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Major depressive disorder (MDD) is characterised by a recurrent course and high comorbidity rates. A lifespan perspective may therefore provide important information regarding health outcomes. The aim of the present study is to examine mental disorders that preceded 12-month MDD diagnosis and the impact of these disorders on depression outcomes.
Data came from 29 cross-sectional community epidemiological surveys of adults in 27 countries (n = 80 190). The Composite International Diagnostic Interview (CIDI) was used to assess 12-month MDD and lifetime DSM-IV disorders with onset prior to the respondent's age at interview. Disorders were grouped into depressive distress disorders, non-depressive
distress disorders, fear disorders and externalising disorders. Depression outcomes included 12-month suicidality, days out of role and impairment in role functioning.
Among respondents with 12-month MDD, 94.9% (s.e. = 0.4) had at least one prior disorder (including previous MDD), and 64.6% (s.e. = 0.9) had at least one prior, non-MDD disorder. Previous non-depressive distress, fear and externalising disorders, but not depressive distress disorders, predicted higher impairment (OR = 1.4–1.6) and suicidality (OR = 1.5–2.5), after adjustment for sociodemographic variables. Further adjustment for MDD characteristics weakened, but did not eliminate, these associations. Associations were largely driven by current comorbidities, but both remitted and current externalising disorders predicted suicidality among respondents with 12-month MDD.
These results illustrate the importance of careful psychiatric history taking regarding current anxiety disorders and lifetime externalising disorders in individuals with MDD.
Previous studies on reporting bias generally examined whether trials were published in stand-alone publications. In this study, we investigated whether pooled-trials publications constitute a specific form of reporting bias. We assessed whether negative trials were more likely to be exclusively published in pooled-trials publications than positive trials and examined the research questions, individual trial results, and conclusions presented in these articles.
Data from a cohort of 105 randomized controlled trials of 16 antidepressants were extracted from earlier publications and the corresponding Food and Drug Administration (FDA) reviews. A systematic literature search was conducted to identify pooled-trials publications.
We found 107 pooled-trials publications that reported results of 23 (72%) of 32 trials not published in stand-alone publications. Only two (3.8%) of 54 positive trials were published exclusively in pooled-trials publications, compared with 21 (41.1%) of 51 negative trials (p < 0.001). Thirteen (12%) of 107 publications had as primary aim to present data on the trial's primary research question (drug efficacy compared with placebo). Only four of these publications, reporting on five (22%) trials, presented individual efficacy data for the primary research question. Additionally, only five (5%) of 107 pooled-trials publications had a negative conclusion.
Compared with positive trials, negative trials of antidepressants for depression were much more likely to be reported exclusively in pooled-trials publications. Pooled-trials publications flood the evidence base with often-redundant articles that, instead of addressing the original primary research question, present (positive) results on secondary questions. Therefore, pooled-trials publications distort the apparent risk–benefit profile of antidepressants.
Improvement in depression within the first 2 weeks of antidepressant treatment predicts good outcomes, but non-improvers can still respond or remit, whereas improvers often do not.
We aimed to investigate whether early improvement of individual depressive symptoms better predicts response or remission.
We obtained individual patient data of 30 trials comprising 2184 placebo-treated and 6058 antidepressant-treated participants. Primary outcome was week 6 response; secondary outcomes were week 6 remission and week 12 response and remission. We compared models that only included improvement in total score by week 2 (total improvement model) with models that also included improvement in individual symptoms.
For week 6 response, the area under the receiver operating characteristic curve and negative and positive predictive values of the total improvement model were 0.73, 0.67 and 0.74 compared with 0.77, 0.70 and 0.71 for the item improvement model. Model performance decreased for week 12 outcomes. Of predicted non-responders, 29% actually did respond by week 6 and 43% by week 12, which was decreased from the baseline (overall) probabilities of 51% by week 6 and 69% by week 12. In post hoc analyses with continuous rather than dichotomous early improvement, including individual items did not enhance model performance.
Examining individual symptoms adds little to the predictive ability of early improvement. Additionally, early non-improvement does not rule out response or remission, particularly after 12 rather than 6 weeks. Therefore, our findings suggest that routinely adapting pharmacological treatment because of limited early improvement would often be premature.
Seasonal affective disorder (SAD) is considered to be a subtype of depression.
To compare the clinical picture of SAD to non-seasonal affective disorders (non-SADs).
Diagnoses according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) were established in 2185 participants of the Netherlands Study of Depression and Anxiety. The Seasonal Pattern Assessment Questionnaire was administered to diagnose SAD. Symptoms of depression and anxiety were measured with the Inventory of Depressive Symptoms, the Beck Anxiety Inventory and the Fear Questionnaire.
