Abstract
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.
Highlights
The results showed that the four groups were significantly different on children’s levels of DAT1 total methylation (F(3,46) = 52.76, p < 0.0001, ηp2 = 0.71), the score of CBCL Dysregulation Profile (DP) (F(3,46) = 266.06, p < 0.0001, ηp2 = 0.85), and mothers score on Global Severity Index (GSI) (F(3,44) = 791.57, p < 0.0001, ηp2 = 0.95), with large effect sizes
With regard to sensory food aversion (SFA) diagnosis, we found a significant association with 10/10 genotype, with large effect size, and DAT1 methylation was at a medium level
Our preliminary findings have supported the importance to considering the complex interaction between DAT1 gene and environment provided by mothers, both in terms of genotype-environment interactions and the possible methylation mechanisms involved
Summary
A greater gene expression has been shown associated with DAT1 10/10 genotype [6,7]. The higher frequency of the short allele (i.e., 7 or 9 repeats, in comparison to the long allele, 10 or 11 repeats) in the DAT1 gene reported by Shinohara and colleagues [13] suggests decreased DAT function in patients who have EDs with binge-eating behaviors. One study [15] found an association between ADHD symptoms and disordered eating in young children, suggesting that the DA path could be involved in the underpinning mechanism explaining both difficulties. Previous research has shown associations between ADHD in children and DAT1 polymorphism and methylation [16,17,18,19]. Undernutrition has been shown to be associated with epigenetic changes in humans and DNA polymorphisms [20,21]
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