Evidence of risk posed by ingestion of processed (manufactured) free glutamic acid (MSG) is undeniable. Retinal damage induced by treatment with monosodium glutamate was demonstrated in 1957 by Lucas and Newhouse. In 1969, Olney demonstrated that treatment with monosodium glutamate causes brain lesions in experimental animals, and that those lesions may be followed by endocrine disorders as the animals approached maturity. During the 1970s, additional research demonstrated that hydrolyzed protein products (which contain MSG just as monosodium glutamate does) will cause brain lesions and neuroendocrine disorders; and that ingestion of monosodium glutamate by the very young will do the same.
The glutamate industry, led by Ajinomoto Co., Inc., the world’s largest producer of monosodium glutamate, responded. Their researchers claimed to replicate the studies that demonstrated MSG-induced neurotoxicity, but did not do so. Delay in examination of potentially damaged tissue beyond the time that damage could be observed, and delay in administering or feeding monosodium glutamate to test animals beyond the age that brain damage would most readily be inflicted, were common to these studies. Researchers also used entirely different (and inappropriate) methods of preservation and staining brain tissue in analysis of results.
As evidence of MSG-induced neurotoxicity became undeniable, the glutamate industry gave up producing its badly flawed animal studies and turned to designing, producing, and publishing human studies that seem to have been carefully designed to guarantee that no difference would be found between subjects given MSG test material and control subjects or between subjects given MSG and subjects given placebos. It was from these studies that they would argue that ingestion of MSG poses no risk to humans.
Today, despite scientific evidence to the contrary, the people who produce and sell products that contain MSG, and their friends at the U.S. Food and Drug Administration (FDA), claim that here are a few people, but only a few people, who will suffer adverse reactions following ingestion of MSG; and that their reactions will be mild and transitory. Similarly, industry claims that it will take a fairly substantial dose of MSG to cause an adverse reaction--a claim that cannot be substantiated because it is literally untrue.
As you read through the studies in this post and in posts that follow, please note that evidence of MSG-induced toxicity rarely comes from researchers in the United States any more. In the United States, researchers who might criticise the safety of MSG are generally not funded, and research done independent of outside funding is generally not published.
MSG Induced Retinal Degeneration
In 1957, Lucas and Newhouse(1) first noticed that severe retinal lesions could be produced in suckling mice (and to some extent in adult mice) by a single injection of glutamate. Studies confirming their findings using neonatal rodents (2-5) and adult rabbits(6) followed shortly, with others being reported from time to time(7-11). These studies concerned themselves not only with the confirmation of monosodium glutamate induced retinal lesions, but with the formulation and testing of hypotheses to explain the phenomenon.
Between 1971 (the date of the last study referenced above) and 2002, there were studies discussing the role of glutamate in diseases of the retina, but no feeding studies. Most, if not all of this research, was done with an eye toward developing pharmaceuticals with which to counter glutamate toxicity related to vision. A number of these studies are cited here as examples of ongoing research(12-18).
In 2002, Ohguro et al.(19) found that rats fed 10 grams of sodium glutamate (97.5% sodium glutamate and 2.5% sodium ribonucleotide) added to a 100 gram daily diet for as little as 3 months had a significant increase in amount of glutamic acid in vitreous, had damage to the retina, and had deficits in retinal function. Ohguro et al. also documented the cumulative effect of damage caused by daily ingestion of MSG.
Subsequently, reports of toxic effects of monosodium glutamate on the retina have come from studies at the University of Pecs, Hungary, where the neuroprotective effects of PACAP in the retina have been studied(20-21).
REFERENCES
________________________________________
1. Lucas DR, Newhouse JP. The toxic effect of sodium-L-glutamate on the inner layers of the retina. AMA Arch Ophthalmol. 1957;58(2):193-201.
2. Potts AM, Modrell RW, Kingsbury C. Permanent fractionation of the electroretinogram by sodium glutamate. Am J Ophthalmol. 1960;50(Nov): 900-907.
