03 Feb Genetic Risk Score Linked To Childhood Weight Gain and Body Fat
MedicalResearch.com Interview with:
Silje Steinsbekk PhD
Associate Professor
Dept. of Pschology
Norwegian University of Science and Technology
Medical Research: What is the background for this study?
Dr. Steinsbekk: More than every third American child is overweight or obese. Childhood obesity is associated with multiple negative health outcomes such as metabolic syndrome and hypertension, as well as mental health problems, reduced self-esteem and impaired quality of life. Further, overweight and obesity tend to persist from childhood into adulthood, and the risk of adult overweight increases the longer a child has been overweight. Identifying modifiable factors contributing to the development and continuity of unhealthy weight is therefore needed.
Genome-wide association studies (GWAS) have identified genetic risks for obesity and these genetic risks have shown to influence development of obesity partly by accelerating weight gain in childhood. Identification of mechanisms through which genetic risks for obesity accelerate weight gain in childhood can therefore provide insight into the developmental pathogenesis of obesity and thus inform intervention. Cross-sectional studies suggest appetite traits as a candidate mechanism. Appetite traits may therefore be targets of intervention to protect children against the effect of genetic predispositions to develop obesity. However, such a preventive approach presupposes that appetite traits indeed transmit the genetic effect upon later development of obesity. Notably, cross-sectional studies cannot establish whether appetite traits precede the development of obesity or are caused by it—a critical piece of information for clinicians seeking treatment targets to prevent childhood obesity. We therefore aimed to test whether genetic risk for obesity was associated with rapid childhood BMI growth and if this genetic effect was mediated by appetite traits, following a representative sample of Norwegian children from age 4 to 8.
Medical Research: What are the main findings?
Dr. Steinsbekk: As expected, we found that children with higher genetic risk scores had higher BMI, BMI SDs and percentage of body fat as compared to children with lower genetic risk score at all measurement points. Children with higher genetic risk scores also gained BMI points and body fat more rapidly as compared to lower genetic risk peers. However, the relationship between genetic risk and accelerated weight gain was not mediated by children’s appetite traits.
Medical Research: What should clinicians and patients take away from your report?
Dr. Steinsbekk: Although our findings did not support appetite as a mediator of genetic influences on children’s weight gain during middle childhood, the results do not diminish the potential value of appetite measures as markers of risk for obesity. In a former study of the same sample, we showed that children’s obesity-related appetite traits indeed predicted increased weight gain from age 6 to 8.Thus, appetite traits are associated with the development of BMI and may still provide targets for interventions to prevent obesity.
Medical Research: What recommendations do you have for future research as a result of this study?
Dr. Steinsbekk: First, studies of early childhood samples are needed to test if appetite traits explain how genetic risks accelerate growth in the first years of life.
Secondly, because our sample is of European descent, replication of findings in non-European populations is needed.
As larger genome-wide association studies uncover addition loci and/or gene-gene interaction effects contributing to the development of obesity, future research may benefit from refined genetic measures of obesity risk. Finally, incorporating identified gene-environment interactions into analyses such as ours may improve precision.
Citation:
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Silje Steinsbekk PhD (2016). Genetic Risk Score Linked To Childhood Weight Gain and Body Fat
Last Updated on February 3, 2016 by Marie Benz MD FAAD