Poor cognitive abilities and low intellectual quotient (IQ) are associated with an increased risk of suicide attempts and suicide mortality. However, knowledge of how this association develops across the life-course is limited. Our study aims to establish whether individuals who died by suicide by mid-adulthood are distinguishable by their child-to-adolescence cognitive trajectories.

Participants were from the 1958 British Birth Cohort and were assessed for academic performance at ages 7, 11, and 16 and intelligence at 11 years. Suicides occurring by September 2012 were identified from linked national death certificates. We compared mean mathematics and reading abilities and rate of change across 7–16 years for individuals who died by suicide v. those still alive, with and without adjustment for potential early-life confounding factors. Analyses were based on 14 505 participants.

Fifty-five participants (48 males) had died by suicide by age 54 years. While males who died by suicide did not differ from participants still alive in reading scores at age 7 [effect size (g) = −0.04, p = 0.759], their reading scores had a less steep improvement up to age 16 compared to other participants. Adjustments for early-life confounding factors explained these differences. A similar pattern was observed for mathematics scores. There was no difference between individuals who died by suicide v. participants still alive on intelligence at 11 years.

While no differences in tests of academic performance and IQ were observed, individuals who died by suicide had a less steep improvement in reading abilities over time compared to same-age peers.

The determinants of quality of life (QoL) in schizophrenia are largely debated, mainly due to methodological discrepancies and divergence about the concepts concerned. As most studies have investigated bi- or tri-variate models, a multivariate model accounting for simultaneous potential mediations is necessary to have a comprehensive view of the determinants of QOL. We sought to estimate the associations between cognitive reserve, cognition, functioning, insight, depression, schizophrenic symptoms, and QoL in schizophrenia and their potential mediation relationships.

We used structural equation modeling with mediation analyses to test a model based on existing literature in a sample of 776 patients with schizophrenia from the FondaMental Foundation FACE-SZ cohort.

Our model showed a good fit to the data. We found better functioning to be positively associated with a better QoL, whereas better cognition, better insight, higher levels of depression, and schizophrenic symptoms were associated with a lower QoL in our sample. Cognitive reserve is not directly linked to QoL, but indirectly in a negative manner via cognition. We confirm the negative relationship between cognition and subjective QoL which was previously evidenced by other studies; moreover, this relationship seems to be robust as it survived in our multivariate model. It was not explained by insight as some suggested, thus the mechanism at stake remains to be explained.

The pathways to subjective QoL in schizophrenia are complex and the determinants largely influence each other. Longitudinal studies are warranted to confirm these cross-sectional findings.

People with bipolar disorder (BPD) are more likely to die prematurely, which is partly attributed to comorbid cardiometabolic traits. Previous studies report cardiometabolic abnormalities in BPD, but their shared aetiology remains poorly understood. This study examined the phenotypic associations and shared genetic aetiology between BPD and various cardiometabolic traits.

In a subset of the UK Biobank sample (N = 61 508) we investigated phenotypic associations between BPD (ncases = 4186) and cardiometabolic traits, represented by biomarkers, anthropometric traits and cardiometabolic diseases. To determine shared genetic aetiology in European ancestry, polygenic risk scores (PRS) and genetic correlations were calculated between BPD and cardiometabolic traits.

Several traits were significantly associated with increased risk for BPD, namely low total cholesterol, low high-density lipoprotein cholesterol, high triglycerides, high glycated haemoglobin, low systolic blood pressure, high body mass index, high waist-to-hip ratio; and stroke, coronary artery disease and type 2 diabetes diagnosis. BPD was associated with higher polygenic risk for triglycerides, waist-to-hip ratio, coronary artery disease and type 2 diabetes. Shared genetic aetiology persisted for coronary artery disease, when correcting PRS associations for cardiometabolic base phenotypes. Associations were not replicated using genetic correlations.

This large study identified increased phenotypic cardiometabolic abnormalities in BPD participants. It is found that the comorbidity of coronary artery disease may be based on shared genetic aetiology. These results motivate hypothesis-driven research to consider individual cardiometabolic traits rather than a composite metabolic syndrome when attempting to disentangle driving mechanisms of cardiometabolic abnormalities in BPD.

It is unclear whether olfactory deficits improve after remission in depressed patients. Therefore, we aimed to assess in drug-free patients the olfactory performance of patients with major depressive episodes (MDE) and its change after antidepressant treatment.

In the DEP-ARREST-CLIN study, 69 drug-free patients with a current MDE in the context of major depressive disorder (MDD) were assessed for their olfactory performances and depression severity, before and after 1 (M1) and 3 (M3) months of venlafaxine antidepressant treatment. They were compared to 32 age- and sex-matched healthy controls (HCs). Olfaction was assessed with a psychophysical test, the Sniffin’ Sticks test (Threshold: T score; Discrimination: D score; Identification: I score; total score: T + D + I = TDI score) and Pleasantness (pleasantness score: p score; neutral score: N score; unpleasantness score: U score).

As compared to HCs, depressed patients had lower TDI olfactory scores [mean (s.d.) 30.0(4.5) v. 33.3(4.2), p < 0.001], T scores [5.6(2.6) v. 7.4(2.6), p < 0.01], p scores [7.5(3.0) v. 9.8(2.8), p < 0.001)] and higher N scores [3.5(2.6) v. 2.1(1.8), p < 0.01]. T, p and N scores at baseline were independent from depression and anhedonia severity. After venlafaxine treatment, significant increases of T scores [M1: 7.0(2.6) and M3: 6.8(3.1), p < 0.01] and p scores [M1: 8.1(3.0) and M3: 8.4(3.3), p < 0.05] were evidenced, in remitters only (T: p < 0.01; P: p < 0.01). Olfaction improvement was mediated by depression improvement.

