PubMed · 226747
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Y Nakai. 1979-06-29. [Dexamethasone suppression test].. https://pubmed.ncbi.nlm.nih.gov/226747/
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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.
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.
Postpartum depression (PPD) affects at least 10% to 15% of postpartum women, including more than 600,000 American mothers in 2003 alone. Dramatic changes in the hypothalamic-pituitary-adrenal (HPA) system in the transition from pregnancy to postpartum coupled with research on the psychobiology of depression provided the foundation for this study. The purpose of this study was to compare the reactivity and regulation of the HPA axis components, adrenocorticotropic hormone (ACTH) and cortisol, in depressed and nondepressed postpartum women. A comparative, longitudinal study design was used with 22 normal, healthy, nondepressed pregnant women. Physiologic and postpartum depression data were collected at 6 and 12 weeks postpartum at a university clinical research center. Maximal treadmill exercise stimulated plasma ACTH and serum cortisol levels which were measured before, during, and after 20 min of exercise. Postpartum depression was measured with the Postpartum Depression Screening Scale. Lag within-subject ACTH levels predicting cortisol regression slopes were significantly different between the depressed and nondepressed groups at both 6 and 12 weeks. The depressed group showed no relationship between their ACTH and cortisol levels, with higher ACTH and lower cortisol levels when compared with the nondepressed group. The expected regulated relationship with cortisol levels rising in response to rising ACTH levels was found in the non-depressed group. These findings indicate that the HPA axis was dysregulated in the depressed group, but regulated in the nondepressed group at 6 and 12 weeks postpartum. This pattern of higher ACTH levels to stimulate less cortisol is similar to patterns found in women with early life stresses.