scholarly journals Sleep Duration and Stroke

Stroke ◽  
2020 ◽  
Vol 51 (11) ◽  
pp. 3279-3285
Author(s):  
Olga E. Titova ◽  
Karl Michaëlsson ◽  
Susanna C. Larsson
Keyword(s):  
Ischemic Stroke ◽  
Intracerebral Hemorrhage ◽  
Prospective Study ◽  
Sleep Duration ◽  
Mendelian Randomization ◽  
Short Sleep ◽  
Mendelian Randomization Analysis ◽  
Increased Risk ◽  
Long Sleep ◽  
Randomization Analysis

Background and Purpose: Studies of sleep duration in relation to specific types of stroke are scarce. Moreover, the results are inconclusive and causality remains unclear. Our objective was to investigate whether sleep duration is associated with risk of stroke and its types using observational and Mendelian randomization designs. Methods: The prospective study included 79 881 women and men (45–79 years of age) who were followed up for incident stroke or death over a mean follow-up of 14.6 years (1 164 646 person-years) through linkage to Swedish Registers. For the Mendelian randomization study, single-nucleotide polymorphisms associated with sleep duration were identified from a genome-wide association study. Summarized data for genetic associations with stroke were obtained from publicly available data of the MEGASTROKE and the International Stroke Genetics Consortia. Results: Compared with normal sleep duration, long sleep (≥9 hours per day) was associated with increased risk of total and ischemic stroke (hazard ratios [95% CI], 1.12 [1.03–1.22] and 1.14 [1.03–1.24], respectively), whereas short sleep (<7 h/d) was linked to higher risk of intracerebral hemorrhage (hazard ratio [95% CI], 1.21 [1.03–1.41]). The 2-sample Mendelian randomization analysis supported no causal association of short or long sleep duration with ischemic stroke as a whole. Conclusions: In a prospective study, long sleep duration was associated with increased risk of total and ischemic stroke, whereas short sleep was linked to increased risk of intracerebral hemorrhage. However, the Mendelian randomization analysis did not show a significant detrimental effect of short or long sleep duration on the risk of total stroke or stroke types.

Causal associations of short and long sleep durations with 12 cardiovascular diseases: linear and nonlinear Mendelian randomization analyses in UK Biobank

2021 ◽  
Author(s):  
Sizhi Ai ◽  
Jihui Zhang ◽  
Guoan Zhao ◽  
Ningjian Wang ◽  
Guohua Li ◽  
...  
Keyword(s):  
Heart Disease ◽  
Arterial Hypertension ◽  
Ischaemic Heart Disease ◽  
Sleep Duration ◽  
Mendelian Randomization ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Causal Risk Factor ◽  
Long Sleep ◽  
Artery Disease

Abstract Aims Observational studies have suggested strong associations between sleep duration and many cardiovascular diseases (CVDs), but causal inferences have not been confirmed. We aimed to determine the causal associations between genetically predicted sleep duration and 12 CVDs using both linear and nonlinear Mendelian randomization (MR) designs. Methods and results Genetic variants associated with continuous, short (≤6 h) and long (≥9 h) sleep durations were used to examine the causal associations with 12 CVDs among 404 044 UK Biobank participants of White British ancestry. Linear MR analyses showed that genetically predicted sleep duration was negatively associated with arterial hypertension, atrial fibrillation, pulmonary embolism, and chronic ischaemic heart disease after correcting for multiple tests (P &lt; 0.001). Nonlinear MR analyses demonstrated nonlinearity (L-shaped associations) between genetically predicted sleep duration and four CVDs, including arterial hypertension, chronic ischaemic heart disease, coronary artery disease, and myocardial infarction. Complementary analyses provided confirmative evidence of the adverse effects of genetically predicted short sleep duration on the risks of 5 out of the 12 CVDs, including arterial hypertension, pulmonary embolism, coronary artery disease, myocardial infarction, and chronic ischaemic heart disease (P &lt; 0.001), and suggestive evidence for atrial fibrillation (P &lt; 0.05). However, genetically predicted long sleep duration was not associated with any CVD. Conclusion This study suggests that genetically predicted short sleep duration is a potential causal risk factor of several CVDs, while genetically predicted long sleep duration is unlikely to be a causal risk factor for most CVDs.

scholarly journals Long Sleep Duration and Risk of Ischemic Stroke and Hemorrhagic Stroke: the Kailuan Prospective Study

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Qiaofeng Song ◽  
Xiaoxue Liu ◽  
Wenhua Zhou ◽  
Ling Wang ◽  
Xiang Zheng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Prospective Study ◽  
Sleep Duration ◽  
Hemorrhagic Stroke ◽  
Long Sleep

scholarly journals Short or Long Sleep Duration and CKD: A Mendelian Randomization Study

2020 ◽  
Vol 31 (12) ◽  
pp. 2937-2947 ◽  
Author(s):  
Sehoon Park ◽  
Soojin Lee ◽  
Yaerim Kim ◽  
Yeonhee Lee ◽  
Min Woo Kang ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Kidney Function ◽  
Sleep Duration ◽  
Genetic Risk ◽  
Mendelian Randomization ◽  
Genetic Risk Score ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Long Duration ◽  
Long Sleep

