Wood1.1 Credits lightning ©istockphoto.com/Soubrette background texture ©istockphoto.com/Hedda Gjerpen person rock climbing ©istockphoto.com/Greg Epperson Wood1.1

Topics 12.1 Digestion, Energy Storage, and Energy Utilization 12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives 12.3 Factors that Determine What, When, and How Much We Eat 12.4 Physiological Research on Hunger and Satiety 12.5 Body Weight Regulation: Set Points versus Settling Points 12.6 Human Obesity: Causes, Mechanisms, and Treatments 12.7 Anorexia and Bulimia Nervosa Credits lightning ©istockphoto.com/Soubrette background texture ©istockphoto.com/Hedda Gjerpen Wood1.

Control of Eating Is there a “set point” for the body’s energy reserves that determines when we eat? The prevalence of eating disorders suggests this may not be the case Over ½ the adult population in the U.S. meets clinical criteria for obesity The average American consumes 3,800 calories per day—about twice the average requirement 3% of U.S. adolescents suffer from anorexia or bulimia L11.26

Digestion, Energy Storage, and Energy Utilization Purpose of eating is to provide the body with molecular building blocks and energy Digestion: breaking down food and absorbing its constituents L12.23

Digestion, Energy Storage, and Energy Utilization

Energy Storage in the Body Energy delivered to the body as lipids, amino acids, and glucose Energy storage in the body as fats, glycogen, and proteins Fats are most efficient for energy storage One gram of fat stores twice as much energy as one gram of glycogen Fat does not attract and hold as much water as glycogen, and so provides denser energy storage L7.1

Three Phases of Energy Metabolism Energy metabolism: Chemical changes that make energy available for use Cephalic phase: preparation for eating Absorptive phase: energy absorbed Fasting phase Withdrawing energy from reserves Ends with next cephalic phase L12.21

Three Phases of Energy Metabolism Energy availability controlled by two pancreatic hormones Insulin: high during cephalic and absorptive phases Glucagon: high during fasting phase Energy availability controlled by two pancreatic hormones Insulin: high during cephalic and absorptive phases Triggers glucose use as fuel by body cells Triggers conversion of blood-borne energy to fat, glycogen, and protein Triggers energy storage in adipose cells, liver, and muscles Glucagon: high during fasting phase Triggers change of stored energy to usable fuel: fat to free fatty acids and then ketones; protein to glucose L12.21

Theories of Hunger and Eating: Set Points vs. Positive Incentives The Set-Point Assumption Hunger is a response to an energy need; we eat to maintain an energy set point Typical assumption: Eating works like a thermostat, a negative feedback system: turns on when energy is needed, off when set point is reached L11.28

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

Glucostatic and Lipostatic Set-Point Theories of Hunger If we eat to maintain an energy level (homeostasis), what is monitored? (c. 1940s and 1950s) Glucostatic theories – glucose levels determine when we eat Lipostatic theories – fat stores determine how much we eat over long term (explaining why weight tends to be constant) Credits ruler ©istockphoto.com/Christopher Hudson woman observing & taking notes ©istockphoto.com/Claudio Arnese

Problems with Set-Point Theories of Hunger and Eating Contrary to evolutionary pressures that favored energy storage for survival Reductions in blood glucose or body fat do not reliably induce eating Do not account for the influence of external factors on eating and hunger Wade6.52

Positive-Incentive Perspective We are drawn to eat by the anticipated pleasure of eating We have evolved to “crave” food Multiple factors interact to determine the positive-incentive value of eating Accounts for the impact of external factors on eating behavior L11.26

Factors that Determine What, When, and How Much We Eat Adaptive species-typical preferences Sweet and fatty foods = high energy Salty = sodium-rich Adaptive species-typical aversions Bitter = often associated with toxins Learned preferences and aversions Rats prefer diet with vitamins, foods they smell in mother’s milk or other rats’ breaths L11.30

