Narrative review explores neurobiological correlates of suicidal behaviors in pediatric populations, suggesting unique mechanisms.
Background Suicide is the second leading cause of death among children and adolescents, with rates of pediatric suicidal behavior rising substantially over the past two decades. The neurobiology of suicide has been extensively studied in adults, yet pediatric-specific evidence remains limited and the extent to which adult findings can be extrapolated to youth is unclear. This review synthesizes current evidence on the neurobiological correlates of suicidal ideation, suicide attempt, and death by suicide in pediatric and adolescent populations across neurological, genetic, epigenetic, inflammatory, metabolic, and endocrine domains. Methods A literature search was conducted in PubMed, Embase, PsycINFO, and Google Scholar for peer-reviewed, English-language human studies. Priority was given to pediatric and adolescent samples, with adult data included where pediatric evidence was lacking. Studies were grouped by biological domain and by suicidal phenotype. Results Suicidal ideation, suicide attempt, and death by suicide showed partially distinct biological signatures rather than lying on a single continuum of severity. Different markers, most notably cortisol regulation and stress-related DNA methylation, differed in direction between pediatric and adult cohorts, indicating that adult biomarker data cannot be directly extrapolated to youth. Findings converged on a developmental cascade in which genetic liability and early-life adversity influence the hypothalamic-pituitary-adrenal axis, with downstream effects on epigenetic regulation, neuroinflammation, neurochemistry, and frontolimbic circuitry. Conclusions Pediatric suicidal behavior reflects developmentally distinct biological processes that cannot be inferred from adult findings. Advancing the field will require longitudinal, multimodal pediatric studies that disaggregate suicidal phenotypes, span the pubertal transition, and apply age-stratified reference ranges, supporting biologically informed stratification and mechanism-targeted intervention.
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Salehi et al. (2026) studied this question.
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