The New Jersey Kids Study (NJKS) is a transdisciplinary statewide initiative to understand influences on child health, development, and disease. We conducted a mixed-methods study of project planning teams to investigate team effectiveness and relationships between team dynamics and quality of deliverables.

Ten theme-based working groups (WGs) (e.g., Neurodevelopment, Nutrition) informed protocol development and submitted final reports. WG members (n = 79, 75%) completed questionnaires including de-identified demographic and professional information and a modified TeamSTEPPS Team Assessment Questionnaire (TAQ). Reviewers independently evaluated final reports using a standardized tool. We analyzed questionnaire results and final report assessments using linear regression and performed constant comparative qualitative analysis to identify central themes.

WG-level factors associated with greater team effectiveness included proportion of full professors (β = 31.24, 95% CI 27.65–34.82), team size (β = 0.81, 95% CI 0.70–0.92), and percent dedicated research effort (β = 0.11, 95% CI 0.09–0.13); age distribution (β = −2.67, 95% CI –3.00 to –2.38) and diversity of school affiliations (β = –33.32, 95% CI –36.84 to –29.80) were inversely associated with team effectiveness. No factors were associated with final report assessments. Perceptions of overall initiative leadership were associated with expressed enthusiasm for future NJKS participation. Qualitative analyses of final reports yielded four themes related to team science practices: organization and process, collaboration, task delegation, and decision-making patterns.

We identified several correlates of team effectiveness in a team science initiative's early planning phase. Extra effort may be needed to bridge differences in team members' backgrounds to enhance the effectiveness of diverse teams. This work also highlights leadership as an important component in future investigator engagement.

People with diabetes are vulnerable to diabetes-related distress and are more likely to experience depressive and anxiety symptoms than the general population. Diabetes distress, depressive, and anxiety symptoms also tend to commonly co-occur.

This study aimed to apply network analysis to explore the associations between diabetes distress, depressive, and anxiety symptoms in a cohort of adults with type 2 diabetes.

Data were from the baseline (2011) assessment of the Evaluation of Diabetes Insulin Treatment (EDIT) study (N = 1,796; 49% female; mean age = 60, SD = 8) from Quebec, Canada. A first network using the 17 items of the diabetes distress scale (DDS-17) was estimated. A second network was estimated using the 17 items of the DDS-17, the 9 depressive items of the PHQ-9, and the 7 anxiety items of the GAD-7. Symptom centrality, network stability, and bridge symptoms were examined.

Regimen-related and physician-related distress symptoms were amongst the most central (highly connected) in the diabetes distress network. Worrying too much (anxiety), Not feeling motivated to keep up diabetes self-management (diabetes distress), and Feeling like a failure (depression) were the most central symptoms in the combined network. Feeling like a failure (depression) was highly connected to diabetes distress symptoms, representing a potential bridge between diabetes distress and depression.

Identifying central and bridge symptoms may provide new insights into diabetes distress, depressive, and anxiety symptom maintenance and comorbidity in people with type 2 diabetes.

No significant relationships.

Adverse childhood experiences (ACEs) have been associated with numerous health consequences in adulthood including cognitive decline. However, the underlying mechanisms implicated remain unclear.

In this study, depressive symptoms and systemic inflammation were investigated as potential independent mediators of the association between ACEs and cognitive decline.

Participants were adults aged 50+ from the English Longitudinal Study of Ageing (N = 3,029; 54.8% female). Measures included self-reported ACEs at wave 3 (2006-2007), C-reactive protein (CRP) and depressive symptoms at wave 4 (2008-2009), and cognitive function at waves 3 and 7 (2014-2015). Mediation analyses examined the direct associations between ACEs and cognitive function at wave 7 and the indirect associations via depressive symptoms and CRP at wave 4 and were conducted using ordinary least squares regression models with the SPSS PROCESS macro. In Step 1, models were adjusted for sociodemographic factors and baseline cognitive function. Models in Step 2 were additionally adjusted for obesity and health behaviours (n = 1,874).

Cumulative ACEs exposure was shown to positively predict later-life depressive symptoms, which in turn predicted cognitive decline. ACEs were also shown to positively predict systemic inflammation as measured by CRP. However, CRP did not mediate the association between ACEs and cognitive decline.

These findings suggest that ACEs are related to cognitive decline partly via depressive symptoms and corroborate prior research linking ACEs with adult systemic inflammation. Efforts towards screening for, preventing, and mitigating the effects of ACEs may therefore represent an important avenue for improving health outcomes in later life.

No significant relationships.

There is a well-established association between anger, hostility, and an increased risk of cardiovascular disease. Emerging evidence also suggests associations between anger/hostility and type 2 diabetes (T2D), though evidence from longitudinal studies has not yet been synthesized.

