Eating disorders (EDs) are complex, multifactorial conditions influenced by biological, psychological and environmental factors. Recent discoveries in genetic epidemiology research have confirmed a genetic component in EDs, particularly in anorexia nervosa. However, the biological processes underlying the causal pathways to disease onset remain poorly understood and biomarker research in this area significantly lags behind. Emerging empirical evidence from the past decade suggests that epigenetic mechanisms serve as key mediators of environmental and genetic risk factors that underlie major mental health conditions, including EDs. This article highlights recent findings from genetic studies on EDs and emphasises the emerging role of epigenetic mechanisms. It introduces epigenetic mechanisms, in particularly DNA methylation, and explores how dynamic DNA methylation changes may influence disordered eating behaviours through alterations in gene expression, offering a fresh perspective on the interplay between genetics, environment and epigenetics in EDs. Recent findings in the field of ED epigenetics provide promising insights into the development of these conditions, despite current limitations in epigenomic coverage, sample size and the identification of reliable biomarkers. Future studies employing comprehensive epigenomic scans across a broader spectrum of ED are crucial for uncovering the mechanistic relevance of epigenetics and advancing biomarker research, ultimately enabling the development of improved, novel and more personalised clinical treatments.
Keywords: epigenetics, eating disorders, anorexia nervosa, binge-eating disorders, gene-environment interaction, epigenome-wide association studies (EWAS)