Mortality from stroke has declined in many countries. This decline may result from a fall in incidence of stroke or a decrease in case fatality from stroke. The present study was conducted to investigate the temporal trends of incidence rate, mortality rate, and case fatality of stroke in an urban and rural Chinese population. A community-based registry study was established in 1983 in defined rural and urban areas of Shanghai with a population aged 35 to 74 years of approximately 86,000 subjects, adhering to the methods and definitions of the World Health Organization MONICA protocol. All stroke events occurring in the population aged 35 to 74 years in these areas were registered by a special three-level case-registration system. From 1984 through 1991, 1391 stroke cases were identified. No significant change in the incidence rate of stroke was observed from 1984 through 1991 in men and women living in rural and urban areas. Age-standardized mortality rates (per 100,000 person years) of stroke declined significantly during this period, except for rural women. The annual changes and 95% confidence intervals of age-standardized mortality rates were: for rural men -4.6% (-5.4, -3.9), for rural women -0.6% (-1.6, 0.5), for urban men -2.5% (-3.5, -1.6), and for urban women -4.7% (-5.2, -4.2). A significant decrease in case fatality from stroke from 1984 through 1991 was found among men living in rural areas (from 62.4% to 46.0%) and among women living in urban areas (from 48.4% to 33.3%). Overall case fatality, however, showed a nonsignificant decline over time. We observed a decline in stroke mortality rate in a rural and urban Chinese population. No significant changes in stroke incidence were found in this study, whereas case fatality appeared to have decreased, in particular among men living in rural areas and women living in urban areas.
INTRODUCTION: The disease burden of nonalcoholic fatty liver disease (NAFLD) increases rapidly, in line with the obesity pandemic. Physical activity has been linked to a lower risk of NAFLD. However, the impact of different intensities of activity and sedentary behavior and whether their effects on NAFLD are explained by metabolic health remain unclear. METHODS: We performed cross-sectional analyses within the population-based Rotterdam Study cohort. Abdominal ultrasound and accelerometry data were collected between 2009 and 2014. NAFLD was defined as hepatic steatosis diagnosed by ultrasound, in the absence of secondary causes for steatosis: viral hepatitis, steatogenic drugs, and excessive alcohol. We categorized accelerometry data into sedentary time and light, moderate, and vigorous physical activities. RESULTS: We included 667 participants (aged 63.3 ± 6.3 years, 53% female individuals), and 34.3% had NAFLD. Total physical activity was associated with lower NAFLD prevalence adjusted for demographic, lifestyle, and socioeconomic factors (odds ratio: 0.958 per 10 min/d, 95% confidence interval [CI]: 0.929–0.986). More intensive physical activity was more strongly associated with lower NAFLD prevalence: odds ratios for light, moderate, and vigorous physical activities were 0.931 (95% CI: 0.882–0.982), 0.891 (95% CI: 0.820–0.967), and 0.740 (95% CI: 0.600–0.906) per 10 min/d, respectively. These associations were explained by metabolic health, particularly homeostatic model assessment of insulin resistance (proportion mediated: 0.59, P < 0.001) and waist circumference (proportion mediated: 1.08, P < 0.001). Beyond this indirect effect, no direct effect could be demonstrated ( P = 0.282–0.827). DISCUSSION: Physical activity at each intensity is inversely associated with NAFLD prevalence, with larger effects for higher intensities of physical activity. This association is mediated by better metabolic health, mainly lower insulin resistance and waist circumference. Physical activity should therefore be incorporated into NAFLD disease management and prevention programs.
