TUESDAY, Oct. 10 (HealthDay News) -- Whether or not you have one or another variant of a particular gene could determine your response to life's ups and downs, a new study finds.
A U.S. team has found a variant of the serotonin transporter gene that may predispose individuals to depression in stressful circumstances.
But the opposite also held true: People without the variant almost seemed to thrive on stress.
The study seemed to confirm previous research and may have added "one more piece of the puzzle," said Dr. Jay Gingrich, an assistant professor of clinical psychiatry at Columbia University and New York State Psychiatric Institute in New York City.
He was not involved in the research, which is published in this week's issue of the Proceedings of the National Academy of Sciences.
While there's been ample clinical data to suggest that certain gene variants predispose a person to depression, this is the first human brain-imaging study supporting that theory, according to lead researcher Turhan Canli, an assistant professor of psychology at Stony Brook University in Stony Brook, N.Y.
"There has been clinical evidence to suggest an association, but it hasn't been described at the level of neurosystems," he explained. "The question was whether we could find evidence for that interaction in the brain as well."
Prior brain-imaging studies had found that certain areas of the brain are activated when depression or stress is present.
For this study, Canli and his colleagues used functional magnetic resonance imaging (fMRI) to measure blood flow in these brain regions in 48 healthy adult volunteers. None of the participants had been diagnosed with any mood disorder, including depression.
Participants were asked to report on any life stresses, including legal or health problems, and childhood stressors.
The amygdala region of the brain, which has been implicated in depression and anxiety, was overactivated in people with the "short" version of the gene and with high levels of life stress, the Stony Brook team reported.
These individuals also showed higher levels of "rumination" (brooding or obsessive thinking), a risk factor for depression.
"Greater life stress seems to increase the level of activation in these brain regions," Canli said.
Interestingly, the opposite was true for others.
"Surprisingly, for the other group of people with a different genetic background, stress is associated with less [amygdala] activation," Canli added.
"It's not just that they are not showing the effect of the other genotype. They are actually showing exactly the opposite pattern," he explained. "These are people to whom the phrase, 'What doesn't kill you makes you stronger,' might actually apply."
At this point, the study raises at least as many questions as it answers.
Canli is currently hunting funds to follow a larger sample of people to see if people with the shorter variant and more life stresses go on to develop depression.
Another direction would be to see if one's genotype influences decisions about seeking out a more or less stressful life.
"I would think that if you happen to have the short [variant], and you do find yourself not responding well to stressful experiences, you would tend to shy away from them as much as you can," Canli said. "It would interesting to see whether there's a difference there in terms of control over life experiences."
For more on depression, visit the U.S. National Institute of Mental Health.
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