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.

The consumption of alcohol within the Australian community continues to rise, impacting care delivery in already over-burdened emergency departments (EDs).

This study aimed to examine the impact of alcohol-related presentations (ARPs) to EDs on days with a public holiday or sporting event.

A retrospective cohort study was undertaken using routinely collected health data pertaining to patient presentations diagnosed with an alcohol-related disorder (ICD-10-AM code F10) to two EDs in Queensland, Australia from January 1, 2016 – December 31, 2020. Descriptive and inferential statistics were used to describe and compare ARPs on event days versus non-event days and uncomplicated versus other ARPs on event days only.

Of all 5,792 ARPs, nine percent (n = 529) occurred on public holidays or sporting event days. When compared by day type, type of presentation, mode of arrival, and day of week differed between event and non-event days. On event days, uncomplicated ARPs differed to other ARPs, with uncomplicated ARPs being younger, having shorter median length-of-stay (LOS), and less likely to be admitted to hospital.

In this multi-site study, public holidays and sporting events had a noteworthy impact on ARPs to EDs. Focused refinement on the clinical management of uncomplicated ARPs is warranted to inform future resource allocation, including on event days.

A significant rise in mental health disorders was expected during the COVID-19 pandemic. However, referrals to mental health services dropped for several months before rising to pre-pandemic levels.

To identify trajectories of incidence and risk factors for common mental disorders among the general population during 14 months of the COVID-19 pandemic, to inform potential mental health service needs.

A cohort of 33 703 adults in England in the University College London COVID-19 Social Study provided data from March 2020 to May 2021. Growth mixture modelling was used to identify trajectories based on the probability of participants reporting symptoms of depression (Patient Health Questionnaire-9) or anxiety (Generalised Anxiety Disorder-7) in the clinical range, for each month. Sociodemographic and personality-related characteristics associated with each trajectory class were explored.

Five trajectory classes were identified for depression and anxiety. Participants in the largest class (62%) were very unlikely to report clinically significant symptom levels. Other trajectories represented participants with a high likelihood of clinically significant symptoms throughout, early clinically significant symptoms that reduced over time, clinically significant symptoms that emerged as the pandemic unfolded and a moderate likelihood of clinically significant symptoms throughout. Females, younger adults, carers, those with existing mental health diagnoses, those that socialised frequently pre-pandemic and those with higher neuroticism scores were more likely to experience depression or anxiety.

Nearly 40% of participants followed trajectories indicating risk of clinically significant symptoms of depression or anxiety. The identified risk factors could inform public health interventions to target individuals at risk in future health emergencies.

Childhood maltreatment is associated with internet addiction, but most evidence is from retrospective studies.

We aimed to investigate the relationship between childhood maltreatment and internet addiction through a prospective cohort design.

In a prospective cohort study, self-reported data on childhood maltreatment (Childhood Trauma Questionnaire – Short Form) at baseline, and internet addiction (Revised Chinese Internet Addiction Scale) at baseline and 6-month follow-up, were collected online from 756 Chinese junior middle school students aged 11–15 years and residing in Changsha, Hunan Province. Demographic data and covariates such as depression, anxiety, stress (Depression, Anxiety, and Stress Scale 21) and insomnia (Athens Insomnia Scale) were also surveyed at baseline. Logistic regression analysis measured the association between childhood maltreatment and internet addiction, and gender-related differences.

Childhood maltreatment was prevalent in Chinese junior middle school students (37.83%), and the incidence rate of internet addiction was 9.26% at the 6-month follow-up. Emotional abuse was a significant risk factor for internet addiction (adjusted odds ratio 2.618, 95% CI 1.194–5.738; P = 0.016) in both males and females.

This study suggests a high prevalence of childhood maltreatment in Chinese junior middle school students, and that emotional abuse plays a significant role in internet addiction. More attention should be paid to parenting style and adolescents’ mental health.

COVID-19 lockdowns increased the risk of mental health problems, especially for children with autism spectrum disorder (ASD). However, despite its importance, little is known about the protective factors for ASD children during the lockdowns.

Based on the Shanghai Autism Early Developmental Cohort, 188 ASD children with two visits before and after the strict Omicron lockdown were included; 85 children were lockdown-free, while 52 and 51 children were under the longer and the shorter durations of strict lockdown, respectively. We tested the association of the lockdown group with the clinical improvement and also the modulation effects of parent/family-related factors on this association by linear regression/mixed-effect models. Within the social brain structures, we examined the voxel-wise interaction between the grey matter volume and the identified modulation effects.

