Anyone who has tried to restrict their eating knows that physiological influences are powerful. Their strength was vividly demonstrated when Ancel Keys and his research team (1950) studied semistarvation among wartime conscientious objectors. After three months of normal eating, they cut in half the food intake of 36 men selected from 200 volunteers. The semistarved men became listless and apathetic as their bodies conserved energy. Eventually, their body weights stabilized at about 25 percent below their starting weights.

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Consistent with Abraham Maslow’s idea of a needs hierarchy, the men became food obsessed. They talked food. They daydreamed food. They collected recipes, read cookbooks, and feasted their eyes on delectable forbidden food. Preoccupied with their unmet basic need, they lost interest in sex and social activities. As one man reported, “If we see a show, the most interesting part of it is contained in scenes where people are eating. I couldn’t laugh at the funniest picture in the world, and love scenes are completely dull.”

The semistarved men’s preoccupations illustrate how powerful motives can hijack our consciousness. When we’re hungry, thirsty, fatigued, or sexually aroused, little else seems to matter. When we’re not, food, water, sleep, or sex just don’t seem like such big things in life, now or ever.

In studies, people in a motivational “hot” state (from fatigue, hunger, or sexual arousal) have easily recalled such feelings in their own past and have perceived them as driving forces in others’ behavior (Nordgren et al., 2006, 2007). (You may recall from Chapter 8 a parallel effect of our current good or bad mood on our memories.) People in another experiment were given $4 cash they could keep or draw from to bid for foods. Hungry people overbid for a snack they would eat later when sated, and sated people underbid for a snack they would eat later when hungry (Fisher & Rangel, 2014). Grocery shop with an empty stomach and you are more likely to see those jelly-filled doughnuts as just what you’ve always loved and will be wanting tomorrow. Motives matter mightily.

10-5 What physiological factors produce hunger?

Deprived of a normal food supply, Keys’ semistarved volunteers were clearly hungry. 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 10.4). 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 and created 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. So the pangs of an empty stomach are not the only source of hunger. What else might trigger hunger?

Body Chemistry and the Brain

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Somehow, somewhere, your body is keeping tabs on the energy it takes in and the energy it uses. If this weren’t true, you would be unable to maintain a stable body weight. A major source of energy in your body is the blood sugar glucose. If your blood glucose level drops, you won’t consciously feel the lower blood sugar, but your stomach, intestines, and liver will signal your brain to motivate eating. Your brain, which is automatically monitoring your blood chemistry and your body’s internal state, will then trigger hunger.

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 10.5). 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 can’t stop eating and will become obese (Duggan & Booth, 1986; Hoebel & 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). Other appetite hormones include insulin, leptin, orexin, and PYY; FIGURE 10.6 below describes how they influence your feelings of hunger.

The interaction of appetite hormones and brain activity suggests that the body has some sort of “weight thermostat.” When semistarved rats fall below their normal weight, this system 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). Hunger increases and energy output decreases. In this way, rats (and humans) tend to hover around a stable weight, or set point, influenced in part by heredity (Keesey & Corbett, 1983).

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We humans (and other species, too) vary in our basal metabolic rate, a measure of how much energy we use to maintain basic body functions when our body is at rest. But we share a common response to decreased food intake: Our basal metabolic rate drops, as it did for participants in Keys’ experiment. After 24 weeks of semistarvation, they stabilized at three-quarters of their normal weight, although they were taking in half their previous calories. How did their bodies achieve this dieter’s nightmare? They reduced their energy expenditure, partly because they were less active, but partly because their basal metabolic rate dropped by 29 percent.

Some researchers have suggested that the idea of a biologically fixed set point is too rigid to explain some things. One thing it doesn’t address is that slow, sustained changes in body weight can alter a person’s set point (Assanand et al., 1998). Another is that when we have unlimited access to a wide variety of tasty foods, we tend to overeat and gain weight (Raynor & Epstein, 2001). And set points don’t explain why psychological factors influence hunger. For all these reasons, some prefer the looser term settling point to indicate the level at which a person’s weight settles in response to caloric intake and energy use. As we will see next, these factors are influenced by environment as well as biology.

10-6 What cultural and situational factors influence hunger?

Our internal hunger games are pushed by our body chemistry and brain activity. Yet there is more to hunger than meets the stomach. This was strikingly apparent when trickster researchers tested two patients who had no memory for events occurring more than a minute ago (Rozin et al., 1998). If offered a second lunch 20 minutes after eating a normal lunch, both patients readily consumed it … and usually a third meal offered 20 minutes after they finished the second. This suggests that one part of our decision to eat is our memory of the time of our last meal. As time passes, we think about eating again, and those thoughts trigger feelings of hunger.