To systematically review findings from existing prospective cohort studies on trait anger/hostility and the risk of T2D and diabetes-related complications.

Electronic searches of MEDLINE (PubMed), PsychINFO, Web of Science, and CINAHL were performed for articles/abstracts published up to December 15, 2020. Peer-reviewed longitudinal studies conducted with adult samples, with effect estimates reported for trait anger or hostility and incident T2D or diabetes-related complications, were eligible for inclusion. Risk of bias/study quality was assessed. The review protocol was published a priori in PROSPERO (CRD42020216356) and was in keeping with PRISMA guidelines. Screening for eligibility, data extraction, and quality assessment was conducted by two independent reviewers.

Four studies with a total of 155,146 participants met the inclusion criteria. A narrative synthesis of extracted data was conducted according to the Synthesis Without Meta-Analysis guidelines. While results were mixed, our synthesis suggested a positive association between high trait-anger/hostility and increased risk of incident T2D. No longitudinal studies were identified relating to anger/hostility and incident diabetes-related complications. Geographical locations of the study samples were limited to the USA and Japan.

Further research is needed to investigate whether trait-anger/hostility predicts incident type 2 diabetes after adjustments for potential confounding factors. Longitudinal studies are needed to investigate trait-anger/hostility and the risk of diabetes-related vascular complications.

No significant relationships.

Substance use disorders are highly prevalent among people with schizophrenia. Dually diagnosed patients present with unfavorable course and poor long-term outcomes. Integrated, motivation-based treatment for both disorders in the same setting is considered the treatment of choice. However, integrated treatment programs are not readily available and effect sizes of the programs are modest.

To evaluate an integrated psychosocial treatment program for people with schizophrenia and substance use disorders in the setting of a community psychiatric hospital.

100 in-patients with schizophrenia and substance use disorders were randomized to Integrated Treatment (IT) or Treatment as usual (TAU). The IT group was initially treated in a specialized open ward; upon discharge they were offered treatment in a specialized out-patient program of the hospital. The TAU group was initially treated in another non-specialized open ward; upon discharge they were offered treatment in the non-specialized out-patient unit of the hospital. TAU included pharmacotherapy, medical treatment, supportive psychotherapy and further aids by nursing staff and social workers. IT included all elements of TAU plus manualized group therapy with motivational interviewing, psychoeducation and cognitive-behavioral approaches. Assessments were performed at baseline and after 3, 6 and 12 months.

The IT group had slightly less drop-outs in the follow-up period (non-significant). The IT group was more satisfied with treatment and they developed a higher motivation to reduce substance use. Both groups succeeded in reducing substance use during follow-up, whereas the IT group did slightly better (non-significant).

To investigate the relationships between work environmental factors and the risk of major depressive disorder (MDD) over one year and to identify factors associated with the outcomes of individuals with MDD.

We conducted a population-based longitudinal study of employees who were randomly selected in Alberta (n = 4239). MDD was assessed using the World Health Organization's Composite International Diagnostic Interview - Auto 2.1.

The one-year incidence of MDD was 3.6% (95% CI: 2.8%-4.6%) overall. It was 2.9% (95% CI: 1.9% - 4.2%) in men and 4.5% (95% CI: 3.3% - 6.2%) in women. The relationships between work environmental factors and MDD differed by sex. In men, high job strain increased the risk of MDD in those who worked 35-40 hours per week; job insecurity and family-work conflict were predictive of MDD. Women who worked 35-40 hours, who reported job insecurity, high effort-reward imbalance and work-family conflict were at higher risk of MDD. Long working hours, negative thinking and having comorbid social phobia were predictive of MDD. Perceived work-family conflict, severity of major depressive episode and symptom of depressed mood were significantly associated with recurrence of MDD.

Job strain, effort-reward imbalance, job insecurity and work-family conflicts are important risk factors for the onset of MDD, and should be targets of primary prevention. However, these work environmental factors appear to operate differently in men and in women. Clinical and psychosocial factors are important in the prognosis of MDD. The factors associated with persistence and recurrence of MDD may be different.

The goals of the present study were to examine the associations between depressive symptoms, sleep problems and the risk of developing heart disease in a Canadian community sample.

Baseline data were from the CARTaGENE study, a community health survey of adults aged 40–69 years in Quebec, Canada. Incidence of heart disease was examined in N = 33 455 participants by linking survey data with administrative health insurance data. Incident heart disease was identified using the World Health Organization's International Classification of Diseases, 9th or 10th edition (ICD-9 and ICD-10) diagnostic codes for heart disease. Sleep problems were assessed with diagnostic codes for sleep disorders within the 2 years preceding the baseline assessment. Average sleep duration was assessed by self-report. Depressive symptoms were assessed with the nine-item Patient Health Questionnaire.

