The DST as a predictor of outcome in depression: a meta-analysis

Ribeiro, Saulo C.M.; Tandon, Rajiv; Grunhaus, Leon; Greden, John F.

doi:10.1176/ajp.150.11.1618

Cited by 291 publications

(41 citation statements)

References 120 publications

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“…The significance of HPA-axis modulation in depression is underscored by reports that successful antidepressant treatment is associated with resolution of impairment in HPA-axis negative feedback. 38, 39 Our data show that the ability of animals to recover from the SC-induced submissive phenotype is critically dependent on intact neurogenesis. Given previous evidence that the HPA-axis is altered by EE exposure and that neurogenesis modulates the HPA-axis stress response, it is plausible that the antidepressant effects of EE in behavioral recovery from SC are mediated via regulation of the HPA axis by neurogenesis.…”

Section: Discussionmentioning

confidence: 71%

Environmental enrichment requires adult neurogenesis to facilitate the recovery from psychosocial stress

et al. 2010

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The subgranular zone of the adult hippocampal dentate gyrus contains a pool of neural stem cells that continuously divide and differentiate into functional granule cells. It has been shown that production of new hippocampal neurons is necessary for amelioration of stress-induced behavioral changes by antidepressants in animal models of depression. The survival of newly born hippocampal neurons is decreased by chronic psychosocial stress and increased by exposure to enriched environments. These observations suggest the existence of a link between hippocampal neurogenesis, stress-induced behavioral changes, and the beneficial effects of enriched environment. To show causality, we subjected transgenic mice with conditionally suppressed neurogenesis to psychosocial stress followed by environmental enrichment. First, we showed that repeated social defeat coupled with chronic exposure to an aggressor produces robust and quantifiable indices of submissive and depressive-like behaviors; second, subsequent exposure to an enriched environment led to extinction of the submissive phenotype, while animals exposed to an impoverished environment retained the submissive phenotype; and third, enrichment was not effective in reversing the submissive and depressive-like behaviors in transgenic mice lacking neurogenesis. Our data show two main findings. First, living in an enriched environment is highly effective in extinguishing submissive behavioral traits developed during chronic social stress, and second, these effects are critically dependent on adult neurogenesis, indicating that beneficial behavioral adaptations are dependent on intact adult neurogenesis.

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Section: Discussionmentioning

confidence: 71%

Environmental enrichment requires adult neurogenesis to facilitate the recovery from psychosocial stress

et al. 2010

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“…Some potential markers include abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis as measured by nonsuppression in the dexamethasone suppression test (DST), impaired lymphocyte glucocorticoid sensitivity and abnormal sleep EEG patterns [114]. While the baseline DST does not predict antidepressant treatment response or outcome after hospital discharge, research has suggested that the DST tends to return to normal as a result of antidepressant treatment [114, 115]or cognitive behavior therapy [116]. Abnormal DST results that persist after treatment and EEG sleep abnormalities have been associated with poor prognosis and higher relapse rates [114, 117].…”

Section: Belief No 3: Antidepressants Are Necessary To Redress a Chementioning

confidence: 99%

Raising Questions about Antidepressants

Antonuccio

Danton

DeNelsky

et al. 1999

Psychother Psychosom

104

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Antidepressant medication has apparently become the most popular treatment for depression in the USA. Several beliefs about the efficacy of antidepressant medications prevail among mental health professionals and the public. This paper explores relevant research data and raises questions about these beliefs. Many of the common beliefs about these medications are not adequately supported by scientific data. The following issues are raised: (1) industry-funded research studies which result in negative findings sometimes do not get published; (2) placebo washout procedures may bias results in some studies; (3) there are serious questions about the integrity of the double-blind procedure; (4) the ‘true’ antidepressant drug effect in adults appears to be relatively small; (5) there is minimal evidence of antidepressant efficacy in children; (6) side effects are fairly common even with the newer antidepressants; (7) combining medications raises the risk for more serious complications; (8) all antidepressants can cause withdrawal symptoms; (9) genetic influences on unipolar depression appear to be weaker than environmental influences; (10) biochemical theories of depression are as yet unproven; (11) biological markers specific for depression have been elusive; (12) dosage and plasma levels of antidepressants have been minimally related to treatment outcome; (13) preliminary evidence suggests that patients who improve with cognitive-behavioral psychotherapy show similar biological changes as those who respond to medication, and (14) the evidence suggests that psychological interventions are at least as effective as pharmacotherapy in treating depression, even if severe, especially when patient-rated measures are used and long-term follow-up is considered.

