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Spinal Fluid Chemical Levels Linked To Suicidal Behavior
An anonymous reader writes "For the first time, researchers have found that a chemical in the brain called glutamate is linked to suicidal behavior. While previous research and drugs have targeted serotonin to fight severe depression, this study shows that more attention should be paid to this chemical."
Glutamate is one of the major neurotransmitters, involved in almost everything the brain does. Reading this summary is kind of like reading "Scientists have discovered that a mysterious substance called 'blood' is involved in heart disease...."
OK then, it's Bush's fault....
The original FA (in the journal) has a reasonable abstract:
The NMDA-receptor antagonist ketamine has proven efficient in reducing symptoms of suicidality, although the mechanisms explaining this effect have not been detailed in psychiatric patients. Recent evidence points towards a low-grade inflammation in brains of suicide victims. Inflammation leads to production of quinolinic acid (QUIN) and kynurenic acid (KYNA), an agonist and antagonist of the glutamatergic N-methyl-D-aspartate (NMDA) receptor, respectively. We here measured QUIN and KYNA in the cerebrospinal fluid (CSF) of 64 medication-free suicide attempters and 36 controls, using gas chromatography mass spectrometry and high-performance liquid chromatography. We assessed the patients clinically using the Suicide Intent Scale and the Montgomery-Åsberg Depression Rating Scale (MADRS). We found that QUIN, but not KYNA, was significantly elevated in the CSF of suicide attempters (p less than 0.001). As predicted, the increase in QUIN was associated with higher levels of CSF interleukin-6. Moreover, QUIN levels correlated with the total scores on Suicide Intent Scale. There was a significant decrease of QUIN in patients who came for follow-up lumbar punctures within 6 months after the suicide attempt. In summary, we here present clinical evidence of increased QUIN in the CSF of suicide attempters. An increased QUIN/KYNA quotient speaks in favor of an overall NMDA-receptor stimulation. The correlation between QUIN and the Suicide Intent Scale indicates that changes in glutamatergic neurotransmission could be specifically linked to suicidality. Our findings have important implications for the detection and specific treatment of suicidal patients, and might explain the observed remedial effects of ketamine.
TL;DR - Suicidally depressed patients seem to have a low level inflammatory process going on. They measure two compounds (out of many) in spinal fluid samples of depressed and control patients that are part of the inflammatory pathway are related to the turnover of glutamate, an amino acid felt to be a neurotransmitter (first link the TFS, a nice short explanation). The glutamate agonist levels were higher in suicidal patients, the glutamate antagonist not.
Potentially a method of quantitating level of suicideality which is a very problematic issue (witness the recent shootings in Connecticut). Very early data. Manuscript submitted but not accepted. At the level of interesting but don't run down to the local Szechuan restaurant and OD on MSG. Oh, and leave the ketamine to the vets.
Faster! Faster! Faster would be better!
Glutamate is a quite common flavour enhancer in processed food. Does that mean processed food can make you suicidal?
No, but it does explain why brains are so tasty.
If God forks the Universe every time you roll a die, he'd better have a damned good memory.
glutamate, an amino acid felt to be a neurotransmitter
Felt to be a neurotransmitter in the same way that hemoglobin is felt to be important to your circulatory system.