(PSYCHIATRIC TIMES) - Suicide persists as a major public health problem in all industrialized countries. More than 90% of people who commit suicide suffered from a psychiatric disorder, mostly a mood disorder (Mann, 2003). Nevertheless, even in psychiatric groups with the highest risk, most individuals never attempt suicide. It has been suggested that stress factors may trigger a suicidal act only in vulnerable individuals (Mann et al., 1999). Clinical vulnerability factors include impulsive aggression, pessimism and a previous history of suicide attempt (Oquendo et al., 2004). Despite the existence of comprehensive models of suicidal behavior (SB), national prevention strategies have yielded variable results and psychiatric assessment is usually insufficient to predict suicide on the basis of risk factors (Work Group on Suicidal Behaviors, 2003). Progress in the field of genomics should improve our understanding of the complex mechanisms involved in the development of SB. Psychiatrists could also benefit from genetic tools to characterize and define suicidal phenotypes (Merikangas and Risch, 2003).
A Genetic Contribution to Suicide?
Results of family studies indicate that SB aggregates within families (for review, see Brent and Mann, 2005). Moreover, these studies support the view of a shared familial transmission for both suicide attempt and completion. However, the existence of a familial transmission does not mean that suicidal behavior is under a genetic influence. Thus, the examination of concordance rates for SB in monozygotic (MZ) and dizygotic (DZ) twins provides arguments for the existence of genetic factors. In a review of all the published twin case reports for suicide, Roy and Segal (2001) reported an increased concordance for suicide in MZ versus DZ twins (18% versus 0.7%). Furthermore, this difference in concordance rates does not seem to be due to greater bereavement reactions in MZ twins (Segal and Roy, 2001), and the higher concordance rate for suicide attempts in the surviving MZ twin suggested that the clinical phenotype for concordance included both completed suicide and suicide attempts (Roy et al., 1995). Lastly, the strongest evidence for the presence of genetic factors comes from Danish adoption studies. Indeed, Schulsinger et al. (1979) reported a sixfold higher rate of suicide in the biological relatives of adoptees who committed suicide and the absence of suicide among the adoptive relatives of the person who committed suicide versus control adoptees.
Overall, these studies provide evidence for a genetic vulnerability to SB that is shared by people who either attempt or complete suicide.
A Specific Genetic Vulnerability?
Does the genetic vulnerability to suicidal behavior simply reflect the genetic vulnerability to psychiatric disorders related to SB? In the Old Order Amish study, while over 90% of the suicide victims had a mood disorder, some pedigrees were both loaded for mood disorder and suicide, whereas others were equally laden for mood disorder but not for suicide (Egeland and Sussex, 1985). This supports the notion that the familial liability for SB could be independent or additive from the genetic vulnerability to psychiatric disorders. Using sophisticated methodologies, several recent studies showed that the familial transmission of SB cannot be explained by the transmission of psychiatric disorder (Brent and Mann, 2005). Moreover, the familial transmission of suicidal ideation is related to the transmission of psychiatric disorder, whereas the familial transmission of SB may be mediated by the transmission of personality traits like impulsive aggression (Brent et al., 2003, 1996). Interestingly, these recent data tend to confirm the initial assumption by Kety (1986), who suggested that genetic predisposition to SB results from an inability to control impulsive behavior, which can be expressed in the presence or absence of psychiatric disorders.
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