Saturday, September 7, 2024
9/7/2024
PROJECT SUMMARY/ABSTRACT Obesity is a key risk factor for several types of cancer. Development of healthy weight and eating behaviors during childhood has the potential to reduce cancer risk in adulthood. Preadolescence is a key risk period, as children become more independent in their food choices and eating behaviors. Non-homeostatic eating, i.e., eating that occurs in response to external cues rather than physiological need, increases in preadolescence and is a risk factor for obesity. Individual differences in interoception, the process by which internal bodily states, like hunger and fullness, are sensed, integrated, interpreted, and regulated, may contribute to propensity for non-homeostatic eating. A number of studies have found that children with obesity have poorer interoceptive awareness than children without obesity, but studies examining the relationship between interoception and eating behavior are lacking. Furthermore, it is unknown if obesity-related impairments in interoception are due to inadequate physiological signaling of internal states (‘bottom up’ processes) and/or impaired cognitive interpretation of these signals (‘top down’ regulation). Levels of ghrelin, a hunger hormone produced by the stomach, typically peak just before a meal and decline following food intake; however, this response to food intake is blunted in individuals with obesity. Altered ghrelin secretion in response to a meal may result in incorrect interoceptive signaling to the brain. The primary goals of this R21 are to better understand how individual differences in multiple features of interoception contribute to objectively-measured non-homeostatic eating in children. To do this, children age 7-10 years with or without obesity (n=60) will complete a series of questionnaire and laboratory-based behavioral measures of interoception. On a separate occasion, children will consume an ad libitum meal followed by a non-homeostatic eating task (Eating in the Absence of Hunger [EAH]), providing saliva samples for measurement of ghrelin and leptin before, during, and after these tasks. For Aim 1, we will determine if interoception is associated with kcal intake in the EAH task; we hypothesize interoception will be inversely associated with intake. For Aim 2, we will examine salivary ghrelin and leptin as interoceptive signals of hunger/satiety; we hypothesize that children with greater postprandial ghrelin suppression will have better interoceptive awareness and will eat less in the EAH task, and that elevated leptin will attenuate the relationship between ghrelin suppression and interoception. For Aim 3 (Exploratory) we will use cluster analysis identify profiles of interoception based on global and system- specific (e.g., cardiac, gastric) interoception, and then examine differences in eating behavior, executive function, and weight between clusters. This project will extend our understanding of the drivers of non- homeostatic eating and reveal how interoceptive awareness impacts food intake, setting the foundation for intervention strategies tailored for children based on individual differences in interoceptive function.
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