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Background <p>Biomarkers distinguishing suicidal from non-suicidal adolescents with major depressive disorder (MDD) remain elusive. This study investigated immune-metabolic dysregulation and its predictive utility for suicide attempt (SA) risk in medication-naïve adolescents.</p> Methods <p>A case-control study compared 168 non-suicidal MDD adolescents with 96 MDD + SA adolescents (recent SA). Peripheral biomarkers included immune cell ratios (neutrophil/HDL [NHR], monocyte/HDL [MHR], lymphocyte/HDL [LHR]), metabolic markers (triglycerides, HDL-C, total protein (TP)), and hematological indices. Analyses employed group comparisons (t-tests/Mann-Whitney U), Spearman correlations, binary logistic regression, and ROC analysis.</p> Results <p>The groups were well-matched demographically and for clinical severity. After adjusting for covariates, the MDD + SA group exhibited significant immune-metabolic dysregulation, including granulocyte hyperactivity, elevated inflammatory ratios, profound HDL-C depletion, hypertriglyceridemia, and reduced total protein (all key findings with adjusted <i>p</i> &lt; 0.05). A post-hoc False Discovery Rate analysis confirmed the robustness of the core lipid findings. Binary logistic regression, adjusted for age, sex, and BMI, identified triglycerides (adjusted OR = 2.17 per mmol/L) and total protein (adjusted OR = 0.93 per g/L decrease) as independent predictors of SA. A model combining triglycerides and total protein significantly outperformed individual biomarkers in ROC analysis (AUC = 0.74, 95% CI: 0.68–0.80).</p> Conclusions <p>Convergent lipid-protein dysregulation represents a novel pathway for adolescent SA risk, identifiable as a significant shift within the normal laboratory range. A simple two-biomarker panel shows promise for risk stratification but requires future validation. These findings highlight metabolic dysfunction as a potential target for preventive strategies, though they do not yet constitute evidence for specific clinical interventions.</p>

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Immune-metabolic dysregulation and suicide risk in adolescents with major depressive disorder: a cross-sectional study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月24日

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  • Yudiao Liang,
  • Chengyi Tan,
  • Ming Liu,
  • Lei Wang,
  • Sha Zhang,
  • Kezhi Liu

摘要

Background

Biomarkers distinguishing suicidal from non-suicidal adolescents with major depressive disorder (MDD) remain elusive. This study investigated immune-metabolic dysregulation and its predictive utility for suicide attempt (SA) risk in medication-naïve adolescents.

Methods

A case-control study compared 168 non-suicidal MDD adolescents with 96 MDD + SA adolescents (recent SA). Peripheral biomarkers included immune cell ratios (neutrophil/HDL [NHR], monocyte/HDL [MHR], lymphocyte/HDL [LHR]), metabolic markers (triglycerides, HDL-C, total protein (TP)), and hematological indices. Analyses employed group comparisons (t-tests/Mann-Whitney U), Spearman correlations, binary logistic regression, and ROC analysis.

Results

The groups were well-matched demographically and for clinical severity. After adjusting for covariates, the MDD + SA group exhibited significant immune-metabolic dysregulation, including granulocyte hyperactivity, elevated inflammatory ratios, profound HDL-C depletion, hypertriglyceridemia, and reduced total protein (all key findings with adjusted p < 0.05). A post-hoc False Discovery Rate analysis confirmed the robustness of the core lipid findings. Binary logistic regression, adjusted for age, sex, and BMI, identified triglycerides (adjusted OR = 2.17 per mmol/L) and total protein (adjusted OR = 0.93 per g/L decrease) as independent predictors of SA. A model combining triglycerides and total protein significantly outperformed individual biomarkers in ROC analysis (AUC = 0.74, 95% CI: 0.68–0.80).

Conclusions

Convergent lipid-protein dysregulation represents a novel pathway for adolescent SA risk, identifiable as a significant shift within the normal laboratory range. A simple two-biomarker panel shows promise for risk stratification but requires future validation. These findings highlight metabolic dysfunction as a potential target for preventive strategies, though they do not yet constitute evidence for specific clinical interventions.