Participants with SAD, participants with a lifetime bipolar disorder and participants with a lifetime comorbid anxiety and depressive disorder scored highest in terms of psychopathology in the past year. The seasonal distribution of major depressive episodes was not different for participants with or without SAD.
SAD may be a measure of severity of depression with a subjectively perceived worsening of symptoms in the winter months.
General anxiety and depressive symptoms following a myocardial infarction are associated with a worse cardiac prognosis. However, the contribution of specific aspects of anxiety within this context remains unclear.
To evaluate the independent prognostic association of cardiac anxiety with cardiac outcome after myocardial infarction.
We administered the Cardiac Anxiety Questionnaire (CAQ) during hospital admission (baseline, n = 193) and 4 months (n = 147/193) after discharge. CAQ subscale scores reflect fear, attention, avoidance and safety-seeking behaviour. Study end-point was a major adverse cardiac event (MACE): readmission for ischemic cardiac disease or all-cause mortality. In Cox regression analysis, we adjusted for age, cardiac disease severity and depressive symptoms.
The CAQ sum score at baseline and at 4 months significantly predicted a MACE (HRbaseline = 1.59, 95% CI 1.04–2.43; HR4-months = 1.77, 95% CI 1.04–3.02) with a mean follow-up of 4.2 (s.d. = 2.0) years and 4.3 (s.d. = 1.7) years respectively. Analyses of subscale scores revealed that this effect was particularly driven by avoidance (HRbaseline = 1.23, 95% CI 0.99–1.53; HR4-months = 1.77, 95% CI 1.04–1.83).
Cardiac anxiety, particularly anxiety-related avoidance of exercise, is an important prognostic factor for a MACE in patients after myocardial infarction, independent of cardiac disease severity and depressive symptoms.
Antidepressants are established first-line treatments for anxiety disorders, but it is not clear whether they are equally effective across the severity range.
To examine the influence of baseline severity of anxiety on antidepressant efficacy for generalised anxiety disorder (GAD), social anxiety disorder (SAD), obsessive–compulsive disorder (OCD), post-traumatic stress disorder (PTSD) and panic disorder.
Fifty-six trials of second-generation antidepressants for the short-term treatment of an anxiety disorder were included. Baseline and change scores were extracted for placebo and treatment groups in each trial. Mixed effects meta-regression was used to investigate the effects of treatment group, baseline severity and their interaction.
Increased baseline severity did not predict greater improvement in drug groups compared with placebo groups. Standardised regression coefficients of the interaction term between baseline severity and treatment group were 0.04 (95% CI –0.13 to 0.20, P = 0.65) for GAD, –0.06 (95% CI –0.20 to 0.09, P = 0.43) for SAD, 0.04 (95% CI –0.07 to 0.16, P = 0.46) for OCD, 0.16 (95% CI –0.22 to 0.53, P = 0.37) for PTSD and 0.002 (95% CI –0.10 to 0.10, P = 0.96) for panic disorder. For OCD, baseline severity did predict improvement in both placebo and drug groups equally (β = 0.11, 95% CI 0.05 to 0.17, P = 0.001).
No relationship between baseline severity and drug–placebo difference was found for anxiety disorders. These results suggest that if the efficacy of antidepressants is considered clinically relevant, they may be prescribed to patients with anxiety regardless of symptom severity.
In this editorial, we propose that the association between depression and
cardiovascular disease may be conceptualised as a continuous, bidirectional
process that originates in youth. The paper by Åberg and colleagues in this
issue adds to this literature showing that low cardiovascular fitness at
adolescence increases the risk of future depression.
Few studies have addressed the relationship between generalised anxiety disorder and cardiovascular prognosis using a diagnostic interview.
To assess the association between generalised anxiety disorder and adverse outcomes in patients with myocardial infarction.
Patients with acute myocardial infarction (n = 438) were recruited between 1997 and 2000 and were followed up until 2007. Current generalised anxiety disorder and post-myocardial infarction depression were assessed with the Composite International Diagnostic Interview. The end-point consisted of all-cause mortality and cardiovascular-related readmissions.
During the follow-up period, 198 patients had an adverse event. Generalised anxiety disorder was associated with an increased rate of adverse events after adjustment for age and gender (hazard ratio: 1.94; 95% confidence interval: 1.14–3.30; P = 0.01). Additional adjustment for measures of cardiac disease severity and depression did not change the results.
Generalised anxiety disorder was associated with an almost twofold increased risk of adverse outcomes independent demographic and clinical variables and depression.
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