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    Biological Aspects Of Obesity Related Eating Disorders111 Biological Aspects Of Obesity Related Eating Disorders111 Presentation Transcript

    • Biological Aspects of Obesity-Related Eating Disorders: Binge Eating Disorder and the Night Eating Syndrome
      Allan Geliebter
      New York Obesity Research Center
      St. Luke's and Roosevelt Hospitals
      Columbia University
      Division of Child and Adolescent Psychiatry
      Grand Rounds
      Columbia University
      February 17, 2010
    • Obesity
      NIGHT EATING
      SYNDROME
      BINGE EATING
      DISORDER
    • Marx J. Science, 2003; 299: 846-849.
    • Controls of Food Intake
      Signals
      Initiation
      Termination
      Differences in BED?
    • Main Criteria for Binge Eating Disorder (BED)
      Recurrent episodes of binge eating 2 days/wk for 6 mos.
      objectively large amount of food in a discrete time period (2 hours)
      sense of loss of control
      without purging afterwards
    • Binge Eating Disorder (BED)
      • Stomach Capacity
      • Gut peptides (leptin, CCK, ghrelin)
      • Brain Imaging
      • Stomach functions as a food reservoir.
      • Stomach capacity could limit meal intake
      and influence satiation.
      Stomach
    • Gastric Capacity
      Estimated by filling a intragastric balloon with water at 100 ml/min through a tube connected to a pump behind the person
      based on maximum volume tolerated
      based on volume required to produce a
      fixed rise in intragastricpressure.
    • Table 1. Characteristics of Overweight Women (M ± SD)
      No differences by group.
      BODPOD
      Geliebter A, Gluck ME, Hashim SA. J Nutr 2005;135:1326-30.
    • *
    • *
    • The two estimates of gastric capacity correlated (r = .60, p = .001) with each other.
    • Test Meal
      Participants ingested a liquid meal through a straw from a large opaque cooler to prevent visual feedback until extremely full.
    • Test meal intake correlated significantly
      (r = .42, p = .03) with gastric capacity.
    • Binge Eating Disorder (BED)
      • Stomach Capacity
      • Gut peptides (leptin, CCK, ghrelin)
      • Brain Imaging
    • Leptin
      • Leptin is secreted primarily by adipose tissue and rises slowly after meals. Leptin administration decreases food intake and weight in animals (Zhang et al., 1994) and modestly inhumans (Heymsfieldet al., 1999).
      Hypothesis
      • Leptin would rise to a lesser extent postprandially in BED.
    • CCK
      • CCK, is secreted primarily by the duodenum, and rises after meals. CCK administration decreases food intake in animals (Gibbs et al., 1973) and humans (Kissileff et al., 1981).
      • Evidence that postmeal CCK rises less in Bulimia Nervosa (Devlin et al., 1997), perhaps contributing to larger meal intake.
      Hypothesis
      • CCK would also rise to a less post meal in BED.
    • Ghrelin
      • Ghrelin, is secreted primarily by the stomach and stimulates food intake in animals (Tschöp et al., 2000) and humans (Wren et al., 2001).
      • Ghrelin is elevated before meals and falls afterwards (Cummings et al, 2002), unlike other peripheral appetite hormones, which rise after meals.
      Hypothesis
      Obese individuals with BED would have high ghrelin levels given their excess meal intake.
    • Methods
      • After a 12 h overnight fast, an intravenous catheter was inserted at 8 am. Subjects rested for 15 minutes before first blood draw at -15 min.
      • Meal was provided at time 0 and consumed at constant rate from graduated beaker in 5 min.
      • The breakfast liquid test meal (600 ml diluted Boost) provided 1254 kJ (300 kcal): 24% protein (19 g), 55% carbohydrate (41 g, including 20 g sugar), and 21% fat (6 g).
    • Methods (cont’)
      Blood samples were assayed for several peptide
      hormones, including leptin, CCK, and ghrelin.
