Quotes from David S. Ludwig

fat cells much more than passive storage sites for excess calories. Fat cells take in or release calories only when instructed to do so by external signals—and the master control is insulin. Too much insulin causes weight gain, whereas too little causes weight loss. So if we think about obesity as a disorder involving fat cells, then a radically different view emerges: Overeating doesn't make us fat. The process of becoming fat makes us overeat.

the ideas presented in this book culminate a century of research questioning the calorie balance model of obesity, and represent a fundamentally different way to understand why we gain weight and what we can do about it.7

fundamental principle of the body's weight-control systems: Impose a change in behavior (for example, by restricting food), and biology fights back (with increased hunger). Change biology, however, and behavior adapts naturally—suggesting a more effective approach to long-term weight management.

researchers from the University of Wales in the United Kingdom gave seventy-one female undergraduate students slow- or fast-digesting carbohydrate-based breakfasts and then tested their cognitive functioning. They found that memory, especially for hard words, was impaired throughout the morning after the fast-digesting breakfast.

Curiously, the stimulant drugs used to treat ADD have broadly similar biological actions to the stress hormone adrenaline. Could it be that these drugs help counteract the swings in blood sugar that occur on the highly processed diets children consume today?

With such limited support, most participants in diet studies don't change their behavior very much, and the comparison groups (for example, people assigned to a low-fat versus a low-carbohydrate diet) don't wind up eating much differently from each other. Not surprisingly, these studies produce very little weight loss in any group.

Such research has sometimes been misinterpreted to mean that "all diets are alike," or "sticking to a diet, any diet, is the only thing that matters." But these conclusions are simply wrong. This sort of faulty reasoning wouldn't withstand scrutiny in other areas of clinical research. Should we abandon a promising new cancer drug, simply because participants in the experimental group didn't take most of the medicine?

But are we really to believe that a cup of Coke would be as healthy as a large apple (both with about 100 calories), if we drank it with a serving of Metamucil and a multivitamin pill?

People with major metabolic problems, like severe insulin resistance or type 2 diabetes, may benefit from long-term carbohydrate restriction— to 25 percent of daily calories as in Phase 1 or sometimes even lower. Preliminary studies report that some individuals experience remarkable improvements in health by eliminating virtually all carbohydrates on a ketogenic diet.4

So for breakfast, you could have a bowl of cornflakes with no added sugar, or a bowl of sugar with no added cornflakes. They would taste different but, below the neck, act more or less the same.

Like many young doctors, I had received virtually no instruction in nutrition. Then, as now, medical schools focused almost exclusively on drugs and surgery, even though lifestyle causes most cases of heart disease and other chronic disabling conditions. In

Several systematic reviews of such studies (called meta-analysis) have been published, and the results are sobering. Low-fat diets produced less weight loss than higher-fat diets, including Mediterranean and low carbohydrate9—raising the possibility that the most widely recommended method for four decades to reduce calorie intake has done more harm than good.

we seem to have a choice—bypass the gastrointestinal tract or bypass the highly processed diet.

Ironically, the standard treatment for diabetes since the 1970s has been a low-fat, high-carbohydrate diet—the same diet that contributed to the problem in the first place! We wouldn't give the milk sugar lactose to someone with lactose intolerance. What's the sense in giving so much carbohydrate to someone who, by definition, has carbohydrate intolerance?

excessive weight in one generation may predispose the next for higher lifetime risk of obesity, apart from genetic inheritance and the tendency of offspring to pick up their parents' lifestyle habits.

Cutting back on calories will cause weight loss for a while, which gives the illusion that we have conscious control of our weight over the long term. However, many bodily functions are within our temporary, but not permanent control. For example, many people can lower the amount of carbon dioxide in the blood for several minutes by breathing fast, but few can do so for much longer.

Conventional diets aim to shrink body fat by restricting calorie intake. But this approach is doomed to fail in the real world, because it targets the symptoms, not the root cause of the problem. After a few weeks of calorie restriction, the body fights back, and makes us feel hungry, tired, and deprived.

Why did basic scientists think one way about obesity and practicing clinicians another? Why did we disregard decades of research into the biological determinants of body weight when treating patients? And why were we using an approach to weight loss based on a "calories in, calories out" model that hadn't changed since the late 1800s, when bloodletting was still in vogue?

Despite consuming the same total calories on each diet, the participants burned about 325 calories a day more on the low-carbohydrate diet than on the low-fat diet, amounting to the energy expended in an hour of moderately vigorous physical activity. So the type of calories we eat can affect the number of calories we burn.

In a sense, the calorie balance view of obesity is like considering fever a problem of heat balance. It's technically not wrong, but also not very helpful.