HUNGER, EATING, & HEALTH

HOMEOSTASIS, AND MOTIVATION

1. Humoral Response
◼ Hypothalamic Neurons detect
signals from sensory neurons and
stimulate or inhibit the release of
pituitary hormones

2. Visceromotor Response
◼ Activates the autonomic nervous
system and the needed
parasympathetic or sympathetic
response

3. Somatic Motor Response

◼ Hypothalamic neurons in the
lateral hypothalamus incite the
appropriate somatic response
Energy Balance

◼ Our brain eats glucose and it needs it as much as it needs

oxygen and just a few minutes without it will render us
unconscious
◼ When the blood has nutrients after eating it stores energy
in two forms Glycogen and Triglycerides
◼ Anabolism: The assembly of macromolecules by small molecules
◼ Catabolism: The process of breaking down macromolecules
◼ Obesity happens when intake consistently exceeds usage
◼ Starvation happens when intake consistently does not meet the
body’s demands
 Homeostasis & Eating

◼BODY WEIGHT IS STABLE AROUND A SET

POINT AND THAT IS WHAT MAKES IT
HARD TO DIET
◼ Glucostatic Hypothesis: We eat to maintain
blood-glucose set point
◼ Lipostatic Hypothesis: We eat to maintain
body fat content
LEPTIN ◼ ob/ob mice lack both copies of the
ob gene
◼ A parabiosis experiment was
designed to see if ob was
responsible for a chemical
messenger in the blood.
◼ Leptin was discovered by Jeffrey
Friedman in 1994 and it is a
hormone released from fat and
acts directly on hypothalamic
neurons to decrease appetite.
◼ Leptin replacement in ob/ob mice
and in leptin deficient humans
prevents obesity
LATERAL HYPOTHALAMIC CONTROL OF FEEDING

◼ Lesions on both sides of the lateral

hypothalamus causes anorexia in rats
(Heatherton & Ranson, 1940)
◼ Lesions on both sides of the ventromedial
hypothalamus causes obesity in rats
◼ The lateral hypothalamus was once referred to
as the hunger center and the ventromedial
hypothalamus the satiety center, but this is
overly simplistic
EFFECTS OF LEPTIN ON THE HYPOTHALAMUS
◼ Arcuate nucleus neurons have
leptin receptors and lies near
the base of the 3rd ventricle
◼ These neurons release two
peptides that have
anorexigenic effects
◼ αMSH is alpha-melanocyte
stimulating hormone
◼ CART is cocaine and
amphetamine regulated transcript
◼ Arcuate neurons project to the
paraventricular nucleus, spinal
cord and the lateral
hypothalamus
EFFECTS OF LEPTIN ON THE
HYPOTHALAMUS

◼ The paraventricular nucleus stimulates

both the humoral and visceromotor
response
◼ The humoral response to leptin consists
of secretion of thyroid stimulating
hormone (TSH) and adrenocorticotropic
hormone (ACTH) and raises metabolism
◼ Increases tone of sympathetic nervous
system increasing metabolic rate
◼ Causing a decrease in food intake
EFFECTS OF LEPTIN ON THE HYPOTHALAMUS

◼ Drops in leptin levels stimulate different

neurons in the arcuate nucleus
◼ NPY is neuropeptide y
◼ AgRP is agouti-related proteins
◼ Stimulates the lateral hypothalamus at the
MC4 receptor (the same receptor that is
excited by CART and aMSH)
◼ The parasympathetic nervous system is
activated
 Ghrelin & Hunger

◼ Ghrelin: Highly concentrated in the

stomach and released into the
bloodstream when the stomach is
empty, then stimulates AGRP and NPY
neurons in the arcuate nucleus.
Satiety
Meals cease when satiety signals including gastric
distention, the release of cholecystokinin, and
insulin

◼ Stretch receptors in the stomach stimulate the

vagus nerve which activates the nucleus of the
solitary tract, this nucleus also receives
gustatory information.
◼ Cholecystokinin or CCK is released in response
to some nutrients, especially fatty foods,
◼ Insulin: released into the blood stream by beta
cells of the pancreas to help break down glucose
in the body
REINFORCEMENT AND REWARD

◼ Reinforcement and Reward

◼ Olds & Milner (1950) Discovered
that rats would self stimulate into
certain regions of the brain
◼ Mesocorticolimbic system or the
reward system
These feeding systems are also
associated with addiction
SEROTONIN, FOOD, & MOOD

