Changes of adrenocorticotropic hormone rhythm and cortisol circadian rhythm in patients with depression complicated with anxiety and their effects on the psychological state of patients

Xie, Zheng; Deng, Yajie; Xie, Chengrong; Yao, Yuanlong

doi:10.3389/fpsyt.2022.1030811

Cited by 2 publications

(1 citation statement)

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“… 122 , 123 For example, flattened diurnal cortisol rhythms have been observed in severe depression, and distinguishable patterns have been identified in depressed patients with comorbid anxiety. 124 , 125 Both higher and lower/blunted cortisol wakening responses have been observed in depression, with the former exhibiting a predictive relationship with major depressive episodes. 122 , 126 , 127 Together, data from cortisol studies suggest that HPA axis impairment can result from either too much or too little cortisol, and HPA axis response and disease characteristics may depend on a variety of moderating influences such as features of the stressor, the person, and timing.…”

Section: Cortisol As a Biomarker Of Hpa Axis Dysfunctionmentioning

confidence: 99%

Targeting the Arginine Vasopressin V1b Receptor System and Stress Response in Depression and Other Neuropsychiatric Disorders

Kanes¹,

Dennie²,

Perera³

2023

NDT

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A healthy stress response is critical for good mental and overall health and promotes neuronal growth and adaptation, but the intricately balanced biological mechanisms that facilitate a stress response can also result in predisposition to disease when that equilibrium is disrupted. The hypothalamic-pituitary-adrenal (HPA) axis neuroendocrine system plays a critical role in the body’s response and adaptation to stress, and vasopressinergic regulation of the HPA axis is critical to maintaining system responsiveness during chronic stress. However, exposure to repeated or excessive physical or emotional stress or trauma can shift the body’s stress response equilibrium to a “new normal” underpinned by enduring changes in HPA axis function. Exposure to early life stress due to adverse childhood experiences can also lead to lasting neurobiological changes, including in HPA axis function. HPA axis impairment in patients with depression is considered among the most reliable findings in biological psychiatry, and chronic stress has been shown to play a major role in the pathogenesis and onset of depression and other neuropsychiatric disorders. Modulating HPA axis activity, for example via targeted antagonism of the vasopressin V 1b receptor, is a promising approach for patients with depression and other neuropsychiatric disorders associated with HPA axis impairment. Despite favorable preclinical indications in animal models, demonstration of clinical efficacy for the treatment of depressive disorders by targeting HPA axis dysfunction has been challenging, possibly due to the heterogeneity and syndromal nature of depressive disorders. Measures of HPA axis function, such as elevated cortisol levels, may be useful biomarkers for identifying patients who may benefit from treatments that modulate HPA axis activity. Utilizing clinical biomarkers to identify subsets of patients with impaired HPA axis function who may benefit is a promising next step in fine-tuning HPA axis activity via targeted antagonism of the V 1b receptor.

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