Gene–diet interactions in childhood obesity: paucity of evidence as the epidemic of childhood obesity continues to rise

Abstract

Childhood obesity is growing rapidly worldwide. Although there have been enormous advances in the genetic underpinnings of obesity in recent years, the pathways that lead to obesity are still not completely understood. One of the ongoing challenges is the lack of a comprehensive definition of the obese phenotype that encompasses intermediary phenotypic expressions of biological and behavioral nature. Interactions between genetic and environmental factors, including nutrient exposures and dietary behaviors, can influence the development of the obese phenotype. Specifically, genes play a decisive role in the etiology of childhood obesity under the permissive circumstances of an obesogenic environment (increase in energy intake with a decrease in physical activity). Like many diseases, the causes of obesity are complex and their investigation requires novel approaches. Given the many contributors to obesity (weight gain, weight loss, weight maintenance, variability in body composition), as well as the dynamic nature of this issue, genomic tools must continue to be employed to evaluate all dimensions of the obesity phenotype, such as biochemical characteristics, susceptibility markers, nutrient intake, feeding practices and gene–environment interactions. Fundamental knowledge of the types of genes involved and available gene–diet interaction studies in children’s obesity are reviewed. Although there is a paucity of existing literature in this specific domain of childhood obesity, ongoing investigations utilizing large cohorts have potential for providing the knowledge needed for targeted interventions in the future.