The_Psychology_of_Eating_and_Drinking_----_(2_Down_the_Hatch_Hunger_and_Satiety) (2).pdf

2 D OW N T H E H AT C H Hunger and Satiety Copyright © 2014. Taylor & Francis Group. All rights reserved. No animal can live without food. Let us then pursue the corollary of this: namely, food is about the most important influence in determining the organization of the brain and the behaviour tha...

2 D OW N T H E H AT C H Hunger and Satiety Copyright © 2014. Taylor & Francis Group. All rights reserved. No animal can live without food. Let us then pursue the corollary of this: namely, food is about the most important influence in determining the organization of the brain and the behaviour that the brain organization dictates. J. Z. Young (1968)1 Many of you reading this book are, I’m certain, interested in weight control (most likely your own). In order to modify one’s weight, it’s extremely helpful to understand the basic factors responsible for the starting and stopping of eating. In other words, you need to understand the basic factors responsible for hunger and satiety. This information will help you understand what might be wrong if someone is eating too much or too little, and will also give you ideas about how to change the amount that someone eats. Perhaps most interestingly, this information will tell you what will not affect the amount that someone eats. For example, this chapter will explain why filling up with water won’t decrease how many calories you eat, something that anyone familiar with the basic laboratory research on eating knows. Given that the focus of this chapter is on hunger and satiety, its material is more closely related to physiology than that of most of the other chapters. However, particularly toward the end of this chapter, I’ll also discuss the relationships of hunger and satiety to aspects of our surroundings. Think of this chapter as providing you with the psychophysiological framework in which to place much of the social and cultural information on eating that you’ll read about in later chapters. The story of the scientific investigation of hunger and satiety reads like a minihistory of psychology laboratory technique. For each time period, the hot theories about what was responsible for hunger and satiety were very much a function of what laboratory techniques had been developed at that time. So, in the early 20th century, scientists investigated the relationship of stomach contractions to hunger because they had a way to measure 11 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. Copyright © 2014. Taylor & Francis Group. All rights reserved. THE PSYCHOLOGY OF EATING AND DRINKING those contractions. Later, in the 1940s and 1950s, as surgical techniques advanced, the effects on hunger of different types of substances in the stomach, substances that had or had not arrived there via the mouth, were investigated. Also around this time, investigations of the brain’s effects on eating began, investigations that still continue and use ever more specific methods to determine which part or aspect of the brain affects which precise type of behavior. Most recently, techniques have advanced to the degree that scientists can show how specific parts of the brain and chemicals elsewhere in the body work together to influence hunger. Now, in the 21st century, the number of different aspects of the body shown to affect hunger and satiety is dazzling and still growing. In this chapter I’ll organize all of the major findings so that you’ll get an idea of the results and the significance of hunger and satiety research over the past 100 years. As we progress through these experiments and their results, it’ll be helpful for you to keep a few principles in mind. First, many animals, including people, don’t eat continuously. Instead, there are periods of time—meals— during which food consumption occurs frequently and periods of time during which there’s little food consumption. So this chapter will be looking at what’s responsible for a meal starting and stopping. Note that all else being equal, more food will be consumed during a long meal than during a short meal. Therefore, investigations of what causes hunger and satiety are also investigations of what determines how much is eaten. Second, investigations of how much is eaten have traditionally been classified into two types: investigations of short-term regulation and long-term regulation, that is, animals’ abilities to consume both what will satisfy their short-term energy needs and their abilities to maintain fairly constant body weight over long periods of time. Before you scoff at your ability to maintain body weight over a long period, consider this: Suppose every day you eat 2% more calories than you need, approximately the number of calories in one extra pat of butter or margarine. After 1 year, this would be equivalent to a 5-pound weight gain. So, even if you find yourself gaining 2 or 3 pounds each year, you’re still doing a pretty good job of eating very close to the amount that your body needs to maintain its current weight. In both short-and long-term regulation, our bodies have been thought to behave in a way that is similar to a household thermostat. A thermostat is set for a particular temperature, and if the temperature becomes too warm or too cold, air conditioning or heat kicks in to bring the temperature back to the ideal level. Many theories of hunger have postulated that, in our bodies, there’s a physiological characteristic (e.g., available energy or stored fat) that has an optimal level, the set point, and whenever there’s a deviation from that optimal level, something happens in the body so that the optimal level is restored. Walter B. Cannon, an early 12 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. CHAPTER 2: DOWN THE HATCH 20th-century American physiologist who is mentioned several times in this chapter, coined the term homeostasis to describe processes such as these.2 In the sections that follow, see if you can identify the theories of hunger and satiety that incorporate the concept of homeostasis, as well as the complications for such theories. One final caution is in order here. In some of the experiments described in this chapter and in subsequent chapters, people are asked to report how hungry they are or what they have eaten. There has been some disagreement about how meaningful such statements are. Do people’s hunger ratings correlate closely with how much they eat, and do people report accurately how much they eat? What people say they felt and what they say they ate don’t necessarily correspond to their actual behaviors. For example, sometimes people report eating significantly less than they really ate, sometimes significantly more, and sometimes they can be quite accurate.3 As long as there are at least some situations in which people’s self-reports help us predict their eating behaviors, experimenters will continue to use self-report data. The number of different factors that have been shown to