Overweight/obesity and loss of control eating (characterized by the sense that one cannot control what or how much one is eating) are prevalent among children and adolescents, and both are associated with serious medical and psychosocial health complications. Although our recently published data suggest that youth with these conditions may have relative deficits in neurocognitive functioning, particularly working memory, understanding of how these processes and their neural correlates are related to change and stability in eating and weight-related outcomes over time is limited, thereby impeding development of targeted, optimally timed interventions. The present study aims to assess prospective associations between general and food-specific executive functioning and underlying neural substrates, and eating and weight outcomes among children at varying levels of risk overweight/obesity and eating disorders, which will help guide research efforts towards the development of effective prevention and intervention strategies.
The current study will examine prospective associations among general and food-specific EF and related neural substrates, and the developmental course of weight gain and LOC eating from middle childhood through early adolescence. Specific aims are to: 1. Investigate prospective associations between general and food-specific EF and z-BMI trajectories. We expect that across risk groups, a) poorer baseline performance on both general and food-specific behavioral EF measures will predict steeper z-BMI gain trajectories; and b) worsening general and food-specific EF will track with the steepest z-BMI gain trajectories. 2. Investigate associations between general and food-specific EF and LOC eating trajectories. We expect that across risk groups, a) poorer baseline performance on general and food-specific behavioral EF measures will predict worsening course of LOC eating; and b) worsening general and food-specific EF will track with worsening course of LOC eating. 3. Investigate prospective associations between EF neural substrates and trajectories of z-BMI and LOC eating. We expect that across risk groups, a) greater activation in prefrontal regions associated with EF (e.g., dorsolateral prefrontal cortex, dorsal cingulate, parietal cortex) during general and food-specific WM tasks, and b) smaller decreases in activation of these regions over 18 months, will predict steeper z-BMI gain trajectories and worsening course of LOC eating.
Study Type
OBSERVATIONAL
Enrollment
180
Observational data will be obtained through self-report measures, parental report measures, cognitive assessments, and a semi-structured interview.
Observational data will be obtained through self-report measures, parental report measures, cognitive assessments, fMRI imaging, and a semi-structured interview.
University of PIttsburgh
Pittsburgh, Pennsylvania, United States
RECRUITINGWeight Control & Diabetes Research Center
Providence, Rhode Island, United States
ACTIVE_NOT_RECRUITINGBMI (Body Mass Index)
BMI will be assessed using height and weight (cm/g)
Time frame: Change in BMI from baseline to 24 months
Eating Behavior
Eating behavior will be assessed using the Eating Disorder Examination (EDE), a semi-structured interview. Global scores are calculated, with higher scores indicating higher disordered eating symptomology.
Time frame: Change in eating behavior from baseline to 24 months
General Executive Functioning
A general n-back task that will involve continuous presentation of neutral stimuli (letters or numbers). Participants indicate via button press whether the target (current) stimulus was presented n items ago.
Time frame: Change in general executive functioning from baseline to 24 months
Food-Specific Executive Functioning
A food-specific WM task that involves continuous presentation of stimuli representing food and non-food items. Participants indicate via button press whether the target (current) stimulus was presented n items ago.
Time frame: Change in food-specific executive functioning from baseline to 24 months
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