title: Bioavailable insulin-like growth factor-I inversely related to weight gain in postmenopausal women regardless of exogenous estrogen.
abstract: BACKGROUND
  Weight gain, insulin-like growth factor-I (IGF-I) levels, and excess exogenous steroid hormone use are putative cancer risk factors, yet their interconnected pathways have not been fully characterized. This cross-sectional study investigated the relationship between plasma IGF-I levels and weight gain according to body mass index (BMI), leptin levels, and exogenous estrogen use among postmenopausal women.
  
  
  METHODS
  This study included 794 postmenopausal women who enrolled in an ancillary study of the Women's Health Initiative Observational Study between February 1995 and July 1998. The relationship between IGF-I levels and weight gain was analyzed using ordinal logistic regression. We used the molar ratio of IGF-I to IGF binding protein-3 (IGF-I/IGFBP-3) or circulating IGF-I levels adjusting for IGFBP-3 as a proxy of bioavailable IGF-I. The plasma concentrations were expressed as quartiles.
  
  
  RESULTS
  Among the obese group, women in the third quartile (Q3) of IGF-I and highest quartile of IGF-I/IGFBP-3 were less likely to gain weight (>3% from baseline) than were women in the first quartiles (Q1). Among the normal-weight group, women in Q2 and Q3 of IGF-I/IGFBP-3 were 70% less likely than those in Q1 to gain weight. Among current estrogen users, Q3 of IGF-I/IGFBP-3 had 0.5 times the odds of gaining weight than Q1.
  
  
  CONCLUSIONS
  Bioavailable IGF-I levels were inversely related to weight gain overall.
  
  
  CONCLUSIONS
  Although weight gain was not consistent with increases in IGF-I levels among postmenopausal women in this report, avoidance of weight gain as a strategy to reduce cancer risk may be recommended.
authors.affiliation: Authors' Affiliations: Division of Cancer Prevention and Population Sciences, Department of Epidemiology; Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston; Department of Nutritional Sciences, The University of Texas at Austin, Austin, Texas; Division of Public Health Sciences, Department of Epidemiology and Prevention, Wake Forest University, School of Medicine, Winston-Salem, North Carolina; and Division of Cancer Prevention and Control, College of Medicine, Ohio State University, Columbus, Ohio.
authors.forename: Su Yon
authors.initials: SY
authors.lastname: Jung
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Hursting
authors.forename: Michele
authors.initials: M
authors.lastname: Guindani
authors.forename: Mara Z
authors.initials: MZ
authors.lastname: Vitolins
authors.forename: Electra
authors.initials: E
authors.lastname: Paskett
authors.forename: Shine
authors.initials: S
authors.lastname: Chang
mesh_terms: D000368:Aged; D015992:Body Mass Index; D003430:Cross-Sectional Studies; D004967:Estrogens / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D020738:Leptin / Q000097:blood; D016015:Logistic Models; D008875:Middle Aged; D009765:Obesity / Q000097:blood; D017698:Postmenopause / Q000097:blood*; D012307:Risk Factors; D016896:Treatment Outcome; D015430:Weight Gain / Q000502:physiology*
chemical_list: D004967:Estrogens; D020738:Leptin; D007334:Insulin-Like Growth Factor I