Daniel Anzia, MD
Chairman, Psychiatry
Advocate Lutheran General Hospital
Presentation Outline
1. Psychiatric Disorders and Obesity
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Obesity and Common Psychiatric Disorders
Primary Eating Disorders
Psychiatric Treatments and Weight Gain
2. Behavioral and Psychological Factors in
Obesity Treatment
3. Obesity: Neurobiology and Addiction
Models
4. Questions and Discussion
Obesity and Psychiatry
 Obesity in Psychiatric Disorders
 Primary Eating Disorders
 Psychiatric Treatments and Obesity
Obesity and Psychiatric Disorders
Depression
Meta-analysis of cross-sectional co-morbidity (DeWit et al):
Odds of being depressed 18% higher in obese persons
Gender effect: Men OR 1.00, Women OR 1.32
Severity of obesity influences the strength of the relationship
Evidence (including meta-analysis) supports both temporal
pathways:
Obesity as risk factor for Depression
Depression as risk factor for Obesity
Binge-Eating Disorder (Research Criteria)
 Recurrent episodes of binge eating, characterized by both:
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Eating, in a discrete period of time, an amount of food that is
definitely larger than most people would eat in a similar period of
time under similar circumstances
A sense of lack of control over eating during the episode (e.g., a feeling
that one cannot stop eating or control what or how much one is
eating)
 Binge eating episodes associated with 3 (or more) of:
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Eating much more rapidly than normal
Eating until feeling 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
From DSM-IV-TR, American Psychiatric Association
 Marked distress regarding binge eating is present.
 The binge eating occurs, on average, at least 2 days a
week for 6 months.
 Binge eating is not associated with the regular use of
inappropriate compensatory behaviors (e.g., purging,
fasting, excessive exercise) and does not occur
exclusively during the course of Anorexia Nervosa or
Bulimia Nervosa.
• From DSM-IV-TR, American Psychiatric Association
Psychotropic Medications, Weight, and Obesity
 Bipolar Disorder, Mood Stabilizers, and Weight Gain
 Likelihood of being overweight or obese correlated with
number of previous depressive episodes
 Lithium, valproate, some antidepressants associated
with weight gain
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Lithium: ¼ to ½ of patients – 5 to 10 % weight gain
Valproate: As frequent as with lithium
Mirtazepine, paroxetine, tricyclics, trazodone
Weight gain and Antipsychotics
 Meta-analysis: Mean weight gain
Clozapine
9.8 #
Olanzapine
9.1 #
Risperidone
4.6 #
Haloperidol
2.4 #
 CATIE study: Greater than 7 % weight gain
Olanzapine
30%
Quetiapine
16 %
Risperidone
14 %
Perphenazine
12 %
Ziprasidone
7%
Risks for weight gain and diabetes
 Greatest effect on weight, increased risk of diabetes
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Clozapine
Olanzapine
 Effect on weight, unclear risk for diabetes
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Quetiapine
Risperidone
 Small to no effect on weight, without risk for diabetes
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Ziprasidone
Aripiprazole
Metabolic Syndrome
 Three or more of the following:
 Waist circumference > 102 cm for men and > 88 cm for
women
 Fasting triglycerides > 150 mg/dL
 HDL cholesterol < 40 mg/dL for men and < 50 mg/dL
for women
 Blood pressure > 130 mm Hg systolic, or > 85 mm Hg
diastolic
 Fasting blood glucose > 100 mg/dL
Baseline in CATIE study:
 > 40 % had metabolic syndrome
 Men 138 % more likely than matched controls
 Women 251 % more likely than matched controls
Weight gain propensity highest the higher the H-1 and
5HT-2C blockade
Irony that unique effectiveness of clozapine must be
balanced with greatest risks
Behavioral and Psychological Factors in Obesity Treatment
 Eating is a Behavior
 Readiness for Change is a Balance between Motivation and
Resistance
 Change-predisposing attributes (Whitlock et al)
 Strongly want and intend to change for clear, personal reasons
 Face a minimum of obstacles to change
 Have the requisite skills and self-confidence to make a change
 Feel positively about change and believe it will result in meaningful
