Biopsychology Biopsychology

Hunger, Eating, and Health Why Do Many People Eat Too Much?

12.1 Digestion, Energy Storage, and Energy Utilization

12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives

12.3 Factors That Determine What, When, and How Much We Eat

12.4 Physiological Research on Hunger and Satiety

12.5 Body Weight Regulation: Set Points versus Settling Points

12.6 Human Obesity: Causes, Mechanisms, and Treatments

12.7 Anorexia and Bulimia Nervosa

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source of serious personal and health problems. Most eating-related health problems in industrialized

nations are associated with eating too much—the average American consumes 3,800 calories per day, about twice the average daily requirement (see Kopelman, 2000). For

example, it is estimated that 65% of the adult U.S. popu- lation is either overweight or clinically obese, qualifying

this problem for epidemic status (see Abelson & Kennedy, 2004; Arnold, 2009). The resulting financial and personal costs are huge. Each year in the United States, about $100 billion is spent treating obesity-related disorders (see Ol- shansky et al., 2005). Moreover, each year, an estimated 300,000 U.S. citizens die from disorders caused by their excessive eating (e.g., diabetes, hypertension, cardiovas- cular diseases, and some cancers). Although the United States is the trend-setter when it comes to overeating and obesity, many other countries are not far behind (Sofsian, 2007). Ironically, as overeating and obesity have reached epidemic proportions, there has been a related increase in disorders associated with eating too little (see Polivy & Herman, 2002). For example, almost 3% of American adolescents currently suffer from anorexia or bulimia, which can be life-threatening in extreme cases.

The massive increases in obesity and other eating- related disorders that have occurred over the last few decades in many countries stand in direct opposition to most people’s thinking about hunger and eating. Many people—and I assume that this includes you—believe that hunger and eating are normally triggered when the

body’s energy resources fall below a prescribed optimal level, or set point. They ap- preciate that many factors in-

fluence hunger and eating, but they assume that the hunger and eating system has evolved to supply the body with just the right amount of energy.

This chapter explores the incompatibility of the set- point assumption with the current epidemic of eating disorders. If we all have hunger and eating systems

whose primary function is to maintain energy resources at optimal levels, then eating disorders should be rare. The fact that they are so prevalent suggests that hunger and eating are regulated in some other way. This chapter will repeatedly challenge you to think in new ways about issues that impact your health and longevity and will provide new insights of great personal relevance—I guarantee it.

Before you move on to the body of the chapter, I would like you to pause to consider a case study. What would a severely amnesic patient do if offered a meal

shortly after finishing one? If his hunger and eating were controlled by energy set points, he would refuse the sec- ond meal. Did he?

The Case of the Man Who Forgot Not to Eat

R.H. was a 48-year-old male whose progress in graduate school was interrupted by the development of severe am- nesia for long-term explicit memory. His amnesia was similar in pattern and severity to that of H.M., whom you met in Chapter 11, and an MRI examination revealed bilateral damage to the medial temporal lobes.

The meals offered to R.H. were selected on the basis of interviews with him about the foods he liked: veal parmi- giana (about 750 calories) plus all the apple juice he wanted. On one occasion, he was offered a second meal about 15 minutes after he had eaten the first, and he ate it. When offered a third meal 15 minutes later, he ate that, too. When offered a fourth meal he rejected it, claiming that his “stomach was a little tight.”

Then, a few minutes later, R.H. announced that he was going out for a good walk and a meal. When asked what he was going to eat, his answer was “veal parmigiana.”

Clearly, R.H.’s hunger (i.e., motivation to eat) did not result from an energy deficit (Rozin et al., 1998). Other cases like that of R.H. have been reported by Higgs and colleagues (2008).

12.1 Digestion, Energy Storage, and Energy Utilization

The primary purpose of hunger is to increase the proba- bility of eating, and the primary purpose of eating is to supply the body with the molecular building blocks and energy it needs to survive and function (see Blackburn, 2001). This section provides the foundation for our con- sideration of hunger and eating by providing a brief overview of the processes by which food is digested, stored, and converted to energy.

Digestion The gastrointestinal tract and the process of digestion are illustrated in Figure 12.1 on page 300. Digestion is the gastrointestinal process of breaking down food and ab- sorbing its constituents into the body. In order to appre- ciate the basics of digestion, it is useful to consider the body without its protuberances, as a simple living tube

29912.1 ■ Digestion, Energy Storage, and Energy Utilization

Thinking CreativelyThinking Creatively

Clinical Clinical Implications Implications

Eating is a behavior that is of interest to virtuallyeveryone. We all do it, and most of us derive greatpleasure from it. But for many of us, it becomes a

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(a simple sugar that is the breakdown product of complex carbohydrates, that is, starches and sugars).

The body uses energy continuously, but its consump- tion is intermittent; therefore, it must store energy for use in the intervals between meals. Energy is stored in three forms: fats, glycogen, and proteins. Most of the body’s energy reserves are stored as fats, relatively little as glycogen and proteins (see Figure 12.2). Thus, changes in the body weights of adult humans are largely a conse- quence of changes in the amount of their stored body fat.

Why is fat the body’s preferred way of storing energy? Glycogen, which is largely stored in the liver and muscles, might be expected to be the body’s preferred mode of energy storage because it is so readily converted to glucose—the body’s main directly utilizable source of energy. But there

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Chewing breaks up food and mixes it with saliva.1 Saliva lubricates food and begins its digestion.2 Swallowing moves food and drink down the esophagus to the stomach.3 The primary function of the stomach is to serve as a storage reservoir. The

hydrochloric acid in the stomach breaks food down into small particles, and pepsin begins the process of breaking down protein molecules to amino acids.

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The stomach gradually empties its contents through the pyloric sphincter into the

duodenum, the upper portion of the intestine, where most of the absorption takes place.

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Digestive enzymes in the duodenum, many of them from the gall bladder and pancreas,

break down protein molecules to amino acids, and starch and complex sugar molecules to simple sugars. Simple sugars and amino acids readily pass through the duodenum wall into the bloodstream and are carried to the liver.

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Fats are emulsified (broken into droplets) by bile, which is manufactured in the liver and

stored in the gall bladder until it is released into the duodenum. Emulsified fat cannot pass through the duodenum wall and is carried by small ducts in the duodenum wall into the lymphatic system.

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Most of the remaining water and electrolytes are absorbed from the waste in

the large intestine, and the remainder is ejected from the anus.

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Steps in Digestion

Parotid gland

Salivary glands

Esophagus

Liver

Stomach

Gall bladder

Pyloric sphincter

Pancreas

Duodenum

Large intestine or colon

Small intestine

Anus

with a hole at each end. To supply itself with energy and other nutrients, the tube puts food into one of its two holes—the one with teeth—and passes the food along its internal canal so that the food can be broken down and partially absorbed from the canal into the body. The leftovers are jettisoned from the other end. Although this is not a particularly appetizing description of eating, it does serve to illustrate that, strictly speaking, food has not been consumed until it has been digested.

Energy Storage in the Body As a consequence of digestion, energy is delivered to the body in three forms: (1) lipids (fats), (2) amino acids (the breakdown products of proteins), and (3) glucose

FIGURE 12.1 The gastrointestinal tract and the process of digestion.

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are two reasons why fat, rather than glycogen, is the pri- mary mode of energy storage: One is that a gram of fat can store almost twice as much energy as a gram of glyco- gen; the other is that glycogen, unlike fat, attracts and holds substantial quantities of water. Consequently, if all your fat calories were stored as glycogen, you would likely weigh well over 275 kilograms (600 pounds).

Three Phases of Energy Metabolism There are three phases of energy metabolism (the chem- ical changes by which energy is made available for an

organism’s use): the cephalic phase, the absorptive phase, and the fasting phase. The cephalic phase is the preparatory phase; it often begins with the sight, smell, or even just the thought of food, and it ends when the food starts to be absorbed into the bloodstream. The absorptive phase is the period during which the energy absorbed into the bloodstream from the meal is meet- ing the body’s immediate energy needs. The fasting phase is the period during which all of the unstored en- ergy from the previous meal has been used and the body is withdrawing energy from its reserves to meet its immediate energy requirements; it ends with the begin- ning of the next cephalic phase. During periods of rapid weight gain, people often go directly from one absorp- tive phase into the next cephalic phase, without experi- encing an intervening fasting phase.

The flow of energy during the three phases of energy metabolism is controlled by two pancreatic hormones: insulin and glucagon. During the cephalic and absorptive phases, the pancreas releases a great deal of insulin into the bloodstream and very little glucagon. Insulin does three things: (1) It promotes the use of glucose as the pri- mary source of energy by the body. (2) It promotes the conversion of bloodborne fuels to forms that can be stored: glucose to glycogen and fat, and amino acids to proteins. (3) It promotes the storage of glycogen in liver and muscle, fat in adipose tissue, and proteins in muscle. In short, the function of insulin during the cephalic phase is to lower the levels of bloodborne fuels, primarily glucose, in anticipation of the impending influx; and its function during the absorptive phase is to minimize the increasing levels of bloodborne fuels by utilizing and storing them.

In contrast to the cephalic and absorptive phases, the fasting phase is characterized by high blood levels of glucagon and low levels of insulin. Without high levels of insulin, glucose has difficulty entering most body cells; thus, glucose stops being the body’s primary fuel. In effect, this saves the body’s glucose for the brain, because insulin is not required for glucose to enter most brain cells. The low levels of insulin also promote the conversion of glycogen and protein to glucose. (The conversion of protein to glucose is called gluconeogenesis.)

On the other hand, the high levels of fasting-phase glucagon promote the release of free fatty acids from adi- pose tissue and their use as the body’s primary fuel. The high glucagon levels also stimulate the conversion of free fatty acids to ketones, which are used by muscles as a source of energy during the fasting phase. After a pro- longed period without food, however, the brain also starts to use ketones, thus further conserving the body’s re- sources of glucose.

Figure 12.3 summarizes the major metabolic events as- sociated with the three phases of energy metabolism.

30112.1 ■ Digestion, Energy Storage, and Energy Utilization

Fat in adipose tissue (85%)

Protein in muscle (14.5%)

Glycogen in muscle and liver (0.5%)

FIGURE 12.2 Distribution of stored energy in an average person.

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12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives

One of the main difficulties I have in teaching the funda- mentals of hunger, eating, and body weight regulation is the set-point assumption. Although it dominates most people’s thinking about hunger and eating (Assanand, Pinel, & Lehman, 1998a, 1998b), whether they realize it or not, it is inconsistent with the bulk of the evidence. What exactly is the set-point assumption?

Set-Point Assumption Most people attribute hunger (the motivation to eat) to the presence of an energy deficit, and they view eating as the means by which the energy resources of the body are returned to their optimal level—that is, to the energy set point. Figure 12.4 summarizes this set-point assumption. After a meal (a bout of eating), a person’s energy resources are assumed to be near their set point and to decline there- after as the body uses energy to fuel its physiological processes. When the level of the body’s energy resources falls far enough below the set point, a person becomes motivated by hunger to initiate another meal. The meal continues, ac- cording to the set-point assumption, until the energy level

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Cephalic Phase Preparatory phase, which is initiated by the sight, smell, or expectation of food

Absorptive Phase Nutrients from a meal meeting the body’s immediate energy requirements, with the excess being stored

Fasting Phase Energy being withdrawn from stores to meet the body’s immediate needs

Promotes • Utilization of blood glucose as a source

of energy • Conversion of excess glucose to

glycogen and fat • Conversion of amino acids to proteins • Storage of glycogen in liver and muscle,

fat in adipose tissue, and protein in muscle

Inhibits • Conversion of glycogen, fat, and protein

into directly utilizable fuels (glucose, free fatty acids, and ketones)

Promotes • Conversion of fats to free fatty acids

and the utilization of free fatty acids as a source of energy

• Conversion of glycogen to glucose, free fatty acids to ketones, and protein to glucose

Inhibits • Utilization of glucose by the body but

not by the brain • Conversion of glucose to glycogen and

fat, and amino acids to protein • Storage of fat in adipose tissue

Glucagon levels low

Insulin levels high

Glucagon levels high

Insulin levels low

FIGURE 12.3 The major events associated with the three phases of energy metabolism: the cephalic, absorptive, and fasting phases.

