34-1 What physiological factors produce hunger?

Keys’ semistarved volunteers felt their hunger because of a homeostatic system designed to maintain normal body weight and an adequate nutrient supply. But what precisely triggers hunger? Is it the pangs of an empty stomach? So it seemed to A. L. Washburn. Working with Walter Cannon (Cannon & Washburn, 1912), Washburn agreed to swallow a balloon attached to a recording device (FIGURE 34.1). When inflated to fill his stomach, the balloon transmitted his stomach contractions. Washburn supplied information about his feelings of hunger by pressing a key each time he felt a hunger pang. The discovery: Washburn was indeed having stomach contractions whenever he felt hungry.

Can hunger exist without stomach pangs? To answer that question, researchers removed some rats’ stomachs, creating a direct path to their small intestines (Tsang, 1938). Did the rats continue to eat? Indeed they did. Some hunger similarly persists in humans whose ulcerated or cancerous stomachs have been removed.

If the pangs of an empty stomach are not the only source of hunger, what else matters?

People and other animals automatically regulate their caloric intake to prevent energy deficits and maintain a stable body weight. This suggests that somehow, somewhere, the body is keeping tabs on its available resources. One such resource is the blood sugar glucose. Increases in the hormone insulin (secreted by the pancreas) diminish blood glucose, partly by converting it to stored fat. If your blood glucose level drops, you won’t consciously feel the lower blood sugar. But your brain, which is automatically monitoring your blood chemistry and your body’s internal state, will trigger hunger. Signals from your stomach, intestines, and liver (indicating whether glucose is being deposited or withdrawn) all signal your brain to motivate eating or not.

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How does the brain integrate these messages and sound the alarm? The work is done by several neural areas, some housed deep in the brain within the hypothalamus, a neural traffic intersection (FIGURE 34.2). For example, one neural arc (called the arcuate nucleus) has a center that secretes appetite-stimulating hormones. When stimulated electrically, well-fed animals begin to eat. If the area is destroyed, even starving animals have no interest in food. Another neural center secretes appetite-suppressing hormones. When electrically stimulated, animals will stop eating. Destroy this area and animals will eat and eat, and become extremely fat (Duggan & Booth, 1986; Hoe-bel & Teitelbaum, 1966).

Blood vessels connect the hypothalamus to the rest of the body, so it can respond to our current blood chemistry and other incoming information. One of its tasks is monitoring levels of appetite hormones, such as ghrelin, a hunger-arousing hormone secreted by an empty stomach. During bypass surgery for severe obesity, surgeons seal off or remove part of the stomach. The remaining stomach then produces much less ghrelin, and the person’s appetite lessens (Ammori, 2013; Lemonick, 2002). Besides insulin and ghrelin, other appetite hormones include leptin, orexin, and PYY; FIGURE 34.3 describes how they influence our feelings of hunger.

Experimental manipulation of appetite hormones has raised hopes for an appetite-reducing medication. Such a nose spray or skin patch might counteract the body’s hunger-producing chemicals or mimic (or even increase) the levels of hunger-dampening chemicals.

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The complex interaction of appetite hormones and brain activity may help explain the body’s apparent predisposition to maintain itself at a particular weight. When semi-starved rats fall below their normal weight, their “weight thermostat” signals the body to restore the lost weight. Fat cells cry out (so to speak) “Feed me!” and grab glucose from the bloodstream (Ludwig & Friedman, 2014). Thus, hunger increases and energy expenditure decreases. This stable weight toward which semistarved rats return is their set point (Keesey & Corbett, 1983). In rats and humans, heredity influences body type and approximate set point.

Our bodies regulate weight through the control of food intake, energy output, and basal metabolic rate—the rate of energy expenditure for maintaining basic body functions when at rest. By the end of their 6 months of semistarvation, the men who participated in Keys’ experiment had stabilized at three-quarters of their normal weight, while taking in half of their previous calories. How did their bodies achieve this dieter’s nightmare? They reduced their energy expenditure, partly through inactivity but partly because of a 29 percent drop in their basal metabolic rate.

Some researchers, however, doubt that our bodies have a preset tendency to maintain optimum weight (Assanand et al., 1998). They point out that slow, sustained changes in body weight can alter one’s set point, and that psychological factors also sometimes drive our feelings of hunger. Given unlimited access to a wide variety of tasty foods, people and other animals tend to overeat and gain weight (Raynor & Epstein, 2001). For these reasons, some researchers have abandoned the idea of a biologically fixed set point. They prefer the term settling point to indicate the level at which a person’s weight settles in response to caloric intake and expenditure (which are influenced by environment as well as biology).