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Learning Objectives

After completing this chapter, you should be able to:

• Identify the areas of the hypothalamus responsible for regulation of body temperature and food and water intake.

• Describe the differences between endotherms and ectotherms. • Explain the mechanisms for shivering and nonshivering thermogenesis. • Illustrate what happens when a person is exposed to a cold or a warm environment. • Explain the relationship between Energy IN, Energy OUT, and body weight. • Differentiate between homeostasis and allostasis. • Describe what happens when the lateral hypothalamus and the ventromedial nucleus of the hypothalamus

are lesioned. • Identify drugs, hormones, and neuropeptides that stimulate or inhibit. • Describe possible causes for obesity, bulimia nervosa, anorexia nervosa, and pica. • Explain the differences between regulation of the intracellular and extracellular fluid compartments in the

human body. • Give examples of secondary versus primary drinking.

9

Eating, Drinking, and Temperature Regulation

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CHAPTER 9Section 9.1 Regulation of Body Temperature

A resident of Fresno, California, Dan decided to visit a friend in Arizona. Rather than take the expressway, he decided to drive along Route 190, which runs through Death Valley. It is a lonely stretch of road, and cars pass by very infrequently. About 20 miles east of Darwin (near the center of Death Valley), smoke began to pour out from under the hood of his car, and the indicator on the car’s temperature gauge warned that the engine’s temperature was dangerously high. Dan pulled off the road quickly and opened the hood. Steaming liquid poured out of a crack in the radiator hose.

Standing outside his car, Dan quickly noticed the intense heat of the afternoon sun. He retreated back inside his car to get out of the sun. Next, Dan devised a fan by folding up a newspaper and fanned himself to cool down. But the sweat just poured off him, and he felt hot and miserable. Less than an hour later, he became aware of the fact that he was extremely thirsty. His lips were dry, his throat was parched, and all he could think about was a cool drink of water.

Once help arrived and Dan was ensconced in air-conditioned luxury with a tall glass of ice water, he suddenly felt hungry and realized that he hadn’t eaten for hours.

Hunger, thirst, and hyperthermia (hyper- means “more than normal” and -thermia means “heat” or “temperature” in Latin) are drive states. A drive is a condition that motivates an individual to perform a particular behavior or set of behaviors in order to eliminate that condition. That is, when you are hungry, you fix a sandwich, open a bag of chips, or drive to a fast-food restaurant to satisfy that drive state. The same is true for being thirsty or overheated (or underheated). You engage in appropriate behaviors to satisfy the state of imbalance produced by the drive.

In this chapter we will look at the regulation of motivated behaviors such as eating, drinking, and managing temperature. These behaviors appear to be controlled by particular regions of the hypothalamus, a brain structure that plays an important role in homeostatic regulation. Homeo- stasis is derived from two Greek words, homeo- (homos) meaning “same” and -statis meaning “to stand.” Thus, homeostasis involves maintaining certain biological variables, such as body tempera- ture, body weight, and body fluid volume, at a constant level. Obviously, homeostatic regulation by the hypothalamus is not perfect. For example, some people overeat and gain weight, thereby overriding their homeostatic mechanism that regulates eating.

Let’s examine how temperature, food intake, and body fluids are regulated. I have placed a greater emphasis on food intake regulation in this chapter because physiological psychologists have con- ducted a vast amount of research on eating behavior.

9.1 Regulation of Body Temperature

We have a number of classification systems that categorize animals according to their ability to regulate their body temperatures. Aristotle proposed one of the earliest classification systems, categorizing animals as either warm-blooded or cold-blooded. According to Aristotle’s classification system, warm-blooded animals are warm to touch, and cold-blooded animals are cool to touch. However, Aristotle’s system runs into trouble when we try to categorize a reptile, like a lizard, that has been lying in the sun. This lizard feels warm to touch after it has been lying in the sun for some time, although it feels cool after it has been lying in the shade. Certainly, an animal cannot be both warm-blooded and cold-blooded. Scientists have developed more precise classification systems since Aristotle’s time.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

One modern classification system categorizes animals as endotherms or ectotherms, based on their body’s source of heat. Endotherms are animals that have an internal source of heat, whereas ectotherms are animals that get their body heat from sources outside their own bodies. Endo- therms produce heat through oxidation of substances such as fats, proteins, and carbohydrates. Oxidation is a process of combustion in which substances are combined with oxygen. Although ectotherms also make use of oxidative processes in their bodies, the heat produced is not con- trolled or harnessed by an ectotherm’s central nervous system. In general, endotherms maintain a constant core body temperature and thus are homeothermic. (Core body temperature refers to the temperature of the body core, which includes the internal organs and the brain.) Birds and mammals are endotherms, and all other animals are ectotherms.

Balancing Heat Production and Heat Loss

It is nearly impossible to think about heat production without also thinking about heat loss, because these two processes are closely linked in homeothermic animals (also called homeo- therms). In order for a homeotherm to maintain the same body temperature, heat production must be equal to heat loss. However, it is easier to discuss the mechanisms of heat production independent from heat loss, so this chapter will present the mechanisms of heat production first, followed by a discussion of heat loss.

Heat Production Endotherms produce heat by means of two mechanisms: shivering thermogenesis and nonshivering thermogene- sis. Shivering thermogenesis is the production of heat by the rhythmic muscular contractions that we call shivering. When the hypothalamus detects that the core body tem- perature has decreased, it stimulates neurons in the cer- ebellum that initiate shivering. The cerebellum coordinates shivering by relaying rhythmic impulses down the spinal cord to motor neurons, which stimulate rhythmic muscle contraction. When muscles contract, they produce a great deal of heat. If you jog for a block or so, you will notice immediately that you start to sweat and feel overheated after a few minutes of exercise. Shivering produces a lot of heat because many muscles are contracting at once, gener- ating much heat. The colder you become, the more vigor- ously you shiver. I was so cold once that I could barely talk because my teeth were chattering so violently.

Nonshivering thermogenesis refers to all the other ways in which we produce heat (besides shivering). The primary mechanism of nonshivering thermogenesis is basal metab- olism. Basal metabolism is the minimum amount of energy expended while a person is at rest. When you are resting, your heart is beating, you are breathing, and a reduced number of neurons in your brain are active, but that’s about all that’s happening in your body. However, the muscles in your chest (that is, your heart muscle and the muscles between your

Blend Images/SuperStock

Photo 9.1 When the hypothalamus detects that the core body temperature has decreased, it stimulates neurons in the cerebellum that initiate shivering.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

ribs) produce heat, even when you are resting. In fact, when you are resting, more than 75% of your body’s heat is produced in your chest and head. In contrast, when you are shivering, more than 75% of your body’s heat is produced by your skeletal muscles. Thus, basal metabolism is an important source of heat production.

Basal metabolism is controlled by thyroid hormones, released by the thyroid gland, that cause an increase in body temperature. The thyroid gland is a butterfly-shaped organ located in the neck (Figure 9.1). Its functioning is controlled by the pituitary gland, like many of the body’s other glands.

Figure 9.1: The location of the thyroid gland and other endocrine glands

The thyroid gland, along with the other glands in the body, is controlled by the pituitary gland. How does the thyroid gland regulate body temperature?

Hypothalamus Pituitary

Thyroid

Pancreas

Adrenals

Ovaries (female gonads)

Testicles (male gonads)

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CHAPTER 9Section 9.1 Regulation of Body Temperature

Recall from Chapter 4 that the hypothalamus regulates the activity of the pituitary gland. When neurons in the hypothalamus detect a drop in the core body temperature, a command is sent from the hypothalamus to the pituitary gland to increase body temperature. In response to the command from the hypothalamus, the pituitary releases thyrotropin-releasing hormone into the bloodstream. Thyrotropin-releasing hormone arrives at the thyroid gland via the bloodstream and stimulates the thyroid gland to release a number of thyroid hormones. Thyroid hormones increase the core body temperature by increasing basal metabolism (Andersson, Ekman, Gale, & Sundsten, 1963). Think for a moment about how this mechanism works: Basal metabolism is the amount of heat produced at rest. If basal metabolism is increased, then heart rate and respiration rate speed up, producing more muscle contractions per minute and thus more heat.

Another mechanism of nonshivering thermogenesis is brown fat metabolism. Human babies are born with very immature nervous systems and are incapable of shivering until they are about 6 months of age. However, newborn humans are born with deposits of brown fat located in stra- tegic areas of their bodies, at the back of the head and in the chest (McCance & Widdowson, 1977). When the hypothalamus of a newborn detects a decrease in core body temperature, the hypothalamus directs the burning of brown fat, which produces a good deal of heat, thereby rais- ing the baby’s core body temperature (Sharma, Ford, & Calvert, 2010; Friedman, 1967). (Most fat in the body is white and produces less heat than brown fat when burned.) Babies burn off most of their brown fat by the age of six months, although some brown fat is found in adults (Tews & Wabitsch, 2011).

Heat Loss Heat loss occurs constantly as we lose heat to the environment in several ways. Evaporation is the most effective mechanism that we have for losing heat. It is the process by which liquid is turned into a gas or vapor. To turn a liquid into vapor requires a lot of heat, approximately one calorie per gram of liquid for each degree of heat. The heat needed to produce evaporation comes from the body, which results in heat loss for the body (Figure 9.2). To enhance heat loss through evapora- tion, humans produce sweat, which is released onto the surface of the skin and subsequently evaporates, producing heat loss.

Most mammals cannot sweat, but they use the mechanism of evaporation in other ways. For exam- ple, dogs and cats (and most other mammals) lose heat through panting. They produce a bolus of saliva on their tongue and breathe fast and rhythmically through their mouths, causing the saliva to evaporate, which causes heat loss. Pigs and hippos wallow in mud and then emerge to cool off by letting the wet mud evaporate from their bodies. In a similar manner, rats, guinea pigs, and kangaroos lick themselves, spreading their saliva all over the surfaces of their bodies. As the saliva evaporates, it removes heat from their bodies, cooling them (Hainsworth & Epstein, 1966).

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CHAPTER 9Section 9.1 Regulation of Body Temperature

Figure 9.2: Mechanisms of heat loss

To enhance heat loss through evaporation, humans produce sweat, which is released onto the surface of the skin and evaporates (Figure A). By contrast, hippos wallow in mud and then emerge to cool off by letting the wet mud evaporate from their bodies (Figure B).

We also lose heat through conduction of body heat to the surrounding air or to solid objects in the environment. For example, when you stand on a cold sidewalk, you lose heat through the soles of your shoes, due to conduction. You might notice that, during the December holiday season, volunteers for the Salvation Army stand out in the cold for long periods of time. Their secret? They stand on a piece of corrugated cardboard, which acts as an insulator between their feet and the frozen sidewalk. The corrugated cardboard traps air between the sheets of cardboard and the cold sidewalk. Air is a poor conductor of heat, which means that heat does not readily flow from the feet through the cardboard to the sidewalk. When you sit in a chair, you lose heat to the chair through radiation. Feel the seat of the chair when you get up. You will notice that the seat is warm. That warmth came from your bottom, which was in contact with the chair.

Vascular Control of Heat Loss Blood vessels play an important role in the regulation of body temperature, particularly the super- ficial blood vessels that are found in the skin. When the blood vessels in the skin dilate, blood flow to the surface of the body increases, and heat loss to the environment is increased. In con- trast, constriction of blood vessels in the skin reduces blood flow to the body’s surface and thus decreases heat loss through the skin. Therefore, when we become cold or when we are exposed to a cold environment, our superficial blood vessels constrict, reducing heat loss. When we are overheated or exposed to a hot environment, our superficial blood vessels dilate, which increases heat loss to the environment.

