4.3 Article

Early Life Adversity and Inflammation in African Americans and Whites in the Midlife in the United States Survey

Journal

PSYCHOSOMATIC MEDICINE
Volume 72, Issue 7, Pages 694-701

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PSY.0b013e3181e9c16f

Keywords

childhood; early life adversity; inflammation; life course epidemiology; race/ethnicity; chronic disease risk

Funding

  1. National Institute on Aging [P01-AG020166]
  2. John D. and Catherine T. MacArthur Foundation
  3. National Center for Research Resources, National Institutes of Health [1UL1RR025011]
  4. Canadian Institutes of Health
  5. National Heart, Lung and Blood Institute [HL092591]

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Objectives: To determine whether early life adversity (ELA) was predictive of inflammatory markers and to determine the consistency of these associations across racial groups. Methods: We analyzed data from 177 African Americans and 822 whites aged 35 to 86 years from two preliminary subsamples of the Midlife in the United States biomarker study. ELA was measured via retrospective self-report. We used multivariate linear regression models to examine the associations between ELA and C-reactive protein, interleukin-6, fibrinogen, endothelial leukocyte adhesion molecule-1, and soluble intercellular adhesion molecule-1, independent of age, gender, and medications. We extended race-stratified models to test three potential mechanisms for the observed associations. Results: Significant interactions between ELA and race were observed for all five biomarkers. Models stratified by race revealed that ELA predicted higher levels of log interleukin-6, fibrinogen, endothelial leukocyte adhesion molecule-1, and soluble intercellular adhesion molecule-1 among African Americans (p < .05), but not among whites. Some, but not all, of these associations were attenuated after adjustment for health behaviors and body mass index, adult stressors, and depressive symptoms. Conclusions: ELA was predictive of high concentrations of inflammatory markers at midlife for African Americans, but not whites. This pattern may be explained by an accelerated course of age-related disease development for African Americans.

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