A Role for the Microbiota‐Gut‐Brain Axis in Avoidant/Restrictive Food Intake Disorder: A New Conceptual Model.

BRAIN physiology; BRAIN metabolism; GASTROINTESTINAL system physiology; FEAR; FOOD consumption; HOMEOSTASIS; GUT microbiome; BRAIN; SENSORY perception; CELLULAR signal transduction; HYDROCORTISONE; EATING disorders; BACTERIA; METABOLITES; FOOD; REWARD (Psychology); AVERSION; INFLAMMATION; DOPAMINE; SEROTONIN; DIET therapy; DIET in disease; BIOPSYCHOSOCIAL model; NEUROTRANSMITTERS

Objective: Avoidant/restrictive food intake disorder (ARFID) is an eating disorder characterized by a severely restrictive diet leading to significant physical and/or psychosocial sequelae. Largely owing to the phenotypic heterogeneity, the underlying pathophysiological mechanisms are relatively unknown. Recently, the communication between microorganisms within the gastrointestinal tract and the brain—the so‐called microbiota‐gut‐brain axis—has been implicated in the pathophysiology of eating disorders. This Spotlight review sought to investigate and conceptualize the possible ways that the microbiota‐gut‐brain axis is involved in ARFID to drive future research in this area. Method: By relating core symptoms of ARFID to gut microbiota and its signaling pathways to the brain, we evaluated how the gut microbiota is potentially involved in the pathophysiology of ARFID. Results: We hypothesized that the restricted type and amount of food intake characteristic of ARFID diminishes gut microbial diversity, including beneficial bacteria and their metabolites capable of signaling to the brain, to modulate biopsychological pathways relevant to ARFID: homeostatic signaling, food reward, interoception, sensory sensitivity, disgust, perseveration, fear‐based learning, and mood. Candidate signaling mechanisms include microbial‐induced effects on inflammation, cortisol, and neurotransmitters such as dopamine and serotonin. Discussion: Through reviewing the extant evidence, we conceptualized a new theoretical framework of ARFID with an emphasis on microbiota‐gut‐brain axis signaling to inform future research. Although more research is necessary to evaluate this theoretical model, the tentative evidence suggests that therapeutics specifically targeting the gut microbiota for the treatment of ARFID symptomatology warrants more investigation. [ABSTRACT FROM AUTHOR]

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