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Am J Clin Nutr 89: 1494S-1501S, 2009. First published March 4, 2009; doi:10.3945/ajcn.2009.27113C
American Journal of Clinical Nutrition, doi:10.3945/ajcn.2009.27113C
Vol. 89, No. 5, 1494S-1501S, May 2009

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© 2009 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

Childhood obesity: are genetic differences involved?1,2,3,4

Claude Bouchard

1 From the Human Genomics Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA.

2 Presented at the workshop "Early Risk Determinants and Later Health Outcomes: Implications for Research Prioritization and the Food Supply," held in Washington, DC, July 8–9, 2008.

3 Supported by the George A Bray Chair in Nutrition and by the National Heart, Blood, and Lung Institute (HL45670). Funds to support the writing of this article were provided in part by the Project Committee on Early Nutrition of the International Life Sciences Institute North American Branch.

4 Reprints not available. Address correspondence to C Bouchard, Human Genomics Laboratory, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808. E-mail: bouchac{at}pbrc.edu.

This brief review focuses on the genetic contribution to childhood obesity. Evidence for a genetic component to excess body weight during growth is presented from the perspective of genetic epidemiology studies. Parental obesity is a predictor of childhood excess weight. The familial risk ratio for childhood obesity when a parent is obese reaches >2.5. Birth weight is characterized by a genetic heritability component on the order of 30%, with significant maternal and paternal effects in addition to the newborn genes. About 5% of childhood obesity cases are caused by a defect that impairs function in a gene, and ≥5 of these genes have been uncovered. However, the common forms of childhood obesity seem to result from a predisposition that primarily favors obesogenic behaviors in an obesogenic environment. Candidate gene and genomewide association studies reveal that these obesogenic genes have small effect sizes but that the risk alleles for obesity are quite common in populations. The latter may translate into a highly significant population-attributable risk of obesity. Gene-environment interaction studies suggest that the effects of predisposing genes can be enhanced or diminished by exposure to relevant behaviors. It is possible that the prevalence of childhood obesity is increasing across generations as a result of positive assortative mating with obese husbands and wives contributing more obese offspring than normal-weight parents.




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