Transcript What are eating disorders?

Eating & Weight
Chapter 4
Why do We Eat?
Models
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Set Point Model
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Genetics Model
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Homeostasis for Weight
Fat Stores Decrease, Hunger Induced
Weight is Largely Hereditary
Positive Incentive Model
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Positive reinforcement: Eating is Pleasurable
(taste)
Role of biological factors & social context
What do we eat?
Gatekeepers
1. Taste
1.
2.
3.
2.
Bitter
Sweet
Sour
Smell
1.
Bad smelling
What Determines How much
We Eat?
1.
2.
3.
4.
5.
Individual experience with food
Availability of Food
Variety of Food
Tasty food
Social Setting
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Eating alone vs together
What time to eat?
Culture encouragement
Cultural ideal for body weight
Sensory Specific Satiety
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Hedonic value
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Role of variety
Faster satiation rates with constant
diet
Digestive System
Peristalsis
 Stomach
 Small intestine
 Large intestine
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Basic Metabolism
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Nutrients: ingredients in food that
provide energy or sustain our cells
and tissues
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Divided into macronutrients
(carbohydrates, protein, and fat) and
micronutrients (vitamins, minerals, etc.)
Basic Metabolism
Carbohydrates
Proteins
Glucose
Amino Acids
Energy Level
Falls
Glycogen
(liver)
Triglycerides
(excess fat)
Triglycerides
(excess fat)
Triglycerides
(excess fat)
Fatty Acids
Glycerol
Local Theories
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Tells us why do we get hungry &
thirsty?
Stomach (S) contractions
 Cutting vagus nerve (Between S and
CNS)
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Central Theories
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Role of Brain
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Hypothalamus
 Sympathetic
and parasympathetic
 Pituitary gland
 Endocrine system
 Behavior: feeding, drinking, sexual,
aggression, fear
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Homeostatic regulation
Regulation of Hunger
Blood Sugar
Glucoreceptors
(Both inhibit & trigger)
Eating
Short term regulation(when and how
much we eat)
 Long term regulation (energy stores)
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Regulation of Hunger
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Short term regulation (STR; when and how
much we eat)
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Ventromedial Hypothalamus (VMH;satiety centre)
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When destroyed hyperphagia
Lateral Hypothalamus (LH;hunger centre)
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When destroyed aphagia and adipsia
Regulation of Hunger
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Glucostatic theory of hunger
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Mayer (1955) Glucoreceptors
Inconsistent support
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Damaging VMH did not result in obesity
LH may be only triggered in extreme stressful situations
Regulation of Hunger
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Peripheral detectors for STR
Stomach
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Duodenum (site of glucoreceptors)
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Ghrelin (hunger signal)and Obestatin
(suppressant)
CCK (halts eating)
Liver (both)
Pancreas (beta cells)
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Insulin (helps transport glucose into cells)
Amyline (satiation)
Regulation of Hunger
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Long term Regulation
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Set-point theory: A Lipostatic Theory of Hunger
LH regulates the normal weight
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Damaging VMH pulls up body’s set point
Leptin (lean people have low leptin levels)
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Damaging LH lowers body’s set point
Low levels signal low fat stores and prompts eating
Insulin (glucose availability and fat storage)
When one diets both Leptin and Insulin goes down
and vice versa
Three Types of Eating
Disorders
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Anorexia nervosa- Characterized by a
pursuit of thinness that leads to selfstarvation
Bulimia nervosa- Characterized by a cycle
of binging followed by extreme behaviors
to prevent weight gain, such as purging.
Eating Disorders
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What are eating disorders?
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Controlling body weight
Anorexia
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DMS-IV-TR
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Types?
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Refuse to maintain body weight
Intense fear of gaining weight
Disturbance in the way the body is perceived
Absence of 3 menstrual cycles
Intentional weight loss to a point weighing less than 85%
BMI of 17.5 or less
Restricting
Purging
Who is anorexic?
