Background Remission has been identified as a top priority by people with type 2 diabetes. Remission is commonly used as an outcome in research studies; however, a widely accepted definition of remission of type 2 diabetes is lacking. A report on defining remission was published (but not formally endorsed) in Diabetes Care, an American Diabetes Association (ADA) journal. This Diabetes Care report remains widely used. It was the first to suggest 3 components necessary to define the presence of remission: (1) absence of glucose-lowering therapy (GLT); (2) normoglycaemia; and (3) for duration ≥1 year. Our aim is to systematically review how remission of type 2 diabetes has been defined by observational and interventional studies since publication of the 2009 report. Methods and findings Four databases (MEDLINE, EMBASE, Cochrane Library, and CINAHL) were searched for studies published from 1 September 2009 to 18 July 2020 involving at least 100 participants with type 2 diabetes in their remission analysis, which examined an outcome of type 2 diabetes remission in adults ≥18 years and which had been published in English since 2009. Remission definitions were extracted and categorised by glucose-lowering therapy, glycaemic thresholds, and duration. A total of 8,966 titles/abstracts were screened, and 178 studies (165 observational and 13 interventional) from 33 countries were included. These contributed 266 definitions, of which 96 were unique. The 2009 report was referenced in 121 (45%) definitions. In total, 247 (93%) definitions required the absence of GLT, and 232 (87%) definitions specified numeric glycaemic thresholds. The most frequently used threshold was HbA1c<42 mmol/mol (6.0%) in 47 (20%) definitions. Time was frequently omitted. In this study, a total of 104 (39%) definitions defined time as a duration. The main limitations of this systematic review lie in the restriction to published studies written in English with sample sizes of over 100. Grey literature was not included in the search. Conclusions We found that there is substantial heterogeneity in the definition of type 2 diabetes remission in research studies published since 2009, at least partly reflecting ambiguity in the 2009 report. This complicates interpretation of previous research on remission of type 2 diabetes and the implications for people with type 2 diabetes. Any new consensus definition of remission should include unambiguous glycaemic thresholds and emphasise duration. Until an international consensus is reached, studies describing remission should clearly define all 3 components of remission. Systematic review registration PROSPERO CRD42019144619

To update and extend a previous cross-sectional international comparison of glycaemic control in people with type 1 diabetes. Methods: Data were obtained for 520,392 children and adults with type 1 diabetes from 17 population and five clinic-based data sources in countries or regions between 2016 and 2020. Median HbA 1c (IQR) and proportions of individuals with HbA 1c < 58 mmol/mol (<7.5%), 58-74 mmol/mol (7.5-8.9%) and ≥75 mmol/mol (≥9.0%) were compared between populations for individuals aged <15, 15-24 and ≥25 years. Logistic regression was used to estimate the odds ratio (OR) of HbA 1c < 58 mmol/mol (<7.5%) relative to ≥58 mmol/mol (≥7.5%), stratified and adjusted for sex, age and data source. Where possible, changes in the proportion of individuals in each HbA 1c category compared to previous estimates were calculated.Results: Median HbA 1c varied from 55 to 79 mmol/mol (7.2 to 9.4%) across data sources and age groups so a pooled estimate was deemed inappropriate. OR (95% CI) for HbA 1c < 58 mmol/mol (<7.5%) were 0.91 (0.90-0.92) for women 18 Joint municipal authority for North Karelia social and health services (Siunsote),

Aims/hypothesis The aim of this study was to investigate the risks of all-cause and cause-specific mortality among participants with neither, one or both of diabetes and depression in a large prospective cohort study in the UK. Methods Our study population included 499,830 UK Biobank participants without schizophrenia and bipolar disorder at baseline. Type 1 and type 2 diabetes and depression were identified using self-reported diagnoses, prescribed medication and hospital records. Mortality was identified from death records using the primary cause of death to define cause-specific mortality. We performed Cox proportional hazards models to estimate the risk of all-cause mortality and mortality from cancer, circulatory disease and causes of death other than circulatory disease or cancer among participants with either depression (n=41,791) or diabetes (n=22,677) alone and with comorbid diabetes and depression (n=3597) compared with the group with neither condition (n=431,765), adjusting for sociodemographic and lifestyle factors, comorbidities and history of CVD or cancer. We also investigated the interaction between diabetes and depression. Results During a median of 6.8 (IQR 6.1–7.5) years of follow-up, there were 13,724 deaths (cancer, n=7976; circulatory disease, n=2827; other causes, n=2921). Adjusted HRs of all-cause mortality and mortality from cancer, circulatory disease and other causes were highest among people with comorbid depression and diabetes (HRs 2.16 [95% CI 1.94, 2.42]; 1.62 [95% CI 1.35, 1.93]; 2.22 [95% CI 1.80, 2.73]; and 3.60 [95% CI 2.93, 4.42], respectively). The risks of all-cause, cancer and other mortality among those with comorbid depression and diabetes exceeded the sum of the risks due to diabetes and depression alone. Conclusions/interpretation We confirmed that depression and diabetes individually are associated with an increased mortality risk and also identified that comorbid depression and diabetes have synergistic effects on the risk of all-cause mortality that are largely driven by deaths from cancer and causes other than circulatory disease and cancer. Graphical abstract

BackgroundThe possible causal association between depression and cardiovascular disease might be partly explained by an increased risk of hypertension. Several epidemiological studies have investigated the role of depression in the development of hypertension but the evidence is inconclusive. A previous systematic review of these studies has a number of shortcomings, including inappropriate pooling of different effect measures and lack of inclusion of all relevant studies. Additional primary studies have also been published since this earlier review was completed. Our aim was to identify, critically appraise, and synthesise evidence on the association between depression and subsequent hypertension.MethodsWe performed a systematic electronic search in PsycINFO, Medline, and EMBASE to identify cohort or longitudinal studies reporting on the risk of hypertension among participants with versus without depressive symptoms and/or clinical depression. We restricted our search to articles published in English. We extracted information on study characteristics, methodology, and results using customised data extraction forms and assessed study quality using the SIGN checklist for cohort studies. We used Stata 14 to perform random effects meta-analyses, to obtain summary effect estimates for the effect of depression on hypertension, pooling hazard ratios and odds ratios separately. We also separately combined studies which defined depression as a categorical or a continuous variable.ResultsAfter de-duplication, the search identified 7402 studies. Twenty-two studies were eligible for inclusion in the review, 17 of which were included in the meta-analyses. Meta-analyses showed an increased hypertension risk among depressed versus non-depressed participants (pooled OR: 1.31, 95% CI: 1.05–1.64; pooled HR: 1.18, 95% CI: 1.02–1.36). Among studies which assessed depressive symptoms on continuous scales meta-analyses indicated an increased risk with every unit increase on the depressive symptoms scale (pooled OR: 1.06, 95% CI: 0.97–1.16; pooled HR: 1.06, 95% CI: 1.01–1.12).DiscussionOur review findings provide evidence that depression may be associated with an increased risk of hypertension. However, existing studies have important limitations and the substantial heterogeneity between studies included in two of the four meta-analyses remained unexplained after performing subgroup analyses. Before concluding that depression is indeed associated with an increased risk of hypertension, future prospective studies should improve the accuracy of exposure and outcome assessment, aim to take all major confounding and effect modifying factors into account, and present effect estimates for subgroups in order to help facilitate more meaningful meta-analyses of study findings. Further research is also needed to determine whether the observed association between depression and hypertension is causal.

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