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returns to its set point and the person feels satiated (no longer hungry).

Set-point models assume that hunger and eating work in much the same way as a thermostat- regulated heating system in a cool climate. The heater increases the house temperature until it reaches its set point (the thermo- stat setting). The heater then shuts off, and the temperature of the house gradually de- clines until it becomes low enough to turn the heater back on. All set-point systems have three components: a set- point mechanism, a detector mechanism, and an effector mechanism. The set-point mechanism defines the set point, the detector mechanism detects deviations from the set point, and the effector mechanism acts to eliminate the deviations. For example, the set-point, detector, and ef- fector mechanisms of a heating system are the thermo- stat, the thermometer, and the heater, respectively.

All set-point systems are negative feedback systems— systems in which feedback from changes in one direction elicit compensatory effects in the opposite direction. Negative feedback systems are common in mammals be- cause they act to maintain homeostasis—a stable internal environment—which is critical for mammals’ survival (see Wenning, 1999). Set-point systems combine negative feedback with a set point to keep an internal environment fixed at the prescribed point. Set-point systems seemed necessary when the adult human brain was assumed to be immutable: Because the brain couldn’t change, energy re- sources had to be highly regulated. However, we now know that the adult human brain is plastic and capable of considerable adaptation. Thus, there is no longer a logical imperative for the set-point regulation of eating. Through- out this chapter, you will need to put aside your precon- ceptions and base your thinking about hunger and eating entirely on the empirical evidence.

Glucostatic and Lipostatic Set-Point Theories of Hunger and Eating In the 1940s and 1950s, researchers working under the as- sumption that eating is regulated by some type of set- point system speculated about the nature of the regulation. Several researchers suggested that eating is

regulated by a system that is designed to maintain a blood glucose set point—the idea being that we become hungry when our blood glucose levels drop significantly below their set point and that we become satiated when eating returns our blood glucose levels to their set point. The various versions of this theory are collectively referred to as the glucostatic theory. It seemed to make good sense that the main purpose of eating is to defend a blood glu- cose set point, because glucose is the brain’s primary fuel.

The lipostatic theory is another set-point theory that was proposed in various forms in the 1940s and 1950s. According to this theory, every person has a set point for body fat, and deviations from this set point produce com- pensatory adjustments in the level of eating that return levels of body fat to their set point. The most frequently cited support for the theory is the fact that the body weights of adults stay relatively constant.

The glucostatic and lipostatic theories were viewed as complementary, not mutually exclusive. The glucostatic theory was thought to account for meal initiation and ter- mination, whereas the lipostatic theory was thought to account for long-term regulation. Thus, the dominant view in the 1950s was that eating is regulated by the inter- action between two set-point systems: a short-term glu- costatic system and a long-term lipostatic system. The simplicity of these 1950s theories is appealing. Remark- ably, they are still being presented as the latest word in some textbooks; perhaps you have encountered them.

Problems with Set-Point Theories of Hunger and Eating Set-point theories of hunger and eating have several seri- ous weaknesses (see de Castro & Plunkett, 2002). You have already learned one fact that undermines these the- ories: There is an epidemic of obesity and overweight,

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FIGURE 12.4 The energy set-point view that is the basis of many people’s thinking about hunger and eating.

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which should not occur if eating is regulated by a set point. Let’s look at three more major weaknesses of set-

point theories of hunger and eating.

● First, set-point theories of hunger and eating are in- consistent with basic eating-related evolutionary pressures as we understand them. The major eating- related problem faced by our ancestors was the incon-

sistency and unpredictability of the food supply. Thus, in order to survive, it was im- portant for them to eat large quantities of

good food when it was available so that calories could be banked in the form of body fat. Any ancestor— human or otherwise—that stopped feeling hungry as soon as immediate energy needs were met would not have survived the first hard winter or prolonged drought. For any warm-blooded species to survive under natural conditions, it needs a hunger and eating system that prevents energy deficits, rather than one that merely responds to them once they have devel- oped. From this perspective, it is difficult to imagine how a set-point hunger and feeding system could have evolved in mammals (see Pinel, Assanand, & Lehman, 2000).

● Second, major predictions of the set-point theories of hunger and eating have not been confirmed. Early studies seemed to support the set-point theories by showing that large reductions in body fat, produced by starvation, or large reductions in blood glucose, pro- duced by insulin injections, induce increases in eating in laboratory animals. The problem is that reductions in blood glucose of the magnitude needed to reliably induce eating rarely occur naturally. Indeed, as you have already learned in this chapter, about 65% of U.S. adults have a significant excess of fat deposits when they begin a meal. Conversely, efforts to reduce meal size by having subjects consume a high-calorie drink before eating have been largely unsuccessful; indeed, beliefs about the caloric content of a premeal drink often influence the size of a subsequent meal more than does its actual caloric content (see Lowe, 1993).

● Third, set-point theories of hunger and eating are de- ficient because they fail to recognize the major influ- ences on hunger and eating of such important factors as taste, learning, and social influences. To convince yourself of the importance of these factors, pause for a minute and imagine the sight, smell, and taste of your favorite food. Perhaps it is a succulent morsel of lobster meat covered with melted garlic butter, a piece of chocolate cheesecake, or a plate of sizzling home- made french fries. Are you starting to feel a bit hun- gry? If the homemade french fries—my personal weakness—were sitting in front of you right now, wouldn’t you reach out and have one, or maybe the whole plateful? Have you not on occasion felt discomfort

after a large main course, only to polish off a substan- tial dessert? The usual positive answers to these ques- tions lead unavoidably to the conclusion that hunger and eating are not rigidly controlled by deviations from energy set points.

Positive-Incentive Perspective The inability of set-point theories to account for the basic phenomena of eating and hunger led to the development of an alternative theoretical perspective (see Berridge, 2004). The central assertion of this perspective, com- monly referred to as positive-incentive theory, is that humans and other animals are not normally driven to eat by internal energy deficits but are drawn to eat by the an- ticipated pleasure of eating—the anticipated pleasure of a behavior is called its positive-incentive value (see Bolles, 1980; Booth, 1981; Collier, 1980; Rolls, 1981; Toates, 1981). There are several different positive-incentive theo- ries, and I refer generally to all of them as the positive- incentive perspective.

The major tenet of the positive-incentive perspective on eating is that eating is controlled in much the same way as sexual behavior: We engage in sexual behavior not because we have an internal deficit, but because we have evolved to crave it. The evolutionary pressures of unexpected food shortages have shaped us and all other warm-blooded an- imals, who need a continuous supply of energy to main- tain their body temperatures, to take advantage of good food when it is present and eat it. According to the positive- incentive perspective, it is the presence of good food, or the anticipation of it, that normally makes us hungry, not an energy deficit.

According to the positive-incentive perspective, the de- gree of hunger you feel at any particular time depends on the interaction of all the factors that influence the positive- incentive value of eating (see Palmiter, 2007). These in- clude the following: the flavor of the food you are likely to consume, what you have learned about the effects of this food either from eating it previously or from other peo- ple, the amount of time since you last ate, the type and quantity of food in your gut, whether or not other people are present and eating, whether or not your blood glucose levels are within the normal range. This partial list illus- trates one strength of the positive-incentive perspective. Unlike set-point theories, positive-incentive theories do not single out one factor as the major determinant of hunger and ignore the others. Instead, they acknowledge that many factors interact to determine a person’s hunger at any time, and they suggest that this interaction occurs through the influence of these various factors on the positive-incentive value of eating (see Cabanac, 1971).

In this section, you learned that most people think about hunger and eating in terms of energy set points and

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were introduced to an alternative way of thinking—the positive-incentive perspective. Which way is correct? If you are like most people, you have an attachment to familiar ways of thinking and a resistance to new ones. Try to put this tendency aside and base your views about this impor- tant issue entirely on the evidence.

You have already learned about some of the major weaknesses of strict set-point theories of hunger and eat- ing. The next section describes some of the things that biopsychological research has taught us about hunger and eating. As you progress through the section, notice the su- periority of the positive-incentive theories over set-point theories in accounting for the basic facts.

12.3 Factors That Determine What, When, and How Much We Eat

This section describes major factors that commonly deter- mine what we eat, when we eat, and how much we eat. No- tice that energy deficits are not included among these factors. Although major energy deficits clearly increase hunger and eating, they are not a common factor in the eating behavior of people like us, who live in food-replete societies. Although you may believe that your body is short of energy just before a meal, it is not. This miscon- ception is one that is addressed in this section. Also, notice how research on nonhumans has played an important role in furthering understanding of human eating.

Factors That Determine What We Eat Certain tastes have a high positive-incentive value for vir- tually all members of a species. For example, most hu- mans have a special fondness for sweet, fatty, and salty tastes. This species-typical pattern of human taste prefer- ences is adaptive because in nature sweet and fatty tastes

are typically characteristic of high-energy foods that are rich in vitamins and miner- als, and salty tastes are characteristic of

sodium-rich foods. In contrast, bitter tastes, for which most humans have an aversion, are often associated with toxins. Superimposed on our species-typical taste prefer- ences and aversions, each of us has the ability to learn specific taste preferences and aversions (see Rozin & Shulkin, 1990).

Learned Taste Preferences and Aversions Animals learn to prefer tastes that are followed by an infusion of calories, and they learn to avoid tastes that are followed by illness (e.g., Baker & Booth, 1989; Lucas & Sclafani, 1989; Sclafani, 1990). In addition, humans and other animals learn what to eat from their conspecifics. For example,

rats learn to prefer flavors that they experience in mother’s milk and those that they smell on the breath of other rats (see Galef, 1995, 1996; Galef, Whishkin, & Bielavska, 1997). Similarly, in humans, many food prefer- ences are culturally specific—for example, in some cul- tures, various nontoxic insects are considered to be a delicacy. Galef and Wright (1995) have shown that rats reared in groups, rather than in isolation, are more likely to learn to eat a healthy diet.

Learning to Eat Vitamins and Minerals How do an- imals select a diet that provides all of the vitamins and minerals they need? To answer this question, researchers have studied how dietary deficiencies influence diet selec- tion. Two patterns of results have emerged: one for sodium and one for the other essential vitamins and min- erals. When an animal is deficient in sodium, it develops an immediate and compelling preference for the taste of sodium salt (see Rowland, 1990). In contrast, an animal that is deficient in some vitamin or mineral other than sodium must learn to consume foods that are rich in the missing nutrient by experiencing their positive effects; this is because vitamins and minerals other than sodium normally have no detectable taste in food. For example, rats maintained on a diet deficient in thiamine (vitamin B1) develop an aversion to the taste of that diet; and if they are offered two new diets, one deficient in thiamine and one rich in thiamine, they often develop a preference for the taste of the thiamine-rich diet over the ensuing days, as it becomes associated with improved health.

If we, like rats, are capable of learning to select diets that are rich in the vitamins and minerals we need, why are dietary deficiencies so prevalent in our society? One reason is that, in order to maximize profits, manufacturers produce foods that have the tastes we prefer but lack many of the nutrients we need to maintain our health. (Even rats prefer chocolate chip cookies to nutritionally complete rat chow.) The second reason is illustrated by the classic study of Harris and associates (1933). When thiamine-deficient rats were offered two new diets, one with thiamine and one without, almost all of them learned to eat the complete diet and avoid the deficient one. However, when they were offered ten new diets, only one of which contained the badly needed thiamine, few developed a preference for the complete diet. The number of different substances, both nutritious and not, con- sumed each day by most people in industrialized societies is immense, and this makes it difficult, if not impossible, for their bodies to learn which foods are beneficial and which are not.

