Psychology of Motivation Chapter 4

Why do we eat? How much do/could/should we eat?

·       Should - 2,000 – 2,005 calories per day

·       Sensory receptors: Taste

o   Sweet, sour, bitter, salty, umami

·       Energy

o   ATP

·       Cues from the environment

o   Sight and smell

·       Memory

Sensory Specific Satiety

·       Eating a particular food till one is satiated – reduces values of that food compared to their foods

·       Consuming less, compared to having a more various diet

·       This constant diet becomes less and less rewarding

·       Hungry individuals show increased activity in the amygdala, suggesting that food-related stimuli are able to increase hunger motivation

·       Related to the characteristics of food

o   Taste (sensory receptors on the tongue)

o   Tactile sensation of the tongue

Basic Metabolism

·       All food separated into 3 groups

o   Carbs

§  Glucose, Glycogen

o   Fats

§  triglycerides

o   Proteins

§  Amino acids

Local Theory

·       Contractions in the stomach – hunger signals in the gastrointestinal tract initiate eating behavior

·       Removing the stomach – still showed signs of food seeking behaviors

·       Severed the vagus nerve – contractions decreased but still showed signs of food seeking behaviors

o   The vagus nerves send and receive information from the stomach to and from the brain

Central Theories

·       Specialized cells in the brain detect changes in the body – then sends messages to trigger the appropriate motivation

·       Homeostatic control center: Hypothalamus

o   Parasympathetic

o   Sympathetic

o   Pituitary gland

o   Endocrine system

·       The hypothalamic-pituitary-adrenal (HPA) axis

·       Monitor internal states – Optimal state (No or Yes) (If yes, stop) – NO – Activate motive – Eat

Regulating Hunger

·       Short-term Regulation (primary function: regulate energy intake with energy output: trigger eating when energy drops)

o   Mechanism that controls when we eat a meal and how much we eat

o   (intermeal interval) x (meal size)

·       Long-term Regulation

o   Maintaining adequate energy stored – detection of changes in the amount of energy stores as fat within the adipose tissue – activates hunger

·       Glucoreceptors

o   Detect imbalance of blood glucose

o   Trigger the motive to eat or inhibits eating

Brain Structures in ST regulation

·       Ventromedial Hypothalamus (VMH): safety center

o   Damaged this area of the hypothalamus:

o   Hyperphagia

§  A condition characterized by excessive eating, where the individual experiences an inability to achieve satiety (full feeling).

·       Lateral Hypothalamus (LH): hunger center

o   Lesions in this region of the hypothalamus

o   Aphasia and Adipsia

§  Inhibition of food intake “Complete failure of eating as well as of drinking”

o   Center hypothesis

§  Damage to the LH should lead to lack of eating

Glucostatic Theory of Hunger (LH and VMH)

·       Not related to glucose as much as a more “emergency system” under “extreme conditions”

·       Regulation of hunger and eating by is based on the fluctuating glucose level

·       LH

o   motivate eating when glucose levels are low

o   Lesions lead to deficit in motivation in general

·       VMH

o   Regulating motivation to stop eating when the body has sufficient amount of glucose

o   Further studies – not entirely the VMH but the fiber bundles adjacent (when damaged leads to obesity)

·       LH and VMH

o   Work together in balancing and regulating hunger and satiety

Peripheral detectors for ST regulation

·       Stomach

o   Stretch receptors on the stomach walls

o   Limits volume/amount intake

o   Ghrelin

§  Brain-stomach hormone

§  Secreted by the stomach – rises sharply before a meal is eaten – drops as food is eaten

o   Not only an appetite stimulant it can also produce thoughts about food

o   When injected (Ghrelin) – there’s an increase in food intake

·       Duodenum

o   Upper small intestine (connected to the stomach)

·       The beginning of the absorption process

o   Sugars (carbs) and amino acids (proteins) enter the bloodstream

·       Travels to the liver

·       Cholecystokinin (CCK)

o   Secreted in response to food

o   Signals the brain to stop eating

·       Glucoreceptors

o   Intestine secretes

o   FIP and FLP-1, letting the brain know that Glucose is available

·       Liver

o   2-deoxyglucose (2-DG)

