The University of Michigan Depression Center Colloquium Series

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The University of Michigan Depression Center
Colloquium Series

• The Colloquium Series is made possible by an
  educational grant from GlaxoSmithKline.

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U-M Depression Center ColloquiumEating
Disorders and DepressionClinical Context

• David S. Rosen, M.D., M.P.H
• University of Michigan Medical School
• Ann Arbor, Michigan, USA

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Spectrum of Eating Disorders
Risk Factors
Healthy Eater
Typical Dieter
Pathological Dieter
ED-NOS
ED
Protective Factors
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Prevalence of Eating Disorders

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Anorexia Nervosa DSM-IV Diagnosis

• Weight loss (or refusal to gain weight) below
  normal for age and height
• Fear of fat, even though underweight
• Body image distortion or overconcern about
  weight or shape even though underweight
• Amenorrhea (abnormal fxn of H-P-G axis)

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Anorexia Nervosa Presentation

• Nutritional deficiency and wasting
• Delusion of being fat
• Obsession to be thinner
• Denial
• High rates of medical complications
• High rates of psychiatric co-morbidity

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Anorexia Nervosa Epidemiology

• Point prevalence lt 1
• Lifetime prevalence 0.6-4.0
• Increasing prevalence in past 30 years
• Females gtgt males
• Typically presents in adolescence
• Increasing presentation among atypical patients
  (e.g., males, children, people of color,
  immigrants, low SES)
• Partial syndromes are common

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Bulimia Nervosa DSM-IV Diagnosis

• Binge eating lack of control over binges
• Abnormal compensatory behavior to manage weight
• Overconcern with body weight or shape
• Symptoms at least 2x/week for 3 mo

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Bulimia Nervosa Presentation

• Recurrent, secretive binge eating
• Awareness that eating is abnormal
• Fear of loss of control over eating
• Short-term relief from compensatory behaviors
• Depression, shame, guilt
• Low, normal, or high weight
• High rates of medical complications
• High rates of psychiatric co-morbidity

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Bulimia Nervosa Epidemiology

• Point prevalence 0.4-3.0
• Lifetime prevalence 1-6
• Increasing prevalence in past 10 years
• Females gtgtgt males
• Occurs primarily in older adolescents and young
  adults
• Partial syndromes are common

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Spectrum of Eating Disorders
Risk Factors
Healthy Eater
Typical Dieter
Pathological Dieter
ED-NOS
ED
Protective Factors
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Eating Disorders Etiology

• Multifactorial Etiology
• Biologic risk factors
• Individual/psychological risk factors
• Familial risk factors
• Sociocultural risk factors

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Etiology Biologic Risk Factors

• EDs aggregate within families with distinct and
  significant genetic effects
• Genetic (and environmental) influences vary
  across adolescence and may be variably expressed
  at different stages of development
• Consistent association of EDs with alteration in
  Serotonin function

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Etiology Biologic Risk Factors

• Native animal models of AN exist among swine,
  sheep, and goats Genetically determined
  physiological response to excessive leanness
  oversensitivity to stress
• Animal models of binge eating have been developed
  in rats Restriction/re-feeding cycles response
  to stress exposure to highly palatable food.
• Binge eating appears to be motivated by reward
  rather than metabolic need

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Etiology Heritable Risk

• AN 11x more likely in female relatives of AN
  proband vs. relatives of controls
• BN 4-5x more likely in female relatives of BN
  proband vs. relatives of controls
• 15 lifetime risk of ED in female relatives of
  AN or BN proband vs. 4 lifetime risk in
  relatives of controls

Strober et al. Am J Psychiatry 2000 157393
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Etiology Individual Characteristics

• Perfectionism
• Over-achieving
• Obsessional thinking
• Low self-esteem
• Depression
• ? History of sexual abuse

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Etiology Sociocultural Pressure

• Societys focus on attractiveness
• Prevailing cultural stereotypes
• Thin is beautiful
• Unhealthy media representationsof women
• Emergence of pro-Ana and pro-mia influences

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Malnutrition

• Decreased metabolic rate
• Inability to maintain body temperature
• Decrease in brain mass (? Reversible)
• Cognitive changes
• Affective symptoms
• Medical sequelae of malnutrition are the leading
  cause of death in anorexia nervosa