benefit
 Perceive the change as congruent with self-image and social group
norms
 Receive encouragement and support to change from valued persons
 First-Line Obesity Treatment is Behavioral
 Structure: Weekly, 4-6 months, usually in group
 Goal Setting
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Objective, easily-measured
 Self-Monitoring
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Food records, weight
Highly correlated with successful weight loss
 Stimulus Control
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Change internal and external cues associated with eating and
activity behaviors
 Longer-term treatment: weight loss maintenance skills
 Profound environmental influences to counter
Best Practices in Behavioral and
Psychological Care in Weight Loss Surgery
 Pre-surgical psychosocial evaluation
 20-60% have current Axis I disorders, mood and anxiety
disorders most common; substance use disorders
 Mental Disorders not necessarily contraindication
 Focused on safety and efficacy of WLS
 In more severe disorders, deferral; compliance with
recommendations as predictor of better outcome
 Behavioralist for psychosocial evaluation and pre- and
postoperative support
 Credentials for specialization not fully formalized
Best Practices (Continued)
 Binge-Eating Disorder: Assessment, address as
potential complication to promote best outcomes
 Night-eating syndrome, emotional eating should be
addressed in similar way to BED
 Substance abuse: While prior lifetime prevalence may
be high, current abuse prevalence low
 Exclusion of current abuse/dependence
 Further research
 Psychotropic medications: 70+% lifetime history
 Further research needed on effects of surgery
 Research opportunities: Psychosocial factors,
treatments, and surgical outcomes
From I Greenberg et al, Obesity, 2009
Criteria for Substance Dependence
 Tolerance (Need for more to get same effect)
 Withdrawal (Characteristic syndrome or consumption to
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avoid withdrawal symptoms)
Substance used more or longer than intended
Persistent desire or unsuccessful attempts to cut down
Great amount of time to obtain, use, or recover from effects
Important social, occupational, or recreational activities
given up or reduced because of use
Use continued despite knowledge of having a persistent or
recurrent physical or psychological problem likely caused or
exacerbated by use
Adapted from DSM-IV-TR, American Psychiatric Association
Eating and Obesity: Neurobiology
 Homeostatic Mechanisms: Hypothalamus
 Ventromedial hypothalamus: Satiety
 Lateral hypothalamus: Feeding
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Connected both through neuronal projections and
neuroendocrine mediators
 Leptin and Insulin inhibit feeding
 Reward-based Mechanisms
 Reactive or Immediate reward: Limbic cortex, amygdala,
ventral striatum; Dopamine and the Nucleus Accumbens
 Reflective or Delayed reward: Prefrontal and lateral
orbitofrontal cortex, central striatum
 Eating is driven by both homeostatic and reward-based
mechanisms, in some balance
Reward Systems, Addiction, and Tolerance
 Dopamine neurons of midbrain ventral tegmentum project
to ventral striatum, nucleus accumbens, and also to the
amygdala, limbic cortex (Mesolimbic Dopamine pathway)
 Brain centers of reward, pleasure, “fun,” and reinforcement
 Many natural triggers: Food
 Many drugs of abuse trigger more explosive (and initially
pleasurable) release of dopamine
 Sensitivity, potentiation, reinforcement
 Tolerance: down-regulation of dopamine receptors in NA
occurs in opiate, alcohol, cocaine addictions; also occurs in
overeaters, correlated with increased BMI
Pros and Cons of an Addiction Model for Obesity
Pros
 Neurobiological and Behavioral Similarities
 Perception (by self and others) as Illness, NOT Weakness
 Possible Reduction of Stigma
 Treatment Models (E.g., 12-step model, future
pharmacology, Deep Brain Stimulation)
 Recognition of Role of Environment
 Possible Public Policy Changes, Resource Allocation
Cons
 Food, unlike substances of abuse, is necessary for survival.
 Possible Increase in Stigma
 One size does not fit all. Obesity has diverse causes
(Genetic, medical, environmental, infectious?).