Taste Preferences: Biology and Culture

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Body cues and environmental factors together influence not only the when of hunger, but also the what—our taste preferences. When feeling tense or depressed, do you tend to take solace in high-calorie foods, as has been found in ardent football fans after a big loss (Cornil & Chandon, 2013)? The carbohydrates in pizza, chips, and sweets help boost levels of the neurotransmitter serotonin, which has calming effects. When stressed, both rats and many humans find it extra rewarding to scarf Oreos (Artiga et al., 2007; Sproesser et al., 2014).

Our preferences for sweet and salty tastes are genetic and universal, but conditioning can intensify or alter those preferences. People given highly salted foods may develop a liking for excess salt (Beauchamp, 1987). People sickened by a food may develop an aversion to it. (The frequency of children’s illnesses provides many chances for them to learn to avoid certain foods.)

Our culture teaches us that some foods are acceptable but others are not. Many Japanese people enjoy nattó, a fermented soybean dish that “smells like the marriage of ammonia and a tire fire,” reports smell expert Rachel Herz (2012). Although many Westerners find this disgusting, Asians, she adds, are often repulsed by what Westerners love—“the rotted bodily fluid of an ungulate” (a.k.a. cheese, some varieties of which have the same bacteria and odor as stinky feet).

But there is biological wisdom to many of our taste preferences. For example, in hot climates (where foods spoil more quickly) recipes often include spices that inhibit bacteria growth (FIGURE 10.7). Pregnancy-related food dislikes—and the nausea associated with them—peak about the tenth week, when the developing embryo is most vulnerable to toxins.

Rats tend to avoid unfamiliar foods (Sclafani, 1995). So do we, especially those that are animal-based. This neophobia (dislike of unfamiliar things) surely was adaptive for our ancestors by protecting them from potentially toxic substances. Disgust works. In time, though, most people who repeatedly sample an initially novel fruit drink or unfamiliar food come to appreciate the new taste (Pliner, 1982, Pliner et al., 1993).

Situational Influences on Eating

To a surprising extent, situations also control our eating—a phenomenon psychologists have called the ecology of eating. Here are five situational influences you may have noticed but underestimated:

10-7 What factors predispose some people to become and remain obese?

Obesity can be socially toxic, by affecting both how you are treated and how you feel about yourself. Obesity has been associated with lower psychological well-being, especially among women, and increased depression (de Wit et al., 2010; Luppino et al., 2010; Riffkin, 2014). Obese 6- to 9-year-olds are 60 percent more likely to suffer bullying (Lumeng et al., 2010). And obesity has physical health risks as well. Yet few overweight people win the battle of the bulge. Why? And why do some people gain weight while others eat the same amount and don’t?

The Physiology of Obesity

Our bodies store fat for good reason. Fat is an ideal form of stored energy—a high-calorie fuel reserve to carry the body through periods when food is scarce—a common occurrence in our prehistoric ancestors’ world. No wonder people in impoverished places have often found heavier bodies attractive. Where food is scarce, plumpness may signal affluence and status (Swami, 2015; Swami et al., 2011).

In parts of the world where food and sweets are now abundantly available, the rule that once served our hungry distant ancestors—When you find energy-rich fat or sugar, eat it!—has become dysfunctional. Pretty much everywhere this book is being read, people have a growing problem. A worldwide study of 188 countries (Ng et al., 2014) revealed that

According to the World Health Organization (WHO), an overweight person has a body mass index (BMI) of 25 or more; someone obese has a BMI of 30 or more. In the United States, the adult obesity rate has more than doubled in the last 40 years, reaching 36 percent, and child-teen obesity has quadrupled (Flegal et al., 2010, 2012). In 1990, no U.S. state had an obesity rate greater than 15 percent. By 2010, no state had an obesity rate of less than 20 percent (CDC, 2012).

In one digest of 97 studies of 2.9 million people, being simply overweight was not a health risk, while being obese was (Flegal et al., 2013). Fitness matters more than being a little overweight. But significant obesity increases the risk of diabetes, high blood pressure, heart disease, gallstones, arthritis, and certain types of cancer, thus increasing health care costs and shortening life expectancy (de Gonzales et al., 2010; Jarrett et al., 2010; Sun et al., 2009). Research also has linked women’s obesity to their risk of late-life cognitive decline, including Alzheimer’s disease and brain tissue loss (Bruce-Keller et al., 2009; Whitmer et al., 2008). One experiment found improved memory performance 12 weeks after severely obese people had weight-loss surgery and lost significant weight. Those not having the surgery showed some further cognitive decline (Gunstad et al., 2011).

SET POINT AND METABOLISM Research on the physiology of obesity challenges the stereotype of severely overweight people being weak-willed gluttons. Once we become fat, we require less food to maintain our weight than we did to attain it. Fat has a lower metabolic rate than does muscle—it takes less food energy to maintain. When an overweight person’s body drops below its previous set (or settling) point, the brain triggers increased hunger and decreased metabolism. The body adapts to what it perceives as starvation by burning off fewer calories and seeking to restore lost weight. Blame your brain for weight regain (Cornier, 2011).

Lean people also seem naturally disposed to move about. They burn more calories than do energy-conserving overweight people, who tend to sit still longer (Levine et al., 2005). Individual differences in resting metabolism help explain why two people of the same height, age, and activity level can maintain the same weight, even if one of them eats much less than does the other.

THE GENETIC FACTOR Do our genes predispose us to eat more or less? To burn more calories by fidgeting or fewer by sitting still? Studies confirm a genetic influence on body weight. Consider two examples:

As with other behavior traits (such as intelligence, sexual orientation, and personality) there is no one “weight gene.” Rather, many genes—including nearly 100 genes identified from a recent DNA analysis of 340,000 people—each contribute small effects (Locke et al., 2015).

THE FOOD AND ACTIVITY FACTORS Genes tell an important part of the obesity story. But environmental factors are mighty important, too.

Studies in Europe, Japan, and the United States show that children and adults who suffer from sleep loss are more vulnerable to obesity (Keith et al., 2006; Nedeltcheva et al., 2010; Taheri, 2004a, b). With sleep deprivation, the levels of leptin (which reports body fat to the brain) fall, and ghrelin (the appetite-stimulating stomach hormone) rise.

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Social influence is another factor. One 32-year study of 12,067 people found them most likely to become obese when a friend became obese (Christakis & Fowler, 2007). If the obese friend was a close one, the odds of likewise becoming obese almost tripled. Moreover, the correlation among friends’ weights was not simply a matter of seeking out similar people as friends. Friends matter.

The strongest evidence that environment influences weight comes from our fattening world (FIGURE 10.8). What explains this growing problem? Changing food consumption and decreased work-related physical activity. We are eating more and moving less, with lifestyles sometimes approaching those of animal feedlots (where farmers fatten inactive animals). Worldwide, 31 percent of adults (including 43 percent of Americans and 25 percent of Europeans) are now sedentary, which means they average less than 20 minutes per day of moderate activity such as walking (Hallal et al., 2012).

The “bottom” line: New stadiums, theaters, and subway cars—but not airplanes—are widening seats to accommodate the girth growth (Hampson, 2000; Kim & Tong, 2010). Washington State Ferries abandoned a 50-year-old standard: “Eighteen-inch butts are a thing of the past” (Shepherd, 1999). New York City, facing a large problem with Big Apple bottoms, has mostly replaced 17.5-inch bucket-style subway seats with bucketless seats (Hampson, 2000). In the end, today’s people need more room.

Note how these findings reinforce a familiar lesson from Chapter 9’s discussion of intelligence: There can be high levels of heritability (genetic influence on individual differences) without heredity explaining group differences. Genes mostly determine why one person today is heavier than another. Environment mostly determines why people today are heavier than their counterparts 50 years ago. Our eating behavior also demonstrates the now-familiar interaction among biological, psychological, and social-cultural factors. For tips on shedding unwanted weight, see TABLE 10.2.

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Learning Objectives

Test Yourself by taking a moment to answer each of these Learning Objective Questions (repeated here from within the chapter). Research suggests that trying to answer these questions on your own will improve your long-term memory of the concepts (McDaniel et al., 2009).

Question

Question

Question

Terms and Concepts to Remember

Test yourself on these terms.

Question

Experience the Testing Effect

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Test yourself repeatedly throughout your studies. This will not only help you figure out what you know and don’t know; the testing itself will help you learn and remember the information more effectively thanks to the testing effect.

Question 10.9

Question 10.10

Question 10.11

Question 10.12

Question 10.13

Question 10.14

Question 10.15

Use to create your personalized study plan, which will direct you to the resources that will help you most in .