To examine the risk of perinatal mental illness, including new diagnoses and recurrent use of mental healthcare, comparing women with and without traumatic brain injury (TBI), and to identify injury-related factors associated with these outcomes among women with TBI.

We conducted a population-based cohort study in Ontario, Canada, of all obstetrical deliveries to women in 2012–2021, excluding those with mental healthcare use in the year before conception. The cohort was stratified into women with no remote mental illness history (to identify new mental illness diagnoses between conception and 365 days postpartum) and those with a remote mental illness history (to identify recurrent illnesses). Modified Poisson regression generated adjusted relative risks (aRRs) (1) comparing women with and without TBI and (2) according to injury-related variables (i.e., number, severity, timing, mechanism and intent) among women with TBI.

There were n = 12,724 women with a history of TBI (mean age: 27.6 years [SD, 5.5]) and n = 786,317 without a history of TBI (mean age: 30.6 years [SD, 5.0]). Women with TBI were at elevated risk of a new mental illness diagnosis in the perinatal period compared to women without TBI (18.5% vs. 12.7%; aRR: 1.31, 95% confidence interval [CI]: 1.24–1.39), including mood and anxiety disorders. Women with a TBI were also at elevated risk for recurrent use of mental healthcare perinatally (35.5% vs. 27.8%; aRR: 1.18, 95% CI: 1.14–1.22), including mood and anxiety, psychotic, substance use and other mental health disorders. Among women with a history of TBI, the number of TBI-related healthcare encounters was positively associated with an elevated risk of new-onset mental illness.

These findings demonstrate the need for providers to be attentive to the risk for perinatal mental illness in women with a TBI. This population may benefit from screening and tailored mental health supports and treatment options.

Secondary stroke prevention can reduce subsequent vascular events, mortality and accumulation of disability. Current rates of adherence to secondary stroke prevention indicators are unknown. Our aim was to evaluate secondary stroke prevention care in Ontario, Canada.

A retrospective cohort study using health administrative databases included all adults discharged alive following an ischemic stroke from April 2010 to March 2019. Indicators of secondary stroke prevention, including laboratory testing, physician visits and receipt of routine influenza vaccinations, were evaluated among survivors in the one year following a stroke event. The use of medication was also assessed among individuals over the age of 65 years and within subgroups of stroke survivors with diabetes and atrial fibrillation.

After exclusions, 54,712 individuals (mean age 68.4 years, 45.7% female) survived at least one year following their stroke event. In the 90 days following discharge from the hospital, most individuals (92.8%) were seen by a general practitioner, while 26.2% visited an emergency department. Within the year following discharge, 66.2% and 61.4% were tested for low-density lipoprotein and glycated hemoglobin, respectively, and 39.6% received an influenza vaccine. Among those over the age of 65 years, 85.5% were prescribed a lipid-lowering agent, and 88.7% were prescribed at least one antihypertensive medication. In those with diabetes, 70.3% were prescribed an antihyperglycemic medication, while 84.9% with atrial fibrillation were prescribed an anticoagulant.

Secondary stroke prevention, especially for important laboratory values, remains suboptimal, despite thorough best practice guidelines. Future studies should explore barriers to better secondary stroke care.

Coercive measures to manage disruptive or violent behaviour are accepted as standard practice in mental healthcare, but systematic knowledge of potentially harmful outcomes is insufficient.

To examine the association of mechanical restraint with several predefined somatic harmful outcomes.

We conducted a population-based, observational cohort study linking data from the Danish national registers from 2007 to 2019. The primary analyses investigated the association of mechanical restraint with somatic adverse events, using panel regression analyses (within-individual analysis) to account for repeated exposures and outcomes. Secondary between-group analyses were performed with a control group exposed to types of coercion other than mechanical restraint.

The study population comprised 13 022 individuals. We report a statistically significant association of mechanical restraint with thromboembolic events (relative risk 4.377, number needed to harm (NNH) 8231), pneumonia (relative risk 5.470, NNH 3945), injuries (relative risk 2.286, NNH 3240) and all-cause death (relative risk 5.540, NNH 4043) within 30 days after mechanical restraint. Estimates from the between-group analyses (comparing the exposed group with a control group of 22 643 individuals) were non-significant or indicated increased baseline risk in the control group. A positive dose–response analysis for cardiac arrest, injury and death supported a causative role of mechanical restraint in the reported associations.

Although the observed absolute risk increases were small, the derived relative risks were non-negligible considering that less restrictive interventions are available. Clinicians and decision makers should be aware of the excess risk in future decisions on the use of mechanical restraint versus alternative interventions.

The association between negative wealth shocks and depression among middle-aged and older individuals remains unclear. Our study aimed to assess the association between negative wealth shocks and depression and its trajectories, and to explore cross-national differences in these associations

Our sample included 21 999 participants, of which 9519 were from the Health and Retirement Study (2012–2020), 4936 from the English Longitudinal Study of Ageing (2012–2020), 2520 from the China Health and Retirement Longitudinal Study (2011–2020), and 5024 from the Mexican Health and Aging Study (2012–2021). We used latent class trajectory models to identify depressive trajectories, alongside mixed-model logistic regression and multinomial logistic regression to evaluate associations.

