The eighteenth century philosopher David Hume knew nothing of epigenetics, so he might have been more right than he knew when he said, “A propensity to hope and joy is real riches; one to fear and sorrow real poverty.” After years of hints, now, with new results from a 3-year study, it is clearer than ever that there is an epigenetic link between poverty and depression.

The new results, which were produced by a team of scientists at Duke University, focused on adolescents who grew up in households with lower socioeconomic status. The scientists followed the adolescents for more than 3 years while collecting genetic, brain imaging, and behavioral data. Ultimately, the scientists determined that these adolescents accumulated greater quantities of a chemical tag on a depression-linked gene. This finding, the scientists noted, could lead to biological predictors that could guide individualized depression-prevention strategies.

Details of the current study appeared May 24 in the journal Molecular Psychiatry, in an article entitled, “An Epigenetic Mechanism Links Socioeconomic Status to Changes in Depression-Related Brain Function in High-Risk Adolescents.” According to this article, the more chemical tags an individual had near a gene called SLC6A4, the more responsive was their amygdala—a brain area that coordinates the body's reactions to threat–to photographs of fearful faces as they underwent functional magnetic resonance imaging (MRI) brain scans. Participants with a more active amygdala were more likely to later report symptoms of depression.

“Using prospective longitudinal epigenetic, neuroimaging and behavioral data from 132 adolescents, we demonstrate that changes in gene methylation associated with lower socioeconomic status (SES) predict changes in risk-related brain function,” wrote the authors of the study. “Specifically, we find that lower SES during adolescence is associated with an increase in methylation of the proximal promoter of the serotonin transporter gene, which predicts greater increases in threat-related amygdala reactivity.”

These initial results, the authors noted, suggest a specific biological mechanism through which adversity contributes to altered brain function, which in turn moderates the emergence of general liability as individual risk for mental illness.

The study included 132 non-Hispanic Caucasian adolescents in the Teen Alcohol Outcomes Study (TAOS) who were between 11 and 15 years old at the outset of the study and came from households that ranged from low to high SES. About half of the participants had a family history of depression.

“The biggest risk factor we have currently for depression is a family history of the disorder,” said study co-author Douglas Williamson, principal investigator of TAOS and professor of psychiatry and behavioral sciences at Duke. “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 2014, Williamson and Ahmad Hariri, a Duke professor of psychology and neuroscience and a co-author of the current study, first showed that the presence of marks near the SLC6A4 gene can predict the way a person's amygdala responds to threat. That study included both Williamson's TAOS and participants in Hariri's Duke Neurogenetics Study, but had looked at the chemical tags at a single point in time.

Looking at the changes in these markers over an extended time is a more powerful way to understand an individual's risk for depression, said Hariri, who is also a member of the Duke Institute for Brain Sciences.

The Duke team is now searching the genome for new markers that would predict depression. Ultimately, a panel of markers used in combination will lead to more accurate predictions. The team also hopes to expand the age ranges of the study to include younger individuals and to continue following the TAOS participants into young adulthood.

“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.”

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