With Aspartame, I understand that there is evidence from both sides, supporting studies from the FDA and the like and a few medical doctors indicating its an excitotoxin.
Why would you disregard something that has decent information behind it?
We also don't inject l-tryptophan into our brains yet it makes it's way there.
You are assuming the blood brain barrier is a 100% full proof iron clad barrier that protects all, nothing could be further from the truth..
As for test and e2 conversion e2 always follows t. Just it is different for every person.. This substance is t something I would he consuming Alot of until it has lasted the o e true test that matters. Time...
mine came with a 3g scoop so i was gonna use 3g every morning with brekky.. how would you recommend dosing?
Excitotoxity and the NMDA receptor
Steven M. Rothmana and John W. Olneyb
aDepartment of Anatomy and Neurobiology, and the Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, USA.
bDepartment of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA.
Available online 5 March 2003.
Abstract
The same receptors for excitatory amino acids (EAA) that mediate direct neuronal depolarization can also be responsible for neuronal injury. Prolonged stimulation of EAA receptors of either the N-methyl-d-aspartate (NMDA) or non-NMDA types eventually results in the death of most central neurons. The exact mechanism(s) of cell injury is complicated, since depolarization and neuronal swelling, calcium influx, and possibly second messengers all contribute. Evidence is accumulating that the brain damage associated with anoxia, stroke, hypoglycemia, epilepsy, and perhaps neurodegenerative illnesses such as Huntington's disease may be at least partially produced by excessive activation of NMDA receptors. To the extent that the pathophysiology can be explained by this mechanism, it may be amenable to rational therapies now under development.
NMDA-dependent superoxide production and neurotoxicity
Mireille Lafon-Cazal*, Sylvia Pietri†, Marcel Culcasi† & Joel Bockaert*
* Centre CNRS-INSERM de Pharmacologie-Endocrinologie, rue de la Cardonille, 34094 Montpellier Cedex 5, France
† CRIPDOM, PO Box 43, 34172 Castelnau-le Lez Cedex, France, and SREP-CNRS URA 1412, Université de Provence, 13397 Marseille Cedex 13, France
NEURONAL injury resulting from acute brain insults and some neurodegenerative diseases implicates N-methyl-D-aspartate (NMDA) glutamate receptors1–4. The fact that antioxidants reduce some types of brain damage suggests that oxygen radicals may have a role5–7. It has been shown that mutations in Cu/Zn-superoxide dismutase (SOD), an enzyme catalysing superoxide (O- 2) detoxification in the cell, are linked to a familial form of amyotrophic lateral sclerosis (ALS)4. Here we report that O- 2 is produced upon NMDA receptor stimulation in cultured cerebellar granule cells. Electron paramagnetic resonance was used to assess O- 2 production that was due in part to the release of arachidonic acid. Activation of kainic acid receptors, or voltage-sensitive Ca2+ channels, did not produce detectable O- 2. We also find that the nitrone DMPO (5,5-dimethyl pyrroline 1-oxide), used as a spin trap, is more efficient than the nitric oxide synthase inhibitor, L-N G-nitroarginine, in reducing NMDA-induced neuronal death in these cultures.
A potential role for excitotoxins in the pathophysiology of spinal cord injury
Dr. Alan I. Faden MD1,*, Roger P. Simon MD2
Issue
Annals of Neurology
Volume 23, Issue 6, pages 623–626, June 1988
Abstract
It has been proposed that endogenously released excitatory amino acids may contribute to injury of the central nervous system in a variety of disorders including certain neurodegenerative diseases, epilepsy, and cerebral ischemia. In the present studies we evaluated the hypothesis that excitatory amino acids, acting at the N-methyl-D-aspartate (NMDA) receptor, contribute to secondary tissue damage following traumatic spinal cord injury. Administration of NMDA, adjacent to the trauma site, significantly worsened the outcome after thoracic cord injury in rats, whereas its stereoisomer, N-methyl-L-aspartate (NMLA), was without effect. Systemic treatment with MK-801—a selective, centrally active, NMDA antagonist—significantly improved neurological outcome after trauma. These findings extend the excitotoxin concept to central nervous system trauma and indicate that NMDA antagonists may be beneficial in the treatment of traumatic spinal cord injury.
The Glutamate Story - British Journal of Pharmacology, Volume 147, Issue S1 (p S100-S108) DOI 10.1038/sj.bjp.0706444
From the abstract:
"Realisation that glutamate and like amino acids (collectively known as excitatory amino acids (EAA)) mediated their excitatory actions via multiple receptors preceded establishment of these receptors as synaptic transmitter receptors. EAA receptors were initially classified as NMDA (N-methyl-D-aspartate) and non-NMDA receptors. In the early 1980s, NMDA receptors were shown to be involved in several central synaptic pathways acting in concert with non-NMDA receptors under conditions where a protracted excitatory postsynaptic potential was effected in response to intense stimulation of presynaptic fibres. Such activation of NMDA receptors together with non-NMDA receptors leads to the phenomenon of long-term potentiation (LTP), associated with lasting changes in synaptic efficacy (synaptic plasticity) and considered to be an important process in memory and learning."
(The NMDA receptor, which is a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function. Aspartate (the conjugate base of aspartic acid) stimulates NMDA receptors, though not as strongly as the amino acid neurotransmitter glutamate. Both aspartate and glutamate serve as an excitatory neurotransmitters in the brain, and are excitotoxins -- meaning that excessively high tissue concentrations can cause nerve cell damage.
* full article: http://www3.interscience.wiley.com/cgi-bin/fulltext/121674911/PDFSTART
99% based on what?
The experts @ bodybuilding.com
Your right, hard to find proof, but a lot of valid points.
As mentioned before, pure speculation - trust me mate 6 months ago this is all the forums were full of - DAA / Excitotoxin / Neurotoxicity / Increased Prolactin / Increased E etc etc...
Besides I trust what PA and Dr P say, these boys know there shit...
In hindsight, they pretty much brought down a company through one epic thread... Do you remember the Slim Xtreme spiking incident? The Divanil issue as well, I'm sure there were others, just don't remember.
Nope i have no idea what you are tlaking about lol, i dont really care about new products. The strongest people in the world never needed them and neither do a bunch of newbies to the strength game.
Yes there are valid points for all sides... and my point is simply "no one knows" so be cautious...
Take some rp6 instead at least there is good research into it
Refresh me on the Divanil issue. I think I already left BB.com before that came up.
Well we have TGA at least..
Thats very true, however the US has the FDA however you still find 'spiked' supps, such as the above Slim Xreme (Designer Stim), ALRI Restore and Jungle Warfare (PH's - although not controlled in the US, there are labelling laws).
FDA is a fucking joke...
We use cookies and similar technologies for the following purposes:
Do you accept cookies and these technologies?
We use cookies and similar technologies for the following purposes:
Do you accept cookies and these technologies?