A recent University analysis points to a possible link between stress and an increased risk for depression.

The findings — released last week by Srijan Sen, an assistant professor of psychiatry at the University’s Medical School, and his colleagues — were based on a comprehensive analysis of 54 published studies that examined the possible genetic correlation between depression and environmental stressors, including health and financial problems.

Sen said he decided to do the analysis after a 2009 report questioned the findings of a study in 2003 that showed a genetic link between the two. The 2003 study was considered a medical breakthrough at the time.

The results of the 2003 study showed that people with a particular version of a serotonin transporter gene, called 5-HTT, exhibited more symptoms of depression, diagnosable depression and suicidal tendencies in reaction to stressful life events than people with a different version of the same gene.

The 5-HTT gene is involved in the reabsorption of serotonin at brain synapses. Seratonin, known as the “happiness hormone,” contributes to general feelings of well-being. And while the gene may not be directly associated with depression, the report states, it could impact the “serotonergic response” to stress.

The researchers hypothesized that variations in the 5-HTT explain why some individuals show have a higher risk of depression after going through stressful experiences while others seem to handle stress relatively easily.

To test their prediction in the 2003 study, the researchers separated 847 men and women into three groups depending on which of the three versions of the 5-HTT gene they had. The researchers asked them to report any stressful experiences such as employment issues, financial troubles, health problems or relationship issues they had between ages 21 and 26.

The researchers then evaluated the participants for symptoms of depression at their current age of 26 and found that those with a particular version of 5-HTT had an elevated risk of depression.

Sen said he and many other scientists in his field felt that the 2009 analysis of the 2003 study was incomplete and biased since it only looked at 14 of the 54 conducted studies. Ten out of the 14, he added, were negative — meaning they didn’t find evidence of an interaction between the gene and an increased risk of depression.

Sen estimated that of the remaining 40 studies omitted from the 2009 analysis, only about eight were negative.

Another shortcoming of the 2009 analysis, Sen said, was its narrow focus. It only considered studies that looked at stressful life events, while other studies on the same genetic interaction have investigated triggers such as abuse during childhood and the first year of medical school.

Over the course of about nine months, Sen and his team looked at all 54 studies published between 2001 and 2010. In total, about 41,000 people participanted in the studies.

While the analysis was a great undertaking, Sen said the real work was done in the original data collection. For example, he said the researchers who conducted the 2003 study worked on it for about 20 years.

Sen said he spoke with the researchers of the 2003 study, and they were very pleased with the results of his team’s analysis.

“They were convinced that the 2003 study was wrong and incomplete,” He said. “So they were happy that somebody was trying to look more completely at the research.”

Sen emphasized that the 5-HTT gene only accounts for a small percentage of variance in symptoms of depression and that this is only the beginning of what he hopes will turn into a genome-wide survey of genetic factors that affect stress.

“I think it’s important to note that this isn’t the depression gene,” he said. “And that there’s going to be dozens of other genes like this, so I don’t think people should go out and find what genotype they have at this gene.”

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