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Influence of culture images
European American Women receive this diagnosis .5% to 1%
15-29 age group
Anorexia Nervosa
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Begins with individuals
restricting certain foods, not
unlike someone who is dieting
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Restrict high-fat foods first
Food intake becomes severely
limited
More on anorexia nervosa
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May exhibit unusual
behaviors with regards to
food.
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Preoccupied with thoughts of
food, and may show
obsessive-compulsive
tendencies related to food
 May
adopt ritualistic behaviors at
mealtime.
 May collect recipes or prepare
elaborate meals for others.
Neurobiology of Anorexia
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Neurobiology
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Serotonin: Low levels
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depression
Heredity
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Cortisol
Blood pressure
Brain atrophy: Cognitive tasks
5-10% prevalence rate
Twin studies (monozygotic twins)
Brain Structures
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Parts of Limbic structure (includes hypothalamus, the amygdala, and
the hippocampus)
These are involved in motivation, emotion, learning, and memory
Anorexia Nervosa
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Treatment
 Poor
motivation
 Resisting suggestions
 Force feeding
 Cognitive Behavioral Therapy
 Attacking irrational beliefs
 Building reasonable habits
Eating Disorders
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Bulimia
Eating huge quantities of food in an uncontrolled manner
(binge) and getting rid of the food by vomiting or using
laxatives (purge)
Two subtypes
 Purging type
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Self-induced vomiting and laxatives as a way to get rid of the
extra calories they have taken in
Non-purging type
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Use a period of fasting and excessive exercise to make up for
the binge
Eating Disorders
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Bulimia
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DSM-IV-TR
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Who is bulimic?
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Recurrent episodes of binging
Sense of lack of control over eating
Inappropriate and drastic measures to
compensate for the binge
Self evaluation is unduly influenced by body
shape
4.1% women
0.2% men
Restricted to western cultures-white upperclass
Is it harmful?
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Large quantities of sweets-Hypoglycemia
Vomiting-Electrolyte imbalance
Anemia
Bulimia Nervosa
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Qualitatively distinct from
anorexia
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A binge may or may not be
planned
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Characterized by binge eating
Marked by a feeling of being out of
control
The binge generally lasts until
the individual is uncomfortably
or painfully full
Bulimia Nervosa
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Common triggers for Binge eating
Behavior
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Difficulty in handling emotions: Dysphoric Mood
Interpersonal Stressors
Restrictive dieting: Intense Hunger After A Period Of
Intense Dieting Or Fasting
Feelings Related To Weight, Body Shape, And Food Are
Common Triggers To Binge Eating
Loss or separation
Uncertain about mood onset
Bulimia Nervosa
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Feelings of being ashamed after a
binge are common
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Behavior is kept a secret
Tend to adhere to a pattern of
restricted caloric intake
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Usually prefer low-calorie foods during
times between binges
More on bulimia nervosa
Later age at the onset of the
disorder
 Are able to maintain a normal
weight
 Will not seek treatment until they
are ready
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 Most
deal with the burden of hiding
their problem for many years,
sometimes well into their 30’s
More on bulimia nervosa
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Life events
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Sexual abuse
Hours of darkness
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Theories
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Socio Cultural Approach
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Clinical Approach
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Low self esteem psychological health
Social Contagion
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Changing body norms
Norms will spread to people experiencing
distress
Serotonin hypotheses
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High level of norepinephrine (eating) low level of
serotonin (satiety)
Eating Disorders
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Bulimia
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Treatment
 Usually
motivated to seek treatment unlike
anorexics
 Interpersonal psychotherapy
 Changes in attitude and food
 Cognitive Behavioral Therapy
 Prevention
Anorexia vs. Bulimia
Anorexia
Diagnostic
Criteria
Bulimia
Anorexia vs. Bulimia
1. There is refusal by the patient to
maintain body weight at or above a
minimally normal weight for age and
height.
2. There is intense fear of gaining
weight or becoming fat even though
they are underweight.