BackgroundStudies have found sleeping behaviors, such as sleep duration, to be associated with kidney function and cardiovascular disease risk. However, whether short or long sleep duration is a causative factor for kidney function impairment has been rarely studied.MethodsWe studied data from participants aged 40–69 years in the UK Biobank prospective cohort, including 25,605 self-reporting short-duration sleep (<6 hours per 24 hours), 404,550 reporting intermediate-duration sleep (6–8 hours), and 35,659 reporting long-duration sleep (≥9 hours) in the clinical analysis. Using logistic regression analysis, we investigated the observational association between the sleep duration group and prevalent CKD stages 3–5, analyzed by logistic regression analysis. We performed Mendelian randomization (MR) analysis involving 321,260 White British individuals using genetic instruments (genetic variants linked with short- or long-duration sleep behavior as instrumental variables). We performed genetic risk score analysis as a one-sample MR and extended the finding with a two-sample MR analysis with CKD outcome information from the independent CKDGen Consortium genome-wide association study meta-analysis.ResultsShort or long sleep duration clinically associated with higher prevalence of CKD compared with intermediate duration. The genetic risk score for short (but not long) sleep was significantly related to CKD (per unit reflecting a two-fold increase in the odds of the phenotype; adjusted odds ratio, 1.80; 95% confidence interval, 1.25 to 2.60). Two-sample MR analysis demonstrated causal effects of short sleep duration on CKD by the inverse variance weighted method, supported by causal estimates from MR-Egger regression.ConclusionsThese findings support an adverse effect of a short sleep duration on kidney function. Clinicians may encourage patients to avoid short-duration sleeping behavior to reduce CKD risk.

scholarly journals Causal Association of Trauma With Subsequent Psychiatric Disorder: A Mendelian Randomization Study

2021 ◽  
Author(s):  
Dongqing Gu ◽  
Shan Ou ◽  
Guodong Liu
Keyword(s):  
Psychiatric Disorder ◽  
Mood Disorder ◽  
Mendelian Randomization ◽  
Association Studies ◽  
Genome Wide Association Studies ◽  
Causal Association ◽  
Post Traumatic Stress ◽  
Mendelian Randomization Analysis ◽  
Increased Risk ◽  
Randomization Analysis

Abstract Objective Trauma has been proposed as a risk factor for the development of psychiatric disorder. This study aimed to determine the causal association between them. Methods Two-sample Mendelian randomization analyses were performed to estimate the causal association between trauma and psychiatric disorder. We obtained summary-level data for genetic variants associated with trauma and the corresponding association with psychiatric disorder from previous genome-wide association studies, and inverse variance weighted was used as the main method in our Mendelian randomization analysis. Results Genetically predisposed trauma was associated with an increased risk of psychiatric disorder (odds ratio [OR] = 1.02, 95% confidence interval [CI], 1.01–1.02,), mood disorder (OR = 1.01, 95% CI, 1.00-1.01) and depression (OR = 1.02, 95% CI, 1.01–1.02) in UK Biobank, as well as increased risk of mood disorder (OR = 1.23, 95% CI, 1.03–1.48), depression (OR = 1.10, 95% CI, 1.04–1.17), bipolar disorder (OR = 1.24, 95% CI, 1.04–1.49) and schizophrenia (OR = 1.47, 95% CI, 1.21–1.78) in data source from MR Base. However, Mendelian randomization evidence did not support an association between trauma and risk of post-traumatic stress disorder, anxiety disorder, sleep disorder, and eating disorder. Conclusions Findings from our Mendelian randomization analysis suggested that trauma might be causally associated with an increased risk of some common psychiatric disorder such as depression.

scholarly journals Genetically Predicted Cardiac Troponin I Concentrations and Risk of Stroke and Atrial Fibrillation

2021 ◽  
Author(s):  
Dandan Liu ◽  
Yue Deng ◽  
Jiao Wang ◽  
Yanan Chen ◽  
Jian Yu ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Ischemic Stroke ◽  
Intracerebral Hemorrhage ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Mendelian Randomization ◽  
Cardiac Troponin I ◽  
Cardioembolic Stroke ◽  
Large Artery ◽  
Increased Risk

