Hepatic function is associated with cognitive function in patients with stable schizophrenia

The liver-brain axis, mediated by inflammatory cytokines, metabolic byproducts, and oxidative stress, shares pathological pathways with schizophrenia neurobiology. Despite this overlap, direct clinical evidence linking hepatic function indicators to psychiatric symptoms or cognitive function in schizophrenia remains limited. Therefore, this study investigated associations between clinical hepatic function indicators and both psychiatric symptoms and cognitive performance in individuals with stable schizophrenia. A cross-sectional study was conducted among 170 inpatients with clinically stable schizophrenia. Liver function indicators were obtained from fasting venous blood samples. Psychiatric symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS), and cognitive function was assessed with the Montreal Cognitive Assessment–Chinese version (MoCA-C). Multiple linear regression models, adjusted for covariates, were used to examine associations between hepatic indicators and outcomes (PANSS total/subscale scores; MoCA-C total score). After covariate adjustment, total bilirubin (TBil) (β = 0.29, 95% CI: 0.08–0.51; P = 0.008) and indirect bilirubin (IDBil) (β = 0.48, 95% CI: 0.17–0.80; P = 0.003) were significantly positively associated with MoCA-C scores. No significant associations were observed between any hepatic indicators and PANSS total/subscale scores. In this cross-sectional study of clinically stable schizophrenia, higher TBil and IDBil levels were associated with better cognitive performance. These findings suggest a potential role of bilirubin metabolism in cognitive function in schizophrenia, highlighting the need for further investigation into its relevance for cognitive impairment management.