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.

Public Health Relevance

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.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD058502-06
Application #
8425987
Study Section
Special Emphasis Panel (ZRG1-RPHB-K (50))
Program Officer
King, Rosalind B
Project Start
2008-12-01
Project End
2014-11-30
Budget Start
2012-12-01
Budget End
2014-11-30
Support Year
6
Fiscal Year
2013
Total Cost
$300,793
Indirect Cost
$106,105
Name
Northwestern University at Chicago
Department
Other Health Professions
Type
Organized Research Units
DUNS #
160079455
City
Evanston
State
IL
Country
United States
Zip Code
60201
Hostinar, Camelia E; Davidson, Richard J; Graham, Eileen K et al. (2016) Frontal brain asymmetry, childhood maltreatment, and low-grade inflammation at midlife. Psychoneuroendocrinology 75:152-163
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
Jiang, Ruiwei; Jones, Meaghan J; Chen, Edith et al. (2015) Discordance of DNA methylation variance between two accessible human tissues. Sci Rep 5:8257
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
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
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

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