Biological Aspects of Obesity-Related Eating Disorders: Binge Eating Disorder and the Night Eating Syndrome <br />Allan Ge...
Obesity<br />NIGHT EATING <br /> SYNDROME<br />BINGE EATING<br />DISORDER<br />
Marx J.   Science, 2003; 299: 846-849. <br />
Controls of Food Intake<br />Signals   <br />Initiation<br />Termination<br />Differences in BED? <br />
Main Criteria for Binge Eating Disorder (BED)<br />   Recurrent episodes of binge eating 2 days/wk for 6 mos.<br />objecti...
Binge Eating Disorder (BED) <br /><ul><li>Stomach Capacity
Gut peptides (leptin, CCK, ghrelin)
Brain Imaging </li></li></ul><li><ul><li>Stomach functions as a food reservoir.
 Stomach capacity could limit meal intake </li></ul>and influence satiation.  	<br />Stomach<br />
Gastric Capacity<br />     Estimated by filling a intragastric balloon with water at 100 ml/min through a tube connected t...
Table 1.   Characteristics of Overweight Women   (M ± SD)<br />   No differences by group. <br />BODPOD<br />Geliebter A, ...
*<br />
*<br />
The two estimates of gastric capacity correlated (r = .60, p = .001) with each other. <br />
   Test Meal <br />Participants ingested a liquid meal through a straw from a large opaque cooler to prevent visual feedba...
Test meal intake correlated significantly <br />   (r = .42, p = .03) with gastric capacity. <br />
Binge Eating Disorder (BED) <br /><ul><li>Stomach Capacity
Gut peptides (leptin, CCK, ghrelin)
Brain Imaging </li></li></ul><li>Leptin<br /><ul><li>Leptin is secreted primarily by adipose tissue and rises slowly after...
Evidence that postmeal CCK rises less in Bulimia Nervosa  (Devlin et al., 1997), perhaps contributing to larger meal intak...
Ghrelin is elevated before meals and falls afterwards (Cummings et al, 2002), unlike other peripheral appetite hormones, w...
Methods<br /><ul><li>After a 12 h overnight fast, an intravenous catheter  was inserted at 8 am. Subjects rested for 15 mi...
 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 ...
meal<br />
meal<br />
meal<br />
Ghrelin Findings<br />BED S’s had lower fasting ghrelin levels than non-BED S’s, contrary to hypothesis. <br />In BED S’s,...
Binge Eating Disorder (BED) <br /><ul><li>Stomach Capacity
Gut peptides (leptin, CCK, ghrelin)
Brain Imaging </li></li></ul><li>Introduction<br />   Only a few studies have employed functional brain imaging underlying...
Participants<br />Women (n = 20)<br />Geliebter A, Logan M, Ladell T, Schneider T, Sharafi M, Hirsh J. Appetite 2006;46:31...
Visual Runs<br />Stimulation<br />Baseline <br />Baseline      <br />Binge<br />Non-binge<br />Non-foods<br />
Auditory Runs<br />Stimulation <br />Baseline <br />Baseline <br />Binge<br />Chocolate<br />Cookies<br />Caramel <br />Su...
Individual Analysis (Method 1)<br />   The analysis used an fMRI program, which identifies brain activation areas for each...
Obese NonBinge Eater<br />Obese Binge Eater<br />L<br />R<br />Lean Binge Eater <br /> Lean NonBinge Eater<br />
Results and Discussion<br /><ul><li>The only brain area activated for all members of a group was the premotor area in the ...
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...
Controls of Food Intake<br />Signals  Stomach PeptidesStress Hormone<br />Initiation Ghrelin    Cortisol              <br ...
Night Eating Syndrome (NES)<br />NES was first described by Stunkard(Stunkard, 1955)<br />
Night Eating<br /><ul><li>Description and Prevalence
Psychological factors
Stress
Sleep Timing
Treatment
Diagnosis </li></li></ul><li>Background<br />  Night eating syndrome (NES) is characterized by: <br />morning anorexia<br ...