§  Blocks glucose usage

§  Monitors glucose availability – sends msg to hypothalamus

o   The portal vein

§  Receive nutrients from the GI tract

§  Hepatic portal vein

·       Source of satiety signals

·       Pancreas

o   Alpha cells produce and release glucagon

o   Beta cells produce and release insulin

o   Insulin

§  Carries glucose into the cells for energy

o   Amylin

§  Slows down food intake

Long Term Regulation

·       Our bodies appear to be relatively well regulated

·       SET-point theory: Lipostatic Theory of Hunger

o   Storage system that acts to monitor body weight and fat, as well as regulate food intake to keep the body fats fairly constant

·       Insulin

o   Hormone produced by the pancreas

o   Sends message to the brain: fat storage – signals the hypothalamus on body’s energy status

o   Insulin resistance:

§  Body’s cells become less responsive to insulin

§  Disrupted hunger regulation increased fat storage

·       High Insulin levels – energy is available

·       Low Insulin levels – energy is low – stimulate hunger

·       Plays a role in the conversion of glucose – fat: fat storage and breakdown system

·       Leptin

o   Hormone produced by (adipocytes)

o   Low levels of fat stored = low leptin levels

§  Increased hunger; reduced energy usage – motivate eating behavior/fat storage

o   High levels of fat store = high leptin levels

§  (Receptors in the Arcuate nucleus) hypothalamus gets a signal to reduce hunger; increase energy metabolism

o   Leptin resistance:

§  Brain does not respond to high levels of Leptin

§  Difficulty regulating hunger and or weight

·       Neuropeptide Y (NPY)

o   Neurotransmitter – produced in the arcuate nucleus

o   Potent stimulator of hunger

o   During weight loss diet or fasting NPY level increase

o   Leptin and Insulin inhibit NPY production

·       Paraventricular Nucleus (PVN)

o   Region in the hypothalamus

o   Critical role in controlling satiety and energy usage

·       Alpha-melanocyte-stimulating hormone (a-MSH)

o   Promotes satiety and encourages the breakdown of fats when energy storage is high

o   High levels of Leptin stimulate the release of (a-MSH)

o   Ghrelin decreases (a-MSH) activity – stimulating food intake

Failure in Regulation

·       Anorexia Nervosa

o   Extreme restriction on food intake

o   In some cases, to the point of starvation

o   Refusal/inability to maintain body weight at/above minimal expected weight

§  As little as less than 85% expected weight

o   Amenorrhea

§  Absence of menstruation, the reproductive cycle (inhibited)

o   Binge eating, Hoard food, show preoccupation with food or cooking

o   Show perfectionism traits obsessive-compulsive behavior, depressed moods, and/or anxiety

o   Body dissatisfaction, Middle socioeconomic household income

·       A neurobiological view

o   Serotonin hypothesis

§  Lower levels of serotonin (metabolite {CSF 5-HIAA})

§  Increased areas of cerebrospinal fluid-filled spaces

§  Lower heart rate, blood pressure, menstrual cycle

§  The GAS

·       Malfunctions in endocrine system

·       Prolonged period of elevated cortisol levels

§  Learning deficits

·       Difficulties in paired-associated tasks

·       The longer the anorexia persisted, the worse their performance

·       Bulimia Nervosa

o   Episodes of Binge eating

§  In a discrete period of time (2-hour) large amount (1,000-5,000 calories)

o   Feelings of loss of control – post binge, Purging behavior

§  Normally appear normal weight

o   Emotion-produced binges

o   40-50% of anorexic will develop bulimia at some point of their disorder

o   Induce vomiting, Abuse laxatives, Overexercise, severely restrictive diets

o   Bulimics reported being sadder; lonelier; weaker; more irritable; more passive; more constrained

·       Different theories

o   Sociocultural Approach

§  Society and culture put pressure on being a certain way

§  Necessity to eat is put under question

§  Conflict with social norms and body image

o   Social Contagion Theory

§  Norms from social groups will be contagious to individuals experiencing psychological distress

