Existing programs which aim to prevent and treat childhood obesity often do not take into account individual variation and the underlying mechanisms that impact child eating behavior. Individual differences in children's appetitive traits have been shown to appear as early as during infancy and become more pronounced as children grow older and become more exposed to the obesogenic food environment. Differences in genetic predispositions interacting with factors in children's early environment account in part for individual differences in appetitive traits. It is very likely that obesogenic eating phenotypes manifest themselves before the onset of childhood obesity. If so, identifying these phenotypes early is expected to move primary prevention strategies in a new direction and holds great potential to significantly enhance our ability to prevent childhood obesity. The aim of this narrative review is to discuss the role of behavioral phenotyping as an innovative approach for the development of more personalized obesity prevention and treatment interventions that are tailored to children's individual predispositions. We describe several examples of appetitive traits which have been linked to overeating and excess weight gain in children and thus may represent modifiable risk factors for future interventions. The review concludes with a comprehensive synthesis of opportunities for future human ingestive behavior research on identifying behavioral phenotypes for childhood obesity.
Objectives: To assess if eating in the absence of hunger (EAH) extends to healthier snacks and examine the relationship between the home food environment and EAH in children with normal weight (NW) or overweight/obesity (OB) who are at low risk (LR) or high risk (HR) for obesity based on maternal obesity. Methods: EAH was assessed after lunch and dinner when children received either low energy dense fruit snacks or high energy dense sweet/savoury snacks. The availability of obesogenic foods in the home was assessed by the Home Food Inventory. Results: Data showed significant main effects of risk group (P=.0003) and snack type (P < .001). EAH was significantly greater in HR-OB (284±8 kcal) than LR-NW (249±9 kcal) or HR-NW (251±8 kcal) children. Serving fruit rather than sweet/ savoury snacks reduced energy intake, on average, by 60% (223 kcal) across risk groups. For each unit increase in the obesogenic home food environment, EAH of sweet/savoury snacks decreased by 1.83 calories. Conclusions: Offering low energy dense snacks after a meal can moderate EAH and increase children's intake of healthy foods. Increased access to obesogenic foods in the home may reduce the salience of high energy dense snacks when they become available in other settings.
BackgroundChildren who have Autism Spectrum Disorder (ASD) show preferences for processed foods, such as salty and sugary snacks (SSS) and sugar-sweetened beverages (SSB), while healthier foods, such as fruits and vegetables (FV), are consumed less. Innovative tools are needed that can efficiently disseminate evidence-based interventions and engage autistic children to improve their diet.AimThe aim of this 3-month randomized trial was to test the initial efficacy of a mobile health (mHealth) nutrition intervention on changing consumption of targeted healthy (FV) and less healthy foods/beverages (SSS, SSB) in children who have ASD, ages 6–10, who were picky eaters.MethodsThirty-eight parent-child dyads were randomly assigned to either an intervention (technology) group or a wait list control (education) group. The intervention included behavioral skills training, a high level of personalization for dietary goals, and involved parents as “agents of change.” Parents in the education group received general nutrition education and the dietary goals but did not receive skills training. Children's intake was assessed at baseline and at 3 months using 24-hour dietary recalls.ResultsWhile there were no significant group-by-time interactions (P > 0.25) for any of the primary outcomes, we found a significant main effect of time for FV intake (P = 0.04) indicating that both groups consumed more FV at 3 months (2.58 ± 0.30 servings/day) than at baseline (2.17 ± 0.28 servings/day; P = 0.03). Children in the intervention group who consumed few FV at baseline and showed high engagement with the technology increased their FV intake by 1.5 servings/day (P < 0.01). Children's taste/smell sensitivity significantly predicted their FV intake (P = 0.0446); for each unit of lower taste/smell sensitivity (indicating greater sensory processing abnormalities), FV intake increased by 0.13 ± 0.1 servings/day.DiscussionThis mHealth intervention did not yield significant between-group differences for changing consumption of targeted foods/beverages. Only children who consumed few FV at baseline and highly engaged with the technology increased their FV intake at 3 months. Future research should test additional strategies to expand the intervention's impact on a wider range of foods while also reaching a broader group of children who have ASD. This trial was registered at clinicaltrials.gov as NCT03424811.Clinical Trial Registration: This study was registered at clinicaltrials.gov as NCT03424811.
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