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.
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|Hostinar, Camelia E; Davidson, Richard J; Graham, Eileen K et al. (2017) Frontal brain asymmetry, childhood maltreatment, and low-grade inflammation at midlife. Psychoneuroendocrinology 75:152-163|
|Hostinar, Camelia E; Ross, Kharah M; Chen, Edith et al. (2017) Early-Life Socioeconomic Disadvantage and Metabolic Health Disparities. Psychosom Med 79:514-523|
|Ehrlich, Katherine B; Ross, Kharah M; Chen, Edith et al. (2016) Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype? Dev Psychopathol 28:1273-1283|
|Chan, Meanne; Miller, Gregory E; Chen, Edith (2016) Early life socioeconomic status and metabolic outcomes in adolescents: The role of implicit affect about one's family. Health Psychol 35:387-96|
|Ehrlich, Katherine B; Miller, Gregory E; Chen, Edith (2015) Harsh parent-child conflict is associated with decreased anti-inflammatory gene expression and increased symptom severity in children with asthma. Dev Psychopathol 27:1547-54|
|Hostinar, Camelia E; Ross, Kharah M; Chen, Edith et al. (2015) Modeling the association between lifecourse socioeconomic disadvantage and systemic inflammation in healthy adults: The role of self-control. Health Psychol 34:580-90|
|Jiang, Ruiwei; Jones, Meaghan J; Chen, Edith et al. (2015) Discordance of DNA methylation variance between two accessible human tissues. Sci Rep 5:8257|
|Murphy, Michael L M; Slavich, George M; Chen, Edith et al. (2015) Targeted rejection predicts decreased anti-inflammatory gene expression and increased symptom severity in youth with asthma. Psychol Sci 26:111-21|
|Hostinar, Camelia E; Lachman, Margie E; Mroczek, Daniel K et al. (2015) Additive contributions of childhood adversity and recent stressors to inflammation at midlife: Findings from the MIDUS study. Dev Psychol 51:1630-44|
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