Compared with the lockdown-free group, the ASD children experienced the longer duration of strict lockdown had less clinical improvement (β = 0.49, 95% confidence interval (CI) [0.19–0.79], p = 0.001) and this difference was greatest for social cognition (2.62 [0.94–4.30], p = 0.002). We found that this association was modulated by parental agreeableness in a protective way (−0.11 [−0.17 to −0.05], p = 0.002). This protective effect was enhanced in the ASD children with larger grey matter volumes in the brain's mentalizing network, including the temporal pole, the medial superior frontal gyrus, and the superior temporal gyrus.

This longitudinal neuroimaging cohort study identified that the parental agreeableness interacting with the ASD children's social brain development reduced the negative impact on clinical symptoms during the strict lockdown.

To identify the optimal weight gain at the end of the second trimester.

This was a population-based cohort study from the antenatal care system in Tianjin, China. We calculated gestational weight gain (GWG) based on the weight measured in the first trimester and the end of the second trimester. Restricted cubic spline analysis was performed to model the possible non-linear relationships between GWG and adverse outcomes. The optimal GWG was defined as the value of the lowest risk. Non-inferiority margins and the shape of the spline curves identified the recommended ranges in Chinese-specific BMI categories.

Tianjin Maternal and Child Health Cohort.

Singleton pregnant women aged 18–45 years.

In total, 69 859 pregnant women were included. Adverse outcome (including stillbirth, preterm birth, hypertensive disorders of pregnancy, gestational diabetes mellitus, small and large for gestational age) was significantly associated with GWG at the end of the second trimester. The risk score was non-linearly correlated with GWG in the underweight, normal weight and overweight groups. GWG at the end of the second trimester should not be < 7 kg in underweight group. For most normal-weight women, a GWG of about 8 kg is optimal. Pregnant women who are overweight should not have a GWG of more than 9 kg. We advised women with overweight and obesity to keep positive growth of GWG (> 0 kg) in the first and second trimesters.

According to the comprehensive adverse maternal and infant outcomes, we recommend the optimal GWG at the end of the second trimester. This study may provide a considerable reference for weight management.

Previous evidence on antidepressant medication and cardiovascular disease (CVD) among patients with posttraumatic stress disorder (PTSD) has been inconclusive. We estimated the association between antidepressant medication and CVD by applying a marginal structural model.

We analyzed medical utilization records of 27 170 people with PTSD without prior major cardiovascular events in the Korean National Health Insurance Database (NHID). PTSD and CVD were defined in accordance with the recorded ICD-10 diagnostic codes. We acquired information on antidepressant use from the NHID and categorized them by medication type. A composite major adverse cardiovascular events (MACE) outcome was defined as coronary artery disease with revascularization, ischaemic stroke, and/or haemorrhagic stroke. We used inverse probability of treatment weighting to estimate the parameters of a marginal structural discrete-time survival analysis regression model, comparing the resulting estimates to those derived from traditional time-fixed and time-varying Cox proportional hazards regression. We calculated cumulative daily defined doses to test for a dose–response relationship.

People exposed to antidepressants showed a higher hazard of MACE [hazard ratio (HR) 1.34, 95% confidence interval (CI) 1.18–1.53]. The estimated effects were strongest for selective serotonin reuptake inhibitors (HR 1.24, 95% CI 1.08–1.44) and TCAs (HR 1.33, 95% CI 1.13–1.56). Exposure to serotonin-norepinephrine reuptake inhibitors did not appear to increase the risk of MACE. People exposed to higher doses of antidepressants showed higher risk of MACE.

In a national cohort of people with PTSD, exposure to antidepressant medications increased the risk of MACE in a dose–response fashion.

It is well-known that childhood attention-deficit hyperactivity disorder (ADHD) is associated with later adverse mental health and social outcomes. Patient-based studies suggest that ADHD may be associated with later cardiovascular disease (CVD) but the focus of preventive interventions is unclear. It is unknown whether ADHD leads to established cardiovascular risk factors because so few cohort studies measure ADHD and also follow up to an age where CVD risk is evident.

