Exposure to trauma during childhood is a non-specific risk factor for psychiatric disorders, including eating disorders (EDs), over the life course. Moreover, an association between stressful life events and the onset/maintenance of EDs has been documented. Therefore, the hypothalamus-pituitary-adrenal (HPA) axis, namely the main component of the endogenous stress response system, has been proposed to be implicated in the pathophysiology of EDs. In this narrative review the current knowledge concerning the effects of early trauma exposure on the HPA axis activity and their putative role in the pathophysiology of EDs will be illustrated. Research findings corroborate the idea that childhood trauma exposure has long-lasting dysregulating effects on the activity of the HPA axis, which may contribute to the biological background of the early trauma-related risk for the development of EDs across the life span. Moreover, literature data support the existence of a "maltreated ecophenotype" in EDs characterized by specific clinic and neuroendocrine features, which may have important implications in treatment programming for such a type of patients.
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