Independent and interactive associations of inflammation, vascular homeostasis markers, and childhood trauma with suicide attempt history.

BACKGROUND

The neurobiological basis of suicidal behaviour remains poorly understood. However, emerging evidence suggests that inflammation and vascular homeostasis factors may play a role in its pathophysiology. Childhood trauma, through immune system dysfunction and increased risk of suicidal behaviours, might influence these associations. This study examined the relationships between immune-inflammatory and vascular homeostasis-related markers and their interaction with childhood trauma in relation to a history of suicide attempts in individuals with depression.

METHODS

A total of 328 patients with major depression were recruited: 166 with a history of suicide attempts and 162 without. Using multivariate binary logistic regression models adjusted for cofounders, we examined the associations between childhood trauma, levels of platelet-related immune markers (serotonin, MCP-1, TSP-1, TSP-2, PDGF-AB, PDGF-BB), and suicide attempt history. Independent associations between PDGF-BB, childhood trauma, and suicide attempts were further assessed using interaction models. Stratified sensitivity analyses based on childhood trauma history were also conducted.

RESULTS

Childhood trauma consistently emerged as associated with suicide attempts across all models. Among the measured biomarkers, higher TSP-2 levels were associated with a suicide attempt history, independent of childhood trauma. Meanwhile, while PDGF-BB alone was not directly linked to suicide attempt history, the interaction analysis revealed that individuals with lower PDGF-BB levels and more severe childhood trauma were more likely to have attempted suicide.

CONCLUSIONS

TSP-2 and PDGF-BB are potential biomarkers linked to suicide attempts, with distinct roles in the interplay between biological processes and early-life adversity. These insights can inform the biomarker-informed development of tailored prevention and treatment strategies.