Psychiatric Aspects of Obesity and Bariatric Surgery

Daniel Anzia, MDChairman, Psychiatry

Advocate Lutheran General Hospital

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

Obesity and Psychiatry

Obesity in Psychiatric Disorders

Primary Eating Disorders

Psychiatric Treatments and Obesity

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

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

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 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

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 %

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

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

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

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

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

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

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

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

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

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

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?).