      Meal
      _________I____I______I______I______I
      -15 0 5 15 30 60 90 120
      min
    • meal
    • meal
    • meal
    • Ghrelin Findings
      BED S’s had lower fasting ghrelin levels than non-BED S’s, contrary to hypothesis.
      In BED S’s, ghrelin levels declined less after meal.
      Results extend and are consistent with findings of lower ghrelin levels in obese individuals.
      Ghrelin may be down-regulated in obese BED S’s due to overeating possibly via stomach capacity.
      Geliebter A, Gluck ME, Hashim SA. J Nutr 2005;135:1326-30
    • Binge Eating Disorder (BED)
      • Stomach Capacity
      • Gut peptides (leptin, CCK, ghrelin)
      • Brain Imaging
    • Introduction
      Only a few studies have employed functional brain imaging underlying binge eating in humans.
    • Participants
      Women (n = 20)
      Geliebter A, Logan M, Ladell T, Schneider T, Sharafi M, Hirsh J. Appetite 2006;46:31-5
    • Visual Runs
      Stimulation
      Baseline
      Baseline
      Binge
      Non-binge
      Non-foods
    • Auditory Runs
      Stimulation
      Baseline
      Baseline
      Binge
      Chocolate
      Cookies
      Caramel
      Sundae
      Pepperoni
      Pizza
      Acorn
      Squash
      Iceberg
      Lettuce
      English
      Cucumbers
      Non-binge
      Looseleaf
      Binder
      Pencil
      Sharpener
      Letter
      Opener
      Non-food
    • Individual Analysis (Method 1)
      The analysis used an fMRI program, which identifies brain activation areas for each individual.
    • Obese NonBinge Eater
      Obese Binge Eater
      L
      R
      Lean Binge Eater
      Lean NonBinge Eater
    • Results and Discussion
      • The only brain area activated for all members of a group was the premotor area in the obese binge eaters in response to the binge type foods.
      • For 80%, it was in the oral premotor region.
      • It is unlikely that this was due to swallowing as the primary motor area was not activated.
      • The premotor area is involved in planning of motor behavior, and may reflect thoughts about ingesting the binge type foods.
    • Groups Analysis (Method 2)
      Another analysis underway is with Statistical Parametric Mapping (SPM), which combines brains from subjects in a group and maps to a reference brain.
    • Controls of Food Intake
      Signals Stomach PeptidesStress Hormone
      Initiation Ghrelin Cortisol
      TerminationCapacity CCK, Leptin
      Emptying
      Differences found in BED
    • Night Eating Syndrome (NES)
      NES was first described by Stunkard(Stunkard, 1955)
    • Night Eating
      • Description and Prevalence
      • Psychological factors
      • Stress
      • Sleep Timing
      • Treatment
      • Diagnosis
    • Background
      Night eating syndrome (NES) is characterized by:
      morning anorexia
      evening hyperphagia
      sleep disturbances
      awakenings from sleep to eat
    • NES Prevalence
    • NSRED
      NES
      -
      +
      Conscious during eating
      +
      -
      Amnesia after eating
      +
      -
      Associated parasomnias
      +
      -
      Consumption of non-food
      -
      +
      Depressed mood
      -
      +
      Evening hyperphagia
      Rare
      Moderate
      Prevalence
      Night Eating Syndrome vs. Nocturnal Sleep-Related Eating Disorder
    • Night Eating
      • Description and Prevalence
      • Psychological factors
      • Stress
      • Sleep Timing
      • Treatment
      • Diagnosis
    • Subject Characteristics(mean + SD)
    • Methods
      • Following 8 h fast, participants completed psychological scales:
      --ZungDepression Self-Rating Scale (Zung, 1965)
      --Rosenberg Self-Esteem Scale (Rosenberg, 1966)
      --Night Eating Diagnostic Questionnaire (Gluck et al., 2001)
      • They then completed ratings of hunger & fullness and ingested a liquid meal until extremely full.