A. B.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

Insulation Responses Recall that air is a poor conductor of heat. The insulation response takes advantage of this prin- ciple in order to reduce heat loss to the environment. Birds and mammals have smooth muscles in their skin that encircle the roots of feathers (birds) or hairs (mammals). When these smooth muscles contract, the feathers or hairs are pulled up to an erect position. This insulation response is called piloerection. When piloerection occurs, air is trapped between the erect hairs or feath- ers. This layer of air insulates the body because air is a poor conductor of heat. Hence, the animal’s body heat is not readily lost to the environment when piloerection occurs.

Piloerection is quite effective in preventing heat loss in hairy animals. For example, the arctic fox has such extremely thick fur insulation that shivering is unnecessary until the temperature falls to –408C (Scholander, Hock, Walters, Johnson, & Irving, 1950). However, in relatively hairless animals like humans, piloerection is not very effective. When we get cold, the insulation reflex is trig- gered in our skin, causing smooth muscles that surround hair follicles to contract. You can see the contraction of these smooth muscles as your skin gets a bumpy appearance when they contract, resulting in what is sometimes referred to as “goose bumps.” Because piloerection is not effective in humans, we make behavioral responses to compensate for our lack of insulation, such as put- ting on more clothes.

The central nervous system of a homeotherm struggles to maintain a stable core body tempera- ture. This is a difficult task because heat loss continues constantly, and the body must produce enough heat, but not too much, to counterbalance the heat lost through evaporation and conduc- tion. Figure 9.3 summarizes the body’s response when it is exposed to a hot environment and a cold environment.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

Figure 9.3: Balancing heat production and heat loss

Figure A: Exposure to a hot environment. When we are exposed to a hot environment or when we become overheated, our bodies make a number of adjustments to prevent hyperthermia. The first response of the body is to dilate superficial blood vessels. The second response of the body is to sweat, which increases heat loss through evaporation. If you remain for an extended period of time in a hot environment, your hypothalamus directs your pituitary gland to decrease basal metabolism by reducing the output of your thyroid gland.

Figure B: Exposure to a cold environment. When exposed to a cold environment, our bodies’ first response is to increase the insulation response, or produce “goose bumps” by piloerection. The second response of the body is to decrease blood flow to the skin by constricting superficial blood vessels. The next response is to shiver, which typically produces a great deal of body heat. If you are a very young infant and are unable to shiver, you would burn brown fat. Finally, if you are exposed to a cold environ- ment for a long time, your hypothalamus directs your pituitary gland to increase basal metabolism by increasing the release of thyroid hormones.

Decrease in basal metabolism

Thyroid

Reduced output

Pituitary gland

Hypothalamus

First Response

Second Response

Fourth Response

First Response

A. B.

Second Response

Third Response

Superficial blood vessels dilate

Body sweats Superficial blood vessels constrict

Insulation response increases— “goose bumps”

Body shivers Increase in basal metabolism

Thyroid

Increasing release of thryroid hormones

Pituitary gland

Hypothalamus

Third Response

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CHAPTER 9Section 9.1 Regulation of Body Temperature

Brain Mechanisms Involved in Temperature Regulation

You’ve already learned about the brain mechanisms that control shivering and the release of thy- roid hormones, which increase basal metabolic rate. Both of these heat production processes are regulated by a region in the anterior hypothalamus called the preoptic area. In fact, heat pro- duction and heat loss are both controlled by the preoptic area of the hypothalamus, as research with nonhuman animal subjects has demonstrated (Ishiwata et al., 2001; Jha, Islam, & Mallick, 2001). For example, when the preoptic area of a rat is lesioned, the rat is unable to maintain a normal core body temperature and will not shiver or show nonshivering thermogenesis when it is exposed to a cool environment (Satinoff, Valentino, & Teitelbaum, 1976). Electrical stimulation of the preoptic area in rats produces both shivering and nonshivering thermogenesis (Thornhill & Halvorson, 1994).

Neurons in the preoptic area appear to be thermosensitive, or sensitive to temperature. Laudenslager (1976) applied heat and cold to neurons in the preoptic area of rhesus monkeys. When Laudenslager cooled the neu- rons in the preoptic area of monkeys, the monkeys pressed a lever con- tinuously to turn on a sunlamp. The monkeys pressed a lever to receive cool air when the preoptic neurons were heated. Forster and Ferguson (1952) demonstrated that warming thermosensitive neurons in the hypo- thalamus of cats produced panting in those animals. Similarly, cooling the preoptic area produces shivering, and warming the same area suppresses shivering in rats (Kanosue, Zhang,

Yanase-Fujiwara, & Hosono, 1994; Zhang, Yanase-Fujiwara, Hosono, & Kanosue, 1995).

Behavioral Regulation of Heat Production and Heat Loss

Ectotherms cannot shiver and thus cannot produce heat by shivering thermogenesis. However, this does not mean that ectotherms cannot regulate body temperature. When ectotherms become cold, they seek shelter in a warm place or they huddle together. I remember, when I was a graduate student at Columbia University and living in New York City, finding a most disgusting cluster of cockroaches gathered around the pilot light of my gas oven one December afternoon. Likewise, ectotherms can also decrease their body temperatures by behavioral means when they become overheated. For example, ants will carry water in their mouths when they get too hot, allowing evaporation of the transported water to cool them off.

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Photo 9.2 The preoptic area in the anterior hypothalamus controls heat production and hear loss.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

Endotherms, too, use behavioral means to increase or decrease body temperature. For example, people will stamp their feet and flap their arms when they are cold. The muscular contractions that are produced when feet are stamped and arms are flapped generate a good deal of heat, although not as much as shivering does. We also put on coats, scarves, and hats when we are cold to prevent heat loss. To enhance heat loss when we are too hot, we might sit in front of a fan (which increases heat loss through convection), take off excess clothing (increasing heat loss through conduction), splash water on our bodies (to increase heat loss through evaporation), or move into a cooler environment.

Disorders of Temperature Regulation

We’ve all experienced a fever. It typically accompanies a cold or the flu, ailments that are caused by infectious microorganisms. A fever is an increase in core body temperature above its normal level. In fact, although we regard a fever as a sign of dysregulation of our body temperature, the spike in temperature that is the hallmark of a fever is actually orchestrated by the hypothala- mus in response to stimulation by the immune system. The function of the immune system, as you will learn in Chapter 12, is to identify foreign agents that threaten the well-being of the body.

When a microorganism infects a region of your body, your immune system mobilizes to deal with the intruder and informs the hypothal- amus that the body is under attack. In response, the preoptic area of the hypothalamus directs an increase in core body temperature (Saper, 1998). Bacteria and viruses are quite fragile and can survive within only a narrow range of tem- peratures. When the body temper- ature rises above 998F, viruses and bacteria begin to die. Thus, the hypothalamus produces a state of fever to fight an infection by microorganisms. We feel quite miserable when we have a fever and our core body temperature is above 998F. But, we can usually survive a slight fever. When the core body temperature goes above 1058F, however, enzymes in our brains and bodies cannot work effectively, and our body systems begin to shut down.

Menopausal Dysregulation The menstrual cycle in women is controlled by hormones produced by the pituitary gland and the ovaries, as you will learn in Chapter 10. Core body temperature in women fluctuates over the course of the menstrual cycle, with the highest temperatures recorded at ovulation and the low- est recorded just before menstruation. Thus, sex hormones appear to influence the regulation of body temperature in women. Some women experience a significant drop in core body tempera- ture, which causes insomnia, 1 or 2 days before menstruation (Manber & Armitage, 1999).

Getty Images/Creatas Images/Creatas/Thinkstock

Photo 9.3 A fever is orchestrated by the hypothalamus in response to stimulation by the immune system.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

When a woman ages and the production of sex hormones ceases, it results in a state called meno- pause, during which regulation of core body temperature can be disrupted. Many menopausal women experience a sudden increase in core body temperature from time to time, referred to as a hot flash. In response to an erratic release of pituitary hormones, the preoptic area of the hypo- thalamus directs an increase in heat production, which produces a sudden rise in body tempera- ture (Archer et al., 2011). Recall what happens when the body becomes overheated: Vasodilation and flushing of the skin occur, followed by profuse sweating. A woman experiencing a hot flash feels overly warm, clammy with sweat, and very uncomfortable. For some women, hot flashes occur so frequently that they are a source of great discomfort. Hormonal supplements, which increase the levels of estrogen and progesterone in a woman’s body, can alleviate the symptoms of temperature dysregulation caused by menopause.

Energy Balance

We’ve just examined how homeotherms balance heat production and heat loss to maintain a constant body temperature. Heat production is also closely associated with food intake. For healthy endotherms that maintain the same body weight over a period of time, the following equation is true:

Energy IN 5 Energy OUT

In this equation, energy is measured in units called calories. Energy IN refers to the calories we take in as food. Energy OUT refers to the many ways in which we expend energy, such as move- ment and exercise, growth, maintenance of body tissues, basal metabolism, and heat production. The food that we eat is burned to produce energy that allows us to move, grow, maintain our tissues, and produce heat. Thus, food intake is closely associated with the regulation of body tem- perature. Healthy, well-nourished endotherms (humans included) will maintain the same body weight if the amount of energy they take in as food is equal to the amount of energy that they need for muscle contractions, growth and maintenance, and heat production.

When food intake exceeds the energy expended (that is, when Energy IN . Energy OUT), weight gain occurs. In the next section of this chapter, we will examine a variety of reasons why peo- ple gain weight. For example, people gain weight when they increase their food intake without increasing their energy output (Energy IN increases, and Energy OUT remains the same). They also gain weight when they switch from an active to a sedentary lifestyle without making a compensa- tory decrease in their food intake (Energy IN remains the same, and Energy OUT decreases). Mov- ing from a cold to a warm climate can also produce a decrease in Energy OUT because the person who has moved to the warmer climate no longer needs to produce as much body heat. The “For Further Thought” box discusses individual differences in weight gain caused by variations in fidg- eting, maintaining good posture, and other activities.

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CHAPTER 9Section 9.1 Regulation of Body Temperature

For Further Thought: Activity and Resistance to Weight Gain

When people consume more calories than they burn, they tend to put on weight. Some individuals resist weight gain when they overeat, whereas others get fat. We all know people who can eat huge amounts of food and remain quite thin. What is their secret?

At the Mayo Clinic, James Levine and his colleagues, Norman Eberhardt and Michael Jensen (1999), have studied how dif- ferent people expend excess calories when they overeat. For 8 weeks, the adult participants in their experiment con- sumed 1,000 extra kcal every day, eating between 2,200 and 3,800 kcal per day. (Human calorie intake is measured in units called kilocalories, abbreviated as kcal.) As a result of daily overconsumption of calories, the participants gained an average of 10.3 pounds over 8 weeks. However, not all people in the study gained the same amount of weight. Some gained as little as 3 pounds, and some gained nearly 16 pounds.

The investigators were able to measure both fat gain and energy expenditure in each of the overfed participants. They found that, on a daily basis, participants stored a mean of

432 kcal of the excess energy consumed as fat and burned a mean of 531 kcal as increased energy expenditure. However, the range among the participants was actually quite large. One person stored only 58 kcal as fat each day, whereas another stored 687 kcal as fat each day.

