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Eating Disorders: Assessment,
Understanding, and Treatment
Strategies
Terry Schwartz MD
Medical Director UCSD Eating Disorders Program
Asst Clinical Professor UCSD
Elise Curry Psy.D.
Program Manager
UCSD IOP
ASSESSMENT AND TREATMENT
STRATEGIES FOR EATING
DISORDERS
Terry Schwartz MD
Medical Director UCSD Outpatient
Eating Disorders Program
Assistant Clinical Professor UCSD
Dept Of Psychiatry
DSM IV Criteria for Anorexia
Nervosa
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Preoccupation with body shape, weight/size
<85% ideal BW
Fear of becoming fat despite low weight
Loss of 3 consecutive periods in women
Types: restricting,binge/purge,purge
Anorexia Nervosa
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Most homogenous psychiatric disorder
90-95% female
Onset teenage years – puberty
Monotonous puzzling symptoms
Poor response to treatment
Highest mortality rate
50% to 80% contribution of genes
Many women diet, few develop AN:
predisposing factors
DSM IV criteria for Bulimia Nervosa
 Recurrent episodes of binge eating, characterized by eating an
excessive amount of food within a discrete period of time and
by a 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 or misuse
of laxatives, diurética, enemas, or other medications (purging);
fasting; or excessive exercise
 The binge eating and inappropriate compensatory behaviors
both occur, on average, at least twice a week for 3 months
• Self-evaluation is unduly influenced by body shape and weight
Psychological Correlates of Anorexia
Nervosa
• Poor self concept
• Obsessive compulsive and avoidant personality style
• Perfectionistic, obsessive, harm avoidant traits
• Family dynamics: enmeshment, anxiety,
over-achievers
• Troubles with major life transitions
• an attempt to regress, avoid development
• Difficulty managing and expressing anger
• Cognitive distortions
• Ego-syntonic nature of disease
Psychological Correlates of Bulimia
Nervosa
• Poor self concept
• Chaotic developmental history, parental
deficit
• ambiguous communication styles
• Affective regulation problems
• Cognitive distortions
• Ego-dystonic nature of disease
• Impulsivity, substance abuse, self harm,
sexual acting out, shop lifting
Cognitive Flexibility
Anorexia Nervosa
•  Perceptual rigidity
•  Cognitive rigidity
AN Weight recovery
No changes
AN Full recovery
• Partial improvement in
cognitive flexibility
tasks
Bulimia Nervosa
• Slowness in cognitive shifting
tasks
• Fluctuations in Perceptual task
Scope of The Problem
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Prevalence increasing
AN: .5-2%
BN: 3-4%
AN BN More common westernized cultures
10% of eating disordered individuals in treatment
are male
• 5%-20% of AN patients die (disorder or suicide)
Scope of the problem: continued
• Highest death rate from any mental health
condition (AN)
• Increasing incidence in elementary age children
(8-11 year old)
• The incidence of bulimia in 10-39 year old women
TRIPLED between 1988 and 1993.
• There has been a rise in incidence of anorexia in
young women 15-19 in each decade since 1930.
