Investigating the Efficacy of Genetic, Environmental, and Multifactorial Risk Information When Communicating Obesity Risk to Parents of Young Children.

BACKGROUND Effectively communicating with parents about children's obesity risk is of critical importance for preventive medicine and public health. PURPOSE The current study investigates the efficacy of communications focused on two primary causes of obesity: genes and environment. METHODS We compared parental feeding responses to messages focused on (i) genetics alone, (ii) family environment alone, (iii) genetics-family environment interaction (G × FE), and (iv) no causal message. We also examined whether parental guilt mediates the effect of message type on feeding. Our sample consisted of 190 parents, half mothers and half fathers, of children 3-7 years old. After receiving one of the four types of messages, parents chose foods for their child using the Virtual Reality Buffet measure. Parents responded to questionnaires in the lab and at 1-week follow-up. RESULTS In the VR Buffet, parents did not feed their children differently in message provision conditions versus control. There were, however, differences among message provision conditions wherein mothers who received any genetic information chose higher-calorie meals in the VR Buffet. At 1-week follow-up, parents who received information about genetics alone reported feeding their child more junk food and fatty meat on self-report food frequency assessments; there were no such differences for sugary beverages, sugary foods, or fast foods. Parental guilt was typically higher for participants who received family environment information alone but did not mediate the relation between information provision and feeding outcomes. CONCLUSIONS While none of the messages improved feeding above the control condition, GxFE messages were associated with a better overall profile of outcomes. As such, it may be beneficial for messaging for parents about children's obesity risk to include content that reflects the complexity of genetic and environmental contributions to obesity risk.