BACKGROUND Clinical studies have reported that patients with gastroesophageal reflux disease(GERD)have a higher prevalence of hypertension.AIM To performed a bidirectional Mendelian randomization(MR)analysis to invest...BACKGROUND Clinical studies have reported that patients with gastroesophageal reflux disease(GERD)have a higher prevalence of hypertension.AIM To performed a bidirectional Mendelian randomization(MR)analysis to investi-gate the causal link between GERD and essential hypertension.METHODS Eligible single nucleotide polymorphisms(SNPs)were selected,and weighted median,inverse variance weighted(IVW)as well as MR egger(MR-Egger)re-gression were used to examine the potential causal association between GERD and hypertension.The MR-Pleiotropy RESidual Sum and Outlier analysis was used to detect and attempt to reduce horizontal pleiotropy by removing outliers SNPs.The MR-Egger intercept test,Cochran’s Q test and“leave-one-out”sen-sitivity analysis were performed to evaluate the horizontal pleiotropy,heterogen-eities,and stability of single instrumental variable.RESULTS IVW analysis exhibited an increased risk of hypertension(OR=1.46,95%CI:1.33-1.59,P=2.14E-16)in GERD patients.And the same result was obtained in replication practice(OR=1.002,95%CI:1.0008-1.003,P=0.000498).Meanwhile,the IVW analysis showed an increased risk of systolic blood pressure(β=0.78,95%CI:0.11-1.44,P=0.021)and hypertensive heart disease(OR=1.68,95%CI:1.36-2.08,P=0.0000016)in GERD patients.Moreover,we found an decreased risk of Barrett's esophagus(OR=0.91,95%CI:0.83-0.99,P=0.043)in essential hypertension patients.CONCLUSION We found that GERD would increase the risk of essential hypertension,which provided a novel prevent and therapeutic perspectives of essential hypertension.展开更多
Background:The relationship between tea intake(TI)and sleep disorders(SDs)has been a topic of interest for some time,but there remains a lack of data showing a causal relationship.We aimed to use a two-sample Mendelia...Background:The relationship between tea intake(TI)and sleep disorders(SDs)has been a topic of interest for some time,but there remains a lack of data showing a causal relationship.We aimed to use a two-sample Mendelian randomization study to determine whether there is a causal link between TI and SDs.Methods:We collected data regarding TI,with a focus on green tea intake(GTI),herbal tea intake(HTI),and rooibos tea intake(RTI);and data regarding SDs and insomnia from genome-wide association studies.We analyzed these data using an inverse variance-weighted two-sample Mendelian randomization study,by means of the TwoSampleMR package in R4.2.3 software.Results:We found no genetic causal relationships of TI,GTI,HTI,or RTI with insomnia.The odds ratios(ORs)for these relationships were as follows:TI:OR=0.61,95%confidence interval(CI):0.29–1.28;GTI:OR=1.04,95%CI:0.95–1.14;HTI:OR=0.98,95%CI:0.82–1.17;and RTI:OR=1.04,95%CI:0.99–1.09.In addition,there were no genetic causal relationships of TI,GTI,HTI,or RTI with SDs.The OR values for these relationships were as follows:TI:OR=0.6,95%CI:0.34–1.06;GTI:OR=1,95%CI:0.93–1.07;HTI:OR=0.89,95%CI:0.66–1.2;and RTI:OR=1.02,95%CI:0.98–1.06.Conclusion:We found no causal relationships of TI with SDs or insomnia,irrespective of the type of tea consumed.However,additional Mendelian randomization studies are required to further explore the relationships of the timing and quantity of tea consumption with SDs and insomnia.展开更多