    • Methods (cont’)
      They then began the weight loss program:
      • 900 kcal, liquid formula diet
      • weekly nutritional counseling sessions
      • weight recorded weekly
    • 50
      45
      NES
      Normal
      p = .04
      40
      35
      30
      p = .003
      25
      20
      15
      10
      5
      0
      Depression
      Low Self-Esteem
    • NES
      Normal
      50
      45
      40
      p = .005
      35
      p = .06
      30
      25
      20
      15
      10
      5
      0
      Hunger
      Fullness
    • Test Meal Intake
      • Night eaters' test meal intake (979 g +417 SD) did not differ significantly from normals (859 g + 459).
      • However, test meal intake was greater later in the day only for the night eaters (F = 11.1, p = .01).
    • Weight Loss (kg)
      9
      8
      7
      p = .006
      6
      5
      4
      3
      2
      1
      0
      NES
      Normal
    • Night Eating
      • Description and Prevalence
      • Psychological factors
      • Stress
      • Sleep Timing
      • Treatment
      • Diagnosis
    • Stress & Eating Disorders
      • Stress plays a role in initiating eating episodes in:
      --Bulimia Nervosa
      --Binge Eating Disorder
      • Does stress also play a role in Night Eating?
    • Stress & Night Eating
      Onset of NES
      • Many develop NES following life stress (Stunkard, 2002)
      • NES often remits if stress alleviated (Stunkard, 2002)
      • Progressive muscle relaxation improves symptoms of NES (Pawlow et al, 2003)
      (Allison & Stunkard, 2004)
    • Stress & Cortisol
      • Cortisol secretion by adrenal gland is a major component of the stress response
      (Ur, 1991).
      • Glucocorticoids can increase food intake & body weight in rats (Dallman et al., 2003)and humans(Tataranni et al., 1996).
      • Cortisol may be a potential mediator of stress-induced eating episodes.
    • HPA Axis
      Yehuda R, N Engl J Med, 346; 2002:108-114.
    • Cortisol in Eating Disorders
      • Several studies have examined cortisol in eating disorders after a laboratory stressor:
      --Exaggerated plasma cortisol response in AN (Abell et al, 1987), BN (Koo-Loeb et al, 2000), and BED (Gluck et al., 2004)
      --Higher 24-h urinary cortisol following a stressor in BN (Koo-Loeb et al, 2000)
      • No studies have examined:
      --cortisol in response to laboratory stress in NES
      --or ghrelin, which has recently been shown to increase in response to a laboratory stressor
    • Hypotheses
      NES would have:
      • higher basal levels of cortisol
      • higher cortisol levels following
      Cold Pressor Test (CPT)
      • less suppression of cortisol after a
      dexamethasone suppression test (DST)
    • Methods
      • Recruited obese women with and without NES
      • Measured basal plasma cortisol at 8:30 am
      • Measured plasma cortisol at 8:30 am in response to dexamethasone the night before
      • Cold Pressor Test (CPT) at about 12:30 pm
    • Group Characteristics (M+SD)
    • Basal Cortisol
      ns
      g/dL
    • Cortisol Following DST
      n.s.
      g/dl
    • Cold Pressor Test
      HAND IMMERSION
      HAND
      WITHDRAWAL
      I
      I
      I
      I
      I
      I
      I
      0
      2
      15
      5
      30
      60
      45
      -10 min
      Blood Draws for Cortisol, Ghrelin, Hunger Ratings
    • Cortisol
      g/dL
      Main effect, p<.05
      Group diff , n.s.
      Baseline (mean of
      -10 and 0 min) NE > Norm, p<.05
      AUC, NE > Norm,p=.02, (n.s. after controlling for baseline.)
    • Ghrelin
      pg/mL
      Main effect, p<.05
      Group diff , n.s.
      Baseline (mean of
      -10 and 0 min), n.s.
      AUC, n.s.
    • Hunger
      Main effect, p<.05
      Group diff, n.s.
      Baseline, n.s.
