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Lecture on Eating Disorders DANIEL STEIN, M.D.

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1 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 * 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 ). 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) – Biological causes (Simmonds Syndrome) – 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, or undue 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-CULTURAL MODEL 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-CULTURAL MODEL 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-CULTURAL MODEL 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:

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 ↑ importance of weight & shape in females
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 Anorexia nervosa restricting type:
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(
Chronic Improved Recovered 20% 35% 45% Anorexia nervosa 30% 50% Bulimia nervosa 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

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45 יומן אכילה- אנורקסיה נרווזה

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47 * Structured, focused, time-limited (treatment manual)
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

48 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

49 * Maladaptive families deteriorates parent- adolescent relationship
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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