The exact cause of ARFID is still unknown. ARFID has been included in the DSM only since 2013, and research on the neurobiology of this disorder is currently limited. It is understood that ARFID can be triggered by a sensitivity to the taste, texture, or smell of food, by negative associations with certain food-related body sensations, or by a lack of interest in food. However the underlying causes of these triggers are not clearly understood, and it is likely that a combination of psychological, environmental, and biological factors contribute to the development of ARFID.
Hypotheses have been proposed based on existing studies of conditions that share similarities with ARFID. Sensory hypersensitivity may contribute to the rejection of food based on taste, smell, or texture, which has been observed both in adults and children identified as “picky eaters”. A decreased activation of the brain’s appetite-regulating centers may be associated with a lack of interest in food. On the other hand, the rejection of food due to fear of adverse events, such as choking or vomiting, may be related to hyperactivation of specific areas of the brain involved in fear responses, such as the amygdala, ventrolateral prefrontal cortex, and anterior cingulate.[1]
Genetics may also play a role in the development of ARFID. One study conducted in Swedish children between the ages of 6 and 12 indicated a heritability rate of up to 79% for ARFID. However, this study has several limitations, and the methodologies used to collect data and diagnose ARFID were not robust, so these results should be interpreted cautiously.[2]