title: Metabolic health reduces risk of obesity-related cancer in framingham study adults.
abstract: BACKGROUND
  It is unknown whether the risk for obesity-related cancers differs between metabolically unhealthy and healthy overweight/obese adults.
  
  
  METHODS
  Data on body mass index (BMI), waist circumference (WC), waist-to-height ratio (WHtR), and random blood glucose in Framingham Heart Study adults (n = 3,763) ages 55 to 69 years were used to estimate risks of obesity-related cancers (n = 385), including postmenopausal breast, female reproductive, colon, liver, gallbladder, pancreas, and kidney cancers, as well as esophageal adenocarcinomas. Multivariable-adjusted Cox proportional hazards models were used to estimate risk for obesity-related cancers associated with body fat and metabolic health (as defined by glucose levels) among subjects in three risk groups (vs. referent group with normal weight/normal glucose): normal weight/elevated glucose, overweight/normal glucose, and overweight/elevated glucose.
  
  
  RESULTS
  Overweight adults [BMI ≥ 25 or WHtR ≥ 0.51 (men) and ≥0.57 (women)] with elevated glucose (≥125 mg/dL) had a statistically significant 2-fold increased risk of developing obesity-related cancer, whereas overweight adults with normal glucose had a 50% increased risk. Normal-weight adults with elevated glucose had no excess cancer risk. The effects of BMI and WHtR were independent of one another. Finally, overweight women with elevated blood glucose had a 2.6-fold increased risk [95% confidence interval (CI), 1.4-4.9] of female reproductive (cervical, endometrial, uterine cancers) and postmenopausal breast cancers, whereas overweight women with normal glucose levels had only a 70% increased risk (95% CI, 1.1-2.5).
  
  
  CONCLUSIONS
  These results suggest that cancer risk may be lower among metabolically healthy overweight/obese older adults than among overweight/obese adults with metabolic dysfunction.
  
  
  CONCLUSIONS
  Metabolic dysfunction and obesity act synergistically to increase cancer risk.
authors.affiliation: Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. Framingham Heart Study, National Heart, Lung, and Blood Institute, Framingham, Massachusetts. llmoore@bu.edu.
authors.forename: Lynn L
authors.initials: LL
authors.lastname: Moore
authors.affiliation: Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
authors.forename: Susan
authors.initials: S
authors.lastname: Chadid
authors.affiliation: Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
authors.forename: Martha R
authors.initials: MR
authors.lastname: Singer
authors.affiliation: Framingham Heart Study, National Heart, Lung, and Blood Institute, Framingham, Massachusetts. General Internal Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
authors.forename: Bernard E
authors.initials: BE
authors.lastname: Kreger
authors.affiliation: Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts. Cancer Research Center, Boston University School of Medicine, Boston, Massachusetts.
authors.forename: Gerald V
authors.initials: GV
authors.lastname: Denis
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000032:analysis / Q000378:metabolism*; D015992:Body Mass Index; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000097:blood* / Q000453:epidemiology*; D009765:Obesity / Q000097:blood / Q000150:complications*; D016016:Proportional Hazards Models; D065927:Waist-Height Ratio
chemical_list: D001786:Blood Glucose