There are recurrent episodes of binge
eating. An episode of binge eating is
characterized by both of the following:
1. Eating, in a discrete period of time
an amount of food that is definitely
larger than most people would eat
during a similar period of time and
under similar circumstances.
2. Sense of lack of control over eating
during the episode. Recurrent
inappropriate compensatory
behavior in order to prevent weight
gain, such as self induced vomiting,
misuse of laxatives or diuretics,
enemas, or other medications;
fasting; or excessive exercise
Weight
Markedly reduced
Usually normal
Sex Hormones level
Low estrogen and testosterone
Usually normal
Glucose levels
Hypoglycemia
Usually normal
Age Onset
Mid adolescence
Late adolescence to late adulthood
Menstruation
(Amenorrhea)
Absent
usually normal
Mortality
5%
Very low
Eating Disorders
PURGE
BINGE
Anorexics may or may not
Anorexics do not
Bulimics do
Bulimics do
Binge eaters only do not
Binge eaters do
Anorexics
Bulimics
Restrictive Type
Purge Type
Binge-purge Type
Non-Purge Type
Some statistics
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Eating disorders have
increased threefold in the last
50 years
10% of the population is
afflicted with an eating
disorder
90% of the cases are young
women and adolescent girls
Up to 21% of college women show sub-threshold symptoms
61% of college women show some sort of eating pathology
Psychological factors
 Low
self-esteem
 Feelings of inadequacy or lack of
control in life
 Depression, anxiety, anger, or
loneliness
Interpersonal Factors
 Troubled
family and personal
relationships
 Difficulty expressing emotions
and feelings
 History of being teased or
ridiculed based on size or weight
 History of physical or sexual
abuse
Social Factors
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Cultural pressures that glorify "thinness"
and place value on obtaining the "perfect
body"
Narrow definitions of beauty that include
only women and men of specific body
weights and shapes
Cultural norms that value people on the
basis of physical appearance and not inner
qualities and strengths
Overeating and Obesity
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What is Obesity?
 Skin fold
 Water Immersion
 Body Mass Index
 It is important to remember that although BMI correlates with the
amount of body fat, BMI does not directly measure body fat.
 It may overestimate body fat in athletes and others who have a
muscular build.
 It may underestimate body fat in older persons and others who
have lost muscle
 http://nhlbisupport.com/bmi/bmicalc.htm
 Waist circumference
 If most of your fat is around your waist rather than at your hips,
you’re at a higher risk for heart disease and type 2 diabetes.
 This risk goes up with a waist size that is greater than 35 inches for
women or greater than 40 inches for men.
Overeating and Obesity
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Other methods of estimating body fat and body fat distribution
include measurements of
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Calculation of waist-to-hip circumference ratios,
Techniques such as ultrasound, computed tomography, and magnetic resonance
imaging (MRI).
For assessing someone's likelihood of developing overweight- or
obesity-related diseases, the National Heart, Lung, and Blood
Institute guidelines recommend looking at two other predictors:
 The individual's waist circumference (because abdominal fat is a
predictor of risk for obesity-related diseases).
 Other risk factors the individual has for diseases and
conditions associated with obesity (for example, high blood
pressure or physical inactivity).
Overeating and Obesity
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Why are some people obese?
 Setpoint Model
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Genetics
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Evolution
Twin studies
Positive incentive
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Internal thermostat which regulates weight
Role of hormones
Positive reinforcement
Availability of food
How unhealthy is obesity?
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Blood pressure
Gall bladder disease
Type 2 diabetes
Processed Foods
Other Obesity Explanations
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Adaptiveness Gone wrong
Genetics-More fat cells
Obesity as maintain obesity
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Role of habituation
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Eating behavior may occur when caloric intake is
not required
Obesity as addiction
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Hyperinsulinmia: Obese people have high insulin
that increases fat storage.
