From Our 2010 Archives
Gene Variant May Help Some Overcome Adversity
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SUNDAY, March 7 (HealthDay News) -- The study of a link between misery and death has helped researchers identify a gene variant fostering resilience in the face of adversity.
The U.S. research team focused on a gene called IL6, which is known to cause inflammation in the body and contributes to cardiovascular disease, neurodegeneration and some types of cancer.
"The IL6 gene controls immune responses but can also serve as 'fertilizer' for cardiovascular disease and certain kinds of cancer," study author Steven Cole, an associate professor of medicine in the division of hematology-oncology at the University of California, Los Angeles and a member of the UCLA Cousins Center for Psychoneuroimmunology, said in a university news release.
"Our studies were able to trace a biochemical pathway through which adverse life circumstances -- fight-or-flight stress responses -- can activate the IL6 gene,' he explained. "We also identified the specific genetic sequence in this gene that serves as a target of that signaling pathway, and we discovered that a well-known variation in that sequence can block that path and disconnect IL6 responses from the effects of stress."
Cole and colleagues also found that people with the most common type of IL6 gene had an increased risk of death for about 11 years after they'd experienced a stressful life event significant enough to trigger depression. But this increased risk of death didn't occur in people with a less common variant of the gene.
The research was released online in advance of publication in an upcoming print issue of the journal Proceedings of the National Academy of Sciences.
In their examination of IL6, Cole and colleagues used a combination of computer modeling, test-tube biochemistry, stress studies in animals, and human genetic epidemiology. This approach could be used to identify other genes that interact with social environment to affect human health, Cole said.
-- Robert Preidt
Copyright © 2010 HealthDay. All rights reserved.
SOURCE: University of California, Los Angeles, news release, February 2010
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