Background:Prior research has established a strong link between cerebral aneurysm(CA)occurrence and inflammation.Tea intake(TI)has been found to have anti-inflammatory properties through multiple mechanisms,potentiall...Background:Prior research has established a strong link between cerebral aneurysm(CA)occurrence and inflammation.Tea intake(TI)has been found to have anti-inflammatory properties through multiple mechanisms,potentially lowering CA incidence.This study aims to employ Mendelian Randomization(MR)methodology to explore the genetic causality between TI and CA.Methods:We collected Genome-wide association study(GWAS)data for CA,TI,Green tea intake(GTI),Herbal tea intake(HTI),and Rooibos tea intake(RTI).The MR analysis employed the TwoSampleMR package and utilized the inverse variance-weighted(IVW)method.Results:The findings suggest no genetic causal relationship between TI and CA(IVW:OR=1.10,95%CI:0.59–2.05,P=0.772).Similarly,there is no genetic causal association between GTI and CA(IVW:OR=1.07,95%CI:0.91–1.26,P=0.388),HTI and CA(IVW:OR=1.00,95%CI:0.89–1.13,P=0.943),or RTI and CA(IVW:OR=1.02,95%CI:0.96–1.09,P=0.472).Conclusion:There is no genetic causal relationship between TI and CA,and the different types of tea do not change this result.Further MR analysis is needed to investigate whether there is a potential genetic causal association between the quantity of TI and CA.展开更多
Background:Previous studies have suggested a potential risk-reducing effect of tea intake(TI)on diabetes.However,the specific impacts of TI on different types of diabetes and its underlying mechanisms remain unclear.T...Background:Previous studies have suggested a potential risk-reducing effect of tea intake(TI)on diabetes.However,the specific impacts of TI on different types of diabetes and its underlying mechanisms remain unclear.To further explore this topic,we conducted a comprehensive investigation to assess the causal relationship between TI and various types of diabetes,as well as its effects on blood glucose(Glu)and glycated hemoglobin(HbA1).Methods:We collected genome-wide association study data for TI,diabetes,type 1 diabetes(T1D),type 2 diabetes(T2D),Glu,HbA1,green tea intake,herbal tea intake,and Rooibos tea intake from the IEU database.Subsequently,we performed two-sample Mendelian randomization analysis using the TwoSampleMR package.Results:Our analysis revealed no evidence of a causal relationship between TI and the incidence of diabetes,T1D,blood Glu,HbA1c,or T2D.Similarly,no genetic causal relationship was found between green tea intake and diabetes,T1D,T2D,Glu,or HbA1c.The same applied to herbal tea intake and Rooibos tea intake,as there was no genetic causal link with diabetes,T1D,T2D,Glu,or HbA1c.Conclusion:Based on our findings,there is no indication of a causal relationship between TI and the incidence of all types of diabetes,regardless of the specific tea type.However,to comprehensively understand the potential effects of TI on diabetes incidence,including the quantity and timing of intake,further evaluation through additional Mendelian randomization studies is warranted.展开更多
Objective: Observational studies have reported malnutrition and vitamin deficiency in patients with schizophrenia (SZ), which can lead to serious metabolic syndromes and decrease anti-psychiatric drug outcomes. Wherea...Objective: Observational studies have reported malnutrition and vitamin deficiency in patients with schizophrenia (SZ), which can lead to serious metabolic syndromes and decrease anti-psychiatric drug outcomes. Whereas, vitamin intake along with psychiatric medication can enhance the medication outcomes. However, it is still unknown if SZ induces vitamin deficiency. Herein, we conduct the Mendelian randomization analysis to explore the causal relationship between schizophrenia and vitamins supplementation.Methods: We retrieved the genome-wide summary statistical data for schizophrenia from recent SZ GWAS data (43,175 cases and 65,166 controls) and vitamins supplementation GWAS data from Neale’s GWAS datasets (more than 337,000 samples from the European population) and performed a two-sample Mendelian randomization analysis to determine the causal association of SZ with vitamin supplementation, in addition, we conduct the sensitivity analysis to obtain reliable results and remove confounding bias.Results: SZ have causal relationships with vitamins A, B, C, D, and E (SZ/vitamin A: β = 0.002, se= 0.001, 95% confidence interval (CI): 0.001 to 0.004,P= 