Primary Causes of Death in Patients with
Eating Disorders
1. Starvation
2. Cardiac
arrhythmia/failure from
hypokalemia of ipecac
abuse
3. Suicide
4. Gastric Dilation
AN, Restricting
Subgroup
AN, Bulimia
Subgroup
Bulimia
Nervosa
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Outcome Data for EDs
• Data mixed results due to design of studies
• AN 10 yr: 50% rec, 20-30% improved but
still symptomatic, 10-20% chronic, up to
10% mortality
• BN 10yr: 50%-70% rec, 30% some
improvement, 20% chronic
Outcomes for EDS
• Some studies show ave of 7 years to rec
• Less than 1 year of treatment has poorer
prognosis
• Chronicity, OCPD, purging in AN
associated with worse outcome
Biological underpinnings of
eating disorders
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Genetics
Neurobiological correlates
Neuropsychiatric
Brain imaging in AN
Genetic Correlates of Bulimia Nervosa
• Twin studies
• 5ht2A receptor gene alteration
• Family history of affective, anxiety,
substance abuse d/o
Genetic Correlates in Anorexia
Nervosa
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Family and twin studies
Serotonin receptor gene
Variation in Dopamine 2 receptor gene
Chrom 1 and 10
Family history of OCD, OCPD, AN
Neuroendocrine correlates of Bulimia
Nervosa
• Serotonin (5HT1A receptor)
• Endogenous opiate response to binge
purge
• ?DA
Neuroendocrine Correlates of
Anorexia Nervosa
• Serotonin (5HT2A receptor)
• Dopamine
• Endogenous opiate response to
starvation
• Hypothalamus dysfunction (satiety,
amenorrhea)
Altered Dopamine function and
psychiatric correlates
• Compare normal to psychiatric conditions
• AN: increased DA sensitivity, hyper
responsive
• Addict: reduced DA sensitivity, takes a lot
to stimulate
• Obesity: DA sensitivity inversely
proportional to weight (high weight, low
DA sensitivity)
Altered Reward Processing in Women
Recovered from Anorexia Nervosa
• RAN may have difficulties differentiating positive and negative
feedback.
• The exaggerated activity of the caudate, a region involved in linking
action to outcome, may constitute an attempt at “strategic” rather than
hedonic means of responding to reward stimuli.
• Researchers hypothesize that individuals with AN have an imbalance
in information processing, with impaired ability to identify the
emotional significance of a stimulus, but increased traffic in
neurocircuits concerned with planning and consequences.
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Wagner A., Aizenstein H., Venkatraman V. ,Fudge J, (2007) Altered Reward Processing in Women recovered from
Anorexia Nervosa. Am J Psychiatry 2007: 164:1842-1849
Neuropsychiatric correlates of
Eating Disorders
• Iowa gambling task: AN vs CW:
Differences seen on fMRI
• AN: Neuropsych testing: difficulties with
set shifting, flexibility
• AN: Detail focus, to the point of missing
global (Janet Treasure)
• AN vs BN
• Use in clinical practice
Dopamine function and
motivation/behavior
• DA cell fires in response to salient environmental
stimuli (rewarding, aversive, novel)
• DA encodes motivation and appropriate choices
• Part of apparatus that makes value judgments and
makes “correct” decision in response to a stimuli
• Disturbances of brain DA - altered activity,
reward, motivation
Iowa Gambling Task
• CW distinguished between wins and losses
• AN have similar response to wins and losses
– Perhaps overactive DA response to both Wins and
Losses
– Difficulty discriminating positive and negative stimuli?
• Clinical implications
– AN may be unable to discriminate pleasurable and
aversive stimuli
– May be very oversensitive to stimuli
– Cannot learn easily learn from experience
– May explain why it is difficult to use reward to
motivate people with AN
Nancy Zucker’s work on Social
Cognition in AN
• Experimental Tasks:
• 1) Rec AN’s rated people as heavier than they are.
Faces less attractive (like Autism)
• 2) Rec AN valued faces less than controls, valued
heavy bodies less, valued thin bodies more.
• 3) Free viewing eye tracking: AN spent less time
on eyes and more time on the mouth (like autism)
Kate Tchanturia’s work on AN and
Theory of Mind
• AN’s were impaired on social cognitive tasks.
• Emotional theory of mind: to know what someone
else is feeling.
• AN’s showed impairment in the ability to infer
about another person’s thoughts, beliefs, or
intentions.
• Similarities to autism: reduced empathy and
increased ability to systematize
Treatment Implications
• Practice social problem solving (process group)
• Assertiveness role plays
• Practice social problem solving in ambiguous
social situations like friend making, dating etc.
• Practice decision making.
