Neglect of Several Important Indexes During the Study of Human Essential Hypertension

ever, these findings only partially explain EH. The Human Genome Project, the International HapMap Project, and the development of molecular genetics have sparked new interest in elucidating the genetic mechanisms underlying EH. However, although hundreds of hypertension-related genes have been identified and some genome-wide association studies (GWAS) have produced interesting results, only 1% of blood pressure (BP) changes can be explained by GWAS. 3–5 One prominent use of GWAS is to identify genetic variants associated with common diseases and complex traits. 6 However, these studies have not provided much information regarding the genetic mechanisms underlying EH. This may be because EH is a multifactor and multigenetic disease, and its progression is affected by many environmental and genetic factors. Typically, for any particular trait, the cumulative effects of multiple single nucleotide polymorphisms explain only a small fraction of each individual’s risk for the trait. Some scientists argue that the methods used for analysis are not necessarily reasonable, only common variants are detected in a given population (>5%), rare variants are untested, or gene-gene and gene-environment interactions are not estimated. 7 However, these may not be the key reasons why GWAS have failed in the study of EH. Other very important characteristics of GWAS relevant to such investigations are discussed below. First, the age of the individuals included in the normotensive and hypertensive groups used in previous