REFRENCE This Course text book in the assignment many citations thank you
Pinel, J. P. (10/2010). Biopsychology, 8th Edition [VitalSource Bookshelf version]. Retrieved from http://online.vitalsource.com/books/9781269533744
12 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
Eating is a behavior that is of interest to virtually everyone. We all do it, and most of us derive great pleasure from it. But for many of us, it becomes a source of serious personal and health problems.
You Are What You Eat
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. population 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 Olshansky 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, cardiovascular 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.
Thinking about Hunger
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 appreciate that many factors influence 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 second 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 amnesia 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 parmigiana (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 probability 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 consideration of hunger and eating by providing a brief overview of the processes by which food is digested, stored, and converted to energy.
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 absorbing its constituents into the body. In order to appreciate the basics of digestion, it is useful to consider the body without its protuberances, as a simple living tube 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.
FIGURE 12.1 The gastrointestinal tract and the process of digestion.
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 (a simple sugar that is the breakdown product of complex carbohydrates, that is, starches and sugars).
The body uses energy continuously, but its consumption 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 consequence 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 are two reasons why fat, rather than glycogen, is the primary mode of energy storage: One is that a gram of fat can store almost twice as much energy as a gram of glycogen; 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).
FIGURE 12.2 Distribution of stored energy in an average person.
Three Phases of Energy Metabolism
There are three phases of energy metabolism (the chemical 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 meeting the body’s immediate energy needs. The fasting phase is the period during which all of the unstored energy 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 beginning of the next cephalic phase. During periods of rapid weight gain, people often go directly from one absorptive phase into the next cephalic phase, without experiencing 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 primary 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 adipose 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 prolonged period without food, however, the brain also starts to use ketones, thus further conserving the body’s resources of glucose.
Figure 12.3 summarizes the major metabolic events associated with the three phases of energy metabolism.
FIGURE 12.3 The major events associated with the three phases of energy metabolism: the cephalic, absorptive, and fasting phases.
12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives
One of the main difficulties I have in teaching the fundamentals 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?
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 thereafter 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, according to the set-point assumption, until the energy level returns to its set point and the person feels satiated (no longer hungry).
FIGURE 12.4 The energy set-point view that is the basis of many people’s thinking about hunger and eating.
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 thermostat setting). The heater then shuts off, and the temperature of the house gradually declines 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 effector mechanisms of a heating system are the thermostat, 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 because 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 resources 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. Throughout this chapter, you will need to put aside your preconceptions 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 assumption 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 glucose 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 compensatory 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 termination, 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 interaction between two set-point systems: a short-term glucostatic system and a long-term lipostatic system. The simplicity of these 1950s theories is appealing. Remarkably, 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 serious weaknesses (see de Castro & Plunkett, 2002). You have already learned one fact that undermines these theories: There is an epidemic of obesity and overweight, 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 inconsistent with basic eating-related evolutionary pressures as we understand them. The major eating-related problem faced by our ancestors was the inconsistency and unpredictability of the food supply. Thus, in order to survive, it was important 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 developed. 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, produced 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 deficient because they fail to recognize the major influences 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 homemade french fries. Are you starting to feel a bit hungry? 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 substantial dessert? The usual positive answers to these questions lead unavoidably to the conclusion that hunger and eating are not rigidly controlled by deviations from energy set points.
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, commonly 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 anticipated 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 theories, 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 animals, who need a continuous supply of energy to maintain 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 degree 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 include 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 people, 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 illustrates 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 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 important issue entirely on the evidence.
You have already learned about some of the major weaknesses of strict set-point theories of hunger and eating. 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 superiority 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 determine what we eat, when we eat, and how much we eat. Notice 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 misconception 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 virtually all members of a species. For example, most humans have a special fondness for sweet, fatty, and salty tastes. This species-typical pattern of human taste preferences is adaptive because in nature sweet and fatty tastes are typically characteristic of high-energy foods that are rich in vitamins and minerals, 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 preferences 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 preferences are culturally specific—for example, in some cultures, 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 animals 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 selection. Two patterns of results have emerged: one for sodium and one for the other essential vitamins and minerals. 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, consumed 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 about nutrition that could have a positive effect on your health: Some popular books on nutrition are dangerous, 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 initiating 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 influenced by cultural norms, work schedules, family routines, personal preferences, wealth, and a variety of other factors. However, in contrast to the usual mammalian preference, 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 concentrate) when they miss a regularly scheduled meal.