• Create social competence training for skill
building (Autism research)
Brain Imaging in OCD
Saxena 2003
• Structural (CT, MRI): variable findings
• Resting PET FDG:
• OFC is involved in sensory integration, in representing the affective
value of reinforcers, and in decision-making and expectation.[2] In
particular, the human OFC is thought to regulate planning behavior
associated with sensitivity to reward and punishment.
– 5 of 9 studies: elevated metabolism in OFC
– 3 found elevated activity in basal ganglia, thalamus
• PET FDG before/after SSRI, CBT, neurosurgery
– 8 of 10 pre to post-treatment studies: decreases in OFC and/or caudate
in responders to treatment
• Symptom provocation using PET, fMRI: consistent increases in
glucose metabolism or rCBF in OFC, caudate, anterior cingulate,
thalamus
• Suggestion of dysfunction of OFC-subcortical circuits
Primary taste cortex (rostral insula) represent taste (temperature, texture) of food in
the mouth that is independent of hunger, and thus of reward value.
Secondary regions (orbitofrontal cortex, OFC) compute the hedonic value of food
Rolls, 2005
Recovered AN
Altered fMRI Response to food
“challenge”
• Pictures food: anterior cingulate cortex and
medial prefrontal (Uher 2003)-anxiety/stress
• Taste sugar and water: insula, caudate-putamen,
anterior cingulate (Wagner 2007)
• Taste sugar and artificial sweetener: insula,
caudate (Oberndorfer, Frank, in preparation)
Psychopharm in EDs
Pharmacology for AN
• No drug has been FDA approved for AN
• No drug has shown major improvement in the
starvation phase
• Meds tried and failed for appetite enhancement
(typical antipsychotic, Li, THC derivatives)
• SSRIs generally not helpful in acute starvation,
though some benefit on comorbid disorders
Pharmacology for AN Continued
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Prozac mixed data for rec-AN
Atypical antipsychotic medications
GI meds to aid physical symptoms
BCP/hormones: no evidence of benefit
Pharmacology for BN
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Serotonin re-uptake inhibitors
?SNRIs
AEDs (topiramate, ?zonisamide)
Antipsychotics
Mood stabilizers
reglan, H2 blockers
?? Stimulants (with caution)
BREAK
Medical Consequences of AN
and BN
Physical Complications of Anorexia
Nervosa
Organ System
Symptoms
Lab Test Results
1. Whole body
Weakness,
lassitude
Low weight/body mass index,
low body fat percentage
2. CNS
Apathy, poor
concentration
CT: ventricular enlargement;
MRI: decreased gray and white
matter
3. CV
Pre-syncope,
palps, dyspnea,
weakness, cold
extremities,
chest pain
ECG: sinus bradycardia, other
arrhythmia, QTc prolongation;
cardiac echo (consider): MVP,
silent pericardial effusion
Physical Complications of Anorexia
Nervosa, Cont.
Organ System
Symptoms
Lab Test Results
4. Muscular
Weakness,
Muscle enzyme abnormalities in
muscle aches severe malnutrition
5. Reproductive
Prepubertal
psychosexually
Hypoestrogenemia; prepubertal
patterns of LH, FSH; lack of
follicular devel.
6. Endocrine,
metabolic
Fatigue, cold
intolerance,
diuresis,
vomiting
Elevated cortisol; euthyroid
sick; dehydration; electrolyte
abnormalities; low phos on
refeeding; hypoglyc.(rare)
Physical Complications of Anorexia
Nervosa, Cont.
