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bread. A calorie-restricted diet that cuts al calories by a third, as John Yudkin noted, wil also cut essential nutrients by a third. A diet that prohibits sugar, flour, potatoes, and beer, but al ows eating to satiety meat, cheese, eggs, and green vegetables wil stil include the essential nutrients, whether or not it leads to a decrease in calories consumed.

in metabolism and physical activity.

10. By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend

9. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we wil be.

6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow tal er. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis?the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and wel -being.

condition known as transient hypercholesterolemia?and that is a consequence of the fact that we store cholesterol along with fat in our fat cel s. When fatty acids are mobilized, the cholesterol is released as wel , and thus serum levels of cholesterol can spike.

sugar appears to induce an exaggerated response in that region of the brain known as the reward center?the nucleus accumbens. This suggests that the relatively intense cravings

The hunger that accompanies calorie restriction is an unavoidable physiological condition; the craving for carbohydrates is not.

In the case of hyperinsulinemia and obesity, however, this happens even between meals, when the cel s should be living off a fuel mixture of predominantly fatty acids. Instead, the insulin traps the fat in the fat tissue, and it signals the cel s to burn glucose. As far as the body is concerned, the elevated insulin is the indication that we?ve just eaten??high levels of insulin herald the ?fed? state,? as George Cahil put it?and the signal that carbohydrates are available to be burned. But in this case, they?re not. Now the homeostatic system that evolved to maintain blood sugar in a healthy range establishes an internal environment in which the cel s are primed to burn glucose for fuel, and only glucose can satisfy that demand, yet there?s no expendable glucose in the system.

hyperinsulinemia in turn leads to increased consumption, which, unless compensated for, could lead to further weight gain,? she wrote. ?Because acute hyperinsulinemia can also be produced in some individuals by simply looking at or thinking about food, it, too, can in turn lead to increased consumption and possible weight gain.?

hyperinsulinemia in turn leads to increased consumption, which, unless compensated for, could lead to further weight gain,? she wrote. ?Because acute hyperinsulinemia can also be produced in some individuals by simply looking at or thinking about food, it, too, can in turn lead to increased consumption and possible weight

demonstrated that rats wil secrete insulin in response to the mere taste of a sweet substance, and it doesn?t matter whether it is sugar or a no-calorie sugar substitute. The perceived taste of sweetness is sufficient to stimulate insulin secretion.

When researchers have measured seasonal variations in insulin levels in humans, they have invariably reported that insulin is highest in late fal and early winter?twice as high, according to one 1984 study?and lowest in late spring and early summer.

the levels of circulating insulin in animals and humans wil be proportional to body fat. ?The leaner an individual, the lower his basal insulin, and vice versa,? as Stephen Woods, now director

In short, nicotine appears to induce weight loss and fat loss not by suppressing appetite but by freeing up fatty acids from the fat cel s and then directing them to the muscle cel s, where they?re taken up and oxidized, providing the body with some excess energy in the process. When smokers quit, they gain weight because their fat cel s respond to the absence of nicotine by significantly increasing lipoprotein-lipase activity. (There?s also evidence that the weight-reduction drug fenfluramine?the ?fen? half of the popular weight-loss drug phen/fen, which was banned by the FDA in 1997?works in a similar manner, by decreasing lipoprotein-lipase activity in the fat tissue.)

The evidence suggests that nicotine induces weight loss by working on fat cel s to increase their insulin resistance, while also decreasing the lipoprotein-lipase activity on these cel s, both of which serve to inhibit the accumulation of fat and promote its mobilization over storage, as we discussed earlier (see Chapter 22). Nicotine also seems to promote the mobilization of fatty acids directly by stimulating receptors on the membranes of the fat cel s that are normal y triggered by hormones such as adrenaline. The drug also increases lipoprotein-lipase activity on muscles, and this may explain the steep rise in metabolic rate that occurs immediately after smoking.

This hypothesis can also explain the infertility associated with obesity in both humans and lab animals. If ?an excessive portion of available calories? is locked away in fat tissue, then the animal wil act as if it?s starving. In

If Neel?s third scenario is correct, however, a likely explanation for why carbohydrate-rich diets appear to facilitate blood-sugar control after meals is that they increase the insulin sensitivity of the fat cel s specifical y, while the muscle tissue remains insulin-resistant.