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Medical Complications of EDs

• Cardiovascular complications
• Gastrointestinal complications
• Fluid/electrolyte complications
• Skeletal complications
• Renal complications
• Endocrine, hormonal,and reproductive
  complications
• Skin and dental complications
• Re-feeding syndrome

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Psychiatric Co-morbidity

• Affective disorders, suicidality
• Anxiety disorders
• Obsessional behavior, OCD
• Substance abuse
• Suicide is the leading cause of deathin bulimia
  nervosa

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Anxiety Disorders and EDs

• Methodologically rigorous controlled study of 271
  women with AN and BN
• Lifetime co-morbidity with at least one anxiety
  d/o 70 (significantly gt controls)
• Most anxiety disorders persist after recovery
• In approximately half of co-morbid cases, the
  anxiety disorder precedes the ED

Godart NT et al. Psychiatr Res 2003 117245
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Depression and EDs

• Longitudinal, community-based, Children in the
  Community study
• Depressive disorders are independent risk factors
  for the development of EDs (OR8.45) and ED Sx.
• Depressive disorders during early adolescence are
  associated with development of later EDs
• EDs during adolescence associated with
  significantly increased risk of depressive
  (OR4.32) and anxiety disorders (OR4.13) during
  early adulthood.

Johnson JG et al. J Consulting and Clin Psychol
2002 51119Johnson JG et al. Arch Gen
Psychiatry 2002 59545
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AN State-of-the-Art Treatment

• Few RCTs and little evidence.
• Interdisciplinary treatment is considered to be
  the standard of care
• Early nutritional rehabilitation is essential
• CBT is the most useful psychotherapy
• In adolescents, evidence strongly supports
  family-oriented treatment
• Limited role for pharmacotherapy

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BN State-of-the-Art Treatment

• Self-help strategies are of limited value
• BN-focused CBT is the most effective treatment
  but short-term outcomes are still poor (lt 50)
• Pharmacotherapy (SSRIs, Topiramate) is a useful
  adjunct to CBT but is less effective as
  monotherapy or when combined with self-help
• Early response to treatment is a useful predictor
  of both short- and long-term outcomes

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Prognosis

• Inadequate data inadequate follow-up
• Variable definitions of recovery and cure
• Long-term outcomes are better than previously
  assumed
• Significant ongoing risk of psychiatric illness
• Relapse prevention is important!
• Mortality is still significant

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Outcome of AN by Age at Onset and Duration of
Follow-up
Both younger age at onset, and longer duration
of follow-up are associated with better outcomes.
Adol Onset
All Ages
Steinhausen HC. Am J Psychiatr 2002 1591284
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Prognosis

• At long-term follow-up, most adolescent patients
  with ED (70) have fully recovered and gt80 have
  normal eating, weight, and menses. However, they
  will have spent more than 1/3 of their lives in
  treatment!
• At long-term follow-up, approximately 10 of
  patients will have persistent AN, 20 will have
  BN, and 5 will have died.

Steinhausen H-C et al. Eur Child Adolesc Psych
2003 1291-98
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Outcome of Adolescent-Onset ED in a Longitudinal
Cohort of Girls

• 982 adolescent girls from a school-based
  Australian cohort 14-15 y/o at entry
• Seven waves over six years
• Point prevalence of ED 2.4 at age 15-18
• Point prevalence of ED 3 at age 20
• Prevalence of ED 8.8 across entire study
• Only 11 of teens with ED still had ED at
  follow-up
• However, nearly half had persistent depression
  and/or anxiety at follow-up

Patton GC et al. Eur Child and Adol Psychiatr.
2003 12 (Suppl 1)I25
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Summary

• Eating disorders are common, even though AN and
  BN are uncommon
• Biology and genetics are fundamental to the
  etiology of eating disorders
• Medical complications of eating disorders may
  affect every organ system and can be serious or
  fatal.
• Significant psychiatric co-morbidity

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Summary

• Early treatment of adolescent ED may be
  associated with a better prognosis
• With excellent treatment, it is reasonable to
  expect a good prognosis (but be prepared to work
  at it for a very long time).
• More effective treatments for ED are urgently
  needed and may be informed by a better
  understanding of their biology