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Randomized trials of vitamin D supplementation in the treatment of cardiovascular disease and all-cause mortality usually report no obvious effects
This study aims to observe and determine the dose-response relationship between 25-hydroxyvitamin D (25[OH]D) concentration and the risk of coronary heart disease, stroke, and all-cause mortality in a Mendelian randomized framework
Observe that the correlation has a similar non-linear shape in all results (Figure 1; Appendix p 28): At low concentrations of 25(OH)D, it is negatively correlated with all results, while at higher concentrations of 25(OH)D , Cardiovascular mortality is not related, and other mortality results are weakly positive
In a random analysis of the Mendelian population (ie, the population average estimate over the entire range of the 25[OH]D concentration distribution), genetically predicted 25(OH)D and coronary heart disease (odds ratio [OR] 0.
However, in the Copenhagen study, there is some evidence that there is an overall inverse association with all-cause mortality (OR 0.
In the British Biobank and the Copenhagen study, Mendelian randomization analysis of mortality from specific causes showed that in the absence of stratification, cardiovascular disease mortality can be observed (OR 0.
In a more finely stratified Mendelian randomization analysis of 25(OH)D concentration, the dose-response curve of all-cause mortality has a clear threshold shape, and there is evidence that 25(OH)D concentration is less than 40 nmol /L is inversely correlated, and there is no correlation when it is higher than 40 nmol/L (Figure 4; Appendix 33); the estimated value below 40 nmol/L has a significant trend, at a concentration lower than 25(OH)D A stronger reverse association is observed
In summary, observational analysis shows that under the condition of low vitamin D concentration in the body , after vitamin D supplementation, the vitamin D concentration in the body is negatively correlated with the results of coronary heart disease, stroke and all-cause mortality
Overall, the study found genetic evidence of a causal relationship between mortality 25 (OH) D concentrations with low vitamin D individuals
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This study aims to observe and determine the dose-response relationship between 25-hydroxyvitamin D (25[OH]D) concentration and the risk of coronary heart disease, stroke, and all-cause mortality in a Mendelian randomized framework
This study aims to observe and determine the dose-response relationship between 25-hydroxyvitamin D (25[OH]D) concentration and the risk of coronary heart disease, stroke, and all-cause mortality in a Mendelian randomized framework
Observe that the correlation has a similar non-linear shape in all results (Figure 1; Appendix p 28): At low concentrations of 25(OH)D, it is negatively correlated with all results, while at higher concentrations of 25(OH)D , Cardiovascular mortality is not related, and other mortality results are weakly positive
Observe that the correlation has a similar non-linear shape in all results (Figure 1; Appendix p 28): At low concentrations of 25(OH)D, it is negatively correlated with all results, while at higher concentrations of 25(OH)D , Cardiovascular mortality is not related, and other mortality results are weakly positive
In a random analysis of the Mendelian population (ie, the population average estimate over the entire range of the 25[OH]D concentration distribution), genetically predicted 25(OH)D and coronary heart disease (odds ratio [OR] 0.
In a random analysis of the Mendelian population (ie, the population average estimate over the entire range of the 25[OH]D concentration distribution), genetically predicted 25(OH)D and coronary heart disease (odds ratio [OR] 0.
However, in the Copenhagen study, there is some evidence that there is an overall inverse association with all-cause mortality (OR 0.
In the British Biobank and the Copenhagen study, Mendelian randomization analysis of mortality from specific causes showed that in the absence of stratification, cardiovascular disease mortality can be observed (OR 0.
In the British Biobank and the Copenhagen study, Mendelian randomization analysis of mortality from specific causes showed that in the absence of stratification, cardiovascular disease mortality can be observed (OR 0.
In a more finely stratified Mendelian randomization analysis of 25(OH)D concentration, the dose-response curve of all-cause mortality has a clear threshold shape, and there is evidence that 25(OH)D concentration is less than 40 nmol /L is inversely correlated, and there is no correlation when it is higher than 40 nmol/L (Figure 4; Appendix 33); the estimated value below 40 nmol/L has a significant trend, at a concentration lower than 25(OH)D A stronger reverse association is observed
In a more finely stratified Mendelian randomization analysis of 25(OH)D concentration, the dose-response curve of all-cause mortality has a clear threshold shape, and there is evidence that 25(OH)D concentration is less than 40 nmol /L is inversely correlated, and there is no correlation when it is higher than 40 nmol/L (Figure 4; Appendix 33); the estimated value below 40 nmol/L has a significant trend, at a concentration lower than 25(OH)D A stronger reverse association is observed
In summary, observational analysis shows that under the condition of low vitamin D concentration in the body , after vitamin D supplementation, the vitamin D concentration in the body is negatively correlated with the results of coronary heart disease, stroke and all-cause mortality
In summary, observational analysis shows that under the condition of low vitamin D concentration in the body , after vitamin D supplementation, the vitamin D concentration in the body is negatively correlated with the results of coronary heart disease, stroke and all-cause mortality
Overall, the study found genetic evidence of a causal relationship between mortality 25 (OH) D concentrations with low vitamin D individuals
Original source:
Ben-Shlomo, Y.
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