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Submitted via IRC for Runaway1956 from a VAI press release:
A collaborative study from research teams in Sweden, the US and Australia published in Translational Psychiatry shows that suicidal patients have a reduced activity of an enzyme that regulates inflammation and its byproducts.
It is known that people who have attempted suicide have ongoing inflammation in their blood and spinal fluid. Now, a collaborative study from research teams in Sweden, the US and Australia published in Translational Psychiatry shows that suicidal patients have a reduced activity of an enzyme that regulates inflammation and its byproducts.
[...] Currently, there are no biomarkers for psychiatric illness, namely biological factors that can be measured and provide information about the patient's psychiatric health. If a simple blood test can identify individuals at risk of taking their lives, that would be a huge step forward, said [Professor Sophie] Erhardt, a Professor at the Department of Physiology and Pharmacology at the Karolinska Institutet, who led the work along with [Professor Lena] Brundin.
The researchers analyzed certain metabolites, byproducts formed during infection and inflammation, in the blood and cerebrospinal fluid [CSF] from patients who tried to take their own lives. Previously it has been shown that such patients have ongoing inflammation in the blood and cerebrospinal fluid. This new work has succeeded in showing that patients who have attempted suicide have reduced activity of an enzyme called ACMSD, which regulates inflammation and its byproducts.
[Continues...]
[...] The substance that the enzyme ACMSD produces, picolinic acid, is greatly reduced in both plasma and in the spinal fluid of suicidal patients. Another product, called quinolinic acid, is increased. Quinolinic acid is inflammatory and binds to and activates glutamate receptors in the brain. Normally, ACMSD produces picolinic acid at the expense of quinolinic acid, thus maintaining an important balance.
[...] Several of the researchers have indicated that they have business interests, which are recognized in the article.
Having found these results in suicidal patients, the researchers are now trying to find out if this imbalance is also present in those with severe depression. They are also seeking to develop drugs that might activate the ACMSD enzyme and restore the balance between quinolinic and picolinic acids.
The full article is available: "An enzyme in the kynurenine pathway That governs vulnerability to suicidal behavior by regulating excitotoxicity and neuroinflammation" Translational Psychiatry, published online August 2, 2016, doi: 10.1038 / TP.2016.133.
(Score: 2) by meustrus on Tuesday August 16 2016, @06:58PM
Could this chemical be the mechanism by which many anti-depressants make users more vulnerable to suicidal thoughts? This makes sense as a chemical foundation that could arise from a chemical modification to our nervous system like anti-depressants. If my hypothesis is correct, we can mitigate one of the nastiest side effects of some of the most effective psychiatric drugs by adding something else to the cocktail. However I shudder to think of the decision that must then be made: buy the generic drug with suicidal side effects, or the one without that, because it is new and still under patent, costs 10x as much or more?
If there isn't at least one reference or primary source, it's not +1 Informative. Maybe the underused +1 Interesting?
(Score: 1, Interesting) by Anonymous Coward on Tuesday August 16 2016, @07:55PM
Anti-depressants make users more vulnerable to suicide because before starting them many users are too depressed to commit suicide. Depression can zap all your energy and willpower to do anything. Anti-depressants recover your energy faster than your mood, so those people will regain the energy to kill themselves before regaining the will to live.
Though that's only for people who are actually depressed. If a non-depressed persons starts taking SSRIs, then they become depressed and that depression could make them suicidal.
Your hypothesis is very likely incorrect. We already know messing around with serotonin messes with your mood. It's far more likely whatever is screwing with serotonin levels has also messed up ACMSD. So we're still not at the root causes of most depression, the thing that put these systems out of wack. What this is is another symptom of depression. It's like your body reacting to a sickness. When you get a cold, your nose runs. When you get depressed, more inflammation agents are released. I think that is far more likely as how would blood inflammation directly lead to thought changes? Serotonin is a neurotransmitter (helps signals move around in your brain).