The extent to which digital media use by adolescents contributes to poor mental health, or vice-versa, remains unclear. The purpose of the present study is to clarify the strength and direction of associations between adolescent internet use and the development of depression symptoms using a longitudinal modeling approach. We also examine whether associations differ for boys and girls.

Data are drawn from (N = 1547) participants followed for the Quebec longitudinal Study of Child Development (QLSCD 1998–2020). Youth self-reported internet use in terms of the average hours of use per week at the ages of 13, 15, and 17. Youth also self-reported depression symptoms at the same ages.

After testing sex-invariance, random intercepts cross-lagged panel models stratified by sex, revealed that internet use by girls was associated with significant within-person (time-varying) change in depression symptoms. Girl's internet use at age 13 was associated with increased depression symptoms at age 15 (ß = 0.12) and internet use at age 15 increased depression at age 17 (ß = 0.10). For boys, internet use was not associated with significant time varying change in depression symptoms.

The present findings support the hypothesis that internet use by adolescents can represent a significant risk factor for the development of depressive symptoms, particularly in girls.

Although most people do not develop mental health disorders after exposure to traumatic events, they may experience subtle changes in cognitive functioning. We previously reported that 2–3 years after the Canterbury earthquake sequence, a group of trauma-exposed people, who identified as resilient, performed less well on tests of spatial memory, had increased accuracy identifying facial emotions and misclassified neutral facial expressions to threat-related emotions, compared with non-exposed controls.

The current study aimed to examine the long-term cognitive effects of exposure to the earthquakes in this resilient group, compared with a matched non-exposed control group.

At 8–9 years after the Canterbury earthquake sequence, 57 earthquake-exposed resilient (69% female, mean age 56.8 years) and 60 non-exposed individuals (63% female, mean age 55.7 years) completed a cognitive testing battery that assessed verbal and visuospatial learning and memory, executive functioning, psychomotor speed, sustained attention and social cognition.

With the exception of a measure of working memory (Digit Span Forward), no significant differences were found in performance between the earthquake-exposed resilient and non-exposed groups on the cognitive tasks. Examination of changes in cognitive functioning over time in a subset (55%) of the original earthquake-exposed resilient group found improvement in visuospatial performance and slowing of reaction times to negative emotions.

These findings offer preliminary evidence to suggest that changes in cognitive functioning and emotion processing in earthquake-exposed resilient people may be state-dependent and related to exposure to continued threat in the environment, which improves when the threat resolves.

The coronavirus disease 2019 (COVID-19) pandemic might affect mental health. Data from population-representative panel surveys with multiple waves including pre-COVID data investigating risk and protective factors are still rare.

In a stratified random sample of the German household population (n = 6684), we conducted survey-weighted multiple linear regressions to determine the association of various psychological risk and protective factors assessed between 2015 and 2020 with changes in psychological distress [(PD; measured via Patient Health Questionnaire for Depression and Anxiety (PHQ-4)] from pre-pandemic (average of 2016 and 2019) to peri-pandemic (both 2020 and 2021) time points. Control analyses on PD change between two pre-pandemic time points (2016 and 2019) were conducted. Regularized regressions were computed to inform on which factors were statistically most influential in the multicollinear setting.

PHQ-4 scores in 2020 (M = 2.45) and 2021 (M = 2.21) were elevated compared to 2019 (M = 1.79). Several risk factors (catastrophizing, neuroticism, and asking for instrumental support) and protective factors (perceived stress recovery, positive reappraisal, and optimism) were identified for the peri-pandemic outcomes. Control analyses revealed that in pre-pandemic times, neuroticism and optimism were predominantly related to PD changes. Regularized regression mostly confirmed the results and highlighted perceived stress recovery as most consistent influential protective factor across peri-pandemic outcomes.

