The expression “stress is a killer” may not be that far off-base. A team of researchers has pinpointed a specific gene that is sensitive to chronic stress and depression and that may also protect against illnesses such as cancer and heart disease.
The study’s first author, Dr. Steven Cole, an associate professor of medicine at the University of California at Los Angeles, and his colleagues studied the IL6 gene and found it becomes hyperactive in response to chronic stress, loneliness or depression.
“This is the first study to show howa person’s emotional state can alter the activity of a specific gene associated with human health,” Cole said.
In 2007, Cole showed that people with chronic feelings of loneliness experienced a change in gene activity, exhibiting more activity in genes linked to inflammation and inflammation-related diseases, such as cancer and heart disease. Cole, however, did not know which genes in particular were susceptible to negative emotions.
In his March study, Cole’s team developed a special computational model, which identified 633,000 variations of different genes that might be vulnerable to environmental influences, such as chronic stress. From the possible candidates, they focused on a gene called IL6 because it is already known to be important for human health. IL6 triggers inflammation in the body and contributes to heart disease and cancers, such as breast and prostate cancer.
The researchers found that 20 percent of people possess a helpful variation of IL6, which appears to be resilient to the effects of negative emotion. Unlike the most common version of the IL6 gene, this variation does not “turn on” in the face of persistent stress, depression or loneliness, and thus may protect the body from inflammation.
Cole’s team confirmed this by measuring IL6 activity and the progression of diseases linked to inflammation in healthy 70- to 80-year-olds, studied over 12 years in the MacArthur Study of Successful Aging. Cole found that as people experienced more intense stress and depression over the years, they exhibited more activity in the most common type of the IL6 gene. These subjects had higher rates of inflammation-related disease and died on average almost three years earlier than those with the rarer variation of the IL6 gene, which remains silent in response to stress.
The study is published in the March edition of Proceedings of the National Academy of Sciences.
“The next step is to see what we can do to identify and protect people who are more vulnerable to inflammation-related diseases, like cancer,” Cole said.