Levine and his colleagues then determined how the participants expended their excess energy intake. They restricted the participants to a low level of sports and fitness types of activities (including walk- ing), which they measured. The remaining energy expenditure of the participants was due to non- exercise activity, such as fidgeting, spontaneous muscle contractions, and maintaining posture. The investigators’ analysis of the data indicated that nonexercise activity determines who gained weight. The change in nonexercise activity for the participants ranged from –98 kcal per day (which represents a decrease in activity) to +692 kcal per day. Those people who spent more time fidgeting, sitting, and standing gained less weight than fellow participants who lounged around and did not exhibit much spontaneous muscular activity. You can view all the data collected by Levine and his colleagues in this study at www.sciencemag.org/feature/data/982662.shl.

Robert Daly/Stone/Getty Images

Photo 9.4 People store weight dif- ferently, depending on their activity levels.

In contrast, when the energy expended exceeds food intake (Energy IN , Energy OUT), weight loss occurs. For example, when a person goes on a diet, Energy IN decreases. In the case of a dieter, Energy OUT can exceed Energy IN if the dieter decreases food intake without simultane- ously decreasing exercise level. You can imagine that, if a person diets and increases exercise out- put (that is, if Energy IN decreases and Energy OUT increases), even more weight loss will occur. However, dieting can induce a reduction in basal metabolism (decreasing Energy OUT), especially in people who have been dieting for a long time (Gingras, Harber, Field, & McCargar, 2000). The hypothalamus responds to a decrease in Energy IN by reducing Energy OUT. Therefore, people who try to lose weight by dieting will typically find it difficult to lose weight due to their reduced

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CHAPTER 9Section 9.2 Regulation of Food Intake

basal metabolic rate. Exercise, on the other hand, increases basal metabolic rate and can enhance weight loss in people who are dieting (Thompson, Manore, & Thomas, 1996).

The interaction between body temperature and food intake is undeniable. However, food intake is influenced by many variables besides temperature regulation. Let’s take a look at the current research on food intake and body weight regulation.

9.2 Regulation of Food Intake

Food intake and food selection are affected by many variables, both biological and psycho-logical. Psychological variables are typically related to individual differences, such as prefer- ences for certain flavors or food textures. We will examine psychological variables briefly in this chapter, but our main focus will be on biological factors that determine food intake. We will look at brain mechanisms, as well as mechanisms in the peripheral nervous system, that control the onset and offset of eating. In addition, we will review the research on the effects of neurotrans- mitters and hormones on eating. Let’s start by exploring the role that homeostasis plays in food intake regulation.

Homeostasis and Allostasis

Homeostasis was first described by Walter Cannon (1929), a professor of physiology at Harvard University, as the set of mechanisms that maintains steady states in the body, including constant levels of glucose and water, among other things. According to Cannon, homeostatic mechanisms cause an individual to drink when water levels in the body fall or to eat when glucose levels decline. However, homeostasis cannot explain fully why individuals begin to eat or drink. That is, we do not always eat because our blood glucose levels have dropped. Sometimes we eat when we have no need for food. A concept called allostasis has been introduced to explain the nonhomeostatic cues that initiate eating and drinking. Allostasis takes into account an individual’s expectations and readiness to alter behavior to meet changing demands in the environment (Schulkin, McEwen, & Gold, 1994). For example, most of us have been forced to nibble a piece of birthday cake after a very filling meal when we were not hungry at all.

Thus, homeostasis is a nonflexible mechanism that requires systems to have set points, or opti- mum levels of various physiological factors, such as body temperature or blood glucose levels, which the nervous system struggles to maintain. When a measure deviates from a set point, as when blood glucose levels drop below some optimal level, homeostatic mechanisms in the brain initiate behavior to bring the level back to the set point level. Allostasis, on the other hand, is a flexible system that allows for learning and adaptation to changing circumstances. Together, homeostasis and allostasis control eating, which means that the regulation of eating is very com- plicated (Power & Schulkin, 2011).

Humans are omnivores, which means they eat a variety of foods, including meats, vegetables, and grains, to obtain the energy and nutrients that they need. Omnivores face a unique predica- ment that vegetarian (strictly plant eating) and carnivorous (strictly meat eating) animals do not: They must carefully select foods in their diet to obtain the complete balance of nutrients that they need. Thus, besides eating to obtain energy, omnivores also eat to obtain needed nutrients, such as protein, fat, carbohydrates, vitamins, and minerals. Table 9.1 gives the recommended minimum daily requirement for selected nutrients for humans.

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CHAPTER 9Section 9.2 Regulation of Food Intake

Table 9.1: Recommended minimum daily requirements for selected nutrients

Nutrient minimum daily requirement Carbohydrates 315 g

Protein 25 g

Fat 65 g

Vitamin A 5000 IU

B vitamins: Thiamin 1.5 mg

Riboflavin 1.7 mg

Niacin 20 mg

B 6

2 mg

Folic acid 400 mcg

B 12

6 mcg

Other vitamins: Vitamin C 60 mg

Vitamin D 400 IU

Vitamin K 30 IU

Potassium 4g

Calcium 1g

Iron 18 mg

Chloride 3.6 g

Zinc 15 mg

Copper 2 mg

Units of measurement: g 5 gram; IU 5 International Unit; mg 5 milligram (10-3 g); mcg 5 microgram (10-6 g).

Food intake consists of two processes: (1) onset of eating and (2) offset of eating. Let’s examine each of these processes separately.

Onset of Eating

The onset of eating is controlled by both homeostatic and allostatic mechanisms. Typically, we do not wait until our energy supplies are depleted before we start eating. Most of us, most of the time, eat in anticipation of our needs. For the most part, we rely on allostatic, rather than homeostatic, mechanisms to begin eating. This allostatic mechanism, which involves learning, is evident in the way eating habits are established. We all have regular, appointed hours at which we consume food. Those of us who eat breakfast every day feel quite hungry by midmorning if we haven’t eaten, whereas those who regularly skip breakfast do not feel like eating until lunchtime. Some people acquire a habit of eating ice cream in the evening before bedtime. If you have this habit and happen to skip your ice cream treat in the evening, you feel hungry at bedtime. This means that some allostatic mechanism “learns” when your regular or habitual eating times occur, and it prompts you to eat when the appointed eating hour approaches.

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CHAPTER 9Section 9.2 Regulation of Food Intake

Allostatic Mechanisms You might be wondering about the location of this allostatic mechanism that prompts you to eat. Some investigators believe that the lateral hypothalamus, working in conjunction with the prefrontal cortex, is responsible for the allostatic mechanism regulating eating behavior (Inglis & Winn, 1995). Many anatomical interconnections exist between the lateral hypothalamus and prefrontal cortex, which means that there is a great deal of communication between these two brain sites.

Early research demonstrated that bilateral lesions of the lateral hypothalamus produced a failure to eat, or aphagia, and weight loss in rats (Anand & Brobeck, 1951). That is, following destruction of the lateral hypothalamus in both hemispheres, rats refused to eat or drink and eventually died from starvation unless measures were taken to provide nutrients to them. Investigators prema- turely concluded that the lateral hypothalamus is responsible for the initiation of eating, referring to the lateral hypothalamus as the feeding center (Grossman, 1967; Stellar, 1954). However, sub- sequent studies showed that dopamine-transmitting axons pass through the lateral hypothalamus on their way from the substantia nigra to the basal ganglia and raised the question of whether lesioning the dopamine axons caused aphagia. Indeed, lesioning this dopamine pathway did pro- duce aphagia and weight loss in rats, despite the fact that no neurons in the lateral hypothalamus were injured (Marshall, Richardson, & Teitelbaum, 1974; Ungerstedt, 1973). After a decade or more of skepticism, the lateral hypothalamus was shown to play an important role in the control of eating. Table 9.2 summarizes the roles of brain structures involved in homeostasis and allostasis.

Table 9.2: Role of brain structures in homeostasis and allostasis of food intake

Brain structure Function

Lateral hypothalamus (allostatic) Initiates eating when the individual is motivated to eat

Prefrontal cortex behavior (allostatic) Organizes attention to food and execution of eating

Orbitofrontal cortex Changes eating behavior in response to learning (allostatic)

Basal ganglia Initiates eating under influence of lateral hypothalamus and prefrontal cortex (allostatic)

Paraventricular nucleus Organizes eating behavior in response to changes in internal body of hypothalamus states (homeostatic)

Ventromedial nucleus Relays information from the nucleus of the solitary tract to the of hypothalamus paraventricular nucleus (homeostatic)

Homeostatic Mechanisms

According to Nigel Lawes (1988), homeostatic regulation takes place in the paraventricular nucleus of the hypothalamus (Figure 9.4). The paraventricular nucleus receives information from the body and organizes behavior to respond to changes in internal body states. For example, the paraventricular nucleus receives information about blood glucose levels and water balance and

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CHAPTER 9Section 9.2 Regulation of Food Intake

directs the brain’s response to changes in these variables. When blood glucose levels fall, the paraventricular nucleus initiates eating to restore optimal blood glucose levels. In contrast, the neurons in the lateral hypothalamus do not respond directly to changes in blood glucose or water balance (Winn, 1995).

Figure 9.4: The paraventricular nucleus in the rat brain

The paraventricular nucleus of the hypothalamus receives information about the peripheral nervous system from the nucleus of the solitary tract and information about fat stores and blood sugar from other areas of the hypothalamus. Together, the paraventricular nucleus (homeostatic control) and the lateral hypothalamus (allostatic control) direct food intake.

A number of theories have been proposed to explain the homeostatic mechanism underlying the regulation of eating behavior. These theories include the glucostatic theory, the thermostatic theory, and the lipostatic theory. You will notice that each of these theories makes use of the suffix -static, which refers to a steady state. Thus, these theories postulate that a steady state is main- tained in the body by a homeostatic mechanism.

The glucostatic theory, first proposed by Mayer (1953), maintains that glucose levels are regulated in the body. According to this theory, whenever blood glucose levels fall below some optimal level, glucose receptors in the brain fire and stimulate eating. When blood glucose levels rise, eating is terminated. This theory has quite a bit of empirical support but has proven to be an inadequate explanation for the control of eating (Chaput & Tremblay, 2009; Smith, 1996). When regulating food intake behavior, the brain is influenced by many factors in addition to blood glucose levels, as you will learn in this chapter. Body fat supplies, hormone levels, and learning are just a few of the many influences that determine when and what an individual eats.

The thermostatic theory postulates that core body temperature drives eating behavior (thermo- means “temperature” or “heat” in Greek). When body temperature falls below some optimal level, eating is triggered. In contrast, a rise in body temperature will cause eating to cease. Accord- ing to this theory, heat is produced during the course of a meal as a result of smooth contractions in the gut following ingestion of food. This rise in body temperature that accompanies ingestion of

Human brain

Vagus nerve

Nucleus of solitary tract

Nucleus of solitary tract

Vagus nerve

Lateral hypothalamic

area

Lateral hypothalamic

area

Arcuate nucleus

Rat brain

Paraventricular nucleus

Paraventricular nucleus

Arcuate nucleus

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CHAPTER 9Section 9.2 Regulation of Food Intake

food triggers a mechanism that terminates eating of a meal. That is, as body temperature begins to rise during a meal, temperature receptors fire in response to the increase in body temperature and excite neurons in parts of the brain that stop eating. Temperature receptors that respond to very small changes in internal body temperature are located in the body cavity along the dorsal wall, where they can detect the heat produced by digestive processes (Riedel, 1976). However, core body temperature alone cannot explain why eating begins and stops.

