Resting state coupling between the amygdala and ventromedial prefrontal cortex is related to household income in childhood and indexes future psychological vulnerability to stress.

Published

Journal Article

While child poverty is a significant risk factor for poor mental health, the developmental pathways involved with these associations are poorly understood. To advance knowledge about these important linkages, the present study examined the developmental sequelae of childhood exposure to poverty in a multiyear longitudinal study. Here, we focused on exposure to poverty, neurobiological circuitry connected to emotion dysregulation, later exposure to stressful life events, and symptoms of psychopathology. We grounded our work in a biopsychosocial perspective, with a specific interest in "stress sensitization" and emotion dysregulation. Motivated by past work, we first tested whether exposure to poverty was related to changes in the resting-state coupling between two brain structures centrally involved with emotion processing and regulation (the amygdala and the ventromedial prefrontal cortex; vmPFC). As predicted, we found lower household income at age 10 was related to lower resting-state coupling between these areas at age 15. We then tested if variations in amygdala-vmPFC connectivity interacted with more contemporaneous stressors to predict challenges with mental health at age 16. In line with past reports showing risk for poor mental health is greatest in those exposed to early and then later, more contemporaneous stress, we predicted and found that lower vmPFC-amygdala coupling in the context of greater contemporaneous stress was related to higher levels of internalizing and externalizing symptoms. We believe these important interactions between neurobiology and life history are an additional vantage point for understanding risk and resiliency, and suggest avenues for prediction of psychopathology related to early life challenge.

Full Text

Duke Authors

Cited Authors

  • Hanson, JL; Albert, WD; Skinner, AT; Shen, SH; Dodge, KA; Lansford, JE

Published Date

  • August 2019

Published In

Volume / Issue

  • 31 / 3

Start / End Page

  • 1053 - 1066

PubMed ID

  • 31084654

Pubmed Central ID

  • 31084654

Electronic International Standard Serial Number (EISSN)

  • 1469-2198

International Standard Serial Number (ISSN)

  • 0954-5794

Digital Object Identifier (DOI)

  • 10.1017/s0954579419000592

Language

  • eng