The present study aims at measuring the association between household food insecurity and psychological distress in adolescents in Inuit communities, concurrently and overtime from childhood to adolescence.

The study used measures of internalising behaviours (anxiety, withdrawn attitude, somatic complaints and depression) as indicators of psychological distress during adolescence, a concurrent measure of household food insecurity in adolescence and an assessment of longitudinal patterns of household food insecurity from childhood to adolescence. We collected descriptive information at birth, childhood and adolescence on potential confounders.

Inuit communities of Nunavik in northern Quebec, Canada

The study consisted of 212 participants from the Nunavik Child Development Study, who have been assessed at birth, childhood (mean age = 11 years, range = 9–13 years) and adolescence (mean age = 18 years, range = 16–21 years).

Concurrent severe household food insecurity in adolescence was associated with higher measures of psychological distress: depression (βstd = 0·26, P < 0·01) and withdrawn attitude (βstd = 0·20, P = 0·04). Persistent household food insecurity (both at childhood and adolescence) was associated with higher levels of adolescent depression (βstd = 0·18, P = 0·02) and anxiety (βstd = 0·17, P = 0·03).

Adolescents from Nunavik living with higher food insecurity and those having experienced food insecurity in both childhood and adolescence were more likely to report symptoms of psychological distress. Considering the high level of distress experienced by young Inuit, existing initiatives to reduce food insecurity in Nunavik communities should be targeted to include children and adolescents.

There are few very brief measures that accurately identify multiple common mental disorders.

The aim of this study was to develop and assess the psychometric properties of a new composite measure to screen for five common mental disorders.

Two cross-sectional psychometric surveys were used to develop (n = 3175) and validate (n = 3620) the new measure, the Rapid Measurement Toolkit-20 (RMT20) against diagnostic criteria. The RMT20 was tested against a DSM-5 clinical checklist for major depression, generalised anxiety disorder, panic disorder, social anxiety disorder and post-traumatic stress disorder, with comparison with two measures of general psychological distress: the Kessler-10 and Distress Questionnaire-5.

The area under the curve for the RMT20 was significantly greater than for the distress measures, ranging from 0.86 to 0.92 across the five disorders. Sensitivity and specificity at prescribed cut-points were excellent, with sensitivity ranging from 0.85 to 0.93 and specificity ranging from 0.73 to 0.83 across the five disorders.

The RMT20 outperformed two established scales assessing general psychological distress, is free to use and has low respondent burden. The measure is well-suited to clinical screening, internet-based screening and large-scale epidemiological surveys.

The antidepressant effect of low-dose ketamine infusion on Taiwanese patients with anxious vs nonanxious treatment-resistant depression (ANX-TRD vs NANX-TRD) has remained unknown.

In total, 71 patients with TRD were randomized to three groups. Each group had participants who received saline infusions mixed with 0 (a normal saline infusion), 0.2, and 0.5 mg/kg of ketamine. Participants were followed up for 2 weeks. Anxious depression was defined as major depressive disorder with a total score of 7 or more on the 17-item Hamilton Depression Rating Scale Anxiety-Somatization factor. Generalized estimating equation models were used to investigate the effects of treatment (ketamine vs placebo) and depression type (ANX-TRD vs NANX-TRD) in the reduction of depressive symptoms during the follow-up period.

Patients with ANX-TRD were less likely to respond to a single low-dose ketamine infusion than those with NANX-TRD. Among patients with NANX-TRD, low-dose ketamine infusion was significantly superior to placebo for reducing depressive symptoms. However, among patients with ANX-TRD, ketamine was not superior to placebo; nonetheless, approximately 30% of the patients responded to ketamine infusion compared to 13% who responded to the placebo.

Low-dose ketamine infusion was effective for Taiwanese patients with NANX-TRD but not so effective for those with ANX-TRD. A higher level of anxiety severity accompanying depression was related to greater depression severity. This may confound and reduce the antidepressant effect of ketamine infusion.

