As dieters know, physiological needs are powerful. Their strength was vividly demonstrated when Ancel Keys and his research team (1950) did a now-classic study with wartime conscientious objectors. First, they fed 200 adult male volunteers normally for three months. Then, for six months, they cut this food level in half for 36 of them. The effects soon became visible. Without thinking about it, these men began conserving energy. They appeared sluggish and dull. Eventually, their body weights stabilized at about 25 percent below their starting weights.

As Maslow might have guessed, the men became obsessed with food. They talked about it. They daydreamed about it. They collected recipes, read cookbooks, and feasted their eyes on tasty but forbidden food. Focused on their unmet basic need, they lost interest in sex and social activities. One man reported, “If we see a show, the most interesting [parts are] scenes where people are eating. I couldn’t laugh at the funniest picture in the world, and love scenes are completely dull.” As journalist Dorothy Dix (1861–1951) observed, “Nobody wants to kiss when they are hungry.”

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Motives can capture 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. (You may recall from Chapter 7 a parallel effect of our current good or bad mood on our memories.) Shop for food on 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.

Deprived of a normal food supply, Keys’ volunteers were clearly hungry. What triggers hunger? Is it the pangs of an empty stomach? So it seemed to A. L. Washburn. Working with Walter Cannon, Washburn agreed to swallow a balloon that was attached to a recording device (Cannon & Washburn, 1912) (FIGURE 9.4). When inflated to fill his stomach, the balloon tracked his stomach contractions. Washburn supplied information about his feelings of hunger by pressing a key each time he felt a hunger pang. The discovery: When Washburn felt hungry, he was indeed having stomach contractions.

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 stomachs have been removed as a treatment for ulcers or cancer. So the pangs of an empty stomach cannot be the only source of hunger. What else might trigger hunger?

Body Chemistry and the Brain

Somehow, somewhere, your body is keeping tabs on the energy it takes in and the energy it uses. This balancing act enables you to maintain a stable body weight. A major source of energy in your body is the glucose circulating in your bloodstream. If your blood glucose level drops, you won’t consciously feel the lower blood sugar. But your brain, which automatically monitors your blood chemistry and your body’s internal state, will trigger your feeling of hunger.

How does the brain sound the alarm? The work is done by several neural areas, some housed deep in the brain within the hypothalamus (FIGURE 9.5). This neural traffic intersection includes areas that influence eating. In one neural area (called the arcuate nucleus), a center pumps out appetite-stimulating hormones, and another center pumps out appetite-suppressing hormones. When researchers stimulate this appetite-enhancing center, well-fed animals will begin to eat. If they destroy the area, even starving animals lose interest in food. The opposite occurs when the appetite-suppressing area is stimulated: The animal will stop eating. Destroy this area and animals can’t stop eating and will become obese (Duggan & Booth, 1986; Hoebel & Teitelbaum, 1966) (FIGURE 9.6).

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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. When people have 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 9.7 describes how they influence your feelings of hunger.

The interaction of appetite hormones and brain activity suggests that the body has a “weight thermostat.” When semistarved rats fall below their normal weight, this system signals their bodies to restore the lost weight. It’s like fat cells cry out, “Feed me!” and start grabbing glucose from the bloodstream (Ludwig & Friedman, 2014). Hunger increases and energy output decreases. If body weight rises—as happens when rats are force-fed—hunger decreases and energy output increases. In this way, rats (and humans) tend to hover around a stable weight, or set point, influenced in part by heredity (Keesey & Corbett, 1983).

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. So it did for the participants in Keys’ experiment. After 24 weeks of semistarvation, they stabilized at three-quarters of their normal weight, although they were taking in only half their previous calories. How did their bodies achieve this dieter’s nightmare? They reduced the amount of energy they were using—partly by being less active, but partly because their basal metabolic rate dropped by 29 percent.

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Some researchers have suggested that the idea of a biologically fixed set point is too rigid to explain why slow, steady changes in body weight can alter a person’s set point (Assanand et al., 1998), or why, when we have unlimited access to various tasty foods, we tend to overeat and gain weight (Raynor & Epstein, 2001). Thus, some researchers 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, environment matters as well as biology.

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 ate 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 that thought triggers feelings of hunger. Psychological influences on eating behavior affect all of us at some point.

Taste Preferences: Biology and Culture

Both body cues and environment influence our feelings of hunger and what we hunger for—our taste preferences. When feeling tense or depressed, do you crave starchy, carbohydrate-laden foods? High-carb foods, such as pasta, 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. Other taste preferences are learned. People given highly salted foods, for example, develop a liking for excess salt (Beauchamp, 1987). People who become violently ill after eating a particular food often develop a dislike of it. (The frequency of children’s illnesses provides many chances for them to learn to avoid certain foods.)

Our culture teaches us what foods are acceptable. 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). Asians, she adds, are often repulsed by what many 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).

