gene

A Genetic Culprit Behind Depressive Disorders

by The Anti Depression Team on

It was never believed that DNA could clearly reflect depressive disorders, until now.

A recent study led by Dr Srijian Sen, professor of Psychiatry at University of Michigan, discovers a gene – which transports serotonin, a brain chemical that regulates mood – responsible for sparking depressive mental conditions such as depression. It is reported that a less functional serotonin-transporter gene inhibits re-absorption of the mood-controlling chemical by nerve cells in an individual’s brain. This makes one more depressive and susceptible to depression later on when faced with stressful life experiences like battling a serious medical illness or suffering from childhood abuse, especially if the poorly functioning transporter is already present during childhood.

Despite the lack of a lucid relationship between this gene, stress, and depressive symptoms, Sen’s results validate those of a revolutionary study in 2003, wherein correlation between genes and environment in depressive disorders is first established. Discoveries in that study of more than 800 subjects show that traumatic life events were more liable to trigger depressive symptoms in individuals with a less functional serotonin transporter gene than those with a more functional one. However, these findings were questioned when 14 studies on relationships between the gene, depression and stress pooled by a 2009 investigation showed no heightened risk of depressive conditions among bearers with different versions of the gene.

To eliminate the sustained controversy, Sen’s team gathered all 54 obtainable studies on the subject, which incorporated information from almost 41,000 volunteers. From this broader analysis, the less functional form of the transporter gene does indeed show that it confers a greater possibility of depressive disorders when coupled with stress.

Additionally, to verify 2009 team’s contrary results, Sen re-examined their data via his analytical model and also found no association between the gene and depressive moods when he limited his investigation to their 14 studies.

He believes that the 2009 findings are not contradictory, but instead reveal a distinction in methodology used in the study. For consistency, using similarly collected information, the 2009 analysis focused only on the 14 studies that included stressful life events, but exempted other stressors, such as childhood abuse or medical illness. The more complete set of 54 studies, which included these stressors as well, showed vigorous interaction between the serotonin-transporting gene, stress and depressive symptoms.

Sen hopes to “settle this story, and move on to looking more broadly across the genome for more factors” related to depressive conditions. Ideally, his team would like to “find a panel of different genetic variations that go together to help predict individuals who respond poorly to stress, and who might respond well to specific types of treatment as opposed to others.”

Nevertheless, Sen stresses that this gene is only one small player in the spread of genetic and environmental factors that contribute to depressive symptoms. For this discovery to be clinically useful, numerous more factors need to be found to “identify new pathways that are involved in depressive conditions in order to derive new and better treatments.”