Biopsychosocial development of avoidant restrictive food intake disorder: an integrative review

Despite the early age of typical Avoidant Restrictive Food Intake Disorder (ARFID) onset and its adverse impacts on development, the biopsychosocial mechanisms underlying its etiology remain poorly understood. The objective of this integrative review is to identify and describe the biological, psychological, and social contributors to the development of ARFID. Systematic searches were conducted across PubMed, PsycINFO, and Web of Science using terms related to parenting and feeding practices and genetic/epigenetic factors. Studies examining ARFID in children and either parenting practices, feeding practices, or biological influences on ARFID development were included. Additional inclusion criteria were peer-review and publication after 2013, when the formal ARFID diagnosis was first introduced. Review of 21 eligible studies indicated that ARFID is potentially associated with distinct neurological and hormonal profiles, including reduced brain volume, atypical appetite hormone signaling, heritable genetic contributions, and epigenetic processes like DAT1 methylation. Maladaptive parenting strategies, poor parent-child relationship quality, and parental accommodation emerged as risk factors, while supportive caregiving strategies appear protective. Maternal psychopathology is associated with child ARFID risk through child emotion dysregulation, a pathway moderated by child genotype. Early developmental difficulties, premature birth, and somatic complaints emerged as salient predictors of ARFID symptom trajectories. Findings support a biopsychosocial framework for understanding ARFID and highlight the need for longitudinal research to examine the complex gene-environment interaction underlying the development of ARFID and its subtypes. Avoidant Restrictive Food Intake Disorder (ARFID) has the earliest age of onset of any eating disorder and the potential to disrupt child development. In addition, eating disorders represent a significant public health burden due to the cost of treatment and high lifetime prevalence rates. More information is needed regarding the parental and biological factors that impact the development of ARFID to inform successful prevention and treatment efforts.