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Enhanced post-awakening cortisol may serve as a biological marker for individuals with major depressive disorder. However, studies comparing post-awakening cortisol between patients with major depressive disorder (MDD) and healthy controls have produced conflicting findings. The aim of this study was to investigate whether this inconsistency could be due to the effects of childhood trauma.
A total of N = 112 patients with MDD and healthy controls were divided into four groups according to the presence of childhood trauma. Saliva samples were collected at awakening and 15, 30, 45, and 60 min later. The total cortisol output and the cortisol awakening response (CAR) were calculated.
The total post-awakening cortisol output was significantly higher in patients with MDD as compared to healthy controls, but only in those individuals reporting childhood trauma. The four groups did not differ regarding the CAR.
Elevated post-awakening cortisol in MDD may be confined to those with a history of early life stress. Tailoring and/or augmenting of currently available treatments may be required to meet the specific needs of this population.
Systematic studies on the outcome of treatment-resistant depression are
To describe the longer-term outcome and predictors of outcome in
Out of 150 patients approached, 118 participants with confirmed
treatment-resistant depression (unipolar, n= 7; bipolar,
n=27; secondary, n=14) treated in a
specialist in-patient centre were followed-up for between 8 and 84 months
The majority of participants attained full remission (60.2%), most of
whom (48.3% of total sample) showed sustained recovery (full remission
for at least 6 months). A substantial minority had persistent
subsyndromal depression (19.5%) or persistent depressive episode (20.3%).
Diagnosis of bipolar treatment-resistant depression and poorer social
support were associated with early relapse, whereas strong social
support, higher educational status and milder level of treatment
resistance measured with the Maudsley Staging Method were associated with
achieving quicker remission. Exploratory analysis of treatment found
positive associations between treatment with a monoamine oxidase
inhibitor (MAOl) in unipolar treatment-resistant depression and attaining
remission at discharge and at final follow-up, and duloxetine use
predicted attainment of remission at final follow-up.
Although many patients with treatment-resistant depression experience
persistent symptomatology even after intensive, specialist treatment,
most can achieve remission. The choice of treatment and presence of good
social support may affect remission rates, whereas those with low social
support and a bipolar diathesis should be considered at higher risk of
early relapse. We suggest that future work to improve the long-term
outcome in this disabling form of depression might focus on social
interventions to improve support, and the role of neglected
pharmacological interventions such as MAOIs.
People with severe depressive illness have raised levels of cortisol and reduced glucocorticoid receptor function.
To obtain a physiological assessment of hypothalamic–pituitary–adrenal (HPA) axis feedback status in an in-patient sample with depression and to relate this to prospectively determined severe treatment resistance.
The prednisolone suppression test was administered to 45 in-patients with depression assessed as resistant to two or more antidepressants and to 46 controls, prior to intensive multimodal in-patient treatment.
The patient group had higher cortisol levels than controls, although the percentage suppression of cortisol output after prednisolone in comparison with placebo did not differ. Nonresponse to in-patient treatment was predicted by a more dysfunctional HPA axis (higher cortisol levels postprednisolone and lower percentage suppression).
In patients with severe depression, HPA axis activity is reset at a higher level, although feedback remains intact. However, prospectively determined severe treatment resistance is associated with an impaired feedback response to combined glucocorticoid and mineralocorticoid receptor activation by prednisolone.
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