NES Prevalence<br />
NSRED<br />NES<br />-<br />+<br />Conscious during eating<br />+<br />-<br />Amnesia after eating<br />+<br />-<br />Assoc...
Night Eating<br /><ul><li>Description and Prevalence
Psychological factors
Stress
Sleep Timing
Treatment
Diagnosis </li></li></ul><li>Subject Characteristics(mean + SD)<br />
Methods<br /><ul><li>Following 8 h fast, participants completed psychological scales:</li></ul>--ZungDepression Self-Ratin...
weekly nutritional counseling sessions
weight recorded weekly</li></li></ul><li>50<br />45<br />NES<br />Normal<br />p = .04<br />40<br />35<br />30<br />p = .00...
NES<br />Normal<br />50<br />45<br />40<br />p = .005<br />35<br />p = .06<br />30<br />25<br />20<br />15<br />10<br />5<...
Test Meal Intake<br /><ul><li>Night eaters' test meal intake (979 g +417 SD) did not differ significantly from normals (85...
However, test meal intake was greater later in the day only for the night eaters (F = 11.1, p = .01).</li></li></ul><li>We...
Night Eating<br /><ul><li>Description and Prevalence
Psychological factors
Stress
Sleep Timing
Treatment
Diagnosis </li></li></ul><li>Stress & Eating Disorders<br /><ul><li>Stress plays a role in initiating eating episodes in:<...
NES often remits if stress alleviated (Stunkard, 2002)
Progressive muscle relaxation improves symptoms of NES           (Pawlow et al, 2003)</li></ul>(Allison & Stunkard, 2004)<...
Stress & Cortisol<br /><ul><li>Cortisol secretion by adrenal gland is a major component of the stress response </li></ul> ...
Cortisol may be a potential mediator of stress-induced eating episodes.</li></li></ul><li> HPA Axis<br />Yehuda R,  N Engl...
Cortisol in Eating Disorders<br /><ul><li>Several studies have examined cortisol in eating disorders after a laboratory st...
             Hypotheses<br />NES would have:<br /><ul><li>  higher basal levels of cortisol
 higher cortisol levels following </li></ul>Cold Pressor Test (CPT)<br /><ul><li> less suppression of cortisol after a</li...
Methods<br /><ul><li>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
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Biological Aspects Of Obesity Related Eating Disorders111

  1. 1. Biological Aspects of Obesity-Related Eating Disorders: Binge Eating Disorder and the Night Eating Syndrome <br />Allan Geliebter<br />New York Obesity Research Center <br /> St. Luke's and Roosevelt Hospitals <br />Columbia University<br />Division of Child and Adolescent Psychiatry <br /> Grand Rounds<br /> Columbia University <br /> February 17, 2010<br />
  2. 2. Obesity<br />NIGHT EATING <br /> SYNDROME<br />BINGE EATING<br />DISORDER<br />
  3. 3. Marx J. Science, 2003; 299: 846-849. <br />
  4. 4. Controls of Food Intake<br />Signals <br />Initiation<br />Termination<br />Differences in BED? <br />
  5. 5. Main Criteria for Binge Eating Disorder (BED)<br /> Recurrent episodes of binge eating 2 days/wk for 6 mos.<br />objectively large amount of food in a discrete time period (2 hours)<br />sense of loss of control <br />without purging afterwards<br />
  6. 6. Binge Eating Disorder (BED) <br /><ul><li>Stomach Capacity
  7. 7. Gut peptides (leptin, CCK, ghrelin)
  8. 8. Brain Imaging </li></li></ul><li><ul><li>Stomach functions as a food reservoir.
  9. 9. Stomach capacity could limit meal intake </li></ul>and influence satiation. <br />Stomach<br />
  10. 10. Gastric Capacity<br /> Estimated by filling a intragastric balloon with water at 100 ml/min through a tube connected to a pump behind the person<br />based on maximum volume tolerated<br />based on volume required to produce a <br /> fixed rise in intragastricpressure.<br />
  11. 11. Table 1. Characteristics of Overweight Women (M ± SD)<br /> No differences by group. <br />BODPOD<br />Geliebter A, Gluck ME, Hashim SA. J Nutr 2005;135:1326-30.<br />
  12. 12. *<br />
  13. 13. *<br />
  14. 14. The two estimates of gastric capacity correlated (r = .60, p = .001) with each other. <br />
  15. 15. Test Meal <br />Participants ingested a liquid meal through a straw from a large opaque cooler to prevent visual feedback until extremely full.<br />
  16. 16.
