I'd like to see the list. Also, I wrote a note to Mark Messina, PhD, who did research on soy for the NIH. I asked him if the glutamate in food, like beans is in the same form and as toxic as the glutamate in MSG and processed soy foods. Robin, if you see this can you repost your information on glutamate?
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The glutamate mystery deepens. Here's a link to the International Food Council's page on glutamate:
http://www.ific.org/publications/brochures/msgbroch.cfm
According to the article, the glutamate in food is the same glutamate as in MSG. Yet, other places are talking about two forms of glutamate, bound (to another molecule) and free, each acting differently in the body. Glutamate is a necessary nutrient. If all glutamate were toxic, why doesn't everyone with seizures react to the many foods high in glutamate. I do not have a good understanding of this and am looking for more information.
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This abstract is rather technical but does explain some aspects of glutamate toxicity. The question now is, do we metabolize the glutamate in food differently than the glutamate in processed foods, like MSG. Feedback?
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1: Neurochem Int. 2006 May-Jun;48(6-7):650-6. Epub 2006 Feb 28.
Short-term fasting, seizure control and brain amino acid metabolism.
Yudkoff M, Daikhin Y, Nissim I, Horyn O, Luhovyy B, Lazarow A, Nissim I.
Department of Pediatrics, Children's Hospital of Philadelphia, University of
Pennsylvania School of Medicine, 19104, USA.
yudkoff@email.chop.edu
The ketogenic diet is an effective treatment for seizures, but the mechanism of
action is unknown. It is uncertain whether the anti-epileptic effect presupposes
ketosis, or whether the restriction of calories and/or carbohydrate might be
sufficient. We found that a relatively brief (24 h) period of low glucose and low
calorie intake significantly attenuated the severity of seizures in young
Sprague-Dawley rats (50-70 gms) in whom convulsions were induced by
administration of pentylenetetrazole (PTZ). The blood glucose concentration was
lower in animals that received less dietary glucose, but the brain glucose level
did not differ from control blood [3-OH-butyrate] tended to be higher in blood,
but not in brain, of animals on a low-glucose intake. The concentration in brain
of glutamine increased and that of alanine declined significantly with
low-glucose intake. The blood alanine level fell more than that of brain alanine,
resulting in a marked increase ( approximately 50%) in the brain:blood ratio for
alanine. In contrast, the brain:blood ratio for leucine declined by about 35% in
the low-glucose group. When animals received [1-(13)C]glucose, a metabolic
precursor of alanine, the appearance of (13)C in alanine and glutamine increased
significantly relative to control. The brain:blood ratio for [(13)C]alanine
exceeded 1, indicating that the alanine must have been formed in brain and not
transported from blood. The elevated brain(alanine):blood(alanine) could mean
that a component of the anti-epileptic effect of low carbohydrate intake is
release of alanine from brain-to-blood, in the process abetting the disposal of
glutamate, excess levels of which in the synaptic cleft would contribute to the
development of seizures.
PMID: 16510212 [PubMed - indexed for MEDLINE]
Related Links
Metabolism of brain amino acids following pentylenetetrazole treatment. [Epilepsy
Res. 2003] PMID:12576176
Seizure resistance is dependent upon age and calorie restriction in rats fed a
ketogenic diet. [Epilepsy Res. 1999] PMID:10232791
A ketogenic diet has different effects upon seizures induced by maximal
electroshock and by pentylenetetrazole infusion. [Epilepsy Res. 2000]
PMID:10642038
Neuronal-glial interactions in rats fed a ketogenic diet. [Neurochem Int. 2006]
PMID:16542760
Ketogenic diet, brain glutamate metabolism and seizure control. [Prostaglandins
Leukot Essent Fatty Acids. 2004] PMID:14769486
