Title: The University of Michigan Depression Center Colloquium Series
1The University of Michigan Depression Center
Colloquium Series
- The Colloquium Series is made possible by an
educational grant from GlaxoSmithKline.
2U-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
3Spectrum of Eating Disorders
Risk Factors
Healthy Eater
Typical Dieter
Pathological Dieter
ED-NOS
ED
Protective Factors
4Prevalence of Eating Disorders
5Anorexia 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)
6Anorexia 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
7Anorexia 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
8Bulimia 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
9Bulimia 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
10Bulimia 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
11Spectrum of Eating Disorders
Risk Factors
Healthy Eater
Typical Dieter
Pathological Dieter
ED-NOS
ED
Protective Factors
12Eating Disorders Etiology
- Multifactorial Etiology
- Biologic risk factors
- Individual/psychological risk factors
- Familial risk factors
- Sociocultural risk factors
13Etiology 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
14Etiology 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
15Etiology 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
16Etiology Individual Characteristics
- Perfectionism
- Over-achieving
- Obsessional thinking
- Low self-esteem
- Depression
- ? History of sexual abuse
17Etiology Sociocultural Pressure
- Societys focus on attractiveness
- Prevailing cultural stereotypes
- Thin is beautiful
- Unhealthy media representationsof women
- Emergence of pro-Ana and pro-mia influences
18(No Transcript)
19Malnutrition
- 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
20Medical 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
21Psychiatric Co-morbidity
- Affective disorders, suicidality
- Anxiety disorders
- Obsessional behavior, OCD
- Substance abuse
- Suicide is the leading cause of deathin bulimia
nervosa
22Anxiety 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
23Depression 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
24AN 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
25BN 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
26Prognosis
- 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
27Outcome 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
28Prognosis
- 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
29Outcome 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
30Summary
- 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
31Summary
- 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