The prefix lipo- refers to fat or fatty tissue. Thus, the lipostatic theory of food intake regulation is based on the notion that a central homeostatic mechanism monitors and maintains an optimal level of body fat. The “optimal” level of body fat appears to depend on a number of factors, includ- ing genetics. That is, some individuals have inherited a predisposition for more fat storage than others. According to the lipostatic theory, the brain stimulates eating when fat stores fall below an optimal level and terminates eating when fat storage is excessive. This theory has some sup- port (Speakman, Stubbs, & Mercer, 2002). Leptin is a hormone that is secreted by fat cells and suppresses food intake (Baile, Della-Fera, & Martin, 2000; Fulton, Woodside, & Shizgal, 2000). Investigators have determined that the more fat an individual has stored, the more leptin that is released. Therefore, leptin regulates fat storage by suppressing food intake when fat stores get too large. Although the action of leptin may explain how fat storage is regulated in the body, it is doubtful whether the lipostatic theory can explain why an individual starts and stops eating a particular meal.

In summary, the glucostatic theory focuses on blood glucose levels as the controlling factor for eating behavior, whereas the thermostatic theory focuses on core body temperature and the lipo- static theory focuses on fat storage. However, none of these theories can, by themselves, explain why an individual starts and stops eating.

Effects of Drugs and Neurotransmitters Two classes of drugs, barbiturates and benzodiazepines, have been shown to stimulate food intake. Recall from Chapter 3 that barbiturates and benzodiazepines are both classes of seda- tives that act as depressants of brain activity. Benzodiazepines increase GABA activity in the brain and have been demonstrated to produce hyperphagia, or overeating (hyper- means “more than normal” and -phagia means “to eat” in Latin), in a wide variety of species, including baboons, cattle, cats, dogs, hamsters, horses, humans, mice, monkeys, pigeons, pigs, rabbits, rats, sheep, and wolves (Cooper & Higgs, 1994). They appear to increase food intake by enhancing the palat- ability (that is, the tastiness) of the ingested food. Recall from earlier in this chapter that the lateral hypothalamus, in conjunction with the frontal cortex, mediates changes in responsiveness to food stimuli. Thus, benzodiazepines act by stimulating the reward system that acts through the lateral hypothalamus, making foods appear to be more tasty and, therefore, increasing their intake.

Morphine, too, produces hyperphagia (Doyle, Berridge, & Gosnell, 1993). In contrast, the opiate antagonist naloxone reduces food intake. This demonstrates that the endorphin system plays a role in food intake regulation. Although the data are not yet conclusive, endorphins appear to increase the palatability of food, just like benzodiazepines do (Cooper & Higgs, 1994). By increas- ing the tastiness of food, the endogenous opioid neurotransmitters stimulate eating through the allostatic system, encouraging individuals to eat even when they are no longer hungry.

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CHAPTER 9Section 9.2 Regulation of Food Intake

Effects of Neuropeptides Two brain peptides, galanin and neuropeptide Y, have been demonstrated to stimulate eating behavior and to control energy balance via the paraventricular nucleus of the hypothalamus (Lei- bowitz, 1995; Leibowitz, Akabayaski, Alexander, & Wang, 1998; Wang et al., 1998). However, these neuropeptides have different effects on eating behavior. Galanin appears to control fat intake, fat metabolism, and fat storage (Leibowitz, 1998). In rats, galanin produces increased fat consump- tion, and it stimulates fat consumption most vigorously at puberty. Neuropeptide Y triggers intake of carbohydrates and promotes the storage of excess carbohydrates as body fat (Leibowitz, 1995; Marston, Hurst, Evans, Burdakov, & Heisler, 2011). Thus, both galanin and neuropeptide Y encour- age fat storage and weight gain.

Another newly discovered class of peptides, called orexins, also stimulates food intake (Barson, Karatayev, Gaysinskaya, Chang, & Leibowitz, 2012; Morganstern, Barson, & Leibowitz, 2011; Saku- rai et al., 1998). Whereas galanin and neuropeptide Y are released in several locations in the brain, orexins are found only in the lateral hypothalamus, which means that their functions are quite limited. You learned about orexins in Chapter 8 when we discussed narcolepsy. Recall that dogs and mice that cannot make orexins become narcoleptic. Although the function of orexins is still unknown, Alasashi Yanagisawa and his colleagues (Sakurai et al., 1998) found that rats ate three to six times more food than did controls after orexins were injected directly into the lateral hypothalamus.

In summary, a number of drugs and neuropeptides stimulate eating, including barbiturates, ben- zodiazepines, morphine, galanin, neuropeptide Y, and orexin. Table 9.3 summarizes the action of these chemicals in the brain.

Table 9.3: Actions of drugs and neuropeptides on the onset of eating Chemical agent Function Allostasis or homeostasis? Drugs

Barbiturates Stimulate eating (increase palatability)

Allostasis

Benzodiazepines Stimulate eating (increase palatability)

Allostasis

Morphine Stimulates eating (increases palatability)

Allostasis

Neuropeptides

Galanin Stimulates eating (increases fat consumption)

Homeostasis

Neuropeptide Y Stimulates eating (increases carbohydrate consumption)

Homeostasis

Orexin Stimulates eating (function unknown) Homeostasis/Allostasis?

Peripheral Onset Mechanisms The peripheral nervous system appears to play an important role in stimulating eating behavior. Signals from the gut are transmitted to the brain by way of the vagus nerve, also known as cranial nerve X (Figure 9.5). This information is relayed to the nucleus of the solitary tract in the hindbrain and from there is sent to the paraventricular nucleus and the lateral nucleus of the hypothalamus.

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CHAPTER 9Section 9.2 Regulation of Food Intake

Information from the mouth, such as information about the taste of food, which can stimulate eating, is also sent to the nucleus of the solitary tract for processing (Zeigler, 1994).

Figure 9.5: The vagus nerve and its pathway

The paraventricular nucleus of the hypothalamus receives information about the peripheral nervous system from the nucleus of the solitary tract and information about fat stores and blood sugar from other areas of the hypothalamus. Together, the paraventricular nucleus (homeostatic control) and the lateral hypothalamus (allostatic control) direct food intake.

A review of the research concerning peripheral factors that trigger eating indicates that no single factor initiates eating by itself. Instead, several signals impact the central nervous system simulta- neously to trigger eating (Mei, 1994). Among these many signals are neural messages relayed to the brain via the vagus nerve and hormonal messages sent from the gut to the brain.

For example, stomach contractions produce feelings of hunger that trigger eating, as research by Walter Cannon (1912) has shown. Cannon had his graduate student swallow a balloon that was inflated in the stomach through a tube that passed down the throat and the esophagus. When the balloon was inflated, Cannon was able to measure the force of smooth muscle contractions as the

Vagus nerve

Nucleus of the solitary tract

Large intestine

Stomach

Duodenum

Spinal cord

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CHAPTER 9Section 9.2 Regulation of Food Intake

stomach squeezed the balloon with each stomach contraction. The student was asked to indicate when he felt hungry, and Cannon discovered that stomach contractions were most vigorous when the student reported feeling very hungry. Thus, Cannon concluded that stomach contractions sig- nal hunger. This finding shouldn’t come as a surprise to you. Certainly, your grumbling stomach must have prompted you to eat on more than one occasion.

However, other factors besides the stomach must signal a need to eat. Research on people who have had their stomachs surgically removed for medical reasons indicates that these individuals begin to eat normally, without external prompting, just like people who have intact stomachs. Therefore, stomach contractions are not necessary to produce eating, but they do stimulate eat- ing in people who have stomachs. Individuals without stomachs rely on other peripheral and cen- tral signals to trigger eating.

Offset of Eating

Did you ever think about why you put down your fork, push yourself away from the table, and stop eating? Brobeck (1955) introduced the concept of satiety to explain why you stop eating. Satiety has the same root as satisfaction, which is satis, a Latin word meaning “enough.” That is, you stop eating when you’ve had enough. But, how does your brain know when you’ve had enough?

Satiation is an unconscious physiological process that stops eating (Blundell, 1979; Smith, 1998). In this section we will look at the various factors that produce satiation and regulate the end of a meal. These factors include brain mechanisms as well as sensory signals from the gut and hor- monal signals. Let’s examine brain mechanisms first.

Central Offset Mechanisms In the previous section you learned that the paraventricular nucleus of the hypothalamus appears to regulate homeostatic eating. Therefore, in addition to the onset of eating, the paraventricular nucleus plays an important role in the offset of homeostatic eating. Closely related to the para- ventricular nucleus in this regard is the ventromedial nucleus of the hypothalamus (VMH). The ventromedial nucleus, as its name implies, is located in the ventral and medial region of the hypo- thalamus. Early research by Hetherington and Ranson (1940) demonstrated that bilateral lesions of the VMH produced hyperphagia and obesity. In contrast, electrical stimulation of the VMH caused a hungry animal to stop eating. As a result of lesioning and stimulation studies, the VMH was regarded as the “satiety center” of the brain that regulates the offset of eating (Stellar, 1954).

However, as with the lateral hypothalamus, many axons pass through the VMH. Lesioning the VMH produces damage to the neurons in the ventromedial nucleus and to the axons that pass through the nucleus. Likewise, electrical stimulation of the VMH excites both the cell bodies located in the VMH and the axons that pass through that region. Most of the axons that pass through the VMH form a pathway between the nucleus of the solitary tract and the paraven- tricular nucleus of the hypothalamus. Thus, damage to this pathway disrupts regulation of eating behavior, producing overeating. Table 9.2 summarizes the roles of the brain structures involved in food intake regulation.

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CHAPTER 9Section 9.2 Regulation of Food Intake

Effects of Drugs Early research on the effects of drugs on eating was conducted in the clinic rather than the labora- tory (Cooper & Higgs, 1994). One of the first published observations was on the appetite-reducing effect of amphetamine (Nathanson, 1937). For many years (before its negative side effects were recognized), amphetamine was widely used therapeutically as a weight-loss drug. Fenfluramine was another drug that was observed to reduce food intake in rodents and people (Munro, Seaton, & Duncan, 1966; Silverstone, Cooper, & Begg, 1970; Woodward, 1970). However, fenfluramine was banned in the United States in 1997, and consequently throughout the world, because it was demonstrated to damage the heart (Connolly et al., 1997; Dahl, Allen, Urie, & Hopkins, 2008; Rothman & Baumann, 2009).

These two drugs, which produce both decreased eating and weight loss, have different effects on the brain. Amphetamine acts through neural pathways that use norepinephrine and dopamine as their neurotransmitters and is believed to inhibit those parts of the brain that initiate eating. In contrast, fenfluramine increases activity in serotonin pathways and stimulates the satiety cen- ter in the ventromedial and paraventricular hypothalamus (Blundell, 1979; Blundell, Latham, & Lesham, 1976). Drugs that enhance activity at serotonin receptors produce satiety and decrease the amount of food eaten at a meal (Simansky, 1998).

Thus, amphetamine reduces food intake by inhibiting the onset of eating, and fenfluramine reduces food intake by stimulating satiety centers in the brain. The actions of these drugs are summarized in Table 9.4.

Table 9.4: Actions of drugs and hormones on the offset of eating

Chemical agent Function Allostasis or homeostasis?

