1. PSY 338: Motivation
Chapter 4:
Physiological Mechanisms of Regulation

2. Hunger Motivation: Why do we eat?
Internal Factors
External Cues

3. Hunger Motivation: Why do we eat?
Memory
Rozin, Dow, Moscovich & Rajaram (1998)
Procedure
Amnesic and non-amnesic participants feed full meal; offered next two meals in 30 minute intervals
Results
Amnesic participants were likely to accept and partially eat both subsequent meals; non-amnesic declined the offer
Interpretation
Memory is a major determinant of when we get hungry

4. What structures are doing the regulating?
Local Theories
Peripheral organs of the body control feeding behavior and bodyweight (e.g., stomach, vagus nerve)

5. Local Theories Cannon & Washburn (1912) Hunger Experiment
Washburn swallowed a balloon to record stomach contractions
Pushed button to report hunger feelings
Hunger feelings came at peak of contractions
Contractions lead to hunger, not vice-versa

6. What structures are doing the regulating?
Central Theories
Specialized cells in the brain control feeding behavior and bodyweight (e.g., hypothalamus)

7. Short-Term Regulation
What controls eating over short periods of time?
Balance energy intake with energy expenditure

8. Short-Term Regulation
What initiates a meal? What terminates a meal?
Center Theory
Ventromedial hypothalamus
Satiety center; Damage caused hyperphagia
Lateral hypothalamus
Hunger center; Damage caused aphagia
VMH lesioned rat is on left

9. Glucostatic Theory of Hunger
Blood Glucose
This is a simple sugar used by most cells in the body for energy - most food ultimately gets converted to blood glucose
Mayer (1955)
Decreasing blood glucose levels  sense of hunger
Receptors in the hypothalamus detect these changes and thus regulate our eating motivations
Many limitations to this theory; receptors are not primarily responsible for short-term regulation

10. Long-Term Regulation of Hunger
Controls a steady bodyweight
Lipostatic Theory
Set-point view: the brain tries to maintain steady lipid (fat) levels
Set point is the weight that your body wants to be
It is a self-regulatory system that maintains your body weight
If you starve yourself the hypothalamus activates compensatory mechanisms, your metabolism slows so that energy stores are used more sparingly and the amount of insulin that is produced increases so that more of the food that you take in remains as fat

11. Long-Term Regulation of Hunger
Dual-Center Theory of feeding behavior
Encompasses the set-point idea but that it’s a dual process
VMH as a "satiety center" and LH as a "Hunger center“
VMH lesion causes hyperphagia & obesity; LH lesion causes aphagia and anorexia

12. Nonhomeostatic Eating Behavior
What other factors affect the initiation and/or the termination of a meal? Hedonic factors must be considered as well.
Learning: anticipation of meals
Taste preferences: Pleasurable effects of food
Taste aversions: Disgust

13. Failure of Regulation: Eating Disorders
Anorexia Nervosa
There are physiological abnormalities that are correlated with the disorder but are these abnormalities causes or effects?
Search for causes:
Homeostatic theory encourages the search for physical deficits in homeostatic mechanisms
Non-homeostatic theory encourages the study of non-regulatory mechanisms such as learning and social influences

14. Anorexia Nervosa Self-starvation and severe weight loss
Usually starts as an innocent diet that went out of control
Often they come from high-achieving or over-protective families
Restricting Type
Binge/Purging Type

15. Case Study: Karen Carpenter
Famous singer died of complications to anorexia (cardiac arrest) in 1983 at the age of 32

16. Anorexia: Facts and Statistics
Lifetime prevalence in US:
Adults: 0.6%
15-24 year old females: 2%
Onset is in childhood

17. Anorexia Nervosa Symptoms Body dissatisfaction; body distortion
Lethargy
Irritability
Depression
Social withdrawal
Obsessiveness (food)

