Purpose of review: Eating disorders are complex psychiatric disorders in which genes, environment, and gene–environment interactions (G×E) have a role. Such G×E may occur in adulthood or during development. They may also be modified by factors such as (mal)nutrition or stress and this may result in acute or long-term epigenetic modifications. This review discusses the potential for recent developments in epigenetics to address ongoing aetiological issues in eating disorders.
Recent findings: Epigenetic studies in eating disorders have focussed on the DNA methylation status of promoter regions of candidate genes: differences have been reported between people with eating disorders and healthy controls, and between subtypes of eating disorders. Animal studies related to eating disorders have focussed on understanding the acute and long-term effects of environmental manipulation on epigenetic changes and on the resultant phenotypes: these studies are promising, but they have also identified some of the complexity of epigenetic processing.
Summary: Because of the difficulties in obtaining brain samples, epigenetic studies in eating disorders (like in other psychiatric illnesses) have used peripheral tissues, usually blood: this raises various problems. It is likely, therefore, that in the immediate future, animal, rather than human studies will guide the progress in epigenetics studies of eating disorders and other psychiatric disorders.