Background Sleep traits are associated with cardiometabolic disease risk, with evidence from Mendelian randomization (MR) suggesting that insomnia symptoms and shorter sleep duration increase coronary artery disease risk. We combined adjusted multivariable regression (AMV) and MR analyses of phenotypes of unfavourable sleep on 113 metabolomic traits to investigate possible biochemical mechanisms linking sleep to cardiovascular disease. Methods We used AMV (N = 17,368) combined with two-sample MR (N = 38,618) to examine effects of self-reported insomnia symptoms, total habitual sleep duration, and chronotype on 113 metabolomic traits. The AMV analyses were conducted on data from 10 cohorts of mostly Europeans, adjusted for age, sex, and body mass index. For the MR analyses, we used summary results from published European-ancestry genome-wide association studies of self-reported sleep traits and of nuclear magnetic resonance (NMR) serum metabolites. We used the inverse-variance weighted (IVW) method and complemented this with sensitivity analyses to assess MR assumptions. Results We found consistent evidence from AMV and MR analyses for associations of usual vs. sometimes/rare/never insomnia symptoms with lower citrate (− 0.08 standard deviation (SD)[95% confidence interval (CI) − 0.12, − 0.03] in AMV and − 0.03SD [− 0.07, − 0.003] in MR), higher glycoprotein acetyls (0.08SD [95% CI 0.03, 0.12] in AMV and 0.06SD [0.03, 0.10) in MR]), lower total very large HDL particles (− 0.04SD [− 0.08, 0.00] in AMV and − 0.05SD [− 0.09, − 0.02] in MR), and lower phospholipids in very large HDL particles (− 0.04SD [− 0.08, 0.002] in AMV and − 0.05SD [− 0.08, − 0.02] in MR). Longer total sleep duration associated with higher creatinine concentrations using both methods (0.02SD per 1 h [0.01, 0.03] in AMV and 0.15SD [0.02, 0.29] in MR) and with isoleucine in MR analyses (0.22SD [0.08, 0.35]). No consistent evidence was observed for effects of chronotype on metabolomic measures. Conclusions Whilst our results suggested that unfavourable sleep traits may not cause widespread metabolic disruption, some notable effects were observed. The evidence for possible effects of insomnia symptoms on glycoprotein acetyls and citrate and longer total sleep duration on creatinine and isoleucine might explain some of the effects, found in MR analyses of these sleep traits on coronary heart disease, which warrant further investigation.
IntroductionPersistent psychiatric symptomatology during childhood and adolescence predicts vulnerability to experience mental illness in adulthood. Physical activity is well-known to provide mental health benefits across the lifespan. However, the underlying mechanisms linking physical activity and psychiatric symptoms remain underexplored. In this context, we aim to systematically synthesise evidence focused on the mechanisms through which physical activity might reduce psychiatric symptoms across all ages.Methods and analysisWith the aid of a biomedical information specialist, we will develop a systematic search strategy based on the predetermined research question in the following electronic databases: MEDLINE, Embase, Web of Science, Cochrane and PsycINFO. Two independent reviewers will screen and select studies, extract data and assess the risk of bias. In case of inability to reach a consensus, a third person will be consulted. We will not apply any language restriction, and we will perform a qualitative synthesis of our findings as we anticipate that studies are scarce and heterogeneous.Ethics and disseminationOnly data that have already been published will be included. Then, ethical approval is not required. Findings will be published in a peer-reviewed journal and presented at conferences. Additionally, we will communicate our findings to healthcare providers and other sections of society (eg, through regular channels, including social media).PROSPERO registration numberCRD42021239440.
BackgroundChronic cough is a debilitating medical condition that is often complicated by psychomorbidities such as depressive symptoms. Nevertheless, little is known about the impact of chronic cough on the risk of developing depression. Therefore, we investigated the association between chronic cough and prevalent, incident, as well as recurrent depression in a population-based sample of middle-aged and older persons.MethodsWithin the Rotterdam Study, a population-based cohort, we defined chronic cough as reporting daily coughing for at least 3 months. Depression was assessed using the Center for Epidemiologic Studies–Depression scale, clinical interviews, and medical records. Associations between chronic cough and depression were determined with linear, logistic and Cox regression analyses.ResultsThe study included 5877 participants (mean age±standard deviation: 72±8 years, 59% female) who contributed 37 287 person-years of follow-up. At baseline, participants with chronic cough reported more depressive symptoms (adjusted standardised mean difference 0.15, 95% CI 0.07–0.22) compared to those without chronic cough. Over time, chronic cough was associated with an increased risk of depression in participants with a history of depression (HR 1.45, 95% CI 1.13–1.84) but not in those without a history of depression (HR 0.91, 95% CI 0.68–1.22).ConclusionsAdults with chronic cough have a disproportionate burden of depressive symptoms and an increased risk of recurrent depression. This highlights the importance of screening for depression in patients with chronic cough.
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