PubMed · 13050910
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H L ALEXANDER. 1953. Allergy.. https://pubmed.ncbi.nlm.nih.gov/13050910/
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Corticotropin-releasing hormone (CRH) is a key mediator of endocrine, autonomic, behavioral, and immune responses to stress. The ability of CRH to induce hormonal stress responses has been used to investigate the functionality of the hypothalamus-pituitary-adrenal axis, and consequently the activity of hypothalamic CRH neuronal systems. Indeed, CRH administration to humans causes prompt release of ACTH, followed by secretion of cortisol, aldosterone and other adrenal steroids. CRH hypersecretion/hyperactivity has been associated to major depression, anxiety-related disorders, anorexia nervosa, Alzheimer's and Parkinson's diseases and progressive supranuclear palsy. During pregnancy the human placenta and its accessory membranes are the major sites of CRH synthesis and secretion. Placental CRH secretion is autonomous, but increasing evidence indicates that maternal or fetal conditions may influence such secretion. Therefore, the emerging concept is that in the event of acute or chronic metabolic, physical or infectious stress, the placenta takes part in a stress syndrome by releasing CRH, which may contribute to restore local blood flow and to influence the timing of delivery. The CRH released by the placenta is measurable in maternal plasma and other biological fluids and may be used to diagnose subclinical processes anteceding pregnancy complications such as pre-eclampsia and preterm delivery.
OBJECTIVE: Fibromyalgia syndrome (FMS) has been associated with decreased cortisol secretion. Patients with posttraumatic stress disorder (PTSD) exhibit similar hypocortisolism in the context of increased negative feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis. Because trauma and PTSD have been associated with fibromyalgia, we evaluated whether patients with fibromyalgia demonstrate increased HPA feedback sensitivity. METHOD: Baseline blood samples were obtained at 0800 h, and 0.5 mg of dexamethasone was administered to 15 female patients with FMS and 20 normal controls at 2300 h. Adrenocorticotropin (ACTH), cortisol, and dexamethasone levels were measured at 0800 h after dexamethasone intake. RESULTS: There were no group differences in mean ACTH or cortisol levels or in ACTH/cortisol ratio at baseline. After dexamethasone intake, patients with FMS exhibited more pronounced suppression of cortisol but not of ACTH, as well as increased ACTH/cortisol ratios compared with controls. Percent cortisol suppression was associated with pain and fatigue, while ACTH/cortisol ratio and dexamethasone availability were associated with stress and anxiety measures. CONCLUSION: Our results suggest increased sensitivity to glucocorticoid feedback, manifested at the adrenal level, in FMS.
Stress is a part of every life to varying degrees, but individuals differ in their stress vulnerability. Stress is usefully viewed from a biological perspective; accordingly, it involves activation of neurobiological systems that preserve viability through change or allostasis. Although they are necessary for survival, frequent neurobiological stress responses increase the risk of physical and mental health problems, perhaps particularly when experienced during periods of rapid brain development. Recently, advances in noninvasive measurement techniques have resulted in a burgeoning of human developmental stress research. Here we review the anatomy and physiology of stress responding, discuss the relevant animal literature, and briefly outline what is currently known about the psychobiology of stress in human development, the critical role of social regulation of stress neurobiology, and the importance of individual differences as a lens through which to approach questions about stress experiences during development and child outcomes.