The apolipoprotein E ε4 allele (APOE*ε4) is indicated as a risk for Alzheimer's disease and other age-related diseases. The risk attributable to APOE*ε4 for depression is less clear and may be because of confounding of the relationship between dementia and depression.

We examined the risk of APOE* ε4 for incident depression and depressive symptomology over a 12-year period across the adult lifespan.

Participants were from the Personality and Total Health Through Life study, aged 20 to 24 (n = 1420), 40 to 44 (n = 1592) or 60–64 (n = 1768) at baseline, and interviewed every 4 years since 1999. Ethnicities other than White, those without genotyping and those with depression at baseline, or who reported strokes and scores on the Mini-Mental State Examination <27 at any observation, were excluded.

Over the study period, there was no evidence that APOE*ε4+ was a risk factor for depression, including any depression (odds ratio (OR) = 0.94, 95% CI 0.77–1.16, P = 0.573), major depression (OR = 0.96, 95% CI 0.60–1.53, P = 0.860), minor depression (OR = 0.94, 95% CI 0.67–1.30, P = 0.695) or depressive symptomology (incidence rate ratio (IRR) = 1.02, 95% CI 0.97–1.08, P = 0.451). APOE*ε4 was unrelated to incident depression. Findings were consistent for all age cohorts.

Among cognitively intact Australian adults who were free of depression at baseline, there was little evidence that APOE*ε4+ carriers are at increased risk for depression over a 12-year period among those who are cognitively intact.

To investigate the effect of maternal depressive symptom trajectories, from 3 months to 11 years postpartum, on the offspring’s body composition at 11 years of age.

Data from the Pelotas 2004 Birth Cohort, from the perinatal interview and from the 3-, 12-, 24- and 48-month and 6- and 11-year follow-ups.

Community-based sample from the city of Pelotas, located in southern Brazil with approximately 350 000 inhabitants. The maternal depression symptom trajectories were identified through a semi-parametric group-based modelling approach, using the Edinburgh Postnatal Depression Scale (EPDS), with data from 3 months to 11 years postpartum.

A total of 3467 (81·9 % of the total cohort).

Five trajectory groups of EPDS scores were identified (‘Low’, ‘Moderate low’, ‘Increasing’, ‘Decreasing’ and ‘Chronic high’). A total of 170 women (4·9 %) from the sample belonged to the ‘Chronic high’ group, having scored ≥13 EPDS points at every follow-up. Mean BMI in the ‘Low’ trajectory group was 0·77 (z-score 1·4), compared with 0·56 (z-score 1·4) in the ‘Chronic high’ group. Children from mothers in the ‘Chronic high’ group had lower fat mass (FM) (–1·34 ± 0·64 kg), FM% (–2·02 ± 0·85 percentage points) and FM index (–0·57 ± 0·27 kg/m2), compared with children from mothers in the ‘Low’ trajectory group. Adjusted analyses showed that sustained or transitory maternal depressive symptoms during childhood had no effect on the offspring’s body composition indices at 11 years of age.

Children raised by chronically depressed mothers have body composition indices at 11 years of age that are similar to those of children whose mothers have never been depressed.

Animal models are critical for the study of mental disorders and their treatments but are repeatedly criticized for problems with validity and reproducibility. One approach to enhance validity and reproducibility of models is to use test batteries rather than single tests. Yet, a question regarding batteries is whether one can expect a consistent individual behavioral phenotype in mice across tests that can be presumed to be part of the same construct.

The present study was designed to explore the relationship between the behaviors of mice across tests in some variations of test batteries for depression- and anxiety-like behaviors.

Female and male healthy, intact and untreated mice from the ICR and black Swiss strains were used in four separate experiments. With some variations, mice were exposed to a battery of behavioral tests representing affective- and anxiety-like behaviors. Data were analyzed for differences between sexes and for correlations between behaviors within and across the tests in the battery.

No differences were found between the sexes. With very few exceptions, we found correlations within tests (when one test has more than one measure or is repeated) but not across different tests within the battery.

