Dataset Information

Circadian Preference as a Moderator of Depression Outcome Following Cognitive Behavioral Therapy for Insomnia Plus Antidepressant Medications: A Report From the TRIAD Study.

ABSTRACT: STUDY OBJECTIVES:We previously presented results from a randomized controlled trial that examined the effects of antidepressant medication plus cognitive behavioral therapy for insomnia (CBT-I) among patients with major depressive disorder (MDD) and insomnia. The current secondary analysis aims to examine whether circadian preference moderated the reduction in depression and insomnia symptom severity during this trial. METHODS:A total of 139 adult participants with MDD and insomnia disorder were treated with antidepressant medication and randomized to receive 7 sessions of CBT-I or a control therapy (CTRL). Circadian preference (eveningness) was measured using the Composite Scale of Morningness (CSM). Depression symptom severity was assessed using the Hamilton Depression Rating Scale (HDRS); insomnia symptom severity was assessed using the Insomnia Severity Inventory (ISI). The moderating role of circadian preference on changes in HRSD and ISI was assessed via latent growth models within the framework of structural equation modeling. RESULTS:Greater evening preference was associated with smaller reduction in HDRS (P = .03) from baseline to week 6 across treatment groups. The interaction between CSM and treatment group was also significant (P = .02), indicating that participants with greater evening preference in the CTRL group had significantly smaller HDRS reduction than those with greater evening preference in the CBT-I group. Circadian preference did not share significant associations with ISI (all P > .30). CONCLUSIONS:Individuals with MDD and insomnia who have an evening preference are at increased risk for poor response to pharmacological depression treatment augmented with either CBT-I or CTRL behavioral insomnia treatment. However, evening types have better depression outcomes when treated with CBT-I than with CTRL for insomnia.

SUBMITTER: Asarnow LD

PROVIDER: S-EPMC6457514 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Circadian Preference as a Moderator of Depression Outcome Following Cognitive Behavioral Therapy for Insomnia Plus Antidepressant Medications: A Report From the TRIAD Study.

Asarnow Lauren D LD Bei Bei B Krystal Andrew A Buysse Daniel J DJ Thase Michael E ME Edinger Jack D JD Manber Rachel R

Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 20190415 4

<h4>Study objectives</h4>We previously presented results from a randomized controlled trial that examined the effects of antidepressant medication plus cognitive behavioral therapy for insomnia (CBT-I) among patients with major depressive disorder (MDD) and insomnia. The current secondary analysis aims to examine whether circadian preference moderated the reduction in depression and insomnia symptom severity during this trial.<h4>Methods</h4>A total of 139 adult participants with MDD and insomni ...[more]

PMID: 30952216

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Project description:Study objectivesThe current archival analyses examine the direct and indirect effects of cognitive behavioral therapy for insomnia (CBT-I) on depression in cancer survivors.MethodsWe report on 67 cancer survivors from a 2 × 2 randomized controlled trial of CBT-I and armodafinil for insomnia, after collapsing across the noneffective study medication conditions (armodafinil/placebo) to create CBT-I (yes/no). Depression and insomnia were assessed before, during the 7-week CBT-I intervention, at postintervention, and 3 months later by the Patient Health Questionnaire and the Insomnia Severity Index, respectively.ResultsMean depression at baseline for all participants was 6.44 (standard error = 0.41, range 0-15). Paired t tests showed that depression improved from baseline to postintervention by 48% (P < .001) in the CBT-I group versus 15% (P = .016) in the non-CBT-I group. Analysis of covariance controlling for baseline found that participants receiving CBT-I had significantly less depression at postintervention (effect size = -0.62; P = .001), compared to those who did not receive CBT-I. These benefits were maintained at the 3-month follow-up. Spearman rank correlations showed that changes in insomnia severity from baseline to postintervention were significantly correlated with concurrent changes in depression (r = .73; P < .001). Path analysis revealed that improvement in depression was mediated by improvement in insomnia severity (P < .001).ConclusionsOur findings provide preliminary support that in cancer survivors, CBT-I reduces depression via improvement in insomnia. Further, this reduction in depression remained stable 3 months after completing CBT-I. This suggests that a CBT-I intervention has a meaningful effect on depression.Clinical trial registrationRegistry: ClinicalTrials.gov; Title: Cognitive Behavioral Therapy +/- Armodafinil for Insomnia and Fatigue Following Chemotherapy; Identifier: NCT01091974; URL: https://clinicaltrials.gov/ct2/show/record/NCT01091974.