Abstract Background: Observational studies have shown that elevated circulating cardiac troponin I (cTnI) concentrations were associated with higher risk of stroke and atrial fibrillation, but the causality remains unclear. Therefore, we conducted a two-sample mendelian randomization study to evaluate the causal effects of cTnI concentrations on the risk of stroke subtypes and atrial fibrillation.Methods: The instrumental variables for circulating cTnI concentrations were selected from a genome-wide association study meta-analysis of 48,115 European individuals. Applying a 2-sample mendelian randomization approach, we examined the associations of circulating cTnI concentrations with stroke (40,585 cases and 406,111 controls), ischemic stroke (34,217 cases and 406,111 controls), ischemic stroke subtypes (cardioembolic, large artery, small vessel stroke), intracerebral hemorrhage (1,545 cases and 1,481 controls) and atrial fibrillation (60,620 cases and 970,216 controls). Results: Genetically predicted elevated circulating cTnI concentrations were associated with increased risk of cardioembolic stroke (odds ratio [OR], 1.80; 95% confidence interval [CI], 1.20-2.68; P = 0.004). However, no significant association was observed for cTnI concentrations with large artery stroke, small vessel stroke, total stroke, ischemic stroke and intracerebral hemorrhage. Additionally, we also found that elevated cTnI concentrations were associated with higher risk of atrial fibrillation (OR, 1.30; 95% CI, 1.10-1.53; P = 0.003).Conclusions: This study provides evidence that genetically predicted circulating cTnI concentrations are causally associated with increased risk of cardioembolic stroke and atrial fibrillation.

scholarly journals The relationship between sleep duration and all-cause mortality in the older people: an updated and dose-response meta-analysis

2020 ◽  
Author(s):  
Mengyang He ◽  
Xiangling Deng ◽  
Yuqing Zhu ◽  
Luyao Huan ◽  
Wenquan Niu
Keyword(s):  
Older People ◽  
Sleep Duration ◽  
Dose Response ◽  
Data Extraction ◽  
Meta Analysis ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Increased Risk ◽  
Long Sleep ◽  
All Cause Mortality

Abstract Background: Short or long sleep duration is proposed as a potential risk factor for all-cause mortality in the older people, yet the results of published studies are not often reproducible. Objectives: We aimed to investigate whether short or long sleep duration was associated with an increased risk of all-cause mortality in the older people via a comprehensive meta-analysis. Methods: Literature retrieval, study selection and data extraction were completed independently and in duplicate. Effect-size estimates are expressed as relative risk (RR) and its 95% confidence interval (CI). Results: Summary data from 35 articles, involving a total of 106990 older people, were meta-analyzed. Overall analyses revealed a significant association between long sleep duration and all-cause mortality (RR=1.27, 95% CI: 1.19-1.35, P <.001), whereas marginal significance was observed for short sleep duration (RR=1.05; 95% CI: 1.00-1.09; P =.045). There was a low probability of publication bias as indicated by Egger’s test for the association between sleep duration and all-cause mortality. In subgroup analyses, the association between long sleep duration and all-cause mortality was relatively strong in women (RR=1.48, 95% CI: 1.18-1.85, P =.002) relative to men (RR=1.30, 95% CI: 1.10-1.50, P =.001) (Two-sample Z test P = .219). Further dose-response regression analyses showed that trend estimation was not obvious for short sleep duration ( P = .016) compared with long sleep duration ( P < .001), indicating a J-shaped relationship between sleep duration and all-cause mortality. Conclusions: Our findings indicate a J-shaped relationship between sleep duration and all-cause mortality in the older people, with long sleep duration significantly associating with all-cause mortality, especially in women.

scholarly journals Association between systemic lupus erythematosus and cancer: findings from cohort studies and Mendelian randomization analysis

2021 ◽  
Author(s):  
Dongqing Gu ◽  
Mingshuang Tang ◽  
Huijie Cui ◽  
Min Zhang ◽  
Yutong Wang ◽  
...  
Keyword(s):  
Cohort Studies ◽  
Lupus Erythematosus ◽  
Odds Ratio ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Meta Analysis ◽  
European Ancestry ◽  
Mendelian Randomization Analysis ◽  
Increased Risk ◽  
Randomization Analysis

Abstract Background Observational studies suggested that systemic lupus erythematosus (SLE) was associated with an increased risk of cancer, however, the causal effect remains unclear. We aim to determine the causality between SLE and cancer using a meta-analysis and Mendelian randomization (MR) approach. Methods A systematic search was conducted using PubMed to identify cohort studies published before January 21, 2021. Meta-analysis was performed to calculate relative risk (RR) and corresponding 95% confidence intervals (CI), and the potentially causal relationships identified by observational studies were further validated using two-sample Mendelian randomization. Results Through meta-analysis of 43 cohort studies involving 231,499 patients, we observed an increased overall cancer risk among SLE patients (RR = 1.62, 95% CI, 1.47–1.79). Site-specific analysis suggested that SLE patients were associated with an increased risk of 17 cancers. Mendelian randomization analysis indicated that genetically predisposed SLE was causally associated with an increased risk of lymphoma (odds ratio = 1.0004, 95% CI, 1.0001–1.0007, P = 0.0035), whereas a decreased risk of bladder cancer (odds ratio = 0.9996, 95% CI, 0.9994–0.9998, P = 0.00004) in European ancestry. However, no relationship was observed between genetically predisposed SLE and risk of colon, pancreatic, lung, cervical and Non-melanoma skin cancer in European ancestry, liver cancer and lung cancer in Asian ancestry. Conclusions Findings from meta-analysis and Mendelian randomization analysis suggested that SLE might be causally associated with an increased risk of lymphoma. However, inconsistent results were observed between SLE and risk of bladder cancer.

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