influence hunger and satiety is truly mind-boggling. To make your comprehension of this material easier, I’m going to divide it into two major categories: investigations of peripheral factors and investigations of central factors. However, as we go along, you’ll see that researchers have increasingly looked at the relationships between these two types of factors. Copyright © 2014. Taylor & Francis Group. All rights reserved. Out of Your Mind (and Brain): Peripheral Factors Peripheral factors that influence hunger and satiety are those factors involving parts of the body other than the central nervous system (the brain and the spinal cord). Let’s follow a piece of chocolate cake as it wends its way from your kitchen table into your mouth, down into your stomach and intestine, to see what peripheral factors might contribute to making you hungry or satiated. Getting from the living room to the kitchen You’re in your living room watching TV. What are some of the factors that might make you start thinking about going into the kitchen to eat the piece of chocolate cake on the table? Thinking about it enough to get up from your nice comfy couch? Let’s suppose that your stomach growls, and it feels as if it’s contracting like crazy. Many people believe that a rumbling stomach is synonymous with hunger and a nonrumbling stomach is synonymous with satiation. Such beliefs led scientists to formulate the stomach contraction theory of 13 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. Copyright © 2014. Taylor & Francis Group. All rights reserved. THE PSYCHOLOGY OF EATING AND DRINKING hunger, which says that the initiation and termination of eating can be predicted on the basis of stomach contractions. Someone whose stomach has been contracting might be more likely to eat and vice versa. Cannon’s 1912 work on this theory with A. L. Washburn was one of the first experimental studies of hunger.4 Cannon and Washburn developed a technique for measuring stomach contractions, and Washburn was the first lucky person to experience it. First, Washburn had to become accustomed to having a long tube inserted down his throat into his stomach and left there for several hours each day. One end of the tube was in his stomach, and the other end was outside his mouth. During the experiment, air was passed into the outer end of the tube to inflate partially a balloon attached to the end of the tube that was in Washburn’s stomach. (Washburn must have been a very dedicated scientist!) Stomach contractions were measured by monitoring changes in air pressure in the balloon. Washburn pressed a telegraph key whenever he felt hungry. His stomach contractions were closely associated with his reports of hunger. Apparently, Washburn would report hunger at the height of a contraction, not at the beginning, which suggested that the stomach contractions caused the feelings of hunger and not the other way around. When Washburn wasn’t hungry there were no contractions. Follow-up studies with additional subjects obtained similar results.5 The stomach contraction theory was the first peripheral theory of hunger to receive experimental support, and it was the dominant peripheral theory for many years. However, subsequent studies showed that neither stomach contractions nor even a stomach are necessary prerequisites for reports of hunger.6 Further, as more sophisticated methods of measuring stomach contractions have been developed, the relationship between hunger and stomach contractions has been found to be extremely weak.7 Therefore the stomach contraction theory of hunger now appears to be primarily of historical interest. You’ve still got to get from that living room into the kitchen. If stomach contractions won’t get you moving, what might? Suppose, in flipping channels, you happen upon a cooking show about how to make the perfect chocolate cake. All of a sudden you’re dying for that piece of chocolate cake on your kitchen table. Have you ever noticed that smelling food, hearing cooking noises, or just looking at food makes you feel hungry? You’re not imagining this. What’s happening to you is related to what happened to Pavlov’s dogs. As you will recall, Pavlov showed that dogs would salivate when they heard or saw something that had previously been associated with food. Similar to the dogs, you also salivate when you hear or see or smell things that have been associated with food. And salivation isn’t the only response that your body has to these situations. Even if you haven’t yet touched the food, your pancreas may secrete insulin, a chemical involved in 14 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. CHAPTER 2: DOWN THE HATCH the metabolism of sugar. The insulin lowers your blood sugar level, which makes you feel hungry. There are several such reflexes that are related to the ingestion and digestion of food and that occur immediately upon—or, with experience, even prior to—our contact with food.8 Understanding how these salivation and insulin responses occur can help in understanding the differences in hunger between Muslim men and women during Ramadan. Ramadan is the month during which devout Muslims fast from sunrise to sunset. Researchers have shown that, during the initial days of Ramadan, women report being significantly more hungry than men. However, during the latter days of Ramadan, women and men report approximately equal levels of hunger. As it turns out, during Ramadan, the men aren’t usually at home during the fasting periods. In contrast, the women are at home and are involved in preparing food for the children to eat during the day and food for the adults to eat after sunset. Thus, during the fasting periods, the women are probably exposed to far more odors, sounds, and sights that are associated with food than are the men. However, as the month of Ramadan proceeds, the food-related phenomena to which the women are exposed during the day are never accompanied by the women ingesting food. Therefore those phenomena are no longer associated with food ingestion.9 This may stop salivation or insulin release and result in decreased hunger. Copyright © 2014. Taylor & Francis Group. All rights reserved. Getting the cake into your mouth You’ve taken the big step and entered the kitchen. Now, with that cake staring you in the face, you’re releasing more insulin and are feeling hungrier. But the kitchen’s window air conditioner breaks, and because it’s July and 95°F (35°C) outside, the kitchen quickly becomes unpleasantly hot and stuffy. Suddenly, you’re no longer so interested in that chocolate cake. The surrounding air temperature is well known to affect hunger. If your kitchen is hot, it’s likely that you’ll eat less than when your kitchen is a little chilly. One explanation for this influence of the surrounding temperature on the amount eaten is that in cold weather the body needs more fuel to keep itself heated to 98.6°F (37°C), and a major source of heat for any animal is the food it consumes. Therefore it’s possible that