This is a thought paper for my Self-Destructive Behaviors class, and is a critique on a paper entitled “Candidate endophenotypes for genetic studies of suicidal behavior” written by Mann et al, linked below.
The purpose of Mann et al (2009) was to elect possible endophenotypes in studying the genetics of suicidal behavior. A review of this nature was called upon due to the difficulty in identifying specific suicide-related genes. Four endophenotypes were named: trait aggression/impulsivity, early-onset major depression, neurocognitive function, and cortisol social stress response. In order to determine if a factor is indeed a valid endophenotype, Mann defined five criterion that must be met: 1) association with illness in the population; 2) heritability greater than 20%; 3) primarily state-dependent; 4) co-segregation of illness and the endophenotype in families; and 5) found in non-affected family members more frequently than in the general population. The review elicited material from a number of different types of studies, including but not limited to psychological autopsies; twin, adoption, and family studies; cognitive functioning exams; and medical testing. Missing from most sections was the fifth criterion, a comparison of nonaffected relatives and the general population.
Interestingly, impulsivity was said to be too broad of a term, at least in genetic studies. It was broken down into three categories: response initiation, which related to suicide attempt history; response inhibition, which has yet to be linked with suicidal behavior (but is with conduct disorder); and consequence sensitivity, which differentiates attempters from nonattempters in self-injury patients. Breaking down impulsivity into its components is a much more effective way to glean information regarding suicidal behavior in a given individual. This could lead to an interesting avenue of study regarding the exact nature of impulsivity and its effect on suicidal behavior, as well as NSSI. Further inquiry could be taken into questioning whether the components are triggered by early-life events, or they are preformed in the combination of certain genomes, possibly leading to more information on the etiology of suicide attempts, conduct disorder, and NSSI. By far, not as much information was provided regarding early-onset major depression, neurocognitive function, and cortisol response to psychosocial stress.
Future implications of this study include easier prediction and tracking of symptoms and warning signs in a person with a known family history of suicidal behavior or psychopathy; and more effective and efficient delivery of interventions. For instance, if a child who had a family history of suicidality were observed to exhibit impulsive characteristics, in particular if he or she appeared to lack sensitivity to consequences, interventions to amend this deficit could be implemented early in life, such as a heavy focus on planning positive goals. Encouraging investment in one’s future may serve to make up for a genetic predisposition to be unable to appreciate the costs of one’s actions. A similar technique could be applied to breaking some of the rigidity associated with attentional fixation, as well as developing the skill to create novel solutions to problems, so suicide doesn’t chronically appear to be the only way out. If a person is more predisposed to act in a maladaptive way due to genetics then perhaps purposeful development of psychological hardiness will serve as a protective factor.
Mann, J. J. et al. (2009). Candidate endophenotypes for genetic studies of suicidal behavior. Biological Psychiatry, 65, 556-563.