Biological Aspects Of Obesity Related Eating Disorders111

1. Biological Aspects of Obesity-Related Eating Disorders: Binge Eating Disorder and the Night Eating Syndrome Allan GeliebterNew York Obesity Research Center St. Luke's and Roosevelt Hospitals Columbia UniversityDivision of Child and Adolescent Psychiatry Grand Rounds Columbia University February 17, 2010

2. ObesityNIGHT EATING SYNDROMEBINGE EATINGDISORDER

3. Marx J. Science, 2003; 299: 846-849.

4. Controls of Food IntakeSignals InitiationTerminationDifferences in BED?

5. 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

6. Binge Eating Disorder (BED) Stomach Capacity

7. Gut peptides (leptin, CCK, ghrelin)

8. Brain Imaging Stomach functions as a food reservoir.

9. Stomach capacity could limit meal intake and influence satiation. Stomach

10. Gastric Capacity Estimated by filling a intragastric balloon with water at 100 ml/min through a tube connected to a pump behind the personbased on maximum volume toleratedbased on volume required to produce a fixed rise in intragastricpressure.

11. Table 1. Characteristics of Overweight Women (M ± SD) No differences by group. BODPODGeliebter A, Gluck ME, Hashim SA. J Nutr 2005;135:1326-30.

14. The two estimates of gastric capacity correlated (r = .60, p = .001) with each other.

15. Test Meal Participants ingested a liquid meal through a straw from a large opaque cooler to prevent visual feedback until extremely full.

17. Test meal intake correlated significantly (r = .42, p = .03) with gastric capacity.

21. Brain Imaging LeptinLeptin 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).HypothesisLeptin would rise to a lesser extent postprandially in BED. CCKCCK, 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).

22. Evidence that postmeal CCK rises less in Bulimia Nervosa (Devlin et al., 1997), perhaps contributing to larger meal intake. HypothesisCCK would also rise to a less post meal in BED. GhrelinGhrelin, is secreted primarily by the stomach and stimulates food intake in animals (Tschöp et al., 2000) and humans (Wren et al., 2001).

23. 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.

24. MethodsAfter 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.

25. Meal was provided at time 0 and consumed at constant rate from graduated beaker in 5 min.

26. 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 peptidehormones, including leptin, CCK, and ghrelin.Meal _________I____I______I______I______I -15 0 5 15 30 60 90 120 min

27. meal

28. meal

29. meal

30. Ghrelin FindingsBED 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

33. Brain Imaging Introduction Only a few studies have employed functional brain imaging underlying binge eating in humans.

34. ParticipantsWomen (n = 20)Geliebter A, Logan M, Ladell T, Schneider T, Sharafi M, Hirsh J. Appetite 2006;46:31-5

36. Visual RunsStimulationBaseline Baseline BingeNon-bingeNon-foods

37. Auditory RunsStimulation Baseline Baseline BingeChocolateCookiesCaramel SundaePepperoniPizzaAcorn SquashIcebergLettuceEnglish CucumbersNon-bingeLooseleafBinderPencil SharpenerLetterOpenerNon-food

38. Individual Analysis (Method 1) The analysis used an fMRI program, which identifies brain activation areas for each individual.

39. Obese NonBinge EaterObese Binge EaterLRLean Binge Eater Lean NonBinge Eater

40. Results and DiscussionThe 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.

41. For 80%, it was in the oral premotor region.

42. It is unlikely that this was due to swallowing as the primary motor area was not activated.

43. 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.

44. Controls of Food IntakeSignals Stomach PeptidesStress HormoneInitiation Ghrelin Cortisol TerminationCapacity CCK, Leptin EmptyingDifferences found in BED

45. Night Eating Syndrome (NES)NES was first described by Stunkard(Stunkard, 1955)

46. Night EatingDescription and Prevalence

47. Psychological factors

48. Stress

49. Sleep Timing

50. Treatment

51. Diagnosis Background Night eating syndrome (NES) is characterized by: morning anorexiaevening hyperphagiasleep disturbancesawakenings from sleep to eat

52. NES Prevalence

53. NSREDNES-+Conscious during eating+-Amnesia after eating+-Associated parasomnias+-Consumption of non-food-+Depressed mood-+Evening hyperphagiaRareModeratePrevalenceNight Eating Syndrome vs. Nocturnal Sleep-Related Eating Disorder

56. Stress

57. Sleep Timing

58. Treatment

59. Diagnosis Subject Characteristics(mean + SD)

60. MethodsFollowing 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

61. weekly nutritional counseling sessions

62. weight recorded weekly5045NESNormalp = .04403530p = .0032520151050DepressionLow Self-Esteem

63. NESNormal504540p = .00535p = .06302520151050HungerFullness

64. Test Meal IntakeNight eaters' test meal intake (979 g +417 SD) did not differ significantly from normals (859 g + 459).

