News Release

Analysis examines genetic obesity susceptibility, association with body size in kids

Peer-Reviewed Publication

JAMA Network

Bottom Line: A review of medical literature appears to confirm an association between genetic obesity susceptibility and postnatal gains in infant weight and length, as well as showing associations with both fat mass and lean mass in infancy and early childhood.

Author: Cathy E. Elks, Ph.D., of the Medical Research Council Epidemiology Unit, University of Cambridge, England, and colleagues.

Background: Identifying indicators and mechanisms in early life related to later life obesity risk is important for preventive strategies.

How the Study Was Conducted: The authors conducted a meta-analysis that included 3,031 children from four birth cohort studies in England, France and Spain. Genetic obesity susceptibility was represented by a combined obesity risk-allele (an alternative form of a gene) score that was calculated in each participant as the sum of 16 different alleles associated with higher adult body-mass index (BMI). Associations between genetic obesity susceptibility and body size or body composition were tested at birth to age 5 years.

Results: The obesity risk-allele score was not associated with infant size at birth but at age 1 year it was associated with weight and length but not with BMI. The associations were stronger at age 2 to 3 years and were also seen for BMI. The allele score was associated with both postnatal fat mass and lean mass but not with the percentage of body fat.

Discussion: "Our findings suggest that genetic susceptibility to obesity promotes early gains in both weight and length/height that are apparent before the positive influence on BMI. This premise is strongly supported by our novel finding of positive associations between the obesity risk-allele score and both fat mass and lean mass, but not relative body fat, in infancy and early childhood."


(JAMA Pediatr. Published online October 20, 2014. doi:10.1001/jamapediatrics.2014.1619. Available pre-embargo to the media at

Editor's Note: This project was funded by a Collaborative Research Grant from the European Society for Paediatric Endocrinology and by the Medical Research Council. The authors made a funding disclosure. Please see article for additional information, including other authors, author contributions and affiliations, etc.

Media Advisory: To contact corresponding author Ken K. Ong, F.R.C.P.C.H., email

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