1.41E-05, heterogeneityP= 0.4486;SZ/vitamin B: β= 0.004, se= 0.001, 95% CI: 0.002-0.005,P= 7.0E-05, heterogeneityP= 0.2217;SZ/vitamin C: β= 0.004, se= 0.001, 95% CI: 0.002-0.007,P= 0.001, heterogeneityP= 0.1349;SZ/vitamin D: β= 0.003, se= 0.001, 95% CI: 0.002-0.005,P= 0.001, heterogeneityP= 0.433;SZ/vitamin E: β= 0.003, se= 0.001, 95% CI: 0.002-0.005,P= 5.0E-05, heterogeneityP= 0.1382).Conclusion: Our findings suggest that vitamin levels and supplementation should be carefully controlled in patients with SZ, which in turn may enhance the therapeutic effects of antipsychotic drug treatments.展开更多
Background:Observational studies have shown that inflammatory bowel disease(IBD),such as ulcerative colitis(UC)and Crohn disease(CD),is associated with gingivitis and periodontal disease(GP).This study aims to investi...Background:Observational studies have shown that inflammatory bowel disease(IBD),such as ulcerative colitis(UC)and Crohn disease(CD),is associated with gingivitis and periodontal disease(GP).This study aims to investigate whether there is a causal relationship between IBD and GP.Methods:This study assessed the causal relationship between IBD and GP through a two-sample Mendelian randomization(MR)study.The required data were obtained through the IEU OpenGWAS project.Instrumental variable screening and the MR and sensitivity analyses were performed using the“TwoSampleMR”R package.Results:IBD,UC,and CD may have a causal effect on GP(IBD,inverse variance weighting[IVW]OR=1.05,95%CI=1.00–1.10,P=0.03;UC,IVWOR=1.05,95%CI=1.00–1.11,P=0.03;CD,weighted median OR=1.06,95%CI=1.00–1.13,P=0.04;simple mode OR=1.15,95%CI=1.02–1.31,P=0.03).Scatterplots,forest plots,and funnel plots showed a significant relationship between IBD and GP and confirmed the robustness of the model.In sensitivity testing,no horizontal pleiotropy or heterogeneity was found in this study.Conclusions:This study found a possible causal relationship between IBD(UC and CD)and GP,which deserves to be considered in clinical practice.展开更多
基金Supported by National Natural Science Foundation of China(General Program),No.82070631.
文摘BACKGROUND Clinical studies have reported that patients with gastroesophageal reflux disease(GERD)have a higher prevalence of hypertension.AIM To performed a bidirectional Mendelian randomization(MR)analysis to investi-gate the causal link between GERD and essential hypertension.METHODS Eligible single nucleotide polymorphisms(SNPs)were selected,and weighted median,inverse variance weighted(IVW)as well as MR egger(MR-Egger)re-gression were used to examine the potential causal association between GERD and hypertension.The MR-Pleiotropy RESidual Sum and Outlier analysis was used to detect and attempt to reduce horizontal pleiotropy by removing outliers SNPs.The MR-Egger intercept test,Cochran’s Q test and“leave-one-out”sen-sitivity analysis were performed to evaluate the horizontal pleiotropy,heterogen-eities,and stability of single instrumental variable.RESULTS IVW analysis exhibited an increased risk of hypertension(OR=1.46,95%CI:1.33-1.59,P=2.14E-16)in GERD patients.And the same result was obtained in replication practice(OR=1.002,95%CI:1.0008-1.003,P=0.000498).Meanwhile,the IVW analysis showed an increased risk of systolic blood pressure(β=0.78,95%CI:0.11-1.44,P=0.021)and hypertensive heart disease(OR=1.68,95%CI:1.36-2.08,P=0.0000016)in GERD patients.Moreover,we found an decreased risk of Barrett's esophagus(OR=0.91,95%CI:0.83-0.99,P=0.043)in essential hypertension patients.CONCLUSION We found that GERD would increase the risk of essential hypertension,which provided a novel prevent and therapeutic perspectives of essential hypertension.
基金supported by 2021 Construction project of key disciplines of Traditional Chinese Medicine(clinical)in Guangdong Province([2021]No.129)2020 Foshan City’s‘14th Five-Year’key specialized projects of traditional Chinese medicine(No.15).Foshan self-financing science and technology plan project(2320001009048).
