Vitamin D and cause-specific vascular disease and mortality: a Mendelian randomisation study involving 99,012 Chinese and 106,911 European adults
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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Vitamin D and cause-specific vascular disease and mortality : a Mendelian randomisation study involving 99,012 Chinese and 106,911 European adults. / Huang, Tao; Afzal, Shoaib; Yu, Canqing; Guo, Yu; Bian, Zheng; Yang, Ling; Millwood, Iona Y.; Walters, Robin G.; Chen, Yiping; Chen, Ningyu; Gao, Ruqin; Chen, Junshi; Clarke, Robert; Chen, Zhengming; Ellervik, Christina; Nordestgaard, Børge G.; Lv, Jun; Li, Liming; Collins, Rory; Peto, Richard; Avery, Daniel; Boxall, Ruth; Bennett, Derrick; Chang, Yumei; Du, Huaidong; Gilbert, Simon; Hacker, Alex; Hill, Mike; Holmes, Michael; Iona, Andri; Kartsonaki, Christiana; Kerosi, Rene; Kong, Ling; Kurmi, Om; Lancaster, Garry; Lewington, Sarah; Lin, Kuang; McDonnell, John; Nie, Qunhua; Radhakrishnan, Jayakrishnan; Ryder, Paul; Sansome, Sam; Schmidt, Dan; Sherliker, Paul; Sohoni, Rajani; Stevens, Becky; Turnbull, Iain; Wang, Jenny; Wang, Lin; Wright, Neil; Yang, Xiaoming; Han, Xiao; Hou, Can; Pei, Pei; Liu, Chao; Tan, Yunlong; Pang, Zengchang; Li, Shanpeng; Wang, Shaojie; Liu, Yongmei; Du, Ranran; Zang, Yajing; Cheng, Liang; Tian, Xiaocao; Zhang, Hua; Zhai, Yaoming; Ning, Feng; Sun, Xiaohui; Li, Feifei; Lv, Silu; Wang, Junzheng; Hou, Wei; Zeng, Mingyuan; Jiang, Ge; Zhou, Xue; Yang, Liqiu; He, Hui; Yu, Bo; Li, Yanjie; Xu, Qinai; Kang, Quan; Guo, Ziyan; Wang, Dan; Hu, Ximin; Chen, Jinyan; Fu, Yan; Fu, Zhenwang; Wang, Xiaohuan; Weng, Min; Guo, Zhendong; Wu, Shukuan; Li, Yilei; Li, Huimei; Fu, Zhifang; Wu, Ming; Zhou, Yonglin; Zhou, Jinyi; Tao, Ran; Yang, Jie; Su, Jian; Liu, Fang; Zhang, Jun; Hu, Yihe; Lu, Yan; Ma, Liangcai; Tang, Aiyu; Zhang, Shuo; Jin, Jianrong; Liu, Jingchao; Tang, Zhenzhu; Chen, Naying; Huang, Ying; Li, Mingqiang; Meng, Jinhuai; Pan, Rong; Jiang, Qilian; Lan, Jian; Liu, Yun; Wei, Liuping; Zhou, Liyuan; Wang, Ping; Meng, Fanwen; Qin, Yulu; Wang, Sisi; Wu, Xianping; Zhang, Ningmei; Zhou, Weiwei; Luo, Guojin; Li, Jianguo; Chen, Xiaofang; Zhong, Xunfu; Liu, Jiaqiu; Sun, Qiang; Ge, Pengfei; Ren, Xiaolan; Dong, Caixia; Zhang, Hui; Mao, Enke; Wang, Xiaoping; Wang, Tao; Zhang, Xi; Zhang, Ding; Zhou, Gang; Feng, Shixian; Chang, Liang; Fan, Lei; Gao, Yulian; He, Tianyou; Sun, Huarong; Hu, Chen; Zhang, Xukui; Wu, Huifang; He, Pan; Yu, Min; Hu, Ruying; Wang, Hao; Qian, Yijian; Wang, Chunmei; Xie, Kaixu; Chen, Lingli; Zhang, Yidan; Pan, Dongxia; Gu, Qijun; Huang, Yuelong; Chen, Biyun; Yin, Li; Liu, Huilin; Fu, Zhongxi; Xu, Qiaohua; Xu, Xin; Zhang, Hao; Long, Huajun; Li, Xianzhi; Zhang, Libo; Qiu, Zhe.
I: BMC Medicine, Bind 17, 160, 08.2019.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Vitamin D and cause-specific vascular disease and mortality
T2 - a Mendelian randomisation study involving 99,012 Chinese and 106,911 European adults
AU - Huang, Tao
AU - Afzal, Shoaib
AU - Yu, Canqing
AU - Guo, Yu
AU - Bian, Zheng
AU - Yang, Ling
AU - Millwood, Iona Y.
