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Title: Lecture on Eating Disorders DANIEL STEIN, M.D.


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
    Bruchs 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-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)
  • SSRIs 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
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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
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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