There is not much about nutrition in this chapter: Although it is critically important to eat a nutritious diet, nutrition seems to have little direct effect on our feelings of hunger. However, while I am on the topic, I would like to direct you to a good source of information

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about nutrition that could have a positive effect on your health: Some popular books on nutrition are dan-

gerous, and even governments, inordinately influenced by economic considerations and special-interest groups, often do not provide the best nutritional advice (see Nestle, 2003). For sound research-based advice on nutrition, check out an article by Willett and Stampfer (2003) and the book on which it is based, Eat, Drink, and Be Healthy by Willett, Skerrett, and Giovannucci (2001).

Factors That Influence When We Eat Collier and his colleagues (see Collier, 1986) found that most mammals choose to eat many small meals (snacks)

each day if they have ready access to a continuous supply of food. Only when there are physical costs involved in initiat-

ing meals—for example, having to travel a considerable distance—does an animal opt for a few large meals.

The number of times humans eat each day is influ- enced by cultural norms, work schedules, family routines, personal preferences, wealth, and a variety of other fac- tors. However, in contrast to the usual mammalian pref- erence, most people, particularly those living in family groups, tend to eat a few large meals each day at regular times. Interestingly, each person’s regular mealtimes are the very same times at which that person is likely to feel most hungry; in fact, many people experience attacks of malaise (headache, nausea, and an inability to concen- trate) when they miss a regularly scheduled meal.

Premeal Hunger I am sure that you have experienced attacks of premeal hunger. Subjectively, they seem to pro- vide compelling support for set-point theories. Your body seems to be crying out: “I need more energy. I cannot function without it. Please feed me.” But things are not al- ways the way they seem. Woods has straightened out the confusion (see Woods, 1991; Woods & Ramsay, 2000; Woods & Strubbe, 1994).

According to Woods, the key to understanding hunger is to appreciate that eating meals stresses the body. Before a meal, the body’s energy reserves are in reasonable homeostatic balance; then, as a meal is consumed, there is a homeostasis-disturbing influx of fuels into the bloodstream. The body does what it can to defend its homeostasis. At the first indication that a person will soon be eating—for example, when the usual mealtime approaches—the body enters the cephalic phase and takes steps to soften the impact of the impending homeostasis- disturbing influx by releasing insulin into the blood and thus reducing blood glucose. Woods’s message is that the strong, unpleasant feelings of hunger that you may expe- rience at mealtimes are not cries from your body for food; they are the sensations of your body’s preparations for the expected homeostasis-disturbing meal. Mealtime

hunger is caused by the expectation of food, not by an en- ergy deficit.

As a high school student, I ate lunch at exactly 12:05 every day and was overwhelmed by hunger as the time approached. Now, my eating schedule is different, and I never experience noontime hunger pangs; I now get hungry just before the time at which I usually eat. Have you had a similar experience?

Pavlovian Conditioning of Hunger In a classic series of Pavlovian conditioning experiments on laboratory rats, Weingarten (1983, 1984, 1985) provided strong sup- port for the view that hunger is often caused by the expec- tation of food, not by an energy deficit. During the conditioning phase of one of his experiments, Weingarten presented rats with six meals per day at irregular inter- vals, and he signaled the impending delivery of each meal with a buzzer-and-light conditional stimulus. This condi- tioning procedure was continued for 11 days. Through- out the ensuing test phase of the experiment, the food was continuously available. Despite the fact that the subjects were never deprived during the test phase, the rats started to eat each time the buzzer and light were presented— even if they had recently completed a meal.

Factors That Influence How Much We Eat The motivational state that causes us to stop eating a meal when there is food remaining is satiety. Satiety mecha- nisms play a major role in determining how much we eat.

Satiety Signals As you will learn in the next section of the chapter, food in the gut and glucose entering the blood can induce satiety signals, which inhibit subse- quent consumption. These signals depend on both the volume and the nutritive density (calories per unit vol- ume) of the food.

The effects of nutritive density have been demon- strated in studies in which laboratory rats have been maintained on a single diet. Once a stable baseline of consumption has been estab- lished, the nutritive density of the diet is changed. Some rats learn to adjust the volume of food they consume to keep their caloric intake and body weights relatively stable. However, there are major limits to this adjustment: Rats rarely increase their intake suffi- ciently to maintain their body weights if the nutritive density of their conventional laboratory feed is reduced by more than 50% or if there are major changes in the diet’s palatability.

Sham Eating The study of sham eating indicates that satiety signals from the gut or blood are not necessary to terminate a meal. In sham-eating experiments, food is chewed and swallowed by the subject; but rather than

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passing down the subject’s esophagus into the stomach, it passes out of the body through an implanted tube (see Figure 12.5).

Because sham eating adds no energy to the body, set-point theories predict that all sham-eaten meals should be huge. But this is not the case. Weingarten and Kulikovsky (1989) sham fed rats one of two differently flavored diets: one that the rats had naturally eaten many times before and one that they had never eaten before. The first sham meal of the rats that had previously eaten the diet was the same size as the previously eaten meals of that diet; then, on ensuing days they began to sham eat more and more (see Figure 12.6). In contrast, the rats that were presented with the unfamiliar diet

sham ate large quantities right from the start. Weingarten and Kulikovsky concluded that the amount we eat is in- fluenced largely by our previous experience with the par- ticular food’s physiological effects, not by the immediate effect of the food on the body.

Appetizer Effect and Satiety The next time you at- tend a dinner party, you may experience a major weak- ness of the set-point theory of satiety. If appetizers are served, you will notice that small amounts of food consumed before a meal actually in- crease hunger rather than reducing it. This is the appetizer effect. Presumably, it occurs because the con- sumption of a small amount of food is particularly effec- tive in eliciting cephalic-phase responses.

Serving Size and Satiety Many experiments have shown that the amount of consumption is influenced by serving size (Geier, Rozin, & Doros, 2006). The larger the servings, the more we tend to eat. There is even evidence that we tend to eat more when we eat with larger spoons.

Social Influences and Satiety Feelings of satiety may also depend on whether we are eating alone or with others. Redd and de Castro (1992) found that their sub- jects consumed 60% more when eating with others. Laboratory rats also eat substantially more when fed in groups.

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FIGURE 12.6 Change in the magnitude of sham eating over repeated sham-eating trials. The rats in one group sham ate the same diet they had eaten before the sham-eating phase; the rats in another group sham ate a diet different from the one they had previously eaten. (Based on Weingarten, 1990.)

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In humans, social factors have also been shown to reduce consumption. Many people eat less than they would like in order to achieve their society’s ideal of slenderness, and others refrain from eating large amounts in front of oth- ers so as not to appear gluttonous. Unfortunately, in our culture, females are influenced by such pressures more than males are, and, as you will learn later in the chapter, some develop serious eating disorders as a result.

Sensory-Specific Satiety The number of different tastes available at each meal has a major effect on meal size. For example, the effect of offering a laboratory rat a varied diet of highly palatable foods—a cafeteria diet—is dramatic. Adults rats that were offered bread and choco- late in addition to their usual laboratory diet increased their average intake of calories by 84%, and after 120 days they had increased their average body weights by 49% (Rogers & Blundell, 1980). The spectacular effects of cafe- teria diets on consumption and body weight clearly run counter to the idea that satiety is rigidly controlled by in- ternal energy set points.

The effect on meal size of cafeteria diets results from the fact that satiety is to a large degree sensory-specific. As you eat one food, the positive-incentive value of all foods de- clines slightly, but the positive-incentive value of that par- ticular food plummets. As a result, you soon become satiated on that food and stop eating it. However, if another food is offered to you, you will often begin eating again.

In one study of sensory-specific satiety (Rolls et al., 1981), human subjects were asked to rate the palatability of eight different foods, and then they ate a meal of one of them. After the meal, they were asked to rate the palata- bility of the eight foods once again, and it was found that their rating of the food they had just eaten had declined substantially more than had their ratings of the other seven foods. Moreover, when the subjects were offered an unexpected second meal, they consumed most of it unless it was the same as the first.

Booth (1981) asked subjects to rate the momentary pleasure produced by the flavor, the smell, the sight, or just the thought of various foods at different times after consuming a large, high-calorie, high-carbohydrate liquid meal. There was an immediate sensory-specific decrease in the palatability of foods of the same or similar flavor as soon as the liquid meal was consumed. This was followed by a general decrease in the palatability of all substances about 30 minutes later. Thus, it appears that signals from taste receptors produce an immediate decline in the positive-incentive value of similar tastes and that signals associated with the postingestive consequences of eating produce a general decrease in the positive-incentive value of all foods.

Rolls (1990) suggested that sensory-specific satiety has two kinds of effects: relatively brief effects that influence the selection of foods within a single meal, and relatively enduring effects that influence the selection of foods from

meal to meal. Some foods seem to be relatively immune to long-lasting sensory-specific satiety; foods such as rice, bread, potatoes, sweets, and green salads can be eaten al- most every day with only a slight decline in their palata- bility (Rolls, 1986).

The phenomenon of sensory-specific satiety has two adaptive consequences. First, it encourages the consump- tion of a varied diet. If there were no sensory-specific sati- ety, a person would tend to eat her or his preferred food and nothing else, and the re- sult would be malnutrition. Second, sensory- specific satiety encourages animals that have access to a variety of foods to eat a lot; an animal that has eaten its fill of one food will often begin eating again if it encoun- ters a different one (Raynor & Epstein, 2001). This en- courages animals to take full advantage of times of abundance, which are all too rare in nature.

This section has introduced you to several important properties of hunger and eating. How many support the set-point assump- tion, and how many are inconsistent with it?

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Are you ready to move on to the discussion of the physiol- ogy of hunger and satiety in the following section? Find out by completing the following sentences with the most appropriate terms. The correct answers are provided at the end of the exercise. Before proceeding, review material related to your incorrect answers and omissions.

1. The primary function of the ______ is to serve as a storage reservoir for undigested food.

2. Most of the absorption of nutrients into the body takes place through the wall of the ______, or upper intestine.

3. The phase of energy metabolism that is triggered by the expectation of food is the ______ phase.

4. During the absorptive phase, the pancreas releases a great deal of ______ into the bloodstream.

5. During the fasting phase, the primary fuels of the body are ______.

6. During the fasting phase, the primary fuel of the brain is ______.

7. The three components of a set-point system are a set-point mechanism, a detector, and an ______.

8. The theory that hunger and satiety are regulated by a blood glucose set point is the ______ theory.

9. Evidence suggests that hunger is greatly influenced by the current ______ value of food.

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10. Most humans have a preference for sweet, fatty, and ______ tastes.

11. There are two mechanisms by which we learn to eat diets containing essential vitamins and minerals: one mechanism for ______ and another mechanism for the rest.

12. Satiety that is specific to the particular foods that produce it is called ______ satiety.

Do the observed reductions in blood glucose before a meal lend support to the glucostatic theory of hunger? I think not, for five reasons:

● It is a simple matter to construct a situation in which drops in blood glucose levels do not precede eating (e.g., Strubbe & Steffens, 1977)—for example, by unex- pectedly serving a food with a high positive-incentive value.

● The usual premeal decreases in blood glucose seem to be a response to the intention to start eating, not the other way round. The premeal decreases in blood glu- cose are typically preceded by increases in blood in- sulin levels, which indicates that the decreases do not reflect gradually declining energy reserves but are actively produced by an increase in blood levels of insulin (see Figure 12.7).

● If an expected meal is not served, blood glucose levels soon return to their previous homeostatic level.

● The glucose levels in the extracellular fluids that sur- round CNS neurons stay relatively constant, even when blood glucose levels drop (see Seeley & Woods, 2003).

