1. 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.

2. 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.

3. 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.

4. 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.

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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.

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

19. 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.

20. 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.

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 © 2011 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 © 2011 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
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.

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 © 2011 Pearson Education, Inc. All rights reserved.

25. 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.

26. 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.

27. 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.

28. 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.

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

31. 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.

32. 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.

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 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.

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

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

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

38. 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.

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 © 2011 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 interacts with both energy input and output
Copyright © 2011 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 © 2011 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 © 2011 Pearson Education, Inc. All rights reserved.

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

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

47. 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.

48. 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.

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
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.