In the USA (OR 1.73, 95% CI 1.40–2.16), England (OR 1.71, 95% CI 1.09–2.70), and China (OR 1.38, 95% CI 1.09–1.75), negative wealth shocks were associated with subsequent depressive symptoms, but not in Mexico (OR 1.06, 95% CI 0.86–1.29). Additionally, negative wealth shocks were associated with several depressive trajectories in the USA and China. This association occurred only in increasing–decreasing trajectory in England, while no significant association was found across any trajectory in Mexico.

Negative wealth shocks were associated with subsequent depressive symptoms, with significant associations observed in some specific depressive trajectories. These associations exhibited cross-national differences, underscoring the importance of considering country-specific contexts when addressing the mental health impacts of wealth shocks.

It remains uncertain whether long-term use of benzodiazepines is associated with age-related cognitive decline, and if cognitive ability in early life is the driver of any association. This study examines the association of cognitive ability in young adulthood with later use of benzodiazepines and explores whether the use of benzodiazepines during adult life is associated with cognitive decline in late midlife.

The study samples include cognitive tests on the Børge Priens Prøve (BPP) from the conscription board examination (age 19 years) from 335 513 men born 1949–1961 and data from re-examinations of 5183 men 44 years later. Cognitive decline was defined as the difference between scores at the conscription board and the re-examination. Information on purchases of benzodiazepines was obtained from the Danish National Prescription Registry, 1995–2022. Associations were analysed using Cox proportional hazards and linear regression.

In total, 120 911 (36%) men purchased benzodiazepines during a follow-up of 20 years. Lower cognitive scores in young adulthood were associated with a higher risk of initiating benzodiazepines (hazard ratio [95% CI] = 0.71[0.68–0.75]). Men with the highest cumulative use of benzodiazepines had larger cognitive decline (β-coefficient [95% CI] = −1.66 [−2.09 to −1.23] BPP scores) compared with never users. Current benzodiazepine users showed a larger cognitive decline than never users (β-coefficient [95% CI] = −2.42[−3.18 to −1.66] BPP scores) and this partially explained the above association. These estimates for cognitive decline were relatively small and may lack clinical relevance.

Low cognitive ability increases the risk of benzodiazepine use in adulthood and cognitive decline is more pronounced in those with the highest benzodiazepine use compared with never-use, but the difference lacks clinical significance.

The prospective association between sleep duration and the development of late-life depressive symptomology is unclear.

To investigate sleep duration from midlife to late life in relation to risk of depressive symptoms in late life.

A total of 14 361 participants from the Singapore Chinese Health Study were included in the present study. Daily sleep duration was self-reported at baseline (mean age of 52.4 years; 1993–98), follow-up 2 (mean age of 65.2 years; 2006–10) and follow-up 3 (mean age of 72.5 years; 2014–16) interviews. Depressive symptoms were evaluated using the Geriatric Depression Scale at follow-up 3 interviews. Modified Poisson regression models were performed to estimate relative risks and 95% confidence intervals of late-life depressive symptoms in relation to sleep duration at baseline and the two follow-up interviews.

Compared with sleeping 7 h per day, a short sleep duration of ≤5 h per day at baseline (i.e. midlife) was related to a higher risk of depressive symptoms (relative risk 1.10, 95% CI 1.06–1.15), and this risk was not affected by subsequent prolongation of sleep. Conversely, a long sleep duration of ≥9 h per day at baseline was not related to risk of depressive symptoms. At follow-up 3 (i.e. late life), both short sleep (relative risk 1.20, 95% CI 1.16–1.25) and long sleep (relative risk 1.12, 95% CI 1.07–1.18) duration were cross-sectionally associated with depressive symptoms.

Short sleep duration in midlife, regardless of subsequent prolongation, is associated with an increased risk of depression in late life. Contrariwise, both short and long sleep duration in late life co-occur with depressive symptoms.

Systemic changes in multiple diseases may influence the onset of dementia. However, the specific temporality between exposure diseases and dementia remains uncertain.

By characterising the full spectrum of temporal disease trajectories before dementia, this study aims to yield a global picture of precursor diseases to dementia and to provide detailed instructions for risk management and primary prevention of dementia.

Using the multicentre, community-based prospective UK Biobank, we constructed disease trajectories before dementia utilising the phenome-wide association analysis, paired directional test and association quantification. Stratified disease trajectories were constructed by dementia subtypes, gender, age of diagnosis and Apolipoprotein E (ApoE) status, respectively.

Our study population comprised 434 266 participants without baseline dementia and 4638 individuals with all-cause dementia. In total, 1253 diseases were extracted as potential components of the disease trajectory before dementia. We identified three clusters of disease trajectories preceding all-cause dementia, initiated by circulatory, metabolic and respiratory diseases occurring approximately 5–15 years before dementia. Cerebral infarction or chronic renal failure following chronic ischaemic heart disease was the specific trajectory before vascular dementia. Apolipoprotein E (ApoE) ε4 non-carriers exhibited more complex trajectories compared with carriers. Lipid metabolism disorders remained in the trajectories regardless of dementia subtypes, gender, age of diagnosis and ApoE status.

