Scientists at the Weizmann Institute of Science have discovered that people who have a hard time turning off their response to stress may be missing a special set of proteins.
That pounding heart, those sweating palms, tensed muscles and that metallic taste in your mouth is normal – when you perceive a threat to your existence.
It's a typical anxiety response, one that often comes along with the “flight or fight” reaction generated by the rush of adrenalin that is produced with any significant stress.
People who have a tough time turning that response off often have suffered a psychological trauma as the result of a frightening experience such as a missile attack or other type of physical threat. Such victims can develp post-traumatic stress disorder (PTSD) as well as other conditions such as anorexia, depression and anxiety disorders.
According to the findings of a new study led by Dr. Alon Chen at the Weizmann Institute's Neurobiology Department, however, there is solid evidence that three related proteins are responsible for the body's ability to turn off the stress response.
The research, which appeared in the Proceedings of the National Academy of Sciences (PNAS), found that urocortin proteins 1, 2, and 3 are crucial for returning the body to normal.
To identify how exactly this is done, Chen and his team tested the gene expression levels of genes involved in the stress response in a group of genetically engineered mice who were lacking the proteins, and a control group of mice.
The levels remained constant both during and after stress in the engineered mice, who were missing the proteins. In contrast, patterns of gene expression in the control mice showed significant change 24 hours after the stress.
In other words, without the urocortin system, the “return to normal” program could not be activated, and the stress genes continued to function.
“This may have implications for anxiety disorders, depression, anorexia and other conditions,” noted Dr. Chen. “The genetically engineered mice we created could be effective research models for these diseases.”