Lipostatic theory of weight loss

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.

4

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.

5

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.

6

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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Hours 1 2 3 4 5 6 7 8 9 10 11

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n er

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s Hunger

Meal

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.

30712.3 ■ Factors That Determine What, When, and How Much We Eat

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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

30912.4 ■ Physiological Research on Hunger and Satiety

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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FIGURE 12.8 The locations in the rat brain of the ventro- medial hypothalamus and the lateral hypothalamus.

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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-