initiation and termination of feeding are related to the maintenance of a specific, optimally efficient body temperature. If this sounds to you like a homeostatic process, you’re exactly right! The temperature theory of hunger was proposed in the late 1940s.10 Since then, experiments with rats and people have supported it—animals do consume more in cold surroundings. Experiments have also shown that exposure to cold surroundings speeds the movement of previously consumed food from the stomach into the intestine. Such a process would, of course, decrease 15 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING whatever it is about food in the stomach that normally inhibits feeding,11 and thus this finding helps to explain why animals eat more in the cold. Copyright © 2014. Taylor & Francis Group. All rights reserved. Cake in the mouth Let’s suppose that you felt hungry enough that you’ve now put the chocolate cake into your mouth. Does the food’s stimulation of your mouth affect your hunger and satiety? In order to determine whether oral factors by themselves contribute to hunger and satiety, over 50 years ago researchers developed a particular type of surgery called an esophagostomy. You may find the description of this surgery difficult and unpleasant to read. Performing an esophagostomy was one of the few then-available techniques that could be used to separate the influence of oral and gastric factors on hunger and satiety. This surgery involves first bringing the subject’s esophagus—the tube through which food passes from the mouth to the stomach—out through the neck. The esophagus is then cut, forming an upper and a lower piece. If an animal that has had this operation eats, the food consumed passes out through the animal’s neck instead of continuing to its stomach. This is known as sham feeding. An animal that is sham fed has all of the usual oral experiences that accompany feeding but none of the sensations that originate in the stomach. The subject tastes, chews, and swallows the food, but the stomach never receives it. Scientists Henry D. Janowitz and M. I. Grossman were among the first researchers to use this surgical technique. They reported that sham fed dogs eventually stop eating, but before they stop they consume much more food than usual.12 Over many sham feedings, the amount of food eaten increases.13 Once the animals learn that food in the mouth is no longer associated with food reaching the stomach, the satiating ability of food in the mouth ceases. Thus, oral factors can contribute to the cessation of eating, but by themselves oral factors don’t precisely regulate food intake. (See Conversation Making Fact #2.) Conversation making fact #2 Chewing gum (sugar-free or regular), or just chewing your food more, can decrease both how hungry you then feel and how much you then eat.14 In middle school my teachers told me that chewing gum would make me look like a cud-chewing cow and I’ve never been able to chew gum since, which now seems very unfortunate! 16 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. CHAPTER 2: DOWN THE HATCH Assuming that you’re not engaging in sham feeding, what characteristics of that piece of food in your mouth might affect whether or not you feel hungry? One food characteristic that has been widely investigated in this regard is whether the food is sweet. Both rats and people eat more of sweet than nonsweet foods, even if the number of calories in these foods is equal. In other words, even if a food is made sweet using a noncaloric sweetener, animals will eat more of it than had it not been sweet. One possible explanation of these findings is that the presence of a sweet taste causes more insulin to be released than if there’s no sweet taste, thus lowering blood sugar to a greater degree and making someone feel hungrier. Another possible explanation is that when we eat food that is sweet, the body makes less of what’s eaten available for immediate use and stores more of it than if what was eaten weren’t sweet. Therefore, when we eat sweet food, in order to have enough energy for our immediate needs, we have to eat relatively large amounts. There may be similar explanations for the fact that we eat lots of any good-tasting food.15 Copyright © 2014. Taylor & Francis Group. All rights reserved. The cake in the gastrointestinal tract You’ve chewed up and swallowed that piece of cake and now it’s in your stomach, on its way to the small and large intestines. What effects does the presence of food within the gastrointestinal (GI) tract have on your feeling hungry or full? In a survey of college students, most said that the reason they stop eating is because they feel full.16 But what’s responsible for that feeling? What can increase or decrease it? Investigation of GI effects is complicated because, ordinarily, food gets to the GI tract by way of the mouth. Therefore, effects of food in the GI tract could be due to either the oral or the GI stimulation provided by the food, or both. Nevertheless, just as with oral factors, researchers have come up with ways to isolate the effects of GI factors. For example, researchers can insert food directly into the lower portion of the esophagus following an esophagostomy, thus bypassing oral factors. Alternatively, they can make a hole by which food or an undigestible substance such as an inflated balloon can be inserted directly into the stomach from outside the body. When what’s inserted is food, this process is known as intragastric feeding. Several scientists, including sham feeding researchers Janowitz and Grossman, have investigated the effects of intragastric feeding on dogs’ eating behaviors. These researchers have put different amounts of food and other substances directly into the stomach. For example, they have studied the effects of inserting an inflated balloon into the stomach. One finding from this research is that intragastric feeding decreases sham feeding only when intragastric feeding is large and occurs at the same 17 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING time as sham feeding. Further, a balloon has no effect on feeding unless the balloon is so inflated that it causes nausea and retching. Finally, dogs with holes directly into the stomach or with esophagostomies can eventually learn to eat less when they have been fed intragastrically.17 In addition, we now know that foods that are very high fat or that have a lot of fiber are more satiating. The precise reasons for this increased satiety aren’t known. It may be that a food’s viscosity or amount of fiber affects absorption of that food’s nutrients or the speed with which that food passes through the GI tract.18 Further, even with the total number of calories consumed held constant, higher volumes of food are more satiating than lower volumes if the foods contain at least some calories.19 If you’re a good detective you’ll have put all of these pieces of evidence together into a fairly consistent story. Here’s my version. Putting something