Citation

Salloum NC. Am. J. Psychiatry Resid. J. 2017; 12(1): 2-4.

Copyright

(Copyright © 2017, American Psychiatric Association Publishing)

DOI

10.1176/appi.ajp-rj.2017.120101

PMID

unavailable

Abstract

Over 800,000 suicide-related deaths are reported around the world every year, with one person committing suicide every 40 seconds (1). Extensive work aimed at improving suicide prevention has yet to deliver objective tools for better assessment and management of suicide risk. One of the hurdles has been a lack of full understanding of the underlying biological manifestations that lead to suicide. In order to conceptualize this complex phenomenon, the stress-diathesis model was proposed almost two decades ago and is still regarded as the most widely accepted hypothesis for understanding suicide. It describes suicidal behavior as the interplay between a stressor (e.g., an acute psychiatric condition or a negative psychosocial event) and an individual's vulnerability to experience suicidality. This vulnerability, or diathesis, potentially results from a genetic predisposition and epigenetic mechanisms related to early-life adversity (2, 3). Within this framework, substantial effort has been made to uncover the pathophysiology that would account for this diathesis. Thus far, findings are indicating that the suicide biological architecture consists of a distinct network of interrelated neural systems at play. Further study may unravel a holistic psychobiological foundation for suicidal behavior. This in turn would add support to the latter as being a discrete psychiatric disorder, a point that was suggested in DSM-5 and will be discussed in more details later. The present article reviews the most salient systems involved in the neurobiology of suicidal behavior and the interactions between them.

Language: en