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Lecture on Eating Disorders DANIEL STEIN, M.D.

Lecture on Eating Disorders DANIEL STEIN, M.D. * Anorexia nervosa (AN) - history, definition, clinical description * Bulimia nervosa (BN) – definition, clinical description * Physical & laboratory findings in AN and BN * Epidemiology of AN and BN

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Lecture on Eating Disorders DANIEL STEIN, M.D.

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  1. Lecture on Eating DisordersDANIEL STEIN, M.D. • * Anorexia nervosa (AN) - history, definition, clinical description • * Bulimia nervosa (BN) – definition, clinical description • * Physical & laboratory findings in AN and BN • * Epidemiology of AN and BN • * Etiology - genetic, biological, socio-cultural, psychological, familial • * Treatment of AN and BN- ambulatory vs. inpatient treatment cognitive-behavioral, family, biological treatments • * Prognosis

  2. References Fairburn Cg, Marcus MD, Wilson GT: Cognitive-behavioral therapy for binge eating and bulimia nervosa: A comprehensive treatment manual. In: Fairburn CG, Wilson TG (Eds), Binge eating: Nature, assessment and treatment (pp 361-404). New York: Guilford Press, 1993. Cooper Z, Fairburn CG, Hawker DM: Cognitive-behavioral Treatment of Obesity: A Clinician Guide. New York: Guilford Press, 2003.

  3. History of anorexia nervosa • Medieval period – Holy anorexia • 1698 – First documentation (Thomas Morton) • 1873 – First clinical descriptions (Laséque, Gull) • 1900-1930 – Biological causes (Simmonds Syndrome) • 1900-1960 – Psychoanalytic explanations (oral impregnation)

  4. History of anorexia nervosa • 1970th – H. Bruch –Severe Ego Pathology • disturbances in body image • overall personality disturbance • alexythymia (not Bruch’s term) • disturbance in interoceptive awareness • ineffectiveness • 1979 – First description of bulimia nervosa • 1982 – description of two types of anorexia nervosa • restricting type • purging/bingeing-purging type • 1993 – First descriptions of binge eating disorder as a separate entity

  5. Diagnostic Criteria of anorexia nervosa (AN) (DSM-IV) • Refusal to maintain body weight at or above a minimally normal weight for age and height (≤85% of expected body weight), or failure to reach expected weight (≤85% of expected body weight) during period of growth • Fear of gaining weight or becoming fat even though underweight • Disturbance in body perception, orundue influence of weight/ shape on self-evaluation, or denial of seriousness of low weight • In post-menarcheal females, amenorrhea – absence of at least three consecutive menstrual cycle (in 33% AN appears before menarche)

  6. Clinical description of anorexia nervosa • * Pre-morbid features: ↑ perfectionism, inhibition, conformity, obsessionality, ineffectiveness, harm avoidance, ↓ self-esteem • * Diet: ↓ in – quantity • type of food (“bad food, “good” food) • number of meals • * Eating & eating-related behaviors highly obsessional • *  physical activity – highly obsessional

  7. Clinical description of anorexia nervosa • Usually prolonged period before discovery (denial, treatment refusal by patient, family problems that reduce parental awareness) • Anorexia nervosa (AN) usually starts as restricting • 30-50% of restricting AN → purging/bingeing- purging AN or bulimia nervosa

  8. Physical changes in anorexia nervosa • * Amenorrhea, ↓ sexual development • * Fatigue (↓ BMR) • * Bradycardia, hypotension, hypothermia • * Osteoporosis, ↓ bone density, ↓ peripheral muscles, cardiomyopathy • * Yellow skin due to Hypercarotenemia (↓ T3)

  9. Physical changes in anorexia nervosa • * Lanugo • * Peripheral edema (↓ albumin, inappropriate ADH secretion) • * ↓ cognitive function (sometimes continuing after recovery) • * ↑ spontaneous abortions, small for date deliveries (even when recovered)

