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86 [95% confidence interval (CI), 0.76�C0.98; http://www.selleckchem.com/products/liproxstatin-1.html P?=?0.02] for IHD and 0.81 (95% CI, 0.66�C0.99; P?=?0.04) for MI, but with corresponding multifactorially adjusted HRs of 0.93 (95% CI, 0.82�C1.06; P?=?0.29) and 0.90 (95% CI, 0.73�C1.12; P?=?0.35). UGT1A1 rs6742078 TT versus GG genotype was associated with 95% increased bilirubin levels (P? http://www.selleckchem.com/products/midostaurin-pkc412.html 4]. However, whether these associations reflect a true atheroprotective effect of bilirubin rather than confounding or reverse causation remains unknown [5, 6]. Mendelian randomization is an epidemiological approach based on the fact that individuals inherit genetic variants randomly from their parents [7]. Genetic variants with effect on plasma bilirubin are therefore ideal for avoiding confounding and reverse causation, limitations that are inherent to observational https://en.wikipedia.org/wiki/Ketanserin epidemiological studies [7]. Genetic variation in the uridine diphosphate glucuronosyltransferase 1A1 gene (UGT1A1) is a common cause of elevated plasma bilirubin [8] and is therefore useful for testing whether a lifelong elevated bilirubin level is a direct cause of reduced risk of IHD and MI using a Mendelian randomization approach. We tested the hypothesis that elevated plasma bilirubin is causally related to decreased risk of IHD and MI, using a Mendelian randomization approach. Accordingly, we first tested whether elevated baseline plasma bilirubin levels predicted decreased risk of IHD and MI in the Copenhagen General Population Study (CGPS), a study of 46?538 white individuals from the Danish general population followed for up to 7.5?years. Secondly, we investigated whether the genetic variant UGT1A1 rs6742078, previously shown to be in strong linkage disequilibrium with the TA repeat polymorphism underlying Gilbert's syndrome [9], was associated with elevated plasma bilirubin in the CGPS.