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)
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)
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
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.
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
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• 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
• 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
• 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
• 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