Link between childhood poverty, neural responsivity predicts inflammation
Poverty during childhood is associated with accentuated neural-immune signaling, a study has shown.
This is consistent with the neuroimmune network hypothesis, which suggests that early-life stress initiates a positive feedback loop between peripheral inflammatory cells and networked brain regions involved in threat and reward processing.
The authors assessed the basic predictions of the neuroimmune network hypothesis in 207 urban children from diverse socioeconomic backgroups (mean age 13.9 years, 63 percent female, 33 percent Black, 30 percent Hispanic), focusing on poverty as a stressor.
The children had fasting blood drawn to measure the following inflammatory biomarkers: C-reactive protein, tumour necrosis factor-α, and interleukins-6, -8, and -10. A composite score was obtained by averaging these biomarkers. The participants also completed two functional magnetic resonance imaging tasks, which measured amygdala responsivity to angry facial expression and ventral striatum responsivity to monetary rewards.
Inflammation was predicted by the statistical interaction between poverty status and neural responsivity. Amygdala threat responsivity positively correlated with inflammation among children living in poverty, as did ventral striatum responsivity to reward. These brain-immune associations weakened as children’s socioeconomic conditions improved.
Sensitivity analyses revealed that the above patterns were robust to alternative measures of socioeconomic status and were independent of age, sex, racial and ethnic identity, and pubertal status. In addition, the correlations were condition-specific; no interactions were evident for amygdala responsivity to neutral faces or striatal responsivity to monetary losses.
“Children exposed to severe, chronic stress are vulnerable to mental and physical health problems across the lifespan,” the authors said.