Genes and cardiovascular risk

This editorial refers to ‘Influence of common genetic variation on blood lipid levels, cardiovascular risk, and coronary events in two British prospective cohort studies’[†][1], by S. Shah et al. , 972 and ‘Impact of common genetic variation on response to simvastatin therapy among 18 705 participants in the Heart Protection Study’[‡][2], by J.C. Hopewell et al. , on page 982 If DNA really is the ‘blueprint’ for life, how can genetic analysis fail to tell us what life has in store for us? One of two excellent articles in this journal shows us that the usual way to calculate risk of cardiovascular disease, such as ascertaining smoking habits and measuring blood pressure and cholesterol, is better than analyses for commonly occurring variations in DNA sequences. From the other article, we learn that a statin drug reduces risk of cardiovascular disease irrespective of whether patients have or do not have common DNA variants that are associated with the degree of the drug's lowering of LDL cholesterol. What the two articles do not tell us is why all of this is so, but that explanation has apparently been published elsewhere since the articles were accepted for publication.. It is a dramatic and profoundly important story for biology and clinical medicine.Sonia Shah and her colleagues in London used data and samples from a subset of the middle-aged men and women ( n = 5059) in the Whitehall II Study … [1]: #fn-2 [2]: #fn-3