in the stomach so that the stomach stretches isn’t very influential in getting us to stop eating unless the stretching is extreme or is accompanied by nutrients in the GI tract.20 This explains why drinking lots of water or inserting an inflated balloon into the stomach aren’t very effective in decreasing food consumption. Although these substances stretch the stomach, they contain no nutrients, and thus they won’t increase satiety effectively. Copyright © 2014. Taylor & Francis Group. All rights reserved. Effects of digestion and storage of the cake You’ve eaten the cake. Now it’ll be digested, and some of it may be stored as fat. What effects might these processes have on hunger and satiety? When you digest food, including chocolate cake, the amounts of certain chemicals in your body increase. Some of these chemicals are the products of the digestion of food. Others are the chemicals produced by the body to aid in the digestion of food. The presence of high levels of chemicals in either group can act as a signal to your body that food has been consumed and so eating should stop. Conversely, when the levels of these chemicals are low, this can signal your body to start eating. A large number of such possible signals have been investigated. A good chemical signal of currently available energy would be one that increases quickly following feeding and slowly decreases with time until the next feeding. Internationally known physiologist and nutritionist Jean Mayer realized that there was such a signal when he formulated the glucostatic theory of hunger in 1953.21 The glucostatic theory postulates that hunger is related to blood sugar level and that information about the energy available to an animal is indicated by the level of sugar in the blood. In addition to rising quickly and then decreasing slowly following feeding, blood sugar is known to be the primary energy source for the central nervous system. Therefore, you would expect animals to have 18 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. Copyright © 2014. Taylor & Francis Group. All rights reserved. CHAPTER 2: DOWN THE HATCH evolved so as to use eating to ensure that adequate levels of blood sugar are maintained. As a refinement to his model, Mayer proposed that it wasn’t the absolute level of blood sugar that was important in the initiation and termination of feeding, but the difference between the levels in the arteries and veins. Arteries take blood to the body’s tissues, and veins return blood from those same tissues. If the blood sugar level is high in the arteries but low in the veins, sugar is being removed from the blood as it passes from the arteries through various tissues and then into the veins. In such cases the body is receiving a fair amount of sugar. If the blood sugar level in both the arteries and veins is low, then the body isn’t receiving much sugar. In support of his theory, Mayer found that the difference between the blood sugar levels in the arteries and veins correlated well with people’s reports of hunger.22 Mayer realized that his glucostatic mechanism would make errors on a daily basis and that some long-term mechanism would be needed to correct those errors. A mechanism related to the fat stores in the body was the obvious choice. Our bodies store excess energy as fat. One pound of fat is equivalent to 3,500 calories. In order to use this storage system to correct errors made by the glucostatic mechanism, the body must have a way of detecting the extent of its energy stores. Lipostatic theories propose that a circulating chemical related to the amount of the body’s stored fat is responsible for long-term regulation of stored fat; when the chemical indicates that fat stores are low or decreasing, eating should increase, and vice versa. In this way, the glucostatic and lipostatic mechanisms could work together to regulate the body’s food intake on both a daily and a long-term basis. Mayer was among the first to propose a lipostatic theory of long-term regulation.23 Over the years since lipostatic theories were first developed, researchers have proposed several candidates for the chemical that signals the amount of stored fat, including leptin, a hormone found in the blood and manufactured by the cells that store fat. The level of leptin in the body is related to the amount of stored fat.24 In the meantime, while lipostatic theories were developing, the glucostatic theory of hunger encountered some bumps. Unfortunately, there hasn’t been extensive evidence supporting the difference in blood sugar between the arteries and veins as a primary determinant of hunger.25 Therefore, researchers have proposed alternatives. One of the most frequently used has become the glycemic index. The glycemic index score for a given food has to do with your body’s metabolic response to that food (see Table 2.1). More specifically, when you eat a certain number of calories of a particular type of food, the glycemic index measures how much total glucose is subsequently added to your blood during a specified period of time (see Figure 2.1).26 19 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING Table 2.1 Typical glycemic index scores for sample foods Food Glycemic Index Bread Rice Bubbles (Rice Krispies) cereal Porridge oats (oatmeal) All-Bran cereal Eggs and bacon 100 116 60 43 24 Source: S. Holt, J. Brand, and C. Soveny, “Relationship of Satiety to Postprandial Glycaemic, Insulin, and Cholecystokinin Responses,” Appetite 18 (1992): 129–141. If a particular food results in a lot of added blood sugar, then that food gets a high glycemic index score and vice versa. High glycemic scores are associated with hunger and low scores with satiety.27 This is an explanation of satiety and blood sugar that takes into account how blood sugar changes over time. (What a daunting thought. It appears that it is not just the amounts of many body chemicals that are involved in hunger and satiety, but the temporal patterns of these chemicals as well.) High Gl Copyright © 2014. Taylor & Francis Group. All rights reserved. Low Gl 0 1 2 T im e A fte r M e al (H o u rs ) Figure 2.1 E  ffects of high and low glycemic index foods on blood glucose over time. (From S. B. Roberts and A. G. Pittas, “The Role of Glycemic Index in Type 2 Diabetes,” Nutrition in Clinical Care 6[2003]: 73–78. Reprinted with permission from S. B. Roberts and A. G. Pittas.) 