Certain variations in a gene that helps regulate stress response offer protection against depression in adults who suffered abuse when they were children, a new study says.
Adults who were abused as children and didn't have the protective variations of the CRHR1 gene had twice the symptoms of moderate to severe depression, compared to those with the variations.
The researchers interviewed more than 400 adults and tested their DNA. About one-third of them had the protective variations in the gene that produces CRHR1, a receptor for the stress hormone corticotropin-releasing hormone (CRH).
Extreme stress in childhood, brought on by factors such as abuse, can hyper-activate the hormone system that regulates stress response, leading to an increased risk of depression in adulthood, the researchers said.
"Our results suggest that genetic differences in CRH-mediated neurotransmission may change the developmental effects that childhood abuse can have on the stress hormone system -- developmental effects that can raise the risk of depression in adults," Dr. Kerry J. Ressler, of Emory University, said in a prepared statement.
"We know that childhood abuse and early life stress are among the strongest contributors to adult depression, and this study brings to light the importance of preventing them," Ressler said. "But when these tragic events do occur, studies like this one ultimately can help us learn how we might be able to better intervene against the pathology that often follows."
The study, funded by the U.S. National Institute of Mental Health (NIMH), is published in the current issue of the journal Archives of General Psychiatry.
NIMH Director Dr. Thomas R. Insel said in a prepared statement: "People's biological variations set the stage for how they respond to different environmental factors, like stress, that can lead to depression. Knowing what those variations are eventually could help clinicians individualize care for their patients by predicting who may be at risk or suggesting more precise avenues for treatment."