Transcript Child and Adolescent Psychopathology

Chapter 12:
Bulimia Nervosa and
Binge Eating Disorder
Linda W. Craighead
Margaret A. Martinez
Kelly L. Klump
DSM-5 Changes for Eating
Disorders
DSM-IV-TR: Eating
Disorders (EDs):
DSM-5: Feeding and
Eating Disorders (FED):
 Anorexia Nervosa (AN)
 Anorexia Nervosa (AN)
 Bulimia Nervosa (BN)
 Bulimia Nervosa (BN)
 Eating Disorder Not
Otherwise Specified (EDNOS)
 Binge Eating Disorder
(BED); in DSM-IV-TR appendix as
provisional
 Separate Chapter had
Disorders Usually First
Diagnosed During Infancy,
Childhood, or Adolescence
 Other specified FED
 Unspecified FED
- Avoidant/restrictive food
intake disorder
- Pica
- Rumination Disorder
Rationale for Changes
 Changes intended to:
 Reduce the frequency of the unspecified diagnosis
 Establish criteria appropriate for clinical presentations at
younger ages
 There is some concern that the new criteria may
dramatically increase the number of individuals
diagnosed with an eating disorder
DSM-5 Diagnostic Criteria for BN
BULIMIA NERVOSA
A. Recurrent episodes of binge eating. Binge eating characterized by BOTH:
1.
2.
Eating an objectively large amount of food, i.e. larger than most people would eat in a similar
period of time and under similar circumstances;
A sense of loss of control over eating during the episode.
B. Recurrent inappropriate compensatory behavior in order to prevent weight
gain (e.g. self-induced vomiting, misuse of laxatives/diuretics/enemas/other
medications)
C. Binge eating and inappropriate compensatory behaviors both occur, on
average, at least once a week for three months
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of Anorexia
Nervosa
Indicates change from DSM-IV-TR criteria
Objective Binge Episode
 To be classified as an objective binge episode
(OBE), individual must:
 Consume an objectively large amount of food, that is
more than most people would eat in a similar situation
and in a discrete period of time (e.g., 2 hours)
• Objectively large ≈ 3x the typical portion for that food
• 1,900 calories on average (Bartholome, Raymond, Lee, Peterson, & Warren, 2006)
 Experience a subjective feeling of loss of control over
eating
Subjective Binge Episode
 Subjective binge episode (SBE):
 Individual experiences loss of control while eating an
amount of food considered normal or small
• For example, one bowl of ice cream (SBE) versus a gallon of ice
cream (OBE)
 700 calories on average
(Bartholome, Raymond, Lee, Peterson, & Warren, 2006)
 Only OBEs count toward frequency criterion for diagnosis
of BN/BED
Characteristics of a Binge
 Typically occur when individual is alone
 May be comprised of high-calorie foods (i.e., ice
cream) or healthy foods (i.e., carrots)
 Restricted intake before and after binge episode
 Can be spontaneous or planned
 Triggered by negative/positive emotions,
interpersonal stressors, presence of tempting food,
violation of a dieting rule, body image
dissatisfaction, excessive hunger, and so on
Obstacles to Treatment in BN
 Bulimia is often not detected until later in the
course of illness, often because:
 Binge/purge episodes feel habitual and are perceived as
problematic
 Function of binge episodes as distracting from negative
emotions
 Conviction that stopping purging behaviors will lead to
weight gain
 Shame and embarrassment associated with binge/purge
behaviors
Medical Complications of BN
 Medical complications typically associated with
purging
 Complications include:
 Electrolyte abnormalities
 Esophageal/gastrointestinal symptoms
 Menstrual irregularities
 Thyroid dysfunction
 Dental problems
 Enlarged parotid glands
 Decreased stomach motility
Proposed DSM-5
Diagnostic Criteria
BINGE EATING DISORDER
A. Recurrent episodes of binge eating. Binge eating characterized by both:
1.
2.
Eating an objectively large amount of food, that is an amount larger than most people would eat
in a similar period of time and under similar circumstances
A sense of loss of control over eating during the episode
B. Binge eating episodes are associated with at least three of the following:
1.
2.
