Abstract: Fibromyalgia is a chronic multisymptom disorder characterized by widespread pain, fatigue, sleep disturbance, cognitive dysfunction, and high comorbidity with mood disorders. Increasing evidence implicates psychological stress and trauma — particularly early-life adverse experiences — in the onset and severity of fibromyalgia. The pathways linking stress and trauma to fibromyalgia risk and expression are complex and likely involve neuroendocrine dysregulation (notably hypothalamic-pituitary-adrenal [HPA] axis and autonomic nervous system dysfunction), neuroinflammation, altered central pain processing (central sensitization), and epigenetic modifications including DNA methylation, histone modifications, and noncoding RNAs (e.g., microRNAs). Epigenetic changes offer a compelling mechanistic bridge between environmental exposures (stress/trauma) and persistent changes in gene expression relevant to pain, immune function, and stress reactivity. This paper synthesizes contemporary evidence linking psychological stress and trauma to epigenetic alterations observed in fibromyalgia, reviews candidate epigenetic biomarkers and mechanisms, discusses implications for diagnosis and treatment, and suggests priorities for future research.

Keywords:Fibromyalgia; Psychological stress; Trauma; Epigenetics; DNA methylation; Neuroinflammation.