To examine associations between childhood ADHD problems and directly measured CVD risk factors at ages 44/45 years in a UK population-based cohort study (National Child Development Study) of individuals born in 1958.

Childhood ADHD problems were defined by elevated ratings on both the parent Rutter A scale and a teacher-rated questionnaire at age 7 years. Outcomes were known cardiovascular risk factors (blood pressure, lipid measurements, body mass index and smoking) at the age 44/45 biomedical assessment.

Of the 8016 individuals assessed both during childhood and at the biomedical assessment 3.0% were categorised as having childhood ADHD problems. ADHD problems were associated with higher body mass index (B = 0.92 kg/m2, s.d. = 0.27–1.56), systolic (3.5 mmHg, s.d. = 1.4–5.6) and diastolic (2.2 mmHg, s.d. = 0.8–3.6) blood pressure, triglyceride levels (0.24 mol/l, s.d. = 0.02–0.46) and being a current smoker (odds ratio OR = 1.6, s.d. = 1.2–2.1) but not with LDL cholesterol.

Childhood ADHD problems predicted multiple cardiovascular risk factors by mid-life. These findings, when taken together with previously observed associations with cardiovascular disease in registries, suggest that individuals with ADHD could benefit from cardiovascular risk monitoring, given these risk factors are modifiable with timely intervention.

To quantify the dose–response relation between yogurt consumption and risk of mortality from all causes, CVD and cancer.

Systematic review and meta-analysis.

We conducted a comprehensive search of PubMed/Medline, ISI Web of Science and Scopus databases through August 2022 for cohort studies reporting the association of yogurt consumption with mortality from all causes, CVD and cancer. Summary relative risks (RR) and 95 % CI were calculated with a random-effects model.

Seventeen cohort studies (eighteen publications) of 896 871 participants with 75 791 deaths (14 623 from CVD and 20 554 from cancer).

High intake of yogurt compared with low intake was significantly associated with a lower risk of deaths from all causes (pooled RR 0·93; 95 % CI: 0·89, 0·98, I2 = 47·3 %, n 12 studies) and CVD (0·89; 95 % CI: 0·81, 0·98, I2 = 33·2 %, n 11), but not with cancer (0·96; 95 % CI: 0·89, 1·03, I2 = 26·5 %, n 12). Each additional serving of yogurt consumption per d was significantly associated with a reduced risk of all-cause (0·93; 95 % CI: 0·86, 0·99, I2 = 63·3 %, n 11) and CVD mortality (0·86; 95 % CI: 0·77, 0·99, I2 = 36·6 %, n 10). There was evidence of non-linearity between yogurt consumption and risk of all-cause and CVD mortality, and there was no further reduction in risk above 0·5 serving/d.

Summarising earlier cohort studies, we found an inverse association between yogurt consumption and risk of all-cause and CVD mortality; however, there was no significant association between yogurt consumption and risk of cancer mortality.

Suicidal behavior and substance use disorders (SUDs) are important public health concerns. Prior suicide attempts and SUDs are two of the most consistent predictors of suicide death, and clarifying the role of SUDs in the transition from suicide attempt to suicide death could inform prevention efforts.

We used national Swedish registry data to identify individuals born 1960–1985, with an index suicide attempt in 1997–2017 (N = 74 873; 46.7% female). We assessed risk of suicide death as a function of registration for a range of individual SUDs. We further examined whether the impact of SUDs varied as a function of (i) aggregate genetic liability to suicidal behavior, or (ii) age at index suicide attempt.

In univariate models, risk of suicide death was higher among individuals with any SUD registration [hazard ratios (HRs) = 2.68–3.86]. In multivariate models, effects of specific SUDs were attenuated, but remained elevated for AUD (HR = 1.86 95% confidence intervals 1.68–2.05), opiates [HR = 1.58 (1.37–1.82)], sedatives [HR = 1.93 (1.70–2.18)], and multiple substances [HR = 2.09 (1.86–2.35)]. In secondary analyses, the effects of most, but not all, SUD were exacerbated by higher levels of genetic liability to suicide death, and among individuals who were younger at their index suicide attempt.

In the presence of a strong predictor of suicide death – a prior attempt – substantial predictive power is still attributable to SUDs. Individuals with SUDs may warrant additional suicide screening and prevention efforts, particularly in the context of a family history of suicidal behavior or early onset of suicide attempt.