Neuroendocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School.
Division of Pediatric Endocrinology, Mass General Hospital for Children.
J Clin Child Adolesc Psychol. 2022 Sep-Oct;51(5):701-714. doi: 10.1080/15374416.2021.1894944. Epub 2021 Mar 26.
Avoidant/restrictive food intake disorder (ARFID) occurs across the weight spectrum, however research addressing the coexistesnce of ARFID with overweight/obesity (OV/OB) is lacking. We aimed to establish co-occurrence of OV/OB and ARFID and to characterize divergent neurobiological features of ARFID by weight.
Youth with full/subthreshold ARFID (12 with healthy weight [HW], 11 with OV/OB) underwent fasting brain fMRI scan while viewing food/non-food images (M age = 16.92 years, 65% female, 87% white). We compared groups on BOLD response to high-calorie foods (HCF) (vs. objects) in food cue processing regions of interest. Following fMRI scanning, we evaluated subjective hunger pre- vs. post-meal. We used a mediation model to explore the association between BMI, brain activation, and hunger.
Participants with ARFID and OV/OB demonstrated significant hyperactivation in response to HCF (vs. objects) in the orbitofrontal cortex (OFC) and anterior insula compared with HW participants with ARFID. Mediation analysis yielded a significant indirect effect of group (HW vs. OV/OB) on hunger via OFC activation (effect = 18.39, SE = 11.27, 95% CI [-45.09, -3.00]), suggesting that OFC activation mediates differences in hunger between ARFID participants with HW and OV/OB.
Compared to youth with ARFID and HW, those with OV/OB demonstrate hyperactivation of brain areas critical for the reward value of food cues. Postprandial changes in subjective hunger depend on BMI and are mediated by OFC activation to food cues. Whether these neurobiological differences contribute to selective hyperphagia in ARFID presenting with OV/OB and represent potential treatment targets is an important area for future investigation.
回避/限制型进食障碍(ARFID)发生在整个体重范围内,然而,关于 ARFID 与超重/肥胖(OV/OB)共存的研究却很少。我们旨在确定 OV/OB 和 ARFID 的共同发生,并通过体重来描述 ARFID 不同的神经生物学特征。
有完全/亚阈值 ARFID 的青少年(12 名体重正常[HW],11 名 OV/OB)在禁食状态下进行 fMRI 扫描,同时观看食物/非食物图像(M 年龄=16.92 岁,65%女性,87%白人)。我们比较了两组在食物线索处理区域的大脑对高热量食物(HCF)(与物体相比)的 BOLD 反应。在 fMRI 扫描后,我们评估了餐前和餐后的主观饥饿感。我们使用中介模型来探索 BMI、大脑激活和饥饿之间的关系。
与 HW 组的 ARFID 参与者相比,OV/OB 组的 ARFID 参与者在眶额叶皮层(OFC)和前岛叶对 HCF(与物体相比)的反应中表现出显著的过度激活。中介分析得出了一个显著的间接效应,即组(HW 与 OV/OB)通过 OFC 激活对饥饿的影响(效应=18.39,SE=11.27,95%置信区间[-45.09,-3.00]),表明 OFC 激活介导了 HW 和 OV/OB 组的 ARFID 参与者之间的饥饿差异。
与 HW 组的 ARFID 参与者相比,OV/OB 组的 ARFID 参与者对食物线索的奖励价值的大脑区域表现出过度激活。餐后主观饥饿感的变化取决于 BMI,并通过 OFC 对食物线索的激活来介导。这些神经生物学差异是否导致了 ARFID 中伴有 OV/OB 的选择性暴食,并代表潜在的治疗靶点,这是未来研究的一个重要领域。