Edited by Ahmad R. Hariri, Duke University, Durham, NC, and accepted by Editorial Board Member Leslie G. Ungerleider November 3, 2016 (received for review April 5, 2016)
Genetic predisposition and sensitivity to environmental cues jointly give rise to maladaptive human behaviors, such as unhealthy eating. Despite the dramatic rise in obesity rates, the relationship between these factors is not well understood. Here we show that children genetically at risk for obesity exhibit stronger reward-related responses to real-world food cues (i.e., food advertisements) in the nucleus accumbens, a brain area canonically associated with reward processing. Additionally, this structure is larger in children at a higher risk for obesity. Taken together, these findings offer one explanation for how genetic risk for obesity may predispose individuals to engage in unhealthy eating behaviors and may inform strategies targeting early intervention.
Obesity is a major public health concern that involves an interaction between genetic susceptibility and exposure to environmental cues (e.g., food marketing); however, the mechanisms that link these factors and contribute to unhealthy eating are unclear. Using a well-known obesity risk polymorphism (FTO rs9939609) in a sample of 78 children (ages 9–12 y), we observed that children at risk for obesity exhibited stronger responses to food commercials in the nucleus accumbens (NAcc) than children not at risk. Similarly, children at a higher genetic risk for obesity demonstrated larger NAcc volumes. Although a recessive model of this polymorphism best predicted body mass and adiposity, a dominant model was most predictive of NAcc size and responsivity to food cues. These findings suggest that children genetically at risk for obesity are predisposed to represent reward signals more strongly, which, in turn, may contribute to unhealthy eating behaviors later in life.
Author contributions: K.M.R., A.L.Z., W.M.K., J.D.S., T.F.H., and D.G.-D. designed research; K.M.R. and A.L.Z. performed research; D.G.-D. contributed new reagents/analytic tools; K.M.R., A.L.Z., and W.M.K. analyzed data; and K.M.R. and W.M.K. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission. A.R.H. is a Guest Editor invited by the Editorial Board.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1605548113/-/DCSupplemental.
Freely available online through the PNAS open access option.
