Biological embedding from adverse childhood experiences in the development of an altered inflammatory state and poor health outcomes in young adults

Abstract

Abstract Exposure to emotional, physical, and/or sexual abuse as a child, cumulatively referred to as Adverse Childhood Experiences (ACEs), has been linked with poor health outcomes in early adulthood. Toward a mechanistic explanation for this link, dysregulated inflammation has garnered attention as a potential ‘social-immunological’ axis. Altered immune profiles are associated with ACEs and may contribute to mental health status, cardiovascular disease, and early mortality. Increases in circulating interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor α (TNFα) have been detected in individuals exposed to ACEs and are proposed to signal an immunological link to these outcomes. While this sets the stage in characterizing the inflammatory profile, gaps remain in the cast of mediators involved, preventing a more refined mechanistic view. We thus aim to expand the associated immunological cast. A sample of young adults from the Niagara Longitudinal Heart Study self-reported early life trauma (ACEs), and serum levels of a panel of immune biomarkers were quantified. We confirm that levels of IL-6, CRP and TNFα are altered, but also further identify new immune biomarkers that are significantly correlated (p<0.05) with ACEs, including pentraxin, chitinase, and interferons. This further refines the nature of ACE-dependent immunological dysregulation and offers new insights into contributing mechanisms, potential early risk-factor detection, and/or therapeutic targets in those exposed to ACEs. This evidence encourages promotion of public health initiatives and psychosocial preventative interventions aimed at limiting early adversity and its sequalae as an investment in later health status/quality of life.