What is Hangry?
What is the emotional connection to
food?
Serotonin rises in the brain in response to
anticipation of food
Serotonergic drugs can suppress
appetite
The effect of carbohydrates on mood are
particularly evident during periods of
stress
Obesity
Obesity is the condition of being very
overweight
BMI: Body Mass Index wt(kg/ht
Basal Metabolic Rate: Resting rate of energy
expenditure
Genetic Factors

Twin Studies reveal that identical twins have a similar wt even when reared
apart
Adoption studies reveal that wt resemble biological parents
Set-Point Theory

◼ The point at which an individual's wt thermostat

is set
◼ When the body falls below that
◼ Increased hunger
◼ Lower metabolic rate
◼ Energy expenditure decreases
◼ What are some issues with this theory?
WHY DO WE EAT?

◼ What motivates us to eat

besides hormones?
◼ Time of day?
◼ Parental commands?
◼ What motivates us to keep
eating?
◼ When or how much you ate last?
◼ How good is the food?
 Anorexia Nervosa
DSM-5 Criteria
◼ Restriction of behaviors that
promote healthy weight; body
weight is significantly below
normal BMI (Body Mass Index)
less than 18.5 for adults
◼ Intense fear of gaining weight
and being fat
◼ Distorted body image or sense
of body shape
Anorexia Nervosa

◼ The term anorexia refers to loss of appetite but this is a misnomer

◼ People with anorexia still have a desire to eat and actually have a preoccupation
with food
◼ Begins during adolescence
◼ Life-time prevalence is less than 1%
Anorexia Nervosa

◼ Usually triggered by dieting and stress

◼ Women 10x as likely to develop disorder as men
◼ Symptomatology in men similar to that of women
◼ Often comorbid with depression, OCD, phobias, panic, alcoholism and personality
disorders

◼ In men, comorbid with substance dependence, mood disorders, or schizophrenia

◼ Suicide rates high in anorexia 5% completing 20% attempting
Consequences of Anorexia

◼ Low blood pressure, heart rate decrease

◼ Kidney and gastrointestinal problems
◼ Loss of bone mass
◼ Brittle nails, dry skin, hair loss
◼ Lanugo, soft body hair
◼ Depletion of potassium and sodium electrolytes
◼ Can cause tiredness, weakness, and death
Prognosis of Anorexia

◼ 50-70% recovery rate

◼ Recovery takes time, may often take 6 or 7 years
◼ Relapse common
◼ Difficult to modify distorted view of self, especially in cultures that highly value thinness
◼ Anorexia is life threatening
◼ Death rates 10x higher than general population
◼ Death rates 2x higher than other psychological disorders
 Bulimia Nervosa

◼ Uncontrollable eating binges followed by

compensatory behavior to prevent weight
gain
DSM-5 Criteria
◼ Recurrent episodes of binge-eating
◼ Recurrent compensatory behaviors to
prevent weight gain
◼ Body shape and weight are extremely
important for self- evaluation
Bulimia Nervosa

◼ Triggered by stress or negative emotions or negative social interactions

◼ Typical food choices : Cakes, cookies, ice cream, other easily consumed, high-calorie
foods

◼ Avoiding a craved food can later increase likelihood of binge

◼ Typically occur in secret
◼ Reports of losing awareness or dissociation
◼ Shame and remorse often follow
Bulimia Nervosa

◼ 1 – 2% prevalence among women

◼ Typically overweight that led to dieting
◼ 90% of cases are women
◼ Comorbid with depression, PD’s, anxiety, substance abuse, conduct disorder
◼ Suicide attempts and completions higher than in general population but much lower
than in anorexia nervosa

◼ Typically have normal BMI

Bulimia Nervosa

◼ Menstrual irregularities
◼ Potassium depletion from purging
◼ Laxative use depletes electrolytes, which can cause cardiac irregularities
◼ Loss of dental enamel from stomach acids in vomit
◼ Mortality rate of 4%
Bulimia Nervosa

◼ Early intervention linked with improved outcomes

◼ Poorer prognosis when depression and substance abuse are comorbid or more
severe symptomatology
◼ 75% of people recover
Binge Eating Disorder
DSM-5 Criteria for Binge Eating Disorder
◼ Recurrent episodes of binge eating
◼ Binge eating episodes include at least three of the
following:
◼ eating more rapidly than normal
◼ eating until uncomfortably full
◼ eating large amounts when not hungry
◼ eating alone due to embarrassment about large food
quantity
◼ feeling disgusted, guilty, or depressed after the binge
◼ No compensatory behavior is present
Binge Eating Vs Bulimia Nervosa

