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Hormones (Athens). 2018 Dec;17(4):507-520. doi: 10.1007/s42000-018-0065-x. Epub 2018 Oct 2.

Early life stress and trauma: developmental neuroendocrine aspects of prolonged stress system dysregulation.

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Department of Psychiatry, Division of Neurosciences, School of Medicine, Faculty of Medical Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Thessaloniki General Hospital "G. Papanicolaou", Psychiatric Hospital of Thessaloniki, Lagkada Str. 196, Stavroupoli, 56430, Thessaloniki, Greece.
Unit of Developmental and Behavioral Pediatrics, First Department of Pediatrics, School of Medicine, "Aghia Sophia" Children's Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Department of Child Psychiatry, School of Medicine, "Aghia Sophia" Children's Hospital, National and Kapodistrian University of Athens, Athens, Greece.


Experience of early life stress (ELS) and trauma is highly prevalent in the general population and has a high public health impact, as it can trigger a health-related risk cascade and lead to impaired homeostatic balance and elevated cacostatic load even decades later. The prolonged neuropsychobiological impact of ELS can, thus, be conceptualized as a common developmental risk factor for disease associated with increased physical and mental morbidity in later life. ELS during critical periods of brain development with elevated neuroplasticity could exert a programming effect on particular neuronal networks related to the stress response and lead to enduring neuroendocrine alterations, i.e., hyper- or hypoactivation of the stress system, associated with adult hypothalamic-pituitary-adrenal axis and glucocorticoid signaling dysregulation. This paper reviews the pathophysiology of the human stress response and provides evidence from human research on the most acknowledged stress axis-related neuroendocrine pathways exerting the enduring adverse effects of ELS and mediating the cumulative long-term risk of disease vulnerability in adulthood.


Autonomic nervous system; Childhood adversity; Childhood trauma; Cortisol; Early life stress; Endocrine system; Glucocorticoids; HPA axis

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