Background: The recent scientific literature has highlighted how factors involved in the onset of under- and over-eating in childhood are related to early emotional dysregulation, dysfunctional relational patterns with caregivers, psychopathological symptoms in parents and genetic and epigenetic correlates. Therefore, there is a need to develop assessment programs that focus on the evaluation of these aspects.
Objectives: The present research project aims to evaluate psychological, genetic and epigenetic risk indicators in the clinical manifestations of Avoidant-Restrictive Feeding Disorder (ARFID) and Overeating (OE), with the goal of providing empirical data to plan specific and targeted interventions.
Methodology: We plan to recruit a total of N=900 families (with children between 24 and 36 months) divided in three samples: N=300 families with children with an ARFID diagnosis; N=300 families with children with an OE diagnosis; N=300 control families with children without medical and/or psychiatric disorders. Subjects of the three samples, depending on their age, will be given observation tools, self-reports and report-forms, to assess possible psychological risk factors. In respect of Istituto Superiore di Sanità research regulation during the Covid-19 pandemic, salivary samples will then be collected from all participants to assess biological risk factors that include specific genetic polymorphisms and global genome methylation.
Data analysis: a model of structural equations will be built, to understand the interaction between the different variables considered.
Discussion and innovation: the present research will allow to understand psychological, genetic and epigenetic risk indicators associated with clinical pictures of ARFID and OE, with the aim of implementing effective intervention programs.
The present study aims to identify the possible psychological processes, and underlying genetic aspects, involved in the ARFID and EO, by analyzing possible risk and/or protection factors. Since studies on adult subjects suggest a shared molecular basis between anorexia nervosa and obesity (Bulik-Sullivan et al., 2015), it is particularly important to study subjects in the first years of life, to investigate the role that gene x environment interaction has in the onset and possible stabilization of eating disorders. The early identification of risk and/or protection factors linked to the adult-subject relationship in the developmental age, to the psychological and/or psychopathological profiles of children and parents, to genetic and epigenetic configurations, will have a strong impact on the international scientific community, because to date there are no multifactorial studies on childhood eating disorders, which take into account the complex interweaving of psychological, genetic and epigenetic variables. In fact, although to date the literature has highlighted how eating disorders are moderately or highly heritable, with estimates of heritability obtained from studies on twins ranging from 28 to 74% for anorexia nervosa, from 54 to 83% for bulimia nervosa and from 41 to 57% for binge eating disorder (Thornton et al., 2011), molecular analysis still needs extensive experimentation to reach conclusions useful for therapeutic interventions. In addition, epigenetic mechanisms provide a recognized substrate for gene x environment interactions and need to be investigated for a better understanding of the clinical pictures under analysis. In fact, environmental influences, especially those typical of early childhood, can induce epigenetic alterations (Strober et al., 2014) that remain stable throughout life, but can be reverted through specific and targeted support and/or therapeutic interventions. The most studied epigenetic modification in the field of eating disorders is DNA methylation. Studies conducted so far have shown that genes involved, among other things, in anxiety, depression and stress responses (Frieling et al., 2008), associative behavior (Kim et al., 2014), gratification circuits (Frieling et al., 2010), are hypermethylated in people with eating disorders. This condition causes a decrease or lack of expression of the modified genes that produces alterations in the activity of neuronal populations directly or indirectly involved in the behavioral disorders under study (Frieling et al., 2007; Saffrey et al., 2014; Tremolizzo et al., 2014). The implementation of this project, in addition to a greater knowledge of the variables associated with these two clinical pictures that appear in the first years of life, will allow the drafting of differentiated guidelines for risk and pathological situations, taking into account the most relevant maladaptive factors on which to focus the intervention: for example, the evaluation of the paternal contribution will provide important indications on possible intervention strategies involving the whole family.