The olfactory signature of MDE is restored after venlafaxine treatment. This olfaction improvement is mediated by depression improvement.

Since 1999, the rate of fatal prescription opioid overdoses and of suicides has dramatically increased in the USA. These increases, which have occurred among similar demographic groups, have led to the hypothesis that the opioid epidemic contributed to increases in suicidal behavior, though the underlying association remains poorly defined. We examine the association between nonmedical use of prescription opioids/opioid use disorder and suicidal ideation/attempts.

We used longitudinal data from a national representative sample of the US adult population, the National Epidemiologic Survey on Alcohol and Related Conditions. Participants (n = 34 653) were interviewed in 2001–2002 (wave 1) and re-interviewed approximately 3 years later (wave 2). A propensity score analysis estimated the association between exposure to prescription opioids at wave 1 and prevalent/incident suicidal behavior at wave 2.

Heavy/frequent (⩾2–3 times a month) prescription opioid use was associated with prevalent suicide attempts [adjusted risk ratio (ARR) = 2.75, 95% CI 1.35–5.60]. Prescription opioid use disorder was associated with prevalent (ARR = 1.98, 95% CI 1.20–3.28) and incident suicidal ideation (ARR = 2.59, 95% CI 1.25–5.37), and prevalent attempts (ARR = 4.19, 95% CI 1.71–10.27). None of the exposures was associated with incident suicide attempts.

Heavy/frequent opioid use and related disorder were associated with prevalent suicide attempts; opioid use disorder was also associated with the incident and prevalent suicidal ideation. Given population increases in nonmedical use of prescription opioids and disorder, the opioid crisis may have contributed to population increases in suicidal ideation.

Studies have shown that there are overlapping traits and symptoms between autism and psychosis but no study to date has addressed this association from an epidemiological approach in the adult general population. Furthermore, it is not clear whether autistic traits are associated with specific symptoms of psychosis or with psychosis in general. We assess these associations for the first time by using the Adult Psychiatric Morbidity Survey (APMS) 2007 and the APMS 2014, predicting an association between autistic traits and probable psychosis, and specific associations between autistic traits and paranoia and strange experiences.

Participants (N = 7353 in 2007 and 7500 in 2014) completed the Psychosis Screening Questionnaire (PSQ) and a 20-item version of the Autism Quotient (AQ-20). Binomial logistic regressions were performed using AQ-20 as the independent variable and probable psychosis and specific symptoms as dependent variables.

In the APMS 2007 dataset, significant associations were found between autism traits and probable psychosis, paranoia, thought insertion, and strange experiences. These results were replicated in APMS 2014 but with the additional significant association between autistic traits and hallucinations. Participants in the highest quartile of the AQ-20, compared with the lowest quartile, had an increased risk of probable psychosis of odds ratio (OR) = 15.5 [95% confidence interval (CI) 4.57–52.6] in APMS 2007 and OR = 22.5 (95% CI 7.64–66.3) in APMS 2014.

Autistic traits are strongly associated with probable psychosis and psychotic experiences with the exception of mania. Limitations such as the cross-sectional nature of the study are discussed.

It has been suggested that screening interventions may be effective for suicide prevention. Few studies, however, have reported their effects on outcome measures, including death by suicide among middle-aged adults.

We used a quasi-experimental parallel cluster design with matched community-based intervention and control municipalities (total eligible population: 90 000) in Japan. At-risk residents within the intervention area were invited for universal depression screening and subsequent care/support. We compared changes in suicide incidence of adults aged 40–64 years for the 4-year pre- and post-implementation periods in the intervention group with the control group and the whole country. Incidence rate ratios (IRRs) of the outcomes were adjusted for age group, gender and interaction terms, using mixed-effects negative binomial regression models. Suicide rates among intervention and control subgroups were compared.

The screening procedure was offered to 52% of the intervention group, and 61% of those contacted responded over the implementation period. Suicide rates decreased more in the intervention group [IRR 0.57, 95% (CI) 0.41–0.78; F1,36 = 12.52, p = 0.001] than the control group (IRR proportion 1.63, 95% CI 1.06–2.48; F1,82 = 5.20, p = 0.025) or the whole country (IRR proportion 1.64, 95% CI 1.16–2.34; F1,42 = 8.21, p = 0.006). Sensitivity analyses confirmed the results from the primary analysis. There were lower suicide rates among both respondents and non-respondents to the screening than in the control group during the implementation period.

Prevention efforts involved in the depression screening intervention were probably successful in reducing suicide rates.

Prior studies have suggested a relationship between atopy and mental health, although methodological barriers have limited the generalizability of these findings. The objective of this study was to investigate the relationship between early-life atopy and vulnerability to mental health problems among youth in the community.

Data were drawn from the Raine Study (N = 2868), a population-based birth cohort study in Western Australia. Logistic regression and generalized estimating equations were used to examine the relationship between atopy at ages 1–5 years [using parent report and objective biological confirmation (sera IgE)], and the range of internalizing and externalizing mental health problems at ages 5–17 years.

Atopy appears to be associated with increased vulnerability to affective and anxiety problems, compared to youth without atopy. These associations remained significant after adjusting for a range of potential confounders. No relationship was evident between atopy and attention deficit hyperactivity disorder or externalizing problems.

Findings are the first linking atopy (measured by both parent report and objective verification) with increased vulnerability to affective and anxiety problems. Therefore, replication is required. If replicated, future research aimed at understanding the possible biological and/or social and environmental pathways underlying these links is needed. Such information could shed light on shared pathways that could lead to more effective treatments for both atopy and internalizing mental health problems.