Organ System
Symptoms
Lab Test Results
7. GI
Vomiting, abdom.
pain, bloating,
constipation
Delayed gastric
emptying; occas. abnl
LFTs
8. Renal
Pitting edema
Elevated BUN/Cr;
renal failure
9. Skeletal
Bone pain w/
exercise
X-ray/bone scan w/ stress
fix; DEXA w/ osteopenia
or osteoporosis
Physical Complications of Bulimia Nervosa
Organ system
Symptoms
Lab Test Results
1. Metabolic
Weakness;
irritability
Dehydration; serum
electrolytes: ↓K+,
↓NA/Cl alkalosis w/
vomiting; ↓Mg,
↓K+, ↓Phos w/
laxative abuse
2. GI
Abdom. pain;
constipation;
bloating; reflux
Physical Complications of Bulimia
Nervosa, cont.
Organ system
Symptoms
Lab Test Results
3. Oropharyngeal
Dental decay;
swollen cheeks
X-rays confirm
erosion of dental
enamel; elevated
serum amylase
4.CV and muscular (in
ipecac abusers)
Palpitations;
weakness
Cardiomyopathy and
arrhythmias;
peripheral myopathy
Amenorrhea and Osteopenia
• Most serious complication of prolonged
amenorrhea is osteopenia, or reduced bone
mass
Osteopenia and Osteoporosis
• Osteopenia refers to decreased quantity of
normally mineralized bone
• Osteoporosis is clinical syndrome consisting of
decreased bone mass, disruption in normal bone
architecture with decreased bone strength,
pathological fractures, pain and disability
• Osteoporosis defined as greater than 2.5 SD below
the mean for young adult women
• Osteopenia 1-2.5 SD below young adult ref
Bone Density and Fractures
• Each SD decrease in bone density doubles
the fracture risk
• DEXA is most widely used method for
measuring bone density
• May be compared with age-matched
children and adolescents (Z scores)
Bone Loss Treatment
Strategies
• No therapies proven effective for bone loss in
women with AN.
• Estrogen/BCP:
Decision on estrogen individualized, but no
convincing data that estrogen alone increases
bone density in AN population.
May give false sense of security!
• Potential therapies under study:
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IGF-I
DHEA
Testosterone
Bisphosphonates
Osteoporosis Treatment
• Weight gain
• Calcium supplementation improves bone
mass (1500-2000mg/day)
• Vitamin D
• Moderate weight-bearing exercise increases
bone mass
• When medically stable, wt bearing
exercises 3-4 times per week
Medical/Psychiatric evaluation and
treatment strategies for Anorexia
Nervosa
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Assess for comorbidity
+/- Serotonin reuptake inhibitors
Atypical antipsychotics
Reglan, h2 blockers
Screening labs: electrolytes, Ca++, Mg+,
Phos, BUN/Cr, CBC, LFTs, TFTs, UA,
hematology
• Bone densomitry (DEXA)
• ECG
Medical evaluation for Bulimia Nervosa
• Assess for comorbidity
• Screening labs: electrolytes, Ca++, Mg+, Phos,
BUN/Cr, CBC, LFTs, TFTs, UA, hematology
• Dexa
• ECG
• Dental
AN: Hospital vs Outpatient Treatment
From American Psychiatric Association Guidelines for the
Treatment of Eating Disorders
Outpatient
Inpatient
Weight
>85%
< 75%
Medical complications
none
 HR, BP, K etc
Not present
severe
Motivation, insight, cooperation
yes
no
Excessive exercise, purging, etc
minimal
severe
Stress, family dynamics
minimal
severe
Local ED treatment resources
available
none
Suicidal, comorbid psych d.o.
Referral to Higher level of care
• Pt is failing lower level.
• Pt’s weight loss is continuing in spite of
treatment
• Pt is unable to stop bingeing/purging.