AU - Walters, Robin G.
AU - Chen, Yiping
AU - Chen, Ningyu
AU - Gao, Ruqin
AU - Chen, Junshi
AU - Clarke, Robert
AU - Chen, Zhengming
AU - Ellervik, Christina
AU - Nordestgaard, Børge G.
AU - Lv, Jun
AU - Li, Liming
AU - Collins, Rory
AU - Peto, Richard
AU - Avery, Daniel
AU - Boxall, Ruth
AU - Bennett, Derrick
AU - Chang, Yumei
AU - Du, Huaidong
AU - Gilbert, Simon
AU - Hacker, Alex
AU - Hill, Mike
AU - Holmes, Michael
AU - Iona, Andri
AU - Kartsonaki, Christiana
AU - Kerosi, Rene
AU - Kong, Ling
AU - Kurmi, Om
AU - Lancaster, Garry
AU - Lewington, Sarah
AU - Lin, Kuang
AU - McDonnell, John
AU - Nie, Qunhua
AU - Radhakrishnan, Jayakrishnan
AU - Ryder, Paul
AU - Sansome, Sam
AU - Schmidt, Dan
AU - Sherliker, Paul
AU - Sohoni, Rajani
AU - Stevens, Becky
AU - Turnbull, Iain
AU - Wang, Jenny
AU - Wang, Lin
AU - Wright, Neil
AU - Yang, Xiaoming
AU - Han, Xiao
AU - Hou, Can
AU - Pei, Pei
AU - Liu, Chao
AU - Tan, Yunlong
AU - Pang, Zengchang
AU - Li, Shanpeng
AU - Wang, Shaojie
AU - Liu, Yongmei
AU - Du, Ranran
AU - Zang, Yajing
AU - Cheng, Liang
AU - Tian, Xiaocao
AU - Zhang, Hua
AU - Zhai, Yaoming
AU - Ning, Feng
AU - Sun, Xiaohui
AU - Li, Feifei
AU - Lv, Silu
AU - Wang, Junzheng
AU - Hou, Wei
AU - Zeng, Mingyuan
AU - Jiang, Ge
AU - Zhou, Xue
AU - Yang, Liqiu
AU - He, Hui
AU - Yu, Bo
AU - Li, Yanjie
AU - Xu, Qinai
AU - Kang, Quan
AU - Guo, Ziyan
AU - Wang, Dan
AU - Hu, Ximin
AU - Chen, Jinyan
AU - Fu, Yan
AU - Fu, Zhenwang
AU - Wang, Xiaohuan
AU - Weng, Min
AU - Guo, Zhendong
AU - Wu, Shukuan
AU - Li, Yilei
AU - Li, Huimei
AU - Fu, Zhifang
AU - Wu, Ming
AU - Zhou, Yonglin
AU - Zhou, Jinyi
AU - Tao, Ran
AU - Yang, Jie
AU - Su, Jian
AU - Liu, Fang
AU - Zhang, Jun
AU - Hu, Yihe
AU - Lu, Yan
AU - Ma, Liangcai
AU - Tang, Aiyu
AU - Zhang, Shuo
AU - Jin, Jianrong
AU - Liu, Jingchao
AU - Tang, Zhenzhu
AU - Chen, Naying
AU - Huang, Ying
AU - Li, Mingqiang
AU - Meng, Jinhuai
AU - Pan, Rong
AU - Jiang, Qilian
AU - Lan, Jian
AU - Liu, Yun
AU - Wei, Liuping
AU - Zhou, Liyuan
AU - Wang, Ping
AU - Meng, Fanwen
AU - Qin, Yulu
AU - Wang, Sisi
AU - Wu, Xianping
AU - Zhang, Ningmei
AU - Zhou, Weiwei
AU - Luo, Guojin
AU - Li, Jianguo
AU - Chen, Xiaofang
AU - Zhong, Xunfu
AU - Liu, Jiaqiu
AU - Sun, Qiang
AU - Ge, Pengfei
AU - Ren, Xiaolan
AU - Dong, Caixia
AU - Zhang, Hui
AU - Mao, Enke
AU - Wang, Xiaoping
AU - Wang, Tao
AU - Zhang, Xi
AU - Zhang, Ding
AU - Zhou, Gang
AU - Feng, Shixian
AU - Chang, Liang
AU - Fan, Lei
AU - Gao, Yulian
AU - He, Tianyou
AU - Sun, Huarong
AU - Hu, Chen
AU - Zhang, Xukui
AU - Wu, Huifang
AU - He, Pan
AU - Yu, Min
AU - Hu, Ruying
AU - Wang, Hao
AU - Qian, Yijian
AU - Wang, Chunmei
AU - Xie, Kaixu
AU - Chen, Lingli
AU - Zhang, Yidan
AU - Pan, Dongxia
AU - Gu, Qijun
AU - Huang, Yuelong
AU - Chen, Biyun
AU - Yin, Li
AU - Liu, Huilin
AU - Fu, Zhongxi
AU - Xu, Qiaohua
AU - Xu, Xin
AU - Zhang, Hao
AU - Long, Huajun
AU - Li, Xianzhi
AU - Zhang, Libo
AU - Qiu, Zhe
PY - 2019/8
Y1 - 2019/8
N2 - Background: Randomised control trials and genetic analyses have demonstrated that vitamin D or 25-hydroxyvitamin D (25[OH]D) levels may not play a causal role in the development of cardiovascular disease. However, it is unclear if 25(OH)D is causally associated with cause-specific vascular disease and lipids. Therefore, we examined the causal association of 25(OH)D with myocardial infarction, stroke, ischaemic heart disease, ischaemic stroke, subarachnoid haemorrhage, intracerebral haemorrhage, and lipid levels among both Chinese and Europeans. Methods: We used a Mendelian randomisation (MR) design in the China Kadoorie Biobank, the Copenhagen City Heart Study, and the Copenhagen General Population Study. The 25(OH)D-related genetic variants in the CYP2R1 and DCHR7 genes were genotyped