This is all pretty interesting stuff for me. If you read through the below citations I'd like to point out a few things:
1-Excitotoxins can come from a variety of sources...even shellfish has levels of glutamine that can cause neuronal damage in susceptible populations!2-glutamine/glutamate is a neurotransmitter AND an excitotoxin! Like I've said before the poison is in the dose. Normal, natrual processes can release or produce levels of glutamate that can damage neurons.
3-Aspartame MAY be en excitotoxin, but I still think it's tough to argue that a regular soda is better than a diet soda. Sugar is BAD news.
4-All of the studies exploring CRAN and intermittent fasting show a marked resistance to neuronal injury from excitotoxins...is the effect we see from thing like shellfish and MSG and artifact of EATING TOO MUCH TOO OFTEN? Insulin resistance increases the severity of excitotoxins, how do co-founders such as this play into these scenarios.
5-in the case of celiac Glutamic acid (glutamine/glutamate) is frequently derived from gluten. This may explain some of the associations folks with celiac make with MSG. Perhaps some of this is not immagined...perhaps not.
1994 Fall;15(3):535-44. Links
Excitotoxins in foods.
Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110.
Evidence is reviewed pertaining to excitatory neurotoxins (excitotoxins) encountered in human food supply. The most frequently encountered food excitotoxin is glutamate (Glu) which is commercially added to many foods despite evidence that it can freely penetrate certain brain regions and rapidly destroy neurons by hyperactivating the NMDA subtype of Glu receptor. Hypersensitivity of NMDA receptors during development makes the immature nervous system especially sensitive to Glu excitotoxicity. On the other hand, elderly consumers are particularly sensitive to domoic acid, a powerful excitotoxic Glu analog that activates both NMDA and non-NMDA receptors. A high content of domoic acid in shell fish caused a recent food poisoning incident that killed some elderly victims and caused brain damage and memory impairment in others. Neurolathyrism is a crippling neurodegenerative condition associated with ingestion of a legume that naturally contains BOAA, an excitotoxic Glu analog that hyperactivates non-NMDA receptors. Thus, the human food supply is a source of excitotoxins that can damage the brain by one type of mechanism to which immature consumers are hypervulnerable, or by other mechanisms to which adult and elderly consumers are peculiarly sensitive.
PMID: 7854587 [PubMed - indexed for MEDLINE]
1: Neurobehav Toxicol Teratol.
1984 Nov-Dec;6(6):455-62. Links
Excitotoxic food additives--relevance of animal studies to human safety.
Evidence is reviewed supporting the view that excitotoxic food additives pose a significant hazard to the developing nervous system of young children. The following points are stressed: (1) although blood-brain barriers protect most central neurons from excitotoxins, certain brain regions lack such protection (a characteristic common to all vertebrate species); (2) regardless of species, it requires only a transient increase in blood excitotoxin levels for neurons in unprotected brain regions to be "silently" destroyed; (3) humans may be at particularly high risk for this kind of brain damage, since ingestion of a given amount of excitotoxin causes much higher blood excitotoxin levels in humans than in other species; (4) in addition to the heightened risk on a species basis, risk may be further increased for certain consumer sub-populations due to youth, disease or genetic factors; (5) despite these reasons for maintaining a wide margin of safety in the use of excitotoxins in foods, no safety margin is currently being observed, i.e., a comparative evaluation of animal (extensive) and human (limited) data supports the conclusion that excitotoxins, as used in foods today, may produce blood elevations high enough to cause damage to the nervous system of young children, damage which is not detectable at the time of occurrence but which may give rise to subtle disturbances in neuroendocrine function in adolescence and/or adulthood.
PMID: 6152304 [PubMed - indexed for MEDLINE]
1: Mol Cell Biochem.
2003 Jan;243(1-2):139-45. Links
Prolonged glutamate excitotoxicity: effects on mitochondrial antioxidants and antioxidant enzymes.
Neurochemistry and Neuroendocrinology Laboratory, Department of Biotechnology, Guru Nanak Dev University, Amritsar, India.
Glutamate, a major excitatory amino acid neurotransmitter is also an endogenous excitotoxin. The present study examined the prolonged and delayed effects of glutamate excitotoxicity on mitochondrial lipid peroxidation and antioxidant parameters in different brain regions, namely, cerebral hemisphere, cerebellum, brain stem and diencephalon. Wistar rats (male) were exposed to monosodium glutamate (MSG) (4 mg x g body wt(-1), i.p.) for 6 consecutive days and sacrificed on 30th and 45th day after last MSG dose. MSG treatment markedly decreased the mitochondrial manganese superoxide-dismutase (Mn-SOD), catalase and reduced glutathione (GSH) content, and increased the lipid peroxidation (LPx), uric acid and glutathione peroxidase (GPx) activity. These results indicate that oxidative stress produced by glutamate in vulnerable brain regions may persist for longer periods and mitochondrial function impairment is an important mechanism of excitatory amino acid mediated neurotoxicity in chronic neurodegeneration.
PMID: 12619899 [PubMed - indexed for MEDLINE]