§  Genetic predisposition x social influence

§  Social learning (body image and sex roles)

o   Clinical/Psychiatric Approach

§  Conflict with social norms and body image

§  Impulsiveness, low self-esteem, history of abuse

o   Epidemiology Logical/Risk Factors

§  Factors that put individuals at risk

§  Unrealistic body image-emotional lability-stressful family relationships

§  Hormonal changes-rigid sex roles-stress-genetic predispositions

o   Escape Theory

§  Escape from self-awareness

·       Physiological changes

o   Neurological changes

o   Serotonin, norepinephrine, dopamine, CCK, beta-endorphin, neuropeptide PYY

o   Lower levels of dopamine and serotonin metabolites in cerebrospinal fluid

·       Obesity

o   Imbalance

§  Energy intake and energy output

§  BMI 25-30 = overweight

§  > 30 = obese

o   2 factors that contribute to increasing body fat

§  Basal metabolism

·       Energy the body consumes to maintain bodily functions at rest

·       Older men who were overfed maintained the additional weight longer than younger men

§  Lean Body Mass (LBM)

·       Body mass – fat mass = LBM

·       LBM decreases with age

Explanations on Obesity

·       Adaptation Gone Wrong

o   Margules (1979) and Pi-Sunyer (1994) view obesity as continued storage of energy

o   Originally – our energy storage system was design to have approximately 1 month’s supply

§  Food was unreliable

§  Nature and environment limits or somewhat controlled obesity

§  Don’t have well-developed mechanisms for limiting fat storage beyond some minimum level

§  Found higher levels beta-endorphin to be associated with obesity in rats

·       Genetic Predisposition

o   Don’t have well-developed mechanisms for limiting fat storage beyond some minimum level

o   300,000 Dutch army draftees

§  Mothers who experienced famine during the first 2 trimesters of their pregnancy (during WW2)

o   Those draftees had higher coincidence of obesity than the population in general

·       Hyperinsulinemia (abnormally high level of insulin in the blood)

o   Pancreas produce excessive amounts of insulin in attempt to maintain blood glucose level

o   Insulin increases the amount of energy stored away as fat

o   As a result of insulin resistance, blood cells become less responsive to insulin’s effects

o   Hyperinsulinemia induces hunger

·       Activity Levels

o   Obese individuals tend to be less active than the normal population

o   Burn less calories due to less activity

o   Adipose (fat) tissue metabolically less active – needs less calories to maintain body weight

o   Regular Exercise

§  Builds muscles, burns more calories than are taken in, needs mor energy to maintain, needs to break down fat storage

·       Dieting Promoting Obesity

o   Food deprivation, the body needs to conserve energy, reduced metabolic rate, each successive dieting episode, larger reductions in metabolic rate

·       Obesity as Addition

o   Eating as an addictive behavior

o   Palatability – rewarding, pleasurable

Homeostatic Regulation of Thirst

·       Weight from water

o   Females: 50%

o   Males: 60%

·       Metabolic water

o   2/3 intracellular fluid

o   1/3 extracellular fluid

§  70% interstitial fluid (fluid between cells)

§  30% intravascular fluid (fluid within blood)

·       Mouth factor

o   Peripheral/local receptors

o   Saliva production increases as a result of drinking

o   Saliva reduces the sensations associated to dry mouth

·       Water loss: urination, sweat, feces evaporation from the skin

·       Resulation of water balance to prevent dehydration

Extracellular and Intracellular Mechanisms

·       Extracellular mechanisms

o   Receptors detecting changes in the fluid surrounding the cells

·       Intracellular mechanisms

o   Receptors detecting changes in the water content inside the cells

·       Frontal area of the brain

o   Impairment in water balance regulation (intracellular)

·       Volumetric thirst

o   Extracellular fluid balance

o   Extracellular thirst

·       Osmometric thirst

o   Intracellular fluid balance

o   Intracellular thirst

The Kidneys

·       Excrete excess fluid that we consume

·       Sodium absorption and remove waste product of metabolism via urine

·       Absorb about 99% of water filtered by the kidneys

·       Anderson (1971) suggested: because control of water balance is closely tied to sodium balance – Thirst controlled by sodium detectors

o   Sodium receptors found in the liver that is involved in water balance

·       Renin +

o   Secreted by the kidney

·       Angiotensinogen

o   Secreted by the liver

·       = Angiotensin II

o   Stimulates adrenal gland to secrete:

o   Aldosterone

§  Kidneys to increase sodium absorption – water

·       Antidiuretic hormone (ADH) vasopressin (VP)

o   Secreted by the posterior pituitary gland

o   The kidney’s capacity to absorb water in the collecting ducts is controlled by vasopressin

o   Produced by neurosecretory cells in the hypothalamus supraoptic and paraventricular nuclei

o   Increase water reabsorption, reduce urine output and maintain blood pressure, to conserve water