18. Anorexia Nervosa Complications Hypothermia may result Amenorrhea
Some will die from heart failure

19. Anorexia Nervosa Treatment
Hospitalization or outpatient care may be a necessary first step
Clinical: Individual, group, and family therapy are then applied
Anti-depressants are often combined with these therapies
Nutrition Therapy can be introduced after patients have recovered enough so that non-compliance is not a major obstacle
Self-help group therapy is an option for those without the financial means or insurance to utilize the above options
Prognosis
There is a good chance for improvement and hopefully recovery
However, it is a life-long process

20. Anorexia Nervosa Theories
Cross-Cultural Evidence
Not seen much in non-white cultures
Serotonin Hypothesis
Higher levels when anorexics are at normal body weight but low levels as they reduce weight
Heredity Factors
5-10% risk in first degree relatives
Holland, Sicotte, & Treasure (1988)
Twin study
Monozygotic twins: 56% concordance
Dizygotic twins: 5% concordance
Brain Structures
Limbic system structures seem primarily involved (hypothalamus, insula)

21. Bulimia Nervosa Purging Type
Disorder characterized by repeated binge-purge episodes of overeating followed by vomiting or using a laxative
Nonpurging Type
Fasting; excessive exercise

22. Bulimia: Facts and Statistics
Gender
89% are female
Appearance
These individuals can be thin, average in weight or even overweight – so this one is more likely to go unnoticed by family or friends
Onset
Childhood
Specific Populations
The incidence is estimated to be 3% in the general population; but as high as 10% of college women may suffer from it

23. Bulimia Nervosa Complications Sore throat Mouth and throat ulcers
Swollen salivary glands
Destruction of tooth enamel
Depression, obsessive-compulsive symptoms
Amenorrhea

24. Bulimia Nervosa Calam & Waller (1998) Procedure
Longitudinal study followed 63 females from age 12 to age 19
Results
Bulimic attitudes in early teenage years were related to bulimic symptoms in early adulthood
Poor family communication also a factor
Interpretation
Good news:
Unhealthy eating attitudes and behaviors can be predicted from early teenage characteristics
Targeting prevention and early intervention programs might be developed
Bad news:
These behaviors may be in place too early
Treatment difficult

25. Theories of Bulimia Sociocultural approach
The primary cause is unrealistic social norms
Clinical/psychiatric approach
The primary cause is an affective disorder
Epidemiological/risk factors approach
This approach looks at the risk factors leading to this disorder
Social contagion
The primary cause is an interaction between unrealistic social norms and affective disorder
Neurotransmitters
Serotonin Hypothesis

26. Obesity
Weight which is 20-40% above the normal standard for a person’s height (BMI over 30)

27. Basal Metabolic Rate
The amount of energy expended while at rest in a neutrally temperate environment, in the post-absorptive state (meaning that the digestive system is inactive, which requires about twelve hours of fasting in humans)
BMR decreases as you age
Depriving yourself of food in hopes of losing weight also decreases your BMR, a foil to your intentions
Exercise increases BMR
Lean body mass (LBM) also decreases with age

28. Obesity Explanations Adaptiveness Gone Wrong
Normal weight has approximately one month of stored energy
In obese, the storage system has continued past normal levels
Genetic predisposition
More fats cells lead to genetically programmed to carry more weight
Problem with one or more homeostatic mechanisms
High sensitivity to one or more nonhomeostatic factors

29. Obesity Explanations Obesity as maintaining obesity Hyperinsulinemia
Insulin involved in fat storage process; increases the amount of energy stored away as fat; the more insulin, the more energy that can be stored away as fat
Activity levels
Obese usually less active so they burn less calories
Fat tissue is metabolically less active than lean tissue
Dieting
Weight cycling
Metabolic rate is reduced during food deprivation
New set-point may be established 

30. Obesity Explanations Schacter (1971) Procedure
Normal weight and obese participants sequestered for a week
Lived in college dorms
Watches taken from participants
Clocks altered
Results
Obese more likely to be hungry than normals when clocks were around mealtimes
Interpretation
The difference between obese and normal weight participants is that the obese are overly responsive to external stimuli (cues for eating)
Externality Hypothesis

