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Psychoneuroendocrinology. 2015 Jan;51:403-13. doi: 10.1016/j.psyneuen.2014.10.016. Epub 2014 Oct 25.

Early origins of inflammation: An examination of prenatal and childhood social adversity in a prospective cohort study.

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Department of Epidemiology and Biostatistics, University of Maryland College Park, School of Public Health, College Park, United States. Electronic address:
Department of Epidemiology, Brown University, Providence, United States.
Department of Epidemiology and Biostatistics, University at Albany, School of Public Health, Rensselaer, United States.
Department of Social and Behavioral Sciences, Harvard School of Public Health, Boston, United States.
Department of Anthropology, Vanderbilt University, Nashville, United States.
Department of Social and Behavioral Sciences, Harvard School of Public Health, Boston, United States; Department of Epidemiology, Harvard School of Public Health, Boston, United States; Department of Psychiatry, Massachusetts General Hospital, Boston, United States.



Children exposed to social adversity carry a greater risk of poor physical and mental health into adulthood. This increased risk is thought to be due, in part, to inflammatory processes associated with early adversity that contribute to the etiology of many adult illnesses. The current study asks whether aspects of the prenatal social environment are associated with levels of inflammation in adulthood, and whether prenatal and childhood adversity both contribute to adult inflammation.


We examined associations of prenatal and childhood adversity assessed through direct interviews of participants in the Collaborative Perinatal Project between 1959 and 1974 with blood levels of C-reactive protein in 355 offspring interviewed in adulthood (mean age=42.2 years). Linear and quantile regression models were used to estimate the effects of prenatal adversity and childhood adversity on adult inflammation, adjusting for age, sex, and race and other potential confounders.


In separate linear regression models, high levels of prenatal and childhood adversity were associated with higher CRP in adulthood. When prenatal and childhood adversity were analyzed together, our results support the presence of an effect of prenatal adversity on (log) CRP level in adulthood (β=0.73, 95% CI: 0.26, 1.20) that is independent of childhood adversity and potential confounding factors including maternal health conditions reported during pregnancy. Supplemental analyses revealed similar findings using quantile regression models and logistic regression models that used a clinically-relevant CRP threshold (>3mg/L). In a fully-adjusted model that included childhood adversity, high prenatal adversity was associated with a 3-fold elevated odds (95% CI: 1.15, 8.02) of having a CRP level in adulthood that indicates high risk of cardiovascular disease.


Social adversity during the prenatal period is a risk factor for elevated inflammation in adulthood independent of adversities during childhood. This evidence is consistent with studies demonstrating that adverse exposures in the maternal environment during gestation have lasting effects on development of the immune system. If these results reflect causal associations, they suggest that interventions to improve the social and environmental conditions of pregnancy would promote health over the life course. It remains necessary to identify the mechanisms that link maternal conditions during pregnancy to the development of fetal immune and other systems involved in adaptation to environmental stressors.


Adult; C-reactive protein; Childhood adversity; Cohort study; Inflammation; Longitudinal; Prenatal exposure; Stress

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