In most trials and systematic reviews that evaluate exercise-based interventions in reducing depressive symptoms, it is difficult to separate treatment from prevention.

To evaluate the effectiveness of exercise-based interventions in reducing depressive symptoms in people without clinical depression.

We searched PubMed, PsycINFO, Embase, WOS, SPORTDiscus, CENTRAL, OpenGrey and other sources up to 25 May 2020. We selected randomised controlled trials (RCTs) that compared exclusively exercise-based interventions with control groups, enrolling participants without clinical depression, as measured using validated instruments, and whose outcome was reduction of depressive symptoms and/or incidence of new cases of people with depression. Pooled standardised mean differences (SMDs) were calculated using random-effect models (registration at PROSPERO: CRD42017055726).

A total of 14 RCTs (18 comparisons) evaluated 1737 adults without clinical depression from eight countries and four continents. The pooled SMD was −0.34 (95% CI −0.51 to −0.17; P < 0.001) and sensitivity analyses confirmed the robustness of this result. We found no statistical evidence of publication bias and heterogeneity was moderate (I2 = 54%; 95% CI 22–73%). Only two RCTs had an overall low risk of bias and three had long-term follow-up. Multivariate meta-regression found that a larger sample size, country (Asia) and selective prevention (i.e. people exposed to risk factors for depression) were associated with lower effectiveness, although only sample size remained significant when adjustment for multiple tests was considered. According to the Grading of Recommendations Assessment, Development and Evaluation tool, the quality of evidence was low.

Exercise-based interventions have a small effect on the reduction of depressive symptoms in people without clinical depression. It could be an alternative to or complement psychological programmes, although further higher-quality trials with larger samples and long-term follow-up are needed.

There are limited studies examining mortality associated with electroconvulsive therapy (ECT), and many studies do not include a control group or method to identify all patient deaths.

We aimed to evaluate the risk of death associated with ECT treatments over 30 days and 1 year.

We conducted a study analysing electronic medical record data from the Department of Veterans Affairs healthcare system between 2000 and 2017. We compared mortality among patients who received ECT with a matched group of patients created through propensity score matching.

Our sample included 123 479 individual ECT treatments provided to 8720 patients (including 5157 initial index courses of ECT). Mortality associated with individual ECT treatments was 3.08 per 10 000 treatments over the first 7 days after treatment. When comparing patients who received ECT with a matched group of mental health patients, those receiving ECT had a relative odds of all-cause mortality in the year after their index course of 0.87 (95% CI 0.79–1.11; P = 0.10), and a relative risk of death from causes other than suicide of 0.79 (95% CI 0.66–0.95; P < 0.01). The similar relative odds of all-cause mortality in the first 30 days after ECT was 1.06 (95% CI 0.65–1.73) for all-cause mortality, and 1.02 (95% CI 0.58–1.8) for all-cause mortality excluding suicide deaths.

There was no evidence of elevated or excess mortality after ECT. There was some indication that mortality may be reduced in patients receiving ECT compared with similar patients who do not receive ECT.

The role of childhood abuse and serum brain-derived neurotrophic factor (BDNF) levels in suicidal behaviour is controversial.

We aimed to investigate the individual and interactive effects of the childhood abuse and serum BDNF on suicidal behaviour before and after pharmacologic treatment in patients with depressive disorders.

At baseline, reported childhood emotional, physical and sexual abuse were ascertained and serum BDNF levels were measured in 1094 patients with depressive disorder, 884 of whom were followed during a 1-year period of stepwise pharmacotherapy. Suicidal behaviours evaluated at baseline were previous suicide attempt and baseline suicide severity, and suicidal behaviours evaluated at follow-up were increased suicide severity and fatal/non-fatal suicide attempt. Individual and interactive associations of any childhood abuse and serum BDNF levels with four types of suicidal behaviours were analysed using logistic regression models, after adjusting relevant covariates.

Individual associations of childhood abuse were significant only with previous suicide attempt, and no significant individual associations were found for serum BDNF with any suicide outcome. However, the presence of both childhood abuse and lower serum BDNF levels was associated with the highest prevalence/incidence of all four suicidal behaviours, with significant interactions for baseline suicide severity and fatal/non-fatal suicide attempt during follow-up.

Synergistic interactive effects of child abuse and serum BDNF levels on suicidal behaviours were found before and after pharmacologic treatment in patients with depressive disorders. Information combining childhood abuse and serum BDNF levels could improve predictions of suicidal behaviour in patients with depressive disorders.

Major depressive disorder (MDD) is a clinically and biologically heterogeneous syndrome. Identifying discrete subtypes of illness with distinguishing neurobiological substrates and clinical features is a promising strategy for guiding personalised therapeutics.

This study aimed to identify depression subtypes with correlated patterns of functional network connectivity and clinical symptoms by clustering patients according to a weighted linear combination of both features in a relatively large, medication-naïve depression sample.

We recruited 115 medication-naïve adults with MDD and 129 matched healthy controls, and evaluated all participants with magnetic resonance imaging. We used regularised canonical correlation analysis to identify component mapping relationships between functional network connectivity and symptom profiles, and K-means clustering was used to define distinct subtypes of patients.

Two subtypes of MDD were identified: insomnia-dominated subtype 1 and anhedonia-dominated subtype 2. Subtype 1 was characterised by abnormal hyperconnectivity within the ventral attention network and sleep maintenance insomnia. Subtype 2 was characterised by abnormal hypoconnectivity in the subcortical and dorsal attention networks, and prominent anhedonia symptoms.

Our study identified two distinct subtypes of patients with specific neurobiological and clinical symptom profiles. These findings advance understanding of the biological and clinical heterogeneity of MDD, offering a pathway for defining categorical subtypes of illness via consideration of both biological and clinical features.