title: Prenatal exposure to maternal cigarette smoking, amygdala volume, and fat intake in adolescence.
abstract: BACKGROUND
  Prenatal exposure to maternal cigarette smoking is a well-established risk factor for obesity, but the underlying mechanisms are not known. Preference for fatty foods, regulated in part by the brain reward system, may contribute to the development of obesity.
  
  
  OBJECTIVE
  To examine whether prenatal exposure to maternal cigarette smoking is associated with enhanced fat intake and risk for obesity, and whether these associations may be related to subtle structural variations in brain regions involved in reward processing.
  
  
  METHODS
  Cross-sectional study of a population-based cohort.
  
  
  METHODS
  The Saguenay Youth Study, Quebec, Canada.
  
  
  METHODS
  A total of 378 adolescents (aged 13 to 19 years; Tanner stage 4 and 5 of sexual maturation), half of whom were exposed prenatally to maternal cigarette smoking (mean [SD], 11.1 [6.8] cigarettes/d).
  
  
  METHODS
  Fat intake was assessed with a 24-hour food recall (percentage of energy intake consumed as fat). Body adiposity was measured with anthropometry and multifrequency bioimpedance. Volumes of key brain structures involved in reward processing, namely the amygdala, nucleus accumbens, and orbitofrontal cortex, were measured with magnetic resonance imaging.
  
  
  RESULTS
  Exposed vs nonexposed subjects exhibited a higher total body fat (by approximately 1.7 kg; P = .009) and fat intake (by 2.7%; P = .001). They also exhibited a lower volume of the amygdala (by 95 mm3; P < .001) but not of the other 2 brain structures. Consistent with its possible role in limiting fat intake, amygdala volume correlated inversely with fat intake (r = -0.15; P = .006).
  
  
  CONCLUSIONS
  Prenatal exposure to maternal cigarette smoking may promote obesity by enhancing dietary preference for fat, and this effect may be mediated in part through subtle structural variations in the amygdala.
authors.affiliation: The Hospital for Sick Children, University of Toronto, Toronto, Canada.
authors.forename: Amirreza
authors.initials: A
authors.lastname: Haghighi
authors.forename: Deborah H
authors.initials: DH
authors.lastname: Schwartz
authors.forename: Michal
authors.initials: M
authors.lastname: Abrahamowicz
authors.forename: Gabriel T
authors.initials: GT
authors.lastname: Leonard
authors.forename: Michel
authors.initials: M
authors.lastname: Perron
authors.forename: Louis
authors.initials: L
authors.lastname: Richer
authors.forename: Suzanne
authors.initials: S
authors.lastname: Veillette
authors.forename: Daniel
authors.initials: D
authors.lastname: Gaudet
authors.forename: Tomáš
authors.initials: T
authors.lastname: Paus
authors.forename: Zdenka
authors.initials: Z
authors.lastname: Pausova
mesh_terms: D000293:Adolescent; D000328:Adult; D000679:Amygdala / Q000473:pathology* / Q000503:physiopathology; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004041:Dietary Fats / Q000008:administration & dosage*; D002149:Energy Intake / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D009765:Obesity / Q000209:etiology* / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000473:pathology / Q000503:physiopathology; D012306:Risk; D012907:Smoking / Q000009:adverse effects*; D055815:Young Adult
chemical_list: D004041:Dietary Fats