We also may learn to prefer some tastes because they are adaptive. In hot climates, where food spoils more quickly, recipes often include spices that slow the growth of bacteria (FIGURE 9.8). India averages nearly 10 spices per meat recipe, Finland 2 spices. Pregnancy-related food dislikes—and the nausea associated with them—are another example of adaptive taste preferences. These dislikes 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 surely was adaptive for our ancestors by protecting them from potentially toxic substances.

Tempting Situations

Would it surprise you to know that situations also control your eating? Some examples:

Obesity has physical health risks, but it can also be socially toxic, by affecting both how you feel about yourself and how others treat you. In fat-disapproving cultures, obese 6- to 9-year olds are 60 percent more likely to suffer bullying (Lumeng et al., 2010). Adult obesity is linked with lower psychological well-being, increased depression, and discrimination in employment (de Wit et al., 2010; Luppino et al., 2010; Riffkin, 2014). 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 seldom add a pound?

The Survival Value—and Health Risks—of Fat

The answers lie partly in our history. Fat is stored energy. It is a fuel reserve that can carry us through times when food is scarce. (Think of that spare tire around the middle as an energy storehouse—biology’s counterpart to a hiker’s waist-borne snack pack.) In impoverished Europe in earlier centuries, and in parts of the world today, plumpness has signaled wealth and social status (Furnham & Baguma, 1994; Swami, 2015; Swami et al., 2011).

Our hungry distant ancestors were well served by a simple rule: When you find energy-rich fat or sugar, eat it! That rule is no longer adaptive in a world where unhealthy processed foods are abundantly available. Pretty much everywhere this book is being read, people have a growing problem. Worldwide, obesity has more than doubled since 1980, with 1.9 billion adults now overweight. Some 600 million are obese, which is defined as a body mass index (BMI) of 30 or more (Swinburn et al., 2011; WHO, 2015). (See tinyurl.com/GiveMyBMI to calculate your BMI.) In the United States, 36 percent of adults are obese (Flegal et al., 2012).

Significant obesity can shorten your life, reduce your quality of life, and increase your health care costs (Kitahara et al., 2014). It increases the risk of diabetes, high blood pressure, heart disease, gallstones, arthritis, and certain types of cancer. Women’s obesity has been linked to a higher risk of late-life cognitive decline, including Alzheimer’s disease and brain tissue loss (Bruce-Keller et al., 2009; Whitmer et al., 2008). In one experiment, memory performance improved 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).

So why don’t obese people just drop that excess baggage? Because their bodies fight back.

A SLUGGISH METABOLISM Once we become fat, we require less food to maintain our weight than we did to gain it. Compared with muscle tissue, fat has a lower metabolic rate—it takes less food energy to maintain. When an overweight person’s body drops below its previous set (or settling) point, the person’s hunger increases and metabolism decreases. The body adapts to what it perceives as starvation by burning fewer calories. Blame your brain for weight regain (Cornier, 2011).

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Lean people and overweight people differ in their rates of resting metabolism. Lean people seem naturally disposed to move about, and in doing so, they burn more calories. Overweight people tend to sit still longer and conserve their energy (Levine et al., 2005). This helps explain why two people of the same height and age can maintain the same weight, even if one of them eats much more than the other does. (Who said life is fair?)

A GENETIC HANDICAP It’s true: Our genes influence the size of our jeans. Consider:

As with other behavior traits, there is no one “weight gene.” Rather, many genes (including nearly 100 genes identified in a recent study) each contribute small effects (Locke et al., 2015).

SLEEP, FRIENDS, FOOD, ACTIVITY—THEY ALL MATTER! 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 at risk for obesity (Keith et al., 2006; Nedeltcheva et al., 2010; Taheri, 2004; Taheri et al., 2004). Deprived of sleep, our bodies produce less leptin (which reports body fat to the brain) and more ghrelin (the appetite-stimulating stomach hormone).

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). The odds of becoming obese almost tripled when the obese friend was a close one. Moreover, the correlation among friends’ weights was not simply a matter of seeking out similar people as friends.

Friends matter, but evidence that environment influences weight comes from eating disorders research (see Chapter 13), and especially from our fattening world (FIGURE 9.9). What explains this growing problem? Changing food consumption and activity levels are at work. Our lifestyles may now approach those of animal feedlots, where farmers fatten animals by giving them lots of food and little exercise. We are eating more and moving less. In the United States, jobs requiring moderate physical activity declined from about 50 percent in 1960 to 20 percent in 2011 (Church et al., 2011).

Stadiums, theaters, and subway cars—but not airplanes—are widening seats to accommodate the new “bottom” line (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.

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The obesity research findings reinforce a familiar lesson from Chapter 8’s study of intelligence. There can be high levels of heritability (genetic influence on individual differences) without heredity being the only explanation of 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 once again demonstrates one of this book’s big ideas: Biological, psychological, and social-cultural factors interact. We have seen many biological and psychological forces working against those who want to shed excess pounds. Indeed, short of drastic weight-loss surgery, what most people lose on weight-loss programs in the short term they regain in the long run (Mann et al., 2015). For tips on shedding unwanted weight, see TABLE 9.2.

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