Socioeconomic status (SES) during early life is an important determinant of vulnerability to cardiovascular disease in adulthood. Because these effects are not simply a result of the more direct influences of social standing in adulthood, they raise challenging mechanistic questions about how early-life SES gets biologically embedded for the long-term. This proposal advances an epigenetic programming hypothesis to explain this process. It posits that psychosocial experiences associated with low early-life SES are programmed in the genome via epigenetic mechanisms, or acquired changes in genomic activity that are not due to changes in DNA sequence. In a study of 420 volunteers, we will evaluate the hypothesis that individuals who spent their early years in low-SES environments were exposed to greater familial turmoil and have developed vigilant, pessimistic outlooks on life. We further expect these experiences to have become embedded in the immune system through epigenetic modifications, and to manifest as a pro-inflammatory phenotype beginning in adolescence and persisting through adulthood. This phenotype will be characterized by activation of pro-inflammatory transcription control pathways and increased concentrations of the inflammatory biomarkers C-reactive protein and interleukin-6. This work will shed light on the biobehavioral mechanisms underlying SES disparities, with implications for preventative interventions.
Individuals who spend the early years of their lives in poverty are more likely to develop heart disease and other medical conditions when they reach adulthood. This research project attempts to identify the mechanisms underlying this phenomenon. It examines the idea that poverty in early childhood changes the way the immune system functions, and does so in a fashion that persists across the lifespan and renders a person vulnerable to diseases in adulthood.
|Miller, Gregory E; Brody, Gene H; Yu, Tianyi et al. (2014) A family-oriented psychosocial intervention reduces inflammation in low-SES African American youth. Proc Natl Acad Sci U S A 111:11287-92|
|Ross, Kharah M; Murphy, Michael L M; Adam, Emma K et al. (2014) How stable are diurnal cortisol activity indices in healthy individuals? Evidence from three multi-wave studies. Psychoneuroendocrinology 39:184-93|
|Ross, Kharah M; McDonald-Jones, Gaye; Miller, Gregory E (2013) Oxytocin does not attenuate the ex vivo production of inflammatory cytokines by lipopolysaccharide-activated monocytes and macrophages from healthy male and female donors. Neuroimmunomodulation 20:285-93|
|Murphy, Michael L M; Slavich, George M; Rohleder, Nicolas et al. (2013) Targeted Rejection Triggers Differential Pro- and Anti-Inflammatory Gene Expression in Adolescents as a Function of Social Status. Clin Psychol Sci 1:30-40|
|Powell, Nicole D; Sloan, Erica K; Bailey, Michael T et al. (2013) Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via *-adrenergic induction of myelopoiesis. Proc Natl Acad Sci U S A 110:16574-9|
|Miller, Gregory E; Chen, Edith (2013) The Biological Residue of Childhood Poverty. Child Dev Perspect 7:67-73|
|Chen, Edith; Miller, Gregory E (2013) Socioeconomic status and health: mediating and moderating factors. Annu Rev Clin Psychol 9:723-49|
|Rueggeberg, Rebecca; Wrosch, Carsten; Miller, Gregory E (2012) The different roles of perceived stress in the association between older adults' physical activity and physical health. Health Psychol 31:164-71|
|Chen, E; Miller, G E; Kobor, M S et al. (2011) Maternal warmth buffers the effects of low early-life socioeconomic status on pro-inflammatory signaling in adulthood. Mol Psychiatry 16:729-37|
|Wrosch, Carsten; Amir, Ella; Miller, Gregory E (2011) Goal adjustment capacities, coping, and subjective well-being: the sample case of caregiving for a family member with mental illness. J Pers Soc Psychol 100:934-46|
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