title: Maternal overweight and obesity and risk of congenital heart defects in offspring.
abstract: OBJECTIVE
  Obesity is a risk factor for congenital heart defects (CHDs), but whether risk is independent of abnormal glucose metabolism remains unknown. Data on whether overweight status increases the risk are also conflicting.
  
  
  METHODS
  We included 121 815 deliveries from a cohort study, the Consortium on Safe Labor (CSL), after excluding women with pregestational diabetes as recorded in the electronic medical record. CHD was identified via medical record discharge summaries. Adjusted odds ratios (ORs) for any CHD were calculated for prepregnancy body mass index (BMI) categories of overweight (25-<30 kg m(-2)), obese (30-<40 kg m(-2)) and morbidly obese (≥40 kg m(-2)) compared with normal weight (18.5-<25 kg m(-2)) women, and for specific CHD with obese groups combined (≥30 kg m(-2)). A subanalysis adjusting for oral glucose tolerance test (OGTT) results where available was performed as a proxy for potential abnormal glucose metabolism present at the time of organogenesis.
  
  
  RESULTS
  There were 1388 (1%) infants with CHD. Overweight (OR=1.15, 95% confidence interval (95% CI): 1.01-1.32), obese (OR=1.26, 95% CI: 1.09-1.44) and morbidly obese (OR=1.34, 95% CI: 1.02-1.76) women had greater OR of having a neonate with CHD than normal weight women (P<0.001 for trend). Obese women (BMI≥30 kg m(-2)) had higher OR of having an infant with conotruncal defects (OR = 1.33, 95% CI: (1.03–1.72) [corrected], atrial septal defects (OR=1.22, 95% CI: 1.04-1.43) and ventricular septal defects (OR=1.38, 95% CI: 1.06-1.79). Being obese remained a significant predictor of CHD risk after adjusting for OGTT.
  
  
  CONCLUSIONS
  Increasing maternal weight class was associated with an increased risk for CHD. In obese women, abnormal glucose metabolism did not completely explain the increased risk for CHD; the possibility that other obesity-related factors are teratogenic requires further investigation.
authors.affiliation: 1] Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA [2] Epidemiology and Biostatistics, CUNY School of Public Health at Hunter College, New York, NY, USA [3] CUNY Institute for Demographic Research (CIDR), New York, NY, USA.
authors.forename: J
authors.initials: J
authors.lastname: Brite
authors.affiliation: Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA.
authors.forename: S K
authors.initials: SK
authors.lastname: Laughon
authors.affiliation: Office of Biostatistics Research, Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD, USA.
authors.forename: J
authors.initials: J
authors.lastname: Troendle
authors.affiliation: Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA.
authors.forename: J
authors.initials: J
authors.lastname: Mills
mesh_terms: D000328:Adult; D015992:Body Mass Index; D015331:Cohort Studies; D005260:Female; D044882:Glucose Metabolism Disorders / Q000453:epidemiology / Q000209:etiology*; D006330:Heart Defects, Congenital / Q000453:epidemiology / Q000209:etiology*; D006801:Humans; D007231:Infant, Newborn; D016015:Logistic Models; D009035:Mothers; D009765:Obesity / Q000150:complications* / Q000453:epidemiology; D016017:Odds Ratio; D011247:Pregnancy; D011248:Pregnancy Complications / Q000453:epidemiology / Q000209:etiology*; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors