Eating Disorders: Assessment, Understanding, and Treatment

Strategies

Terry Schwartz MDMedical 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

• 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

• 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 rigidityAN 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

• 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

AN, Restricting Subgroup

AN, Bulimia Subgroup

Bulimia Nervosa

1. Starvation+ + +

2. Cardiac arrhythmia/failure from hypokalemia of ipecac abuse

+ + + + +

3. Suicide+ + + + +

4. Gastric Dilation+ +

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

• 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

 

• 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.

• 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 OCDSaxena 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 foodRolls, 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

• Prozac mixed data for rec-AN

• Atypical antipsychotic medications

• GI meds to aid physical symptoms

• BCP/hormones: no evidence of benefit

Pharmacology for BN

• 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 aches

Muscle enzyme abnormalities in severe malnutrition

5. Reproductive Prepubertal psychosex-ually

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:– 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

• 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 TreatmentFrom American Psychiatric Association Guidelines for the

Treatment of Eating Disorders

Outpatient Inpatient

Weight >85% < 75%

Medical complications none HR, BP, K etc

Suicidal, comorbid psych d.o. 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

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– 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 adolescence• Little net gain in bone mass after 2 yrs post-menarche• Peak bone mass achieved by end of second decade

– Stereotypic food choices, ritualized eating, calorie counting– Delusionary quality – Nothing else is more important

Methods of TreatmentA. Regular Weight restoration

• 2 to 3 lbs/wk inpatient

• 1 to 2 lbs/wk day-hospital

• 1 lb/wk outpatient

B. Nutritional Teaching• Provide patient support

• Prevention from vitamin and mineral deficiency

• Prevention of osteoporosis• 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

EDsTerry 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:– 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

• 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

• CBT

• CBT plus BWL

• BWL alone

• Group therapy

• Indiv therapy

• 12 step/self help

Medical treatments for BED/obesity

• No magic pill!

• Sibutramine

• Orlastat

• Acomplia

• Phentermine

• Gastric Bipass

• Stimulants

Medical treatments for BED/obesity continued

• No magic pill!

• ? SSRIs, SNRIs

• ?Wellbutrin

• ? Topiramate

• ? Zonisamide

What about psych meds and weight gain

• 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 NervosaDSM-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• 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

• Anorexia nervosa

• Food avoidant emotional disorder

• Selective eating

• Functional dysphagia

• Bulimia nervosa

• Pervasive refusal syndrome

Early behavioral risk factors for EDs

• 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

SocialPsychological

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– 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

• 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

• 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