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Research has suggested a relationship between early life stress, and depression in particular longer episodes of depression with treatment resistant outcomes. However, the underlying mechanisms for this association remain poorly understood. Molecular studies indicate that, in general, the hereditary character of psychiatric disorders are polygenic, multifactorial and highly complex, with innumerable low-effect genetic variants interacting with each other. In addition, the importance of the environment and its interaction with genes has pointed to a fundamental role of epigenetic mechanisms in psychiatric disorders, such as methylation of deoxyribonucleic acid (DNA), alterations, histone actions and regulation of gene expression by non-coding ribonucleic acids (RNAs). This article provides an overview of the interplay of epigenetics, the HPA axis, early life stress and the development of depression. Advances in our knowledge of epigenetics in the context of early life stress and depression provide a new understanding of the genetic influence on psychopathology and could lead to the identification of new targets for clinical intervention.
•Early stressful life events play an important role in the pathogenesis of depression.•A better understanding of the mechanisms of Early Life Stress leading to HPA axis impairment and vulnerability to depression.•Early life trauma alters inflammation and causes HPA axis abnormalities increasing vulnerability to stress and depression.•Epigenetic approaches to early intervention will provide new pharmacological and psychoeducational strategies.•Neuroendocrine-stress effects and cognitive vulnerability-stress model studies are needed for a better understanding.