Dieting: Low metabolic rate makes weight loss
difficult
Low metabolic rates (burn few calories)
Pleasure of eating
Lack of control
Stress
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Chronic stress increased ghrelin levels
Obesity Prevalence
http://www.iaso.org/resources/world-mapobesity/?map=adults
2010 State Obesity Rates
State
%
State
%
State
%
State
%
State
%
Mississip
pi
34.0
Arkansas
30.1
South
Dakota
27.3
Rhode
Island
25.5
New
Jersey
23.8
West
Virginia
32.5
Georgia
29.6
North
Dakota
27.2
Washingt
on
25.5
Vermont
23.2
Alabama
32.2
Indiana
29.6
Maryland
27.1
New
Mexico
25.1
Montana
23.0
South
Carolina
31.5
Kansas
29.4
Nebraska
26.9
Wyoming
25.1
Massachu
setts
23.0
Kentucky
31.3
Ohio
29.2
Oregon
26.8
25.0
Hawaii
22.7
Texas
31.0
Pennsylv
ania
28.6
Maine
26.8
New
Hampshir
e
Minnesot
a
24.8
Connectic
ut
22.5
Louisiana
31.0
Iowa
28.4
Florida
26.6
Alaska
24.5
Utah
22.5
Michigan
30.9
Illinois
28.2
Idaho
26.5
Arizona
24.3
Nevada
22.4
Tennesse
e
30.8
Delaware
28.0
Wisconsi
n
26.3
California
24.0
22.2
Oklahom
a
30.4
North
Carolina
27.8
Virginia
26.0
New York
23.9
District
of
Columbia
Colorado
21.0
Dieting
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Approaches to losing weight
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Food restriction
 Low
carbohydrate diet
 Have high drop out rates
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B-Mod
 Healthy
eating habits
 Use of diaries, self-rewards and penalties
 Dieters main 60% of weight loss.
Dieting
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Approaches to losing weight
 Exercise
 Speeds body metabolism
 Drastic means
 Diet pills, fasting and laxatives
 Gastric bypass or gastric banding surgery
 Liposuction
 Maintenance
 Problem of relapse
 Keeping ideal weight by fruits, vegetables and whole
grain cereals
Is dieting a good choice?
 Some do not recommend
 Some gain benefits
Regulation of Thirst
Intra cellular fluid
 Extra cellular Fluid
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Interstitial fluid
 Intravascular fluid
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Dry Mouth
Regulation of Thirst
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Intra cellular fluid
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Extra cellular Fluid
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Osmometric thirst
Volumetric thirst
Kidney (absorbs 99% of the fluid)
Renin
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Angiotensin-stimulates adrenal cortex to secrete
aldosterone (reabsorption of SODIUM & Water)
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Angiotensin II
The ability of kidney to do this is called ADH and VP
Regulation of Thirst
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Osmometric thirst
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Volumetric thirst
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Osmosis (equalize concentration of fluids)
Osmoreceptors –trigger drinking
OVLT controls water intake
Hypovolemia-reduction in fluid balance
Angiotensin stimulates thirst motivation
Non-homeostatic Drinking
Inhibitory control of drinking
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Inhibitory mechanisms are less developed
Sexual Motivation
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Sex Hormones: Organization and Activation
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Mammalian Brain is female unless altered
Sexual Dimorphism
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Y and X chromosome
Sexual Motivation
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Hypothalmic Regulation
Tumors in hypothalamus lead to early sexual
development
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Spinal cord damage represses
Mating behavior increases activity in the preoptic area
Aggression Motivation
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Limbic system
Destruction of parts of limbic system leads to low
aggression
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LH stimulation biting attack
VMH stimulation
Amygdala inhibits
Destroying thalamus inhibits
Affective attack-cats hissing high emotionality
Quiet biting attack-low emotionality
Types of Aggression
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Predator Aggression
Intermale aggression
Fear-induced aggression
Territorial defense
Maternal aggression
Instrumental aggression
Serotonin suppresses
Intermittant explosive disorder
HAA & PAG controls aggression