In total, 2448 (7.3%) participants developed heart disease over an average follow-up period of 4.6 years. Compared to those without depressive symptoms and with no sleep disorders, those with elevated depressive symptoms and a sleep disorder (HR = 2.60, 95% CI 1.83–3.69), those with depressive symptoms alone (HR = 1.40, 95% CI 1.25–1.57) and those with sleep disorders alone (HR = 1.33, 95% CI 1.03–1.73) were more likely to develop heart disease. Test of additive interaction suggested a synergistic interaction between depressive symptoms and sleep disorders (synergy index = 2.17 [95% CI 1.01–4.64]). When sleep duration was considered, those with long sleep duration and elevated depressive symptoms were more likely to develop heart disease than those with long sleep alone (HR = 1.77, 95% CI 1.37–2.28; and HR = 1.16, 95% CI 0.99–1.36, respectively).

Depression and diagnosed sleep disorders or long sleep duration are independent risk factors for heart disease and are associated with a stronger risk of heart disease when occurring together.

Bulimia nervosa (BN), a mental disorder that causes significant impairment, can be treated with psychological, pharmacological, nutrition-based and self-help interventions. We conducted a pre-registered meta-analysis of randomized-controlled trials (RCTs) to assess the efficacy of these interventions in up to 19 different interventions.

Database search terms were combined for BN and RCTs from database inception to March 2017. Abstinence from binge eating episodes, compensatory behaviors, the absence of a BN diagnosis and reduction of symptom severity were considered as primary outcome variables, reduction of self-reported eating pathology and depression served as secondary outcome variables. Retrieved RCTs were meta-analyzed using fixed and random effects models.

RCT (79 trials; 5775 participants) effects post-treatment revealed moderate to large intervention effects for psychotherapy [mostly cognitive-behavioral therapy (CBT)] for primary outcome variables. Slightly reduced effects were obtained for self-help and moderate effects for pharmacotherapy. Similarly, psychotherapy yielded large to very large effects in regard to secondary outcome variables, while moderate to large effects were observed for self-help, Pharmacotherapy and combined therapies. Meta-analyses for the pre to post changes within group confirmed these findings. Additionally, follow-up analyses revealed the sustainability of psychotherapies in terms of large effects in primary outcome criteria, while these effects were moderate for self-help, pharmacotherapy, and combined therapies.

Most psychological and pharmacological interventions revealed to be effective in BN treatment. Taking effect size, sustainability of the intervention, as well as the consistency of findings and available evidence into consideration, CBT can be recommended as the best intervention for the initial treatment of BN.

Previous studies have examined associations of cardiometabolic factors with depression and cognition separately.

To determine if depressive symptoms mediate the association between cardiometabolic factors and cognitive decline in two community studies.

Data for the analyses were drawn from the Rotterdam Study, the Netherlands (n = 2940) and the Whitehall II study, UK (n = 4469).

Mediation analyses suggested a direct association between cardiometabolic factors and cognitive decline and an indirect association through depression: poorer cardiometabolic status at time 1 was associated with a higher level of depressive symptoms at time 2 (standardised regression coefficient 0.07 and 0.06, respectively), which, in turn, was associated with greater cognitive decline between time 2 and time 3 (standardised regression coefficient of −0.15 and −0.41, respectively).

Evidence from two independent cohort studies suggest an association between cardiometabolic dysregulation and cognitive decline and that depressive symptoms tend to precede this decline.

None.

The aim of this study was to evaluate the dynamic association between depressive symptoms and glycated hemoglobin A1c (HbA1c) levels using data from the English Longitudinal Study of Ageing (ELSA).

The sample was comprised of 2886 participants aged ⩾50 years who participated in three clinical assessments over an 8-year period (21% with prediabetes and 7% with diabetes at baseline). Structural equation models were used to address reciprocal associations between depressive symptoms and HbA1c levels and to evaluate the mediating effects of lifestyle-related behaviors and cardiometabolic factors.

We found a reciprocal association between depressive symptoms and HbA1c levels: depressive symptoms at one assessment point predicted HbA1c levels at the next assessment point (standardized β = 0.052) which in turn predicted depressive symptoms at the following assessment point (standardized β = 0.051). Mediation analysis suggested that both lifestyle-related behaviors and cardiometabolic factors might mediate the association between depressive symptoms and HbA1c levels: depressive symptoms at baseline predicted lifestyle-related behaviors and cardiometabolic factors at the next assessment, which in turn predicted HbA1c levels 4 years later. A similar association was observed for the other direction: HbA1c levels at baseline predicted lifestyle-related behaviors and cardiometabolic factors at the next assessment, which in turn predicted depressive symptoms 4 years later.

Our results suggest a dynamic relationship between depressive symptoms and HbA1c which might be mediated by both lifestyle and cardiometabolic factors. This has important implications for investigating the pathways which could link depressive symptoms and increased risk of diabetes.