We identified several psychological risk and protective factors related to PD outcomes during the COVID-19 pandemic. A comparison of pre-pandemic data stresses the relevance of longitudinal assessments to potentially reconcile contradictory findings. Implications and suggestions for targeted prevention and intervention programs during highly stressful times such as pandemics are discussed.

Severe mental illness (SMI) is associated with increased stroke risk, but little is known about how SMI relates to stroke prognosis and receipt of acute care.

To determine the association between SMI and stroke outcomes and receipt of process-of-care quality indicators (such as timely admission to stroke unit).

We conducted a cohort study using routinely collected linked data-sets, including adults with a first hospital admission for stroke in Scotland during 1991–2014, with process-of-care quality indicator data available from 2010. We identified pre-existing schizophrenia, bipolar disorder and major depression from hospital records. We used logistic regression to evaluate 30-day, 1-year and 5-year mortality and receipt of process-of-care quality indicators by pre-existing SMI, adjusting for sociodemographic and clinical factors. We used Cox regression to evaluate further stroke and vascular events (stroke and myocardial infarction).

Among 228 699 patients who had had a stroke, 1186 (0.5%), 859 (0.4%), 7308 (3.2%) had schizophrenia, bipolar disorder and major depression, respectively. Overall, median follow-up was 2.6 years. Compared with adults without a record of mental illness, 30-day mortality was higher for schizophrenia (adjusted odds ratio (aOR) = 1.33, 95% CI 1.16–1.52), bipolar disorder (aOR = 1.37, 95% CI 1.18–1.60) and major depression (aOR = 1.11, 95% CI 1.05–1.18). Each disorder was also associated with marked increased risk of 1-year and 5-year mortality and further stroke and vascular events. There were no clear differences in receipt of process-of-care quality indicators.

Pre-existing SMI was associated with higher risks of mortality and further vascular events. Urgent action is needed to better understand and address the reasons for these disparities.

It is not clear to what extent associations between schizophrenia, cannabis use and cigarette use are due to a shared genetic etiology. We, therefore, examined whether schizophrenia genetic risk associates with longitudinal patterns of cigarette and cannabis use in adolescence and mediating pathways for any association to inform potential reduction strategies.

Associations between schizophrenia polygenic scores and longitudinal latent classes of cigarette and cannabis use from ages 14 to 19 years were investigated in up to 3925 individuals in the Avon Longitudinal Study of Parents and Children. Mediation models were estimated to assess the potential mediating effects of a range of cognitive, emotional, and behavioral phenotypes.

The schizophrenia polygenic score, based on single nucleotide polymorphisms meeting a training-set p threshold of 0.05, was associated with late-onset cannabis use (OR = 1.23; 95% CI = 1.08,1.41), but not with cigarette or early-onset cannabis use classes. This association was not mediated through lower IQ, victimization, emotional difficulties, antisocial behavior, impulsivity, or poorer social relationships during childhood. Sensitivity analyses adjusting for genetic liability to cannabis or cigarette use, using polygenic scores excluding the CHRNA5-A3-B4 gene cluster, or basing scores on a 0.5 training-set p threshold, provided results consistent with our main analyses.

Our study provides evidence that genetic risk for schizophrenia is associated with patterns of cannabis use during adolescence. Investigation of pathways other than the cognitive, emotional, and behavioral phenotypes examined here is required to identify modifiable targets to reduce the public health burden of cannabis use in the population.

Psychiatric disorders are associated with increased risk of ischaemic heart disease (IHD) and stroke, but it is not known whether the associations or the role of sociodemographic factors have changed over time.

To investigate the association between psychiatric disorders and IHD and stroke, by time period and sociodemographic factors.

We used Scottish population-based records from 1991 to 2015 to create retrospective cohorts with a hospital record for psychiatric disorders of interest (schizophrenia, bipolar disorder or depression) or no record of hospital admission for mental illness. We estimated incidence and relative risks of IHD and stroke in people with versus without psychiatric disorders by calendar year, age, gender and area-based deprivation level.

