Stress Gene 5HTR2C Linked to Increased Heart Attack Risk

There's no doubt that stress may exacerbate health problems. Yet a recent study suggests that a newly discovered 'stress gene' could also increase an individual's risk of dying from a heart attack or heart disease by up to 38 percent.

According to researchers at Duke University, they linked the gene to the body overproducing the hormone cortisol, which is responsible for the regulation of blood pressure and insulin release of blood sugar maintenance.

This new gene, which scientists are calling 5HTR2C gene, has also been linked to bipolar disorder.

"This is very exciting, but it's very preliminary. It certainly merits further investigation," lead study author and university professor Beverly Brummett notes, via WebMD. He discovered 5HTR2C gene. "Down the line, if the findings were replicated, then the next step would be to test people (on a widespread basis) for the gene and watch them more closely."

Researchers analyzed the medical records of 6,000 patients diagnosed with heart disease. Their findings showed that approximately 17 percent of male participants had shown a genetic change as a result of being under so much stress. However, 3 percent of female participants also showed similar signs.

After a seven-year follow up period that also considered various factors such as age, obesity and smoking, researchers concluded that the stress gene increased the risk of patients dying from a heart attack.

For those that carry the stress gene, researchers believe these findings may hold new insight into making improvements on stress therapies and drug treatments that could potentially minimize a patient's risk.

"This is one step towards the day when we will be able to identify people on the basis of this genotype who are at higher risk of developing heart disease in the first place," said Dr. Redford Williams, director of the Behavioral Medicine Research Center at Duke University School of Medicine, via BBC.

More information regarding the study can be found via the journal PLOS One.