Could there be connections between socio-economic status, epigenetics, and one’s likelihood of developing depression? Previous and current research has long revealed a relationship between poverty and depression, and now new research suggests that there could be an underlying epigenetic influence. This new finding may help mediate the association between lower socioeconomic status and the risk of developing the disease. The study, published in Molecular Psychiatry, utilizes epigenetics, brain imaging, and behavioral data of adolescents collected over three years as part of a larger study. The results may help progress individualized strategies for preventing depression based on biological predictors.
In a study conducted by researchers at Duke University, results showed that youths growing up in homes with lower socioeconomic status (SES) had higher amounts of an epigenetic tag on genes related to depression. This mark is specifically known as DNA methylation, which is defined as the addition of a methyl group to DNA, typically suppressing gene expression. In general, increased DNA methylation of gene promoters has been linked to stressors, including low SES. Furthermore, recent studies have shown that DNA methylation of the proximal promoter region of the serotonin transporter gene, SLC6A4, could lead to heightened risk for mental illness. SLC6A4 encodes a protein that plays a crucial role in transporting serotonin molecules, which are neurotransmitters implicated in depression, anxiety, and OCD.
When the gene SLC6A4 was more methylated, the researchers found that an individual’s amygdala – an area of the brain that plays a role in a person’s threat reaction, or “fight or flight” response – was more active. The increased responsivity of the amygdala was measured with an fMRI as the participants were shown photographs of fearful faces. Later on, those who had higher amygdala activity were more likely to report depressive symptoms. Ultimately, the researchers reported that “changes in gene methylation associated with lower socioeconomic status (SES) predict changes in risk-related brain function.”
Johnna Swartz, the study’s first author and post-doctoral researcher in the Duke lab of Ahmad Hariri, commented, “This is some of the first research demonstrating that low socioeconomic status can lead to changes in the way genes are expressed, and it maps this out through brain development to the future experience of depression symptoms.”
SES is a metric that assesses parents’ income, occupation, and level of education, according to the American Psychological Association. It has been associated with numerous physical and psychological health issues, such as chronic stress, cardiovascular disease, poor nutrition and high body mass index. Adolescence is considered difficult for anyone and even more so for those growing up in a family with low SES.
“These small daily hassles of scraping by are evident in changes that build up and affect children’s development,” Swartz said.
Their research involved 132 adolescents who were between the ages of 11 and 15 at the beginning of a study known as TAOS (Teen Alcohol Outcomes Study). Their SES ranged from low to high and about half of the individuals had a history of depression in their families.
Professor of Psychiatry and Behavioral Sciences at Duke, Douglas Williamson, who is also co-author of this study and principal investigator of TAOS, said the biggest risk factor for depression is family history of the disorder. “Our new work reveals one of the mechanisms by which such familial risk may be manifested or expressed in a particular group of vulnerable individuals during adolescence.”
In one of the group’s previous studies, published in Neuron, they found that scanning the amygdala with an fMRI could indicate who is more likely to have anxiety and depression in response to stress years later. In the current study, they found a connection between high activity in the amygdala and depression about one year later, when the individuals were between the ages of 14 and 19.
“Notably, we found that sensitized amygdala reactivity only predicted increases in depressive symptoms among adolescents with a positive family history of depression,” the team concluded.
Swartz explained that their research assessed a range of SES scores and did not focus exclusively on the adolescents who faced extreme poverty or neglect. The findings hint that there is a link between those even with just a slightly lower socioeconomic status and biological differences, which in turn increases the individual’s risk for depression.
A previous study that Williamson and Hariri conducted demonstrated that epigenetic tags near the SLC6A4 gene were associated with the amygdala’s sensitivity. They included participants from the Duke Neurogenetics Study (DNS) and TAOS, but only looked at the levels of DNA methylation at one point in time.
It is more powerful to look at the changes in these epigenetic markers over a long period of time in order to know more about an individual’s risk for depression, according to Hariri, who is a member of the Duke Institute for Brain Sciences.
The group of scientists is now scrutinizing the genome for novel markers that would predict depression. Swartz noted that more accurate predictions could be made if a panel of markers were used in combination. In the future, they hope to investigate younger individuals in regard to depression.
“As they enter into young adulthood they are going to be experiencing more problems with depression or anxiety – or maybe substance abuse,” Hariri said. “The extent to which our measures of their genomes and brains earlier in their lives continue to predict their relative health is something that’s very important to know and very exciting for us to study.”
Bailey Kirkpatrick
Source: Swartz, J.R., Hariri, A.R., Williamson, D.E. (2016). An epigenetic mechanism links socioeconomic status to changes in depression-related brain function in high-risk adolescents. Mol Psychiatry, 1-6.
Reference: Duke University. Poverty Marks a Gene, Predicting Depression. Duke Today. 24 May 2016. Web.
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