Volume 67, January 2018, Pages 211-217
aMRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
bDepartment of Psychology and Neuroscience, Duke University, Durham, NC, USA
cDepartment of Psychiatry and Behavioral Sciences, Duke University, Durham, NC, USA
dDepartment of Psychology and Social Behavior, University of California, Irvine, Irvine, CA, USA
eSanford School of Public Policy, Duke University, Durham, NC, USA
fDepartment of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
gDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
hNational and Specialist CAMHS Trauma and Anxiety Clinic, South London and Maudsley NHS Foundation Trust, London, UK
Received 22 June 2017, Revised 15 August 2017, Accepted 24 August 2017, Available online 1 September 2017.
Under a Creative Commons license open access
•Childhood victimization predicted elevated levels of CRP at age 18
•The association between child victimization and CRP levels was specific to females.
•Latent genetic influences on CRP levels did not explain the association in females.
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.
Participants were 2232 children followed from birth to age 18 years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12 years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18 years. Latent genetic liability for high inflammation levels was assessed through a twin-based method.
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.
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.