Factors That Influence When We Eat We tend to get hungry at mealtime As mealtime approaches, the body enters the cephalic phase leading to a decrease in blood glucose Pavlovian conditioning of hunger demonstrated experimentally L7.1

Factors that Influence How Much We Eat Satiety: may stop a meal, “being full” Satiety signals: food in gut and glucose in the blood can induce satiety signals Sham eating studies demonstrate that satiety signals are not necessary for meal termination Rats initially sham eating eat normal-sized meal if food is familiar L4.13

Factors that Influence How Much We Eat FIGURE 12.5: The sham-eating preparation. L4.13

Factors that Influence How Much We Eat FIGURE 12.6: Change in the magnitude of sham eating over repeated sham-eating trials. The rats in one group sham ate the same diet they had eaten before the sham eating phase; the rats in another group sham ate a diet different from the one they had previously eaten. (Based on Weingarten, 1990.) L4.13

Factors that Influence How Much We Eat Appetizer effect: small amounts of food may increase hunger Serving size: the larger the serving, generally the more consumed Social influences Even rats eat more when in a group L11.28

Sensory-Specific Satiety Tasting a food immediately decreases the positive-incentive value of similar tastes and decreases the palatability of all foods about 30 minutes later Adaptive – encourages a varied diet Some foods are resistant to sensory-specific satiety: rice, bread, potatoes, sweets, and green salads Credit person thinking ©istockphoto.com/akurtz

Physiological Research on Hunger and Satiety Role of blood glucose levels Myth of hypothalamic centers Role of the GI tract Hunger and satiety peptides Serotonin and satiety Credit book ©istockphoto.com/Carmen Martínez Banús 21

Role of Blood Glucose Levels in Hunger and Satiety Blood glucose drops prior to a meal as preparation to eat – not a cue to eat Must decrease blood glucose by 50% to trigger feeding Premeal glucose infusions often do not suppress eating Reduced blood glucose may contribute to hunger, but changes in blood glucose do not prevent hunger or satiety Myth of Hypothalamic Hunger and Satiety Centers Experiments suggested two hypothalamic centers Ventromedial (VMH): a satiety center Lateral (LH): a hunger center Lesions of VMH produce hyperphagia Lesions of LH produce aphagia and adipsia Wood1. Credit brain ©istockphoto.com/Stephen Kirklys

Myth of Hypothalamic Hunger and Satiety Centers Experiments suggested two hypothalamic centers Ventromedial (VMH): a satiety center Lateral (LH): a hunger center Lesions of VMH produce hyperphagia Lesions of LH produce aphagia and adipsia

Myth of Hypothalamic Hunger and Satiety Centers The VMH likely is not a satiety center VMH lesion rats maintain a new higher weight VMH lesions may non-specifically destroy other brain regions (noradrenergic bundle; paraventricular nucleus) The LH likely is not a feeding center LH lesioned rats will recover if kept alive by tube feeding LH lesions may produce sensory and motor disturbances that affect food seeking Most supported role of the hypothalamus: regulation of energy metabolism Myth of Hypothalamic Hunger and Satiety Centers Experiments suggested two hypothalamic centers Ventromedial (VMH): a satiety center Lateral (LH): a hunger center Lesions of VMH produce hyperphagia Lesions of LH produce aphagia and adipsia Wood1. Credit brain ©istockphoto.com/Stephen Kirklys

Role of Gastrointestinal Tract in Satiety Cannon and Washburn (1912) Studies suggested stomach contractions led to hunger, distension to satiety However, hunger is still experienced with no stomach (but rest of GI tract remaining) In a rat study, rats with a transplanted stomach and intestine expressed sated behavior when food was injected Led to hypothesis of blood borne satiety signal(s) L1.20

Role of Gastrointestinal Tract in Satiety

Hunger and Satiety Peptides Gut peptides that decrease meal size: cholecystokinin (CCK), bombesin, glucacon, alpha- melanocyte-stimulating hormone, somatostatin Must first establish that peptide does not merely create illness CCK causes nausea at high doses, but suppresses food intake at doses insufficient to induce taste aversions Wade6.25