      AUC, n.s.
    • Controls of Food Intake
      Signals Stress HormoneTime Cues
      Initiation Cortisol Evening/Night
      Termination
      Differences found in NES
    • Night Eating
      • Description and Prevalence
      • Psychological factors
      • Stress
      • Sleep Timing
      • Treatment
      • Diagnosis
    • Timing of Sleep Onset and Offset
      NES Control
      Sleep onset time (Lab) 23:38 ± 1:5922:52 ± 1:04
      Sleep onset time (home) 23:57 ± 1:3323:32 ±1:06
      Sleep offset time (Lab) 7:04 ± 0:48 7:06 ± 0:41
      Sleep offset time (home) 7:35 ± 1:11 6:59± 1:12
      NES and Control Ss did not differ in sleep periods in the laboratory (Rogers et al., 2006 ) or at home (diary and actigraphy) (O ’Reardon et al., 2004).
    • Food Intake
      NES > Controls
      Inpatient study reflects night eating (20 h- 08 h) in NES subjects (Allison et al,. 2005)
      Outpatient study shows shifted calorie intake curve in NES (O’Reardon et al., 2004)
    • Night Eating
      • Description and Prevalence
      • Psychological factors
      • Stress
      • Sleep Timing
      • Treatment
      • Diagnosis
    • Randomized Controlled Trial of Sertraline
      Patients randomized to sertraline(n=17)
      or placebo (n = 17) for 8 weeks.
      O’Reardon et al., 2006
    • Night Eating Symptom Scale
    • Nocturnal ingestions/week
    • % Caloric Intake after Dinner
    • Weight change
    • Discussion
      NES – altered circadian food intake
      • SSRIs could be acting on the SCN to synchronize food intake and sleep-wake cycle rhythms
      • SSRIs may also act to control the compulsion to eat as they do in BN & BED
    • Control
      NES
      Lundgren et al., 2008
    • Behavioral Treatment
      No Formal Studies
      Useful Strategies
      • Reduce triggers, e.g., stress that induce eating
      • Keep tempting foods out of reach
      • Increase breakfast consumption
      Recommended Manual
      Overcoming Night Eating Syndrome
      Kelly Allison, Albert Stunkard, Sarah Tier
      New Harbinger, 2004
    • Night Eating
      • Description and Prevalence
      • Psychological factors
      • Stress
      • Sleep Timing
      • Treatment
      • Diagnosis
    • Proposed Research Diagnostic Criteria for NES(First International Night Eating Symposium, April 26, 2008, Minneapolis, MN)
      I.    The daily pattern of eating demonstrates a significantly increased intake in the
      evening and/or nighttime, as manifested by one or both of the following:
      A. > 25% of food consumed after the evening meal
      B. > 2 episodes of nocturnal eating per week
      II. Awareness and recall of evening and nocturnal eating episodes 
      III.  > 3 of the following:
      A. Lack of desire to eat in the morning and/or breakfast is omitted on four or more
      mornings per week
      B. Presence of a strong urge to eat between dinner and sleep onset and/or during
      the night
      C. Sleep onset and/or sleep maintenance insomnia are present four or more nights
      per week
      D. Presence of a belief that one must eat in order to initiate or return to sleep
      E. Mood is frequently depressed and/or mood worsens in the evening
      IV.  The disorder is associated with significant distress and/or impairment in functioning.
      V.   The disordered pattern of eating has been maintained for at least 3 months.
      VI.  The disorder is not secondary to substance abuse or dependence, medical disorder,
      medication, or another psychiatric disorder.
      Allison et al, 2009
    • Acknowledgements
      Co-Investigators
      Marci Gluck, Sami Hashim, Eric Yahav, Dennis Gage, Joy Hirsch, Susan Carnell
      Resources
      NY Obesity Research Center provided hormone assays and body composition
      measurements
      Grant Support
      NIH Grants RO1 DK 554318, R01 DK074046, R03 DK068392, and MO1 RR0064529