Post-traumatic stress disorder (PTSD) is a debilitating, psychiatric disorder that can occur following exposure to trauma or extreme stress. While anyone who has experienced trauma can develop PTSD, it is most often associated with military veterans. Not everyone who has experienced trauma will develop PTSD—in fact, the majority of people exposed to trauma do not develop the disorder. Whether or not someone develops PTSD depends on a person’s perception of stress, which is shaped by life experiences, genetics and behavior.
The genetic aspect of PTSD has two parts: genes and environmental factors such as life experiences. The idea that genes play a role in PTSD is getting a lot of attention lately. The effect of genes and environmental factors together is called gene-environment interaction. Scientists have identified a gene that may contribute to PTSD, particularly in people who have experienced early-life trauma.
Researchers think that variations in genes can play a role in determining how someone responds to a traumatic event or can even make them more likely to develop PTSD. One type of gene variation is on a particular gene called FKBP5 that has been associated with PTSD. FKBP5 has a related protein that is involved in the body’s response to stress. If a variation occurs in FKBP5 that causes irregular function of its associated protein, it will affect a person’s stress response. This in turn could influence the development or severity of PTSD symptoms. Studies of people with PTSD who have a FKBP5 variation and also experienced early-life trauma, such as childhood abuse, show a significant gene-environment interaction. More specifically, the combination of the gene variation plus early-life trauma resulted in more severe PTSD symptoms compared to people who had not experienced trauma.
Scientists hope the results of studies like these will lead to new and more effective PTSD treatments.
Donna Cioffi, PhD, is an associate professor in the department of biochemistry and molecular biology at the University of South Alabama. She studies the role of the protein FKBP51 in calcium signaling in pulmonary endothelial cells.