Much of the effective treatment of depression lies in the accurate identification of its origin and triggers. While stressful life events are an obvious trigger, a specific gene variation that has been identified as increasing the risk in conjunction with stressful life events may actually have no impact at all. This surprising finding is the result of research funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. The study, published in the Journal of the American Medical Association, challenges the widely accepted assumption in identifying risk factors for depression. Scientists believe that most mental disorders are the result of a combination of many genetic risk factors that interact with environmental triggers. Identifying the exact combinations continues to present significant challenges in the research, keeping absolute treatments at bay. As a result of advances in scientific understanding and technologies in the last decade, mental health researchers found in 2003 that a gene involved in serotonin activity increased over a five-year period. This groundbreaking research received wide acclaim and produced far-reaching influence. The problem with this study is scientists have been unable to replicate its findings as follow-up studies have produced inconsistent results. To challenge the 2003 findings in an effort to either confirm or contradict the results, Kathleen Merikangas, Ph.D., of the NIMH Intramural Research Program, led a group of scientists from NIMH and six universities in a meta-analysis, re-analyzing data on 14,250 participants in 14 studies published from 2003 through March 2009. This original data was analyzed to also identify potential gender differences associated with serotonin genotype, stressful life events, and depression. While the workgroup did find a strong association between the number of stressful life events and risk of depression across the studies, the presumed high-risk version of the serotonin transporter gene failed to show a relationship to increased risk for major depression. The relationship was not shown alone or in interaction with stressful life events. The findings proved to be the same in men and women. Researchers within the workgroup suggest these findings may account for the difficulty others have had in attempting to replicate the 2003 study. The analysis certainly brings into question the validity of the 2003 study and highlights earlier reviews that had also questioned the actual impact the gene had on depression risk. “Even though our re-analysis did not confirm an association between the serotonin gene and depression, the finding that the environmental factor was strongly associated with depression in several studies reminds us that environmental factors are also involved in the complex pathways leading to mental disorders,” noted Merikangas in a NIMH statement. “Future progress will require thoughtful integration of the tools of genetics, epidemiology, and clinical and behavioral sciences.” Serotonin is a neurotransmitter in the brain which helps brain cells to communicate with one another. This particular neurotransmitter is involved in regulating mood. A person’s inability to make or use the right amount of serotonin has been linked to a number of mental disorders, including depression, bipolar disorder, anxiety disorder, autism, and schizophrenia.
