Thank you everybody for sharing your opinion on this topic. In the present post I'd like to comment on the following part of Quantum's reply.
When I read about that neurotoxicity/excitotoxicity thing, I have started to use even more NMDA receptors blockers in my anti-POIS pre-E pack. In fact, I was already using magnesium for years, which is a a good NMDA receptor blocker, but didn't know it could be the reason why it was helping reduce my POIS symptoms ( anybody else have tried magnesium for POIS relief ?). NMDA receptors blockers act as neuroprotectors against the excitotoxins, so they prevent brain inflammation. Apart from magnesium, the other NMDA receptors blockers I have found useful for me are flaxseed oil ( the lignam in it is the NMDAR blocker), L-theanine, taurine, and ibuprofen. I didn't try yet cat's claw and huperzine A. I have tried acetyl-L-carnitine, but not sure if it helps me or not.
My remark is simple. In the articles I linked in my initial post, the physicians (both in the English team and in the French team) explain that the problem comes from auto-antibodies wrongly blocking NMDA receptors. But when describing your vision and your cure you're saying the exact contrary, i.e. you take substances that are going to block NMDA receptors.
So, to block or not to block, that is the question :-)
Your remark is very interesting, superfrancais. I think the confusion came because of the words used by the journalists who were referring to the studies, without mastering the subject. Words and expressions like "immobilizing the NMDA receptors" in the French account, and the phrase "When the immune system attacks the NMDA receptor, it becomes inflamed", are not accurate, because those journalist are not specialists. For example, you can talk about inflammation for a tissue or an organ, but not for a single receptor, which is a the protein/molecule level, so the English phrase in not correct.
That being said, I went back to read the original article, in order to hear it "straight from the horse's mouth" and understand what has been really been found by this research team, I have found the article at
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065649/ . I think the relevant part is the following: " These preliminary data show that some patients with schizophrenia have potentially pathogenic autoantibodies to relevant membrane proteins. " , the relevant membrane proteins being parts of the NMDA receptors structures. So, it says that the antibodies are "pathogenic" to the receptors, meaning they cause some sort of dysfunctions leading to schizophrenia symptoms, according to their hypothesis. But there is no more precision on the nature of this pathogenic effect, apart form the fact that they know they binds to the NMDA receptors. Do they block them in "on" position, or in "off" position? Do they have another effect? I think they do not have these answers yet.
What is well known form other sources is the excitotoxicity effect (
https://en.wikipedia.org/wiki/Excitotoxicity ), where an excessive stimulation NMDA receptors leads to nerve cell death, and, on a brain tissue level, to inflammation. Quinolinic acid, a potent NMDA receptor agonist ( it stimulates it), is known to being able to cause excitotoxicity ( see at
https://en.wikipedia.org/wiki/Quinolinic_acid ). This bad effect occurs in the microglia, which is the first line immune defence cells of the brain tissue. Quinolinic acid is known to cause emotional symptoms.
On the other end, kynurenic acid is a potent NMDA antagonist ( it blocks the NMDA receptors). It can leads to too much blocking , but on another type of brain support cells, the astrocytes. In this case, it is known taht high levels of kynurenic acids leads to cognitive deficit, confusion and psychotic symptoms (
https://en.wikipedia.org/wiki/Kynurenic_acid#Role_in_disease )
So, too much is no better than not enough. You can have toxic effects both ways, on different type of brain cells.
You can see a good graphic synthesis of this on the image at
http://fr.slideshare.net/adonissfera/tryptophan-and-madness/17-Cytokines_Come_in_Two_FlavorsProInflammatory . In bottom center of the slide, you will see that the a higher kynurenines ( KYN ) production can than lead to a raise concentration of quinolinic acid (QUIN), leading to a + effect on the NMDA receptors of the microglia cells, which manifests in depression, anxiety and impulsivity, as noted on the slide. You can also see that the kynurenines ( KYN) can also be transformed in kynurenic acid ( KYNA on the slide), and this raise in KYNA concentration affects the astrocytes, having a - effect on the NMDA receptors, and lead to cognitive deficits ( yes, brain fog, memory problems, mental focus problems, .....).
Moreover, the concept of "blocking" a receptor is not always a on-off reality - it is often a modulation of the receptor activity. If you are really interested on all those interactions at the NMDA receptors, take a look at
https://en.wikipedia.org/wiki/NMDA_receptor , and you will see it is more complicated that it appears.
So, not having all the information, sometime all is left is our personal response to a particular supplement, to see if it helps or not ( through trials with safe doses, of course). In my case, the fact that I had no cognitive symptoms, it was clear that it was better for me to try NMDA blockers ( which, anyway, are good for anxiety, something I have been living with since childhood). Having just myself as "guinea pig", I don't know for sure if a POIS sufferer with both cognitive symptoms and emotional symptoms, would have less emotional symptoms and more cognitive symptoms if using NMDA blockers, but it do not seems to be the case. From what have been share on the forum so far, I do not recall any member noticing worse cognitive symptoms after using flaxseed oil, l-theanine, magnesium, taurine, or another NMDAR blocker.
For me, at the least, my answer to your question, "to block or not to block" the NMDAR, is to block, and use NMDAR blockers. Moreover, when I used to eat food containing aspartame, which ends in the brain as glutamate ( a NMDA agonist/stimulator), I would always have a typical dull and constant headache, sign of a certain level of neurotoxicity ( actually, aspartame is known to be a migraine trigger for many people).
I hope my answer is not too long and is clear enough, but there was no simple answer to this question :-)