·       Lack of ADH or VP – Diabetes insipidus

Osmometric Thirst

·       When solute concentration (like salt) in the body’s fluids rises, it creates an imbalance, prompting a desire to drink water to restore balance

·       Osmosis

o   Movement of water across a semi-permeable membrane (like a cell membrane) from an area of lower solute concentration to an area of higher solute concentration

§  Sodium cannot pass into the cell body

·       Osmoreceptors

o   Specialize cells in the structure at base of the third ventricle – outside of the blood-brain barrier

o   As a result, the cell decreases in size

·       Trigger drinking behavior in order to restore intracellular water balance

·       Organum Vasculum laminae terminalis (OVLT) detect changes in osmolarity of the blood and hormonal changes (e.g. angiotensin)

o   Stimulate cells in Median preoptic area

o   Initiate thirst and drinking

·       Anderson (1971) suggested: because control of water balance is closely tied to sodium balance

o   Thirst controlled by sodium detectors

·       Sodium receptors found in the liver that are involved in water balance

o   Sends signal to area postrema (AP)

o   Stop drinking

o   Distension of throat, esophagus, stomach, and duodenum

·       Organum vasculum laminae terminalis (OVLT)

o   Controls water intake

o   It takes 10-20 mins for ingested water to reduce osmolarity

Volumetric Thirst

·       The body’s response to decrease in blood volume

·       Hypovolemia

o   Decrease in the volume of blood plasma

§  Increase in blood pressure and adjust heart rate

o   Causes:

§  Severe dehydration

§  Blood less

§  Excessive fluid loss (vomiting/diarrhea)

o   Stimulate release of renin – Produce angiotensin II

·       Low-pressure baroreceptors, Atrial volume receptors

o   Stretch receptors located on the walls of the great veins (blood return to heart) and right atrium

o   Sends message to the hypothalamus to stimulate thirst – drink fluid

o   Trigger release of ADH from posterior pituitary

o   Telling kidneys to conserve water

Non homeostatic Drinking

·       Drinking is closely linked to eating

o   Eating appears to be a stimulus for drinking

·       FI tract changes (food enters) stimulate drinking behavior that is non-homeostatic

o   Histamine released by stomach cells

o   Cause production of renin in the kidneys

§  Interacts with angiotensinogen

§  Angiotensin

o   Stimulate drinking

·       Amylin

o   Hormone produced in the pancreas

o   Produced when food is eaten – injected into rats

§  Rats initiated drinking

Regulation of Sexual Motivation

·       Sexual Dimorphism

o   Differences in appearance, size or behavior of the male and female of species

§  Genetic makeup

§  Hormone makeup

§  Reproductive organs

§  Body size

§  Behavioral differences

·       The mammalian brain is developed as female

o   Only with the presence of testosterone (male hormone) during a critical period in development (is sex determined)

·       Sex-determining region Y (SRY gene)

o   Located on the Y chromosome

o   Initiating development of male characteristics during the embryonic period (of pregnancy)

o   Formation of testes (from undifferentiated gonadal tissue)

o   Production of testosterone

o   Male secondary sexual characteristics

·       Sex hormones

o   Activating gender specific behaviors as the organism reaches puberty

§  Attractivity

·       Behavior that attracts a male to a receptive female

§  Proceptivity

·       Species-specific behavior that sexually around the male and lead to mounting

§  Receptivity

·       Behaviors that lead to the successful transfer of sperm to the female

§  Intromission

·       Penetration of the vagina by the penis

§  Thrusting

·       Produces friction between the sex organs

§  Ejaculation

·       Introduction of the sperm to the vagina

·       Injecting sex hormones into rats

o   Castration – signs on female physiology

§  Sex organs decreased in size

§  No longer produce egg cells

§  Ovulation cycle was disrupted

§  Lordosis

·       Arching back and elevating pelvis in order to permit mounting by the male

o   Stress and hormones and early life experiences can have long-term effects on the development of sexual behavior and reproductive physiology

