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Association Between Circulating Cytokines and Psychosomatic Syndromes in Patients with Mood Disorders.

Year: 2025

Type: article

Abstract: Objective: elevated levels of pro-inflammatory cytokines are frequently observed in mood disorders, but their relationship with psychosomatic symptomatology remains underexplored. This study aimed to examine whether interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) are associated with psychosomatic syndromes in patients with major depression (MD) and bipolar depression (BD), and whether these associations are moderated by sex. Method: seventy-seven outpatients with MD or BD were assessed using the Diagnostic Criteria for Psychosomatic Research-Revised (DCPR-R) and the Patient Health Questionnaire-15 (PHQ-15) to evaluate psychosomatic symptoms. Depression and mania severity were measured with the Beck Depression Inventory-II (BDI-II) and the Mania Rating Scale (MRS). Circulating levels of IL-6 and TNF-α were analyzed. Associations were tested using multivariate regression and mediation analyses, controlling for demographic and health-related variables. Results: both IL-6 and TNF-α were significantly associated with psychosomatic syndromes (as per DCPR-R) and PHQ-15 scores. IL-6, in particular, showed a strong association with persistent somatization (PS). These relationships remained significant after adjusting for affective-cognitive depressive symptoms and potential confounders. No significant moderating effect of sex was identified. Mediation analyses suggested that psychosomatic syndromes mediate the relationship between inflammatory cytokines and depressive symptomatology. Conclusions: findings suggest that the link between inflammation and mood disorders is more closely related to psychosomatic syndromes than to mood symptoms alone. Elevated IL-6 levels may reflect somatization processes within depression rather than being directly pro-depressive. Psychosomatic syndromes may thus represent a key clinical and therapeutic target in mood disorders with elevated inflammation.

Source: PubMed

DOI: 10.36131/cnfioritieditore20250605