Type 2 diabetes is an established risk factor for dementia. However, the roles of glycemic control and diabetic complications in the development of dementia have been less well substantiated. This large-scale cohort study aims to examine associations of longitudinal HbA 1c levels and diabetic complications with the risk of dementia incidence among patients with type 2 diabetes. RESEARCH DESIGN AND METHODSData of eligible patients with diabetes, aged $50 years in the U.K. Clinical Practice Research Datalink from 1987 to 2018, were analyzed. Time-varying Cox regressions were used to estimate adjusted hazard ratios (HRs) and 95% CIs for dementia risk. RESULTSAmong 457,902 patients with diabetes, 28,627 (6.3%) incident dementia cases were observed during a median of 6 years' follow-up. Patients with recorded hypoglycemic events or microvascular complications were at higher risk of dementia incidence compared with those without such complications (HR 1.30 [95% CI 1.22-1.39] and 1.10 [1.06-1.14], respectively). The HbA 1c level, modeled as a time-varying exposure, was associated with increased dementia risk (HR 1.08 [95% CI 1.07-1.09] per 1% HbA 1c increment) among 372,287 patients with diabetes with postdiagnosis HbA 1c records. Similarly, a higher coefficient of variation of HbA 1c during the initial 3 years of follow-up was associated with higher subsequent dementia risk (HR 1.03 [95% CI 1.01-1.04] per 1-SD increment). CONCLUSIONSHigher or unstable HbA 1c levels and the presence of diabetic complications in patients with type 2 diabetes are associated with increased dementia risk. Effective management of glycemia might have a significant role in maintaining cognitive health among older adults with diabetes.

INTRODUCTION Midwifery care meets the triple aims of health system improvement, i.e. good health outcomes, high client satisfaction, and low per capita costs. Scaling up access to midwifery care is a global priority yet the growth and sustainability of the profession is threatened by high levels of burnout and attrition. This scoping review provides a comprehensive review of the existing literature on burnout in midwifery, with a focus on prevalence, associated factors and potential solutions. METHODS Four electronic databases were searched to locate relevant literature up to July 2019. A total of 1034 articles were identified and reduced to 27 articles that met inclusion criteria. We summarize sample sizes, settings, study designs, burnout measures, prevalence of burnout, associated factors and potential solutions, and recommendations. RESULTS Prevalence of burnout was highest among Australian, Western Canadian and Senegalese midwives and lowest among Dutch and Norwegian midwives. Midwives working in caseload/continuity models reported significantly lower burnout compared to midwives working in other models. We identified 26 organizational and personal factors that were significantly associated with burnout, such as high workload, exposure to traumatic events, and fewer years in practices. Organizational support to improve work-life balance and emotional well-being, as well as more continuing education to raise awareness about burnout and how to cope with it, emerged as common strategies to prevent and address burnout. CONCLUSIONS Burnout is a serious and complex occupational phenomenon. More qualitative research is needed in this area, to better understand the lived experience of burnout. AFFILIATION

BackgroundRehabilitation programmes are used to improve hip fracture outcomes. There is little published trial clinical trial or population-based data on the effects of the type or provider of rehabilitation treatments on hip fracture outcomes. We evaluated the associations of rehabilitation interventions with post-operative hip fracture outcomes.MethodsCross-sectional (2013–2015) analysis of data from the English National Hip Fracture Database (NHFD) from all 191 English hospitals treating hip fractures. Of 62,844 NHFD patients, we included 17,708 patients with rehabilitation treatment and 30-day mobility data, and 34,142 patients with rehabilitation treatment and discharge destination data. The intervention was early mobilisation rehabilitation treatments delivered by a physiotherapist (PT, physical therapist in North America) or other clinical staff as identifiable in NHFD. We used ordinal logistic and propensity scoring regression models to adjust for confounding variables including age, sex, pre-fracture mobility, operative delay, and cognitive function and peri-operative risk scores.ResultsIn both the adjusted multivariate and propensity-weighted analyses, mobilisation on the day or the day following surgery is associated with better mobility function 30 days after discharge. However patients mobilised by a PT did not have better mobility compared to mobilisation by other professionals. Patients who received a PT assessment were not protected from poorer mobility 30 days after discharge, compared with those who did not receive an assessment. The discharge destination outcome is also better in mobilised than unmobilised patients, whether done by a PT or another health professional, and the difference persists, slightly attenuated, after propensity weighting.ConclusionsIn addition to the type of health professional initiating mobilisation, data on rehabilitation treatment activity and post-operative gait speed is needed to determine optimum rehabilitation dosage and functional outcome. After adjustment patients mobilised by non-PTs did as well as patients mobilised by PTs, suggesting that PTs’ current roles in very early rehabilitation should be reconsidered, with a view to redeploying them to more specialised later rehabilitation activity.Electronic supplementary materialThe online version of this article (10.1186/s12891-018-2093-8) contains supplementary material, which is available to authorized users.

Elevated cortisol as a measure of hypothalamic-pituitary-adrenal-axis hyperactivity has emerged as a predictor of clinical progression of Alzheimer's disease (AD), in conjunction with amyloid-␤ (A␤) abnormalities. Yet factors exist which have the propensity to delay AD symptomatic expression in the face of an AD-type biomarker-based pathological profile. This study sought to determine whether abnormal cerebrospinal fluid (CSF) A␤ and elevated cortisol levels are associated with clinical transition to mild cognitive impairment (MCI) and AD in cognitively normal (CN) individuals, and if this association is modified by reserve proxies. Data from 91 CN individuals participating in the Alzheimer's Disease Neuroimaging Initiative (ADNI) with available morning CSF cortisol and A␤ 42 were evaluated. Reserve was modelled as a latent composite score of standardized intracranial volume and lifetime experience proxies. Cox regressions were used to test associations between baseline CSF cortisol/A␤ 42 , reserve score and AD progression, adjusting for age, sex, apolipoprotein E genotype, and depressive symptoms. Individuals with elevated cortisol + abnormal A␤ 42 levels at baseline showed highest risk of clinical progression. After a median of 84 months follow-up, significant cortisol/A␤ reserve interaction for clinical 1 Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report.

Metformin, a diabetes drug with anti-aging cellular responses, has complex actions that may alter dementia onset. Mixed results are emerging from prior observational studies. To address this complexity, we deploy a causal inference approach accounting for the competing risk of death in emulated clinical trials using two distinct electronic health record systems. In intention-to-treat analyses, metformin use associates with lower hazard of all-cause mortality and lower cause-specific hazard of dementia onset, after accounting for prolonged survival, relative to sulfonylureas. In parallel systems pharmacology studies, the expression of two AD-related proteins, APOE and SPP1, was suppressed by pharmacologic concentrations of metformin in differentiated human neural cells, relative to a sulfonylurea. Together, our findings suggest that metformin might reduce the risk of dementia in diabetes patients through mechanisms beyond glycemic control, and that SPP1 is a candidate biomarker for metformin’s action in the brain.