daniel anzia, md chairman, psychiatry advocate lutheran general hospital
TRANSCRIPT
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Psychiatric Aspects of Obesity and Bariatric Surgery
Daniel Anzia, MDChairman, Psychiatry
Advocate Lutheran General Hospital
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Presentation Outline1. Psychiatric Disorders and Obesity
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
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Obesity and Psychiatry
Obesity in Psychiatric Disorders
Primary Eating Disorders
Psychiatric Treatments and Obesity
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Obesity and Psychiatric DisordersDepression
Meta-analysis of cross-sectional co-morbidity (DeWit et al):
Odds of being depressed 18% higher in obese personsGender 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
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Binge-Eating Disorder (Research Criteria)
Recurrent episodes of binge eating, characterized by both:
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: 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
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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
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Psychotropic Medications, Weight, and Obesity
Bipolar Disorder, Mood Stabilizers, and Weight GainLikelihood of being overweight or obese
correlated with number of previous depressive episodes
Lithium, valproate, some antidepressants associated with weight gain Lithium: ¼ to ½ of patients – 5 to 10 % weight gain Valproate: As frequent as with lithium Mirtazepine, paroxetine, tricyclics, trazodone
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Weight gain and AntipsychoticsMeta-analysis: Mean weight gain
Clozapine 9.8 #Olanzapine 9.1 #Risperidone 4.6 #Haloperidol 2.4 #
CATIE study: Greater than 7 % weight gainOlanzapine 30%Quetiapine 16 %Risperidone 14 %Perphenazine 12 %Ziprasidone 7 %
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Risks for weight gain and diabetes
Greatest effect on weight, increased risk of diabetes
Clozapine Olanzapine
Effect on weight, unclear risk for diabetes Quetiapine Risperidone
Small to no effect on weight, without risk for diabetes
Ziprasidone Aripiprazole
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Metabolic Syndrome Three or more of the following:
Waist circumference > 102 cm for men and > 88 cm for women
Fasting triglycerides > 150 mg/dLHDL cholesterol < 40 mg/dL for men and < 50
mg/dL for womenBlood pressure > 130 mm Hg systolic, or > 85
mm Hg diastolicFasting blood glucose > 100 mg/dL
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Baseline in CATIE study:> 40 % had metabolic syndromeMen 138 % more likely than matched controlsWomen 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
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Behavioral and Psychological Factors in Obesity TreatmentEating is a BehaviorReadiness for Change is a Balance between Motivation and
ResistanceChange-predisposing attributes (Whitlock et al)
Strongly want and intend to change for clear, personal reasons
Face a minimum of obstacles to changeHave the requisite skills and self-confidence to make a changeFeel positively about change and believe it will result in
meaningful benefitPerceive the change as congruent with self-image and social
group normsReceive encouragement and support to change from valued
persons
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First-Line Obesity Treatment is BehavioralStructure: Weekly, 4-6 months, usually in groupGoal Setting
Objective, easily-measuredSelf-Monitoring
Food records, weight Highly correlated with successful weight loss
Stimulus Control Change internal and external cues associated with
eating and activity behaviors
Longer-term treatment: weight loss maintenance skillsProfound environmental influences to counter
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Best Practices in Behavioral and Psychological Care in Weight Loss Surgery
Pre-surgical psychosocial evaluation20-60% 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 WLSIn more severe disorders, deferral; compliance
with recommendations as predictor of better outcome
Behavioralist for psychosocial evaluation and pre- and postoperative supportCredentials for specialization not fully
formalized
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Best Practices (Continued)Binge-Eating Disorder: Assessment, address as
potential complication to promote best outcomesNight-eating syndrome, emotional eating should
be addressed in similar way to BEDSubstance abuse: While prior lifetime prevalence
may be high, current abuse prevalence lowExclusion of current abuse/dependenceFurther research
Psychotropic medications: 70+% lifetime historyFurther research needed on effects of surgery
Research opportunities: Psychosocial factors, treatments, and surgical outcomes
From I Greenberg et al, Obesity, 2009
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Criteria for Substance Dependence Tolerance (Need for more to get same effect) Withdrawal (Characteristic syndrome or consumption
to 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
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Eating and Obesity: NeurobiologyHomeostatic Mechanisms: Hypothalamus
Ventromedial hypothalamus: SatietyLateral hypothalamus: Feeding
Connected both through neuronal projections and neuroendocrine mediators
Leptin and Insulin inhibit feedingReward-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
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Reward Systems, Addiction, and ToleranceDopamine 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: FoodMany drugs of abuse trigger more explosive (and
initially pleasurable) release of dopamineSensitivity, potentiation, reinforcement
Tolerance: down-regulation of dopamine receptors in NA occurs in opiate, alcohol, cocaine addictions; also occurs in overeaters, correlated with increased BMI
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Pros and Cons of an Addiction Model for ObesityProsNeurobiological and Behavioral SimilaritiesPerception (by self and others) as Illness, NOT WeaknessPossible Reduction of StigmaTreatment Models (E.g., 12-step model, future
pharmacology, Deep Brain Stimulation)Recognition of Role of EnvironmentPossible Public Policy Changes, Resource AllocationConsFood, unlike substances of abuse, is necessary for
survival.Possible Increase in StigmaOne size does not fit all. Obesity has diverse causes
(Genetic, medical, environmental, infectious?).