20 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. Copyright © 2014. Taylor & Francis Group. All rights reserved. CHAPTER 2: DOWN THE HATCH Many factors contribute to the glycemic index score. These factors include the chemical structure of a food, the amount of fiber in that food, and how the food has been processed. For example, oatmeal, which is high in fiber, has a lower glycemic index score than Rice Bubbles(Rice Krispies) cereal, which contains finely milled grains.28 Similarly, adding salad to your meal or flax seed to your food can also help to increase satiation.29 In an intriguing experiment, scientists J. H. Lavin and N. W. Read gave 10 young men a radioactive, 300-calorie, orange-tasting, glucose drink and then measured the amounts of glucose and insulin in the men’s blood for the next 3 hours, as well as the men’s hunger ratings, fullness ratings, and amounts of radioactivity in the men’s stomachs. Each man came to the laboratory twice; on one day he had the basic glucose drink, and on the other day he had that drink with the addition of guar gum. Guar gum is an inert substance that isn’t digested. The results showed that after consuming the guar gum as compared to the regular drink, the participants’ glycemic index scores, plasma insulin levels, and hunger were all lower. These results indicate that slowing the absorption of glucose, in this case by the use of guar gum, makes people feel more full. Lavin and Read also showed that there were no significant differences over time in the changes of the amounts of radioactivity in the stomach; there was no difference in how long the drink stayed in the stomach with and without the guar gum. Based on this evidence, the researchers believed that the guar gum drink was more satiating because it extended the contact between the molecules of glucose and the glucose receptor cells in the small intestine, the next location after the stomach on the drink’s trip through the gastrointestinal tract.30 I do have one question about this experiment, however. Did the guar gum change the taste of the drink? We know that eating good-tasting foods results in the release of more insulin than eating not-so-goodtasting foods. Perhaps the guar gum drink resulted in a lower glycemic index score because the drink didn’t taste as good with the guar gum. The authors don’t discuss this possibility or report any data on the taste of the two drinks, so unfortunately, at present, there’s no answer to my question. Among the chemicals produced by the body to aid in food digestion, three of the most investigated in terms of their import for hunger and satiety are insulin, cholecystokinin (CCK), and glucagon. There is a great deal of evidence that insulin outside of the central nervous system is a satiating agent—insulin produced by the pancreas during the digestion of food does reduce subsequent food intake.31 Experiments also suggest that CCK, which is produced in the small intestine during digestion, may help to terminate feeding.32 In one experiment, rat pups 21 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING were first administered a chemical that causes the release of CCK from the small intestine. These experimental rats subsequently ate less than untreated rats.33 Similar to insulin, glucagon is produced in the pancreas. One experiment gave small doses of glucagon (like the levels that occur naturally after food consumption) intravenously to people. These people subsequently ate less food than if they had not been given glucagon.34 Therefore glucagon may be another naturally occurring substance that plays an influential role in satiety. Copyright © 2014. Taylor & Francis Group. All rights reserved. Types of foods By this point, you’re probably pretty well satiated with the effects on hunger and satiation of different levels of your body’s different chemicals. So let’s turn to something else. What sorts of foods increase and decrease hunger? You already know that foods that have a lot of fiber are more satiating. Does a food’s caloric density affect how much we eat? A gram of one food can have a lot more, or a lot fewer, calories than a gram of another food. Consider our infamous piece of chocolate cake. The cake could be made with a high proportion of fat (which contains 9 calories per gram) or with a high proportion of sugar (which contains 4 calories per gram). Will we eat different amounts of chocolate cake (or other food) depending on the relative proportions of fat and sugar in it? This is a question to which I would personally like an answer because I have been known to buy and eat low-fat, low-calorie chocolate truffle cake. A great many experiments have been conducted to answer this question. In general, these experiments find that, when single meals are examined, eating a high-calorie food can cause us to eat less soon afterward.35 Similarly, over the long term and many meals, if animals are fed foods that are relatively low in caloric density as part of their regular diet, they will eat more so that their total caloric intake remains the same.36 This is disappointing news—after all, what’s the point of buying that low-calorie chocolate truffle cake? But this news shouldn’t be that surprising. When we were evolving, in order to maintain adequate fat stores, our bodies had to be able to compensate by eating more when food supplies were relatively poor in calories. Nevertheless, psychologists repeatedly tantalize us with experiments showing that certain foods under certain conditions result in more shortterm satiation than other foods. For example, with calories held constant, eating a meal of meatballs is more satiating that eating a meal of pasta; tomato soup is more satiating than crackers with cheese or than melon; prunes are more satiating than low-fat cookies; protein is more satiating than carbohydrates; and eating the exact same food in liquid form isn’t 22 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. CHAPTER 2: DOWN THE HATCH as satiating as eating it in solid form (perhaps because there’s less chewing— see Conversation Making Fact #2).37 In general, these sorts of experiments seem to indicate that the lower the glycemic index score, then the less insulin released, the more cholecystokinin released in the small intestine, the higher the satiety, and the less food that’s eaten. Certain foods fill us up faster. Enjoy a meal of dehydrated tomato soup with meatballs and prunes for dessert! Conclusion to peripheral factors I hope that, by learning about the many different factors that contribute to our starting and ending meals, you’re also learning to appreciate how exquisitely constructed our bodies are. Eating the right amount of food is absolutely essential to survival. Therefore it’s not surprising that our bodies have apparently evolved with a number of different, sometimes redundant, mechanisms that each help to ensure that the correct amount of food is consumed. Should one of these mechanisms fail for any reason, another will still be in effect so that we are unlikely to starve or eat ourselves to death. These different mechanisms work together to guarantee that eating is basically within normal limits. You’ll see more examples of our bodies’ exquisite construction and redundancy as we now turn to the central nervous system factors that are involved in hunger and satiety. Copyright © 2014. Taylor & Francis Group. All rights reserved. Food on Your Mind: Central Factors Ever since scientists began investigating the influence of the central nervous system on the initiation and termination of feeding, they have viewed the brain as first receiving