The mechanism behind how human genes interact with their environment to boost disease risk has been detailed in a new UCLA study.
Published in the Feb. 18 online edition of the
American Journal of Human Genetics, the findings shed light on why the search for specific gene variants linked to human diseases can only partly explain common disorders.
"We know that genes and environmental factors influence common human diseases like heart disease, diabetes and cancer," explained principal investigator Jake Lusis, professor of medicine, human genetics and microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA. "Most research, however, has focused on unraveling the genetic component of disease risk while ignoring the effect of environmental stimuli. Our study examined how the molecular interaction between the two helps lead to disease."
"Smoking and high cholesterol, for example, each increase a person's risk for heart disease," he said. "But when you add them together, the total risk exceeds its parts. Their interaction creates a dangerous synergy that causes damage beyond what the two can cause independently."
Unlike earlier studies that focused on a single gene, the UCLA team scrutinized the activity of thousands of human genes both at rest and under stress. In particular, the scientists zeroed in on gene expression—the process by which a gene's DNA sequence is converted into cellular proteins.