Neural correlates of children with avoidant restrictive food intake disorder symptoms: large-scale neuroanatomical analysis of a paediatric population

Date published: 02/12/24
Authors: Michelle Sader, Holly Harris, Gordon Waiter, Pauline Jansen, Justin H.G. Williams & Tonya White
Published in: Journal of Child Psychology and Psychiatry

Objective

Avoidant restrictive food intake disorder (ARFID) is a recently recognised feeding and eating disorder and is characterised by a lack of interest and motivation to eat. Despite burgeoning research, few studies to date have explored the underlying neurobiology of ARFID. Research examining the neural underpinnings of ARFID can greatly assist in understanding different mechanisms that play disorder-specific roles. 


Method

We studied a total of 1,977 10-year-old participants from the Generation R Study, a population-based Dutch cohort, to cross-sectionally examine neuroanatomical differences between those with versus without ARFID-like symptoms. Children were classified with versus without ARFID symptoms using the ARFID Index, a validated evaluative tool comprised of parent-reported and researcher-assessed measurements of picky eating, energy intake, diet quality, growth and psychosocial impact to characterise ARFID symptoms in the paediatric population. Global and regional values of surface area, cortical thickness, and volume from T1-weighted structural magnetic resonance imaging (MRI) scans in those with ARFID symptoms were compared with children not exhibiting symptoms.


Results

We identified 121 (6.1%) individuals with ARFID symptoms relative to 1,856 (93.9%) individuals without ARFID symptoms. Neuroanatomical findings identified significantly greater frontal (p = .00743; d = 0.21) and superior frontal (p = 6.56E-04; d = 0.28) cortical thickness among children with ARFID symptoms. 


Conclusions

This first large-scale study of the neural correlates of ARFID identified greater thickness of frontal cortical regions in children with ARFID symptoms, suggesting a role for executive function in the aetiology of the condition.

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