● Injections of insulin do not reliably induce eating un- less the injections are sufficiently great to reduce blood glucose levels by 50% (see Rowland, 1981), and large premeal infusions of glucose do not suppress eating (see Geiselman, 1987).

Myth of Hypothalamic Hunger and Satiety Centers In the 1950s, experiments on rats seemed to suggest that eating behavior is controlled by two different re- gions of the hypothalamus: satiety by the ventromedial

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Scan Your Brainanswers: (1) stomach, (2) duodenum, (3) cephalic, (4) insulin, (5) free fatty acids, (6) glucose, (7) effector, (8) glucostatic, (9) positive- incentive, (10) salty, (11) sodium, (12) sensory-specific.

12.4 Physiological Research on Hunger and Satiety

Now that you have been introduced to set-point theories, the positive-incentive perspective, and some basic factors that affect why, when, and how much we eat, this section introduces you to five prominent lines of research on the physiology of hunger and satiety.

Role of Blood Glucose Levels in Hunger and Satiety As I have already explained, efforts to link blood glucose levels to eating have been largely unsuccessful. However, there was a renewed interest in the role of glucose in the regulation of eating in the 1990s, following the develop- ment of methods of continually monitoring blood glucose levels. In the classic experiment of Campfield and Smith (1990), rats were housed individu- ally, with free access to a mixed diet and water, and their blood glucose levels were continually monitored via a chronic intravenous catheter (i.e., a hypodermic needle located in a vein). In this situation, baseline blood glucose levels rarely fluctuated more than 2%. However, about 10 minutes before a meal was initiated, the levels suddenly dropped about 8% (see Figure 12.7).

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hypothalamus (VMH) and feeding by the lateral hypo- thalamus (LH)—see Figure 12.8. This theory turned out to be wrong, but it stimulated several important discoveries.

VMH Satiety Center In 1940, it was discovered that large bilateral electrolytic lesions to the ventromedial hypothala- mus produce hyperphagia (excessive eating) and extreme obesity in rats (Hetherington & Ranson, 1940). This VMH syndrome has two different phases: dynamic and static. The dynamic phase, which begins as soon as the subject regains consciousness after the operation, is characterized by several weeks of grossly excessive eating and rapid weight gain. However, after that, consumption gradually declines to a level that is just sufficient to maintain a stable level of obe- sity; this marks the beginning of the static phase. Figure 12.9 illustrates the weight gain and food intake of an adult rat with bilateral VMH lesions.

The most important feature of the static phase of the VMH syndrome is that the animal maintains its new

body weight. If a rat in the static phase is deprived of food until it has lost a substantial amount of weight, it will re- gain the lost weight once the deprivation ends; conversely, if it is made to gain weight by forced feeding, it will lose the excess weight once the forced feeding is curtailed.

Paradoxically, despite their prodigious levels of con- sumption, VMH-lesioned rats in some ways seem less hungry than unlesioned controls. Although VMH-lesioned rats eat much more than normal rats when palatable food is readily available, they are less willing to work for it (Teitelbaum, 1957) or to consume it if it is slightly un- palatable (Miller, Bailey, & Stevenson, 1950). Weingarten, Chang, and Jarvie (1983) showed that the finicky eating of VMH-lesioned rats is a consequence of their obesity, not a primary effect of their lesion; they are no less likely to consume unpalatable food than are unlesioned rats of equal obesity.

LH Feeding Center In 1951,Anand and Brobeck reported that bilateral electrolytic lesions to the lateral hypothala- mus produce aphagia—a complete cessation of eating. Even rats that were first made hyperphagic by VMH le- sions were rendered aphagic by the addition of LH le- sions. Anand and Brobeck concluded that the lateral region of the hypothalamus is a feeding center. Teitelbaum and Epstein (1962) subsequently discovered two impor- tant features of the LH syndrome. First, they found that the aphagia was accompanied by adipsia—a complete cessa- tion of drinking. Second, they found that LH-lesioned rats partially recover if they are kept alive by tube feeding. First, they begin to eat wet, palatable foods, such as chocolate chip cookies soaked in milk, and eventually they will eat dry food pellets if water is concurrently available.

Reinterpretation of the Effects of VMH and LH Lesions The theory that the VMH is a satiety center crumbled in the face of two lines of evidence. One of these lines showed that the primary role of the hypothalamus is the regulation of energy metabolism, not the regulation of eating. The initial interpretation was that VMH-lesioned animals become obese because they overeat; however, the evidence suggests the converse—that they overeat because they become obese. Bilateral VMH le- sions increase blood insulin levels, which increases lipogenesis (the pro- duction of body fat) and decreases lipolysis (the break- down of body fat to utilizable forms of energy)—see Powley et al. (1980). Both are likely to be the result of the increases in insulin levels that occur following the lesion. Because the calories ingested by VMH-lesioned rats are converted to fat at a high rate, the rats must keep eating to ensure that they have enough calories in their blood to meet their immediate energy requirements (e.g., Hustvedt & Løvø, 1972); they are like misers who run to the bank each time they make a bit of money and deposit it in a sav- ings account from which withdrawals cannot be made.

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The second line of evidence that undermined the theory of a VMH satiety center has shown that many of the effects of VMH lesions are not at- tributable to VMH damage. A large fiber bundle, the ventral noradrener- gic bundle, courses past the VMH and is thus inevitably damaged by large electrolytic VMH lesions; in particu- lar, fibers that project from the nearby paraventricular nuclei of the hypothalamus are damaged (see Figure 12.10). Bilateral lesions of the noradrenergic bundle (e.g., Gold et al., 1977) or the paraventricular nu- clei (Leibowitz, Hammer, & Chang, 1981) produce hyperphagia and obe- sity, just as VMH lesions do.

Most of the evidence against the notion that the LH is a feeding cen-

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ter has come from a thorough analysis of the effects of bi- lateral LH lesions. Early research focused exclusively on the aphagia and adipsia that are produced by LH lesions, but subsequent research has shown that LH lesions pro- duce a wide range of severe motor disturbances and a general lack of responsiveness to sensory input (of which food and drink are but two examples). Consequently, the idea that the LH is a center specifically dedicated to feed- ing no longer warrants serious consideration.

Role of the Gastrointestinal Tract in Satiety One of the most influential early studies of hunger was published by Cannon and Washburn in 1912. It was a perfect collaboration: Cannon had the ideas, and Wash- burn had the ability to swallow a balloon. First, Washburn swallowed an empty balloon tied to the end of a thin tube. Then, Cannon pumped some air into the balloon and connected the end of the tube to a water-filled glass U-tube so that Washburn’s stomach contractions pro- duced a momentary increase in the level of the water at

FIGURE 12.10 Location of the paraventricular nucleus in the rat hypothalamus. Note that the section through the hypothala- mus is slightly different than the one in Figure 12.8.

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the other end of the U-tube. Washburn re- ported a “pang” of hunger each time that a large stomach contraction was recorded (see Figure 12.11).

Cannon and Washburn’s finding led to the theory that hunger is the feeling of contractions caused by an empty stomach, whereas satiety is the feeling of stomach dis- tention. However, support for this theory and interest in the role of the gastroin- testinal tract in hunger and satiety quickly waned with the discovery that human pa- tients whose stomach had been surgically removed and whose esophagus had been hooked up directly to their duodenum (the first segment of the small intestine, which normally carries food away from the stomach) continued to report feelings of hunger and satiety and continued to maintain their normal body weight by eating more meals of smaller size.

In the 1980s, there was a resurgence of interest in the role of the gastrointestinal tract in eating. It was stimulated by a se- ries of experiments that indicated that the gastrointestinal tract is the source of satiety signals. For example, Koopmans (1981) transplanted an extra stomach and length of intes- tine into rats and then joined the major arteries and veins of the implants to the recipients’ circulatory systems (see Figure 12.12). Koopmans found that food injected into the transplanted stomach and kept there by a noose around the pyloric sphincter decreased eating in propor- tion to both its caloric content and volume. Because the transplanted stomach had no functional nerves, the gas- trointestinal satiety signal had to be reaching the brain through the blood. And because nutrients are not ab- sorbed from the stomach, the bloodborne satiety signal could not have been a nutrient. It had to be some chemi- cal or chemicals that were released from the stomach in response to the caloric value and volume of the food— which leads us nicely into the next subsection.

Hunger and Satiety Peptides Soon after the discovery that the stomach and other parts of the gastrointestinal tract release chemical signals to the brain, evidence began to accumulate that these chemicals

were peptides, short chains of amino acids that can func- tion as hormones and neurotransmitters (see Fukuhara et al., 2005). Ingested food interacts with receptors in the gastrointestinal tract and in so doing causes the tract to release peptides into the bloodstream. In 1973, Gibbs, Young, and Smith injected one of these gut peptides, cholecystokinin (CCK), into hungry rats and found that they ate smaller meals. This led to the hypothesis that circulating gut peptides provide the brain with information about the quantity and nature of food in the gastrointestinal tract and that this information plays a role in satiety (see Bad- man & Flier, 2005; Flier, 2006).

There has been considerable support for the hypothesis that peptides can function as satiety signals (see Gao & Horvath, 2007; Ritter, 2004). Several gut peptides have been shown to bind to receptors in the brain, particularly in areas of the hypothalamus involved in energy metabolism, and a dozen or so (e.g., CCK, bombesin, glucagon, alpha- melanocyte-stimulating hormone, and somatostatin) have been reported to reduce food intake (see Batterham et al., 2006; Zhang et al., 2005). These have become known as satiety peptides (peptides that decrease appetite).

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FIGURE 12.11 The system developed by Cannon and Washburn in 1912 for measuring stomach contractions. They found that large stomach contractions were related to pangs of hunger.

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In studying the appetite-reducing effects of peptides, researchers had to rule out the possibility that these ef- fects are not merely the consequence of illness (see Moran, 2004). Indeed, there is evidence that one pep- tide in particular, CCK, induces illness: CCK adminis- tered to rats after they have eaten an unfamiliar substance induces a conditioned taste aversion for that substance, and CCK induces nausea in human subjects. However, CCK reduces appetite and eating at doses substantially below those that are required to induce taste aversion in rats, and thus it qualifies as a legitimate satiety peptide.

Several hunger peptides (peptides that increase appetite) have also been discovered. These peptides tend to be syn- thesized in the brain, particularly in the hypothalamus. The most widely studied of these are neuropeptide Y, galanin, orexin-A, and ghrelin (e.g., Baird, Gray, & Fischer, 2006; Olszewski, Schiöth & Levine, 2008; Williams et al., 2004).

The discovery of the hunger and satiety peptides has had two major effects on the search for the neural mechanisms of hunger and satiety. First, the sheer number of these hunger and satiety peptides indicates

that the neural system that controls eating likely reacts to many different signals (Nogueiras & Tschöp, 2005; Schwartz & Azzara, 2004), not just to one or two (e.g., not just to glucose and fat). Second, the discovery that many of the hunger and satiety peptides have receptors in the hypothalamus has renewed interest in the role of the hypothalamus in hunger and eating (Gao & Horvath, 2007; Lam, Schwartz, & Rossetti, 2006; Luquet et al., 2005). This interest was further stimulated by the dis- covery that microinjection of gut peptides into some sites in the hypothalamus can have major effects on eat- ing. Still, there is a general acceptance that hypothalamic circuits are only one part of a much larger system (see Berthoud & Morrison, 2008; Cone, 2005).

Serotonin and Satiety The monoaminergic neurotransmitter serotonin is an- other chemical that plays a role in satiety. The initial evi- dence for this role came from a line of research in rats. In these studies, serotonin- produced satiety was found to have three major properties (see Blundell & Halford, 1998):

● It caused the rats to resist the powerful attraction of highly palatable cafeteria diets.

● It reduced the amount of food that was consumed during each meal rather than reducing the number of meals (see Clifton, 2000).

● It was associated with a shift in food preferences away from fatty foods.