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“…Hyperactivity of the HPA axis has been observed in patients with major depressive disorder and with poorer antidepressant outcome [8,9]. Moreover, elevated cortisol levels and no suppression of cortisol secretion after dexamethasone suppression test (DST) have been associated with worse antidepressant treatment outcome, relating the HPA axis dysregulation to the response [10]. This suggests that patients resistant to antidepressant treatment may represent a biologically distinct group [8,9].…”

Section: Introductionmentioning

confidence: 99%

Relationship of cortisol levels and genetic polymorphisms to antidepressant response to placebo and fluoxetine in patients with major depressive disorder: a prospective study

et al. 2014

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BackgroundIncreased cortisol levels and genetic polymorphisms have been related to both major depressive disorder and antidepressant treatment outcome. The aim of this study is to evaluate the relationship between circadian salivary cortisol levels, cortisol suppression by dexamethasone and genetic polymorphisms in some HPA axis-related genes to the response to placebo and fluoxetine in depressed patients.MethodsThe diagnosis and severity of depression were performed using the Mini International Neuropsychiatric Interview (M.I.N.I.) and Hamilton depression scale (HAM-D17), respectively. Euthyroid patients were treated with placebo (one week) followed by fluoxetine (20 mg) (two months). Severity of depression was re-evaluated after placebo, three weeks and two months of fluoxetine treatments. Placebo response was defined as HAM-D17 score reductions of at least 25% and to < 15. Early response and response were reductions of at least 50% after three weeks and two months, and remission with ≤ 7 after two months. Plasma TSH, free-T4, circadian salivary cortisol levels and cortisol suppression by dexamethasone were evaluated. Seven genetic polymorphisms located in the Corticotrophin-releasing-hormone-receptor-1 (rs242939, rs242941, rs1876828), Corticotrophin-releasing-hormone-receptor-2 (rs2270007), Glucocorticoid-receptor (rs41423247), FK506-binding-protein-5 (rs1360780), and Arginine-vasopressin (rs3729965) genes were determined. Association analyses between response to placebo/fluoxetine and polymorphism were performed by chi-square or Fisher exact test. Cortisol levels were compared by t-test, ANOVA and the general linear model for repeated measures.Results208 depressed patients were recruited, 187 of whom were euthyroid. Placebo responders, fluoxetine responders and remitters exhibited significantly lower circadian cortisol levels than those who did not respond (p-values of 0.014, 0.008 and 0.021 respectively). Patients who abandoned treatment before the third week also exhibited a trend to low cortisol levels (p = 0.057). The polymorphisms rs242939 (CRHR1) and rs2270007 (CRHR2) were not in Hardy-Weinberg equilibrium. Only the rs242939 polymorphism (CRHR1) exhibited association with early response (three weeks) to fluoxetine (p-value = 0.043). No other association between outcomes and polymorphisms was observed.ConclusionsThese results support the clinical relevance of low salivary cortisol levels as a predictor of antidepressant response, either to placebo or to fluoxetine. Only one polymorphism in the CRHR1 gene was associated with the early response. Other factors may be involved in antidepressant response, although further studies are needed to identify them.Electronic supplementary materialThe online version of this article (doi:10.1186/s12888-014-0220-0) contains supplementary material, which is available to authorized users.

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The DST as a predictor of outcome in depression: a meta-analysis

Cited by 291 publications

References 120 publications

Environmental enrichment requires adult neurogenesis to facilitate the recovery from psychosocial stress

Environmental enrichment requires adult neurogenesis to facilitate the recovery from psychosocial stress

Raising Questions about Antidepressants

Relationship of cortisol levels and genetic polymorphisms to antidepressant response to placebo and fluoxetine in patients with major depressive disorder: a prospective study

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