Chapter 4: Physiological Mechanisms of Regulation
PSY 338: Motivation
Hunger Motivation: Why do we eat?
Internal Factors
External Cues
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
What structures are doing the regulating?• Local Theories
• Peripheral organs of the body control feeding behavior and bodyweight (e.g., stomach, vagus nerve)
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
What structures are doing the regulating? • Central Theories
• Specialized cells in the brain control feeding behavior and bodyweight (e.g., hypothalamus)
Short-Term Regulation
What controls eating over short periods of time? •Balance energy intake with energy expenditure
Short-Term Regulation
Center Theory•Ventromedial hypothalamus
• Satiety center; Damage caused hyperphagia
•Lateral hypothalamus• Hunger center; Damage caused
aphagia
What initiates a meal? What terminates a meal?
VMH lesioned rat is on left
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
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
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
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
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
Anorexia NervosaSelf-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
Case Study: Karen Carpenter• Famous singer died of complications to anorexia (cardiac
arrest) in 1983 at the age of 32
Anorexia: Facts and Statistics
Lifetime prevalence in US: •Adults: 0.6%•15-24 year old females: 2%•Onset is in childhood
Anorexia Nervosa
Symptoms•Body dissatisfaction; body distortion•Lethargy•Irritability
•Depression
•Social withdrawal
•Obsessiveness (food)
Anorexia Nervosa
Complications
•Hypothermia may result
•Amenorrhea
•Some will die from heart failure
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
Anorexia Nervosa TheoriesCross-Cultural Evidence•Not seen much in non-white culturesSerotonin Hypothesis•Higher levels when anorexics are at normal body weight but low levels as they reduce weightHeredity 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)
Bulimia Nervosa
Purging Type•Disorder characterized by repeated binge-purge episodes of overeating followed by vomiting or using a laxativeNonpurging Type•Fasting; excessive exercise
Bulimia: Facts and Statistics
Gender •89% are femaleAppearance•These individuals can be thin, average in weight or even overweight – so this one is more likely to go unnoticed by family or friendsOnset•ChildhoodSpecific Populations•The incidence is estimated to be 3% in the general population; but as high as 10% of college women may suffer from it
Bulimia Nervosa
Complications•Sore throat•Mouth and throat ulcers•Swollen salivary glands•Destruction of tooth enamel•Depression, obsessive-compulsive symptoms•Amenorrhea
Bulimia NervosaCalam & 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
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
ObesityWeight which is 20-40% above the normal standard for a person’s height (BMI over 30)
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
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
Obesity ExplanationsObesity 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
Obesity ExplanationsSchacter (1971)Procedure•Normal weight and obese participants sequestered for a week•Lived in college dorms •Watches taken from participants•Clocks alteredResults•Obese more likely to be hungry than normals when clocks were around mealtimesInterpretation•The difference between obese and normal weight participants is that the obese are overly responsive to external stimuli (cues for eating)•Externality Hypothesis
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
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
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
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
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
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
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
Regulation of Thirst
Two different kinds of homeostatic thirst include:
1. Osmometric thirst – a thirst resulting from eating salty foods
2. Volmetric thirst – a thirst resulting from loss of fluids due to bleeding or sweating
Each kind of thirst motivates different kinds of behaviors
Nonhomeostatic DrinkingEating 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)
Regulation of Sexual Motivation
Sex Hormones•Testosterone (males)•Estrogen (females)
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
Hypothalmic Regulation
Damage to hypothalamus•Hypogonadal conditions: Lack of sexual motivation
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
Limbic SystemAmygdala•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)
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
Neurotransmitters
Serotonin •Low levels increase aggression
GABA•Low levels increase aggression
Opioids•Low levels increase aggression
Dopamine•High levels increase aggression
Credits
Some slides prepared with the help of the following websites:• http://pirate.shu.edu/~vigorimi/Motivation_and_Emotion/chapter4.htm• plaza.ufl.edu/laurajf/lectures/Chapter%2012.ppt• web.campbell.edu/faculty/asbury/ppt/chapter10.ppt• http://www.futuresofpalmbeach.com/anorexia-treatment/facts-
statistics/• http://www.anred.com/stats.html