The results cast some doubt on the utility of behavioral test batteries to represent different facets of emotional behavior in healthy intact outbred mice, without any interventions or treatments. Additional studies are designed to explore whether stronger relationship between the tests will appear after manipulations or drug treatments.

Across international contexts, people with serious mental illnesses (SMI) experience marked reductions in life expectancy at birth. The intersection of ethnicity and social deprivation on life expectancy in SMI is unclear. The aim of this study was to assess the impact of ethnicity and area-level deprivation on life expectancy at birth in SMI, defined as schizophrenia-spectrum disorders, bipolar disorders and depression, using data from London, UK.

Abridged life tables to calculate life expectancy at birth, in a cohort with clinician-ascribed ICD-10 schizophrenia-spectrum disorders, bipolar disorders or depression, managed in secondary mental healthcare. Life expectancy in the study population with SMI was compared with life expectancy in the general population and with those residing in the most deprived areas in England.

Irrespective of ethnicity, people with SMI experienced marked reductions in life expectancy at birth compared with the general population; from 14.5 years loss in men with schizophrenia-spectrum and bipolar disorders, to 13.2 years in women. Similar reductions were noted for people with depression. Across all diagnoses, life expectancy at birth in people with SMI was lower than the general population residing in the most deprived areas in England.

Irrespective of ethnicity, reductions in life expectancy at birth among people with SMI are worse than the general population residing in the most deprived areas in England. This trend in people with SMI is similar to groups who experience extreme social exclusion and marginalisation. Evidence-based interventions to tackle this mortality gap need to take this into account.

We evaluated processing-speed and shift-cost measures in adults with depression or ADHD and monitored the effects of treatment. We hypothesized that cognitive-speed and shift-cost measures might differentiate diagnostic groups.

Colour, form, and colour-form stimuli were used to measured naming times. The shift cost (s) were calculated as colour-form naming time minus the sum of colour and form naming times. Measurements were done at baseline and endpoint for 42 adults with depression and 42 with ADHD without depression. Patients with depression were treated with Transcranial Pulsed Electromagnetic Fields and patients with ADHD with methylphenidate IR.

During depression treatment, reductions in naming times were recorded weekly. One-way ANOVA indicated statistical between-group differences with effect sizes in the medium range for form and colour-form. In both groups, naming times were longer before than after treatment. For the ADHD group, shift costs exceeded the average-normal range at baseline but were in the average-normal range after stabilization with stimulant medication. For the depression group, shift costs were in the average-normal range at baseline and after treatment. Baseline colour-form naming times predicted reductions in naming times for both groups with the largest effect size and index of forecasting efficiency for the ADHD group.

The cognitive-processing speed (colour-form) and shift-cost measures before treatment proved most sensitive in differentiating patients with depression and ADHD. Reductions in naming times for the depression group were suggested to reflect improved psycho-motor skills rather than improved cognitive control.

The etiology of depression remains poorly understood. Changes in blood lipid levels were reported to be associated with depression and suicide, however study findings were mixed.

We performed a two-sample Mendelian randomisation (MR) analysis to investigate the causal relationship between blood lipids and depression phenotypes, based on large-scale GWAS summary statistics (N = 188 577/480 359 for lipid/depression traits respectively). Five depression-related phenotypes were included, namely major depression (MD; from PGC), depressive symptoms (DS; from SSGAC), longest duration and number of episodes of low mood, and history of deliberate self-harm (DSH)/suicide (from UK Biobank). MR was conducted with inverse-variance weighted (MR-IVW), Egger and Generalised Summary-data-based MR (GSMR) methods.

There was consistent evidence that triglyceride (TG) is causally associated with DS (MR-IVW β for one-s.d. increase in TG = 0.0346, 95% CI 0.0114–0.0578), supported by MR-IVW and GSMR and multiple r2 clumping thresholds. We also observed relatively consistent associations of TG with DSH/suicide (MR-Egger OR = 2.514, CI 1.579–4.003). There was moderate evidence for positive associations of TG with MD and the number of episodes of low mood. For HDL-c, we observed moderate evidence for causal associations with DS and MD. LDL-c and TC did not show robust causal relationships with depression phenotypes, except for weak evidence that LDL-c is inversely related to DSH/suicide. We did not detect significant associations when depression phenotypes were treated as exposures.

