Neurobiological and psychosocial mechanisms linking early life stress to the pathogenesis of eating disorders

Early life stress (ELS) is a significant factor in the development of eating disorders (ED), not as a single cause, but as a powerful influence that creates a vulnerability across an individual's biology and psychology. This review explains how various forms of ELS, such as trauma, neglect, and chronic adversity, can permanently alter brain systems. For example, chronic stress hormone exposure can dysregulate the hypothalamic-pituitary-adrenal (HPA) axis, leading to abnormal cortisol levels and impaired stress self-regulation later in life. This dysregulation can lead to difficulties in managing emotions and coping with stress later in life. Furthermore, ELS impacts the brain's neurochemical systems, including serotonin, dopamine, and norepinephrine, which are responsible for mood, reward, and impulse control. Lasting changes to these systems can explain why some people use food to cope with distress, leading to behaviors like binge eating or extreme restriction. ELS also leaves a biological memory via epigenetic modifications, notably DNA methylation, altering gene expression without changing the DNA sequence to link early experiences to long-term risk. From a psychological perspective, ELS often leads to low self-esteem, self-criticism, and an impaired ability to regulate emotions. These psychological traits, along with a person's neurobiological profile, can make them more susceptible to developing an eating disorder as a way to gain a sense of control over their lives. By integrating genetic, epigenetic, neurobiological, and psychosocial factors, this review clarifies how ELS acts as a multifaceted embedder of vulnerability, contributing to the onset and persistence of EDs.