Scientists Spot Another Group of Genes That May Raise Depression Risk
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TUESDAY, March 25, 2014 (HealthDay News) -- Scientists report that they have found another group of genes that might increase a person's risk of developing depression.
The genes' effect appears to be small, but scientists hope their discovery will one day provide new targets for drug development.
"Further research may identify people who are at risk of depression after life stresses due to specific personality traits and genetic variations," said study author Gyorgy Bagdy, chairman of the department of pharmacodynamics at Semmelweis University in Budapest, Hungary.
Experts are still trying to figure out how to improve depression treatments by drawing on a growing understanding of how different genes affect human resilience -- the way a person copes with life.
Research suggests that 9 percent of American adults suffer from depression, with almost half of that group suffering severe cases. The people most prone to depression include middle-aged people, blacks, Hispanics, women, those who are unemployed or unable to work, and those with little education.
The genes you inherit from your parents are thought to account for about 30 percent to 40 percent of the risk of depression, with life stresses accounting for much of the rest, said Dr. Srijan Sen, an assistant professor of psychiatry, neuroscience and bioinformatics at the University of Michigan.
"But we haven't had too much success in finding specific genes," Sen said, and those that have been discovered appear to be responsible for only a small percentage of overall risk.
In the new study, an international team of researchers looked at the genes of nearly 2,400 white people from the United Kingdom and Hungary. They found that those with genetic variations linked to a brain chemical called galanin were more likely to suffer from depression and anxiety after suffering high levels of stress.
Galanin is involved in the regulation of pain, sleeping, waking mood and blood pressure, according to the U.S. National Institutes of Health, and scientists suspect it plays a role in stress and anxiety disorders.
The overall effect was small, however, with the gene variants involving galanin explaining less than 2 percent of moods in both healthy people and those suffering from depression, study co-author Bagdy said.
The findings don't confirm that these variants directly contribute to a higher risk of depression, but Bagdy said it's possible that they raise the risk by how they interact with stressors in the worlds in which the study participants live.
How common are the genetic variations?
Study co-author Bill Deakin, a professor of psychiatry at the University of Manchester, in the United Kingdom, said that's not the right question because the percentage of people who have the traits "doesn't say anything about how much risk it confers if you carry it. Some are more potent than others."
In general, though, riskier genetic variations "tend to occur in a few percent of the population," Deakin said, and they can work together to raise the risk of depression.
Although the study found an association between these gene variants and depression risk, it did not prove a cause-and-effect link.
Sen praised the study but cautioned that "most of the genetic risk for depression out there is still undiscovered."
More research is needed into this possible genetic link to depression, Sen said, because it's too early to know if it's actually valid. One approach could be to stress people out and see how they react when they do -- or don't -- have the genetic variations, he said.
"If this turns out to be involved, it will be one of hundreds or thousands of genes," he said. "This isn't going to be the gene for depression, but it might help us with the puzzle."
And, he said, the research could bring scientists closer to the ultimate goal: better treatments for depression. More knowledge about genetics and depression, he said, "could help predict who will respond to Prozac or Zoloft or psychotherapy."
The study appears in this week's issue of the journal Proceedings of the National Academy of Sciences.
SOURCES: Gyorgy Bagdy, Ph.D., chairman, department of pharmacodynamics, Semmelweis University, Budapest, Hungary; Srijan Sen, M.D., Ph.D., assistant professor, psychiatry, neuroscience and bioinformatics, University of Michigan, Ann Arbor; March 24 to 28, 2014, Proceedings of the National Academy of Sciences