31. The Role of Habituation in Obesity
A decrease in the magnitude of a response as the result of repeated stimulation
Organisms decrease responding to a stimulus after repeated exposures
A simple form of learning in which the organism learns something about a single stimulus
Common examples:
Noises in your house
Traffic
Air conditioning/furnace

32. The Role of Habituation
Dishabituation
Habituation to a stimulus can be temporarily blocked by a novel stimulus
The novel stimulus increases the response to the original stimulus when the original is re-presented

33. Dishabituation Siddle (1985)
Participants receive 15 presentations of 4-second tone
Response to tone decreases to almost nothing as the result of habituation
New stimulus (patch of red light) is presented
New response specific to light occurs
Tone is then presented again (16th time overall)
Response increases as compared to 15th presentation; dishabituation has taken place
Presenting the tone again will lead to the reappearance of habituation; response returns to previous low level

34. The Role of Habituation
Epstein, Temple, Bouton, & Roemmich (2009)
Many stimuli associated with eating food making habituation likely; eating that food should decrease
However, if dishabituating stimulus occurs then eating behavior is also likely to return
When we vary what we eat, habituation is less likely to occur

35. Obesity as Addiction Palatability of food may be addictive
Pleasurable, rewarding part nor related to homeostatic system
Related to hedonic system that appears to promote addiction-like behaviors

36. Stress leads to Obesity
Animal studies demonstrate that stress can produce overeating
Seems to cause elevation of ghrelin levels and reduce levels of leptin leading to overeating, increased hunger for high fat diets, and increased body weight

37. Regulation of Thirst Water constitutes 70% of the mammalian body
Water in the body must be regulated within narrow limits
The concentrations of chemicals in water determines the rate of all chemical reactions in the body

38. Regulation of Thirst
Two different kinds of homeostatic thirst include:
Osmometric thirst – a thirst resulting from eating salty foods
Volmetric thirst – a thirst resulting from loss of fluids due to bleeding or sweating
Each kind of thirst motivates different kinds of behaviors

39. Nonhomeostatic Drinking
Eating seems to be a potent stimulus for drinking; nonhomeostatic influence
Kraly (1984)
Normal drinking occurs around meals for people and animals
Lab rats: as much as 90% of daily water intake occurs near mealtime (10:00 before to 30:00 after)

40. Regulation of Sexual Motivation
Sex Hormones
Testosterone (males)
Estrogen (females)

41. Sexual Dimorphism
Refers to sexual differences between males and females
This is the result of the action of a gene found on the Y (male) chromosome
For first 6 weeks, fetal development is the same for both males and females
Then SRY male gene starts producing a protein that causes the testes to develop

42. Hypothalmic Regulation
Damage to hypothalamus
Hypogonadal conditions: Lack of sexual motivation

43. Regulation of Aggressive Motivation
Nonhomeostatic motivation
Cortex of the brain is unnecessary for the expression of anger
Cannon (1929)
Decorticate cats displayed “sham rage”
Lesions in cortex yet displays of anger accompanied by normal autonomic arousal

44. Limbic System Amygdala
Emotional control center of the brain – major influence on aggression and fear
Kluver & Bucy (1939)
Aggressive monkeys became tame after lesions in this area
Olvera (2002)
Intermittent explosive disorder has been traced to amygdala (as well as the prefrontal cortex)

45. Limbic System Hypothalamus
Pleasure center may be involved in the spontaneity of aggressive behavior
Flynn et al. (1970)
Affective attack – high emotionality; can be elicited by electric stimulation of VMH
Quiet biting attack – low emotionality, predatory behavior; can be elicited by electric stimulation of LH and thalamus

46. Neurotransmitters Serotonin Low levels increase aggression GABA
Opioids
Dopamine
High levels increase aggression

47. Credits Some slides prepared with the help of the following websites:
plaza.ufl.edu/laurajf/lectures/Chapter%2012.ppt
web.campbell.edu/faculty/asbury/ppt/chapter10.ppt