Childhood victimization and inflammation in young adulthood: A genetically sensitive cohort study.

Published

Journal Article

OBJECTIVE:Childhood victimization is an important risk factor for later immune-related disorders. Previous evidence has demonstrated that childhood victimization is associated with elevated levels of inflammation biomarkers measured decades after exposure. However, it is unclear whether this association is (1) already detectable in young people, (2) different in males and females, and (3) confounded by genetic liability to inflammation. Here we sought to address these questions. METHOD:Participants were 2232 children followed from birth to age 18years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18years. Latent genetic liability for high inflammation levels was assessed through a twin-based method. RESULTS:Greater exposure to childhood victimization was associated with higher CRP levels at age 18 (serum-equivalent means were 0.65 in non-victimized Study members, 0.74 in those exposed to one victimization type, and 0.81 in those exposed to poly-victimization; p=0.018). However, this association was driven by a significant association in females (serum-equivalent means were 0.75 in non-victimized females, 0.87 in those exposed to one type of victimization, and 1.19 in those exposed to poly-victimization; p=0.010), while no significant association was observed in males (p=0.19). Victimized females showed elevated CRP levels independent of latent genetic influence, as well as childhood socioeconomic status, and waist-hip ratio and body temperature at the time of CRP assessment. CONCLUSION:Childhood victimization is associated with elevated CRP levels in young women, independent of latent genetic influences and other key risk factors. These results strengthen causal inference about the effects of childhood victimization on inflammation levels in females by accounting for potential genetic confounding.

Full Text

Duke Authors

Cited Authors

  • Baldwin, JR; Arseneault, L; Caspi, A; Fisher, HL; Moffitt, TE; Odgers, CL; Pariante, C; Ambler, A; Dove, R; Kepa, A; Matthews, T; Menard, A; Sugden, K; Williams, B; Danese, A

Published Date

  • January 2018

Published In

Volume / Issue

  • 67 /

Start / End Page

  • 211 - 217

PubMed ID

  • 28867281

Pubmed Central ID

  • 28867281

Electronic International Standard Serial Number (EISSN)

  • 1090-2139

International Standard Serial Number (ISSN)

  • 0889-1591

Digital Object Identifier (DOI)

  • 10.1016/j.bbi.2017.08.025

Language

  • eng