Eating Disorders: Assessment, Understanding, and Treatment Strategies

1. 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

2. ASSESSMENT AND TREATMENT STRATEGIES FOR EATING DISORDERS Terry Schwartz MD Medical Director UCSD Outpatient Eating Disorders Program Assistant Clinical Professor UCSD Dept Of Psychiatry

3. 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

4. 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

5. 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

6. 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

7. 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

8. Anorexia Nervosa  Perceptual rigidity  Cognitive rigidity ANWeight recovery No changes ANFull recovery Partial improvement in cognitive flexibility tasks Bulimia Nervosa Slowness in cognitive shifting tasks Fluctuations in Perceptual task Cognitive Flexibility

9. 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)

10. 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.

11. Primary Causes of Death in Patients with Eating Disorders

12. 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

13. 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

14. Biological underpinnings of eating disorders • Genetics • Neurobiological correlates • Neuropsychiatric • Brain imaging in AN

15. Genetic Correlates of Bulimia Nervosa • Twin studies • 5ht2A receptor gene alteration • Family history of affective, anxiety, substance abuse d/o

16. 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

17. Neuroendocrine correlates of Bulimia Nervosa • Serotonin (5HT1A receptor) • Endogenous opiate response to binge purge • ?DA

18. Neuroendocrine Correlates of Anorexia Nervosa • Serotonin (5HT2A receptor) • Dopamine • Endogenous opiate response to starvation • Hypothalamus dysfunction (satiety, amenorrhea)

19. 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)

20. 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

21. 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

22. 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

23. 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

24. 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)

25. 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

26. 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)

27. 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

28. 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

29. 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)

30. Psychopharm in EDs

31. 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

32. 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

33. Pharmacology for BN • Serotonin re-uptake inhibitors • ?SNRIs • AEDs (topiramate, ?zonisamide) • Antipsychotics • Mood stabilizers • reglan, H2 blockers • ?? Stimulants (with caution)

34. BREAK

35. Medical Consequences of AN and BN

36. Physical Complications of Anorexia Nervosa

37. Physical Complications of Anorexia Nervosa, Cont.

38. Physical Complications of Anorexia Nervosa, Cont.

39. Physical Complications of Bulimia Nervosa

40. Physical Complications of Bulimia Nervosa, cont.

41. Amenorrhea and Osteopenia • Most serious complication of prolonged amenorrhea is osteopenia, or reduced bone mass

42. 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

43. 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)

44. 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

45. 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

46. 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

47. Medical evaluation for Bulimia Nervosa • Assess for comorbidity • Screening labs: electrolytes, Ca++, Mg+, Phos, BUN/Cr, CBC, LFTs, TFTs, UA, hematology • Dexa • ECG • Dental

48. AN: Hospital vs Outpatient TreatmentFrom American Psychiatric Association Guidelines for the Treatment of Eating Disorders

49. 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

50. 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