Hunger and Satiety Peptides Hunger peptides usually synthesized in the hypothalamus: neuropeptide Y, galanin, orexin-A, ghrelin Overall, many different neural signals control eating (not just glucose and fat) Hypothalamus plays a central role in eating behaviors Microinjections of some peptides have major effects on eating Wade6.25

Serotonin agonists consistently reduce rats’ food intake Serotonin and Satiety Serotonin agonists consistently reduce rats’ food intake Even intake of palatable food is affected Reduces amount eaten per meal Preferences shift away from fatty foods Similar effects seen in humans Credit hand holding rat ©iStockphoto.com/sidsnapper

Prader-Willi Syndrome: Patients with Insatiable Hunger Symptoms: Food-related: insatiable appetite, extremely slow metabolism; eventual death in adulthood from obesity related diseases Other symptoms: weak muscles, small hands and feet, triangular mouth, stubbornness, feeding difficulties in infancy, tantrums, compulsivity, skin picking Damage or absence of a section of chromosome 15 Study of the syndrome may lead to advances in understanding eating behaviors in humans L11.26

Body Weight Regulation: Set Points vs. Settling Points Variability of body weight According to the set-point assumption, it should be very difficult to gain weight Set points and health Free-feeding does not lead to optimum health Positive effects seen with caloric restriction Diet-induced thermogenesis – body temperature drops with fat loss, making weight-loss diets gradually less effective L11.29

Set Points and Settling Points in Weight Control Body weight drifts around a natural settling point – “the level at which the various factors that influence body weight achieve an equilibrium” A new body weight will be established if conditions remain constant A loose kind of homeostatic regulation Modeled by “The leaky-barrel” L11.29

Set Points and Settling Points in Weight Control FIGURE 12.13: The diminishing effects on body weight of a low-calorie diet and a high-calorie diet. L11.29

Set Points and Settling Points in Weight Control FIGURE 12.14: The leaky-barrel model: a settling-point model of eating and body weight homeostasis. L11.29

Who Needs to Be Concerned about Obesity? Everyone, as rates of obesity are increasing in most parts of the world Obesity is related to many other health problems L11.6

Human Obesity: Causes, Mechanisms, and Treatments Why Is There an Epidemic of Obesity? Evolution favored preferring high- calorie food, eating to capacity, storing fat, and using energy efficiently Cultural practices and beliefs promote consumption L11.6

Why Do Some People Become Obese While Others Do Not? Energy input differences Craving for high-calorie foods Cultural norms Large cephalic-phase response to sight and smell of food Energy output differences Exercise Diet-induced thermogenesis NEAT (nonexercise activity thermogenesis) Genetics interacts with both energy input and output L12.19

Why Are Weight-Loss Programs Typically Ineffective? Considering the leaky-barrel model, long-term weight loss will require a permanent lifestyle change Exercise also can make you hungry Often people eat more calories after the workout than they burned during the workout L12.30

Leptin and the Regulation of Body Fat Leptin – a negative feedback fat signal Hormone released by fat cells Leptin receptors found in the brain ob/ob mice are three times normal weight Homozygous for a mutant gene ob Lack leptin Eat more, and store fat more efficiently than controls Human leptin research However, most obese humans have high leptin levels. Leptin injections help the few ob/ob humans L1.20

Leptin, Insulin, and the Melanocortin System Insulin brain levels reflect visceral fat; leptin levels reflect subcutaneous fat Both insulin and leptin receptors found in the arcuate nucleus of the hypo-thalamus Leptin and insulin in the brain have some effects on eating behavior, but are (again) not the only eating/sating signals Wood1. Credit brain ©istockphoto.com/Stephen Kirklys

Treatment of Obesity: Serotonergic Agonists Serotonin appears to increase short-term satiety signals associated with the consumption of a meal and decrease… Urge to eat high-calorie foods Consumption of fat Intensity of hunger Size of meals Number of snacks and bingeing Early serotonin agonists produced heart disease in some patients and were withdrawn from the market L12.31

