Citation

Lengvenyte A, Sebti E, Courtet P. Minerva Psychiatry 2022; 63(4): 397-406.

Copyright

(Copyright © 2022)

DOI

10.23736/S2724-6612.22.02369-7

PMID

unavailable

Abstract

Suicidal ideation and behaviors, as devastating as they are, are extremely hard to prevent. Their pathophysiology is complex and not fully clear. However, mounting amount of evidence has emerged in recent years, pointing to multiple points of connection between inflammatory dysregulation and suicidal ideation and behaviors. A PubMed search was made to look for the most relevant studies. A narrative evidence synthesis was made to succinctly present the major recent findings regarding the association between inflammation and suicidal ideation, behaviors, and associated phenotypes. Strong evidence suggest that suicidal ideation and behaviors are associated with increased concentration of pro-inflammatory proteins in blood, with the strongest evidence for C-reactive protein and interleukin-6, both of which however lacking specificity. Post-mortem and imaging studies suggest that increased inflammation in specific brain regions, most notably prefrontal cortex and default mode network, are also linked to suicidal behaviors and ideation. This association is possibly mediated via intermediate phenotypes, notably anhedonia, impulsivity/aggressivity and impaired decision making. Stressful life experiences, especially in early life, have been implicated in this association. The present review briefly presents the latest advances in research on the association between various immune and inflammatory factors and suicidal behaviors, as well as related behavioral and cognitive factors. © 2022 EDIZIONI MINERVA MEDICA.

Language: en

Keywords

human; Suicide; Review; decision making; bipolar disorder; suicidal ideation; depression; Inflammation; suicidal behavior; hospitalization; C reactive protein; inflammation; Cytokines; risk factor; obesity; death; mental disease; pathophysiology; impulsiveness; sleep disorder; hepatitis C; psychosocial withdrawal; brain region; anhedonia; interleukin 2; interleukin 6; nervous system development; homeostasis; aminotransferase; interleukin 1beta; phenotype; brain derived neurotrophic factor; microglia; interleukin 8; interleukin 4; transforming growth factor beta1; tumor necrosis factor; protein S100B; anterior cingulate; vasculotropin; kynurenic acid; quinolinic acid; default mode network; lipopolysaccharide; glycogen synthase kinase 3; kynurenine aminotransferase