This chapter explores the neurological link between trauma and eating disorders (EDs) by describing one of humans’ basic functions: response to stressors. Adverse life events interact with the genome and developmental processes, leading to biological changes that predispose one to a broad range of psychiatric problems, including EDs. The mechanisms involved include abnormalities in the stress response, changes in appetite, altered reward sensitivity, and increased sensitivity to rejection. Specific genes increase one’s susceptibility to stressful experiences, and stressful experiences have the ability to alter one’s genes (i.e., epigenetics). Epigenetics refers to the way in which environmental exposures have the capacity to influence the genome in a way that affects later gene expression. Findings from epigenetic research and neural-based interventions offer evidence against the long-standing understanding of genes and neurocircuitry as “rigid” structures.

Feeding and eating disorders (EDs) are severe mental illnesses. This chapter gives a concise overview regarding EDs, their diagnostic configuration, and comorbidity with other mental illnesses. Moreover, the focus included vulnerability and psychological aspects of EDs, with particular attention given to the impact of dysfunctional attachment dynamics and relational trauma on the onset of each type of ED. The chapter covers EDs such as anorexia nervosa, bulimia nervosa, binge eating disorder, and other specified feeding or eating disorder (OSFED). Types of EDs also included those that are not present in Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5), but are frequently found in clinical practice. Such disorders (e.g., bulimarexia or orthorexia) are symptomatological manifestations that require further investigation to clarify risk factors related to their onset and to shed light on their mechanism of action.