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MSG as a slow neurotoxin

There is sound science that suggests that the glutamic acid in MSG may act as a "slow neurotoxin," not resulting in observable damage such as dementia until years after the MSG is ingested.  Mercury, for example, is a slow neurotoxin – manifesting its toxic effects years after being ingested.  It is entirely possible that the concept of a “slow neurotoxin” may be relevant to the production of human adverse reactions to MSG in some MSG-sensitive people.

The work of Dr. Peter Spencer is particularly relevant(1-3).  In more recent work (2002), Ohguro et al.(4) found that rats fed 10 grams of sodium glutamate added to a 100 gram daily diet for as little as 3 months had a significant increase in the amount of glutamic acid in vitreous, had damage to the retina, and had deficits in retinal function, potentially leading to blindness.  Ohguro et al. also documented the cumulative effect of damage caused by daily ingestion of MSG.

Consumers have reported being able to ingest an MSG-containing food on a given day without having an MSG-type reaction; but upon eating that same food two or three days in a row, a reaction will occur.


1. Spencer PS, Kisby GE, Ludolph AC. Long-latency neurodegenerative disease in the western Pacific. Geriatrics. 1991 Aug;46 Suppl 1:37-42. PMID:1894143

2. Spencer PS, Kisby GE, Ludolph AC. Slow toxins, biologic markers, and long-latency neurodegenerative disease in the western Pacific region.
Neurology. 1991 May;41(5 Suppl 2):62-6; discussion 66-8. PMID:2041595

3. Spencer PS. Guam ALS/parkinsonism-dementia: a long-latency neurotoxic disorder caused by "slow toxin(s)" in food? Can J Neurol Sci. 1987 Aug;14(3 Suppl):347-57. PMID:3315142

4. Ohguro H, Katsushima H, Maruyama I, et al. A high dietary intake of sodium glutamate as flavoring (Ajinomoto) causes gross changes in retinal morphology and function. Exp Eye Res. 2002;75(3):307-15.