Co-Occurrence of Avoidant/Restrictive Food Intake Disorder (ARFID) and Schizophrenia-Spectrum Disorders: A Comprehensive Review

TL;DR

This paper reviews how eating disorder ARFID and schizophrenia-spectrum disorders can co-occur, complicating diagnosis and treatment.

Contribution

The paper identifies shared mechanisms like pathological avoidance and sensory sensitivity linking ARFID and psychosis.

Findings

Abnormalities in interoception and sensory sensitivity are common to both ARFID and psychosis.

Psychosis can mimic or worsen ARFID, and malnutrition from ARFID may trigger psychotic symptoms.

Shared mechanisms suggest a need for integrated treatment approaches in comorbid patients.

Abstract

Background/Objectives: Avoidant/restrictive food intake disorder (ARFID) and psychotic disorders are clinically distinct conditions yet occasionally co-occur in ways that complicate assessment and treatment. ARFID is characterised by avoidance of food due to sensory sensitivities, fear of aversive consequences, or low interest in eating, without body-image distortion. Recent meta-analytic evidence suggests that ARFID affects a substantial proportion of the population and is associated with a considerable social burden. Psychosis is characterised by positive symptoms (hallucinations and delusions), negative symptoms (avolition, blunted affect, and social withdrawal), and cognitive impairments affecting thought, perception, and behaviour. Methods: Across the limited literature, shared mechanisms between ARFID and psychotic disorders appear to converge on pathological avoidance, which may arise from sensory overstimulation, obsessive–compulsive features, or delusional beliefs about food. Case reports indicate that psychosis may both mimic ARFID and exacerbate food avoidance, while severe malnutrition can itself precipitate or worsen psychotic symptoms, blurring diagnostic boundaries. Results: Abnormalities in interoception, sensory sensitivity, and disrupted perception of bodily signals are manifestations of both ARFID and psychosis, suggesting a potential bridging pathway contributing to vulnerability and clinical overlap. Conclusions: Given the paucity of empirical studies and the reliance on isolated case reports, systematic investigation is mandatory and necessary to clarify shared mechanisms, refine differential diagnosis, and guide integrated treatment approaches. Given the heterogeneity of symptoms in comorbid patients, a personalised approach is suggested for treating these patients.

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