Redox dysregulation, inflammation and mental health in adults with high risk of childhood maltreatment
摘要
Childhood maltreatment (CM) increases the risk of lifelong mental illness, yet the underlying biochemical mechanisms remain unclear. Oxidative stress (OS), alongside inflammation, may contribute to this link. This study examined whether OS mediates the link between CM and mental health in a highly vulnerable group of formerly out-of-home placed young adults and explored associations between OS and inflammatory markers. Data were collected from 131 participants (31% women, M age = 26.29 ± 3.5 years) with histories of youth residential care. CM was assessed using the Childhood Trauma Questionnaire (CTQ), and mental health via the Achenbach System of Empirically Based Assessment (ASEBA). Biomarkers of OS (Superoxide Dismutase [SOD], Glutathione Peroxidase/Glutathione Reductase ratio [GPx/GRed]) and inflammation (Interleukin-1 Receptor Antagonist [IL-1RA], Interleukin-6 [IL-6], Interleukin-10 [IL-10], C-Reactive Protein [CRP], Tumor Necrosis Factor [TNF𝛼]) were analyzed. Multiple regression models examined associations among CM, OS, inflammation, and mental health, adjusting for covariates. Greater CM exposure was associated with poorer mental health (b = 0.34, p < .001). Initial analyses indicated that GPx/GRed (b = 0.20, p = .04), —but not SOD— was related to CM, particularly emotional abuse (b = 0.21, p = .03). However, this association did not remain significant after adjusting for medication use, suggesting that medication may confound links between CM and redox biology. TNF𝛼 predicted current mental health problems (b = 0.22, p = .02), and OS and inflammatory markers were significantly interrelated. Neither OS nor inflammation mediated the CM–mental health relationship. These findings highlight a complex interplay between CM, OS, and inflammation in young adults with histories of residential care. They underscore the importance of considering medication effects when studying redox mechanisms and indicate that further research is needed to clarify the biological pathways linking CM to long-term mental health outcomes.