title: Changes in estradiol and testosterone levels in postmenopausal women after changes in body mass index.
abstract: BACKGROUND
  Endogenous sex hormones are risk factors for postmenopausal breast cancer. A potential route for favorable hormonal modification is weight loss.
  
  
  OBJECTIVE
  The objective of the study was to measure change in plasma estradiol and testosterone levels in postmenopausal women in relation to change in body mass index (BMI) and plasma leptin.
  
  
  METHODS
  The setting was a cohort study of over 100,000 female volunteers from the general population, United Kingdom.
  
  
  METHODS
  The participants were a sample of 177 postmenopausal women aged over 45 years who provided blood samples during 2004-2005 and again during 2010-2011.
  
  
  METHODS
  Outcomes were percentage change in plasma estradiol and testosterone levels per 1 kg/m² change in BMI and per 1 ng/mL change in plasma leptin.
  
  
  RESULTS
  Among women with reduction in BMI, estradiol decreased 12.7% (95% confidence interval: [6.4%, 19.5%]; P < .0001) per kg/m² and among women with increased BMI estradiol increased 6.4% [0.2%, 12.9%] (P = .042). The corresponding figures for testosterone were 10.7% [3.0%, 19.0%] (P = .006) and 1.9% [-5.4%, 9.7%] (P = .61) per kg/m². For women with decreases and increases in leptin, estradiol decreased by 3.6% [1.3%, 6.0%] (P = .003) per ng/mL and increased by 1.7% [-0.3%, 3.6%] (P = .094), respectively. The corresponding figures for testosterone were 4.8% [2.0%, 7.8%] (P = .009) and 0.3% [-2.0%, 2.6%] (P = .82) per ng/mL.
  
  
  CONCLUSIONS
  In postmenopausal women, changes in BMI and plasma leptin occurring over several years are associated with changes in estradiol and testosterone levels. The results suggest that fat loss by an individual can result in substantial decreases in postmenopausal estradiol and testosterone levels and provides support for weight management to lessen breast cancer risk.
authors.affiliation: Division of Genetics and Epidemiology, The Institute of Cancer Research, University of London, Sutton SM2 5NG and London SW3 6JB, United Kingdom. Michael.Jones@ICR.AC.UK
authors.forename: Michael E
authors.initials: ME
authors.lastname: Jones
authors.forename: Minouk
authors.initials: M
authors.lastname: Schoemaker
authors.forename: Megan
authors.initials: M
authors.lastname: Rae
authors.forename: Elizabeth J
authors.initials: EJ
authors.lastname: Folkerd
authors.forename: Mitch
authors.initials: M
authors.lastname: Dowsett
authors.forename: Alan
authors.initials: A
authors.lastname: Ashworth
authors.forename: Anthony J
authors.initials: AJ
authors.lastname: Swerdlow
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000368:Aged; D015992:Body Mass Index; D001943:Breast Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control; D015331:Cohort Studies; D015536:Down-Regulation; D004958:Estradiol / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D020738:Leptin / Q000378:metabolism; D008875:Middle Aged; D050177:Overweight / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D017698:Postmenopause; D012307:Risk Factors; D013739:Testosterone / Q000097:blood*; D006113:United Kingdom / Q000453:epidemiology; D015854:Up-Regulation; D015430:Weight Gain; D015431:Weight Loss
chemical_list: D020738:Leptin; D013739:Testosterone; D004958:Estradiol