UCLA. US: Heredity may influence people’s predisposition for post-traumatic stress disorder (PTSD). Why
do some people develop post-traumatic stress disorder while others who
suffered the same ordeal do not? A new UCLA discovery may shed light on
the answer.
UCLA scientists have linked two genes to the debilitating mental
disorder, suggesting that heredity influences a person’s risk of
developing PTSD. Published in the February 2015 edition of the Journal
of Affective Disorders, the findings could provide a biological basis
for diagnosing and treating PTSD more effectively in the future.
“Many people suffer with post-traumatic stress disorder after
surviving a life-threatening ordeal like war, rape or a natural
disaster,” explained lead author Dr. Armen Goenjian, a researcher at the
Semel Institute for Neuroscience and Human Behavior
at UCLA. “But not everyone who experiences trauma suffers from PTSD. We
investigated whether PTSD has genetic underpinnings that make some
people more vulnerable to the syndrome than others.”
In 1988, Goenjian, an Armenian American, rushed to Spitak, Armenia,
after a 6.8 magnitude earthquake devastated the country. The temblor
leveled entire towns and cities, killing more than 25,000 people,
two-thirds of them children.
With support from the Armenian Relief Society, Goenjian and his
colleagues helped establish a pair of psychiatric clinics that treated
earthquake survivors for 21 years. A dozen multigenerational
families in northern Armenia agreed to allow their blood samples to be
sent to UCLA, where Goenjian and his colleagues combed the DNA of 200
individuals for genetic clues to psychiatric vulnerability.
In 2012, his team discovered
that PTSD was more common in survivors who carried two gene variants
associated with depression. In the current study, Goenjian and first
author Julia Bailey, an adjunct assistant professor of epidemiology at
the UCLA Fielding School of Public Health, focused on two genes, COMT
and TPH-2, which play important roles in brain function.
COMT is an enzyme that degrades dopamine, a neurotransmitter that
controls the brain’s reward and pleasure centers and helps regulate
mood, thinking, attention and behavior. Too much or too little dopamine
can influence various neurological and psychological disorders.
TPH-2 controls the production of serotonin, a neurotransmitter that
regulates mood, sleep and alertness — all of which are disrupted in
PTSD. Serotonin is the target of a group of drugs called selective
serotonin reuptake inhibitors, or SSRIs, which were designed to treat
depression. Now, more physicians are prescribing SSRIs to treat
disorders beyond depression, including PTSD.
“We found a significant association between variants of COMT and
TPH-2 with PTSD symptoms, suggesting that these genes contribute to the
onset and persistence of the disorder,” Goenjian said. “Our results
indicate that people who carry these genetic variants may be at higher
risk of developing PTSD.”
The team used the most recent PTSD criteria from the American
Psychiatric Association’s diagnostic manual to measure genes’ role in
predisposing someone to the disorder. The new criteria increased
estimates of the degree to which PTSD is genetic to 60 percent;
estimates based on older criteria reached only 41 percent.
“Assessments of patients based upon the latest diagnostic criteria
may boost the field’s chances of finding new genetic markers for PTSD,”
Goenjian said. “We hope our findings will lead to molecular methods for
screening people at risk for this disorder and identify new drug
therapies for prevention and treatment.”
Goenjian cautioned that PTSD is likely caused by multiple genes, and
that more research must be done to find more of the genes involved.
PTSD affects about 7 percent of Americans. It has been a pressing
health issue for many veterans returning from tours in Iraq and
Afghanistan.
The study’s co-authors were Ernest Noble and Sugandha Dandekar, both
of UCLA; Alan Steinberg of the UCLA–Duke National Childhood Center for
Traumatic Stress; David Walling of the Collaborative Neuroscience
Network; and Sofia Stepanian of UC Riverside.