• Pt’s physical symptoms warrant greater
supervision (fainting, dehydration, heart
palpitations)
• Pt is resisting current level of care
REFEEDING COMPLICATIONS
• Normal food
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Peripheral edema
Bloating or discomfort
Reflux
Rare gastric dilitation
• Nasogastric feeding
– Seldom indicated
– Nasal, esophageal erosion
• Central hyperalimentation
– Rarely indicated
– Pneumothorax, infection, metabolic disturbances
Eating behavior in AN – After weight
restoration
• Hypermetabolic even after weight restoration
– RAN need 50 to 60 kcal/kg/day
– BAN need 40 to 50 kcal/kg/day
– 50 kg women = 2000 to 3000 kcal/day
• Probably normalizes in long term
• Probable contribution to high rate of relapse
• Degree of osteopenia depends on age of onset and
duration of amenorrhea
• Adolescence is critical time for bone mass
acquisition
• Approx 60% of peak bone mass is accrued during
Methods of Treatment
A. Regular Weight restoration
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2 to 3 lbs/wk inpatient
1 to 2 lbs/wk day-hospital
1 lb/wk outpatient
B. Nutritional Teaching
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Provide patient support
Prevention from vitamin and mineral deficiency
Prevention of osteoporosis
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Aim for high Ca++ intake
Vitamin D to aid in Ca++ absorption; vegetarians may need
supplements
Eat iron-containing foods, especially important for vegetarians
lunch
Countertransference Issues
• Feeling angry at the patient for not
recovering
• Thinking this is “willful” behavior
• Blaming the parents
• Feeling incompetent
• Giving up hope for the patient
• Not taking the disorder seriously
Coping with Countertransference
Issues
• Practice patient acceptance: The average
recovery rate is 7 years.
• Have compassion for the suffering
of the patient.
• See their behavior as part of the disorder,
not personal toward you.
• Practice good self-care.
Important tips for physicians
when talking to patients with
EDs
Terry Schwartz MD
Live Demo
Process live demo
Obesity/BED
Binge Eating Disorder
• Recurrent episodes of binge eating (see BN)
• The binge eating episodes are associated with three (or more)
of the following:
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Eating much more rapidly than normal
Eating until feeling uncomfortably full
Eating large amounts of food when not feeling physically hungry
Eating alone because of being embarrassed by how much one is eating
Feeling disgusted with oneself, depressed, or very guilty after
overeating
• Marked distress regarding binge eating is present
• 2 days/week for 6 months
Obesity
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BMI > 30
32.2% of American adults, increasing in children
Increasing in past 30 years by 50% per decade
Major successful treatment advances in treatment
of complications of obesity, but minimal success
in treatments for obesity itself
Is Obesity a psychiatric disorder
(BED)?
• Medical/Metabolic issues
• Am J Psych 2007: Issues for DSM –V: Should
obesity be included as a brain Disorder
• Major limitation to treatment of obesity is long
term behavioral compliance
• Diets major cause of ED, including BED (recall
starvation study)
• Individual biological risks: genetic/heritability
BED and Neurochemistry
• Serotonin, endogenous opiates,
cannabinoids
• Certain foods impact nucleus accombens:
DA, opiate
• Neuropsych: similar to addicts; ie; follow
immed reward over long term results during
gambling type tasks (with excitable reward)
Food for affect regulation
• Neurochemical stimulation
• Anxiety, depression, anger, boredom,
agitation etc
• Endogenous response to food (or starvation)
may predispose to AN or BED/BN
Literature Review: Treatment for
BED
• International J of EDs May 2007
• 26 studies reviewed: Med plus BWL, meds
alone, BWL alone
• Meds plus BWL best, short term
Psychosocial treatments
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CBT
CBT plus BWL
BWL alone
Group therapy
Indiv therapy
12 step/self help
Medical treatments for
BED/obesity
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No magic pill!
Sibutramine
Orlastat
Acomplia
Phentermine
Gastric Bipass
Stimulants
Medical treatments for
BED/obesity continued
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No magic pill!
? SSRIs, SNRIs
?Wellbutrin
? Topiramate
? Zonisamide
What about psych meds and
weight gain
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Need to know and be truthful with ED patients!
SSRIs
SNRIs
Atypical Antipsychotic Medications
Typical Antipsychotic Medications
Mood Stabilizers
TCAs, MAOIs
BREAK
Eating Disorders in special
populations
• Children
• Teens
• Males
ED IN KIDS TEENS
What about the kids?