Project description:Late-life depression frequently co-occurs with cognitive impairment. To inform clinical management of these conditions, we examined the hypotheses that, relative to cognitively normal elders meeting DSM-IV criteria for major depressive disorder, those with cognitive impairment would require greater intensity of pharmacotherapy to reach criteria for antidepressant response and would take longer to respond.Using data from the MTLD-3 study, we conducted a series of secondary analyses examining the implications of cognitive impairment for short-term, open-trial pharmacotherapy of late-life depression (major depressive disorder in individuals 65 years and older). The treatment algorithm consisted of 3 steps: initial treatment with a selective serotonin reuptake inhibitor (SSRI), a switch to a serotonin-norepinephrine reuptake inhibitor (SNRI) if the patient did not respond, and addition of an atypical antipsychotic if the patient did not respond to the SNRI. The first subject entered the protocol in April 2004, and the last subject exited in September 2009. We examined data for participants who completed the acute phase of MTLD-3 as responders and received a cognitive diagnosis (N = 153) based on National Alzheimer's Coordinating Center (NACC) Uniform Data Set criteria. We divided participants into 3 groups on the basis of NACC cognitive diagnosis: no cognitive disorder (n = 74), mild cognitive impairment (n = 60), and dementia (n = 19). For each group, we calculated the proportion of participants requiring first- (SSRI), second- (SNRI), or third-step (add-on atypical antipsychotic) treatment to meet criteria for response (17-Item Hamilton Depression Rating Scale score ? 10 for 3 consecutive weeks). We compared time to response across groups and correlates of nonresponse.The 3 groups did not differ in intensity of pharmacotherapy (P = .68) or time to response (P = .84). Nonresponse was more strongly correlated with longer major depressive episode duration (P = .0015), presence of recurrent depression (P = .002), and younger current age (P = .047), rather than cognitive status (P = .61).Cognitive status does not appear to impact short-term pharmacotherapy response variability in individuals whose depression responds to treatment with open-trial antidepressants delivered in a supportive, university-based medication clinic.

Project description:BackgroundBrain derived neurotrophic factor (BDNF) is one of the most important regulatory proteins in the pathophysiology of major depressive disorder (MDD). Increasing numbers of studies have reported the relationship between serum/plasma BDNF and antidepressants (ADs). However, the potential effects of several classes of antidepressants on BDNF concentrations are not well known. Hence, our meta-analyses aims to review the effects of differential antidepressant drugs on peripheral BDNF levels in MDD and make some recommendations for future research.MethodsElectronic databases including PubMed, EMBASE, the Cochrane Library, Web of Science, and PsycINFO were searched from 1980 to June 2016. The change in BDNF levels were compared between baseline and post-antidepressants treatment by use of the standardized mean difference (SMD) with 95% confidence intervals (CIs). All statistical tests were two-sided.ResultsWe identified 20 eligible trials of antidepressants treatments for BDNF in MDD. The overall effect size for all drug classes showed that BDNF levels were elevated following a course of antidepressants use. For between-study heterogeneity by stratification analyses, we detect that length of treatment and blood samples are significant effect modifiers for BDNF levels during antidepressants treatment. While both SSRIs and SNRIs could increase the BDNF levels after a period of antidepressant medication treatment, sertraline was superior to other three drugs (venlafaxine, paroxetine or escitalopram) in the early increase of BDNF concentrations with SMD 0.53(95% CI = 0.13-0.93; P = 0.009).ConclusionsThere is some evidence that treatment of antidepressants appears to be effective in the increase of peripheral BDNF levels. More robust evidence indicates that different types of antidepressants appear to induce differential effects on the BDNF levels. Since sertraline makes a particular effect on BDNF concentration within a short amount of time, there is potential value in exploring its relationship with BDNF and its pharmacological mechanism concerning peripheral blood BDNF. Further confirmatory trials are required for both observations.

Project description:BackgroundMajor depressive disorder (MDD) is often comorbid with metabolic diseases such as obesity, cardiovascular disease, and type 2 diabetes. A potential link between these disorders is adiponectin, an adipocyte-derived circulating hormone with insulin-sensitizing, anti-inflammatory, and neuroplasticity effects. Reductions in plasma levels of adiponectin have been reported in both humans with depression and in the chronic-defeat mouse model of depression. However, the predictive value of adiponectin for treatment response to depression has not been determined.MethodsWe investigated the potential predictive effect of baseline adiponectin levels in patients who provided plasma and were undergoing one of three pharmacological treatments (escitalopram monotherapy; escitalopram plus bupropion; and venlafaxine plus mirtazapine) in the Combining Medications to Enhance Depression Outcomes clinical trial (n=160). Specifically, we assessed whether adiponectin moderates-that is, differentially predicts-treatment response among the treatment arms. Improvements with treatment were assessed using change in the clinician-rated 30-item Inventory of Depressive Symptomatology (IDS-C) from baseline through week 12. Moderator effects were tested using separate pairwise repeated measures mixed-effects models with a treatment-arm-by-adiponectin interaction.ResultsBaseline adiponectin levels moderated treatment outcome between two combination therapies. Specifically, low adiponectin predicted better response to escitalopram plus bupropion compared to venlafaxine plus mirtazapine, whereas high adiponectin predicted better response to venlafaxine plus mirtazapine compared to escitalopram plus bupropion (F=4.84, p=0.03). Adiponectin levels did not correlate with baseline depression severity (r=-0.03, p=.59).ConclusionsAntidepressant selection for patients with MDD can be personalized using pre-treatment blood-based biomarkers, such as adiponectin, thereby improving treatment outcomes.

Dataset Information

Circadian Preference as a Moderator of Depression Outcome Following Cognitive Behavioral Therapy for Insomnia Plus Antidepressant Medications: A Report From the TRIAD Study.

Publications

Circadian Preference as a Moderator of Depression Outcome Following Cognitive Behavioral Therapy for Insomnia Plus Antidepressant Medications: A Report From the TRIAD Study.

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