This profile of effects suggested that serotonin might be useful in combating obesity in humans. Indeed, serotonin agonists (e.g., fenfluramine, dexfenfluramine, fluoxetine) have been shown to reduce hunger, eating, and body weight under some conditions (see Blundell & Halford, 1998). Later in this chapter, you will learn about the use of serotonin to treat human obesity (see De Vry & Schreiber, 2000).

Prader-Willi Syndrome: Patients with Insatiable Hunger Prader-Willi syndrome could prove critical in the discov- ery of the neural mechanisms of hunger and satiety (Goldstone, 2004). Individuals with Prader-Willi syn- drome, which results from an accident of chromosomal replication, experience insatiable hunger, little or no sati- ety, and an exceptionally slow metabolism. In short, the Prader-Willi patient acts as though he or she is starving. Other common physical and neurological symptoms in- clude weak muscles, small hands and feet, feeding diffi- culties in infancy, tantrums, compulsivity, and skin picking. If untreated, most patients become extremely obese, and they often die in early adulthood from dia- betes, heart disease, or other obesity-related disorders. Some have even died from gorging until their stomachs

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FIGURE 12.12 Transplantation of an extra stomach and length of intestine in a rat. Koopmans (1981) im- planted an extra stomach and length of intestine in each of his experimental subjects. He then connected the major blood vessels of the implanted stomachs to the circulatory systems of the recipients. Food injected into the extra stomach and kept there by a noose around the pyloric sphincter decreased eating in pro- portion to its volume and caloric value.

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split open. Fortunately, Miss A. was diagnosed in infancy and received excellent care, which kept her from becom- ing obese (Martin et al., 1998).

Prader-Willi Syndrome: The Case of Miss A.

Miss A. was born with little muscle tone. Because her sucking reflex was so weak, she was tube fed. By the time she was 2 years old, her hypotonia (below-normal muscle tone) had resolved itself, but a number of characteristic deformities and developmental delays began to appear.

At 31/2 years of age, Miss A. suddenly began to display a voracious appetite and quickly gained weight. Fortu- nately, her family maintained her on a low-calorie diet and kept all food locked away.

Miss A. is moderately retarded, and she suffers from psychiatric problems. Her major problem is her tendency to have tantrums any time anything changes in her envi- ronment (e.g., a substitute teacher at school). Thanks largely to her family and pediatrician, she has received ex- cellent care, which has minimized the complications that arise with Prader-Willi syndrome—most notably those related to obesity and its pathological effects.

Although the study of Prader-Willi syndrome has yet to provide any direct evidence about the neural mecha- nisms of hunger and eating, there has been a marked surge in its investigation. This increase has been stimu- lated by the recent identification of the genetic cause of the condition: an accident of reproduction that deletes or disrupts a section of chromosome 15 coming from the fa- ther. This information has provided clues about genetic factors in appetite.

12.5 Body Weight Regulation: Set Points versus Settling Points

One strength of set-point theories of eating is that they explain body weight regulation. You have already learned that set-point theories are largely inconsistent with the facts of eating, but how well do they account for the reg- ulation of body weight? Certainly, many people in our culture believe that body weight is regulated by a body-fat set point (Assanand, Pinel, & Lehman, 1998a, 1998b). They believe that when fat deposits are below a person’s set point, a person becomes hungrier and eats more, which results in a return of body-fat levels to that person’s set point; and, conversely, they believe that when fat de- posits are above a person’s set point, a person becomes less hungry and eats less, which results in a return of body-fat levels to their set point.

Set-Point Assumptions about Body Weight and Eating You have already learned that set-point theories do a poor job of explaining the characteristics of hunger and eating. Do they do a better job of accounting for the facts of body weight regulation? Let’s begin by looking at three lines of evidence that challenge fundamental aspects of many set- point theories of body weight regulation.

Variability of Body Weight The set-point model was expressly designed to explain why adult body weights re- main constant. Indeed, a set-point mechanism should make it virtually impossible for an adult to gain or lose large amounts of weight. Yet, many adults experience large and lasting changes in body weight (see Booth, 2004). Moreover, set-point thinking crumbles in the face of the epidemic of obesity that is currently sweeping fast- food societies (Rosenheck, 2008).

Set-point theories of body weight regulation suggest that the best method of maintaining a constant body weight is to eat each time there is a motivation to eat, be- cause, according to the theory, the main function of hunger is to defend the set point. However, many people avoid obesity only by resisting their urges to eat.

Set Points and Health One implication of set-point theories of body weight regulation is that each person’s set point is optimal for that person’s health—or at least not incompatible with good health. This is why popular psychologists commonly advise people to “listen to the wisdom of their bodies” and eat as much as they need to satisfy their hunger. Experimental results indicate that this common prescription for good health could not be further from the truth.

Two kinds of evidence suggest that typical ad libitum (free-feeding) levels of consumption are unhealthy (see Brownell & Rodin, 1994). First are the results of studies of humans who consume fewer calories than others. For ex- ample, people living on the Japanese island of Okinawa seemed to eat so few calories that their eating habits be- came a concern of health officials. When the health offi- cials took a closer look, here is what they found (see Kagawa, 1978). Adult Okinawans were found to consume, on average, 20% fewer calories than other adult Japanese, and Okinawan school children were found to consume 38% fewer calories than recommended by public health officials. It was somewhat surprising then that rates of morbidity and mortality and of all aging-related diseases were found to be substantially lower in Okinawa than in other parts of Japan, a country in which overall levels of caloric intake and obesity are far below Western norms. For example, the death rates from stroke, cancer, and heart disease in Okinawa were only 59%, 69%, and 59%, respectively, of those in the rest of Japan. Indeed, the pro- portion of Okinawans living to be over 100 years of age

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was up to 40 times greater than that of inhabitants of var- ious other regions of Japan.

The Okinawan study and the other studies that have reported major health benefits in humans who eat less (e.g., Manson et al., 1995; Meyer et al., 2006; Walford &

Walford, 1994) are not controlled experiments; therefore, they must be interpreted with caution. For ex-

ample, perhaps it is not simply the consumption of fewer calories that leads to health and longevity; per- haps in some cultures people who eat less tend to eat healthier diets.

Controlled experimental demonstrations in over a dozen different mammalian species, including monkeys (see Coleman et al., 2009), of the beneficial effects of calo-

rie restriction constitute the second kind of evidence that ad libitum levels of con- sumption are unhealthy. Fortunately, the

results of such controlled experiments do not present the same problems of interpretation as do the findings of the Okinawa study and other similar correlational studies in humans. In typical calorie-restriction experiments, one group of subjects is allowed to eat as much as they choose, while other groups of subjects have their caloric intake of the same diets substantially reduced (by between 25% and 65% in various studies). Results of such experiments have been remarkably consistent (see Bucci, 1992; Masoro, 1988; Weindruch, 1996; Weindruch & Walford, 1988): In experiment after experiment, substantial reductions in the caloric intake of balanced diets have improved nu- merous indices of health and increased longevity. For ex- ample, in one experiment (Weindruch et al., 1986), groups of mice had their caloric intake of a well-balanced commercial diet reduced by either 25%, 55%, or 65% after weaning. All levels of dietary restriction substantially improved health and increased longevity, but the benefits

were greatest in the mice whose intake was reduced the most. Those mice that con- sumed the least had the lowest incidence of

cancer, the best immune responses, and the greatest maxi- mum life span—they lived 67% longer than mice that ate as much as they liked. Evidence suggests that dietary restriction can have beneficial effects even if it is not initi- ated until later in life (Mair et al., 2003; Vaupel, Carey, & Christensen, 2003).

One important point about the results of the calorie- restriction experiments is that the health benefits of the restricted diets may not be entirely attributable to loss of body fat (see Weindruch, 1996). In some dietary restric- tion studies, the health of subjects has improved even if they did not reduce their body fat, and there are often no significant correlations between amount of weight loss and improvements in health. This suggests excessive en- ergy consumption, independent of fat accumulation, may accelerate aging with all its attendant health problems (Lane, Ingram, & Roth, 2002; Prolla & Mattson, 2001).

Remarkably, there is evidence that dietary restriction can be used to treat some neurological conditions. Caloric restriction has been shown to reduce seizure susceptibility in human epileptics (see Maalouf, Rho, & Mattson, 2008) and to improve memory in the elderly (Witte et al., 2009). Please stop and think about the impli- cations of all these findings about calorie restriction. How much do you eat?

Regulation of Body Weight by Changes in the Effi- ciency of Energy Utilization Implicit in many set- point theories is the premise that body weight is largely a function of how much a person eats. Of course, how much someone eats plays a role in his or her body weight, but it is now clear that the body controls its fat levels, to a large degree, by changing the efficiency with which it uses energy. As a person’s level of body fat declines, that person starts to use energy resources more efficiently, which lim- its further weight loss (see Martin, White, & Hulsey, 1991); conversely, weight gain is limited by a progressive decrease in the efficiency of energy utilization. Rothwell and Stock (1982) created a group of obese rats by main- taining them on a cafeteria diet, and they found that the resting level of energy expenditure in these obese rats was 45% greater than in control rats.

This point is illustrated by the progressively declining effectiveness of weight-loss programs. Initially, low-calorie diets produce substantial weight loss. But the rate of weight loss diminishes with each successive week on the diet, until an equilibrium is achieved and little or no fur- ther weight loss occurs. Most dieters are familiar with this disappointing trend. A similar effect occurs with weight- gain programs (see Figure 12.13 on page 316).

The mechanism by which the body adjusts the effi- ciency of its energy utilization in response to its levels of body fat has been termed diet-induced thermogenesis. Increases in the levels of body fat produce increases in body temperature, which require additional energy to maintain them—and decreases in the level of body fat have the opposite effects (see Lazar, 2008).

There are major differences among humans both in basal metabolic rate (the rate at which energy is utilized to maintain bodily processes when resting) and in the ability to adjust the metabolic rate in response to changes in the levels of body fat. We all know people who remain slim even though they eat gluttonously. However, the re- search on calorie-restricted diets suggests that these peo- ple may not eat with impunity: There may be a health cost to pay for overeating even in the absence of obesity.

Set Points and Settling Points in Weight Control The theory that eating is part of a system designed to de- fend a body-fat set point has long had its critics (see

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Booth, Fuller, & Lewis, 1981; Wirtshafter & Davis, 1977), but for many years their arguments were largely ignored and the set-point assumption ruled. This situa- tion has been changing: Several promi- nent reviews of research on hunger and weight regulation generally acknowledge that a strict set-point model cannot ac-

count for the facts of weight regulation, and they argue for a more

flexible model (see Berthoud, 2002; Mercer & Speakman, 2001; Woods et al., 2000). Because the body-fat set-point model still dominates the thinking of many people, I want to review the main advantages of an alternative and more flexible regulatory model: the settling-point model. Can you change your thinking?

According to the settling-point model, body weight tends to drift around a natu- ral settling point—the level at which the various factors that influence body weight achieve an equilibrium. The idea is that as body-fat levels increase, changes occur that tend to limit further increases until a balance is achieved between all factors that encourage weight gain and all those that discourage it.

The settling-point model provides a loose kind of homeostatic regulation, without a set-point mechanism or mechanisms to return body weight to a set point. Ac- cording to the settling-point model, body weight remains stable as long as there are no long-term changes in the factors that influence it; and if there are such changes, their impact is limited by negative feedback. In the settling- point model, the negative feedback merely limits further changes in the same direction, whereas in the set-point model, negative feedback triggers a return to the set point. A neuron’s resting potential is a well-known bio- logical settling point—see Chapter 4.