3.
4.
5.
Eating more rapidly than normal;
Eating until 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
C. Marked distress regarding binge eating is present
D. Binge eating occurs, on average, at least once a week for 3 months
E. The disturbance does not occur exclusively during episodes of anorexia
nervosa and is not accompanied by inappropriate compensatory behaviors,
as in bulimia nervosa.
**Indicates change from provisional DSM-IV-TR criteria
Distinction Between BN and BED
 Both BN and BED require the presence of
objectively large binge episodes (at least 1x/week
for 3 months) in individuals who are not
significantly underweight
 In BED, no inappropriate compensatory behaviors
 BED does not require concern about shape/weight,
although this is often reported
 Both BN and BED can be chronic conditions
exacerbated by life stressors
Medical complications of BED
 Medical complications less common in BED
 Most common complaint is gastrointestinal distress
associated with binge episodes
 Individuals with BED are more often affected by
complications of comorbid obesity
 Many (but not all) individuals with BED are also
overweight/obese
 Those individuals with BED who are not overweight are at
risk of developing obesity
History of Binge Eating
Ancient
Greek
physicians
describe
ravenous
hunger, or
boulimos
James (1743)
described
case
accounts of
overeating at
times
followed by
vomiting
Stunkard et
al. called
attention to
night-eating
syndrome
(1955) and
binge eating
syndrome
(1959)
BoskindLodahl and
White (1973)
published
feminist
formulation of
“bulimarexia”
Russell
(1979)
labeled this
syndrome as
“bulimia
nervosa”
DSM-5 (2013)
recognizes
both BN and
BED
Transdiagnostic Model
of Eating Disorders
 Proposed by Fairburn et al., a diagnostic approach
that focuses on the similarities between various
types of eating disorders
 Views overevaluation of eating, shape, and weight as the
core pathology underlying all eating disorders
 Hypothesizes that overevaluation leads to
restriction/dieting that, in turn, leads to disordered eating
 May explain the high rate of diagnostic crossover in
eating disorders
 Limitations of the transdiagnostic model:
 Many individuals with BED report onset of binge eating
before development of weight concerns
Epidemiology
 Using DSM-IV criteria, prevalence of BN is ~0.5%
to1.0%
 Prevalence of any binge eating symptoms is 5.7%
 Using DSM-5 criteria, prevalence of BN is ~2%
 ~90% of those diagnosed are women
 Using DSM-IV criteria, prevalence of BED is ~2% to
5%
 Prevalence among individuals seeking weight-loss
interventions is higher, ~30%
 Using DSM-5 criteria, prevalence of BED is ~3.6% in women
and 2.1% in men
 More equitable gender distribution (~65% female, 35% male)
 Binge eating may be more common among certain
minority groups
Course
 Typical age of onset for BN is late
adolescence/early adulthood
 Individuals with BN often have a history of AN (~10% to
14% of community samples, ~25% to 37% of clinical
samples)
 Onset of OBEs may be earlier than the age at which the
individual meets full diagnostic criteria for BN or BED
 Both BN and BED have a chronic course and high
relapse rates
Comorbidity
 Common Axis I cormorbidities include:
 Mood disorders
• Especially major depression and dysthymia
 Anxiety disorders
• Posttraumatic stress disorder is more common in BN and BED than
AN
 Substance abuse
 Common Axis II comorbidities include:
 Borderline personality disorder
 Avoidant, dependent, histrionic, and paranoid personality
disorders
Genetic Risk Factors
 AN, BN, and BED have moderate-to-large
heritabilities, similar to biologically based illnesses
 In girls, genetic risk activated during puberty
 In boys, genetic risk remains constant across the lifespan
 Estrogen may account for difference in pubertal risk
 Some genes have been implicated, including
serotonin, neurotrophic, estrogen receptor, and
dopamine genes
 Dieting and other environmental factors may
increase genetic risk
Neurobiological Risk Factors
 Overactivity in opioid and dopaminergic systems in
binge eating resembles that seen in substance use
 Neural patterns may vary over course of illness
 Hypothesized that overactive reward networks may
increase risk for developing binge eating…
 …once binge eating develops, binge behaviors may
result in down-regulation and hyposensitivity of neural
reward pathways
Personality Traits
 Impulsivity