  17. 17. Test meal intake correlated significantly <br /> (r = .42, p = .03) with gastric capacity. <br />
  18. 18.
  19. 19. Binge Eating Disorder (BED) <br /><ul><li>Stomach Capacity
  20. 20. Gut peptides (leptin, CCK, ghrelin)
  21. 21. Brain Imaging </li></li></ul><li>Leptin<br /><ul><li>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).</li></ul>Hypothesis<br /><ul><li>Leptin would rise to a lesser extent postprandially in BED. </li></li></ul><li>CCK<br /><ul><li>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).
  22. 22. Evidence that postmeal CCK rises less in Bulimia Nervosa (Devlin et al., 1997), perhaps contributing to larger meal intake. </li></ul>Hypothesis<br /><ul><li>CCK would also rise to a less post meal in BED. </li></li></ul><li>Ghrelin<br /><ul><li>Ghrelin, is secreted primarily by the stomach and stimulates food intake in animals (Tschöp et al., 2000) and humans (Wren et al., 2001).
  23. 23. Ghrelin is elevated before meals and falls afterwards (Cummings et al, 2002), unlike other peripheral appetite hormones, which rise after meals. </li></ul>Hypothesis<br /> Obese individuals with BED would have high ghrelin levels given their excess meal intake. <br />
  24. 24. Methods<br /><ul><li>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.
  25. 25. Meal was provided at time 0 and consumed at constant rate from graduated beaker in 5 min.
  26. 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).</li></li></ul><li>Methods (cont’)<br />Blood samples were assayed for several peptide<br />hormones, including leptin, CCK, and ghrelin.<br />Meal <br />_________I____I______I______I______I <br />-15 0 5 15 30 60 90 120 <br />min<br />
  27. 27. meal<br />
  28. 28. meal<br />
  29. 29. meal<br />
  30. 30. Ghrelin Findings<br />BED S’s had lower fasting ghrelin levels than non-BED S’s, contrary to hypothesis. <br />In BED S’s, ghrelin levels declined less after meal.<br />Results extend and are consistent with findings of lower ghrelin levels in obese individuals.<br />Ghrelin may be down-regulated in obese BED S’s due to overeating possibly via stomach capacity.<br />Geliebter A, Gluck ME, Hashim SA. J Nutr 2005;135:1326-30<br />
  31. 31. Binge Eating Disorder (BED) <br /><ul><li>Stomach Capacity
  32. 32. Gut peptides (leptin, CCK, ghrelin)
  33. 33. Brain Imaging </li></li></ul><li>Introduction<br /> Only a few studies have employed functional brain imaging underlying binge eating in humans.<br />
  34. 34. Participants<br />Women (n = 20)<br />Geliebter A, Logan M, Ladell T, Schneider T, Sharafi M, Hirsh J. Appetite 2006;46:31-5<br />
  35. 35.
  36. 36. Visual Runs<br />Stimulation<br />Baseline <br />Baseline <br />Binge<br />Non-binge<br />Non-foods<br />
  37. 37. Auditory Runs<br />Stimulation <br />Baseline <br />Baseline <br />Binge<br />Chocolate<br />Cookies<br />Caramel <br />Sundae<br />Pepperoni<br />Pizza<br />Acorn <br />Squash<br />Iceberg<br />Lettuce<br />English <br />Cucumbers<br />Non-binge<br />Looseleaf<br />Binder<br />Pencil <br />Sharpener<br />Letter<br />Opener<br />Non-food<br />
  38. 38. Individual Analysis (Method 1)<br /> The analysis used an fMRI program, which identifies brain activation areas for each individual.<br />
  39. 39. Obese NonBinge Eater<br />Obese Binge Eater<br />L<br />R<br />Lean Binge Eater <br /> Lean NonBinge Eater<br />
  40. 40. Results and Discussion<br /><ul><li>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.