  10. Mortality in anorexia nervosa • Lifetime mortality restricting anorexia nervosa – 5-10% (illness complications & suicide) • Lifetime mortality bingeing/purging anorexia nervosa – 10-20% (illness complications & suicide)

  11. Laboratory changes in anorexia nervosa • * Anemia, leucopenia • * ↓ glucose, ↑ cholesterol (due to ↓ T3) • * Disturbances in liver function tests • * ↓ Mg, zinc • * TSH, T4 normal, ↓ T3 • * Hypercarotenemia (↓ T3) • Most changes related to starvation, reversible

  12. Laboratory changes in anorexia nervosa • ↑ response to ADH • ↓ FSH, LH, estrogens, testosterone (males) • ↑ CRH, cortisol • ↑ endogenous opiates • ↓ leptin, neuropeptides • ↓brain volume, gray, white matter changes Most changes related to starvation, reversible

  13. Diagnostic Criteria of bulimia nervosa (BN) (DSM-IV) • Recurrent episodes of binge-eating, characterized by: 1. Eating in a discrete period of time an amount of food that is definitively larger than most people would (e.g., ≥1000 calories in 30 minutes). 2. Lack of control over eating during binge. • Recurrent inappropriate compensatory behaviors to prevent weight gain (purging – self-induced vomiting, misuse of laxatives, diuretics, enemas, or other medications, fasting, excessive exercise) • Bingeing & purging occur at least 2 twice a week for 3 months. • Undue influence of weight/ shape on self-evaluation • Not associated with low weight for age and height (i.e., not occurring exclusively during AN episodes).

  14. Clinical description of bulimia nervosa – Bingeing • Planning ahead • Obsessional planning • Bingeing high calorie food (sweet, fat) • ↑ pace compared to normal eating • Feeling that one is bingeing (sense of lack of control, unable to stop) – automatic, dissociation (bingeing in front of TV) • Hiding binges

  15. Clinical description of bulimia nervosa – Bingeing • Between binges ↓ of food intake (weight fluctuations) • Stress, negative feelings ↑ bingeing • In binges eating until feeling full/uncomfortable/pain • Immediately following binge ↓ dysphoria, later – ↑ dysphoria, disgusted, guilty • Bingeing not associated with hunger • Binges ↑ late in evening/night (D.D – DSPS)

  16. Clinical description of bulimia nervosa – Purging • Self-induced vomiting – 80-90% • Immediately following vomiting ↓ dysphoria, later –↑ dysphoria, disgusted, guilty • Laxatives, enemas – 30%

  17. Physical changes in bulimia nervosa • ↑ parotid glands (due to vomiting) • ↑ gastric dilatation (due to binges) • Congestive heart failure (due to binges) • Irregular menstruation • Peripheral edema (inappropriate ADH secretion) • Erosion of dental enamel • Lifetime mortality – 10%

  18. Laboratory changes in bulimia nervosa • Hypokalemia, metabolic alkalosis ( HCL ↑ bicarbonate) (due to vomiting) • Hyponathremia, metabolic acidosis (laxative-induced) • ↑ parotid diastase (due to vomiting) • Most changes related to starvation, reversible

  19. Multi-impulsive bulimia nervosa •  rates of a combination of several • impulsive behaviors • * Multiple purging behaviors (self-induced vomiting & laxatives) • * Substance use disorders • * Impulse control disorders (kleptomania, gambling) • * Suicidal behavior, self-mutilation • * Promiscuity • * Borderline personality disorder

  20. Epidemiology • Lifetime Prevalence • Anorexia nervosa – 0.2 – 1% • Bulimia nervosa – 1 – 4% • Binge Eating Disorder – not known (apparently ↑ than BN) • Partial eating disorders – 5 – 15%

  21. Epidemiology • Anorexia nervosa (AN) – mainly adolescents • Bulimia nervosa (BN) – mainly young adults • Binge Eating Disorder - mainly young adults • AN & BN – males: 5-10% • In recent years – ↑ males • ↓ age of onset

