Prepared by Jeffrey W. Grimm Western Washington University PowerPoint Presentation for Biopsychology, 8th Edition by John P.J. Pinel Prepared by Jeffrey W. Grimm Western Washington University This multimedia product and its contents are protected under copyright law. The following are prohibited by law: any public performance or display, including transmission of any image over a network; preparation of any derivative work, including the extraction, in whole or in part, of any images; any rental, lease, or lending of the program. Copyright © 2011 Pearson Education, Inc. All rights reserved.

Why Do Many People Eat Too Much? Chapter 12 Hunger, Eating, and Health Why Do Many People Eat Too Much? Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. 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 that this may not be the case Over half of 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.1 The gastrointestinal tract and the process of digestion. Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Three Phases of Energy Metabolism Continued 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.3 The major events associated with the three phases of energy metabolism: the cephalic, absorptive, and fasting phases. Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.4 The energy set-point view that is the basis of many people’s thinking about hunger and eating. Copyright © 2011 Pearson Education, Inc. All rights reserved.

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) Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Factors That Influence What 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.5 The sham-eating preparation. Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. 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.) Copyright © 2011 Pearson Education, Inc. All rights reserved.

Factors That Influence How Much We Eat Continued Appetizer effect: small amounts of food may increase hunger Due to cephalic-phase responses? Serving size: the larger the serving, generally the more consumed Social influences Even rats eat more when in a group Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Physiological Research on Hunger and Satiety (outline) Role of blood glucose levels Myth of hypothalamic centers Role of the GI tract Hunger and satiety peptides Serotonin and satiety Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.8 The locations in the rat brain of the ventromedial hypothalamus and the lateral hypothalamus. Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.9 Postoperative hyperphagia and obesity in a rat with bilateral VMH lesions. (Based on Teitelbaum, 1961.) Copyright © 2011 Pearson Education, Inc. All rights reserved.

Myth of Hypothalamic Hunger and Satiety Centers Continued 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Role of the 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) Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.12 Transplantation of an extra stomach and length of intestine in a rat. Koopmans (1981) implanted an extra stomach and length of intestine in each of his experimental subjects. Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Hunger and Satiety Peptides Continued 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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” Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.13 The diminishing effects on body weight of a low-calorie diet and a high-calorie diet. Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.14 The leaky-barrel model: a settling-point model of eating and body weight homeostasis. Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Copyright © 2011 Pearson Education, Inc. All rights reserved. FIGURE 12.16 An ob/ob mouse and a control mouse. Copyright © 2011 Pearson Education, Inc. All rights reserved.

Leptin, Insulin, and the Arcuate 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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.

Anorexia and Positive Incentives It is not clear whether anorexics find food less appealing Some evidence suggests the opposite Copyright © 2011 Pearson Education, Inc. All rights reserved.

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 Copyright © 2011 Pearson Education, Inc. All rights reserved.