  41. 41. For 80%, it was in the oral premotor region.
  42. 42. It is unlikely that this was due to swallowing as the primary motor area was not activated.
  43. 43. The premotor area is involved in planning of motor behavior, and may reflect thoughts about ingesting the binge type foods. </li></li></ul><li>Groups Analysis (Method 2)<br /> Another analysis underway is with Statistical Parametric Mapping (SPM), which combines brains from subjects in a group and maps to a reference brain.<br />
  44. 44. Controls of Food Intake<br />Signals Stomach PeptidesStress Hormone<br />Initiation Ghrelin Cortisol <br />TerminationCapacity CCK, Leptin <br />Emptying<br />Differences found in BED <br />
  45. 45. Night Eating Syndrome (NES)<br />NES was first described by Stunkard(Stunkard, 1955)<br />
  46. 46. Night Eating<br /><ul><li>Description and Prevalence
  47. 47. Psychological factors
  48. 48. Stress
  49. 49. Sleep Timing
  50. 50. Treatment
  51. 51. Diagnosis </li></li></ul><li>Background<br /> Night eating syndrome (NES) is characterized by: <br />morning anorexia<br />evening hyperphagia<br />sleep disturbances<br />awakenings from sleep to eat<br />
  52. 52. NES Prevalence<br />
  53. 53. NSRED<br />NES<br />-<br />+<br />Conscious during eating<br />+<br />-<br />Amnesia after eating<br />+<br />-<br />Associated parasomnias<br />+<br />-<br />Consumption of non-food<br />-<br />+<br />Depressed mood<br />-<br />+<br />Evening hyperphagia<br />Rare<br />Moderate<br />Prevalence<br />Night Eating Syndrome vs. Nocturnal Sleep-Related Eating Disorder<br />
  54. 54. Night Eating<br /><ul><li>Description and Prevalence
  55. 55. Psychological factors
  56. 56. Stress
  57. 57. Sleep Timing
  58. 58. Treatment
  59. 59. Diagnosis </li></li></ul><li>Subject Characteristics(mean + SD)<br />
  60. 60. Methods<br /><ul><li>Following 8 h fast, participants completed psychological scales:</li></ul>--ZungDepression Self-Rating Scale (Zung, 1965)<br />--Rosenberg Self-Esteem Scale (Rosenberg, 1966) <br />--Night Eating Diagnostic Questionnaire (Gluck et al., 2001) <br /><ul><li>They then completed ratings of hunger & fullness and ingested a liquid meal until extremely full.</li></li></ul><li>Methods (cont’)<br /> They then began the weight loss program:<br /><ul><li>900 kcal, liquid formula diet
  61. 61. weekly nutritional counseling sessions
  62. 62. weight recorded weekly</li></li></ul><li>50<br />45<br />NES<br />Normal<br />p = .04<br />40<br />35<br />30<br />p = .003<br />25<br />20<br />15<br />10<br />5<br />0<br />Depression<br />Low Self-Esteem<br />
  63. 63. NES<br />Normal<br />50<br />45<br />40<br />p = .005<br />35<br />p = .06<br />30<br />25<br />20<br />15<br />10<br />5<br />0<br />Hunger<br />Fullness<br />
  64. 64. Test Meal Intake<br /><ul><li>Night eaters' test meal intake (979 g +417 SD) did not differ significantly from normals (859 g + 459).
