PTSD Risk Rooted in Stress
Tuesday, December 9, 2008; 12:00 AM
TUESDAY, Dec. 9 (HealthDay News) -- A decade-long study into post-traumatic stress disorder among combat veterans and their identical twins has yielded critical information on the root causes of this devastating condition.
The researchers found that both genetic and environmental factors increase the risk of developing post-traumatic stress disorder (PTSD). The work, to be presented Tuesday at the American College of Neuropsychopharmacology annual meeting in Scottsdale, Ariz., was sponsored by both the U.S. National Institute of Mental Health and the Veterans Administration.
"In addition to building our understanding of how PTSD comes to exist, we may have useful signs for PTSD prevention and treatment," study author Dr. Roger Pitman, a professor of psychiatry at Harvard Medical School, said during a recent teleconference on the research. "For example, persons with recognized PTSD risk factors may be best advised to avoid occupations that would have them serve in highly stressful situations, such as serving in military forces. Things acquired as a result of stress are more likely to be reversed by treatment and could be taken as targets of PTSD treatment."
Pitman's group studied more than 100 combat veterans of the Vietnam War, each of whom have an identical twin who did not serve in combat.
"We made the assumption that, because twins have the same genes and the same family upbringing, that the twin who did not serve in combat represents what the combat-exposed twin would be like except for the combat exposure," Pitman explained.
Prior to this research, experts had noted a smaller hippocampal volume (the hippocampus is a part of the brain involved in memory) in people with PTSD.
Now it appears that the smaller volume exists in both the exposed and unexposed twin, indicating that this may be a preexisting risk factor for PTSD.
"This suggests this 'fragile egg' hypothesis -- that some people are probably genetically a little bit less resilient [to PTSD] than other people," said Dr. Julie Fudge, an associate professor of psychiatry and neurobiology and anatomy at the University of Rochester Medical Center, in New York.
However, the ventromedial prefrontal cortex area of the brain (involved in decision-making) is smaller in the combat-exposed brothers, compared to their unexposed twins.
"We discovered a number of abnormalities in PTSD combat veterans not shared with their twins and . . . we infer that the abnormality was caused by combat," Pitman said. "One of these is increased heart rate response when the combat veteran is startled. Another example is loss of gray matter in the rostral anterior cingulated cortex, which plays a role in inhibiting the fear response."
"The assumption for the last 10 years has been that the hippocampus has shrunken due to stress basically because this is what happens in animals. But the Pitman study shows that this is probably not the case for the hippocampus," said Dr. Keith A. Young, vice chair for research at Texas A&M Health Science Center College of Medicine and Neuroimaging and Genetics Core Leader for the VA Center of Excellence for Research on Returning War Veterans. "In other areas of the brain they may very well be being damaged by the excess stress," he said.
A thus-far unpublished finding, Pittman added, is that combat-exposed men had a broad array of psychiatric symptoms that were not seen in their brothers.
"This tends to refute that persons with PTSD would have had psychiatric problems if they hadn't been exposed to a traumatic event," he said.
For more on this condition, visit Root Cause of PTSD.
SOURCES: Keith A. Young, Ph.D., vice chair, research at Texas A&M Health Science Center College of Medicine, and Neuroimaging and Genetics Core Leader, VA Center of Excellence for Research on Returning War Veterans; Julie Fudge, M.D., associate professor, psychiatry and neurobiology and anatomy, University of Rochester Medical Center; Dec. 4, 2008, teleconference with Roger Pittman, M.D., professor, psychiatry, Harvard Medical School, Massachusetts General Hospital, Boston; Dec. 8, 2008, presentation, American College of Neuropsychopharmacology annual meeting, Scottsdale, Ariz.