"It's like using four different cops to find the same culprit," Chakravarti says. "The more ways we search for blood pressure genes, the better our ability to understand hypertension, whose affects are not uni-causal."
For the billion-plus people worldwide with hypertension, even small elevations in blood pressure are associated with increased risk of cardiovascular disease. Although it's generally known that hypertension has a familial component, the genetic regulatory mechanisms of blood pressure have been challenging to pin down so far, Chakravarti says, citing similar genetic studies three years ago that failed to detect any genes. He credits the recent spate of genetic discoveries more than 300 genes for cardiovascular diseases have been identified in just the last few years to the collective analyses of long-term prospective research efforts such as the pioneering Framingham Heart Study, begun in 1948, the Cardiovascular Heath Study, started in 1989, and the Atherosclerosis Risk in Communities (ARIC) study, started in 1987.
"Too often, people look at these studies that have a long provenance and wonder what is it doing for them today," says Chakravarti, who compares the studies to a retirement account. "Researchers visit them time and time again. Without them, this feat of genetic studies would be impossible."
Each genome-wide association study, often referred to as GWAS, reported what effects were observed at which locations on the genome in a scan of single nucleotide polymorphisms (SNPs) throughout the genome. Pronounced snips, SNPs are sites where a sing
|Contact: Maryalice Yakutchik|
Johns Hopkins Medical Institutions