• Pre-pubertal Eating
Disorder
• Childhood Onset
Eating Disorder
• Early Onset Eating
Disorder
What Are We NOT
Talking About?
• DSM-IV Feeding and Eating Disorders of
Infancy or Early Childhood
– Pica
– Rumination Disorder
– Feeding disorder of infancy or childhood
Anorexia Nervosa
DSM-IV
• Refusal to maintain body weight above a
minimally normal weight for age and height.
<85% of IBW
• Intense fear of gaining weight or becoming fat
• Disturbance in the way one’s body weight or
shape is experienced
• Amenorrhea: absence of at least three consecutive
menstrual cycles
Weight Loss vs Weight Maintenance
• DSM-IV criteria
excludes children who
have not reached the
critical level of <85%
• Failure to gain
appropriate weight
with growth
• Malnutrition can lead
to poor growth
Body Image
• May be more tricky to assess
• How can it be evaluated?
– Children’s expression of body image
– Standard tools
– Clinical Interview
• Somatic symptoms
– Abdominal pain or discomfort
– Feeling of fullness
– Nausea
– Loss of appetite
Amenorrhea
• Primary vs Secondary
• Pubertal delay
– Evaluation may include pelvic ultrasound
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Height
Weight
Weight/height ratio
Ovarian volume
Uterine volume
– Conventional target weight and weight/height may be
too low to ensure ovarian and uterine maturity
Alternative Criteria for ED in
Children: Byant-Waugh and Lask
1995
• Alternative classification for the range of eating
disorders of childhood
• “Excessive preoccupation with weight or shape
and/or food intake which is accompanied by
grossly inadequate, irregular or chaotic food
intake”
Byant-Waugh and Lask 1995
:Criteria for Anorexia Nervosa
• Failure to make appropriate weight gains, or
significant weight loss
• Determined weight loss (e.g., food avoidance,
self-induced vomiting, excessive exercising, abuse
of laxatives).
• Abnormal cognitions regarding weight and/or
shape.
• Morbid preoccupation with weight and/or shape.
Related ED Behaviors in
Children
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Anorexia nervosa
Food avoidant emotional disorder
Selective eating
Functional dysphagia
Bulimia nervosa
Pervasive refusal syndrome
Early behavioral risk factors for
EDs
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PICA – BN
Picky Eater – BN, some AN
Digestive problems – AN
Subsyndromal symptoms of EDs can
predate
Incidence and Demographics
• Anorexia in this age range is considered to
be rare, but appears to be increasing
• Males may constitute a higher proportion of
cases in childhood as opposed to in
adolescence or adulthood
– 19-30% of childhood cases
– 5-10% of adolescent or adult cases
Biological
Psychological
Social
Biological
• Genetics
– Higher rate of AN, BN and
ED NOS in first degree
relatives
– Cross-transmitted
– High heritability
• Medication
– Trials suggest serotonin and
dopamine systems contribute
• Imaging
– Gordon et al, 1997
• 15 girls ages 8-16 with AN
• Regional cerebral blood blow
radioisotope scans
• 13/15 had unilateral temporal
lobe hypoperfusion
– Lask et al, 2005
• significant association
between unilateral reduction
of blood flow in the temporal
region and
– impaired visuospatial
ability,
– impaired visual memory
– enhanced speed of
information processing
Psychological
• Personality traits
– Anxious
– Obsessional
– Perfectionistic
• Susceptibility factors
– Obsessions
• Perfectionism
• Symmetry
• Exactness
– Negative affect, harm avoidance
– Preoccupations with weight, body image and food
Prognosis
• Long term follow up of patients with early onset
anorexia nervosa (Bryant-Waugh et al, 1987)
– 30 children with anorexia nervosa followed for mean
duration of 7.2 years
– Mean age at onset 11.7 years
• 19/30 (60%) with a “good” outcome
• 10/30 remained moderately to severely impaired
• Poor prognostic factors included
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Early age at onset (<11 years)
Depression during the illness
Disturbed family life and one parent families
Families in which one or both parents had been married before
Treatment Challenges (especially
for the very young)
• Very little data or literature on treatment
• Few inpatient or outpatient programs for
kids under 12 or 13 years old
• Only 1 we are aware of.
