1. Prepared by Jeffrey W. Grimm Western Washington University
PowerPoint Presentation for Biopsychology, 9th 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 © 2014 PEARSON EDUCATION, INC.
ALL RIGHTS RESERVED.

2. Why Do Many People Eat Too Much?
Chapter 12
Hunger, Eating,
and Health
Why Do Many People Eat Too Much?
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

3. Copyright © 2014 Pearson Education, Inc.
Learning Objectives
LO1: Describe how energy is stored in the body.
LO2: Summarize the process of digestion.
LO3: Explain the 3 phases of energy metabolism.
LO4: Compare set point and positive incentive theories of hunger, and summarize relevant evidence.
LO5: Summarize the factors that influence what, when, and how much we eat.
LO6: Discuss the role of blood glucose in hunger.
LO7: Critically evaluate the concept of hypothalamic hunger and satiety centers.
LO8: Discuss the role of the gastrointestinal tract in hunger and satiety.
LO9: Compare and evaluate set-point and settling-point models of body weight regulation.
LO10: Discuss human obesity, its causes, and treatments.
LO12: Compare anorexia and bulimia.
LO13: Starving anorexics do not appear to be as hungry as they should: Discuss.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

4. Copyright © 2014 Pearson Education, Inc.
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 percent of U.S. adolescents suffer from anorexia or bulimia.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

5. Digestion, Energy Storage, and Energy Utilization
The purpose of eating is to provide the body with molecular building blocks and energy.
Digestion: breaking down food and absorbing its constituents
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

6. Copyright © 2014 Pearson Education, Inc.
FIGURE 12.1 The gastrointestinal tract and the process of digestion.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

7. Energy Storage in the Body
Energy is delivered to the body as lipids, amino acids, and glucose.
Energy is stored 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 © 2014 Pearson Education, Inc.
All rights reserved.

8. 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 © 2014 Pearson Education, Inc.
All rights reserved.

9. Three Phases of Energy Metabolism (Con’t)
Energy availability is 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 © 2014 Pearson Education, Inc.
All rights reserved.

10. Copyright © 2014 Pearson Education, Inc.
FIGURE 12.3 The major events associated with the three phases of energy metabolism: the cephalic, absorptive, and fasting phases.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

11. 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; it turns on when energy is needed and off when the set point is reached.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

12. Copyright © 2014 Pearson Education, Inc.
FIGURE 12.4 The energy set-point view that is the basis of many people’s thinking about hunger and eating.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

13. 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 © 2014 Pearson Education, Inc.
All rights reserved.

14. Problems with Set-Point Theories of Hunger and Eating
These theories are contrary to evolutionary pressures that favored energy storage for survival.
Reductions in blood glucose or body fat do not reliably induce eating.
These theories do not account for the influence of external factors on eating and hunger.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

15. 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.
This accounts for the impact of external factors on eating behavior.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

16. 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 a diet with vitamins, as well as foods they smell in mother’s milk or on other rats’ breath.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

17. Factors That Influence What, When, and How Much 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 has been demonstrated experimentally.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

18. Factors That Influence What, When, and How Much We Eat (Con’t)
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 a normal-sized meal if the food is familiar.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

19. Copyright © 2014 Pearson Education, Inc.
FIGURE 12.5 The sham-eating preparation.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

20. Factors That Influence What, When, and How Much We Eat
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 © 2014 Pearson Education, Inc.
All rights reserved.

21. 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 © 2014 Pearson Education, Inc.
All rights reserved.

22. 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 © 2014 Pearson Education, Inc.
All rights reserved.

23. 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.
Blood glucose must decrease by 50 percent 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 © 2014 Pearson Education, Inc.
All rights reserved.

24. 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 © 2014 Pearson Education, Inc.
All rights reserved.