The seductiveness of the set-point mechanism is attrib- utable in no small part to the existence of the thermostat model, which provides a vivid means of thinking about it. Figure 12.14 presents an analogy I like to use to think about the settling-point mechanism. I call it the leaky-barrel model: (1) The amount of water entering the hose is analogous to the amount of food available to the subject; (2) the water pressure at the nozzle is analogous to the

positive-incentive value of the available food; (3) the amount of water entering the barrel is analogous to the amount of

energy consumed; (4) the water level in the barrel is analo- gous to the level of body fat; (5) the amount of water leak- ing from the barrel is analogous to the amount of energy being expended; and (6) the weight of the barrel on the hose is analogous to the strength of the satiety signal.

The main advantage of the settling-point model of body weight regulation over the body-fat set-point model is that it is more consistent with the data. Another advan- tage is that in those cases in which both models make the same prediction, the settling-point model does so more parsimoniously—that is, with a simpler mechanism that requires fewer assumptions. Let’s use the leaky-barrel analogy to see how the two models account for four key facts of weight regulation.

● Body weight remains relatively constant in many adult animals. On the basis of this fact, it has been argued that body fat must be regulated around a set point. However, constant body weight does not require, or even imply, a set point. Consider the leaky-barrel model. As water from the tap begins to fill the barrel, the weight of the water in the barrel increases. This in- creases the amount of water leaking out of the barrel and decreases the amount of water entering the barrel by increasing the pressure of the barrel on the hose. Eventually, this system settles into an equilibrium where the water level stays constant; but because this level is neither predetermined nor actively defended, it is a settling point, not a set point.

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● Many adult animals experience enduring changes in body weight. Set-point systems are designed to main- tain internal constancy in the face of fluctuations of the external environment. Thus, the fact that many adult animals experience long-term changes in body weight is a strong argument against the set-point model. In contrast, the settling-point model predicts that when there is an enduring change in one of the parameters that affect body weight—for example, a major increase in the positive-incentive value of available food—body weight will drift to a new settling point.

● If a subject’s intake of food is reduced, metabolic changes that limit the loss of weight occur; the oppo- site happens when the subject overeats. This fact is often cited as evidence for set-point regulation of body weight; however, because the metabolic changes merely limit further weight changes rather than eliminating those that have occurred, they are more consistent with a settling-point model. For example, when water intake in the leaky-barrel model is reduced, the water

level in the barrel begins to drop; but the drop is lim- ited by a decrease in leakage and an increase in inflow attributable to the falling water pressure in the barrel. Eventually, a new settling point is achieved, but the re- duction in water level is not as great as one might ex- pect because of the loss-limiting changes.

● After an individual has lost a substantial amount of weight (by dieting, exercise, or the surgical removal of fat), there is a tendency for the original weight to be re- gained once the subject returns to the previous eating- and energy-related lifestyle. Although this finding is often offered as irrefutable evidence of a body-weight set point, the settling-point model readily accounts for it. When the water level in the leaky-barrel model is reduced—by temporarily decreasing input (dieting), by temporarily increasing output (exercising), or by scoop- ing out some of the water (surgical removal of fat)— only a temporary drop in the settling point is produced. When the original conditions are reinstated, the water level inexorably drifts back to the original settling point.

31712.5 ■ Body Weight Regulation: Set Points versus Settling Points

1The amount of water entering the hose is analogous to the amount of available food.

2 The water pressure at the nozzle is analogous to the incentive value of the available food.

3 The amount of water entering the barrel is analogous to the amount of consumed energy.

4 The water level in the barrel is analogous to the level of body fat.

5 The amount of water leaking from the barrel is analogous to the amount of energy being expended.

6 The weight of the barrel on the hose is analogous to the strength of the satiety signal.

FIGURE 12.14 The leaky-barrel model: a settling-point model of eating and body weight homeostasis.

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Does it really matter whether we think about body weight regulation in terms of set points or settling points— or is making such a distinction just splitting hairs? It cer- tainly matters to biopsychologists: Understanding that

body weight is regulated by a settling- point system helps them better under- stand, and more accurately predict,

the changes in body weight that are likely to occur in vari- ous situations; it also indicates the kinds of physiological mechanisms that are likely to mediate these changes. And it should matter to you. If the set-point model is correct, at- tempting to change your body weight would be a waste of time; you would inevitably be drawn back to your body- weight set point. On the other hand, the leaky-barrel model suggests that it is possible to permanently change your body weight by permanently changing any of the factors that influence energy intake and output.

11. ______ models are more consistent with the facts of body-weight regulation than are set-point models.

12. ______ are to set points as leaky barrels are to settling points.

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Are you ready to move on to the final two sections of the chapter, which deal with eating disorders? This is a good place to pause and scan your brain to see if you under- stand the physiological mechanisms of eating and weight regulation. Complete the following sentences by filling in the blanks. The correct answers are provided at the end of the exercise. Before proceeding, review material related to your incorrect answers and omissions.

1. The expectation of a meal normally stimulates the release of ______ into the blood, which reduces blood glucose.

2. In the 1950s, the ______ hypothalamus was thought to be a satiety center.

3. A complete cessation of eating is called ______. 4. ______ is the breakdown of body fat to create usable

forms of energy. 5. The classic study of Washburn and Cannon was the

perfect collaboration: Cannon had the ideas, and Washburn could swallow a ______.

6. CCK is a gut peptide that is thought to be a ______ peptide.

7. ______ is the monoaminergic neurotransmitter that seems to play a role in satiety.

8. Okinawans eat less and live ______. 9. Experimental studies of ______ have shown that typi-

cal ad libitum (free-feeding) levels of consumption are unhealthy in many mammalian species.

10. As an individual grows fatter, further weight gain is minimized by diet-induced ______.

Scan Your Brainanswers: (1) insulin, (2) ventromedial, (3) aphagia, (4) Lipolysis, (5) balloon, (6) satiety, (7) Serotonin, (8) longer, (9) calorie restriction, (10) thermogenesis, (11) Settling-point, (12) Thermostats.

12.6 Human Obesity: Causes, Mechanisms, and Treatments

This is an important point in this chapter. The chapter opened by describing the current epidemic of obesity and overweight and its adverse effects on health and longevity and then went on to discuss behavioral and physiological factors that influence eating and weight. Most importantly, as the chapter progressed, you learned that some common beliefs about eating and weight regulation are incompati- ble with the evidence, and you were challenged to think about eating and weight regulation in unconventional ways that are more consistent with current evidence. Now, the chapter completes the circle with two sections on eat- ing disorders: This section focuses on obesity, and the next covers anorexia and bulimia. I hope that by this point you realize that obesity is currently a major health problem and will appreciate the relevance of what you are learning to your personal life and the lives of your loved ones.

Who Needs to Be Concerned about Obesity? Almost everyone needs to be concerned about the prob- lem of obesity. If you are currently overweight, the reason for concern is obvious: The relation between obesity and poor health has been repeatedly documented (see Eilat- Adar, Eldar, & Goldbourt, 2005; Ferrucci & Alley, 2007; Flegal et al., 2007; Hjartåker et al., 2005; Stevens, McClain, & Truesdale, 2006). Moreover, some studies have shown that even individuals who are only a bit overweight run a greater risk of developing health problems (Adams et al., 2006; Byers, 2006; Jee et al., 2006), as do obese individuals who manage to keep their blood pressure and blood cho- lesterol at normal levels (Yan et al., 2006). And the risk is not only to one’s own health: Obese women are at in- creased risk of having infants with health problems (Nohr et al., 2007).

Even if you are currently slim, there is cause for con- cern about the problem of obesity. The incidence of obe- sity is so high that it is almost certain to be a problem for somebody you care about. Furthermore, because weight tends to increase substantially with age, many people who are slim as youths develop serious weight problems as they age.

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There is cause for special concern for the next genera- tion. Because rates of obesity are increasing in most parts of the world (Rosenheck, 2008; Sofsian, 2007), public health officials are concerned about how they are going to handle the growing problem. For example, it has been es- timated that over one-third of the children born in the United States in 2000 will eventually develop diabetes, and 10% of these will develop related life-threatening conditions (see Haslam, Sattar, & Lean, 2006; Olshansky et al., 2005).

Why Is There an Epidemic of Obesity? Let’s begin our analysis of obesity by considering the pressures that are likely to have led to the evolution of our eating and weight-regulation systems (see Flier & Maratos-Flier, 2007; Lazar, 2005; Pinel et al., 2000). Dur-

ing the course of evolution, inconsistent food supplies were one of the main threats to survival. As a result, the fittest individu-

als were those who preferred high-calorie foods, ate to ca- pacity when food was available, stored as many excess calories as possible in the form of body fat, and used their stores of calories as efficiently as possible. Individuals who did not have these characteristics were unlikely to survive a food shortage, and so these characteristics were passed on to future generations.

The development of numerous cultural practices and beliefs that promote consumption has augmented the ef- fects of evolution. For example, in my culture, it is com- monly believed that one should eat three meals per day at regular times, whether one is hungry or not; that food should be the focus of most social gatherings; that meals should be served in courses of progressively increasing palatability; and that salt, sweets (e.g., sugar), and fats (e.g., butter or cream) should be added to foods to im- prove their flavor and thus increase their consumption.

Each of us possesses an eating and weight-regulation system that evolved to deal effectively with periodic food shortages, and many of us live in cultures whose eating- related practices evolved for the same purpose. However, our current environment differs from our “natural” envi- ronment in critical food-related ways. We live in an envi- ronment in which an endless variety of foods of the highest positive-incentive and caloric value are readily and continuously available. The consequence is an ap- pallingly high level of consumption.

Why Do Some People Become Obese While Others Do Not? Why do some people become obese while others living under the same obesity-promoting conditions do not? At a superficial level, the answer is obvious: Those who are obese are those whose energy intake has exceeded their energy output; those who are slim are those whose energy intake

has not exceeded their energy output (see Nestle, 2007). Although this answer provides little insight, it does serve to emphasize that two kinds of individual differences play a role in obesity: those that lead to differences in energy input and those that lead to differences in energy output.

Differences in Consumption There are many factors that lead some people to eat more than others who have comparable access to food. For example, some people consume more energy because they have strong prefer- ences for the taste of high-calorie foods (see Blundell & Finlayson, 2004; Epstein et al., 2007); some consume more because they were raised in families and/or cultures that promote excessive eating; and some consume more because they have particu- larly large cephalic-phase re- sponses to the sight or smell of food (Rodin, 1985).

Differences in Energy Expenditure With respect to energy output, people differ markedly from one another in the degree to which they can dissipate excess consumed energy. The most obvious difference is that people differ substantially in the amount of exercise they get; however, there are others. You have already learned about two of them: differences in basal metabolic rate and in the ability to react to fat increases by diet-induced thermogenesis. The third factor is called NEAT, or nonexercise activity thermo- genesis, which is generated by activities such as fidgeting and the maintenance of posture and muscle tone (Ravussin & Danforth, 1999) and can play a small role in dissipating excess energy (Levine, Eberhardt, & Jensen, 1999; Ravussin, 2005).

Genetic Differences Given the number of factors that can influence food consumption and energy metabolism, it is not surprising that many genes can influence body weight. Indeed, over 100 human chromosome loci (regions) have already been linked to obesity (see Fischer et al., 2009; Rankinen et al., 2006). However, because body weight is influenced by so many genes, it is proving difficult to under- stand how their interactions with one another and with ex- perience contribute to obesity in healthy people. Although it is proving difficult to unravel the various genetic factors that influence variations in body weight among the healthy, single gene mutations have been linked to pathological con- ditions that involve obesity. You will encounter an example of such a condition later in this section.

Why Are Weight-Loss Programs Typically Ineffective? Figure 12.15 describes the course of the typical weight- loss program. Most weight-loss programs are unsuccess- ful in the sense that, as predicted by the settling-point model, most of the lost weight is regained once the dieter

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stops following the program and the original conditions are reestablished. The key to permanent weight loss is a permanent lifestyle change.