Hypothalamic Regulation of Sexual Behavior

·       Sexually dimorphic nucleus of the preoptic area (SDN-POA)

o   Larger in males

o   Regulating male sexual behavior

§  Mounting

§  Intromission

§  Ejaculation

o   Damaged – impairments in these behaviors

·       Medial preoptic area (MPOA)

o   Regulating sexual behavior in both:

§  Males: mounting copulation

§  Females: maternal behavior and sexual behavior

o   Responsible for both inhibitory and excitatory function

·       VMH

o   Regulating sexual behaviors in females

o   Sending signal to periaqueductal gray area (PAG)

§  Controls lordosis

§  Sensitive to estrogen and progesterone

o   Damaged/removed VMH = decreased female sexual behavior

·       Bed nucleus of stria terminalis (BNST)

o   Sexually dimorphic

o   Larger in males

o   Modulating emotional responses and reproductive behavior – sexual arousal and motivational aspects (in expressive behavior)

Regulation of Aggressive Motivation

·       Removal of the cortex in cats (decorticate) = sham rage (true emotional behavior)

o   Lashing tail, arched back, snarling, slowing, biting, pupil dilation, piloerection, rapid heartbeat, increase in adrenaline and blood sugar

·       Needs intact hypothalamus (posterior portion)

·       The cortex – acts to suppress aggressive emotional behavior

The Limbic System

·       The Papez circuit

o   Emotions are not solely generated by external sensor inputs

o   Internal circuit of interconnected brain area that process emotional experiences

·       Hippocampus

o   Emotional processing

o   Regulating emotional memories

o   Linking emotion to cognition

·       Hypothalamus

o   Center for emotional expression

o   Influence autonomic behavior during emotional states

·       Anterior Thalamic Nuclei

o   Relay station

o   Transmit emotional signal to/from cingulate cortex and hypothalamus

·       Cingulate Cortex

o   Subjective experience of emotion

o   Interpret emotional signals from hypothalamus and generating experience

·       Signals travel from Hippocampus – Via the fornix – To the mammillary bodies (of the hypothalamus) – Signals move to the anterior thalamic nuclei – Cingulate cortex – (repeat)

·       Periaqueductal gray (PAG)

o   Area in the midbrain involved in aggressive behavior

o   Role in pain modulation and coordinating defensive behaviors in response to threat

·       Thalamus

o   Neural system for fight/flight

o   Lesions lead to elimination of flight behavior (when pain was inflicted)

·       Amygdala

o   Damages lead to loss of social dominance behavior in monkeys

o   Significant for normal expression of aggressive behavior

o   Supports that the amygdala is crucial in emotional responses to threat

The Limbic System: Aggressive Behavior

·       Hypothalamus

o   Neural mechanisms underlying aggressive behaviors

o   Brain regions controlling different types of attack behaviors

o   Affective (defensive) attack

§  Emotional and defensive reactions

§  Autonomic arousal: heart rate and vigilance

o   Predatory attack quiet biting attack

§  Calm, focused and goal-directed

§  Aim at capture/killing prey

§  Little to no autonomic arousal associated

o   VMH stimulated

§  Defensive in nature

§  Ward off threats

§  Intimidate/repel

o   LH stimulated

§  Stalking and biting behavior

§  Methodical and purposeful

·       Feeding and hunting (no emo defense)

Different types of Aggression

·       Predatory Aggression: aggression elicited by a natural object of prey (basal nucleus inhibits) Predatory Attack, Quiet biting attack

·       Intermale Aggression: aggression typically released by the presence of another male; the attack is usually without provocation

·       Fear-Induced Aggression: aggression that occurs when escape is blocked (facilitated by basal nucleus of amygdala

·       Irritable Aggression: aggression usually described as either anger or rage; attack occurs in response to a broad range of stimuli either animate or inanimate (basal nucleus inhibits) Affective (defensive) attack

·       Territorial Defense: aggression in defense of territory; the aggression is usually against member of the animal’s own species

·       Maternal Aggression: aggression involving defense of the young, typically performed by the female in mammals

·       Instrumental Aggression: aggressive behavior that is learned response and is performed when that response is reinforced