Suicide is chemical biomedical. Suicide is in our genes.
In Essential Papers on Suicide, Maltsberger and Goldblatt introduce the field of biochemical study with the following:
Plasma cortisol levels, the dexamethasone suppression test, imipramine binding on platelets, thyroid function tests, dopamine, and the hypothalamic-pituitary-adrendal axis are all under examination. No avenue has aroused greater interest or shown greater promise, however, than the investigation of the serotonin system
In “5-HIAA in the Cerebrospinal Fluid: A Biochemical Suicide Predictor,” Marie Asberg, Lil Traskman, and Peter Thoren advance one of the first biochemical readings of suicide, first published in 1976.[1]
They begin the study with a puzzle. “The frequency of suicide is high in psychiatric patients, particularly in those suffering from depressive illness. But only a minority of depressed patients commit or attempt suicide.”
They wish to know what accounts for the suicidal impetus. Why suicide in some depressives but not others? They continue: “Additional risk factors have mainly been sought among demographic, sociocultural, and psychological variables.”
They pursue a different line of inquiry and offers their findings: “Evidence for the role of this neurotransmitter [serotonin] in depressive illness is derived, inter alia, from findings of low levels of serotonin in brains from suicide victims and low levels of its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in the cerebrospinal fluid (CSF) of depressed patients.”
They conclude: “This suggested the existence of a biochemical subgroup within the depressive disorders, characterized by a lower level of 5-HIAA in the CSF. (343-4).”
In “Family History of Suicide,” first published in 1984, Alec Roy delves even deeper, into one’s very stars.[2] Maltsberger and Goldblatt note that a patient with a family history of suicide is twice as likely to attempt suicide, compared to those without such a history. Roy, then, studies possible connections between genetic suicide and genetic makeup in first- and second-degree relatives: parents, twins, adoptees, and the like.
In “Serotonin 1A Receptor Genetic Variations, Suicide, and Life Events in the Iranian Population,” Bahram Samadi Rad et al., draw the biochemical and genetic paths together.[3]
Aim: The association of serotonin 1A receptor (5-HTR1A) gene polymorphisms with suicidal behavior has been reported in several previous studies, but the results have been inconsistent, which might be due to ethnic differences. The aim of the present study was therefore to investigate the association between polymorphisms -1019C>G, 47C>T (Pro16Leu) and 815G>A (Gly272Asp) and suicidal behavior, taking into account age, gender, and the presence of stressful life and loss events in 1 year prior to suicide.
Methods: A total of 191 suicide victims and 218 healthy control subjects were included in the present study. 5-HT1RA gene polymorphisms were determined on polymerase chain reaction–restriction fragment length polymorphism.
Results: The distribution of -1019C>G genotypes was significantly different in suicide victims and healthy controls (P = 0.002), and the GG genotype was associated with a significantly higher number of more stressful life and loss events in the suicide victims (P = 0.017, P = 0.037, respectively). The distribution of 47C>T (Pro16Leu) and 815G>A (Gly272Asp) genotypes was not significantly different in the suicide victims and control subjects (P>0.05). Moreover, these genotypes were not asso- ciated with stressful life and loss events (P>0.05).
Conclusion: The frequency of the -1019G allele in the 5-HTR1A gene was higher in suicide victims (with stressful life events) as compared with the control group. In contrast, neither 47C>T (Pro16Leu) nor 815G>A (Gly272Asp) polymorphisms were related with suicide and stressful life events. (337)
That is, if serotonin levels enter individuals in a suicide sub-group, as Asberg et al. indicate, then genetic polymorphism as genotype helps to explain serotonin levels, which help to explain suicide as a genetic-to-biochemical-to-phenomenal chain reaction. And, Boom.
But of course bombs can be defused. The Neurobiology of Suicide offers multiple techniques to defuse the petard including anti-depressants to bring you up and lithium to bring you down.[4]
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[1] Marie Asberg, Lil Traskman, and Peter Thoren, “5-HIAA in the Cerebrospinal Fluid: A Biochemical Suicide Predictor,” in Essential Papers; and, in Archives of General Psychiatry 33 (1976): 1193-7.
[2] Alec Roy, “Family History of Suicide,” in Essential Papers; and, in Archives of General Psychiatry 40 (1983): 971–4.
[3] Bahram Samadi Rad et al., “Serotonin 1A Receptor Genetic Variations, Suicide, and Life Events in the Iranian Population,” in Psychiatry and Clinical Neuroscience 66, no. 4 (2012): 337-43.
[4] David Stoff andJ. John Mann, The Neurobiology of Suicide: From the Bench to the Clinic (New York: New York Academy of Sciences, 1997).