in 99,012 Chinese adults and 106,911 Danish adults. Results: In Chinese adults, plasma 25(OH)D levels were not significantly associated with cause-specific vascular disease or mortality, with the exception of intracerebral haemorrhage (HR, 1.09 [95% CI, 1.01,1.18] per 25 nmol/L higher plasma 25(OH)D). In Europeans, plasma 25(OH)D levels were inversely associated with all types of vascular diseases and mortality. However, MR analysis did not demonstrate causal associations of genetically increased 25(OH)D levels with cause-specific vascular diseases, or mortality in both Chinese and European adults. In addition, each 25 nmol/L higher 25(OH)D was observationally associated with lower total cholesterol and low-density lipoprotein cholesterol levels, but higher high-density lipoprotein cholesterol levels. Likewise, MR analysis showed that 25(OH)D levels were not causally associated with lipids in both Chinese and European adults after Bonferroni correction. Conclusions: We found no evidence to support that genetically increased 25(OH)D was associated with a lower risk of ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and lipid levels in both Chinese and European adults. These results suggest that the inverse associations of vitamin D with vascular disease could be the result of confounding.
AB - Background: Randomised control trials and genetic analyses have demonstrated that vitamin D or 25-hydroxyvitamin D (25[OH]D) levels may not play a causal role in the development of cardiovascular disease. However, it is unclear if 25(OH)D is causally associated with cause-specific vascular disease and lipids. Therefore, we examined the causal association of 25(OH)D with myocardial infarction, stroke, ischaemic heart disease, ischaemic stroke, subarachnoid haemorrhage, intracerebral haemorrhage, and lipid levels among both Chinese and Europeans. Methods: We used a Mendelian randomisation (MR) design in the China Kadoorie Biobank, the Copenhagen City Heart Study, and the Copenhagen General Population Study. The 25(OH)D-related genetic variants in the CYP2R1 and DCHR7 genes were genotyped in 99,012 Chinese adults and 106,911 Danish adults. Results: In Chinese adults, plasma 25(OH)D levels were not significantly associated with cause-specific vascular disease or mortality, with the exception of intracerebral haemorrhage (HR, 1.09 [95% CI, 1.01,1.18] per 25 nmol/L higher plasma 25(OH)D). In Europeans, plasma 25(OH)D levels were inversely associated with all types of vascular diseases and mortality. However, MR analysis did not demonstrate causal associations of genetically increased 25(OH)D levels with cause-specific vascular diseases, or mortality in both Chinese and European adults. In addition, each 25 nmol/L higher 25(OH)D was observationally associated with lower total cholesterol and low-density lipoprotein cholesterol levels, but higher high-density lipoprotein cholesterol levels. Likewise, MR analysis showed that 25(OH)D levels were not causally associated with lipids in both Chinese and European adults after Bonferroni correction. Conclusions: We found no evidence to support that genetically increased 25(OH)D was associated with a lower risk of ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and lipid levels in both Chinese and European adults. These results suggest that the inverse associations of vitamin D with vascular disease could be the result of confounding.
KW - Cardiovascular diseases
KW - Causal effect
KW - Lipids
KW - Mendelian randomisation
KW - Vitamin D
U2 - 10.1186/s12916-019-1401-y
DO - 10.1186/s12916-019-1401-y
M3 - Journal article
C2 - 31466528
AN - SCOPUS:85071610534
VL - 17
JO - BMC Medicine
JF - BMC Medicine
SN - 1741-7015
M1 - 160
ER -
ID: 241215020