DAT1 and Its Psychological Correlates in Children with Avoidant/Restrictive Food Intake Disorder: A Cross-Sectional Pilot Study

International research has underlined the role played by children’s and maternal psychopathological symptoms on the onset of avoidant/restrictive food intake disorder (ARFID) in early childhood. No study has considered the possible interplay between children’s dopamine transporter (DAT1) genotype and methylation, dysregulation problems and maternal psychopathological risk. This study aimed to investigate the complex relationship between these variables, considering the possible mediation role played by children’s DAT1 methylation on the relationship between mothers’ psychopathological risk and children’s dysregulation problems, moderated by children’s DAT1 genotype. Our sample consisted of 94 early children and their mothers, divided into four subgroups, based on children’s ARFID subtypes (irritable/impulsive (I/I), sensory food aversions (SFA), post-traumatic feeding disorders subtypes (PTFD), and a non-clinical group (NC)). We addressed children’s dysregulation problems and maternal psychopathological risk, and collected children’s DNA through buccal swabs. Results showed that children’s 9/x genotype was associated with PTFD and NC groups, whereas the 10/10 genotype was associated with the SFA group, with large effect size. There were significant large differences in the study groups on children’s DAT1 total methylation, children’s dysregulation problems, and maternal psychopathological risk. Children’s DAT1 methylation did not mediate the relationship between mother’s psychopathological risk and children’s dysregulation problems, but there was a significant large direct effect. Children’s 9/x genotype moderated the relationship between maternal psychopathological risk and children’s DAT1 methylation but, respectively, with a large and small effect. Our pilot study suggested that the relationship between children’s DAT1 genotype and methylation, dysregulation problems, and maternal psychopathological risk has a crucial contribution to ARFID.