Neuroendocrine Alterations in Major Depressive Disorder

doi:10.1016/B978-0-323-58131-8.00005-7

Major Depressive Disorder

2020, Pages 63-74

https://doi.org/10.1016/B978-0-323-58131-8.00005-7 Get rights and content

Abstract

Several alterations in neuroendocrine systems have been demonstrated to exhibit altered activity in patients with major depression compared to normal healthy volunteers. The most robust and best replicated findings are studies of the hypothalamic–pituitary–adrenal (HPA) axis, and more specifically the corticotropin-releasing hormone (CRH) neuropeptide system. Increased neuronal CRH activity in extrahypothalamic and hypothalamic areas and increased HPA axis activity has been implicated in the development of depression during adulthood, in part a consequence of exposure to early-life stress as demonstrated in both in clinical and preclinical studies. In addition other neuroendocrine aberrations in depressed patients have also been demonstrated, most notably the hypothalamic–pituitary–thyroid axis and to a lesser extent, the hypothalamic–pituitary–gonadal axis. This chapter is a brief overview of the research findings over the last 50 or so years highlighting the neuroendocrine abnormalities and their putative role in the pathogenesis of major depression.

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Increased HPA activity, including elevated levels of cortisol, has long been linked with depression (Ali and Nemeroff, 2020; Pariante and Lightman, 2008; Russell and Lightman, 2019; Stetler and Miller, 2011), although more recent meta-analyses and models associate elevated HPA activity with only subgroups of patients (Gold, 2015; Lombardo et al., 2019; Menke, 2019), such as with melancholic but not atypical depression (Gold, 2015). Successful treatment of depression tends to normalize the HPA axis disruptions (reviewed in Ali and Nemeroff, 2020), and, importantly, reduction of stress or cortisol can reverse the neural and psychological impairments caused by elevated HPA activity (Lupien et al., 2009; McEwen and Gianaros, 2011). Thus, interventions that can reduce stress and excess sympathetic and HPA activity are considered particularly effective at boosting resilience.
Although research has identified dozens of behavioral and psychosocial strategies for boosting resilience in adults, little is known about the common underlying pathways. A comprehensive review of these strategies using an affective neuroscience approach indicates three distinct general routes to resilience: 1) down-regulating the negative (e.g., exposure, cognitive reappraisal) by reducing distress-related responses of the amygdala, hypothalamic-pituitary-adrenal axis, and autonomic nervous system; 2) up-regulating the positive (e.g., optimism, social connectedness) by activating mesostriatal reward pathways, which in turn can buffer the effects of stress; and 3) transcending the self (e.g., mindfulness, religious engagement) by reducing activation in the default mode network, a network associated with self-reflection, mind-wandering, and rumination. Some strategies (e.g., social support) can boost resilience via more than one pathway. Under- or over-stimulation of a pathway can result in vulnerability, such as over-stimulation of the reward pathway through substance abuse. This tripartite model of resilience-building is testable, accounts for a large body of data on adult resilience, and makes new predictions with implications for practice.
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Major Depressive Disorder

Chapter 5 - Neuroendocrine Alterations in Major Depressive Disorder

Abstract

An affective neuroscience model of boosting resilience in adults

The Relative Importance of Internal Cognitive Processes in Explaining Depressive Symptoms in University Students