Aberrant functional connectivity between reward and inhibitory control networks in pre-adolescent binge eating
Stuart B Murray1, Celina Alba2, Christina J Duval1
1Department of Psychiatry & Behavioral Sciences, Keck School of Medicine of USC, University of Southern California, Los Angeles, CA, USA.
Insights
Pediatric binge eating disorder (BED) shows altered brain connectivity between reward and control networks. This study reveals reduced functional connectivity in children with BED, impacting their ability to regulate food desires.
Area of Science:
- Neuroscience
- Developmental Psychology
- Pediatric Psychiatry
Background:
- Behavioral symptoms of binge eating disorder (BED) suggest issues with reward processing and inhibitory control.
- Adult BED studies show functional brain network abnormalities, but the neurobiology in children is unstudied.
- Behavioral markers for BED emerge in childhood, highlighting the need to investigate pediatric neurobiology.
Purpose of the Study:
- To investigate neurobiological differences in pediatric BED.
- To examine functional connectivity (FC) within and between reward and inhibitory control networks in pre-adolescent children with BED.
- To identify potential neural underpinnings of early-onset BED.
Main Methods:
- Utilized data from 58 pre-adolescent children with BED and 66 controls from the ABCD Study.
- Employed resting-state functional MRI to assess functional connectivity (FC).
- Conducted seed-based analyses targeting reward (OFC, nucleus accumbens, amygdala) and inhibitory control (dlPFC, ACC) networks.
Main Results:
- Children with BED exhibited reduced FC between the dorsolateral prefrontal cortex (dlPFC) and amygdala.
- A decrease in FC was observed between the anterior cingulate cortex (ACC) and orbitofrontal cortex (OFC) in children with BED.
- Whole-brain analyses corroborated these findings of aberrant connectivity between inhibitory control and reward networks.
Conclusions:
- Early-onset BED may involve widespread abnormalities in the synergy between reward and cognitive control networks.
- These connectivity deficits between networks, rather than within them, may underlie difficulties in regulating hedonic food intake in BED.
- Dysconnectivity between reward and inhibitory control networks could be a key factor in the pathophysiology of pediatric BED.
Background:
Behavioral features of binge eating disorder (BED) suggest abnormalities in reward and inhibitory control. Studies of adult populations suggest functional abnormalities in reward and inhibitory control networks. Despite behavioral markers often developing in children, the neurobiology of pediatric BED remains unstudied.
Methods:
58 pre-adolescent children (aged 9-10-years) with BED (mBMI = 25.05; s.d. = 5.40) and 66 age, BMI and developmentally matched control children (mBMI = 25.78; s.d. = 0.33) were extracted from the 3.0 baseline (Year 0) release of the Adolescent Brain Cognitive Development (ABCD) Study. We investigated group differences in resting-state functional MRI functional connectivity (FC) within and between reward and inhibitory control networks. A seed-based approach was employed to assess nodes in the reward [orbitofrontal cortex (OFC), nucleus accumbens, amygdala] and inhibitory control [dorsolateral prefrontal cortex, anterior cingulate cortex (ACC)] networks via hypothesis-driven seed-to-seed analyses, and secondary seed-to-voxel analyses.
Results:
Findings revealed reduced FC between the dlPFC and amygdala, and between the ACC and OFC in pre-adolescent children with BED, relative to controls. These findings indicating aberrant connectivity between nodes of inhibitory control and reward networks were corroborated by the whole-brain FC analyses.
Conclusions:
Early-onset BED may be characterized by diffuse abnormalities in the functional synergy between reward and cognitive control networks, without perturbations within reward and inhibitory control networks, respectively. The decreased capacity to regulate a reward-driven pursuit of hedonic foods, which is characteristic of BED, may in part, rest on this dysconnectivity between reward and inhibitory control networks.
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