. Lowering cortisol, by contrast, lowers insulin and results in weight loss. A study of Cushing’s, an illness that results in high levels of cortisol, found that 97% of patients gained weight, regardless of diet and exercise (92). People without Cushing’s but with high cortisol levels are also prone to weight gain, particularly around the abdomen.

Stress causes cortisol to rise, and by extension, stress causes weight gain. Mindfulness, exercise, and therapy may reduce work- or relationship-related stress, however, sleep deprivation, a major cause of chronic stress, is more difficult to treat. Sleep duration has declined dramatically in the last 100 years. In 1910, people slept an average of nine hours per night. Currently, 30% of adults report sleeping fewer than six hours per night (94). Sleep deprivation drives obesity by causing stress, which raises cortisol levels. A good weight loss plan, then, requires regular sleep.

Chapter 9 focuses on the Atkins Diet, a low-carbohydrate, high-fat diet named after the man who popularized it, Dr. Robert Atkins. In the early 1960s, Atkins lost a significant amount of weight by following a low-carb diet. In 1972, he published Dr. Atkins’ Diet Revolution, which recommended restricting carbohydrates to reduce insulin levels and hunger and to promote weight loss. The book became an instant best seller, as did similar books over the following decades. By 2004, more than 26 million Americans claimed to follow low-carb diets (99). Food corporations reacted by producing a variety of low-carb foods.

Health authorities have largely rejected the Atkins diet, claiming that its high fat content increases the risk of heart disease. Indeed, the American Heart Association (AHA) denounced the diet as a fad and continued to promote the low-fat diet as the sole dietary path to weight loss. Tellingly, obesity rates soared in the four decades the AHA promoted eating less fat. Rather than abandon the ineffective approach, doctors blamed patients for failing to lose weight.

A 2007 article in the Journal of the American Medical Association compared four popular weight loss plans: 1) the Atkins Diet; 2) the very low-fat Ornish Diet; 3) the Zone Diet, which balances carbohydrates, proteins, and fats in a 30:40:30 ratio; and 4) the standard low-fat diet. The Atkins Diet emerged as the clear winner. Later studies confirmed the efficacy of low-carb diets in lowering blood pressure, cholesterol, and blood sugar in the short term. Long-term studies, however, reveal that the Atkins Diet does not produce lasting benefits. Indeed, Fung’s systematic review of all the dietary trials shows that most of the benefits of low-carb diets disappear after one year. Compliance is partially to blame. According to Fung, though, the real problem lies in the incompleteness of the carbohydrate-insulin hypothesis. Pointing to low obesity rates in Asia and the South Pacific, he argues that sugar contributes more to obesity than other refined carbohydrates. For example, indigenous people in Papua New Guinea have low obesity rates despite eating a high-carbohydrate diet of yams, taro, sweet potato, and cassava (104). Residents of Okinawa, Japan, also eat starchy vegetables, yet have low rates of obesity. Carbohydrates cause weight gain, but sugar is an equally important part of the equation.