Sader Michelle, Harris Holly A, Waiter Gordon D, Jansen Pauline W, Williams Justin H G, White Tonya
University of Aberdeen, Aberdeen, UK.
Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.
J Child Psychol Psychiatry. 2025 Jun;66(6):785-795. doi: 10.1111/jcpp.14086. Epub 2024 Dec 2.
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.
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 T-weighted structural magnetic resonance imaging (MRI) scans in those with ARFID symptoms were compared with children not exhibiting symptoms.
We identified 121 (6.1%) individuals with ARFID symptoms relative to 1,865 (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.
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.
回避性限制性食物摄入障碍(ARFID)是一种最近才被认识到的进食障碍,其特征是对进食缺乏兴趣和动力。尽管研究不断涌现,但迄今为止,很少有研究探讨ARFID的潜在神经生物学机制。研究ARFID的神经基础有助于深入理解发挥疾病特异性作用的不同机制。
我们对来自荷兰基于人群的队列研究“Generation R Study”中的1977名10岁参与者进行了研究,以横断面方式检查有或没有ARFID样症状的儿童之间的神经解剖学差异。使用ARFID指数对儿童进行ARFID症状分类,该指数是一种经过验证的评估工具,由家长报告和研究人员评估的挑食、能量摄入、饮食质量、生长和心理社会影响等测量指标组成,用于描述儿科人群中的ARFID症状。将有ARFID症状儿童的T加权结构磁共振成像(MRI)扫描的表面积、皮质厚度和体积的全局和区域值与未出现症状的儿童进行比较。
我们确定了121名(6.1%)有ARFID症状的个体,相对于1865名(93.9%)没有ARFID症状的个体。神经解剖学研究结果显示,有ARFID症状的儿童额叶(p = 0.00743;d = 0.21)和额上回(p = 6.56E - 04;d = 0.28)皮质厚度显著更大。
这项关于ARFID神经相关性的首次大规模研究发现,有ARFID症状的儿童额叶皮质区域厚度更大,表明执行功能在该疾病的病因学中起作用。