  22. CURRENT CONCEPTS OF THE SOCIO-CULTURALMODEL IN ANOREXIA NERVOSA (AN) • Messages and norms that are of importance for the development of AN • * Social influences of body image and perception • * The thin body ideal • * Denigration of obesity • * Importance of weight and appearance for success and self-esteem • (e.g., ↓ Weight is critical for ↑ self-esteem; we can change our life with dieting & physical activity; “all-American” woman)

  23. SUPPORT FOR THE ROLE OF THE SOCIO-CULTURALMODEL IN ANOREXIA NERVOSA • * AN does not appear in all cultures but in specific groups (e.g., young females, who are particularly influenced by weight-related social norms) • * AN ↑ in Western than non-Western cultures • * ↑ incidence of AN in recent years that parallels ↑ influence of weight-related social norms

  24. SUPPORT FOR THE ROLE OF THE SOCIO-CULTURALMODEL IN ANOREXIA NERVOSA • * ↑ rate of AN in specific vulnerable sub-populations (e.g., dancers) • * Recent appearance of AN in places only recently exposed to Western weight-related social norms (e.g., Fiji Islands, Curacao) • * Young females at risk to develop disordered eating will adopt more rigidly weight-related social norms expressed by media, family/peers

  25. Heritability of anorexia nervosa (AN) and bulimia nervosa (BN( • Family studies: ↑ rates of AN, BN, ED-NOS in 1st degree relatives of AN & BN patients • Twin studies: ↑ concordance rates of AN, BN, or both in monozygotic twins in whom the afflicted twin has AN or BN • compared to dyzygotic twins • Heritablity estimates for AN & BN: 0.54-0.80

  26. Findings supporting genetic transmission in eating disorders (EDs) • * ↑ rates of ↑/↓ weight in 1st degree relatives of AN & BN patients • * Limited influence of shared environmental factors in the variance of disordered eating among family members • * Genotypic influences may determine the nature of experiences to which the individual is attracted (non-shared environment) • * Infrequency of full-blown EDs in the face of robust cultural influences

  27. Biological aspects of eating disorders • ↑ food intake (hunger) • endogenous opioids, neuropeptide Y, NE, grhelin, adiponectin • food intake (satiety) • cholecystokinin, leptin, 5HT • High rates of dissatisfaction with weight & shape in young female adolescents & young adults • BUT • AN & BN – relatively rare

  28. Differences in rates of eating disorders between females & males –Psychological, sociocultural & biological factors • ↑ importance of weight & shape in females • Females more influenced by media & societal directives • ↑ food more available to women • ↑ in number of fat cells in females but not males during puberty • Centrifugal (females) vs. centripetal (males) weight increase

  29. Lifetime comorbid disorders in Eating Disorders (EDs) • Depressive disorders– • Prevalence 40-80% • Not necessarily associated with starvation & bingeing/purging • ↑ prevalence in 1st degree relatives of patients with eating disorders

  30. Lifetime comorbid disorders in Eating Disorders (EDs( • Substance use disorders (SADs) • 50% of BN & AN-P/BP patients • ↑ prevalence of SADs in 1st degree relatives of patients with BN & AN-P/BP who also have SADs

  31. Lifetime comorbid disorders in Eating Disorders (EDs) • Anxiety disorders • Social phobia & panic disorder – 30– 80% • ↑ prevalence of panic disorder in 1st degree relatives of patients with AN & BN • ↑ prevalence of social phobia in 1st degree relatives of patients with AN

  32. Lifetime comorbid disorders in Eating Disorders (EDs) • Obsessive compulsive disorder • 10-70% in anorexia nervosa • 5-45% in bulimia nervosa • obsessive compulsive symptoms in acutely ill & recovered patients – symmetry, ordering, perfectionism • ↑ prevalence of obsessive compulsive disorder in 1st degree relatives of patients with AN & BN

  33. Psychological factors – personality disorders (PDs) and personality features in eating disorders (EDs) • Anorexia nervosa restricting type: • * ↑ rates of pre-morbid avoidant, dependent, obsessive compulsive, narcissistic PDs • *↑ rates of pre-morbid conformism, rigidity, inhibition, harm-avoidance, perfectionism, low self-esteem, selflessness, alexithymia • * Secondary vs. primary anorexia nervosa