文摘Background:The relationship between tea intake(TI)and sleep disorders(SDs)has been a topic of interest for some time,but there remains a lack of data showing a causal relationship.We aimed to use a two-sample Mendelian randomization study to determine whether there is a causal link between TI and SDs.Methods:We collected data regarding TI,with a focus on green tea intake(GTI),herbal tea intake(HTI),and rooibos tea intake(RTI);and data regarding SDs and insomnia from genome-wide association studies.We analyzed these data using an inverse variance-weighted two-sample Mendelian randomization study,by means of the TwoSampleMR package in R4.2.3 software.Results:We found no genetic causal relationships of TI,GTI,HTI,or RTI with insomnia.The odds ratios(ORs)for these relationships were as follows:TI:OR=0.61,95%confidence interval(CI):0.29–1.28;GTI:OR=1.04,95%CI:0.95–1.14;HTI:OR=0.98,95%CI:0.82–1.17;and RTI:OR=1.04,95%CI:0.99–1.09.In addition,there were no genetic causal relationships of TI,GTI,HTI,or RTI with SDs.The OR values for these relationships were as follows:TI:OR=0.6,95%CI:0.34–1.06;GTI:OR=1,95%CI:0.93–1.07;HTI:OR=0.89,95%CI:0.66–1.2;and RTI:OR=1.02,95%CI:0.98–1.06.Conclusion:We found no causal relationships of TI with SDs or insomnia,irrespective of the type of tea consumed.However,additional Mendelian randomization studies are required to further explore the relationships of the timing and quantity of tea consumption with SDs and insomnia.
文摘Background:Prior research has established a strong link between cerebral aneurysm(CA)occurrence and inflammation.Tea intake(TI)has been found to have anti-inflammatory properties through multiple mechanisms,potentially lowering CA incidence.This study aims to employ Mendelian Randomization(MR)methodology to explore the genetic causality between TI and CA.Methods:We collected Genome-wide association study(GWAS)data for CA,TI,Green tea intake(GTI),Herbal tea intake(HTI),and Rooibos tea intake(RTI).The MR analysis employed the TwoSampleMR package and utilized the inverse variance-weighted(IVW)method.Results:The findings suggest no genetic causal relationship between TI and CA(IVW:OR=1.10,95%CI:0.59–2.05,P=0.772).Similarly,there is no genetic causal association between GTI and CA(IVW:OR=1.07,95%CI:0.91–1.26,P=0.388),HTI and CA(IVW:OR=1.00,95%CI:0.89–1.13,P=0.943),or RTI and CA(IVW:OR=1.02,95%CI:0.96–1.09,P=0.472).Conclusion:There is no genetic causal relationship between TI and CA,and the different types of tea do not change this result.Further MR analysis is needed to investigate whether there is a potential genetic causal association between the quantity of TI and CA.
文摘Background:Previous studies have suggested a potential risk-reducing effect of tea intake(TI)on diabetes.However,the specific impacts of TI on different types of diabetes and its underlying mechanisms remain unclear.To further explore this topic,we conducted a comprehensive investigation to assess the causal relationship between TI and various types of diabetes,as well as its effects on blood glucose(Glu)and glycated hemoglobin(HbA1).Methods:We collected genome-wide association study data for TI,diabetes,type 1 diabetes(T1D),type 2 diabetes(T2D),Glu,HbA1,green tea intake,herbal tea intake,and Rooibos tea intake from the IEU database.Subsequently,we performed two-sample Mendelian randomization analysis using the TwoSampleMR package.Results:Our analysis revealed no evidence of a causal relationship between TI and the incidence of diabetes,T1D,blood Glu,HbA1c,or T2D.Similarly,no genetic causal relationship was found between green tea intake and diabetes,T1D,T2D,Glu,or HbA1c.The same applied to herbal tea intake and Rooibos tea intake,as there was no genetic causal link with diabetes,T1D,T2D,Glu,or HbA1c.Conclusion:Based on our findings,there is no indication of a causal relationship between TI and the incidence of all types of diabetes,regardless of the specific tea type.However,to comprehensively understand the potential effects of TI on diabetes incidence,including the quantity and timing of intake,further evaluation through additional Mendelian randomization studies is warranted.
基金This work was supported by the National Key Research and Development Project of China(No.2016 YFC1306903to YS)+9 种基金National Natural Science Foundation of China(No.81501154to YS)Shanghai Hospital Development Center(No.SHDC12016115to YS)Shanghai Key Laboratory of Psychotic Disorders(No.13dz2260500to YS)Shanghai Mental Health Center(No.2016-fx-02to YS)Shanghai Science and Technology Committee(Nos.17JC1402900,17490712200to YS).