Drugs

Amphetamine Appetite-reducing (inhibits initiation of eating)

Allostasis

Fenfluramine Appetite-reducing (stimulates satiation)

Homeostasis

Hormones

Cholecystokinin Appetite-reducing (stimulates satiation)

Homeostasis

Glucagon Appetite-reducing (stimulates satiation)

Homeostasis

Insulin Appetite-reducing (stimulates satiation)

Homeostasis

Leptin Appetite-reducing (reduces palatability)

Allostasis

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CHAPTER 9Section 9.2 Regulation of Food Intake

Peripheral Offset Mechanisms As food passes through the upper part of the digestive tract (that is, through the mouth, down the throat and esophagus, through the stomach and small intestine), it stimulates receptors located in the lining of these structures (Figure 9.6). These receptors send sensory messages about the presence of food by way of several cranial nerves (cranial nerves V, VII, IX, and X) to the central nervous system, which signal satiation and, therefore, cause eating to stop. It is interesting that these peripheral signals occur and satiation begins before nutrients are absorbed into the blood. Satiety is apparently elicited by food in the digestive tract before absorption has occurred and energy stores have been replaced (Smith, 1998).

Figure 9.6: Major organs of the digestive tract

Can you explain the relationship between the digestive tract and the central nervous system?

Oral cavity

Trigeminal nerve (V)

Facial nerve (VII)

Esophagus

Salivary glands

Pharynx

Glossopharangeal nerve (IX)

Vagus nerve

Stomach

Pancreas

Small intestine

Large intestine

Rectum

Anus

Duodenum

Gallbladder

Liver

Hypothalamus

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CHAPTER 9Section 9.2 Regulation of Food Intake

Oral Cues Food placed into the mouth stimulates receptors that line the oral cavity and the throat and starts the development of satiety. Research with dogs and rats has demonstrated that stimula- tion of receptors in the mouth and throat can produce satiety (Kraly, Carty, & Smith, 1978; Smith, 1995). Some people, due to accident or disease, are unable to swallow and must feed themselves through a stomach tube that is inserted directly into the stomach. Interviews with these individu- als indicate that people with stomach tubes feel more satisfied with a meal when they can chew the food and spit it out before inserting food in the stomach tube. Thus, stimulation of receptors in the mouth contributes to the experience of satisfaction during a meal.

Stomach Cues Food in the stomach can also produce satiety (Smith, 1998). Think about how you feel after you’ve consumed an enormous meal, like Thanksgiving dinner. Your stomach is distended from all the mashed potatoes and stuffing you’ve consumed, and you feel that you can’t eat another bite. This same effect can be produced in the laboratory. An inflatable cuff, devised by Young and Deutsch (1981), is placed around the constriction between the stomach and the small intestine, called the pyloric sphincter. When the cuff is inflated, food cannot pass from the stomach to the small intes- tine. Satiety is readily produced in an animal when the pyloric cuff is inflated just prior to a meal. Rats with an inflated pyloric cuff stop eating immediately after consuming a normal-sized meal, indicating that satiety can occur before food has been absorbed into the blood from the small intestine (Phillips & Powley, 1996).

Intestinal Cues The small intestine, which is located between the stomach and the large intestine, also plays an important role in the development of satiety (Greenberg, 1998). The duodenum (the section of the small intestine nearest the stomach) provides a good deal of information to the central ner- vous system that induces feelings of satiety in the individual (Figure 9.6). Research with dogs, rats, pigs, and human participants has shown that food injected directly into the duodenum of a hungry individual inhibits food intake (Ehman, Albert, & Jamieson, 1971; Houpt, 1982; Welch, Saunders, & Read, 1985; Yin & Tsai, 1973.) Thus, food in the duodenum stimulates receptors that signal the brain, producing satiety.

Effects of Hormones and Neurotransmitters The mechanisms by which receptors in the stomach and intestines produce satiation are largely unknown. Certainly, neural messages transmitted by way of the vagus nerve to the nucleus of the solitary tract and the paraventricular nucleus of the hypothalamus play a role in the inhibition of eating. There is also evidence that chemical substances that act as hormones are released into the blood when food stimulates receptors in the stomach and duodenum. A number of hormones released in the gut induce the termination of eating behavior. These hormones are peptides, which means that they can also act as neurotransmitters and bind with receptors on neurons. We will examine the role of cholecystokinin, glucagon, insulin, and leptin in this section.

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CHAPTER 9Section 9.3 Eating Disorders

Cholecystokinin (CCK) is a peptide that is released from the duodenum in response to ingested food. Gibbs, Young, and Smith (1973) demonstrated that intraperitoneal injections of CCK (that is, administration of CCK into the abdomen via a needle) produced inhibition of eating in rats. Since then, research with rats and other animals (including people) has demonstrated that CCK has a satiating effect and can regulate meal size (Smith & Gibbs, 1992, 1998). This suggests that food in the duodenum triggers the release of CCK, which in turn inhibits eating.

Two hormones produced by the pancreas, glucagon and insulin, are also implicated in the offset of eating. The primary role of glucagon is to break down glycogen, which is stored in the liver, into glucose to raise blood glucose levels. In contrast, insulin lowers blood glucose levels by transport- ing glucose out of the bloodstream and into cells. However, they both appear to play a role in the offset of eating.

Glucagon inhibits food intake and produces satiety when it is injected into rats and people (Geary, 1998). In addition, glucagon is released in the body during a meal, immediately after onset of the meal, which means that it could act as a signal that induces satiety and termination of the meal. Glucagon appears to stimulate the vagus nerve, which transmits information to the nucleus of the solitary tract, producing satiation. Glucagon receptors have also been found in the brain, particu- larly in the nucleus of the solitary tract and in the medial and paraventricular areas of the hypo- thalamus (Geary, 1998). Secretion of glucagon also appears to stimulate the release of insulin.

Insulin appears to produce satiation, too. Insulin is released during a meal as soon as food enters the mouth (Strubbe & Steffens, 1975). As the meal continues, more and more insulin is released, increasing insulin’s ability to produce satiety. VanderWeele (1998) maintains that insulin is one of many factors that works to terminate a meal. These factors send redundant signals to the brain by way of the vagus nerve, reducing appetite and decreasing the palatability or tastiness of the consumed food.

Another hormone that suppresses food intake is leptin, which you learned about earlier in this chapter. Leptin is secreted by fat cells and circulates in the blood to reach the lateral and the ventromedial hypothalamus, where it has its principal effects. The role of leptin is to regulate fat storage by suppressing food intake when fat stores get too large. The effect of leptin on the lateral hypothalamus appears to be opposite the effect of benzodiazepines and endorphins. Whereas benzodiazepines and endorphins increase the palatability and reward value of food (which induces food intake), leptin reduces the reward value of food in the lateral hypothalamus (Fulton, Woodside, & Shizgal, 2000). Receptors for leptin are also found in the ventromedial hypothala- mus, where leptin directly triggers termination of eating behavior.

Cholecystokinin, glucagon, insulin, and leptin are hormones that have been demonstrated to sup- press food intake. The specific actions of these hormones are summarized in Table 9.4.

9.3 Eating Disorders

Overeating and its consequence, obesity, are the most prominent eating disorders in our soci-ety. Other important eating disorders include pica, anorexia nervosa, and bulimia nervosa. We will examine each of these disorders in this section.

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CHAPTER 9Section 9.3 Eating Disorders

Obesity

A person is considered to be obese when his or her body weight is 20% above the normal weight for his or her height and body frame. The rate of obesity is steadily increasing, with 12.5% of the American population meeting the criteria for obesity in 1991 and nearly 34% meeting the same criteria in 2010 (Centers for Disease Control and Prevention, 2010). The cause of obesity is unknown, but investigators in the field are certain that a number of factors play a role in its development. These factors include overeating, hormonal disorders, genetic predisposition, and behavioral explanations.

Hormonal Factors Contributing to Obesity When I was a child, I remember an obese neighbor telling my mother, “I have a hormone prob- lem. That’s why I can’t lose weight.” I’ve thought about my former neighbor’s words many times since I began studying eating behavior and eating disorders over 20 years ago. I’ve often won- dered, “What hormone could she have been referring to?” To this day, I don’t know what, if any, hormonal disorder my neighbor had. Let’s consider the hormones that have been implicated in obesity.

Insulin has been investigated as a factor in the development of obesity. In the laboratory overeat- ing and obesity can be produced in rats by administration of large amounts of insulin (Lovett & Booth, 1970; Panksepp & Ritter, 1975). Conversely, overeating is accompanied by increased levels of insulin because insulin release is directly tied to the amount of food consumed. People who chronically overeat secrete massive amounts of insulin. According to what you learned in the previous section, increased amounts of insulin in the blood should lead to reduced food intake. However, people with high amounts of insulin in their blood become insensitive to their own insu- lin and thus do not respond to it normally. That is, high levels of insulin in the blood cause people to react as if they don’t produce insulin any longer. In Chapter 2 you learned about type 1 diabetes, a disorder in which an individual does not produce adequate amounts of insulin. High levels of insulin in the blood produce a type of diabetes, called type 2 diabetes, in which an individual produces insulin but does not respond to it. For that reason, overeating and obesity can predis- pose a person to type 2 diabetes.

When a person overproduces insulin, hypoglycemia (or low blood sugar) results. Hypoglycemia occurs when insulin transports glucose out of the blood and into cells. Obviously, the more insulin that is secreted, the more glucose is transported out of the blood. The net result is that cells in the hypothalamus that moni- tor blood glucose levels detect lower than normal lev- els of glucose in the blood and initiate eating in order to increase blood glucose levels (Figure 9.7). Thus, hypoglycemia can produce overeating.

Blend Images/SuperStock

Photo 9.5 People who overeat or are over- weight are at risk for developing diabetes due to constantly elevated insulin levels.

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CHAPTER 9Section 9.3 Eating Disorders

This mechanism explains how weight gain occurs in women who have recently given birth. A preg- nant woman produces insulin in increasing amounts over the course of her pregnancy to meet her own needs plus the needs of her growing fetus, which is unable to produce its own insulin. After the woman gives birth, her pancreas continues to produce high levels of insulin for several weeks until her body adjusts to the loss of the fetus. This means that, whenever the new mother eats, she overproduces insulin, which causes hypoglycemia and, consequently, overeating. This is especially true when the woman eats a snack of carbohydrates, such as cookies, pretzels, or potato chips. In the woman who has recently given birth, consumption of carbohydrates causes overproduction of insulin, which in turn produces hypoglycemia, feelings of hunger, and eating soon after a snack or meal has ended. This vicious cycle can cause a weight gain after the birth of a baby unless the woman learns to control her appetite and avoid carbohydrate snacks.

Figure 9.7: Mechanisms of hyperglycemia and hypoglycemia

What are the differences between hyperglycemia and hypoglycemia?

Thyroid hormones have been implicated in weight gain in older individuals. After age 25, thyroid hormone production begins to slow down, a little more each year. This means that by age 45 or so, thyroid hormone levels are quite a bit lower than they were at age 25. Recall that thyroid hor- mones control metabolic rate. When thyroid hormone levels are high, metabolic rates are high, and Energy OUT is high. As we age, thyroid hormone levels decline, which means that metabolic rates are lower, and Energy OUT is lower. Thus, older individuals require less food intake (or Energy IN) than younger people because their metabolic rates are slower. Most people, however, do not decrease food intake as they age, and they gain weight as a consequence.

Glucose in blood

a. Hyperglycemia: glucose in blood cannot get into neurons due to inadequate insulin

b. Hypoglycemia: low or no glucose in blood due to high levels of insulin

Stimulation of eating

Stimulation of eating

Cells in hypothalamus register starvation

Cells in hypothalamus register low blood sugar

No glucose in blood

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CHAPTER 9Section 9.3 Eating Disorders

The type of food consumed may affect hormone release, appetite, and weight gain. Recall that the neuropeptide galanin stimulates the intake of fatty foods, whereas neuropeptide Y stimulates carbohydrate consumption. Unfortunately, eating fatty foods increases the production of galanin, which in turn stimulates the consumption of even more fat. This same vicious cycle is evident for neuropeptide Y. Intake of carbohydrates increases the release of neuropeptide Y, which produces cravings for more carbohydrates (Morris, Chen, Watts, Shulkes, & Cameron-Smith, 2008). There is evidence from research with female rats that increased levels of galanin and neuropeptide Y contribute to overeating and increased weight gain (Leibowitz et al., 1998).