 Impulsivity associated with binging and purging
 Impulsivity abates with recovery
 Obsessionality
 Individuals with eating disorders tend to have obsessivecompulsive traits
 Perfectionism
 May mediate the relationship between eating disorders
and obsessive-compulsive symptoms
Emotion Dysregulation
 Binge eating conceptualized as emotion regulation
strategy
 Negative affect precedes and maintains onset of binge
eating
 Negative affect also associated with body dissatisfaction and
dieting behaviors, which may compound the relationship
between negative affect and binge eating
 Although binge eating may momentarily reduce
negative affect, episode is often followed by increased
negative affect
 Compensatory behaviors may reduce negative affect
and thus increase as a result of negative reinforcement
Cognitive Dysfunction
 Cognitive symptoms of BN include:
 Appearance overvaluation
• Self-worth is disproportionately affected by body shape and weight
 Internalization of the thin ideal
• Thin cultural standard is fully adopted
 Cognitive biases
• Attention and memory biased towards information regarding food,
weight, and shape
 Rigid and obsessive thinking patterns
• Thinking characterized by strict and dichotomous patterns
Risk Factors
 Body dissatisfaction
 Leads to negative affect and dieting behavior, which in turn
may produce disordered eating
 Dieting
 Excessive caloric deprivation may trigger binge eating
 Interoceptive awareness
 Deficits in ability to monitor internal states predicts onset of
eating disorder symptoms
 Body mass
 Higher body mass may contribute to disordered eating through
increased body dissatisfaction and dieting behaviors
Environmental Factors
 Sociocultural pressure
 No clear causal relationship between media exposure
and onset of eating disorders
 Family
 Family attitudes and behavior may contribute to thin ideal
internalization and the failure to develop effective coping
strategies
 Childhood sexual abuse
 History of abuse is a risk factor for general
psychopathology, not specific to eating disorders
Assessment
 Interview measure of eating disorder symptoms
 Eating Disorder Examination (EDE): Assesses disordered
attitudes and behaviors over past 4 weeks
• Four subscales assess restraint, concern about eating, concern
about shape, and concern about weight
• Structured format ensures assessment of a variety of constructs are
assessed
• Takes time to complete interview and the extensive training
required to use it limits use in clinical settings
Assessment, cont
 Self-report measures of eating disorder symptoms
 Questionnaire version of EDE (EDE-Q)
• Can be used for diagnostic purposes or to assess dimensions of
eating pathology
 Eating Disorder Inventory (EDI) and Bulimia Test–
Revised (BULIT-R)
• Global measures with multiple subscales, often used to assess
treatment outcome
 Children’s Eating Attitudes Test (Ch-EAT)
• Used to assess eating disorders in children
Treatment of BN
 Psychological interventions
 Clinical trials have established Cognitive Behavioral Therapy
(CBT) and Interpersonal Therapy (IPT) as optimal treatments
• Although CBT may initially be more effective, individuals receiving IPT
continue to show improvement over follow-up so no difference in long
run
 Interventions may be delivered in guided self-help format to
increase treatment access
 Pharmacological interventions
 Antidepressant medications to prevent relapse when
medication stopped effective but best to use in combination
with CBT
 Further research required to determine best treatments
for males, older women, and adolescents
Treatment of BED
 Psychological interventions
 As with BN, CBT and IPT are effective treatments
 Self-help treatments also effective
 Behavioral Weight Loss (BWL) often used to treat
comorbid obesity, but weight loss is minimal
 Pharmacological interventions
 Fluoxetine may reduce binge episodes in BED, as in BN,
but does not contribute to weight loss
 Topirimate thought to control impulsive tendencies
 Medications do not seem to confer additional benefit
beyond psychotherapy
Prevention of Eating Disorders
 Programs targeting high-risk individuals more
effective than those implemented universally
 Prevention programs generally effective in raising
awareness of eating disordered symptoms, less
effective in reducing risk factors
 Novel programs capitalize on cognitive dissonance
by asking participants to critique the thin ideal