文摘Objective: Observational studies have reported malnutrition and vitamin deficiency in patients with schizophrenia (SZ), which can lead to serious metabolic syndromes and decrease anti-psychiatric drug outcomes. Whereas, vitamin intake along with psychiatric medication can enhance the medication outcomes. However, it is still unknown if SZ induces vitamin deficiency. Herein, we conduct the Mendelian randomization analysis to explore the causal relationship between schizophrenia and vitamins supplementation.Methods: We retrieved the genome-wide summary statistical data for schizophrenia from recent SZ GWAS data (43,175 cases and 65,166 controls) and vitamins supplementation GWAS data from Neale’s GWAS datasets (more than 337,000 samples from the European population) and performed a two-sample Mendelian randomization analysis to determine the causal association of SZ with vitamin supplementation, in addition, we conduct the sensitivity analysis to obtain reliable results and remove confounding bias.Results: SZ have causal relationships with vitamins A, B, C, D, and E (SZ/vitamin A: β = 0.002, se= 0.001, 95% confidence interval (CI): 0.001 to 0.004,P= 1.41E-05, heterogeneityP= 0.4486;SZ/vitamin B: β= 0.004, se= 0.001, 95% CI: 0.002-0.005,P= 7.0E-05, heterogeneityP= 0.2217;SZ/vitamin C: β= 0.004, se= 0.001, 95% CI: 0.002-0.007,P= 0.001, heterogeneityP= 0.1349;SZ/vitamin D: β= 0.003, se= 0.001, 95% CI: 0.002-0.005,P= 0.001, heterogeneityP= 0.433;SZ/vitamin E: β= 0.003, se= 0.001, 95% CI: 0.002-0.005,P= 5.0E-05, heterogeneityP= 0.1382).Conclusion: Our findings suggest that vitamin levels and supplementation should be carefully controlled in patients with SZ, which in turn may enhance the therapeutic effects of antipsychotic drug treatments.
基金the Training Project of Key Talents of Youth Medicine in Jiangsu Province of China(No.QNRC2016330)the Graduate Research-Innovation Project in Jiangsu Province(No.SJCX21_1644)+5 种基金the Academic Science and Technology Innovation Fund for College Students(No.202011117056Y)the Social Development-Health Care Project of Yangzhou,Jiangsu Province(No.YZ2018087)the Social Development-Health Care Project of Yangzhou,Jiangsu Province(No.YZ2021075)the High-Level Talent“Six One Projects”Top Talent Scientific Research Project of Jiangsu Province(No.LGY2019034)the Graduate Research-Innovation Project in Jiangsu Province(No.SJCX22_1816)the Social development project of the key R&D plan of Jiangsu Provincial Department of Science and Technology(No.BE2022773).
文摘Background:Observational studies have shown that inflammatory bowel disease(IBD),such as ulcerative colitis(UC)and Crohn disease(CD),is associated with gingivitis and periodontal disease(GP).This study aims to investigate whether there is a causal relationship between IBD and GP.Methods:This study assessed the causal relationship between IBD and GP through a two-sample Mendelian randomization(MR)study.The required data were obtained through the IEU OpenGWAS project.Instrumental variable screening and the MR and sensitivity analyses were performed using the“TwoSampleMR”R package.Results:IBD,UC,and CD may have a causal effect on GP(IBD,inverse variance weighting[IVW]OR=1.05,95%CI=1.00–1.10,P=0.03;UC,IVWOR=1.05,95%CI=1.00–1.11,P=0.03;CD,weighted median OR=1.06,95%CI=1.00–1.13,P=0.04;simple mode OR=1.15,95%CI=1.02–1.31,P=0.03).Scatterplots,forest plots,and funnel plots showed a significant relationship between IBD and GP and confirmed the robustness of the model.In sensitivity testing,no horizontal pleiotropy or heterogeneity was found in this study.Conclusions:This study found a possible causal relationship between IBD(UC and CD)and GP,which deserves to be considered in clinical practice.
基金supported by grants from the National Natural Science Foundation of China(81872682)the Young Taishan Scholars Program of Shandong Province of China(tsqn20161046)+2 种基金the Academic Promotion Programme of Shandong First Medical University(2019RC010)the Shandong Province Higher Educational Young and Innovation Technology Supporting Program(2019KJL004)the Doctoral Scientific Research Foundation of Shandong First Medical University.