In summary, insulin, thyroid hormone, galanin, and neuropeptide Y are all associated with weight gain. Increased levels of insulin and decreased levels of thyroid hormone have been implicated in weight gain. Galanin and neuropeptide Y contribute to weight gain by increasing intake of fats and carbohydrates, respectively.

Genetic Factors Contributing to Obesity The link between genetics and obesity is still unclear. Certainly, researchers have observed that obese people are more likely to have obese children than are people of normal weight. However, obese people are also more likely to have obese adopted children and obese pets, which calls into question a genetic explanation of obesity. That word of caution aside, investigators have discov- ered two animal strains that are genetically obese: the ob/ob mouse and the Zucker fatty yellow rat. Both strains of animals produce offspring that, due to a defective gene, are grossly obese. The Zucker fatty yellow rat gets its name from the fact that this rat produces so much fat that the excess fat literally oozes through the animal’s skin and coats its hair.

In the ob/ob mouse, the defective gene, called the obesity or ob gene, has been identified and cloned. Research with the ob gene has indicated that body fat in adult rats and mice is regu- lated by leptin acting on the hypothalamus to inhibit eating (Kiess et al., 1998). As you learned in the previous section, the release of leptin increases as fat stores increase. In genetically obese rodents, the defective ob gene produces a leptin deficiency, which causes a failure to inhibit eating as fat stores increase. That is, as the rodents get fatter and fatter, correspondingly large amounts of leptin are not secreted because of the leptin deficiency, and eating is not inhibited. A defective ob gene has been shown to produce severe obesity in human children (Kiess et al., 1998). These children have a leptin deficiency due to a mutation in the ob gene (de Luis, Castrillón, & Dueñas, 2009; Körner et al., 2005).

Behavioral Factors Contributing to Obesity Personality and eating habits can certainly play a role in the way we eat, the foods we select, and our attitudes toward food, although these variables have received relatively little study. For example, individuals who eat rapidly consume a great deal of food before satiety signals terminate a meal. Members of a subclass of the population, called restrained eaters, control their eating behavior very rigorously in a manner that predisposes them to obesity when their controls break down (Polivy & Herman, 1976; Wardle, 1990). Stanley Schachter and his colleagues at Columbia University compared the eating behaviors of obese humans and hyperphagic rats with lesions in the ventromedial nucleus of the hypothalamus. They found that, compared to normal con- trols, obese rats and humans were finicky eaters who avoid bad-tasting food, did not like to work to obtain their food, and were highly emotional. Most importantly, Schachter and Rodin (1974)

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CHAPTER 9Section 9.3 Eating Disorders

discovered that obese rats and humans did not respond as much to internal signals as they did to external cues to eat, whereas normal controls were more aware of their internal signals. An obese person who had just eaten a large meal had more difficulty passing up delicious-smelling pastries than did a normal control with a similarly full stomach.

In addition, the environment can affect food intake. Normal rats typically eat the same amount of lab chow every day and rarely get obese. However, when they are offered a variety of foods (marshmallows, peanut butter, crackers, sausage, cheese, and so forth) and allowed to eat cafete- ria style, rats overeat and gain weight (Kanarek & Hirsch, 1977). This effect has also been demon- strated in people. Cafeteria-style eating might explain why freshman college students often gain weight when they enter college. Like rats offered a cafeteria-style diet, students who dine in the college cafeteria select a wide variety of foods to consume and overeat.

Other environmental stimuli have been shown to produce overeating or hyperphagia in rats. For example, a mild tail pinch elicits overeating in rats (Antelman & Szechtman, 1975), and white noise has also been shown to produce hyperphagia (Kupfermann, 1964; Wilson & Cantor, 1986). Schedule- induced hyperphagia has been produced in rats that press a lever for pleasurable brain stimula- tion on an intermittent reinforcement schedule. That is, when pleasurable brain stimulation is available once every 90 seconds, rats will spend the first 60 seconds or so of that waiting period eating, if food is made available. During the last 20 to 30 seconds, the rats go to the lever and begin pressing it in anticipation of receiving pleasurable brain stimulation. Rats that are placed in an experimental chamber for several hours a day and permitted to press for rewarding brain stimulation with food available will overeat and gain weight (Wilson & Cantor, 1987). Although these phenomena have not been demonstrated in people to date, it is extremely probable that environmental stimuli like noise or schedules can affect eating behavior in people, too.

Bulimia Nervosa

Bulimia nervosa occurs in less than 4% of the population, and its occurrence is limited mostly to adolescent girls and women (Garfinkel et al., 1995; Masheb, Grilo, & White, 2011). Athletes, par- ticularly those who need to maintain low body weights for competitive reasons, are much more likely to develop this eating disorder than the general population (Anderson, Petrie, & Neumann, 2011; Beekley et al., 2009; Greenleaf, Petrie, Carter, & Reel, 2009; Monthuy-Blanc, Maïano, & Therme, 2011). Bulimia nervosa is characterized by binge eating followed by self-induced vomiting or laxative use. A person with bulimia may eat normally much of the time, although she often diets for extended periods of time. However, cycles of uncontrollable binging and purging interrupt the bulimic individual’s day, producing a sense of distress and shame (Lavender et al., 2011; Mitchell et al., 2011). A bulimic college student told me once, “I can be sitting in a friend’s house or my boyfriend’s apartment, and this feeling will come over me, and I will tell a lie, anything, so I can go back to my house and binge.”

During binge-eating episodes, people eat enormous quantities of foods, typically foods high in carbohydrates and fats, like cake, ice cream, or pizza, but they also will eat bizarre food items, such as a bag of flour or a frozen TV dinner. Sometimes so much food can be consumed that the stomach will rupture (Casper, 1998). Depending on the purging method used, a number of physi- cal problems can emerge as a result of bulimia, including erosion of enamel from the teeth and digestive system disorders involving the stomach, small intestine, or large intestine. Vomiting and laxative use can also deplete potassium levels in the blood, which can interfere with heart and kidney function.

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CHAPTER 9Section 9.3 Eating Disorders

Studies of bulimic individuals indicate that they have reduced serotonin activity compared to anorexic patients and normal controls (Kaye, 2001; Kaye, Gendall, & Strober, 1998; Kaye, Klump, Frank, & Strober, 2000). Drugs that increase serotonin activity, such as selective serotonin reup- take inhibitors (SSRIs, as you learned in Chapter 3), are useful in reducing bingeing episodes, although relapse occurs when use of these drugs is continued over a long period of time or when use of these drugs is discontinued (Halmi, 1995; Mauri et al., 1996; Walsh & Devlin, 1995). Cognitive- behavioral therapy is the treatment of choice for bulimia nervosa (Wilson & Fairburn, 1999).

Anorexia Nervosa

Anorexia nervosa is rarer than bulimia nervosa and is found in one of two forms: restricting anorexia and anorexia nervosa-bulimic subtype. Restricting anorexia is characterized by severe reduction in food intake, which produces an emaciated appearance due to a loss of body fat, especially fat stored under the skin (Photo 9.6). People with restricting anorexia lose from 15 to 60% of their body weight due to reduced caloric intake, and they also eat selectively, avoiding certain “forbidden” foods, which leads to malnutri- tion and vitamin deficiencies. In contrast, individuals with the bulimic subtype of anorexia nervosa engage in abnormal eating behavior patterns that resemble bulimic behavior, including gorging followed by vomit- ing or other forms of purging, in addition to periodic bouts of severe food restriction.

Research on treatments for anorexia nervosa lags far behind research on treatments for bulimia nervosa (Wilson & Fairburn, 1999). Nutritional and cognitive- behavioral counseling can help the anorexic patient

gain weight, and SSRIs have been demonstrated to be helpful in controlling depression and compulsive behaviors associated with anorexia (Kaye, 1997; Kaye et al., 1998; Wilson & Fair- burn, 1999). Treatment can be given in either an inpatient or outpatient setting. The “Case Study” describes the case of a woman who required hospitalization, or inpatient treatment, for her severe restricting anorexia.

Susan Rosenberg /Science Source

Photo 9.6 What psychological factors con- tribute to the development of anorexia nervosa?

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CHAPTER 9Section 9.3 Eating Disorders

Case Study: Anorexia

Laura was quite popular in elementary school, but her social life flagged when she made the transition to junior high school. The “cool” kids no longer called her and invited her on their outings, and Laura was stuck hanging out with the less popular girls, who tended to be a bit overweight. When Laura’s mother made an off- hand comment one day about one of Laura’s best friends (“That poor girl would be so much prettier if she lost some weight”), Laura looked in a mirror and said to herself, “I’m ugly. I need to lose weight.” She immediately began restricting her food intake. Laura made up a secret list of foods that she could not eat because they contained too much fat. Before eating anything, she studied the package label carefully to see how much fat the food contained.

While she was in high school, Laura had to work hard to deceive her mother, who always seemed to be watching her. She was able to skip breakfast by getting up late and claiming there was no time to eat. When her mother forced her to take something to eat on the way to school, Laura promptly dumped it into the nearest trash can she passed. She didn’t eat lunch at school, either. Dinner was a problem because her family always sat down to eat together, and she was forced to pretend to eat, although most food ended up in her napkin, which Laura tossed into the trash. Laura became involved in athletics: field hockey in the fall, basketball in the winter, and track in the spring. Because practice took place during dinnertime, she was able to skip most dinners.

When she arrived at college, Laura weighed about 98 pounds, which was much too thin for her 5’6” frame. However, college provided Laura with a good deal of freedom. No one was concerned with whether she ate or not, although at first her roommate would invite her to come to the dining hall with her and sometimes brought back food for her, which Laura never touched. Laura was extremely proud of her ability to resist food and of her self-control. However, she was afraid that, if she started to eat, she would lose control and not be able to stop eating.

Laura’s parents were startled at her gauntness when she came home the summer after her first year. Laura had lost nearly 10 pounds in college, and her hair was thin and had lost its natural sheen. When she refused to take off her favorite sweatshirt on a very warm day in July, claiming she was cold (which she was), her mother took her to talk with a local psychologist.

Laura insisted to the psychologist and her mother that her appetite was good and that she ate regu- larly. She saw the psychologist every week over the summer and ate more than she wanted to, to please her mother and the psychologist.

Laura was relieved to go back to college at the end of the summer so that she could eat the way she wanted, which amounted to a handful of vitamins, one cup of chicken broth, and a tablespoon or so of applesauce each day. At Thanksgiving, she weighed about 85 pounds, and her parents promptly called the health center at her college and asked for help. The physician who examined Laura was alarmed. She looked absolutely skeletal and was weak and apathetic. He told Laura that she had to come to the health center every day and, if her weight dropped below 85 pounds, she would have to leave the col- lege to get treatment. The physician also insisted that Laura see the school counselor twice a week.

(continued)

AJPhoto/Science Source

Photo 9.7 Those who suffer from anorexia tend to avoid foods that are “off limits.”

