The relationship between adverse childhood experiences and pro-inflammatory analytes and the mediating role of cortisol

Abstract

Adverse childhood experiences (ACEs) are harmful experiences that have occurred during the developing years of life. ACEs often include maltreatment, household dysfunctions and other traumatic events. People with ACEs have been found to be at greater risk of pulmonary, cardiovascular and auto-immune diseases. Recent research has suggested that the epigenetic regulation occurring as a result of these ACEs can program macrophages to sustain inflammatory processes and therefore contribute to the development of these diseases. As one of the primary responders to stress, cortisol is also a suppressor of inflammation. Therefore, dysregulation of the cortisol levels, chronically high or low, also brought forth by ACEs exposure can affect inflammation. The purpose of the current study was to investigate the relationship between ACEs exposure and physiological measures including cortisol and different pro-inflammatory analytes. This cross-sectional study included follow-up data from 156 participants as part of the Niagara Longitudinal Heart Study. Out of the 156 participants, a final sample of 101, with 23 males and 78 females, complete with physiological measures was included in the analyses. The current study collected ACEs data from questionnaire, cortisol from hair, and inflammatory analytes including CRP, IL-6Rα, gp130, sTNFr1, sTNFr2, IFN-γ, and IL-10 from blood. Total ACEs score was negatively associated with cortisol levels. Every additional exposure to a type of ACEs decreased cortisol levels by 21.2 (pg/mg) on average. Exposure to ACEs was positively associated with IL-6Rα but was not associated with all other inflammatory analytes. Every additional exposure to a type of ACEs increased IL-6Rα levels by 284.6 (pg/mL) on average. In contrast to previous literature, sex differences from the regression analyses were also found in the current study among the inflammatory analytes CRP, IL-6Rα, sTNFr1, and IL-10. Cortisol did not mediate the relationship between exposure to ACEs and the different inflammatory analytes. The current study was limited in properly detecting associations as the pilot sample was underpowered. The proportion of cortisol availability in males was much lower than in females. The current study found that ACEs were associated with lowered chronic cortisol and elevated IL-6Rα.