  65. 65. However, test meal intake was greater later in the day only for the night eaters (F = 11.1, p = .01).</li></li></ul><li>Weight Loss (kg)<br />9<br />8<br />7<br />p = .006<br />6<br />5<br />4<br />3<br />2<br />1<br />0<br />NES<br />Normal<br />
  66. 66. Night Eating<br /><ul><li>Description and Prevalence
  67. 67. Psychological factors
  68. 68. Stress
  69. 69. Sleep Timing
  70. 70. Treatment
  71. 71. Diagnosis </li></li></ul><li>Stress & Eating Disorders<br /><ul><li>Stress plays a role in initiating eating episodes in:</li></ul>--Bulimia Nervosa<br />--Binge Eating Disorder<br /><ul><li>Does stress also play a role in Night Eating?</li></li></ul><li>Stress & Night Eating<br /> Onset of NES<br /><ul><li>Many develop NES following life stress (Stunkard, 2002)
  72. 72. NES often remits if stress alleviated (Stunkard, 2002)
  73. 73. Progressive muscle relaxation improves symptoms of NES (Pawlow et al, 2003)</li></ul>(Allison & Stunkard, 2004)<br />
  74. 74. Stress & Cortisol<br /><ul><li>Cortisol secretion by adrenal gland is a major component of the stress response </li></ul> (Ur, 1991).<br /><ul><li>Glucocorticoids can increase food intake & body weight in rats (Dallman et al., 2003)and humans(Tataranni et al., 1996).
  75. 75. Cortisol may be a potential mediator of stress-induced eating episodes.</li></li></ul><li> HPA Axis<br />Yehuda R, N Engl J Med, 346; 2002:108-114.<br />
  76. 76. Cortisol in Eating Disorders<br /><ul><li>Several studies have examined cortisol in eating disorders after a laboratory stressor:</li></ul>--Exaggerated plasma cortisol response in AN (Abell et al, 1987), BN (Koo-Loeb et al, 2000), and BED (Gluck et al., 2004) <br />--Higher 24-h urinary cortisol following a stressor in BN (Koo-Loeb et al, 2000)<br /><ul><li>No studies have examined:</li></ul>--cortisol in response to laboratory stress in NES<br />--or ghrelin, which has recently been shown to increase in response to a laboratory stressor <br />
  77. 77. Hypotheses<br />NES would have:<br /><ul><li> higher basal levels of cortisol
  78. 78. higher cortisol levels following </li></ul>Cold Pressor Test (CPT)<br /><ul><li> less suppression of cortisol after a</li></ul>dexamethasone suppression test (DST)<br />
  79. 79. Methods<br /><ul><li>Recruited obese women with and without NES
  80. 80. Measured basal plasma cortisol at 8:30 am
  81. 81. Measured plasma cortisol at 8:30 am in response to dexamethasone the night before
  82. 82. Cold Pressor Test (CPT) at about 12:30 pm</li></li></ul><li>Group Characteristics (M+SD)<br />
  83. 83. Basal Cortisol<br />ns<br />g/dL<br />
  84. 84. Cortisol Following DST<br />n.s.<br />g/dl<br />
  85. 85. Cold Pressor Test<br />HAND IMMERSION<br />HAND<br />WITHDRAWAL<br /> I<br />I<br />I<br />I<br />I<br />I<br />I<br />0<br />2 <br />15<br />5<br />30<br />60<br />45<br />-10 min<br />Blood Draws for Cortisol, Ghrelin, Hunger Ratings<br />
  86. 86. Cortisol<br />g/dL<br />Main effect, p<.05<br />Group diff , n.s.<br />Baseline (mean of<br />-10 and 0 min) NE > Norm, p<.05<br />AUC, NE > Norm,p=.02, (n.s. after controlling for baseline.)<br />
  87. 87. Ghrelin<br />pg/mL<br />Main effect, p<.05<br />Group diff , n.s.<br />Baseline (mean of<br />-10 and 0 min), n.s.<br />AUC, n.s.<br />
  88. 88. Hunger<br />Main effect, p<.05<br />Group diff, n.s.<br />Baseline, n.s.<br />AUC, n.s.<br />
  89. 89. Controls of Food Intake<br />Signals Stress HormoneTime Cues <br />Initiation Cortisol Evening/Night <br />Termination<br />Differences found in NES <br />
  90. 90. Night Eating<br /><ul><li>Description and Prevalence
  91. 91. Psychological factors
  92. 92. Stress
  93. 93. Sleep Timing
  94. 94. Treatment
