Relationships between childhood adversity and inflammatory biomarkers in adulthood: A cross-sectional analysis of a middle-to older-aged population

Abstract

BackgroundExposure to adverse childhood experiences (ACEs) has been linked with increased cardiometabolic risk in adulthood. Low-grade systemic inflammation may underlie this association. Thus far, however, there has been limited investigation of later life inflammatory biomarkers in the context of childhood adversity. ObjectivesTo assess ACE history, and ACE subcategory, relationships with a broad range of inflammatory biomarkers in middle-to older-aged adults to test the hypothesis that ACE exposure is associated with an unfavourable inflammatory profile in adulthood and determine whether associations vary by ACE subtype and sex. MethodsThis study used data from a random sample of 1,839 men and women aged 46–74 years. Participant exposure to ACEs (overall and subtypes including abuse, neglect and household dysfunction) was determined using a validated 10-item ACE questionnaire. Inflammatory biomarkers (pro-inflammatory cytokines, adipocytokines, acute-phase response proteins, white blood cell counts and their constituents, coagulation factors and glycoprotein acetyl) were measured from participant blood samples. Linear regression analyses examined relationships between ACE history (overall and each subcategory) and inflammatory biomarkers in adulthood, controlling for potential confounders. Sex-stratified and mediation analyses were also conducted. ResultsIn age and sex-adjusted models, ACE history was significantly associated with higher c-reactive protein (p = 0.027), resistin (p = 0.024), white blood cell count (WBC) (p = 0.034), monocyte (p = 0.044), eosinophil (p = 0.031) and plasminogen activator inhibitor-1 (p = 0.047) concentrations, and lower adiponectin (p = 0.025) levels. Results from stratified analyses indicated sex differences and ACE subtype specific associations, with household dysfunction identified as the main driver of positive ACE associations with WBCs and constituents (all p < 0.05). Mediation analyses suggested that BMI and smoking mediate relationships between ACE exposures and increased inflammation. ConclusionsThis study provides evidence that ACE exposure may be associated with more pro-inflammatory and pro-thrombotic profiles in adulthood. Associations differed according to ACE subtype, and sex differences exist, which may influence cardiometabolic risk.