I am sure that you have experienced attacks of premeal hunger. Subjectively, they seem to provide 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 always 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 experience 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 energy 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 support for the view that hunger is often caused by the expectation 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 intervals, and he signaled the impending delivery of each meal with a buzzer-and-light conditional stimulus. This conditioning procedure was continued for 11 days. Throughout 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 mechanisms play a major role in determining how much we eat.
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 subsequent consumption. These signals depend on both the volume and the nutritive density (calories per unit volume) of the food.
The effects of nutritive density have been demonstrated in studies in which laboratory rats have been maintained on a single diet. Once a stable baseline of consumption has been established, 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 sufficiently 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.
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 passing down the subject’s esophagus into the stomach, it passes out of the body through an implanted tube (see Figure 12.5).
FIGURE 12.5 The sham-eating preparation.
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 influenced largely by our previous experience with the particular food’s physiological effects, not by the immediate effect of the food on the body.
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.)
Appetizer Effect and Satiety
The next time you attend a dinner party, you may experience a major weakness of the set-point theory of satiety.
If appetizers are served, you will notice that small amounts of food consumed before a meal actually increase hunger rather than reducing it. This is the appetizer effect. Presumably, it occurs because the consumption of a small amount of food is particularly effective 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 subjects consumed 60% more when eating with others. Laboratory rats also eat substantially more when fed in groups.
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 others 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.
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 chocolate 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 cafeteria diets on consumption and body weight clearly run counter to the idea that satiety is rigidly controlled by internal 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 declines slightly, but the positive-incentive value of that particular 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 palatability 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 almost every day with only a slight decline in their palatability (Rolls, 1986).
The phenomenon of sensory-specific satiety has two adaptive consequences. First, it encourages the consumption of a varied diet. If there were no sensory-specific satiety, a person would tend to eat her or his preferred food and nothing else, and the result 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 encounters a different one (Raynor & Epstein, 2001). This encourages 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 assumption, and how many are inconsistent with it?
Scan Your Brain
Are you ready to move on to the discussion of the physiology 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.
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.
Scan Your Brain answers:
(5) free fatty acids,
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 development of methods of continually monitoring blood glucose levels. In the classic experiment of Campfield and Smith (1990), rats were housed individually, 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).
FIGURE 12.7 The meal-related changes in blood glucose levels observed by Campfield and Smith (1990).
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 unexpectedly 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 glucose are typically preceded by increases in blood insulin 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 surround CNS neurons stay relatively constant, even when blood glucose levels drop (see Seeley & Woods, 2003).
• Injections of insulin do not reliably induce eating unless 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 regions of the hypothalamus: satiety by the ventromedial hypothalamus (VMH) and feeding by the lateral hypothalamus (LH)—see Figure 12.8. This theory turned out to be wrong, but it stimulated several important discoveries.
FIGURE 12.8 The locations in the rat brain of the ventromedial hypothalamus and the lateral hypothalamus.
VMH Satiety Center
In 1940, it was discovered that large bilateral electrolytic lesions to the ventromedial hypothalamus 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 obesity; 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 regain 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 consumption, 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 unpalatable (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 hypothalamus produce aphagia—a complete cessation of eating. Even rats that were first made hyperphagic by VMH lesions were rendered aphagic by the addition of LH lesions. Anand and Brobeck concluded that the lateral region of the hypothalamus is a feeding center. Teitelbaum and Epstein (1962) subsequently discovered two important features of the LH syndrome. First, they found that the aphagia was accompanied by adipsia—a complete cessation 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 lesions increase blood insulin levels, which increases lipogenesis (the production of body fat) and decreases lipolysis (the breakdown 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 savings account from which withdrawals cannot be made.
FIGURE 12.9 Postoperative hyper-phagia and obesity in a rat with bilateral VMH lesions. (Based on Teitelbaum, 1961.)
