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Interesting slideshow on excitotoxins, methylation, glutathione and glutamate. http://dramyyasko.com/wp-content/uploads/2010/06/17-A1-Excitotoxins.pdfYasko seems to believe that glutamate imbalances cause seizures in autistic kids. While I'm a bit skeptical about some of these claims, there are some useful papers referenced and I do think there's something to the idea that methylation problems (and related like Vit D deficiency) lead to systemic diseases by preventing the body from balancing levels of amino acids (such as glutamic acid) and minerals (e.g. calcium)She says that she's seen symptoms such as vision problems, migraines and tension, bladder problems and irritable bowel which reminds me of POIS as many sufferers have talked about similar symptoms.
Folks, let me share what's going on with my niacin experiments.I'm still using a batch of few-months-old 500mg full-flush niacin (Nicotinic Acid), while I'm waiting to receive fresh 100mg caspules.It's been a couple of times that I wake-up early morning and, being sure this way that I've had enough fasting hours and I'm far from any other supplements, I take 500mg of that niacin and wait in bed for the flush to happen. Well, something very weak happens 30 mins after, but eventually I fall deeply asleep again. Then I wake up (later than usual) in the morning 2-3 hours after, and a small flush happens again as I take my supplements or eat something. In other words, I never get a full-blown flush this way, especially on empty stomach when it's supposed to happen.500mg are quite a bit, and I'm using this big amount because it's not so fresh, the flush doesn't occur right away nonetheless.Also, the fact that a small flush occurs few hours after when I eat something means that some of that niacin is still around, waiting to be fully metabolized, is my assumption wrong? As if niacin metabolization is somehow slowed down. Or is it normal this way?Finally, I slept in and didn't wake-up very refreshed. Not so unusual for me, but something to be considered anyway.I'll wait for the fresh batch and test with smaller doses, but does this all say anything to any of you?Thanks,Andrea
Quote from: kurtosis on 13/03/2013 14:02:09Interesting slideshow on excitotoxins, methylation, glutathione and glutamate. http://dramyyasko.com/wp-content/uploads/2010/06/17-A1-Excitotoxins.pdfYasko seems to believe that glutamate imbalances cause seizures in autistic kids. While I'm a bit skeptical about some of these claims, there are some useful papers referenced and I do think there's something to the idea that methylation problems (and related like Vit D deficiency) lead to systemic diseases by preventing the body from balancing levels of amino acids (such as glutamic acid) and minerals (e.g. calcium)She says that she's seen symptoms such as vision problems, migraines and tension, bladder problems and irritable bowel which reminds me of POIS as many sufferers have talked about similar symptoms.I don't fully understand few points, but it's possibly because of my poor knowledge. Why proteins like whey are among the excitotoxins? Why L-Cystein can be an issue, and not NAC, and in what sense sulphur-containing aminos (thus including methionine) can cause glutammate excess, if I understand well? If limiting calcium will help limit inflammation, would vit D which improves calcium absorption and decreases calcium excretion be an issue? Is glutammine intake an issue, what decides if it will be to Glutammate or to GABA? Is supplementing magnesium and zinc always beneficial in this sense?In few words, I don't fully get what the strategy for balancing glutamate/GABA would be, apart from obviously ingesting directly too much glutammate.
modulation of NMDA glutamate receptors or by increasing glutathione
Glutamate transporters[11] are found in neuronal and glial membranes. They rapidly remove glutamate from the extracellular space. In brain injury or disease, they can work in reverse, and excess glutamate can accumulate outside cells. This process causes calcium ions to enter cells via NMDA receptor channels, leading to neuronal damage and eventual cell death, and is called excitotoxicity. The mechanisms of cell death includeDamage to mitochondria from excessively high intracellular Ca2+[12]Glu/Ca2+-mediated promotion of transcription factors for pro-apoptotic genes, or downregulation of transcription factors for anti-apoptotic genes
Anyway, the point I was trying to make was that zinc+b6 and methylfolate+mb12 are possibly all related treatments for a similar problem. The same problem that Nathan took flunarazine for.
