FUNCTIONAL NEUROANATOMY OF SOCIAL ECONOMIC STRESS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Persons in the bottom decile of income are at 3-4 times higher risk of morbidity and premature mortality than persons of in the top decile. While a portion of this risk is attributed to behavioral and environmental factors, the biological mechanism mediating this response is not well understood. Recently, evidence has surfaced that psychological stress associated with perceived low socio-economic position (SEP) can disrupt neuroendocrine and immune function. It is plausible that these distruptions account for the biological changes underpinning the association between poverty and mortality. However, it is not known how an individual's perceptions of SEP are neurologically transduced into physiological changes. The aim of this investigation is to examine the relationship between low SEP and the function of neural circuits that mediate the physiological stress response. Limited funds have been received to conduct a pilot cross-sectional neuroimaging and physiologic monitoring study on persons raised in low income households versus persons raised in high income households. However, this funding does not include subject participation incentive costs or release time from teaching needed to perform administrative funcitons and project oversight. If differences in neural activity in brain circuits mediating the stress response are found, further funding for a prospective study will be sought. Hypothesis: We hypothesize that images with socioeconomic content coupled with a cognitive task will produce differential levels of stress by social class. This will be measured by activation of areas in the brain that mediate the stress response and will also lead to subsequent increases in autonomic output. Moreover, we hypothesize that recall tasks of neutral content will produce no difference in stress response by SEP.