This study provides a comprehensive view of the longitudinal disease trajectories before dementia and highlights the potential targets of midlife cardiometabolic dysfunction for dementia screening and prevention.

Different aspects of social relationships (e.g., social network size or loneliness) have been associated with dementia risk, while their overlap and potentially underlying pathways remain largely unexplored. This study therefore aimed to (1) discriminate between different facets of social relationships by means of factor analysis, (2) examine their associations with dementia risk, and (3) assess mediation by depressive symptoms.

Thirty-six items from questionnaires on social relationships administered in Wave 2 (2004/2005) of the English Longitudinal Study of Ageing (n = 7536) were used for exploratory and confirmatory factor analysis. Factors were then used as predictors in Cox proportional hazard models with dementia until Wave 9 as outcome, adjusted for demographics and cardiovascular risk factors. Structural equation modeling tested mediation by depressive symptoms through effect decomposition.

Factor analyses identified six social factors. Across a median follow-up time of 11.8 years (IQR = 5.9–13.9 years), 501 people developed dementia. Higher factor scores for frequency and quality of contact with children (HR = 0.88; p = 0.021) and more frequent social activity engagement (HR = 0.84; p < 0.001) were associated with lower dementia risk. Likewise, higher factor scores for loneliness (HR = 1.13; p = 0.011) and negative experiences of social support (HR = 1.10; p = 0.047) were associated with higher dementia risk. Mediation analyses showed a significant partial effect mediation by depressive symptoms for all four factors. Additional analyses provided little evidence for reverse causation.

Frequency and quality of social contacts, social activity engagement, and feelings of loneliness are associated with dementia risk and might be suitable targets for dementia prevention programs, partly by lowering depressive symptoms.

Evidence linking air pollutants and the risk of schizophrenia remains limited and inconsistent, and no studies have investigated the joint effect of air pollutant exposure and genetic factors on schizophrenia risk.

To investigate how exposure to air pollution affects schizophrenia risk and the potential effect modification of genetic susceptibility.

Our study was conducted using data on 485 288 participants from the UK Biobank. Cox proportional hazards models were used to estimate the schizophrenia risk as a function of long-term air pollution exposure presented as a time-varying variable. We also derived the schizophrenia polygenic risk score (PRS) utilising data provided by the UK Biobank, and investigated the modification effect of genetic susceptibility.

During a median follow-up period of 11.9 years, 417 individuals developed schizophrenia (mean age 55.57 years, s.d. = 8.68; 45.6% female). Significant correlations were observed between long-term exposure to four air pollutants (PM2.5; PM10; nitrogen oxides, NOx; nitrogen dioxide, NO2) and the schizophrenia risk in each genetic risk group. Interactions between genetic factors and the pollutants NO2 and NOx had an effect on schizophrenia events. Compared with those with low PRS and low air pollution, participants with high PRS and high air pollution had the highest risk of incident schizophrenia (PM2.5: hazard ratio = 6.25 (95% CI 5.03–7.76); PM10: hazard ratio = 7.38 (95% CI 5.86–9.29); NO2: hazard ratio = 6.31 (95% CI 5.02–7.93); NOx: hazard ratio = 6.62 (95% CI 5.24–8.37)).

Long-term exposure to air pollutants was positively related to the schizophrenia risk. Furthermore, high genetic susceptibility could increase the effect of NO2 and NOx on schizophrenia risk.

This study aimed to estimate networks of depressive symptoms among Irish adults with and without diabetes at two time points and compare between the two groups at each time point using data from the Irish Longitudinal Study on Ageing (TILDA).

Participants were from Wave 1 (2009–2011) and Wave 4 (2016) of TILDA, with n = 639 participants with diabetes and n = 7,837 without diabetes at Wave 1, and n = 1,151 with diabetes and n = 4,531 without diabetes at Wave 4. Depressive symptoms were measured using the 8 items of the Center for Epidemiologic Studies Depression Scale. Network psychometric analysis was used to examine symptom centrality, symptom-level associations, and network comparisons at each time point.

Stable, strongly connected networks emerged for people with and without diabetes at both time points. The symptoms of feeling depressed, feeling like everything’s an effort, not enjoying life, feeling sad, and couldn’t get going were the most central nodes in all networks, which did not differ between people with and without diabetes. However, for people with diabetes, the network was more densely connected at Wave 4, when the sample was predominately people with newly diagnosed diabetes. Furthermore, the relationship between ‘felt lonely’ and ‘couldn’t get going’ and between ‘not enjoying life’ and ’sad’ was significantly stronger for people with diabetes than for those without.

This study provides a more detailed understanding of the structure of depressive symptoms at two time points in older Irish adults with and without type 1 or type 2 diabetes.