information about what’s going on inside and outside of the body and then causing the body to take some action. The initial experiments tried to identify the many individual parts of the brain, each made up of millions of neurons, that were responsible for these sorts of central functions. In recent years, investigations of the role of the central nervous system in hunger and satiety have grown far more complex. These more recent investigations include examinations of the combined effects of activity in several parts of the brain, as well as examinations of the effects of a variety of chemical substances present in the brain. What follows is a semihistorical review of the highlights of the research on central factors. Hunger and satiety centers This story begins with a now famous case of obesity in an adolescent boy with a large tumor of the pituitary gland around 1900: 23 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING Copyright © 2014. Taylor & Francis Group. All rights reserved. R. D., a boy, was born in 1887…. Since March 1899 the patient, who previously had been slim, had been rapidly gaining weight. In January 1901 he complained about diminishing eyesight on the left.… Later, vision in the right eye also began to fail.… Since the patient suffered from severe headaches and his eyesight was rapidly decreasing, an operative procedure appeared justified. The operation by the nasal route was performed by von Eiselsberg on June 21 [1907]. In the depth of the sphenoid sinus the whitish membrane of a cyst the size of a hazelnut was encountered. After incision in the midline, several spoonfuls of a fluid resembling old blood drained out. By measuring with the finger and comparison with the roentgenogram, it could be ascertained that the cyst which contained this fluid corresponded to the hypophysis [the pituitary gland, connected to and near the hypothalamus]. The walls of the cavity were cut away as far as could be done without damaging the optic chiasm and the carotid arteries.… The postoperative course was favorable.… There was considerable improvement in the general condition.38 Information such as this suggested that the hypothalamus might be involved in satiety; interference with the hypothalamus apparently resulted in overeating and obesity. By 1940 science had advanced far enough that scientists A.W. Hetherington and S. W. Ranson were able to conduct a detailed physiological study of the brain and the control of feeding.39 They inserted small electrodes into the brains of anesthetized rats, more specifically, into the area of the hypothalamus. When an electrode was in the proper place, an electrical current was passed through it, thereby destroying the surrounding cells. Several such small lesions were made in each rat’s brain. The rats subjected to this procedure usually recovered after the operation and appeared fairly normal. However, they ate excessively and became obese, behavior known as hyperphagia. The most likely place, if lesioned, that would result in obesity was the ventromedial hypothalamus (VMH). Therefore the researchers concluded that the VMH was involved in the control of satiety. Additional research showed that stimulation of the VMH (activating the cells with an electrical current, rather than destroying them with lesions) inhibits eating,40 which seemed to confirm that the VMH functions as a satiety center. Further, it was discovered that there are cells in the VMH that are sensitive to one kind of sugar, glucose, and that destroying these cells caused rats to behave similarly to VMH-lesioned rats.41 This suggested that the VMH receives information about blood sugar levels, thus allowing it to serve as a central collection center for information about the body energy level. (See Figure 2.2.) 24 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. CHAPTER 2: DOWN THE HATCH cortex cortex p araventricular nucleus dorsom edial nucleus dorsom edial nucleus lateral hypothalam us lateral hypothalam us :l h : (LH1 (a) ventrom edial hypothalam us (VMH) third ventricle ventrom edial hypothalam us (VMH) cortex brain stem Copyright © 2014. Taylor & Francis Group. All rights reserved. (b ) Figure 2.2 D  iagram of some of the parts of the rat brain that have been found to be important in the initiation and termination of feeding. The top panel (a) is a vertical cross section of the brain. The bottom panel (b) gives a side view of the brain in which the front part of the brain is to the left. The vertical line drawn through this side view shows the location of the cross section. The shaded rectangle in panel b is the part of the caudal (that is, posterior) brain stem containing the area postrema. (Adapted from R. J. Martin, B. D. White, and M. G. Hulsey, “The Regulation of Body Weight,” American Scientist 79[1991]: 528–541.) During the next decade, scientists reasoned that if there were a location in the VMH that controls satiety, there might also be a location in the hypothalamus that’s involved in hunger. Physiologists Bal K. Anand and John R. Brobeck’s 1951 report42 identified such a location as the lateral hypothalamus (LH). Their research seemed to show that destruction of this specific area of the hypothalamus resulted in rats that would never eat again, rats that eventually die of starvation. Further, it was shown that stimulation of the LH induced rats to eat.43 Together, the data that had been collected through the 1950s seemed to form a tidy package, as indicated in Table 2.2. Based on this evidence, 25 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING Copyright © 2014. Taylor & Francis Group. All rights reserved. Table 2.2 Summary of findings involving the hypothalamus in the mid-1950s Area of Hypothalamus Lesion Stimulation Ventromedial hypothalamus Lateral hypothalamus Increases eating Decreases eating Decreases eating Increases eating in 1954 psychologist Eliot Stellar formally proposed that the VMH is the brain’s satiety center and the LH is its hunger center.44 According to Stellar, these centers, essentially little brains within a larger brain, gather information about, for example, the body’s temperature and blood sugar level using a variety of sensory receptors in the hypothalamus; synthesize this information; and then may cause the body to do something, such as eat. Stellar saw brain centers as major locations in the brain that integrate information. However, he stated specifically that areas of the brain other than the hypothalamus are probably involved in the initiation and termination of feeding. Note that Stellar’s concept of brain centers did not eliminate the peripheral theories that we talked about earlier. Instead, Stellar’s concept of brain centers integrated peripheral theories with central theories of hunger. The brain centers theory dominated study of the initiation and termination of feeding for many years. Unfortunately, in the 55 years since Stellar first proposed the hunger and satiety centers hypothesis, a number of research findings have