Exercise has many health-promoting effects; however, despite the general belief that exercise is the most effective method of losing weight, several studies have shown that it often contributes little to weight loss (e.g., Sweeney et al., 1993). One reason is that physical exercise normally accounts for only a small proportion of total en- ergy expenditure: About 80% of the energy you expend is used to maintain the resting physiological processes of your body and to digest your food (Calles-Escandon & Horton, 1992). Another reason is that our bodies are effi- cient machines, burning only a small number of calories during a typical workout. Moreover, after exercise, many people feel free to consume extra drinks and foods that contain more calories than the relatively small number that were expended during the exercise.

Leptin and the Regulation of Body Fat Fat is more than a passive storehouse of energy; it actively releases a peptide hormone called leptin. The discovery of leptin has been extremely influential (see Elmquist & Flier, 2004). The following three subsections describe (1) the discovery of leptin, (2) how its discovery has fu- eled the development of a new approach to the treatment

of human obesity, and (3) how the understanding that leptin (and insulin) are feedback signals led to the discov- ery of a hypothalamic nucleus that plays an important role in the regulation of body fat.

Obese Mice and the Discovery of Leptin In 1950, a spontaneous genetic mutation occurred in the mouse colony being maintained in the Jackson Laboratory at Bar Harbor, Maine. The mutant mice were homozygous for the gene (ob), and they were grossly obese, weighing up to three times as much as typical mice. These mutant mice are commonly referred to as ob/ob mice. See Figure 12.16.

Ob/ob mice eat more than control mice; they convert calories to fat more efficiently; and they use their calories more efficiently. Coleman (1979) hypothesized that ob/ob mice lack a critical hormone that normally inhibits fat production and maintenance.

In 1994, Friedman and his colleagues characterized and cloned the gene that is mutated in ob/ob mice (Zhang et al., 1994). They found that this gene is expressed only in fat cells, and they characterized the protein that it nor- mally encodes, a peptide hormone that they named leptin. Because of their mutation, ob/ob mice lack leptin. This finding led to an exciting hypothesis: Perhaps leptin is a negative feedback signal that is normally released from fat

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1 Weight lossoccurs rapidly at beginning of diet

2 As weightdeclines, the amount of energy “leakage” is automatically reduced, and this reduces the rate of weight loss

3 Gradually thereduced rate of intake is matched by the reduced energy output, and a new stable settling point is achieved

4 When the dietis terminated, weight gain is rapid because of the high incentive value of food and the low level of energy leakage

5 As weightaccumulates, the incentive value of food gradually decreases and the energy leakage increases until the original settling point is regained

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stores to decrease appetite and increase fat metabolism. Could leptin be administered to obese humans to reverse the current epidemic of obesity?

Leptin, Insulin, and the Arcuate Melanocortin System There was great fanfare when leptin was dis- covered. However, it was not the first peptide hormone to be discovered that seems to function as a negative feed- back signal in the regulation of body fat (see Schwartz, 2000; Woods, 2004). More than 25 years ago, Woods and colleagues (1979) suggested that the pancreatic peptide hormone insulin serves such a function.

At first, the suggestion that insulin serves as a negative feedback signal for body fat regulation was viewed with skepticism. After all, how could the level of insulin in the body, which goes up and then comes back down to nor- mal following each meal, provide the brain with infor- mation about gradually changing levels of body fat? It turns out that insulin does not readily penetrate the blood–brain barrier, and its levels in the brain were found to stay relatively stable—indeed, high levels of glu- cose are toxic to neurons (Tomlinson & Gardiner, 2008). The following findings supported the hypothesis that in- sulin serves as a negative feedback signal in the regula- tion of body fat:

● Brain levels of insulin were found to be positively cor- related with levels of body fat (Seeley et al., 1996).

● Receptors for insulin were found in the brain (Baura et al., 1993).

● Infusions of insulin into the brains of laboratory ani- mals were found to reduce eating and body weight (Campfield et al., 1995; Chavez, Seeley, & Woods, 1995).

Why are there two fat feedback signals? One reason may be that leptin levels are more closely correlated with subcutaneous fat (fat stored under the skin), whereas insulin levels are more closely correlated with visceral

fat (fat stored around the internal organs of the body cavity)—see Hug & Lodish (2005). Thus, each fat signal provides different information. Visceral fat is more common in males than females and poses the greater threat to health (Wajchenberg, 2000). Insulin, but not leptin, is also involved in glucose regulation (see Schwartz & Porte, 2005).

The discovery that leptin and insulin are signals that provide information to the brain about fat levels in the body provided a means for discovering the neural cir- cuits that participate in fat regulation. Receptors for both peptide hormones are located in many parts of the nervous system, but most are in the hypothalamus, par- ticularly in one area of the hypothalamus: the arcuate nucleus.

A closer look at the distribution of leptin and insulin receptors in the arcuate nucleus indicated that these re- ceptors are not randomly distributed throughout the nu- cleus. They are located in two classes of neurons: neurons that release neuropeptide Y (the gut hunger peptide that you read about earlier in the chapter), and neurons that release melanocortins, a class of peptides that includes the gut satiety peptide α-melanocyte-stimulating hormone (alpha-melanocyte-stimulating hormone). Attention has been mostly focused on the melanocortin-releasing neurons in the arcuate nucleus (often referred to as the melanocortin system) because injections of α-melanocyte-stimulating hormone have been shown to suppress eating and pro- mote weight loss (see Horvath, 2005; Seeley & Woods, 2003). It seems, however, that the melanocortin system is only a minor component of a much larger system: Elimi- nation of leptin receptors in the melanocortin system produces only a slight weight gain (see Münzberg & Myers, 2005).

Leptin as a Treatment for Human Obesity The early studies of leptin seemed to confirm the hypothesis that it could function as an effective treatment for obesity. Re- ceptors for leptin were found in the brain, and injecting it into ob/ob mice reduced both their eating and their body fat (see Seeley & Woods, 2003). All that remained was to prove leptin’s effectiveness in human patients.

However, when research on leptin turned from ob/ob mice to obese humans, the program ran into two major snags. First, obese humans—unlike ob/ob mice—were found to have high, rather than low, levels of leptin (see Münzberg & Myers, 2005). Second, injections of leptin did not reduce either the eating or the body fat of obese humans (see Heymsfield et al., 1999).

Why the actions of leptin are different in humans and ob/ob mice has yet to be explained. Nevertheless, efforts to use leptin in the treatment of human obesity have not been a total failure. Although few obese humans have a genetic mutation to the ob gene, leptin is a panacea for those few who do. Consider the following case.

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FIGURE 12.16 An ob/ob mouse and a control mouse.

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The Case of the Child with No Leptin

The patient was of normal weight at birth, but her weight soon began to increase at an excessive rate. She demanded food continually and was disruptive when denied food. As a result of her extreme obesity, deformities of her legs de- veloped, and surgery was required.

She was 9 when she was referred for treatment. At this point, she weighed 94.4 kilograms (about 210 pounds), and her weight was still increasing at an alarming rate. She was found to be homozygous for the ob gene and had no detectable leptin. Thus, leptin therapy was com- menced.

The leptin therapy immediately curtailed the weight gain. She began to eat less, and she lost weight steadily over the 12-month period of the study, a total of 16.5 kilograms (about 36 pounds), almost all in the form of fat. There were no obvious side effects (Farooqi et al., 1999).

Treatment of Obesity Because obesity is such a severe health problem, there have been many efforts to develop an effective treatment. Some of these—such as the leptin treatment you just read about—have worked for a few, but the problem of obesity continues to grow. The following two subsections discuss two treatments that are at different stages of de- velopment: serotonergic agonists and gastric surgery.

Serotonergic Agonists Because—as you have already learned—serotonin agonists have been shown to reduce food consumption in both human and nonhuman sub- jects, they have considerable potential in the treatment of obesity (Halford & Blundell, 2000a). Serotonin agonists seem to act by a mechanism different from that for leptin and insulin, which produce long-term satiety signals based on fat stores. Serotonin agonists seem to increase short-term satiety signals associated with the consump- tion of a meal (Halford & Blundell, 2000b).

Serotonin agonists have been found in various studies of obese patients to reduce the following: the urge to eat high- calorie foods, the consumption of fat, the subjective inten-

sity of hunger, the size of meals, the number of between-meal snacks, and bingeing. Because of this extremely posi-

tive profile of effects and the severity of the obesity problem, serotonin agonists (fenfluramine and dexfenfluramine) were rushed into clinical use. However, they were subse- quently withdrawn from the market because chronic use was found to be associated with heart disease in a small, but significant, number of users. Currently, the search is on for serotonergic weight-loss medications that do not have dan- gerous side effects.

Gastric Surgery Cases of extreme obesity sometimes warrant extreme treatment. Gastric bypass is a surgical treatment for extreme obesity that involves short-circuiting the normal path of food through the digestive tract so that its absorption is reduced. The first gastric bypass was done in 1967, and it is currently the most commonly pre- scribed surgical treatment for extreme obesity. An alter- native is the adjustable gastric band procedure, which involves surgically positioning a hollow silicone band around the stomach to reduce the flow of food through it; the circumference of the band can be adjusted by inject- ing saline into the band through a port that is implanted in the skin. One advantage of the gastric band over the gastric bypass is that the band can readily be removed.

The gastric bypass and adjustable gastric band are illustrated in Figure 12.17. A meta-analysis of studies comparing the two procedures found both to be highly effective (Maggard et al., 2005). However, neither proce- dure is effective unless patients change their eating habits.

12.7 Anorexia and Bulimia Nervosa

In contrast to obesity, anorexia nervosa is a disorder of underconsumption (see Södersten, Bergh, & Zandian, 2006). Anorexics eat so little that they experience health- threatening weight loss; and despite their emaciated appearance, they often perceive themselves as fat (see Benning- hoven et al., 2006). Anorexia nervosa is a serious condition; In approximately 10% of diagnosed cases, complications from starvation result in death (Birmingham et al., 2005), and there is a high rate of suicide among anorexics (Pompili et al., 2004).

Anorexia nervosa is related to bulimia nervosa. Bulimia nervosa is a disorder characterized by periods of not eating interrupted by bingeing (eating huge amounts of food in short periods of time) followed by efforts to immediately eliminate the consumed calories from the body by voluntary purging (vomiting); by excessive use of laxatives, enemas, or diuretics; or by extreme exercise. Bu- limics may be obese or of normal weight. If they are un- derweight, they are diagnosed as bingeing anorexics.

Relation between Anorexia and Bulimia Are anorexia nervosa and bulimia nervosa really different disorders, as current convention dictates? The answer to this question depends on one’s perspective. From the perspec- tive of a physician, it is important to distinguish between these disorders because starvation pro- duces different health problems than does repeated bingeing and purging.

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For example, anorexics often require treatment for reduced metabolism, bradycardia (slow heart rate), hypotension (low blood pressure), hypothermia (low body temperature), and anemia (deficiency of red blood cells) (Miller et al., 2005). In contrast, bulimics often require treatment for irritation and inflammation of the esophagus, vitamin and mineral defi- ciencies, electrolyte imbalance, dehydration, and acid reflux.

Although anorexia and bulimia nervosa may seem like very different disorders from a physician’s perspective, sci- entists often find it more appropriate to view them as vari- ations of the same disorder. According to this view, both anorexia and bulimia begin with an obsession about body image and slimness and extreme efforts to lose weight. Both anorexics and bulimics attempt to lose weight by strict diet- ing, but bulimics are less capable of controlling their ap- petites and thus enter into a cycle of starvation, bingeing, and purging (see Russell, 1979). The following are other similarities that support the view that anorexia and bulimia are variants of the same disorder (see Kaye et al., 2005):

● Both anorexics and bulimics tend to have distorted body images, seeing themselves as much fatter and

less attractive than they are in reality (see Grant et al., 2002).

● In practice, many patients seem to straddle the two di- agnoses and cannot readily be assigned to one or the other categories and many patients flip-flop between the two diagnoses as their circumstances change (Lask & Bryant-Waugh, 2000; Santonastaso et al., 2006; Ten- coni et al., 2006).

