Diurnal cortisol and CAR in depression Sample Clauses

Diurnal cortisol and CAR in depression. Whilst it is clearly evident that dysregulation of the HPA axis is a key feature of depression, the exact nature of this dysfunction is not fully understood. Studies investigating atypical diurnal HPA patterns in depressed individuals have produced mixed results, with a wealth of studies reporting hypercortisolemia (Bhagwagar, Xxxxxx, & Cowen, 2003, 2005; Xxxxxxxx et al., 2009), but others reporting hypoactivity (Xxxxxx, Xxxxxxx, Xxxxxx-Xxxxx, Xxxxxxxxx, & Xxxxx, 2013). For example, in a study of 20 non-medicated depressed patients and 40 healthy controls, depressed patients were found to secrete approximately 25% more cortisol than controls at 30 minutes post-awakening, but had similar cortisol levels 60 minutes after waking (Bhagwagar et al., 2005). In another study of 1,588 Dutch adults, depressed and remitted individuals showed an elevated CAR compared to healthy controls. Evening cortisol levels were also found to be higher amongst depressed individuals at 10pm, but not 11pm, in comparison with controls (Xxxxxxxx et al., 2009). In contrast, Xxxxxx and colleagues (2013) found in sample of 23 depressed women and 26 matched controls, that depressed women exhibited lower cortisol at 30 minutes post awaking, as well as in the evening, in comparison with controls. Depressed patients also showed less suppression of cortisol following dexamethasone administration than non-depressed women, suggesting GC resistance in these women. One potential explanation for these seemingly paradoxical findings could be that GC output may not be a linear correlate to all functional activity of the HPA axis. That is, whilst impairment in GR-mediated feedback may indeed be present, this could manifest differently depending on the chronicity and severity of disturbance, with a blunted CAR perhaps being indicative of fatigue and exhaustion. These discrepancies could also be explained by methodological differences such as sampling, type of depression, co-morbid conditions, age and early life experiences. What is clear, however, from all of these studies, is that dysfunction in GC secretion is a key facet of depression.
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