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Abstract

Background: Current management of Crohn’s Disease (CD) prioritizes mucosal healing (“treat-to-target”); however, many treated patients continue to experience debilitating symptoms driven by maladaptive eating behaviours. This phenomenon, known as Conditioned Food Avoidance and Sensitivity Trap (C-FAST) or Avoidant/Restrictive Food Intake Disorder (ARFID), involves the restriction of food due to a fear of inducing worsening gastrointestinal (GI) symptoms. While the impact of diet on the bacterial microbiome is well-established, fungi also play a critical role in gut homeostasis and inflammation, and are highly responsive to dietary changes. However, the relationship between restrictive eating, specific nutritional deficits, and the fungal mycobiome remains largely unexplored. This study investigated whether fear-based food avoidance drives fungal alterations and contributes to poor nutritional status and quality of life (QoL) in CD. Methods: A cross-sectional analysis was conducted on 40 adult patients with CD recruited as part of an ongoing prospective clinical cohort study (the OPTIMIST study). Participants were stratified by disease activity (Remission vs. Flare) and food avoidance severity (Low vs. High Avoidance) using a composite questionnaire score. Validated instruments were used to assess QoL (IBDQ-32) and disordered eating traits (Nine-Item ARFID Screen [NIAS]). Nutritional intake was quantified using 3-day weighed diet records, and total fungal load was measured via quantitative PCR (qPCR) of the ITS1 region in stool samples. Results: A distinct “False Remission” phenotype was identified, where 25% of patients in clinical remission exhibited High Avoidance behaviours with some experiencing ongoing GI symptoms. These patients reported significantly lower QoL scores on the IBDQ (p = 0.018) comparable to those with active disease. High Avoidance was associated with a significantly lower intake of dietary tryptophan (p = 0.046), a key precursor for serotonin and pathways involved in mood regulation and gut-brain signaling, while total dietary fibre intake remained stable across groups. Contrary to the hypothesis that restriction would drive fungal overgrowth, total fungal load remained stable across all disease and avoidance states, suggesting mycobiota community resilience. Interestingly, in patients with active inflammation, higher fungal load correlated with better systemic symptom scores on the IBDQ (p = 0.038). Conclusion: Maladaptive food avoidance behaviours create a state of “False Remission” characterized by severe psychosocial impairment, especially in those with ongoing GI symptoms, and tryptophan depletion independent of biological inflammation. The observed stability of the mycobiota suggests that the fungal community is resilient to these dietary restrictions. Consequently, dietary reintroduction interventions in remission patients should be prioritized to correct nutritional deficits and improve QoL, alongside further research to determine whether restrictive eating impacts specific fungal taxa.