Dysregulation of the Stress Response System in Childhood: Long-Term Psychological Consequences of Neuroendocrine Mechanisms

Abstract

Early life stress can profoundly disrupt the development of the body’s stress response system, particularly through neuroendocrine mechanisms such as the hypothalamic-pituitary-adrenal axis and glucocorticoid signaling. This topic is of particular relevance because dysregulation of these systems during sensitive periods of development is associated with long-term psychological and physical health outcomes. Research suggests that childhood trauma, neglect, or chronic adversity can “program” neural networks, leading to persistent hyper- or hypoactivation of the stress system. Researchers typically assess neuroendocrine regulation by measuring biomarkers such as cortisol (e.g., in blood) before and after stressful events. They can also use quantitative measures of psychopathology, behavioral observations, and neurobiological analyses to capture the multidimensional effects of early stress. The subjects of these studies are wide-ranging—including children exposed to institutional care, nonhuman primates exposed to maternal neglect, and rodent models of early adversity—with the “object” (focus) being the neuroendocrine stress system, and the “subject” (field) being the long-term psychological outcomes. Early dysregulation of stress systems increases vulnerability to a range of mental health disorders, such as anxiety, depression, and posttraumatic stress disorder, as well as to physiological conditions later in life, such as metabolic syndrome and inflammation. These findings suggest that early life stress does not simply produce transient impairment, but also has long-term “programming” effects at the neuroendocrine level, increasing allostatic load and reducing adaptive stress regulation capacity throughout life.