title: Cortisol Measures Across the Weight Spectrum.
abstract: BACKGROUND
  There are conflicting reports of increased vs decreased hypothalamic-pituitary-adrenal (HPA) activation in obesity; the most consistent finding is an inverse relationship between body mass index (BMI) and morning cortisol. In anorexia nervosa (AN), a low-BMI state, cortisol measures are elevated.
  
  
  OBJECTIVE
  This study aimed to investigate cortisol measures across the weight spectrum.
  
  
  METHODS
  This was a cross-sectional study at a clinical research center.
  
  
  METHODS
  This study included 60 women, 18-45 years of age: overweight/obese (OB; N = 21); AN (N = 18); and normal-weight controls (HC; N = 21).
  
  
  METHODS
  HPA dynamics were assessed by urinary free cortisol, mean overnight serum cortisol obtained by pooled frequent sampling every 20 minutes from 2000-0800 h, 0800 h serum cortisol and cortisol-binding globulin, morning and late-night salivary cortisol, and dexamethasone-CRH testing. Body composition and bone mineral density (BMD) were assessed by dual-energy x-ray absorptiometry.
  
  
  RESULTS
  Cortisol measures demonstrated a U-shaped relationship with BMI, nadiring in the overweight-class I obese range, and were similarly associated with visceral adipose tissue and total fat mass. Mean cortisol levels were higher in AN than OB. There were weak negative linear relationships between lean mass and some cortisol measures. Most cortisol measures were negatively associated with postero-anterior spine and total hip BMD.
  
  
  CONCLUSIONS
  Cortisol measures are lowest in overweight-class I obese women-lower than in lean women. With more significant obesity, cortisol levels increase, although not to as high as in AN. Therefore, extreme underweight and overweight states may activate the HPA axis, and hypercortisolemia may contribute to increased adiposity in the setting of caloric excess. Hypercortisolemia may also contribute to decreased BMD and muscle wasting in the setting of both caloric restriction and excess.
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
authors.forename: Melanie
authors.initials: M
authors.lastname: Schorr
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Lawson
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
authors.forename: Laura E
authors.initials: LE
authors.lastname: Dichtel
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
authors.forename: Anne
authors.initials: A
authors.lastname: Klibanski
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
authors.forename: Karen K
authors.initials: KK
authors.lastname: Miller
mesh_terms: D000293:Adolescent; D000328:Adult; D000856:Anorexia Nervosa / Q000097:blood* / Q000503:physiopathology; D001835:Body Weight / Q000502:physiology; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000503:physiopathology; D050177:Overweight / Q000097:blood* / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D055815:Young Adult
chemical_list: D006854:Hydrocortisone