scholarly journals Causal effects of the early caregiving environment on development of stress response systems in children

2015 ◽  
Vol 112 (18) ◽  
pp. 5637-5642 ◽  
Author(s):  
Katie A. McLaughlin ◽  
Margaret A. Sheridan ◽  
Florin Tibu ◽  
Nathan A. Fox ◽  
Charles H. Zeanah ◽  
...  

Disruptions in stress response system functioning are thought to be a central mechanism by which exposure to adverse early-life environments influences human development. Although early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis in rodents, evidence from human studies is inconsistent. We present results from the Bucharest Early Intervention Project examining whether randomized placement into a family caregiving environment alters development of the autonomic nervous system and HPA axis in children exposed to early-life deprivation associated with institutional rearing. Electrocardiogram, impedance cardiograph, and neuroendocrine data were collected during laboratory-based challenge tasks from children (mean age = 12.9 y) raised in deprived institutional settings in Romania randomized to a high-quality foster care intervention (n = 48) or to remain in care as usual (n = 43) and a sample of typically developing Romanian children (n = 47). Children who remained in institutional care exhibited significantly blunted SNS and HPA axis responses to psychosocial stress compared with children randomized to foster care, whose stress responses approximated those of typically developing children. Intervention effects were evident for cortisol and parasympathetic nervous system reactivity only among children placed in foster care before age 24 and 18 months, respectively, providing experimental evidence of a sensitive period in humans during which the environment is particularly likely to alter stress response system development. We provide evidence for a causal link between the early caregiving environment and stress response system reactivity in humans with effects that differ markedly from those observed in rodent models.

2014 ◽  
Vol 10 (2) ◽  
pp. 20131010 ◽  
Author(s):  
David Costantini ◽  
Pat Monaghan ◽  
Neil B. Metcalfe

It is increasingly recognized that hormetic environmental priming of stress responses can improve resilience to later life stress exposure. However, such phenotypic adjustments may be costly, particularly if the subsequent environment does not match that to which the adjustment was made. Here, we show that hormetic priming to mild heat stress in early life increases survival only when heat stress is again experienced in adulthood; it reduces survival if the stressor is not encountered again. That such costs can occur explains both why the stress response system is not maintained in an upregulated state and why the hormetic adjustment of responses has evolved.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Manuel Martinez-Lavin

Fibromyalgia is a painful stress-related disorder. A key issue in fibromyalgia research is to investigate how distress could be converted into pain. The sympathetic nervous system is the main element of the stress response system. In animal models, physical trauma, infection, or distressing noise can induce abnormal connections between the sympathetic nervous system and the nociceptive system. Dorsal root ganglia sodium channels facilitate this type of sympathetic pain. Similar mechanisms may operate in fibromyalgia. Signs of sympathetic hyperactivity have been described in this condition. Genetic factors and/or distressful lifestyle may lead to this state of sympathetic hyperactivity. Trauma and infection are recognized fibromyalgia triggers. Women who suffer from fibromyalgia have catecholamine-evoked pain. Sympathetic dysfunction may also explain nonpain-related fibromyalgia symptoms. In conclusion, in fibromyalgia, distress could be converted into pain through forced hyperactivity of the sympathetic component of the stress response system.


2021 ◽  
Author(s):  
Aurelie Cohas ◽  
Coraline Bichet ◽  
Rebecca Garcia ◽  
Sylvia Pardonnet ◽  
Sophie Lardy ◽  
...  

Stress responses have evolved to quickly and appropriately deal with environmental stressors in order to secure or restore homeostasis. Since the regulation of stress hormones plays a key adaptive role, the regulatory processes controlling stress hormones levels may be under high selective pressure. The social environment during early life (parents and litter characteristics) strongly affects ontogeny of the hypothalamic-pituitary-adrenal (HPA) axis. In cooperative breeders, offspring are also confronted with helpers but whether and how variation in the helping context can affect HPA axis responsiveness of offspring remains unanswered. Combining dexamethasone suppression and adrenocorticotropic hormone stimulation tests, we investigated the link between the social environment and the characteristics of the HPA axis at the early stages of life in wild Alpine marmots. We show that when raised in the presence of helpers, marmot pups exhibit a greater capacity not only to mount, but also to turn off a stress response. The capacity to mount a stress response was also higher as the pups were raised in large litters. Determining impacts of such social modulation of the HPA axis functioning on individual fitness would make an important contribution to our understanding of the evolution of cooperative breeding.


2017 ◽  
Vol 21 (4) ◽  
pp. 330-353 ◽  
Author(s):  
Michael P. Hengartner

The present work proposes an evolutionary model of externalizing personality that defines variation in this broad psychobiological phenotype resulting from genetic influences and a conditional adaptation to high-risk environments with high extrinsic morbidity-mortality. Due to shared selection pressure, externalizing personality is coadapted to fast life history strategies and maximizes inclusive fitness under adverse environmental conditions by governing the major trade-offs between reproductive versus somatic functions, current versus future reproduction, and mating versus parenting efforts. According to this model, externalizing personality is a regulatory device at the interface between the individual and its environment that is mediated by 2 overlapping psychobiological systems, that is, the attachment and the stress-response system. The attachment system coordinates interpersonal behavior and intimacy in close relationships and the stress-response system regulates the responsivity to environmental challenge and both physiological and behavioral reactions to stress. These proximate mechanisms allow for the integration of neuroendocrinological processes underlying interindividual differences in externalizing personality. Hereinafter I further discuss the model's major implications for personality psychology, psychiatry, and public health policy.


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