We read with enthusiasm the recent articles by Martin et al. 1 and Mikhael-Moussa et al. 2, which provide valuable insights into the relationship between avoidant/restrictive food intake disorder (ARFID) and disorders of gut–brain interaction (DGBI). Both highlight the difficulty of identifying ARFID in clinical settings and the need for greater diagnostic clarity. These challenges reflect broader conceptual uncertainties about the mechanisms underlying dietary restriction in patients with gastrointestinal symptoms. Unlike eating disorders driven by body image disturbance, ARFID involves avoidance related to sensory characteristics of food or concerns about aversive consequences. In patients with DGBI, dietary restriction often emerges from interactions between biological symptoms and psychological responses within the biopsychosocial model. In clinical practice, biologically driven avoidance may resemble ARFID, complicating assessment and patient communication. To address these challenges, we propose a conceptual framework informed by the Conditioned Food Avoidance and Sensitivity Theory (C-FAST), which emphasizes food–illness associations as key drivers of eating behavior. These associations may develop through implicit learning and threat conditioning, whereby repeated experiences of gastrointestinal discomfort become linked to specific foods or eating contexts. Over time, this process can lead to persistent avoidance patterns that may continue even after biological triggers have resolved. Within this framework, we distinguish between two related but conceptually distinct phenomena. Conditioned food avoidance, dietary restriction driven by learned food–illness associations, may be accurate, reflecting a biologically driven response (e.g., lactose intolerance), or inaccurate, resulting in unnecessary or excessive restriction. Conditioned food sensitivity describes the emergence or amplification of physical symptoms driven by fear, expectation, or heightened symptom monitoring, consistent with nocebo-related mechanisms 3, 4. These processes may interact to create self-reinforcing cycles of avoidance, symptom perception and exacerbation. Restrictive eating may also influence biological processes relevant to gut–brain signaling. Reduced dietary diversity and altered composition can affect the gut microbiota, visceral sensitivity, and interoceptive processing, potentially reinforcing symptom persistence and conditioned responses 5. Within the C-FAST Model, these biological factors are viewed as modulators rather than primary drivers. This integrative perspective has important clinical implications. Framing restrictive eating as a learned and potentially adaptive response, rather than inherently pathological, may improvepatient engagement and support nuanced assessment. Future research should prioritize developing screening tools which capture the conditioning processes, food-related beliefs, and maintaining factors. Patient feedback should be utilized to develop multidisciplinary care integrating nutrition and behavioral strategies to interrupt the C-FAST cycle and promote intentional food choices. W.B. developed the C-FAST model. W.B, L.A. and E.V. conducted the literature search. W.B. and L.A. drafted the letter. All authors critically revised the letter. The authors have nothing to report. Wendy Busse owns the FAST Freedom Program. Research data are not shared.
Busse et al. (Wed,) studied this question.