revealed problems with it. One major problem concerns the methods that were used to collect much of the data on which the hypothesis was based. These experiments used lesions or stimulation of particular parts of the brain. It can be very difficult to be precisely certain about what particular behavior has been affected by lesions or stimulation. Every action consists of many component actions. The act of eating a forkful of peas after being instructed to do so by one of your parents involves hearing and understanding the instruction, seeing the peas, bringing the fork to the peas, balancing the peas on the tines of the fork, bringing the fork to your mouth, scooping the peas into your mouth, chewing the peas, swallowing them, and in some way finding this act worth doing (if only to avoid your parent’s wrath). A brain lesion, or brain stimulation that interfered with eating peas, might do so by interfering with any one or several of these components of the act of pea eating. Psychologists are now aware that interfering with what seems to be a very small part of the brain can have profound effects on general arousal or on complex sensory functions.45 Thus, with regard to the brain centers theory of hunger, it’s possible that the brain lesions and/or stimulation affected motor or sensory behavior instead of interfering with hunger and satiety. Another major difficulty with the hunger and satiety centers hypothesis is the degree to which the lesions and stimulation were actually limited to 26 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. Copyright © 2014. Taylor & Francis Group. All rights reserved. CHAPTER 2: DOWN THE HATCH the parts of the brain where they were supposed to be. These manipulations may have affected larger areas than were intended. In part this may have been due to the shape of neurons; a neuron can have a central part (the cell body) and extensions (fibers) as long as 1 meter. As a result, the lesions and stimulation may have affected neuronal fibers passing through the lesion/stimulation areas, and not just cell bodies at those locations. There seems to be some validity to such criticisms. For example, it appears that lesions strictly confined to the VMH are less effective at inducing the VMH syndrome than lesions not strictly confined to the VMH.46 Still another problem with the hunger and satiety centers hypothesis is that experiments have shown that other parts of the brain, including all of those named in Figure 2.2, are also very important in detecting aspects of the surroundings and initiating behaviors related to feeding.47 Research has shown how these areas of the brain work together in starting and stopping eating. For example, it’s now believed that areas of the brain, such as the paraventricular nucleus, monitor and regulate what’s going on in the body and then pass their information to the lateral hypothalamus. The LH then influences the brain’s frontal cortex, which then affects how the animal plans and performs specific behaviors.48 Recent research has also been pointing to a part of the brain called the amygdala, which sends projections to the hypothalamus, as essential in the control of feeding.49 Not all experimental results have been incompatible with the hunger and satiety centers hypothesis. For example, data from one study50 showed that putting food in the small intestine quickly results in less activity in the LH and more activity in the VMH. These changes in brain activity were probably the result of information conveyed by the vagus nerve, which projects between the intestine and the part of the brain containing the hypothalamus. The hypothalamus is one of the major integrators of information about what’s going on inside and outside of the body, and of activity from higher and lower brain structures.51 However, the little brains within a brain that would have so neatly explained the initiation and termination of eating simply don’t exist. Chemical substances in the brain It’s not just the anatomy of the brain that influences the initiation and termination of feeding; the chemical substances present in the brain are also very important. In fact, the effects of brain chemistry on feeding may be particularly intriguing because a thorough understanding of the influence of brain chemistry on feeding might allow us to develop drugs that would be highly effective in treating anorexia or overeating. One group of brain chemicals that has received intense scrutiny is the neurotransmitters, 27 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING the chemical substances released in the small gaps between two adjoining neurons. These chemicals are necessary for the occurrence of the electrical impulses by which neurons communicate. Two types of neurotransmitters that have been extensively investigated are dopamine and serotonin. It has been known for many years that both of these neurotransmitters inhibit feeding.52 Recent experiments have examined how these two neurotransmitters might work together in this regard. For example, a review of data from several studies indicated that the interaction of dopamine and serotonin within the LH affects the size of the meals that an animal eats, and that the dopamine and serotonin within the VMH affect the frequency with which an animal eats. These aren’t the only mechanisms by which meal size and meal frequency are determined, but they’re important ones.53 Other chemical substances present in the brain can also affect the initiation and termination of feeding. One example is neuropeptide Y. This substance modulates the effects of neurotransmitters. Ultimately, it increases eating, primarily by affecting the hypothalamus. Research suggests that when excess neuropeptide Y is present for extended periods, significant overeating and obesity can result. In contrast, inactivation of neuropeptide Y inhibits eating.54 Another example is a protein called apolipoprotein A-IV, which is naturally present in the fluid within the central nervous system. When this protein is infused into the third ventricle of the brain, eating decreases.55 These are just some of the great many chemical substances involved in the initiation and termination of feeding within the central nervous system. Copyright © 2014. Taylor & Francis Group. All rights reserved. Putting It all Together: Combinations and Interactions of Different Factors We’ve spent most of this chapter pulling apart and examining separately the various peripheral and central factors that affect hunger and satiety. Now it’s time to try to put things back together. How do different mechanisms work as a team to determine when we start and stop eating? The answers are complex, and continuously developing. It’s extremely exciting research because we can finally see how influences inside and outside of the body combine in determining how much and how frequently we eat. Combinations of peripheral and central factors You’ve already been given some hints about how peripheral and central factors can work together. One such case was when we discussed how the hypothalamus detects the presence of blood sugar, thus integrating the glucostatic (peripheral) and the VMH (central) theories of hunger. Lots of other similar connections have been investigated. 