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 attributable to VMH damage. A large fiber bundle, the ventral noradrenergic bundle, courses past the VMH and is thus inevitably damaged by large electrolytic VMH lesions; in particular, 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 nuclei (Leibowitz, Hammer, & Chang, 1981) produce hyperphagia and obesity, just as VMH lesions do.
Most of the evidence against the notion that the LH is a feeding center has come from a thorough analysis of the effects of bilateral 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 produce 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 feeding no longer warrants serious consideration.
FIGURE 12.10 Location of the paraventricular nucleus in the rat hypothalamus. Note that the section through the hypothalamus is slightly different than the one in Figure 12.8.
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 Washburn 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 produced a momentary increase in the level of the water at the other end of the U-tube. Washburn reported a “pang” of hunger each time that a large stomach contraction was recorded (see Figure 12.11).
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.
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 distention. However, support for this theory and interest in the role of the gastrointestinal tract in hunger and satiety quickly waned with the discovery that human patients 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 series 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 intestine 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 proportion to both its caloric content and volume. Because the transplanted stomach had no functional nerves, the gastrointestinal satiety signal had to be reaching the brain through the blood. And because nutrients are not absorbed from the stomach, the bloodborne satiety signal could not have been a nutrient. It had to be some chemical 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 function 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 Badman & 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).
FIGURE 12.12 Transplantation of an extra stomach and length of intestine in a rat. Koopmans (1981) implanted 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 proportion to its volume and caloric value.
In studying the appetite-reducing effects of peptides, researchers had to rule out the possibility that these effects are not merely the consequence of illness (see Moran, 2004). Indeed, there is evidence that one peptide in particular, CCK, induces illness: CCK administered 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 synthesized 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 discovery that microinjection of gut peptides into some sites in the hypothalamus can have major effects on eating. 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 another chemical that plays a role in satiety. The initial evidence 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 discovery of the neural mechanisms of hunger and satiety (Goldstone, 2004). Individuals with Prader-Willi syndrome, which results from an accident of chromosomal replication, experience insatiable hunger, little or no satiety, 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 include weak muscles, small hands and feet, feeding difficulties in infancy, tantrums, compulsivity, and skin picking. If untreated, most patients become extremely obese, and they often die in early adulthood from diabetes, heart disease, or other obesity-related disorders. Some have even died from gorging until their stomachs split open. Fortunately, Miss A. was diagnosed in infancy and received excellent care, which kept her from becoming 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. Fortunately, 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 environment (e.g., a substitute teacher at school). Thanks largely to her family and pediatrician, she has received excellent 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 mechanisms of hunger and eating, there has been a marked surge in its investigation. This increase has been stimulated 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 father. 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 regulation 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 deposits 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 remain 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, because, 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 example, people living on the Japanese island of Okinawa seemed to eat so few calories that their eating habits became a concern of health officials. When the health officials 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 proportion of Okinawans living to be over 100 years of age was up to 40 times greater than that of inhabitants of various 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 example, perhaps it is not simply the consumption of fewer calories that leads to health and longevity; perhaps 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 calorie restriction constitute the second kind of evidence that ad libitum levels of consumption 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 numerous indices of health and increased longevity. For example, 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 consumed the least had the lowest incidence of cancer, the best immune responses, and the greatest maximum 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 initiated 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 restriction 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 energy 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 implications of all these findings about calorie restriction. How much do you eat?
Regulation of Body Weight by Changes in the Efficiency 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 limits 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 maintaining 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 further 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 efficiency 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 research on calorie-restricted diets suggests that these people 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 defend a body-fat set point has long had its critics (see
FIGURE 12.13 The diminishing effects on body weight of a low-calorie diet and a high-calorie diet.
Booth, Fuller, & Lewis, 1981; Wirtshafter & Davis, 1977), but for many years their arguments were largely ignored and the set-point assumption ruled. This situation has been changing: Several prominent reviews of research on hunger and weight regulation generally acknowledge that a strict set-point model cannot account 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 natural 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. According 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 biological settling point—see Chapter 4.
The seductiveness of the set-point mechanism is attributable 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 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; 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 advantage 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 increases 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.