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Interplay between Stressful Life Events and Interleukin-1β on 12-week Antidepressant Response in Depressive Patients

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Objective: This study aimed to investigate the moderating effects of interleukin-1 (IL-1) on the relationship between stressful life events (SLEs) and antidepressant treatment outcomes over 12 weeks in patients with depressive disorders. Methods: Baseline assessments of SLEs, IL-1 levels, and other covariates were conducted for 1,094 depressive out patients with 1,086 followed up for 12 weeks. Antidepressant treatment was tailored according to clinician recom mendations and patient preferences, with outcomes evaluated at 12 weeks using the Hamilton depression rating scale. Logistic regression analyses explored the individual and interactive effects of SLEs and IL-1 on depression remission. Results: SLEs alone did not predict 12-week remission (OR = 0.93, 95% CI [0.82, 1.06]). However, IL-1 levels sig nificantly influenced outcomes (OR = 0.67, 95% CI [0.53, 0.87]), particularly in conjunction with high SLE exposure (Wald = 13.29, p < 0.001). Higher IL-1 levels were associated with lower odds of achieving remission in the group with two or more SLEs (OR = 0.46, 95% CI [0.33, 0.65]), whereas in the group with fewer than two SLEs, the odds were not significantly different (OR = 1.13, 95% CI [0.77, 1.65]). Conclusion: These findings highlight the critical role of both biological markers and environmental stressors in anti depressant treatment. IL-1 could serve as a biomarker for customizing antidepressant strategies, particularly in patients experiencing high SLE exposure, thereby enhancing treatment efficacy and personalized care. Future studies should include longitudinal assessments of IL-1 to further elucidate its dynamic role in depression pathology and treatment response.

Abstract

Objective: This study aimed to investigate the moderating effects of interleukin-1 (IL-1) on the relationship between stressful life events (SLEs) and antidepressant treatment outcomes over 12 weeks in patients with depressive disorders. Methods: Baseline assessments of SLEs, IL-1 levels, and other covariates were conducted for 1,094 depressive out patients with 1,086 followed up for 12 weeks. Antidepressant treatment was tailored according to clinician recom mendations and patient preferences, with outcomes evaluated at 12 weeks using the Hamilton depression rating scale. Logistic regression analyses explored the individual and interactive effects of SLEs and IL-1 on depression remission. Results: SLEs alone did not predict 12-week remission (OR = 0.93, 95% CI [0.82, 1.06]). However, IL-1 levels sig nificantly influenced outcomes (OR = 0.67, 95% CI [0.53, 0.87]), particularly in conjunction with high SLE exposure (Wald = 13.29, p < 0.001). Higher IL-1 levels were associated with lower odds of achieving remission in the group with two or more SLEs (OR = 0.46, 95% CI [0.33, 0.65]), whereas in the group with fewer than two SLEs, the odds were not significantly different (OR = 1.13, 95% CI [0.77, 1.65]). Conclusion: These findings highlight the critical role of both biological markers and environmental stressors in anti depressant treatment. IL-1 could serve as a biomarker for customizing antidepressant strategies, particularly in patients experiencing high SLE exposure, thereby enhancing treatment efficacy and personalized care. Future studies should include longitudinal assessments of IL-1 to further elucidate its dynamic role in depression pathology and treatment response.

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