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

HORMONES ◽  
2018 ◽  
Vol 17 (4) ◽  
pp. 507-520 ◽  
Author(s):  
Agorastos Agorastos ◽  
Panagiota Pervanidou ◽  
George P. Chrousos ◽  
Gerasimos Kolaitis
2011 ◽  
Vol 23 (4) ◽  
pp. 1001-1016 ◽  
Author(s):  
Brittany R. Howell ◽  
Mar M. Sanchez

AbstractThe mechanisms through which early life stress leads to psychopathology are thought to involve allostatic load, the “wear and tear” an organism is subjected to as a consequence of sustained elevated levels of glucocorticoids caused by repeated/prolonged stress activations. The allostatic load model described this phenomenon, but has been criticized as inadequate to explain alterations associated with early adverse experience in some systems, including behavior, which cannot be entirely explained from an energy balance perspective. The reactive scope model has been more recently proposed and focuses less on energy balance and more on dynamic ranges of physiological and behavioral mediators. In this review we examine the mechanisms underlying the behavioral consequences of early life stress in the context of both these models. We focus on adverse experiences that involve mother–infant relationship disruption, and dissect those mechanisms involving maternal care as a regulator of development of neural circuits that control emotional and social behaviors in the offspring. We also discuss the evolutionary purpose of the plasticity in behavioral development, which has a clear adaptive value in a changing environment.


2020 ◽  
Vol 10 (3) ◽  
pp. 169 ◽  
Author(s):  
Panagiota Pervanidou ◽  
Gerasimos Makris ◽  
George Chrousos ◽  
Agorastos Agorastos

Traumatic stress exposure during critical periods of development may have essential and long-lasting effects on the physical and mental health of individuals. Two thirds of youth are exposed to potentially traumatic experiences by the age of 17, and approximately 5% of adolescents meet lifetime criteria for posttraumatic stress disorder (PTSD). The role of the stress system is the maintenance of homeostasis in the presence of real/perceived and acute/chronic stressors. Early-life stress (ELS) has an impact on neuronal brain networks involved in stress reactions, and could exert a programming effect on glucocorticoid signaling. Studies on pediatric PTSD reveal diverse neuroendocrine responses to adverse events and related long-term neuroendocrine and epigenetic alterations. Neuroendocrine, neuroimaging, and genetic studies in children with PTSD and ELS experiences are crucial in understanding risk and resilience factors, and also the natural history of PTSD.


2018 ◽  
Author(s):  
Adrian Dahl Askelund ◽  
Susanne Schweizer ◽  
Ian M. Goodyer ◽  
Anne-Laura van Harmelen

Depression is the leading cause of ill health and disability worldwide1. A known risk factor of depression is exposure to early life stress2. Such early stress exposure has been proposed to sensitise the maturing psychophysiological stress system to later life stress3. Activating positive memories dampens acute stress responses with resultant lower cortisol response and improved mood in humans4 and reduced depression-like behaviour in mice5. It is unknown whether recalling positive memories similarly reduces adolescent vulnerability to depression. Here we used path modelling to examine the effects of positive autobiographical memory specificity on later morning cortisol and negative self-cognitions during low mood in adolescents at risk for depression due to early life stress (n = 427, age: 14 years)6. We found that experimentally assessed positive but not negative memory specificity was associated with lower morning cortisol and less negative self-cognitions during low mood one year later. Moderated mediation analyses demonstrated that positive memory specificity reduced later depressive symptoms through lowering negative self-cognitions in response to negative life events reported in the one-year interval. Positive memory specificity actively dampened the negative effect of stressors over time, thereby operating as a resilience factor reducing the risk of subsequent depression7. These findings suggest that developing methods to improve positive memory specificity in at-risk adolescents may counteract vulnerability to depression.


2019 ◽  
Vol 25 (1) ◽  
pp. 78-97 ◽  
Author(s):  
Peter M McInnis ◽  
Taylor A Braund ◽  
Zhi Kai Chua ◽  
Kasia Kozlowska

Accumulating evidence indicates that psychological and neurophysiological processes interconnect and interact to activate the body’s stress system and to trigger and maintain functional somatic symptoms. This study used the Early Life Stress Questionnaire, Depression Anxiety Stress Scales and biological markers (heart rate, heart rate variability, skin conductance, C-reactive protein (CRP) titre, respiratory rate, and accuracy and reaction time in an emotion-face identification task), to examine childhood adversity, psychological distress and stress-system activation in 35 children and adolescents (23 girls and 12 boys, 9–17 years old) disabled by chronic pain (vs two groups of age- and sex-matched healthy controls). Patients reported more early-life stress ( U = 798.5, p = .026) and more psychological distress ( U = 978, p < .001). They showed activation of the autonomic system: elevated heart rate ( U = 862.5, p = .003), elevated electrodermal activity ( U = 804.5, p = .024) and lower heart rate variability in the time domain ( U = 380.5, p = .007) and frequency domain ( U = 409.5, p = .017). The group showed an upward shift of CRP titres (with 75th and 90th CRP percentiles of 4.5 and 10.5 mg/L, respectively), suggesting the activation of the immune–inflammatory system. Elevated CRP titres were associated with elevated heart rate ( p = .028). There were no differences in respiratory rate or in accuracy and reaction time in the emotion-face identification task. The results indicate that interventions for children and adolescents with chronic pain need a multidisciplinary mind–body approach that concurrently addresses psychological distress, physical impairment and stress-system dysregulation.


2019 ◽  
Vol 133 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Nathalie D. Elliott ◽  
Rick Richardson

2002 ◽  
Vol 7 (2) ◽  
pp. 89-95 ◽  
Author(s):  
David A Gutman ◽  
Charles B. Nemeroff

2019 ◽  
Vol 39 (5) ◽  
pp. 329-342
Author(s):  
Jamie Y. Choe ◽  
Maya Nair ◽  
Riyaz Basha ◽  
Byung-Jin Kim ◽  
Harlan P. Jones

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