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.

An ‘ethnic’ or ‘group’ density effect in psychosis has been observed, whereby the risk of psychosis in minority group individuals is inversely related to neighbourhood-level proportions of others belonging to the same group. However, there is conflicting evidence over whether this effect differs between minority groups and limited investigation into other moderators.

To conduct a comprehensive systematic review and meta-analysis of the group density effect in psychosis and examine moderators.

Four databases were systematically searched. A narrative review was conducted and a three-level meta-analysis was performed. The potential moderating effect of crudely and specifically defined minority groups was assessed. Country, time, area size and whether studies used clinical or non-clinical outcomes were also tested as moderators.

Thirty-two studies were included in the narrative review and ten in the meta-analysis. A 10 percentage-point decrease in own-group density was associated with a 20% increase in psychosis risk (OR = 1.20, 95% CI 1.09−1.32, P < 0.001). This was moderated by crudely defined minority groups (F6,68 = 6.86, P < 0.001), with the strongest associations observed in Black populations, followed by a White Other sample. Greater heterogeneity was observed when specific minority groups were assessed (F25,49 = 7.26, P < 0.001).

This is the first review to provide meta-analytic evidence that the risk of psychosis posed by lower own-group density varies across minority groups, with the strongest associations observed in Black individuals. Heterogeneity in effect sizes may reflect distinctive social experiences of specific minority groups. Potential mechanisms are discussed, along with the implications of findings and suggestions for future research.

After remission, antidepressants are often taken long term to prevent depressive relapse or recurrence. Whether psychological interventions can be a viable alternative or addition to antidepressants remains unclear.

To compare the effectiveness of psychological interventions as an alternative (including delivered when tapering antidepressants) or addition to antidepressants alone for preventing depressive relapse.

Embase, PubMed, the Cochrane Library and PsycINFO were searched from inception until 13 October 2019. Randomised controlled trials (RCTs) with previously depressed patients in (partial) remission where preventive psychological interventions with or without antidepressants (including tapering) were compared with antidepressant control were included. Data were extracted independently from published trials. A random-effects meta-analysis on time to relapse (hazard ratio, HR) and risk of relapse (risk ratio, RR) at the last point of follow-up was conducted. PROSPERO ID: CRD42017055301.

Among 11 included trials (n = 1559), we did not observe an increased risk of relapse for participants receiving a psychological intervention while tapering antidepressants versus antidepressants alone (RR = 1.02, 95% CI 0.84–1.25; P = 0.85). Psychological interventions added to antidepressants significantly reduced the risk of relapse (RR = 0.85, 95% CI 0.74–0.97; P = 0.01) compared with antidepressants alone.

This study found no evidence to suggest that adding a psychological intervention to tapering increases the risk of relapse when compared with antidepressants alone. Adding a psychological intervention to antidepressant use reduces relapse risk significantly versus antidepressants alone. As neither strategy is routinely implemented these findings are relevant for patients, clinicians and guideline developers.

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.