DOI 10.1016/j.sjpmh.2026.02.003
Associations between social cognition and inflammatory markers in eating disorders and borderline personality disorder.
Аннотация
INTRODUCTION/
OBJECTIVES
Eating disorders (EDs) and borderline personality disorder (BPD) are severe psychiatric conditions characterized by emotional dysregulation and impairments in social cognition. Growing evidence suggests that inflammatory and oxidative stress pathways may contribute to their pathophysiology. The present study aimed to explore the association between social cognition performance and immune-inflammatory and oxidative stress biomarkers in individuals with BPD, restrictive ED (EDR), and purging ED (EDP) vs healthy controls (HC), using a pathway-based psychoneuroimmunological approach.
METHODS
We studied a total of 100 adult women (EDR, EDP, BPD, and HC) using the Movie for the Assessment of Social Cognition (MASC) and a comprehensive clinical battery. Blood samples were drawn to quantify inflammatory, oxidative stress, and antioxidant biomarkers, including intracellular signaling pathways. Group comparisons and group-specific Bayesian Lasso regression analyses were conducted to examine within-group associations between biomarkers and social cognition outcomes, controlling for relevant clinical and demographic covariates.
RESULTS
Participants with BPD and EDP showed greater psychological dysregulation, higher impulsivity, and increased activation of pro-inflammatory and oxidative stress pathways vs HC. The EDR group displayed an intermediate biological and clinical profile. Social cognition impairments were observed across clinical groups, with BPD participants exhibiting the highest hypomentalization. Exploratory regression analyses revealed diagnosis-specific associations between social cognition performance and immune-inflammatory pathways, particularly involving markers related to p38 MAPK, JNK, COX-2, and oxidative stress, with no significant associations observed in healthy controls.
CONCLUSIONS
The findings support a psychoneuroimmunological model in which social cognition impairments are associated with diagnosis-specific interactions between immune-inflammatory regulation and clinical phenotype in EDs and BPD. Because of the exploratory and cross-sectional design, these results should be considered hypothesis-generating and warrant replication in longitudinal studies.
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