25. Copyright © 2014 Pearson Education, Inc.
FIGURE 12.6 The locations in the rat brain of the ventromedial
hypothalamus and the lateral hypothalamus.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

26. Copyright © 2014 Pearson Education, Inc.
FIGURE 12.7 Postoperative hyperphagia and obesity in a rat with bilateral VMH lesions. (Based on Teitelbaum, 1961.) Disturbances in feeding and drinking behavior after hypothalamic lesions. In M. R. Jones (Ed.), Nebraska symposium on motivation (pp. 39–69). Lincoln: University of Nebraska Press.)
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

27. Myth of Hypothalamic Hunger and Satiety Centers (Con’t)
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.
The most supported role of the hypothalamus is the regulation of energy metabolism.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

28. Role of the Gastrointestinal Tract in Satiety
Cannon and Washburn (1912)
Studies suggested that stomach contractions led to hunger, and distension to satiety.
However, hunger is still experienced by those 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 © 2014 Pearson Education, Inc.
All rights reserved.

29. Copyright © 2014 Pearson Education, Inc.
FIGURE Transplantation of an extra stomach and length of intestine in a rat. Koopmans (1981) implanted an extra stomach and length of intestine in each of his experimental subjects. He then connected the major blood vessels of the implanted stomachs to the circulatory systems of the recipients. Food injected into the extra stomach and kept there by a noose around the pyloric sphincter decreased eating in proportion to its volume and caloric value.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

30. 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 © 2014 Pearson Education, Inc.
All rights reserved.

31. Hunger and Satiety Peptides (Con’t)
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).
The hypothalamus plays a central role in eating behaviors.
Microinjections of some peptides have major effects on eating.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

32. Copyright © 2014 Pearson Education, Inc.
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 are seen in humans.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

33. 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 to or Absence of a Section of Chromosome 15
Study of the syndrome may lead to advances in understanding eating behaviors in humans.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

34. 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 © 2014 Pearson Education, Inc.
All rights reserved.

35. 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 © 2014 Pearson Education, Inc.
All rights reserved.

36. Copyright © 2014 Pearson Education, Inc.
FIGURE The diminishing effects on body weight of a low-calorie diet and a high-calorie diet.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

37. Copyright © 2014 Pearson Education, Inc.
FIGURE The leaky-barrel model: a settling-point model of eating and body weight homeostasis.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

38. Who Needs to Be Concerned about Obesity?
Everyone: rates of obesity are increasing in most parts of the world.
Obesity is related to many other health problems.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

39. 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 © 2014 Pearson Education, Inc.
All rights reserved.

40. 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 interact with both energy input and output.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

41. 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 © 2014 Pearson Education, Inc.
All rights reserved.

42. 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 © 2014 Pearson Education, Inc.
All rights reserved.

43. Copyright © 2014 Pearson Education, Inc.
FIGURE An ob/ob mouse and a control mouse.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

44. Leptin, Insulin, and the Arcuate Melanocortin System
Insulin brain levels reflect visceral fat; leptin levels reflect subcutaneous fat.
Both insulin and leptin receptors are found in the arcuate nucleus of the hypothalamus.
Leptin and insulin in the brain have some effects on eating behavior, but are (again) not the only eating/sating signals.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

45. 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 © 2014 Pearson Education, Inc.
All rights reserved.

46. 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 © 2014 Pearson Education, Inc.
All rights reserved.

47. Anorexia and Bulimia Nervosa
Voluntary self-starvation
Fatal in 10 percent of patients
Bulimia: bingeing and purging
The two illnesses have similar symptoms, and can be difficult to distinguish.
Distorted body image
Most often affects educated, affluent young females
Associated with obsessive-compulsive disorder and depression
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

48. Anorexia and Positive Incentives
It is not clear whether anorexics find food less appealing.
Some evidence suggests the opposite.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.

49. 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.
The implication is that anorexics should eat small amounts of food throughout the day as part of their therapy.
Copyright © 2014 Pearson Education, Inc.
All rights reserved.