Major Depression in Late Life Is Associated with Both Hypo- and Hypercortisolemia

Depression gets old fast: do stress and depression accelerate cell aging?

“…[45,56] It is possible but not proven that hyper-and hypocortisolism identify different subtypes of depression or map onto different symptom clusters. [45,54,[57][58][59] It should also be recognized that the effects of either state are likely to differ, depending on the target tissue involved and that ''relative'' conditions of either hyper-or hypocortisolism may exist at the same time within organisms, making any global statements a simplification of the underlying endocrine state. [60][61][62][63] For example, different GR polymorphisms can significantly affect individuals' responses to GCs, [35,64] and alternative splicing of the GR mRNA can lead to different GR isoforms with different actions in different tissues.…”

Hypothalamus-Pituitary-Adrenal Axis Hypersuppression Is Associated with Gastrointestinal Symptoms in Major Depression

“…5,7,8 The present study focuses on the HPA-axis, which plays a central role in the neuroendocrine response to stress with cortisol being it's main effector constituent, since both IBS and depression have been reported to exhibit HPAaxis dysregulation and that stress-dysregulation has been suggested as one important etiologic factor in both conditions. [9][10][11][12][13][14][15][16][17][18] While stress has traditionally been associated with increased cortisol levels and HPA-axis hyperactivity, there is a growing body of literature describing lowered cortisol levels and hypoactivity of the HPA-axis in a number of stress related disorders [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] ; eg, posttraumatic stress disorder (PTSD), 30,31 chronic fatigue syndrome, [22][23][24] burnout, 25,26 as well as in fibromyalgia and chronic somatic pain conditions of unknown or uncertain etiology. 28,29,[32][33][34] Dysfunction of the HPA-axis, including hypoactivity, has also been reported in IBS.…”

“…Early studies in depression, mainly investigating younger inpatients, typically reported the existence of an HPA-axis hyperactivity, [12][13][14] whereas more recent studies in older outpatients have in addition to findings of hypercortisolism also discovered patients exhibiting hypocortisolism. [15][16][17][18] An exaggerated negative feedback response (also denoted hypersuppression) of the HPA-axis as captured by a low cortisol value, post a low dose dexamethasone suppression test (DST), is believed to be the earliest and most common characteristic of hypocortisolism according to Fries et al 19 Measurements of the negative feedback sensitivity of the HPA-axis commonly employ different DSTs. The use of a low dose or a very low dose regimen (0.5 mg dexamethasone or lower) allows for the discrimination of hypersuppression from normal and decreased suppression (denoted here intermediate or normal suppression and hyposuppression, respectively).…”

Acute Inhibition of 11β-Hydroxysteroid Dehydrogenase Type-1 Improves Memory in Rodent Models of Cognition

“…One approach may involve targeting glucocorticoid function. Abnormally high levels of glucocorticoids are correlated with memory impairment in some patients with AD (Pomara et al, 2003) and depression (Bremmer et al, 2007). Increased glucocorticoid activity is also associated with greater hippocampal atrophy and memory impairment in the elderly (Lupien et al, 1998) and more rapid AD disease progression (Csernansky et al, 2006).…”