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CHAPTER 9Section 9.3 Eating Disorders

A number of physiological and neurochemical abnormalities accompany anorexia nervosa. For the restricting subtype of the disorder, these abnormalities resemble the effects of starvation and include slowed metabolic rate, lowered body temperature, abnormal EEG record, and disorders of the digestive system, the cardiovascular system, and the kidneys. The changes in body tempera- ture and metabolic rate reflect dysfunction of the hypothalamus (Casper, 1998).

Other problems associated with anorexia that indicate hypothalamic involvement are sleep dis- orders, including insomnia and early morning wakening, changes in pituitary gland function, reduced gonadal function, including absence of menstruation in women, and depression. Reduc- tion in body fat, as signaled by reduced levels of leptin and other hormones, affects hypothalamic function, which in turn affects activity of the pituitary gland (Baranowska, Wasilewska-Dziubinska, Radzikowska, Plonowski, & Roguski, 1997; Casper, 1998; Kiess et al., 1998). For example, a loss of body fat can interfere with reproductive function, which is adaptive in times of starvation because it prevents a starving woman from getting pregnant.

Brain-imaging studies have revealed that adolescent girls with anorexia nervosa may develop per- manent brain cell loss due to their illness. Katzman and his colleagues (1996) in Toronto compared MRI scans of the brains of 13 low-weight adolescent girls with anorexia nervosa with the brains of 8 healthy, age-matched controls. The brains of the anorexic subjects had significantly enlarged ventricles and associated reductions in gray matter and white matter. That is, the brains of ado- lescents with restricting anorexia had significantly less brain matter than did the brains of healthy controls. A year later, 6 of the 13 girls had recovered and gained weight. MRI scans were conducted for all 13 original patients and 18 healthy controls (Katzman, Zipursky, Lambe, & Mikulis, 1997). Although white matter volume in the recovered anorexic patients had increased significantly, gray matter was still severely reduced in the brains of recovered anorexics.

Another MRI study comparing the brain scans of 12 women who had recovered from anorexia 1 to 23 years prior to the study with MRI scans of 18 healthy controls and 13 low-weight anorexic patients demonstrated that the former anorexics had a significantly smaller volume of gray matter in their brains than did the healthy controls (Lambe, Katzman, Mikulis, Kennedy, & Zipursky, 1997). Both the former anorexics and the low-weight anorexics had reduced amounts of gray matter in their brains, which suggests that anorexia causes permanent changes in the brain that are not affected by treatment and recovery.

Case Study: Anorexia (continued)

Every day, Laura reported for her weigh-in at the health center. Often she would consume two cups of broth right before the weigh-in and then promptly vomit it up after she left the health center. In January Laura came down with the flu and was “too sick” to come to the health center for the daily weigh-in. When she did come in, 4 days later, her weight had slipped to 82 pounds. Her parents were called, and they came and took Laura home, where she immediately was enrolled in an inpatient eat- ing disorder clinic at a local university hospital. Laura was promptly placed on intravenous (IV) nutrition therapy to restore needed nutrients and electrolytes to her body. Psychotherapy, nutritional therapy, and occupational therapy were soon added to her treatment. Laura was released after 3 weeks of inpa- tient treatment, but she remained in treatment as an outpatient for 3 more years while she attended a local college near her parents’ home.

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CHAPTER 9Section 9.4 Regulation of Water Intake

9.4 Regulation of Water Intake

Water intake is intimately linked to temperature regulation and food intake. For example, sweating depletes the body’s water supplies, causing thirst. Eating highly salty food can also affect water levels within the cells of the body and produce thirst. Ingestion of cold water causes heat loss because it takes one calorie to raise one gram of water one degree Centigrade. Thus, you burn a large number of calories for every 8 ounces of ice cold water that you drink.

Controlling water levels in the body is important because two-thirds of the body is composed of water. All of the water in the body can be divided into two components: the intracellular compart- ment and the extracellular compartment. Most of the body’s water, about 70%, is found in the intracellular compartment. As its name implies, the intracellular compartment refers to all the water located inside the cells of the body. The remaining 30 to 35% of the body’s water supply is found outside of cells in the extracellular compartment, such as in the blood, glands, lymph sys- tem, and cavities of body organs like the stomach or bladder. This means that you lose water from your extracellular compartment whenever you sweat, vomit, bleed, or urinate.

The central nervous system, particularly neurons in the anterior hypothalamus, controls water bal- ance in the intracellular and extracellular compartments. Two different homeostatic mechanisms regulate water levels in these compartments. For the intracellular compartment, the homeostatic mechanism involves preserving a constant concentration of solutes (particles such as salts, acids, and other chemical molecules) in the water within the cell. For the extracellular compartment, the homeostatic mechanism involves maintaining a constant volume of fluid in the extracellular com- partment. Thus, water intake is regulated by two homeostatic mechanisms: one that preserves a constant concentration in the intracellular compartment and one that maintains a constant vol- ume of water in the extracellular compartment.

Osmotic Thirst

The preoptic area of the hypothalamus maintains the internal concentration of cells at a constant concentration. Whenever the concentration within cells rises above this specified concentration, osmotic thirst occurs in the affected individual. Think about what happens when you eat a large bag of salty chips. The salty chips are digested, and the salt passes from your small intestine into your bloodstream. If you eat a lot of this salty food, the concentration of salt in your blood increases to a higher level than normal. Because the concentration of salt in the blood is elevated above normal, water is drawn from the cells into the blood. When water is pulled from the cells, the internal concentration of the cells increases above the level set by hypothalamus, producing osmotic thirst (Figure 9.8).

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CHAPTER 9Section 9.4 Regulation of Water Intake

Figure 9.8: Osmotic thirst

In normal state (Figure A), the concentrations of ions in the blood and inside of cells (intracellular com- partment) are equal. After a salty meal (Figure B), water is drawn out of the cells and goes into the blood because the concentration of ions in the blood is greater than in the cells, producing osmotic thirst.

When osmotic thirst occurs, it sets off a series of events that results in drinking behavior. Spe- cial receptors, called osmoreceptors, in the anterior hypothalamus monitor the intracellular con- centration (Ramsay & Thrasher, 1990; Verney, 1947). When the concentration increases, these osmoreceptors fire and excite neurons in the paraventricular nucleus of the hypothalamus, which in turn stimulate the pituitary gland. The pituitary gland reacts to stimulation from the hypothala- mus by releasing a hormone called antidiuretic hormone (ADH) (Bargmann & Scharrer, 1951). Antidiuretic hormone travels in the blood to the kidneys, where it signals to the kidneys to stop producing urine (Nielsen et al., 2002). The purpose of antidiuretic hormone, then, is to regulate water loss, through suppressing urination, from the body. Information about increased osmotic pressure is also relayed to the preoptic area of the hypothalamus, which induces drinking behav- ior. Thus, osmotic thirst produces two end results: It stops water loss through the kidneys, and it initiates drinking.

Hypovolemic Thirst

A second type of thirst, called hypovolemic thirst, is produced when the volume of water in the extracellular compartment becomes reduced (Stricker, 1966; Stocker, Stricker, & Sved, 2001). Loss of fluid from the extracellular compartment through profuse sweating, vomiting, diarrhea, or hemorrhage can produce hypovolemic thirst. For example, a bad case of the flu or a heavy men- strual flow can result in hypovolemic thirst. A nursing mother feels thirsty more often and drinks more due to depletion of her fluid stores caused by lactation.

The most important reason for monitoring the volume of the extracellular compartment is to maintain blood pressure at an optimal level. Obviously, blood pressure must be high enough to permit blood to flow against the force of gravity to reach the brain. When blood pressure is drasti- cally reduced, blood cannot get to the brain, causing unconsciousness, seizures, and even death.

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A. Normal state B. Osmotic thirst

Cells Blood vessel

Shrunken cells (higher-than- normal intracellular concentration)

Swollen blood vessel

In normal state, the concentrations of ions in the blood and inside of cells (intracellular compartment) are equal.

After a salty meal, the concentration of ions in the blood is greater than that inside cells.

Water is drawn out of cells into the blood, producing osmotic thirst.

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CHAPTER 9Section 9.4 Regulation of Water Intake

Therefore, the body needs a mechanism like hypovolemic thirst to maintain blood pressure in order that the brain receives the nourishment that it needs.

To maintain the volume of fluid in the extracellular compartment, receptors called baroreceptors, which are located in large veins, monitor blood pressure. When blood pressure drops, the barore- ceptors fire, initiating drinking behavior. A reduction in blood pressure also stimulates the kidney to release a hormone called renin (Ramsay & Thrasher, 1990). Renin is secreted into the blood, where it binds with another hormone called angiotensin I to produce a third hormone called angiotensin II. Angiotensin II is the active form of angiotensin. In the bloodstream it causes blood vessels to constrict, which increases blood pressure. Angiotensin II also binds with receptors in the hypothalamus, which in turn stimulates drinking behavior (Fitzsimons, 1998). Thus, hypovolemic thirst causes angiotensin II to become activated, which in turn increases blood pressure and initi- ates drinking, restoring blood pressure to normal levels.

For example, after running a marathon, a runner’s extracellular fluid volume will be reduced due to excessive sweating. Baroreceptors in the runner’s body will fire, causing the kidneys to release renin, which binds with angiotensin I to produce angiotensin II. Angiotensin II will cause the run- ner to feel thirsty and drink.

Nonhomeostatic Drinking

As with eating, not all drinking occurs when an individual has a need for water. That is, people do not ordinarily wait until their blood pressure drops or their intracellular concentration rises before they start to drink. Most of our drinking behavior is nonhomeostatic or secondary drinking. Pri- mary drinking occurs when an individual experiences osmotic or hypovolemic thirst. In contrast, secondary drinking occurs in the absence of thirst.

What stimulates secondary drinking? For many people, eating acts as a cue for drinking behav- ior. In fact, most drinking is prandial drinking, or drinking that occurs when an individual is eat-

ing. Personally, I find it impossible to eat unless I have some liquid to sip on during the meal. However, this is just a habit because some people are able to eat very com- fortably without drinking during the meal. Other types of second- ary drinking include drinking when the mouth feels dry or drinking a cool beverage on a hot day or a hot beverage on a cool day. Drinking something because it tastes good is yet another example of second- ary drinking.

In the laboratory secondary drink- ing can be produced when an indi- vidual is working for a reward on a schedule. In the previous section

Jupiterimages/Pixland/Thinkstock

Photo 9.8 Most drinking is prandial drinking, or drinking that occurs when an individual is eating.

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CHAPTER 9Section 9.5 Chapter Summary

on obesity, you learned about schedule-induced eating. Schedule-induced drinking (usually referred to as schedule-induced polydipsia) was first demonstrated in rats and has since been reported in many other species, including humans (Falk, 1961, 1971, 1977). Animals, including people, will often drink huge quantities of liquids when they are working for food or other rewards (such as money or pleasurable brain stimulation) that become available every minute or so.

Likewise, some people will drink large quantities of alcohol in order to get drunk. This, too, is an example of secondary drinking. We will examine alcohol drinking in greater detail in Chapter 11. As we conclude this chapter, it is important to keep in mind that not all eating and drinking are controlled by homeostatic mechanisms. Eating and drinking disorders arise when homeostatic mechanisms break down, but they also arise as a result of environmental or behavioral causes. Investigators are just beginning to understand how these disorders occur, especially those disor- ders that develop as a result of psychological, rather than purely biological, triggers.

Section 9.5 Chapter Summary Regulation of Body Temperature

• The hypothalamus plays an important role in homeostatic regulation of body temperature and food and water intake.

