PROJECT SUMMARY
The preschool years (2-5 years of age) is a critical timeframe to shape the lifetime risk of obesity. While the
causes of obesity are complex, appetitive traits related to overeating, such as high food approach and low food
avoidance, are robustly associated with a greater BMI among children. Some children are genetically pre-
disposed to expressing obesogenic appetitive traits, and those traits may mediate a genetic risk for obesity.
Separately, parental feeding practices are emerging as an important, yet modifiable, influence on children’s
obesity risk. Coercive control feeding practices, such as strictly limiting a child’s intake of highly palatable foods
(restriction) and using food to control children’s negative emotions (emotional feeding), are believed to be
detrimental for young children because they impede self-regulatory skills around eating and may increase the
saliency of highly palatable foods. Our goal for this project is to disentangle the inter-relationships between
coercive control feeding practices, children’s obesogenic appetitive traits, and children’s dietary intake across
the preschool years to understand how coercive control feeding practices ultimately impact children’s adiposity
gain over time. Importantly, we aim to understand how those effects differ based on children’s underlying genetic
risk for obesity. We hypothesize that parents will respond to children’s obesogenic appetitive traits by exhibiting
more coercive control feeding practices (restriction, emotional feeding), which in turn, will promote future
increase in obesogenic appetitive traits and overconsumption, leading to excess adiposity gain among children.
Importantly, we hypothesize children with a high genetic risk for obesity will be most susceptible to the negative
effects of coercive control feeding practices because food is highly salient for them. We will test our hypotheses
among a cohort of children aged 2.5 years old using a longitudinal study design with repeated assessments
every 6 months until children are 5 years old. We include validated assessments of parental feeding practices,
child appetitive traits and usual dietary intake. We will assess children’s genetic risk for obesity via candidate
single-nucleotide polymorphisms (SNPs) and a polygenic risk score. Importantly, our novel approach expands
upon previous research by including our lab’s proven, objective paradigm to measure children’s food approach
and overconsumption. Specifically, we will use eye-tracking to measure children’s attentional bias to food, an
objective metric of food approach. We also include an eating in the absence of hunger paradigm to objectively
measure children’s overconsumption. Study findings can be leveraged to develop tailored strategies to help
parents support healthy eating behaviors among their young children that consider the heterogeneity in
obesogenic appetitive traits among young children due to genetic risk factors.