◼ Absence of weight loss in Binge Eating Disorder

◼ Binge Eating Disorder vs. Bulimia: Absence of compensatory behaviors (purging,
fasting, or excessive exercise) in Binge Eating Disorder
Binge Eating Disorder

◼ Associated with obesity and history of dieting

◼ Body mass index (BMI) > 30
◼ Not all obese people meet criteria for binge eating disorder
◼ Must report binge eating episodes and a feeling of loss of control over eating to qualify
◼ Approximately 2-25% of obese may qualify
◼ Risk factors include : Childhood obesity, early childhood weight loss attempts, having been
taunted about their weight, low self-concept, depression, and childhood physical or sexual
abuse
Binge Eating Disorder

◼ Between 25 and 82% recover

◼ Binge Eating Disorder is the most common and lasts the longest of the three Eating
Disorders

◼ Lasts on average: 14.4 years

Genetic Factors for eating disorders

◼ Family and twin studies support genetic link

◼ First-degree relatives of individuals with both disorders more likely to have the disorder
◼ Higher MZ concordance rates for both anorexia and bulimia
◼ Body dissatisfaction, desire for thinness, binge eating, and weight preoccupation all
heritable

◼ Environmental factors (e.g., family interactions) play an even greater role in etiology
◼ Further research on genetic/environmental interaction is needed
Neurobiological Factors

◼ Low levels of endogenous opioids

◼ Substances that reduce pain, enhance mood, DO NOT suppress appetite
◼ Released during starvation
◼ May reinforce restricted eating of anorexia
◼ Exercise increases opioids
◼ Low levels of opioids (beta-endorphins) in bulimia promote craving
◼ Reinforce binging
◼ Serotonin related to feelings of satiety (feeling full)
◼ Low levels of serotonin metabolites in people with eating disorders
◼ Antidepressants that increase serotonin often effective in treatment of eating
disorders
Neurobiological Factors
◼ Participants in a PET study who scored higher on dietary
restraint showed greater dopamine activity in the dorsal
striatum when presented with food
◼ Women with anorexia and bulimia showed greater expression of
dopamine transporter gene
◼ Dopamine related to feelings of pleasure and motivation
◼ Women with anorexia show more active reward centers &
feel more positive when viewing pictures of underweight
Cognitive Behavioral Factors: Anorexia
◼ Focus on body dissatisfaction and fear of fatness
◼ Certain behaviors (e.g., restrictive eating, excessive exercise) negatively reinforcing
◼ Reduce anxiety about weight gain
◼ Feelings of self control brought about by weight loss are positively reinforcing
◼ Perfectionism and personal inadequacy lead to excessive concern about weight
◼ Criticism from family and peers regarding weight can also play a role
◼ Self-worth strongly influenced by weight
◼ Low self-esteem
◼ Rigid restrictive eating triggers lapses, which can become binges
Cognitive Behavioral Factors: Bulimia
◼ Many “off-limit” foods
◼ After binging, disgust with oneself and fear of gaining weight lead to compensatory behavior
e.g., vomiting, laxative use

◼ Purging temporarily reduces anxiety about weight gain

◼ Negative feelings about purging lead to lowered self-esteem, which triggers further bingeing
◼ Stress, negative affect trigger binges
◼ Restrained eating plays central role in bulimia
◼ Restraint Scale measures dieting and overeating
◼ People with anorexia and bulimia are more distracted by food words on an emotional stroop task
Sociocultural Factors
◼ American society values thinness in women, muscularity in men
◼ Dieting, especially among women, has become more prevalent and often precedes onset
◼ Body dissatisfaction and preoccupation with thinness also predict eating disorders
◼ Societal objectification of women
◼ Women viewed as sexual objects
◼ Unrealistic media portrayals
◼ Women may feel shame when they don’t match the ideal
◼ Overweight individuals are viewed with disdain, creating more pressure to be thin
Gender Factors
◼ Objectification of women’s bodies
◼ Women defined by their bodies; men defined by their accomplishments
◼ Societal objectification of women leads to “self- objectification”
◼ Women see their own bodies through the eyes of others
◼ Leads to more shame when fall short of cultural ideals
◼ Aging and changes in life roles (having a life partner, or having children) associated with decreased
eating-disorder symptoms
Cognitive Behavioral Factors