Given energy’s central role in sustaining life, it is not surprising that obtaining and storing energy has a complex physiological regulation. Our bodies will let us know when we are hungry, and when we have eaten enough (if we pay attention). Through this complex physiological control system, which involves a constant dialogue between our brains and our gastrointestinal tract, we are able to obtain and maintain sufficient energy stores to power our activities.

There are two different ways of regulating energy balance and food intake, a short-term system and a long-term system. The short-term system is mediated by hormones and stomach pressure and is responsible for triggering hunger and satiety before and after individual meals. The long-term system, mediated by a different set of hormones, adjusts food intake and energy expenditure to maintain adequate fat stores.

When we haven’t eaten for a while, our stomach begins to grumble. That grumbling is a sign that a hormone called ghrelin is racing into action. Ghrelin, nicknamed the “hunger hormone,” is a 28–amino acid peptide hormone that is produced primarily in the stomach. It is the only hormone that has been found to increase hunger. Circulating ghrelin levels in the blood surge just before meals and decrease after eating. Ghrelin stimulates hunger by activating specific neurons in the brain. Ghrelin secretion decreases only once nutrients from the meal are absorbed into the blood. Its secretion is most effectively inhibited by carbohydrates, and then by proteins; fat is least effective.

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Satiation is the process that leads to the termination of a meal and refers to the sense of fullness that we feel while eating. Satiety is the effect that the meal has on our interest in food after a meal; it operates in the interval between meals and affects when we feel hungry again. The primary factors affecting these two processes are gastric distention—how much our stomach has expanded to let food in—and the release of hormones produced by specialized cells in the gastrointestinal tract. Nerves in the stomach sense its expansion and relay signals to the brain to communicate a sense of fullness. At the same time, several gut peptide hormones are produced by specialized cells in the small intestine in response to the detection of nutrients in the gut.

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Importantly, calories in beverages appear to bypass mechanisms of satiation. A number of studies have demonstrated that soft-drink calories are less satiating than calories from solid foods.

Over the long term, energy balance is affected by a hormone called leptin. Leptin is produced primarily by adipose (fat) tissue. Its circulating concentration is closely associated with total body fat. When fat stores increase, more leptin is produced. The leptin level increase in the blood acts on the brain to suppress hunger, and increases energy expenditure to avoid excess weight gain. (INFOGRAPHIC 15.4)

If leptin suppresses hunger, and fat people have more leptin, then why do people ever become obese? It turns out that obese individuals have higher levels of circulating leptin than lean individuals, but they seem to be resistant to the effects of leptin. Thus, they don’t experience the same suppressed hunger or increased expenditure of energy. Some evidence suggests that a high-fructose diet may contribute to leptin resistance in humans.

In addition to the internal cues that regulate energy balance, there are also many environmental cues that influence food intake and energy expenditure. It is critical to differentiate between hunger and appetite. Hunger is the biological impulse that drives us to seek out food and consume it to meet our energy needs. Appetite, however, is often viewed as the liking and wanting of food for reasons other than, or in addition to, hunger. Appetite is often a product of sensory stimuli (the sight or smell of appealing foods) and the perceived pleasure we will experience as we satisfy our appetite and eat the desired food.

Most of us live in an environment in which we are surrounded by a plethora of palatable foods that are readily accessible. Hunger is certainly not the only reason (and perhaps not the dominant one) that motivates us to eat on many occasions. (See Chapter 19 to learn more about determinants of eating behavior.) We often eat because it is pleasurable to do so. Furthermore, food manufacturers spend billions of dollars in research designing foods that will trigger our “bliss point”—with just the right balance of salt, fat, and sugar that we find nearly irresistible. Similarly, large sums of money are spent marketing these products to us. We are often surrounded by cues (such as advertisements) that stimulate our appetite and make us not only want to eat, but to eat specific foods—and more of them as portion sizes increase. In the end, we often eat when we are not hungry, causing us to consume more calories than we expend, and therefore, to gain weight. This is often referred to as the “toxic food environment” because the easy accessibility of highly palatable, energy-dense foods, and the resulting overconsumption of those foods, is a significant factor in the obesity epidemic.

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We also eat for many other reasons, such as in response to stress, boredom, and difficult emotions. All of these reasons for eating can, to some degree, override the satiety signals that are designed to keep us in energy balance.

So is overconsumption of food the cause of our obesity epidemic? Are we simply being goaded into eating more food than we used to, and paying the price in wider waistlines? Levine and his colleagues think that there is more to this story than just an increase in energy intake.