Abstract
BACKGROUND: Childhood trauma is a well-established risk factor for greater severity and poorer prognosis of bipolar depression. While anhedonia particularly in the social domain is theorized to link early adversity to depressive symptoms, this specific pathway remains underexplored in bipolar disorder. METHODS: A cross-sectional study was conducted with 201 patients diagnosed with bipolar I disorder (current depressive episode). Childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ). Anhedonia was evaluated multidimensionally, including Revised Social Anhedonia Scale-Chinese Version (RSAS-C) and Revised Physical Anhedonia Scale-Chinese Version (RPAS-C). Depressive symptom severity was rated using the 17-item Hamilton Rating Scale for Depression (HAMD-17). Mediation analyses were performed using the PROCESS macro, controlling for age, sex, years of education, age of onset, illness duration, and psychotropic medication. RESULTS: Mediation analysis revealed that social anhedonia showed a significant indirect effect in the association between childhood trauma and depression severity (indirect effect B = 0.02, 95% CI [0.00, 0.04]). This mediating effect was most robust for emotional abuse (indirect effect B = 0.06, 95% CI [0.01, 0.14]). Notably, the direct path from emotional abuse to depression became non-significant after controlling for social anhedonia, suggesting that the effect of emotional abuse on depression is largely statistically accounted for by social anhedonia. In contrast, physical anhedonia showed no significant mediation effect. CONCLUSIONS: This study identifies social anhedonia as a critical mediator in the pathway from childhood emotional abuse to depressive severity in bipolar disorder. These findings highlight a specific psychosocial mechanism, suggesting that deficits in social reward processing may serve as a key link between early relational trauma and adult mood pathology. CLINICAL TRIAL NUMBER: Not applicable. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12888-026-08004-1.