  34. Psychological factors – personality disorders (PDs) and personality features in eating disorders (Eds) • Anorexia nervosa purging type & bulimia nervosa: • * ↑ rates of pre-morbid narcissistic, borderline, antisocial PDs • * ↑ rates of pre-morbid impulsivity, novelty seeking • * Difference between uni-impulsive and multi-impulsive BN * Importance of sexual abuse (not necessarily ↑ rates of PTSD)

  35. Family factors in eating disorders (EDs( • The Psychosomatic Family (Anorexia Nervosa) (Minuchin, 1978) • * Enmeshment – overly close relationship between IP & mother, father distant • * Overprotection • * Lack of distinct boundaries between parents & children subunits (“parental child”) • * Conflict avoidance • * Illness of IP maintains conflict avoidance • * Rigidity of family structure hampers change

  36. Outcome of eating disorders (EDs( Eating disorders are chronic: mean duration for recovery 4-7 years 30-50% relapse rate in BN after 6 months-6 years

  37. Factors associated with negative outcome of AN • * Earlier onset in adolescent patients (not definite), particularly prepubertal • * Onset in adulthood compared to adolescence • * ↑ duration of illness • * ↑ duration until receiving treatment • * Severe disturbance in body image

  38. Factors associated with negative outcome of AN • * Obsessionality in eating & physical exercise • * Appearance of bingeing/purging symptoms in restricting AN • * Illness starts at normal vs. overweight • * Comorbid DSM Axis I & Axis II disorders • * Maladaptive relations with family members • * Decreased social skills

  39. Treatment • Multidimensional interventions (pediatrician, psychiatrist, psychologist, dietician, social worker, nurse, art therapist, school) • Ambulatory ↔ day/partial treatment ↔ Inpatient • Behavioral weight restoration program

  40. Treatment • Indications for hospitalization– • severe weight ↓ (>30% IBW) • rapid weight ↓ • failure of ambulatory treatment • severe pathology in family • suicidality

  41. Treatment • Psychotherapy: dynamic – anorexia nervosa • Cognitive behavioral – bulimia nervosa, binge eating disorder • Family therapy – in adolescent non-chronic patients (particularly AN, but also BN) • SSRI’s – bulimia nervosa, binge eating disorder • only weight restored anorexia nervosa to decrease relapse

  42. Principles of cognitive behavioral treatment (CBT) in eating disorders Three stages 1. Psychoeducation on cognitive model Introduction of behavioral techniques to replace maladaptive with adaptive behavior Cognitive technique to modify dysfunctional cognitions .2  3. Maintenance of change, relapse prevention

  43. יומן אכילה – בולמיה נרווזה

  44. יומן אכילה- אנורקסיה נרווזה

  45. Evidence based family therapy for adolescent anorexia nervosa (AN) (Dare & Isler, 1997; Lock et al, 2001) • * Structured, focused, time-limited (treatment manual) • * Mobilization of adolescent & family for therapy • * Family not he source of AN, but is the best resource for change • * Psychoeducation

  46. Evidence based family therapy for adolescent anorexia nervosa (AN) (Dare & Isler, 1997; Lock et al, 2001) • * Active, consistent, non-blaming parental involvement in nutritional rehabilitation. *  parental efficacy is important for adolescent development. • * Family has a meal in the presence of therapist – direct observation food considered medication • * Upon  in weight – focus transfers to age appropriate developmental tasks (adolescent gradually takes control over her life) • * Relapse prevention

  47. Evidence based family therapy for adolescent anorexia nervosa (AN) (Dare & Isler, 1997; Lock et al, 2001) • Contraindications for parental involvement in nutritional rehabilitation • * Maladaptive families • deteriorates parent- adolescent relationship • if ineffective - ↓ motivation • * Not recommended in the case of binging, self-induced vomiting

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