title: Associations between genetic obesity susceptibility and early postnatal fat and lean mass: an individual participant meta-analysis.
abstract: OBJECTIVE
  Patterns of body size and body composition associated with genetic obesity susceptibility inform the mechanisms that increase obesity risk.
  
  
  OBJECTIVE
  To test associations between genetic obesity susceptibility, represented by a combined obesity risk-allele score, and body size or body composition at birth to age 5 years.
  
  
  METHODS
  A total of 3031 children from 4 birth cohort studies in England, France, and Spain were included in a meta-analysis.
  
  
  METHODS
  A combined obesity risk-allele score was calculated from genotypes at 16 variants identified by genome-wide association studies of adult body mass index (BMI).
  
  
  METHODS
  Outcomes were age- and sex-adjusted SD scores (SDS) for weight, length/height, BMI, fat mass, lean mass, and percentage of body fat at birth as well as at ages 1, 2 to 3, and 4 to 5 years.
  
  
  RESULTS
  The obesity risk-allele score was not associated with infant size at birth; at age 1 year it was positively associated with weight (β [SE], 0.020 [0.008] SDS per allele; P = .009) and length (β [SE], 0.020 [0.008] SDS per allele; P = .01), but not with BMI (β [SE], 0.013 [0.008] SDS per allele; P = .11). At age 2 to 3 years these associations were stronger (weight: β [SE], 0.033 [0.008] SDS per allele; P < .001; height: β [SE], 0.025 [0.008] SDS per allele; P < .001) and were also seen for BMI (β [SE], 0.024 [0.008] SDS per allele; P = .003). The obesity risk-allele score was positively associated with both postnatal fat mass (1 year: β [SE], 0.032 [0.017] SDS per allele; P = .05; 2-3 years: β [SE], 0.049 [0.018] SDS per allele; P = .006; and 4-5 years: β [SE], 0.028 [0.011] SDS per allele; P = .009) and postnatal lean mass (1 year: β [SE], 0.038 [0.014] SDS per allele; P = .008; 2-3 years: β [SE], 0.064 [0.017] SDS per allele; P < .001; and 4-5 years: β [SE], 0.047 [0.011] SDS per allele; P < .001), but not with the percentage of body fat (P > .15 at all ages).
  
  
  CONCLUSIONS
  Genetic obesity susceptibility appears to promote a normally partitioned increase in early postnatal, but not prenatal, growth. These findings suggest that symmetrical rapid growth may identify infants with high life-long susceptibility for obesity.
authors.affiliation: Medical Research Council Epidemiology Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge, England.
authors.forename: Cathy E
authors.initials: CE
authors.lastname: Elks
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Center for Research in Epidemiology and Population Health, Lifelong Epidemiology of Obesity, Diabetes and Renal Disease Team, Villejuif, France3Medical Faculty, University Paris-Sud, Villejuif, Fr.
authors.forename: Barbara
authors.initials: B
authors.lastname: Heude
authors.affiliation: Paediatric Endocrinology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium.
authors.forename: Francis
authors.initials: F
authors.lastname: de Zegher
authors.affiliation: Medical Research Council Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, England.
authors.forename: Sheila J
authors.initials: SJ
authors.lastname: Barton
authors.affiliation: Institut de Cardiometabolism and Nutrition, Centre de Recherche en Nutrition Humaine lle de France, Pitié-Salpêtrière Hospital, Paris, France7Institut National de la Santé et de la Recherche Médicale U872 team Nutriomique, Paris, France.
authors.forename: Karine
authors.initials: K
authors.lastname: Clément
authors.affiliation: Medical Research Council Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, England.
authors.forename: Hazel M
authors.initials: HM
authors.lastname: Inskip
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Center for Research in Epidemiology and Population Health, Lifelong Epidemiology of Obesity, Diabetes and Renal Disease Team, Villejuif, France3Medical Faculty, University Paris-Sud, Villejuif, Fr.
authors.forename: Yves
authors.initials: Y
authors.lastname: Koudou
authors.affiliation: Medical Research Council Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, England8National Institute of Health Research, Nutrition Biomedical Research Centre, University of Southampton, Southampton, Engla.
authors.forename: Cyrus
authors.initials: C
authors.lastname: Cooper
authors.affiliation: Department of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Cambridge, England.
authors.forename: David B
authors.initials: DB
authors.lastname: Dunger
authors.affiliation: Department of Endocrinology, Hospital Sant Joan de Déu, University of Barcelona, Barcelona, Spain11Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid, Spain.
authors.forename: Lourdes
authors.initials: L
authors.lastname: Ibáñez
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Center for Research in Epidemiology and Population Health, Lifelong Epidemiology of Obesity, Diabetes and Renal Disease Team, Villejuif, France3Medical Faculty, University Paris-Sud, Villejuif, Fr.
authors.forename: Marie-Aline
authors.initials: MA
authors.lastname: Charles
authors.affiliation: Medical Research Council Epidemiology Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge, England9Department of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Cambridge, England.
authors.forename: Ken K
authors.initials: KK
authors.lastname: Ong
mesh_terms: D000273:Adipose Tissue; D001835:Body Weight / Q000235:genetics*; D002675:Child, Preschool; D004739:England; D005260:Female; D005602:France; D020022:Genetic Predisposition to Disease; D006801:Humans; D007223:Infant; D008297:Male; D009765:Obesity / Q000235:genetics*; D012307:Risk Factors; D013030:Spain