65. However, test meal intake was greater later in the day only for the night eaters (F = 11.1, p = .01).Weight Loss (kg)987p = .0066543210NESNormal

68. Stress

69. Sleep Timing

70. Treatment

71. Diagnosis Stress & Eating DisordersStress plays a role in initiating eating episodes in:--Bulimia Nervosa--Binge Eating DisorderDoes stress also play a role in Night Eating?Stress & Night Eating Onset of NESMany develop NES following life stress (Stunkard, 2002)

72. NES often remits if stress alleviated (Stunkard, 2002)

73. Progressive muscle relaxation improves symptoms of NES (Pawlow et al, 2003)(Allison & Stunkard, 2004)

74. Stress & CortisolCortisol 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).

75. Cortisol may be a potential mediator of stress-induced eating episodes. HPA AxisYehuda R, N Engl J Med, 346; 2002:108-114.

76. Cortisol in Eating DisordersSeveral 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

77. HypothesesNES would have: higher basal levels of cortisol

78. higher cortisol levels following Cold Pressor Test (CPT) less suppression of cortisol after adexamethasone suppression test (DST)

79. MethodsRecruited obese women with and without NES

80. Measured basal plasma cortisol at 8:30 am

81. Measured plasma cortisol at 8:30 am in response to dexamethasone the night before

82. Cold Pressor Test (CPT) at about 12:30 pmGroup Characteristics (M+SD)

83. Basal Cortisolnsg/dL

84. Cortisol Following DSTn.s.g/dl

85. Cold Pressor TestHAND IMMERSIONHANDWITHDRAWAL IIIIIII02 155306045-10 minBlood Draws for Cortisol, Ghrelin, Hunger Ratings

86. Cortisolg/dLMain effect, p<.05Group diff , n.s.Baseline (mean of-10 and 0 min) NE > Norm, p<.05AUC, NE > Norm,p=.02, (n.s. after controlling for baseline.)

87. Ghrelinpg/mLMain effect, p<.05Group diff , n.s.Baseline (mean of-10 and 0 min), n.s.AUC, n.s.

88. HungerMain effect, p<.05Group diff, n.s.Baseline, n.s.AUC, n.s.

89. Controls of Food IntakeSignals Stress HormoneTime Cues Initiation Cortisol Evening/Night TerminationDifferences found in NES

92. Stress

93. Sleep Timing

94. Treatment

95. Diagnosis Timing of Sleep Onset and Offset NES ControlSleep onset time (Lab) 23:38 ± 1:5922:52 ± 1:04Sleep onset time (home) 23:57 ± 1:3323:32 ±1:06Sleep offset time (Lab) 7:04 ± 0:48 7:06 ± 0:41Sleep offset time (home) 7:35 ± 1:11 6:59± 1:12NES 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).

96. Food IntakeNES > ControlsInpatient 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)

99. Stress

100. Sleep Timing

101. Treatment

102. Diagnosis Randomized Controlled Trial of SertralinePatients randomized to sertraline(n=17)or placebo (n = 17) for 8 weeks.O’Reardon et al., 2006

103. Night Eating Symptom Scale

104. Nocturnal ingestions/week

105. % Caloric Intake after Dinner

106. Weight change

107. DiscussionNES – altered circadian food intake SSRIs could be acting on the SCN to synchronize food intake and sleep-wake cycle rhythms

108. SSRIs may also act to control the compulsion to eat as they do in BN & BEDControlNES Lundgren et al., 2008

109. Behavioral TreatmentNo Formal Studies Useful StrategiesReduce triggers, e.g., stress that induce eating

110. Keep tempting foods out of reach

111. Increase breakfast consumptionRecommended ManualOvercoming Night Eating Syndrome Kelly Allison, Albert Stunkard, Sarah TierNew Harbinger, 2004

114. Stress

115. Sleep Timing

116. Treatment

117. 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 weekII. 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

118. AcknowledgementsCo-InvestigatorsMarci Gluck, Sami Hashim, Eric Yahav, Dennis Gage, Joy Hirsch, Susan CarnellResourcesNY Obesity Research Center provided hormone assays and body compositionmeasurements Grant SupportNIH Grants RO1 DK 554318, R01 DK074046, R03 DK068392, and MO1 RR0064529

Biological Aspects Of Obesity Related Eating Disorders111

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Biological Aspects Of Obesity Related Eating Disorders111