The International journal of eating disorders · 2026
An Exploratory Study of Neural Response to Food Cues Following Cognitive-Behavioral Therapy for Avoidant/Restrictive Food Intake Disorder.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Becker Kendra R, Graver Haley, Van De Water Avery L, Dalton Abigail G, Karlson Rebecca, Palmer Lilian P, Stern Casey, Breithaupt Lauren, Burton-Murray Helen, Kuhnle Megan, Kristine Hauser N P, Misra Madhusmita, Lawson Elizabeth A, Eddy Kamryn T, Holsen Laura, Thomas Jennifer J
Аннотация
OBJECTIVE: Avoidant/restrictive food intake disorder (ARFID) is characterized by limited dietary volume and/or variety due to fear of aversive consequences, lack of interest in eating, and/or sensory sensitivity. Uncontrolled studies suggest that cognitive-behavioral therapy for ARFID (CBT-AR) is beneficial, but neural mechanisms remain unknown. Prior work has shown hyperactivation in regions of the salience network (SN) during the presentation of food stimuli in ARFID compared to healthy controls, and the SN shows reduction from pre- to post-CBT in anxiety disorders. We tested hypotheses that (1) higher pre-treatment food-related activation in the SN (anterior cingulate cortex [ACC], anterior insula, amygdala) would be prospectively associated with greater reductions in ARFID severity at post-treatment, and (2) food-related activation in the SN would decrease from pre- to post-treatment.
METHOD: In a validated functional magnetic resonance imaging (fMRI) food cue paradigm, youth with ARFID viewed images of food and non-food in a fasted state at pre-treatment (N = 24) and a subset (N = 14) also completed post-treatment scans.
RESULTS: Pre-treatment activation in response to food versus objects was not associated with changes in ARFID severity or remission post-treatment. However, hyperactivation in the right ACC (MNI coordinates: 3, 53, 17; k(E) = 579, p(FWEcorr) = 0.013) decreased from pre- to post-treatment with a large effect size (d = 1.1).
CONCLUSION: These pilot findings raise the possibility that changes in SN neural activity may be candidate mechanisms through which CBT-AR exerts its effects. Randomized controlled trials are needed to replicate and extend these results.
TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02963220.
METHOD: In a validated functional magnetic resonance imaging (fMRI) food cue paradigm, youth with ARFID viewed images of food and non-food in a fasted state at pre-treatment (N = 24) and a subset (N = 14) also completed post-treatment scans.
RESULTS: Pre-treatment activation in response to food versus objects was not associated with changes in ARFID severity or remission post-treatment. However, hyperactivation in the right ACC (MNI coordinates: 3, 53, 17; k(E) = 579, p(FWEcorr) = 0.013) decreased from pre- to post-treatment with a large effect size (d = 1.1).
CONCLUSION: These pilot findings raise the possibility that changes in SN neural activity may be candidate mechanisms through which CBT-AR exerts its effects. Randomized controlled trials are needed to replicate and extend these results.
TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02963220.