This study provides evidence to a causal relationship between TG, and to a lesser extent, altered cholesterol levels with depression phenotypes. Further studies on its mechanistic basis and the effects of lipid-lowering therapies are warranted.

Sleep disturbance has been consistently identified as an independent contributor to suicide risk. Inflammation has emerged as a potential mechanism linked to both sleep disturbance and suicide risk. This study tested associations between sleep duration, insomnia, and inflammation on suicidal ideation (SI) and history of a suicide attempt (SA).

Participants included 2329 adults with current or remitted depression and/or anxiety enrolled in the Netherlands Study of Depression and Anxiety. Sleep duration, insomnia, past week SI, and SA were assessed with self-report measures. Plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α were obtained.

Short sleep duration (⩽6 h) compared to normal sleep duration (7–9 h) was associated with reporting a prior SA, adjusting for covariates [adjusted odds ratio (AOR) 1.68, 95% CI 1.13–2.51]. A higher likelihood of SI during the past week was observed for participants with long sleep duration (⩾10 h) compared to normal sleep duration (AOR 2.22, 95% CI 1.02–4.82), more insomnia symptoms (AOR 1.44, 95% CI 1.14–1.83), and higher IL-6 (AOR 1.31, 95% CI 1.02–1.68). Mediation analyses indicated that the association between long sleep duration and SI was partially explained by IL-6 (AOR 1.02, 95% CI 1.00–1.05).

These findings from a large sample of adults with depression and/or anxiety provide evidence that both short and long sleep duration, insomnia symptoms, and IL-6 are associated with the indicators of suicide risk. Furthermore, the association between long sleep duration and SI may operate through IL-6.

This systematic review examines the effectiveness and cost-effectiveness of behavioural health integration into primary healthcare in the management of depression and unhealthy alcohol use in low- and middle-income countries. Following PRISMA guidelines, this review included research that studied patients aged ≥18 years with unhealthy alcohol use and/or depression of any clinical severity. An exploration of the models of integration was used to characterise a typology of behavioural health integration specific for low- and middle-income countries.

Fifty-eight articles met inclusion criteria. Studies evidenced increased effectiveness of integrated care over treatment as usual for both conditions. The economic evaluations found increased direct health costs but cost-effective estimates. The included studies used six distinct behavioural health integration models.

Behavioural health integration may yield improved health outcomes, although it may require additional resources. The proposed typology can assist decision-makers to advance the implementation of integrated models.

Network analysis (NA) conceptualizes psychiatric disorders as complex dynamic systems of mutually interacting symptoms. Major depressive disorder (MDD) is a heterogeneous clinical condition, and very few studies to date have assessed putative changes in its psychopathological network structure in response to antidepressant (AD) treatment.

In this randomized trial with adult depressed outpatients (n = 151), we estimated Gaussian graphical models among nine core MDD symptom-domains before and after 8 weeks of treatment with either escitalopram or desvenlafaxine. Networks were examined with the measures of cross-sectional and longitudinal structure and connectivity, centrality and predictability as well as stability and accuracy.

At baseline, the most connected MDD symptom-domains were fatigue–cognitive disturbance, whereas at week 8 they were depressed mood–suicidality. Overall, the most central MDD symptom-domains at baseline and week 8 were, respectively, fatigue and depressed mood; in contrast, the most peripheral symptom-domain across both timepoints was appetite/weight disturbance. Furthermore, the psychopathological network at week 8 was significantly more interconnected than at baseline, and they were also structurally dissimilar.

Our findings highlight the utility of focusing on the dynamic interaction between depressive symptoms to better understand how the treatment with ADs unfolds over time. In addition, depressed mood, fatigue, and cognitive/psychomotor disturbance seem to be central MDD symptoms that may be viable targets for novel, focused therapeutic interventions.