3. Freedman JK, Potts AM. Repression of glutaminase I in the rat retina by administration of sodium-L-glutamate. Invest Ophthalmol Vis Sci. 1962;1(Feb):118-121.
4. Freedman JK, Potts AM. Repression of glutaminase I in the rat retina by administration of sodium-L-glutamate II. Invest Ophthal Vis Sci. 1963;2(June):252-258.
5. Potts AM. Selective action of chemical agents on individual retinal layers. In: Graymore CN, ed. Biochemistry of the retina. New York: Academic Press; 1965:155-161.
6. Hamatsu T. Experimental studies on the effect of sodium iodate and sodium L-glutamate on ERG and histological structure of retina in adult rabbits. Acta Soc Ophthalmol Jpn. 1964;68(11):1621-1636. (Abstract)
7. Hansson HA. Ultrastructure studies on long-term effects of MSG on rat retina. Virchows Arch [Zellpathol]. 1970;6(1):1-11.
8. Cohen AI. An electron microscopic study of the modification by monosodium glutamate of the retinas of normal and "rodless" mice. Am J Anat. 1967;120(2): 319-356.
9. Olney JW. Glutamate-induced retinal degeneration in neonatal mice. Electron-microscopy of the acutely evolving lesion. J Neuropathol Exp Neurol 1969;28(3):455-474.
10. Hansson HA. Scanning electron microscopic studies on the long term effects of sodium glutamate on the rat retina. Virchows Arch ABT B (Zellpathol). 1970; 4(4): 357-367.
11. Arees E, Sandrew B, Mayer J. MSG-induced optic pathway lesions in infant mice following subcutaneous injection. Fed Proc. 1971;30(2):287Abs (Abstract # 521).
12.Casper DS, Trelstad RL, Reif-Lehrer L. Glutamate-induced cellular injury in isolated chick embryo retina: Müller cell localization of initial effects. J Comp Neurol. 1982 Jul 20;209(1):79-90.
13. Katz A, Kruger EF, Minko G, Liu CH, Rosen RB, Alfano RR. Detection of glutamate in the eye by Raman spectroscopy. J Biomed Opt. 2003 Apr;8(2):167-72.
14. Van Rijn CM, Marani E, Rietveld WJ. The neurotoxic effect of monosodium glutamate (MSG) on the retinal ganglion cells of the albino rat. Histol Histopathol. 1986 Jul;1(3):291-5.
15. Azuma N, Kawamura M, Kohsaka S. [Morphological and immunohistochemical studies on degenerative changes of the retina and the optic nerve in neonatal rats injected with monosodium-L-glutamate]. Nippon Ganka Gakkai Zasshi. 1989 Jan;93(1):72-9. [Article in Japanese]
16. Bellhorn RW, Lipman DA, Confino J, Burns MS. Effect of monosodium glutamate on retinal vessel development and permeability in rats. Invest Ophthalmol Vis Sci. 1981 Aug;21(2):237-47.
17. Fang JH, Wang XH, Xu ZR, Jiang FG. Neuroprotective effects of bis(7)-tacrine against glutamate-induced retinal ganglion cells damage. BMC Neurosci. 2010 Mar 3;11:31.
18. Varga B, Szabadfi K, Kiss P, Fabian E, Tamas A, Griecs M, Gabriel R, Reglodi D, Kemeny-Beke A, Pamer Z, Biro Z, Tosaki A, Atlasz T, Juhasz B. PACAP improves functional outcome in excitotoxic retinal lesion: an electroretinographic study. J Mol Neurosci. 2011 Jan;43(1):44-50. Epub 2010 Jun 22.
19. 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.
20. Babai N, Atlasz T, Tamas A, et al. Search for the optimal monosodium glutamate treatment schedule to study the neuroprotective effects of PACAP in the retina. Ann N Y Acad Sci. 2006;1070(July):149-155.
21. Szabadfi K, Atlasz T, