Psychiatry Research · Mar 10, 2026
Longitudinal associations among childhood trauma, oxytocin, and metabolic risk in schizophrenia
By Goh KK, Chen PY, Chang HM et al.
Childhood trauma has been consistently associated with adverse physical and metabolic outcomes in schizophrenia, yet the neurobiological mechanisms translating early-life adversity into long-term metabolic risk remain unclear. Oxytocin, a stress-sensitive neuropeptide involved in metabolic regulation, may modulate stress-related metabolic vulnerability. In this 24-month prospective cohort study, 90 individuals with schizophrenia receiving stable antipsychotic monotherapy and 60 age- and sex-matched healthy controls underwent assessments of anthropometric measures, metabolic parameters, and plasma oxytocin levels at baseline and follow-up. Metabolic outcomes included Continuous Metabolic Syndrome Severity Scores (cMetS-S) and metabolic syndrome (MetS) incidence, while childhood trauma was assessed using the Childhood Trauma Questionnaire-Short Form with cross-validation interviews. Generalized estimating equations were applied to evaluate longitudinal associations, and moderation analyses tested oxytocin × childhood trauma interactions. Greater childhood trauma exposure was associated with lower plasma oxytocin levels (p = .001), higher body mass index (p < .001), and greater metabolic burden over time (p = .009). At 24-month follow-up, individuals with schizophrenia exhibited higher MetS incidence (p = .043) and higher cMetS-S (p = .006) compared with healthy controls.Lower oxytocin levels predicted increased MetS risk (OR = 0.27, p = .009). Importantly, a significant childhood trauma × oxytocin interaction (OR = 0.95, p = .018) indicated that higher oxytocin levels attenuated trauma-related metabolic deterioration. These findings suggest that oxytocinergic dysregulation may be involved in the association between early-life trauma and metabolic risk in schizophrenia and support oxytocin as a candidate biomarker associated with trauma-related metabolic vulnerability.
doi.org/10.1016/j.psychres.2026.117088PubMed 41855641Populations