When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders.

By Charles L Raison, Andrew H. Miller. American Journal of Psychiatry, 2011

670 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/3068e09fab98b6e276c604644f530d314675de62

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Citations in the corpus

Biological and Psychosocial Predictors of Postpartum Depression: Systematic Review and Call for Integration (2015, background): “This is of concern because insensitivity to glucocorticoid signals has been suggested as a central mechanism in the development of depression and other stress-related disorders (Raison & Miller 2003).”
From inflammation to sickness and depression: when the immune system subjugates the brain (2008, background): “This increased inflammatory response in the brain results in a decreased inhibitory feedback on CRH by glucocorticoids, thereby intensifying the stress-response syste”
Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms (2011, background): “…of theoretical perspectives from the fetal-origins literature (Barker, 1992), life-course epidemiology (Lynch & Smith, 2005), socioemotional development (Pollak, 2008; Repetti et al., 2002), stress physiology (McEwen, 1998), and behavioral immunology (Coe & Lubach, 2007; Raison & Miller, 2003).”
Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “It should be noted that although glucocorticoids are well known to suppress T cell function, no relationship has been found between increased cortisol secretion and decreased in vitro proliferative responses to T cell mitogens in depressed patients (Kronfol et al., 1986; Raison and Miller, 2003).”
Cytokines sing the blues: inflammation and the pathogenesis of depression. (2006, background): “These effects might contribute to therapeutic efficacy, given recent data that antidepressant-like effects of desipramine in the forced swim test (an animal model frequently used to evaluate antidepressant efficacy) depend on the ability of the drug to inhibit CNS production of TNF-α [82].”
The link between childhood trauma and depression: insights from HPA axis studies in humans. (2008, positive): “Specifically, the combination of increased stress responsiveness with insufficient glucocorticoid signaling due to glucocorticoid receptor deficiency might have adverse effects in target systems that are regulated by glucocorticoids (Heim et al., 2000a; Raison and Miller, 2003).”
A new view on hypocortisolism. (2005, background): “Based on the literature, one may preliminarily suggest that early innate and inflammatory immune responses may be overactive, whereas adaptive immunity seems to be unchanged or depressed (see Raison and Miller, 2003; Rohleder et al., 2004).”
If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans. (2007, methodology): “These models are generally advanced to explain how stress could exacerbate conditions in which deficient cortisol signaling contributes to disease pathogenesis (Raison & Miller, 2003).”
Benefit Finding and Physical Health: Positive Psychological Changes and Enhanced Allostasis (2008, background): “…allostasis assume that the adrenal is not hyposensitized, which would lead to inefficient cortisol output in response to stress, increasingly recognized as a common phenotype of stress-related dysregulation or allostatic load (Fries, Hesse, Hellhammer, & Hellhammer, 2005; Raison & Miller, 2003).”
Early-Life Adversity and Physical and Emotional Health across the Lifespan: A Neuro-Immune Network Hypothesis (2015, background): “This insensitivity to glucocorticoids may be adaptive during acute threats but if sustained would facilitate the kind of low-grade chronic inflammation implicated in many emotional and physical health problems (1,48).”
The molecular neurobiology of depression (2008, neutral): “Neuroendocrine and neuroimmune interactions Early clinical studies identifying reproducible but small increases in serum glucocorticoid concentrations in depressio”
Effect of Compassion Meditation on Neuroendocrine, Innate Immune and Behavioral Responses to Psychosocial Stress (2008, background): “Moreover, as the end product of HPA axis activation and a primary physiological restraint upon immune activity, cortisol is especially relevant in terms of stress physiology and health (Raison and Miller, 2003).”