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posted by martyb on Tuesday August 16 2016, @02:44PM   Printer-friendly
from the wishing-them-success dept.

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.


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  • (Score: 0) by Anonymous Coward on Wednesday August 17 2016, @10:07AM

    by Anonymous Coward on Wednesday August 17 2016, @10:07AM (#389060)

    It makes it easier to sell SSRIs and trivializes the issues to something that can be fixed by a pill.

    We can't check levels of neurotransmitters in living creatures, we can only do it though dissecting the brain. It was noticed that SSRIs (before they were called that) were helping some people with depression and that they (temporally*) increase serotonin levels thus depression must be caused by low serotonin. Some of those people were dissected when they died and screwed up levels of neurotransmitters was confirmed (remember these people we already on the meds. No one has dissected a depressed person who has never sought treatment! At least not knowingly). That was the logic for the basis of the anti-depressants industry. And it is an industry, they make billions and spend tons on marketing. They quietly ignored the fact that giving to SSRIs to people who aren't depressed causes those people to become depressed. So does that mean too much serotonin causes depression too? Or that SSRIs can cause lower levels of functional serotonin molecules? Or that something completely different is going on? (There doesn't need to a single root causes of depression, it could be a symptom of different things just like many things can give you a rash.)

    If you've even been on anti-depressants you know its all bullshit. You take one med and if it doesn't work you up the dose until it does. Eventually your body builds up a tolerance/resistance to the med (just like it does to any addictive drug). Once you hit the max dosage, you switch to something else. There's no blood tests or anything. It's all guess work and these meds have serious effects on your body.

    *Everything is way more complex than that. The leftover, degrading molecules get stuck in and thus damage their receptors, so the brain starts making more receptors to replace the failed ones. Eventually you end up with too many receptors being triggered too often so the brain ramps down serotonin production. So taking SSRIs means you'll end up with tons of receptors crowding out the space for other receptors, many of them degraded, and your body's production of serotonin drops further than it was before you started taking the meds. It is a downward spiral. Never take anti-depressants long term. They aren't treating the cause of your depression. They only manage the symptoms. Use that extra energy they give you to fix the underlying cause of the depression then stop taking them as quickly as you can.