In all cohorts, incidence of IHD (645 393 events) and stroke (276 073 events) decreased over time, but relative risks decreased for depression only. In 2015, at the mean age at event onset, relative risks were 2- to 2.5-fold higher in people with versus without a psychiatric disorder. Age at incidence of outcome differed by cohort, gender and socioeconomic status. Relative but not absolute risks were generally higher in women than men. Increasing deprivation conveys a greater absolute risk of IHD for people with bipolar disorder or depression.

Despite declines in absolute rates of IHD and stroke, relative risks remain high in those with versus without psychiatric disorders. Cardiovascular disease monitoring and prevention approaches may need to be tailored by psychiatric disorder and cardiovascular outcome, and be targeted, for example, by age and deprivation level.

BACTOT, Quebec’s healthcare-associated bloodstream infection (HABSI) surveillance program has been operating since 2007. In this study, we evaluated the changes in HABSI rates across 10 years of BACTOT surveillance under a Bayesian framework.

A retrospective, cohort study of eligible hospitals having participated in BACTOT for at least 3 years, regardless of their entry date. Multilevel Poisson regressions were fitted independently for cases of HABSI, catheter-associated bloodstream infections (CA-BSIs), non–catheter-associated primary BSIs (NCA-BSIs), and BSIs secondary to urinary tract infections (BSI-UTIs) as the outcome and log of patient days as the offset. The log of the mean Poisson rate was decomposed as the sum of a surveillance year effect, period effect, and hospital effect. The main estimate of interest was the cohort-level rate in years 2–10 of surveillance relative to year 1.

Overall, 17,479 cases and 33,029,870 patient days were recorded for the cohort of 77 hospitals. The pooled 10-year HABSI rate was 5.20 per 10,000 patient days (95% CI, 5.12–5.28). For HABSI, CA-BSI, and BSI-UTI, there was no difference between the estimated posterior rates of years 2–10 compared to year 1. The posterior means of the NCA-BSI rate ratios increased from the seventh year until the tenth year, when the rate was 29% (95% confidence interval, 1%–89%) higher than the first year rate.

HABSI rates and those of the most frequent subtypes remained stable over the surveillance period. To achieve reductions in incidence, we recommend that more effort be expended in active interventions against HABSI alongside surveillance.

Healthcare-associated bloodstream infections (HABSI) are a significant cause of morbidity and mortality worldwide. In Québec, Canada, HABSI arising from acute-care hospitals have been monitored since April 2007 through the Surveillance des bactériémies nosocomiales panhospitalières (BACTOT) program, but this is the first detailed description of HABSI epidemiology.

This retrospective, descriptive study was conducted using BACTOT surveillance data from hospitals that participated continuously between April 1, 2007, and March 31, 2017. HABSI cases and rates were stratified by hospital type and/or infection source. Temporal trends of rates were analyzed by fitting generalized estimating equation Poisson models, and they were stratified by infection source.

For 40 hospitals, 13,024 HABSI cases and 23,313,959 patient days were recorded, for an overall rate of 5.59 per 10,000 patient days (95% CI, 5.54–5.63). The most common infection sources were catheter-associated BSIs (23.0%), BSIs secondary to a urinary focus (21.5%), and non–catheter-associated primary BSIs (18.1%). Teaching hospitals and nonteaching hospitals with ICUs often had rates higher than nonteaching hospitals without ICUs. Annual HABSI rates did not exhibit statistically significant changes from year to year. Non–catheter-associated primary BSIs were the only HABSI type that exhibited a sustained change across the 10 years, increasing from 0.69 per 10,000 patient days (95% CI, 0.59–0.80) in 2007–2008 to 1.42 per 10,000 patient days (95% CI, 1.27–1.58) in 2016–2017.

Despite ongoing surveillance, overall HABSI rates have not decreased. The effect of BACTOT participation should be more closely investigated, and targeted interventions along alternative surveillance modalities should be considered, prioritizing high-burden and potentially preventable BSI types.