28 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. CHAPTER 2: DOWN THE HATCH For example, several researchers now believe that insulin links both peripheral and central control of feeding (see Figure 2.3a). As you’ll recall, the level of insulin released by the pancreas increases either when an animal eats food or experiences things, such as the smell of chocolate, that have been previously associated with food consumption. An additional fact is that, when nothing associated with food is present, insulin levels are higher in individuals with more body fat. Finally, insulin circulating in the peripheral blood supply can enter the brain, and the more insulin that enters the brain, the less the central nervous system causes eating, and body weight decreases. Together, all of this information indicates that insulin level is an important factor in the short-term initiation and termination of feeding as well as in the long-term control of body weight, with both peripheral and central mechanisms at work.56 Figure 2.3b shows another pathway that links peripheral and central controls of feeding. The more fat someone has, the higher the level of leptin in that person’s bloodstream. It’s believed that special cells in the brain (e.g., in the paraventricular nucleus in the hypothalamus) detect these leptin levels. Further, leptin inhibits the production of neuropeptide Y. Therefore, when leptin levels are high, levels of neuropeptide Y decrease, causing decreased eating.57 Finally, let’s consider the example of CCK (Figure 2.3c). When first we met CCK in this chapter, it was described as an intestinal chemical involved in the peripheral control of hunger and satiety. We now also know that there are special cells both in the periphery and in the brain that are sensitive to—in other words, behave differently in—the presence of CCK. Further, it appears that CCK released in the periphery affects the vagus nerve, which then sends information to the brain, resulting in the termination of feeding.58 Copyright © 2014. Taylor & Francis Group. All rights reserved. The effects of our surroundings, memory, and learning It’s essential, in all of this discussion of anatomy and chemicals, not to forget the influence of our surroundings on eating behavior. The presence or absence of food and things associated with food ultimately cause all of the bodily reactions that we’ve been discussing. Furthermore, the act of eating, or of not eating, is by definition an act that involves interaction with the world around us. At least partly for these reasons, it has been argued that the only way to determine an animal’s homeostatic set point is to know what’s going on around that animal. For example, even though hens eat 20% less than usual when they’re incubating eggs, we shouldn’t describe this behavior as nonhomeostatic. There are so many ways in which our surroundings affect what should be considered homeostatic behavior that it has been suggested that the whole concept of homeostasis be abandoned.59 29 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. THE PSYCHOLOGY OF EATING AND DRINKING taste, odors, sounds, and sights associated with food inc rea ses enters insulin in blood s ase CNS decreases feeding cre in increased body fat (a) its ib inh ses rea inc leptin in blood de te es feeding cte increased body fat neuropeptide Y decr eas db y ses rea paraventicular nucleus in hypothalamus dec (b) s ect aff CCK in small intestine de vagus nerve dec rea ses feeding tec ted by periphery and brain ses rea dec (c) Copyright © 2014. Taylor & Francis Group. All rights reserved. Figure 2.3 T  hree examples of combinations of peripheral and central factors: (a) insulin; (b) leptin; (c) CCK. Not only current surroundings, but experience with past surroundings (memory and learning), greatly influence hunger and satiety. In fact, similar memory and learning processes that operate in other contexts also affect when we start and stop eating. For example, reminders of the previous meal—of how much and what was eaten—influence the next meal.60 Brain-damaged patients with no memory for events more than 1 minute ago will eat a second lunch 10 minutes after a first lunch, but people with no brain damage won’t.61 For an example involving undamaged memory processes, consider an experiment conducted by Suzanne Higgs and Jessica E. Donohue. These researchers asked some female undergraduates to focus on the sensory aspects of their food while eating lunch, other female undergraduates 30 Logue, Alexandra W.. The Psychology of Eating and Drinking, Taylor & Francis Group, 2014. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mqu/detail.action?docID=1873771. Created from mqu on 2023-11-06 09:47:37. Copyright © 2014. Taylor & Francis Group. All rights reserved. CHAPTER 2: DOWN THE HATCH to read a food-related newspaper article while eating lunch, and a third group to just eat lunch. Higgs and Donohue measured each student’s cookie eating later that afternoon. As it turned out, students who were in the food-focused group ate significantly fewer cookies than those in the other two groups. Not surprisingly, students in the food-focused group also remembered their lunches better than students in the other two groups. Thus, activities that increase memory of a meal may also serve to decrease food intake following a meal.62 As another example, I’ve already explained how odors, sounds, and sights previously associated with food can affect what goes on in the body concerning hunger and satiety. More specifically, you’ll recall that just as food you’ve eaten will cause insulin to be released, so will aspects of your surroundings that have been previously associated with food. Such an explanation can help us understand the differences between men’s and women’s hunger levels during Ramadan. These learned reactions of the body to upcoming meals have been described as the body’s way of anticipating and decreasing the large, potentially harmful, ups and downs in homeostatic functions that are caused by eating food.63 As a fourth example, if rats have learned to associate a particular odor such as almond or violet with the later stages of a meal of a highly caloric carbohydrate solution, they will drink less of another carbohydrate solution if that odor is present than if a novel odor is present.64 The rats apparently learn that the odor indicates that they have consumed a lot of calories. Thus learning associated with an odor can help to control meal volume. As a final example, psychologist Leann Birch and her colleagues first repeatedly gave preschool children snacks in a specific location where they could see a rotating red light and hear a certain song, but not in another location with other sights and sounds. Later, even