• Little data or clinical experience
• Family Therapy
Family therapy
• Maudsley Family Therapy
• Systemic Family Therapy
Family Therapy
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Required with Adolescents
Maudsley Family Therapy
Systemic Family Therapy
Couples
Family involvement to motivate pt for
treatment (case example)
Systemic Family Therapy
• Underlying belief: if you fix the system, the
symptom will no longer be needed.
• The eating disorder is serving a function in
the family.
• The symptom bearer is trying to help the
family (unconsciously).
Methods for Systemic Family Therapy
• Circular questioning
• Therapist is curious observer, not expert.
• Discuss communication patterns within the
family.
• Involve all family members in the
discussion, even small children.
• Do not pathologize family or symptom
bearer.
Maudsley Family Therapy
“Behavioral Family Therapy”
Maudsley Family Therapy
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Agnostic toward etiology
Involves parents, rather than a parent-ectomy
Food is medicine
Initial focus on symptoms
Parents are responsible for weight restoration.
Non-authoritarian therapist stance
Separation of child from illness
Maudsley Family Therapy
• Phase I: (sessions 1 - 10) Weight
restoration, re-feeding focus.
• Phase II: (sessions 11 - 16) Transfer control
back to adolescent gradually.
• Phase III: (sessions 17 - 20) Focus on
adolescent developmental issues,
termination.
Maudsley Family Therapy
• Session 1: Funeral session
• Goals: engage the family, obtain history of how
AN came to be, find out how AN has affected each
family member, assess family functioning, reduce
blame, raise anxiety concerning AN.
• Interventions: Greet family in sincere but grave
manner, externalize the AN, orchestrate intense
scene, charge parents with the task of re-feeding.
Session 2: Family Meal
• Instructions to parents: bring a meal that would be
appropriate for your child’s nutritional needs.
• Goals: assess family structure as it may affect
ability of parents to re-feed patient, provide an
opportunity for parents to successfully feed
patient, assess family process during meal.
• Interventions: bring the symptom alive and present
in the room, one more bite, align patient with
siblings for support.
Males and EDS
Males and EDs
• Less common than in females, but
increasing (approx 10% of EDS occur in
men)
• They have a job or profession that
demands thinness. Male models,
actors.
• Cultural pressures to be V shaped
Males and EDS
• More in common with female EDs than
differences
• Lower testosterone may predispose to ED
• Fears regarding sexuality
• More common in homosexual men
• Conflict over sexual identity
• Avoidant, passive, negative reactions from
peers as children
Males and EDs
• Athletes/profession with weight
requirements
• 1:10 male to female ratio
• BED similar rates male/female, though
women more distressed about it, more guilt
Males and EDs
• They were fat or overweight as children
(different than females).
• They have been dieting. Dieting is one
of the most powerful eating disorder
triggers for both males and females.
Males and EDs
• They participate in a sport that demands
thinness. Runners and jockeys are at higher
risk than football players and weight lifters.
• Wrestlers who try to shed pounds quickly
before a match so they can compete in a
lower weight.
• Body builders are at risk if they deplete body
fat and fluid reserves to achieve high
definition
Special Assessment and
Treatment Strategies for Chronic
AN
• Problems accumulate, may become
irreversible after as early as 6 mos
• Poor Prognosis
• Risk benefit assessment of ED
• Harm reduction
Treatment issues in Chronic EDs
• Legal aspects
• Case examples
Q and A, discussion