Low socioeconomic status (SES) has been associated with distinct patterns of reward processing, which appear to have adverse implications for health outcomes, well-being, and human capital. However, most studies in this literature have used complex tasks that engage more than reward processing and/or retrospectively studied childhood SES in samples of adults. To clarify how SES relates to the development of reward processing tendencies, we measured income-to-poverty ratio (IPR) in 172 youth who subsequently underwent functional MRI while completing a passive avoidance task to assess neural responses to reward and loss information. Participants were 12–15 years old (mean = 13.94, SD = .52; 65.7% female) from a sample broadly representative of the Chicago area in terms of SES (IPR range = 0.1–34.53; mean = 3.90; SD = 4.15) and racial makeup (40.1% White 30.8% Black; 29.1% Hispanic). To the extent they had lower IPR, children displayed a trend toward worse behavioral performance on the passive avoidance task. Lower IPR also was associated with a greater response in attention brain regions to reward and loss cues and to reward and loss feedback. Lower IPR also was associated with reduced differentiation between reward and loss feedback in the ventromedial prefrontal and parietal cortex. The current data suggest that both increased salience of reward/loss information and reduced discrimination between reward and loss feedback could be factors linking SES with the development of human capital and health outcomes.

Growing up in poverty is associated with a heightened risk for mental and physical health problems across the life span, and there is a growing recognition of the role that social determinants of health play in driving these outcomes and inequities. How do the social conditions of poverty get under the skin to influence biology, and through what mechanisms do the stressors of poverty generate risk for a broad range of health problems? The growing field examining the neuroscience of socioeconomic status (SES) proposes that the brain is an entry point or pathway through which poverty and adversity become embedded in biology to generate these disparities. To date, however, the majority of research on the neuroscience of SES has focused on cognitive or executive control processes. However, the relationship between SES and brain systems involved in affective or emotional processes may be especially important for understanding social determinants of health. Accordingly, this Special Focus on The Affective Neuroscience of Poverty invited contributions from authors examining the relationship between SES and brain systems involved in generating and regulating emotions. In this editorial introduction, we (a) provide an overview of the neuroscience of SES; (b) introduce each of the articles in this Special Focus; and (c) discuss the scientific, treatment, and policy implications of studying the affective neuroscience of poverty.

Anxiolytic effects of perceived control have been observed across species. In humans, neuroimaging studies have suggested that perceived control and cognitive reappraisal reduce negative affect through similar mechanisms. An important limitation of extant neuroimaging studies of perceived control in terms of directly testing this hypothesis, however, is the use of within-subject designs, which confound participants' affective response to controllable and uncontrollable stress. To compare neural and affective responses when participants were exposed to either uncontrollable or controllable stress, two groups of participants received an identical series of stressors (thermal pain stimuli). One group (“controllable”) was led to believe they had behavioral control over the pain stimuli, whereas another (“uncontrollable”) believed they had no control. Controllable pain was associated with decreased state anxiety, decreased activation in amygdala, and increased activation in nucleus accumbens. In participants who perceived control over the pain, reduced state anxiety was associated with increased functional connectivity between each of these regions and ventral lateral/ventral medial pFC. The location of pFC findings is consistent with regions found to be critical for the anxiolytic effects of perceived control in rodents. Furthermore, interactions observed between pFC and both amygdala and nucleus accumbens are remarkably similar to neural mechanisms of emotion regulation through reappraisal in humans. These results suggest that perceived control reduces negative affect through a general mechanism involved in the cognitive regulation of emotion.