Sex-specific associations between childhood trauma and adult systemic inflammation in daily life.

OBJECTIVE: Childhood trauma may contribute to lifelong health through chronic systemic inflammation. However, associations between childhood trauma and inflammation are mixed, indicating that distinct types of childhood trauma may relate to inflammation differently. Moreover, most studies use a single assessment of inflammatory markers that may not reliably estimate stable interindividual differences. The current study is the first to examine relationships between childhood trauma and an ecologically valid measure of inflammation derived from repeated assessments of interleukin (IL)-6 in daily life. We also examine the possibility that glucocorticoid sensitivity and patterns of daily cortisol may contribute to observed associations. Finally, we explore whether biological sex moderates relationships between childhood trauma and IL-6. METHOD: Participants were 283 healthy adults aged 40-64 (57% female, 23% Black, Indigenous, and People of Color) who completed the Childhood Trauma Questionnaire and self-collected dried blood spots at home on 4 days to measure IL-6. Measures of salivary cortisol and blood-based glucocorticoid sensitivity were also assessed. RESULTS: Childhood trauma was not associated with IL-6 in the sample as a whole. However, exploratory analyses showed that childhood trauma related to IL-6 differently for males and females, such that total trauma and emotional neglect predicted higher IL-6 for males but not females. Results persisted after adjustment for covariates. There was no evidence for indirect effects via cortisol or glucocorticoid sensitivity. CONCLUSIONS: Childhood trauma and, specifically, emotional neglect were associated with IL-6 in daily life among middle-aged males. Additional research is needed to elucidate biological and behavioral pathways underlying these associations. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

A systematic review and meta-analysis of the stability of peripheral immune markers in healthy adults.

Peripheral immune markers are widely used to predict risk for inflammatory disease. However, whether single assessments of inflammatory biomarkers represent stable individual differences remains unclear. We reviewed 50 studies (N = 48,674; 57 % male; mean age 54 (range 13-79) years) that assessed markers of inflammation on >1 occasion, with time between measures ranging from 24 h to 7+ years. Separate random effects meta-analyses were conducted for each inflammatory marker and time interval. Markers that had broad coverage across most time intervals included C-reactive protein (CRP; k = 37), interleukin (IL)-6 (k = 22), TNF-α (k = 10), and fibrinogen (Fg; k = 9). For CRP, IL-6, and TNF-α, stability estimates generally decreased with time, with strong to moderate stability over intervals <6 months (r's = 0.80-0.61), modest to moderate stability over 6 months - 3 years (r's = 0.60-0.51), and low stability for >3 years (r's = 0.39-0.30). Estimates were less reliable for Fg for time intervals ≤ 3 years although they generally followed the same pattern; more reliable findings suggested greater stability for Fg than other markers for intervals >3 years (r = 0.53). These findings suggest that single measures of inflammatory biomarkers may be an adequate index of stable individual differences in the short term (<6 months), with repeated measures of inflammatory biomarkers recommended over intervals ≥ 6 months to 3 years, and absolutely necessary over intervals >3 years to reliably identify stable individual differences in health risk. These findings are consistent with stability estimates and clinical recommendations for repeated measurement of other cardiovascular measures of risk (e.g., blood lipids, blood pressure).