Quote from: kurtosis on 13/03/2013 19:36:54Anyway, the point I was trying to make was that zinc+b6 and methylfolate+mb12 are possibly all related treatments for a similar problem. The same problem that Nathan took flunarazine for.To keep it simple, maybe reguarly supplementing magnesium and Vit K2 would help with calcium excess related issues?
Quote from: urano75 on 14/03/2013 19:47:17Quote from: kurtosis on 13/03/2013 19:36:54Anyway, the point I was trying to make was that zinc+b6 and methylfolate+mb12 are possibly all related treatments for a similar problem. The same problem that Nathan took flunarazine for.To keep it simple, maybe reguarly supplementing magnesium and Vit K2 would help with calcium excess related issues?Yes. Or using a multi without copper but with zinc and magnesium You can get K2 from eggs and I eat an egg a day.
urano75No I did not suffer from flu like symptoms all the time after an O like you do. That would be really bad, but there is a immunological effect going on for me. Whenever there were cold/flus going around (family, friends coworkers, passengers on the train, etc), I would be fine until I had an O, then I would always get the cold/flu the next day. With all the theories being discussed we need to remember that there seems to something wrong that is unique to the male biology. Why would being an under-methylator or weak adrenals not also cause women to have the POIS.
Quote from: kurtosis on 14/03/2013 21:33:10Quote from: urano75 on 14/03/2013 19:47:17Quote from: kurtosis on 13/03/2013 19:36:54Anyway, the point I was trying to make was that zinc+b6 and methylfolate+mb12 are possibly all related treatments for a similar problem. The same problem that Nathan took flunarazine for.To keep it simple, maybe reguarly supplementing magnesium and Vit K2 would help with calcium excess related issues?Yes. Or using a multi without copper but with zinc and magnesium You can get K2 from eggs and I eat an egg a day.I eat 2 raw egg yolks everyday, but I supplement K2 anyway especially since I discovered elevated serum calcium. Possibly caused by D supplementation (to be determined).
Quote from: urano75 on 14/03/2013 22:01:22Quote from: kurtosis on 14/03/2013 21:33:10Quote from: urano75 on 14/03/2013 19:47:17Quote from: kurtosis on 13/03/2013 19:36:54Anyway, the point I was trying to make was that zinc+b6 and methylfolate+mb12 are possibly all related treatments for a similar problem. The same problem that Nathan took flunarazine for.To keep it simple, maybe reguarly supplementing magnesium and Vit K2 would help with calcium excess related issues?Yes. Or using a multi without copper but with zinc and magnesium You can get K2 from eggs and I eat an egg a day.I eat 2 raw egg yolks everyday, but I supplement K2 anyway especially since I discovered elevated serum calcium. Possibly caused by D supplementation (to be determined).Unless you have very high serum levels of vitamin D then it's overreaching to believe that you're taking too much vitamin D. You may simply be taking in too much calcium? What's your diet like?
T3 therapy? That's interesting. One of the main causes of elevated serum calcium is hyperparathyroidism. http://en.wikipedia.org/wiki/HyperparathyroidismYou could have this but have low vitamin D which masks it. See http://www.acssurgerynews.com/fileadmin/content_pdf/fpn/archive_pdf/vol37iss4/70214_main.pdfI take around 5000-6000IU of vitamin D / day. How much were you taking?
Cysteine assists in the regulation of neuronal intra- and extracellular exchange of glutamate through the cystine–glutamate antiporter. Whereas this antiporter is ubiquitous throughout all cell types, in the brain it is preferentially located on glial cells.25 The dimer, cystine, is taken up by astrocytes and exchanged for glutamate, which is released into the extracellular space. This free glutamate appears to stimulate inhibitory metabotropic glutamate receptors on glutamatergic nerve terminals and thereby reduce the synaptic release of glutamate.26 Given that relation, the amount of cysteine in the system as well as the feedback via GSH production by neurons may directly regulate the amount of glutamate present in the extracellular space
Yes, I understand now. That rT3 theory is controversial but then again, this is the POIS forum. T