Treatment of Obesity: Gastric Surgery Gastric bypass and the adjustable gastric band create a smaller stomach Treatments are for extreme obesity These treatments are effective in some patients L12.31

Anorexia Bulimia Nervosa Voluntary self-starvation Fatal in 10% of patients Bulimia: bingeing and purging Similar symptoms, difficult to distinguish Distorted body image Most often affects educated, affluent young females Associated with obsessive-compulsive disorder and depression It is not clear whether anorexics find food less appealing; some evidence suggests the opposite L11.29

Anorexia Nervosa: A Hypothesis A person out of homeostatic balance might find a full meal to be aversive Eating a meal would then lead to development of food aversions For example, feeding meals to famine victims sometimes leads to anorexia Implication is for anorexics to eat small amounts of food throughout the day as part of therapy L1.27

Watch: Thinking About Hunger Watch: Eating and the Brain Watch: Anorexia Animation: Leptin and Obesity Note: To view the MyPsychLab assets, please make sure you are connected to the internet and have a browser opened and logged into www.mypsychlab.com.

Acknowledgments Slide Image Description Image Source template lightning ©istockphoto.com/Soubrette background texture ©istockphoto.com/Hedda Gjerpen Ch12 image eating ©istockphoto.com/aldomurillo 3, 13 head ©istockphoto.com/Suzanne Tucker 3, 13, 30 food - burger & fries ©istockphoto.com/Adolfo Lazo 4 blue sky & clouds, open arms ©istockphoto.com/kertlis 5 Figure 12.1 Pinel 8e, p. 300 6 messy files ©istockphoto.com/Jelena Popic 7 laughing ©istockphoto.com/Stratesigns, Inc. 8 Figure 12.3 Pinel 8e, p. 302 9, 19 hungry ©istockphoto.com/Neil Wysocki bowl ©istockphoto.com/Jill Chen dish of noodles ©istockphoto.com/Jamesmcq24 10 Figure 12.4 Pinel 8e, p. 303 11 woman observing & taking notes ©istockphoto.com/Claudio Arnese 12 Man's head ©istockphoto.com/Nicolas Hansen 14 box of chocolates ©istockphoto.com/The Desktop Studio 15 pressure gauge ©istockphoto.com/Mark Evans 16 bucket of popcorn ©iStockphoto.com/PMSI Web Hosting and Design 17 Figure 12.5 Pinel 8e, p. 307 18 Figure 12.6 Pinel 8e, p. 308 20 person thinking ©istockphoto.com/akurtz

Acknowledgments Slide Image Description Image Source 21 book ©istockphoto.com/Carmen Martínez Banús 22, 24, 40 brain ©istockphoto.com/Stephen Kirklys 23 Figure 12.8 Pinel 8e, p. 310 Figure 12.9 Pinel 8e, p. 311 25, 39 white rat ©iStockphoto.com/Elena Butinova 25, 26, 39 blue sky & clouds ©istockphoto.com/kertlis 26 Figure 12.12 Pinel 8e, p. 313 27, 28 head - woman ©istockphoto.com/Angel Herrero de Frutos 29 hand holding rat ©iStockphoto.com/sidsnapper 31, 32, 33, 34 DNA ©istockphoto.com/HooRoo Graphics 31, 32, 43 scale ©istockphoto.com/Luca di Filippo 33 Figure 12.13 Pinel 8e, p. 316 34 Figure 12.14 Pinel 8e, p. 317 35, 36 globe w/ flags ©istockphoto.com/Stay Media Productions 37 friends sitting on a bench ©istockphoto.com/Aldo Murillo 38 people on treadmills ©istockphoto.com/ShaneKato 41, 42 medical clipboard ©istockphoto.com/Anastasia Pelikh 44 notebook ©istockphoto.com/stockcam yellow pad ©istockphoto.com/DNY59 45 laptop ©istockphoto.com/CostinT table and wall ©istockphoto.com/David Clark