Citation

Klempan T, Turecki G. Rev. Bras. Psiquiatr. 2005; 27(3): 172-173.

Vernacular Title

Suicídio: um ponto de vista neurobiológico

Copyright

(Copyright © 2005, Associacao Brasileira de Psiquiatria)

DOI

10.1590/s1516-44462005000300002

PMID

16224601

Abstract

Despite the prominence of suicide as a leading cause of death throughout most countries of the world and the substantial evidence supporting the role of biological factors in suicide predisposition and risk mediation/moderation, its biological basis remains poorly understood and inadequately studied. While several psychosocial factors associated with suicide have been described in detail, numerous studies have also documented an inherited basis for suicidal behaviour, suggesting that the discovery of such genetic factors could lead, in the long run, to some improvements in prevention. The etiology of suicidal behaviour is likely to overlap with that of other psychiatric disorders, owing to the high rates of mood disorders and other psychiatric diagnoses amongst victims of suicide. However, numerous studies controlling for the presence of psychiatric conditions have indicated that the liability for suicide is independent from (but conditional on) the genetic factors mediating susceptibility for major psychiatric disorders. Impulsive-aggressive behaviors also play a critical role in suicide predisposition. Perspectives on the neurobiological basis of suicide have begun to converge in recent years on several key areas, which will be elaborated on below.

The primary biological focus in studies of suicide has been oriented upon the serotonin system, following the observation of an inverse correlation between CSF 5-HIAA levels and suicide risk in depression,1 as well as the finding of an increased density of serotonin binding sites in the frontal cortex of suicide victims. These observations, combined with reports of a blunted prolactin response to challenge with D-fenfluramine in suicide attempters, as well as fewer presynaptic serotonin transporter sites and upregulated levels of the 5-HT1A receptor in ventromedial prefrontal cortex of suicide completers collectively imply a role for both serotonin and this brain region in suicide. However, multiple systems appear to play a role in regulating the risk of suicide, and under this perspective, recent findings pointing to the possible implication of protein kinase A and C in the suicide neurobiology are encouraging.2 Another interesting lead that, in spite of much controversy, is supported by several lines of evidence concerns the relationship between low cholesterol levels and suicidal behaviour. This is an intriguing association with unclear candidate mediating mechanisms to explain how serum cholesterol levels may have an effect on behaviour. In any case, the investigation of components of the lipid metabolisms in the neurobiology of suicide and related behaviours has gained renewed interest in light of the growing evidence demonstrating essential roles for cholesterol in brain synaptogenesis, as well as evidence suggesting that alterations in brain sterol composition may mediate this association.3