Does Sexual Trauma Accelerate Biological Aging? A Narrative Review of Epigenetic, Cellular, Endocrine, Inflammatory and Metabolic Pathways

Survivors of sexual violence carry a disproportionate burden of age-related morbidity, including cardiovascular disease, type 2 diabetes and inflammatory conditions, raising the possibility that sexual trauma accelerates the biology of aging rather than acting solely through psychological distress or health behaviors. This narrative review synthesizes translational, epidemiological and biomarker evidence across five mechanistic domains. Epigenetically, posttraumatic stress disorder (PTSD) is associated with accelerated DNA-methylation age, most consistently on the mortality-calibrated GrimAge clock, whereas meta-analytic evidence for cumulative childhood adversity on first- and second-generation clocks is weak. At the cellular level, severe childhood sexual abuse is associated with shorter leukocyte telomeres in several, though not all, studies, and PTSD with telomere(definition) attrition, T-cell senescence(definition) and oxidative DNA damage. Endocrinologically, childhood sexual abuse produces enduring hypothalamic-pituitary-adrenal axis sensitization and earlier pubertal maturation in girls. Inflammatory evidence is the most robust: childhood maltreatment prospectively predicts adult C-reactive protein, and PTSD is consistently associated with elevated pro-inflammatory cytokines. Metabolically, PTSD is associated with a high prevalence of metabolic syndrome, and childhood sexual abuse with obesity and type 2 diabetes in women. Glucocorticoid-FKBP5-NF-κB signaling and allostatic load emerge as bridges between domains, and we propose an integrated six-step model. Causal inference remains limited by retrospective trauma assessment, confounding by co-occurring adversity and scarce trauma-type-specific analyses. Priorities include prospective, sexual-trauma-specific multi-omic studies and trials testing whether trauma-focused, anti-inflammatory or metabolic interventions can slow the pace of biological aging in survivors.