Today, Mendelian randomization may have settled some of the thorniest issues of cause and effect facing heart doctors—including not just HDL (not causal) and homocysteine (not causal) but also the LDL particles that carry "bad" cholesterol (causal) and even C reactive protein, a measure of the inflammatory process that got considerable media attention as a potential cause of heart disease and now, also, seems to be no more than an association. Mendelian randomisation is being used by pharmaceutical companies to mimic large-scale drug trials, using the genetic differences between people to discover whether certain traits are causal to disease. For example, a 2012 study into the correlation between HDL and heart disease found people born with genes that raise HDL cholesterol do not have fewer heart attacks that those without the gene, explaining the failure of HDL-raising drugs. George Davey Smith and Shah Ebrahim at the University of Bristol, England are among pioneers of the technique. The researchers analysed data from more than 1 million patients in Britain who had been diagnosed with cardiovascular disease, including about half of all deaths during this period.
Mendelian randomisation is being used by pharmaceutical companies to mimic large-scale drug trials, using the genetic differences between people to discover whether certain traits are causal to disease. For example, a 2012 study into the correlation between HDL and heart disease found people born with genes that raise HDL cholesterol do not have fewer heart attacks that those without the gene, explaining the failure of HDL-raising drugs. George Davey Smith and Shah Ebrahim at the University of Bristol, England are among pioneers of the technique. The researchers analysed data from more than 1 million patients in Britain who had been diagnosed with cardiovascular disease, including about half of all deaths during this period.