• Endotherms are homeothermic animals that can produce their own heat and maintain a constant core body temperature. Ectotherms cannot generate their own body heat.

• Shivering thermogenesis and nonshivering thermogenesis are two mechanisms used by endotherms to produce heat. The primary mechanism of nonshivering thermogenesis is basal metabolism.

• Under the influence of the hypothalamus, the pituitary gland releases thyrotropin- releasing factor, which stimulates the thyroid gland to release thyroid hormones.

• Brown fat metabolism is used by newborn humans to produce heat. • Heat loss occurs through evaporation and conduction. The most effective mechanism for

losing heat is evaporation. • To reduce loss of body heat, blood vessels in the skin constrict in response to cold

environments. • Piloerection occurs when smooth muscles contract in response to cold, pulling hairs or

feathers up on end to trap air and reduce loss of body heat. • Heat production and heat loss are regulated by the preoptic area of the hypothalamus. • Fever and menopausal dysregulation are the most common examples of disorders of tem-

perature regulation. • Energy balance is affected by both heat production and food intake. Energy is measured

in units called calories.

Regulation of Food Intake • Homeostasis maintains steady states in the body, whereas allostasis involves nonhomeo-

static cues that initiate eating and drinking. • As omnivores, we have to select carefully to obtain needed macronutrients (protein, fat,

and carbohydrates, which we need in large supply) and micronutrients (vitamins and min- erals, which we need in tiny amounts).

• Both the onset and offset of eating are controlled by peripheral and central mechanisms. • The lateral hypothalamus, together with the prefrontal cortex, regulates allostatic food

intake mechanisms.

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CHAPTER 9Section 9.5 Chapter Summary

• Bilateral lesions of the lateral hypothalamus produce aphagia. • Homeostatic regulation of food intake involves the paraventricular nucleus of the

hypothalamus. • Barbiturates, benzodiazepines, and endorphins stimulate food intake by enhancing the

palatability of the ingested food. • The brain peptides, galanin, neuropeptide Y, and orexin, also stimulate food intake. • Signals from the gut stimulate eating by way of the vagus nerve, which relays information

to the nucleus of the solitary tract. • The ventromedial nucleus of the hypothalamus, together with the paraventricular nucleus,

is involved in the homeostatic offset of eating. • Amphetamine and fenfluramine reduce food intake. • The stomach and the small intestine, particularly the duodenum (the section of the small

intestine nearest the stomach) play an important role in satiety. • Several hormones, including cholecystokinin (released by the duodenum), glucagon and

insulin (both released by the pancreas), and leptin (secreted by fat cells) are involved in the offset of eating.

Eating Disorders • Eating disorders include obesity, bulimia nervosa, and anorexia nervosa. • People who chronically overeat show high levels of blood insulin, due to secretion of large

amounts of insulin, producing type 2 diabetes, in which a person fails to respond to the insulin he or she produces.

• When a person overproduces insulin, hypoglycemia results because the large amounts of insulin cause more glucose than normal to be transported out of the blood. As a result of hypoglycemia, the hypothalamus detects an abnormally low level of blood glucose and initiates eating, which can produce overeating and weight gain.

• In older people thyroid gland function is reduced, which can produce weight gain in those who do not reduce their food intake.

• In genetically obese mice, the defective ob gene produces a deficiency of leptin, a hor- mone that inhibits food intake.

• Bulimia nervosa is characterized by binge eating followed by self-induced purging. • The two forms of anorexia nervosa are restricting anorexia (severe reduction in food

intake) and anorexia nervosa-bulimic subtype (food restriction plus periodic binging and purging).

• When an individual is deprived of one or more essential nutrients, the eating of nonnutri- tive substances, called pica, may occur.

Regulation of Water Intake • About 70% of the body’s water is found in the intracellular compartment, which is located

inside the cells of the body. • The extracellular compartment refers to water found in the blood, glands, lymph system,

and cavities of body organs. • Osmotic thirst arises when the internal concentration within a cell becomes higher than

normal, which occurs when salty food is ingested.

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CHAPTER 9Web Links

• In response to firing of osmoreceptors, the pituitary gland releases antidiuretic hormone (ADH), which causes the kidneys to stop production of urine, and encourages drinking.

• Hypovolemic thirst is produced when fluid in the extracellular compartment becomes reduced in volume, due to hemorrhage, sweating, vomiting, or diarrhea.

• Baroreceptors monitor blood pressure and fire when blood pressure drops, initiating drinking behavior. In addition, the kidneys release the hormone renin in response to low blood pressure. Renin is secreted into the blood, where it binds with angiotensin I (the inactive form) to produce angiotensin II (the active form), which causes constriction of blood vessels, increasing blood pressure.

• Most of our drinking is nonhomeostatic in nature. Primary drinking occurs when a per- son experiences osmotic or hypovolemic thirst, whereas secondary drinking occurs in the absence of thirst.

Questions for Thought

1. How do whales manage to stay warm in cold ocean waters? 2. Why are so many people in this country overweight? 3. Give several examples of secondary drinking. 4. Explain how the controls of eating, drinking, and body temperature are interrelated. 5. How does the pituitary gland control body temperature regulation? What role does the

pituitary gland play in water intake regulation? 6. Contrast shivering thermogenesis with nonshivering thermogenesis. 7. Which drugs increase food intake? Which decrease food intake? What is the mechanism

by which these drugs affect eating? 8 List the hormones involved in eating, drinking, and temperature regulation. Where is

each hormone produced? What role does each play?

Web Links

Information on eating disorders, including anorexia nervosa and bulimia nervosa, can be found on the Medline Plus website, a service of the U.S. National Library of Medicine and the National Institutes of Health. http://medlineplus.gov

The Centers for Disease Control and Prevention (CDC) supplies excellent information on obesity on their website. Here you can find data and statistics, a list of state and community programs, and other resources that can help you understand the biological and psychological elements of obesity. http://www.cdc.gov

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CHAPTER 9

allostasis A concept that explains the non- homeostatic cues that initiate eating and drinking; it takes into account an individual’s expectations and readiness to alter behavior to meet changing demands in the environment.

angiotensin II The active form of angioten- sin; it causes blood vessels to constrict, which increases blood pressure, and also binds with receptors in the hypothalamus, which in turn stimulates drinking behavior.

anorexia nervosa An eating disorder in which the affected individual restricts food intake and loses significant body weight.

antidiuretic hormone (ADH) A hormone that travels in the blood to the kidneys, where it signals to the kidneys to stop producing urine, thereby regulating water loss from the body.

aphagia A failure or refusal to eat.

baroreceptors Receptors that maintain the volume of fluid in the extracellular compart- ment; when blood pressure drops, barorecep- tors fire and initiate drinking behavior.

basal metabolism The minimum amount of energy expended while a person is at rest.

brown fat metabolism Deposits of brown fat at the back of the head and in the chest of human babies; when a newborn’s core body temperature drops, the hypothalamus directs the burning of brown fat, which produces heat and thereby raises the baby’s temperature.

bulimia nervosa An eating disorder character- ized by binge eating followed by self-induced vomiting or laxative use.

calorie A unit of energy.

drive A condition that motivates an individual to perform a particular behavior or set of behaviors in order to eliminate that condition.

duodenum The section of the small intestine nearest the stomach; it provides information to the central nervous system that induces feelings of satiety in the individual.

ectotherms Animals that get their body heat from sources outside their own bodies.

endotherms Animals that have an internal source of heat; they produce heat through oxidation of substances such as fats, proteins, and carbohydrates.

evaporation The process by which liquid is turned into a gas or vapor; it is an effective mechanism for losing heat.

extracellular compartment Refers to the 30 to 35% of the body’s water supply that is found outside of cells, such as in the blood, glands, lymph system, and cavities of body organs like the stomach or bladder.

fever An increase in core body temperature above its normal level.

galanin A brain peptide that appears to con- trol fat intake, fat metabolism, and fat storage.

glucagon A hormone that breaks down glyco- gen, which is stored in the liver, into glucose to raises blood glucose levels.

glucostatic theory The theory that glucose levels are regulated in the body. According to this theory, whenever blood glucose levels fall below some optimal level, glucose receptors in the brain fire and stimulate eating; when blood glucose levels rise, eating is terminated.

homeostasis The process of maintaining certain biological variables, such as body tem- perature, body weight, and body fluid volume, at a constant level.

homeotherms Homeothermic animals, or endotherms; animals that maintain a constant core body temperature.

Key Terms

Key Terms

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CHAPTER 9Key Terms

hyperphagia Overeating.

hypoglycemia Having lower than normal lev- els of glucose in the blood.

hypovolemic thirst A type of thirst that is produced when the volume of water in the extracellular compartment becomes reduced; for example, through profuse sweating, vomit- ing, diarrhea, or hemorrhage.

insulin A hormone that lowers blood glu- cose levels by transporting glucose out of the bloodstream and into cells.

intracellular compartment Refers to the majority of the body’s water, about 70%, that is found inside the cells of the body,

lateral hypothalamus A region of the hypo- thalamus believed to be connected to regulat- ing eating behavior.

leptin A hormone that is secreted by fat cells and suppresses food intake.

lipostatic theory A theory of food intake regulation that is based on the notion that a central homeostatic mechanism monitors and maintains an optimal level of body fat.

menopause A period in a woman’s life fol- lowing the cessation of the production of sex hormones.

neuropeptide Y A brain peptide that triggers intake of carbohydrates and promotes the storage of excess carbohydrates as body fat.

nonshivering thermogenesis Refers to all the ways in which we produce heat besides shiver- ing; the primary mechanism of nonshivering thermogenesis is basal metabolism, or the minimum amount of energy expended while a person is at rest.

nucleus of the solitary tract A nucleus in the medulla that receives information from the gut and other receptors by way of cranial nerves VII, IX, and X.

ob gene A defective gene found in genetically obese mice.

obese A term that describes a person whose body weight is 20% above the normal weight for his or her height and body frame.

omnivores Animals that eat a variety of foods, including meats, vegetables, and grains, to obtain the energy and nutrients that they need; humans are omnivores.

orexins A newly discovered class of peptides that also stimulate food intake.

osmoreceptors Special receptors in the ante- rior hypothalamus that monitor the intracel- lular concentration.

osmotic thirst A type of thirst produced when the concentration of the blood becomes greater than the concentration within cells.

piloerection A reflex that occurs when smooth muscles contract in response to cold, pulling hairs or feathers up on end to trap air and reduce loss of body heat.

prandial drinking Drinking that occurs when an individual is eating.

preoptic area A region in the anterior hypo- thalamus that regulates heat production and heat loss.

primary drinking Drinking that occurs when an individual experiences osmotic or hypovole- mic thirst.

renin A hormone that is released by the kid- neys and secreted into the blood.

satiety The condition of fullness that signals a person to stop eating.

secondary drinking Drinking that occurs in the absence of thirst.

set points Optimum levels of various physi- ological factors, such as body temperature or blood glucose levels.

shivering thermogenesis The production of heat by the rhythmic muscular contractions called shivering.

superficial blood vessels Blood vessels that are found in the skin.

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CHAPTER 9Key Terms

thermostatic theory A theory that postulates that core body temperature drives eating behavior.

thyroid gland A butterfly-shaped organ located in the neck that is controlled by the pituitary gland.

vagus nerve Cranial nerve X, which carries sensory information from the upper abdomen, chest, and neck to the brain and carries motor information from the brain to smooth muscles in those areas of the body.

ventromedial nucleus of the hypothalamus (VMH) An area of the hypothalamus that is regarded as the “satiety center” of the brain and regulates the offset of eating.

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