P BED

 A

Key Points: Adolescent Obesity, Binge Eating Disorder (BED), Cortical Thickness, and Appetite Hormones

Category	Findings
Study Objective	To investigate brain cortical thickness and appetite-regulating hormones (NPY and ghrelin) in adolescents with obesity and BED.
Participants	70 adolescents (ages 12–18): 24 with BED + obesity, 24 with obesity without BED, 22 healthy controls (HCs).
Brain Imaging Method	Structural MRI (3.0 T) with FreeSurfer cortical thickness analysis.
Hormones Measured	Fasting serum Neuropeptide Y (NPY) and ghrelin levels.
Psychological Assessments	EAT-40, EDE-Q, CDI (depression), STAI-C (anxiety).

Hormonal Findings

Finding	Interpretation
Elevated NPY in both obesity groups compared with healthy controls	NPY appears linked to obesity itself rather than specifically to BED.
No NPY difference between obesity-only and BED groups	BED does not add additional NPY elevation beyond obesity.
Ghrelin levels similar across all groups	Fasting ghrelin may not distinguish BED from obesity or healthy adolescents.

Brain Structure Findings

Brain Region	Finding
Right Posterior Cingulate Cortex (PCC)	Significantly thinner only in adolescents with BED.
Left Posterior Cingulate Cortex	Thinner in both obesity groups compared with healthy controls.
Insula	No significant group differences in thickness.
Anterior Cingulate Cortex (ACC)	No significant group differences in thickness.

Psychological Findings

Measure	Result
Depression (CDI)	Higher in both obesity groups than healthy controls.
Disordered Eating Attitudes	Higher in both obesity groups.
Eating-related Psychopathology	Greater in both obesity groups than controls.
Anxiety	Increased psychological burden associated with obesity.

Regression Analysis

Variable	Association with Higher NPY
Higher BMI	Strong positive association (β = 0.47).
Lower Left Insular Thickness	Independent negative association (β = -0.45).
Diagnostic Group (BED vs Obesity)	Less important than BMI and insular thickness for predicting NPY.

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Neurobiological Interpretation

Finding	Possible Meaning
Elevated NPY	Increased hunger signaling, energy conservation, and appetite drive associated with obesity.
Left PCC thinning in obesity	Altered self-referential processing, reward evaluation, and internal state monitoring associated with obesity.
Right PCC thinning specific to BED	May reflect impaired self-regulation, altered craving processing, and vulnerability to binge-eating behaviors.
Insular-NPY relationship	Suggests interaction between appetite signaling and brain regions involved in interoception (awareness of hunger/fullness).

Clinical Takeaway

• Elevated NPY appears to be a neurobiological marker of adolescent obesity in general.

• Reduced right posterior cingulate cortical thickness may be a more specific neural signature of binge eating disorder (BED).

• BED is not simply "more obesity"; it may involve distinct alterations in brain networks related to self-awareness, craving regulation, and eating behavior.

• These findings support the idea that adolescent BED has identifiable neurobiological correlates rather than being solely a behavioral problem.

One-Sentence Summary

In adolescents, obesity is associated with elevated appetite-promoting NPY levels, while binge eating disorder appears additionally linked to thinning of the right posterior cingulate cortex, suggesting a distinct brain-based component to loss-of-control eating.