title: Predicting the development of the metabolically healthy obese phenotype.
abstract: OBJECTIVE
  The metabolically healthy (MHO) and unhealthy obese (MUHO) differ in terms of cardiovascular risk. However, little is known about predicting the development of these phenotypes and the future stability of the MHO phenotype. Therefore, we examined these two issues in the San Antonio Heart Study.
  
  
  METHODS
  Longitudinal, population-based study of cardiometabolic risk factors among Mexican Americans and non-Hispanic whites in San Antonio.
  
  
  METHODS
  The study sample included 2368 participants with neither MUHO nor diabetes at baseline. Median follow-up was 7.8 years. MHO was defined as obesity with ⩽1 metabolic abnormality; MUHO, as obesity with ⩾2 abnormalities.
  
  
  RESULTS
  At baseline, 1595 and 498 individuals were non-obese with ⩽1 and ⩾2 metabolic abnormalities, respectively, and 275 were MHO. Among non-obese individuals, independent predictors of incident MHO (odds ratio (OR) for 1 s.d. change (95% confidence interval)) included body mass index (8.12 (5.66-11.7)), triglycerides (0.52 (0.39-0.68)) and high-density lipoprotein cholesterol (HDL-C) (1.41 (1.11-1.81)), whereas independent predictors of incident MUHO included body mass index (5.97 (4.58-7.77)) and triglycerides (1.26 (1.05-1.51)). Among participants with ⩽1 metabolic abnormality, obesity was associated with greater odds of developing multiple metabolic abnormalities (OR 2.26 (1.74-2.95)).
  
  
  CONCLUSIONS
  Triglycerides and HDL-C may be useful for predicting progression to MHO. MHO may not be a stable condition, because it confers an increased risk of developing multiple metabolic abnormalities.
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: I
authors.initials: I
authors.lastname: Achilike
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: H P
authors.initials: HP
authors.lastname: Hazuda
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: S P
authors.initials: SP
authors.lastname: Fowler
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: K
authors.initials: K
authors.lastname: Aung
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: C
authors.initials: C
authors.lastname: Lorenzo
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology; D008076:Cholesterol, HDL / Q000378:metabolism*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D017058:Mexican Americans / Q000706:statistics & numerical data*; D008875:Middle Aged; D009765:Obesity / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology; D010641:Phenotype; D011159:Population Surveillance; D012307:Risk Factors; D014280:Triglycerides / Q000378:metabolism*; D014481:United States / Q000453:epidemiology; D044465:White People / Q000706:statistics & numerical data*
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D014280:Triglycerides