● Anorexia and bulimia show the same pattern of distri- bution in the population. Although their overall inci- dence in the population is low (lifetime incidence estimates for American adults are 0.6% and 1.0% for anorexia and bulimia, respectively; Hudson et al., 2007), both conditions occur more commonly among educated females in affluent cultural groups (Lind- berg & Hjern, 2003).

● Both anorexia and bulimia are highly correlated with obsessive-compulsive disorder and depression (Kaye et al., 2004; O’Brien & Vincent, 2003).

● Neither disorder responds well to existing therapies. Short-term improvements are common, but relapse is usual (see Södersten et al., 2006).

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From esophagus From esophagusStaples create a smaller stomach pouch

Stitches

Stitches

Skin

To colon To colon

Staples

Adjustable band slows passage of food through stomach

Skin

Access port to inflatable band

Gastric Bypass Adjustable Gastric Band

FIGURE 12.17 Two surgical methods for treating extreme obesity: gastric bypass and adjustable gastric band. The gastric band can be tightened by injecting saline into the access port implanted just beneath the skin.

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Anorexia and Positive Incentives The positive-incentive perspective on eating suggests that the decline in eating that defines both anorexia (and bulimia) is likely a consequence of a corresponding de- cline in the positive-incentive value of food. However, the

positive-incentive value of food for anorexia patients has received little attention—in part, because anorexic

patients often display substantial interest in food. The fact that many anorexic patients are obsessed with food— continually talking about it, thinking about it, and preparing it for others (Crisp, 1983)—seems to suggest that food still holds a high positive-incentive value for them. However, to avoid confusion, it is necessary to keep in mind that the positive-incentive value of interacting with food is not necessarily the same as the positive-incentive value of eating food—and it is the positive-incentive value of eating food that is critical when considering anorexia nervosa.

A few studies have examined the positive-incentive value of various tastes in anorexic patients (see, e.g., Drewnowski et al., 1987; Roefs et al., 2006; Sunday & Halmi, 1990). In general, these studies have found that the positive-incentive value of various tastes is lower in anorexic patients than in control participants. However, these studies grossly under- estimate the importance of reductions in the positive- incentive value of food in the etiology of anorexia nervosa, because the anorexic participants and the normal-weight control participants were not matched for weight—such matching is not practical.

We can get some insight into the effects of starvation on the positive-incentive value of food by studying starva- tion. That starvation normally triggers a radical increase in the positive-incentive value of food has been best docu- mented by the descriptions and behavior of participants voluntarily undergoing experimental semistarvation. When asked how it felt to starve, one participant replied:

I wait for mealtime. When it comes I eat slowly and make the food last as long as possible. The menu never gets mo- notonous even if it is the same each day or is of poor quality. It is food and all food tastes good. Even dirty crusts of bread in the street look appetizing. (Keys et al., 1950, p. 852)

Anorexia Nervosa: A Hypothesis The dominance of set-point theories in research into the regulation of hunger and eating has resulted in wide- spread inattention to one of the major puzzles of anorexia: Why does the adaptive massive increase in the positive-incentive value of eating that occurs in victims of starvation not occur in starving anorexics? Under condi- tions of starvation, the positive-incentive value of eating normally increases to such high levels that it is difficult to imagine how anybody who was starving—no matter how

controlled, rigid, obsessive, and motivated that person was—could refrain from eating in the presence of palat- able food. Why this protective mechanism is not activated in severe anorexics is a pressing question about the etiol- ogy of anorexia nervosa.

I believe that part of the answer lies in the research of Woods and his colleagues on the aversive physiological effects of meals. At the beginning of meals, people are nor- mally in reasonably homeostatic bal- ance, and this homeostasis is disrupted by the sudden infusion of calories. The other part of the answer lies in the finding that the aversive effects of meals are much greater in people who have been eating little (Brooks & Melnik, 1995). Meals, which produce adverse, but tolerable, effects in healthy individuals, may be extremely aversive for individuals who have undergone food deprivation. Evidence for the extremely noxious effects that eating meals has on starving humans is found in the re- actions of World War II concentration camp victims to refeeding—many were rendered ill and some were even killed by the food given to them by their liberators (Keys et al., 1950; see also Soloman & Kirby, 1990).

So why do severe anorexics not experience a massive in- crease in the positive-incentive value of eating, similar to the increase experienced by other starving individuals? The answer may be meals—meals forced on these patients as a result of the misconception of our society that meals are the healthy way to eat. Each meal consumed by an anorexic may produce a variety of conditioned taste aversions that reduce the motivation to eat. This hypothesis needs to be addressed because of its implication for treatment: Anorexic patients—or anybody else who is severely under- nourished—should not be encouraged, or even permitted, to eat meals. They should be fed—or infused with—small amounts of food intermittently throughout the day.

I have described the preceding hypothesis to show you the value of the new ideas that you have encountered in this chapter: The major test of a new theory is whether it leads to innovative hypotheses. A while ago, as I was perusing an article on global famine and malnutrition, I noticed an in- triguing comment: One of the clinical complications that results from feeding meals to famine victims is anorexia (Blackburn, 2001). What do you make of this?

The Case of the Anorexic Student In a society in which obesity is the main disorder of con- sumption, anorexics are out of step. People who are struggling to eat less have difficulty understanding those who have to struggle to eat. Still, when you stare anorexia in the face, it is diffi- cult not to be touched by it.

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She began by telling me how much she had been enjoy- ing the course and how sorry she was to be dropping out of the university. She was articulate and personable, and her grades were high—very high. Her problem was anorexia; she weighed only 82 pounds, and she was about to be hospitalized.

“But don’t you want to eat?” I asked naively.“Don’t you see that your plan to go to medical school will go up in smoke if you don’t eat?”

“Of course I want to eat. I know I am terribly thin— my friends tell me I am. Believe me, I know this is wreck- ing my life. I try to eat, but I just can’t force myself. In a strange way, I am pleased with my thinness.”

She was upset, and I was embarrassed by my insensi- tivity. “It’s too bad you’re dropping out of the course be- fore we cover the chapter on eating,” I said, groping for safer ground.

“Oh, I’ve read it already,” she responded. “It’s the first chapter I looked at. It had quite an effect on me; a lot of things started to make more sense. The bit about posi-

tive incentives and learning was really good. I think my problem began when eating started to lose its positive- incentive value for me—in my mind, I kind of associ- ated eating with being fat and all the boyfriend problems I was having. This made it easy to diet, but every once in a while I would get hungry and binge, or my parents would force me to eat a big meal. I would eat so much that I would feel ill. So I would put my fin- ger down my throat and make myself throw up. This kept me from gaining weight, but I think it also taught my body to associate my favorite foods with illness— kind of a conditioned taste aversion. What do you think of my theory?”

Her insightfulness impressed me; it made me feel all the more sorry that she was going to discontinue her studies. After a lengthy chat, she got up to leave, and I walked her to the door of my office. I wished her luck and made her promise to come back for a visit. I never saw her again, but the image of her emaciated body walking down the hallway from my office has stayed with me.

325Think about It

Themes Revisited

Three of the book’s four themes played prominent roles in this chapter. The thinking creatively theme was prevalent as you were challenged to critically evaluate your own beliefs and ambiguous research findings, to consider the

scientific implications of your own experiences, and to think in new ways about phenomena with major personal

and clinical implications. The chapter ended by using these new ideas to develop a potentially important hypothesis about the etiology of anorexia nervosa. Because of its emphasis on thinking, this chapter is my personal favorite.

Both aspects of the evolutionary perspective theme were emphasized repeatedly. First, you saw how thinking about hunger and eating from an evolutionary perspective leads to important insights. Second, you saw how controlled research on nonhuman species has contributed to our current understanding of human hunger and eating.

Finally, the clinical implications theme pervaded the chapter, but it was featured in the cases of the man who forgot not to eat, the child with Prader-Willi syndrome, the child with no leptin, and the anorexic student.

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Think about It

1. Set-point theories suggest that attempts at permanent weight loss are a waste of time. On the basis of what you have learned in this chapter, design an effective and per- manent weight-loss program.

2. Most of the eating-related health problems of people in our society occur because the conditions in which we live are different from those in which our species evolved. Discuss.

3. On the basis of what you have learned in this chapter, de- velop a feeding program for laboratory rats that would lead to obesity. Compare this program with the eating habits prevalent in your culture.

4. What causes anorexia nervosa? Summarize the evidence that supports your view.

5. Given the weight of evidence, why is the set-point theory of hunger and eating so prevalent?

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Biopsychology Biopsychology homewotk help

326 Chapter 12 ■ Hunger, Eating, and Health

Set point (p. 299)

12.1 Digestion, Energy Storage, and Energy Utilization Digestion (p. 299) Lipids (p. 300) Amino acids (p. 300) Glucose (p. 300) Cephalic phase (p. 301) Absorptive phase (p. 301) Fasting phase (p. 301) Insulin (p. 301) Glucagon (p. 301) Gluconeogenesis (p. 301) Free fatty acids (p. 301) Ketones (p. 301)

12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives Set-point assumption (p. 302) Negative feedback systems

(p. 303)

Homeostasis (p. 303) Glucostatic theory (p. 303) Lipostatic theory (p. 303) Positive-incentive theory

(p. 304) Positive-incentive value (p. 304)

12.3 Factors That Determine What, When, and How Much We Eat Satiety (p. 306) Nutritive density (p. 306) Sham eating (p. 306) Appetizer effect (p. 307) Cafeteria diet (p. 308) Sensory-specific satiety (p. 308)

12.4 Physiological Research on Hunger and Satiety Ventromedial hypothalamus

(VMH) (p. 309) Lateral hypothalamus (LH)

(p. 310) Hyperphagia (p. 310)

Dynamic phase (p. 310) Static phase (p. 310) Aphagia (p. 310) Adipsia (p. 310) Lipogenesis (p. 310) Lipolysis (p. 310) Paraventricular nuclei (p. 311) Duodenum (p. 312) Cholecystokinin (CCK) (p. 312) Prader-Willi syndrome (p. 313)

12.5 Body Weight Regulation: Set Points versus Settling Points Diet-induced thermogenesis

(p. 315) Basal metabolic rate (p. 315) Settling point (p. 316) Leaky-barrel model (p. 316)

12.6 Human Obesity: Causes, Mechanisms, and Treatments NEAT (p. 319) Leptin (p. 320)

Ob/ob mice (p. 320) Subcutaneous fat (p. 321) Visceral fat (p. 321) Arcuate nucleus (p. 321) Neuropeptide Y (p. 321) Melanocortins (p. 321) Melanocortin system (p. 321) Gastric bypass (p, 322) Adjustable gastric band

procedure (p. 322)

12.7 Anorexia and Bulimia Nervosa Anorexia nervosa (p. 322) Bulimia nervosa (p. 322)

Key Terms

Test your comprehension of the chapter with this brief practice test. You can find the answers to these questions as well as more practice tests, activities, and other study resources at www.mypsychlab.com.

1. The phase of energy metabolism that often begins with the sight, the smell, or even the thought of food is the a. luteal phase. b. absorptive phase. c. cephalic phase. d. fasting phase. e. none of the above

2. The ventromedial hypothalamus (VH) was once believed to be a. part of the hippocampus. b. a satiety center. c. a hunger center. d. static. e. dynamic.

3. Patients with Prader-Willi syndrome suffer from a. anorexia nervosa. b. bulimia. c. an inability to digest fats. d. insatiable hunger. e. lack of memory for eating.

4. In comparison to obese people, slim people tend to a. have longer life expectancies. b. be healthier. c. be less efficient in their use of body energy. d. all of the above e. both a and b

5. Body fat releases a hormone called a. leptin. b. glucagon. c. insulin. d. glycogen. e. serotonin.

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