  95. 95. Diagnosis </li></li></ul><li>Timing of Sleep Onset and Offset <br />NES Control<br />Sleep onset time (Lab) 23:38 ± 1:5922:52 ± 1:04<br />Sleep onset time (home) 23:57 ± 1:3323:32 ±1:06<br />Sleep offset time (Lab) 7:04 ± 0:48 7:06 ± 0:41<br />Sleep offset time (home) 7:35 ± 1:11 6:59± 1:12<br />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).<br />
  96. 96. Food Intake<br />NES > Controls<br />Inpatient study reflects night eating (20 h- 08 h) in NES subjects (Allison et al,. 2005)<br />Outpatient study shows shifted calorie intake curve in NES (O’Reardon et al., 2004)<br />
  97. 97. Night Eating<br /><ul><li>Description and Prevalence
  98. 98. Psychological factors
  99. 99. Stress
  100. 100. Sleep Timing
  101. 101. Treatment
  102. 102. Diagnosis </li></li></ul><li>Randomized Controlled Trial of Sertraline<br />Patients randomized to sertraline(n=17)<br />or placebo (n = 17) for 8 weeks.<br />O’Reardon et al., 2006<br />
  103. 103. Night Eating Symptom Scale<br />
  104. 104. Nocturnal ingestions/week<br />
  105. 105. % Caloric Intake after Dinner <br />
  106. 106. Weight change<br />
  107. 107. Discussion<br />NES – altered circadian food intake <br /><ul><li>SSRIs could be acting on the SCN to synchronize food intake and sleep-wake cycle rhythms
  108. 108. SSRIs may also act to control the compulsion to eat as they do in BN & BED</li></li></ul><li>Control<br />NES<br /> Lundgren et al., 2008 <br />
  109. 109. Behavioral Treatment<br />No Formal Studies <br />Useful Strategies<br /><ul><li>Reduce triggers, e.g., stress that induce eating
  110. 110. Keep tempting foods out of reach
  111. 111. Increase breakfast consumption</li></ul>Recommended Manual<br />Overcoming Night Eating Syndrome <br />Kelly Allison, Albert Stunkard, Sarah Tier<br />New Harbinger, 2004<br />
  112. 112. Night Eating<br /><ul><li>Description and Prevalence
  113. 113. Psychological factors
  114. 114. Stress
  115. 115. Sleep Timing
  116. 116. Treatment
  117. 117. Diagnosis </li></li></ul><li>Proposed Research Diagnostic Criteria for NES(First International Night Eating Symposium, April 26, 2008, Minneapolis, MN)<br />I.    The daily pattern of eating demonstrates a significantly increased intake in the<br /> evening and/or nighttime, as manifested by one or both of the following:<br />A. > 25% of food consumed after the evening meal<br /> B. > 2 episodes of nocturnal eating per week<br />II. Awareness and recall of evening and nocturnal eating episodes <br />III.  > 3 of the following:<br /> A. Lack of desire to eat in the morning and/or breakfast is omitted on four or more <br /> mornings per week<br /> B. Presence of a strong urge to eat between dinner and sleep onset and/or during <br /> the night<br /> C. Sleep onset and/or sleep maintenance insomnia are present four or more nights <br /> per week<br /> D. Presence of a belief that one must eat in order to initiate or return to sleep <br /> E. Mood is frequently depressed and/or mood worsens in the evening <br />IV.  The disorder is associated with significant distress and/or impairment in functioning. <br />V.   The disordered pattern of eating has been maintained for at least 3 months.<br />VI.  The disorder is not secondary to substance abuse or dependence, medical disorder, <br /> medication, or another psychiatric disorder.<br />Allison et al, 2009<br />
  118. 118. Acknowledgements<br />Co-Investigators<br />Marci Gluck, Sami Hashim, Eric Yahav, Dennis Gage, Joy Hirsch, Susan Carnell<br />Resources<br />NY Obesity Research Center provided hormone assays and body composition<br />measurements <br />Grant Support<br />NIH Grants RO1 DK 554318, R01 DK074046, R03 DK068392, and MO1 RR0064529 <br />

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