“[I]f replicated, the risk pathway identified here could represent a discrete biomarker that could be targeted by novel strategies for personalized treatment and prevention,” Johnna Swartz, Ph.D., a postdoctoral associate in the Department of Psychology and Neuroscience at Duke University, and colleagues wrote.
For the study, the researchers analyzed epigenetic, neuroimaging, and behavioral data collected from 132 youth who were participants in the Teen Alcohol Outcomes Study (a multiyear study examining the association between the development of depression and alcohol use disorders in adolescence). Adolescents were between 11 and 15 years old during the first wave of data collection, 13 and 18 at Wave 2, and 14 and 19 at Wave 3.
Lower socioeconomic status—as defined by parental education and income—at Wave 1 predicted greater increase in methylation of the proximal promoter region of the serotonin transporter gene SLC6A4 two years later (Wave 2), with or without a family history of mental illness. Analysis of fMRI data revealed that increases in SLC6A4 methylation from Wave 1 to Wave 2 were also associated with increases in threat-related amygdala reactivity over the same period. In adolescents with a positive family history of depression, greater increases in reactivity from Wave 1 to Wave 2 prospectively predicted greater increases in depressive symptoms from Wave 2 to Wave 3; there was no such relationship in adolescents without a family history of depression.
“It is possible that these high-risk adolescents experience additional forms of chronic adversity such as parental neglect or familial discord uncommon among their low-risk counterparts and that this additional exposure is necessary to trigger symptoms of depression,” Swartz and colleagues concluded. “[O]ur results identify a specific biological pathway through which broader environmental adversity may act to drive individual vulnerability for depression among at-risk adolescents.”
For related information, see the Psychiatric News article “Researchers Tackle Complexity of Intergenerational Stress Transmission.”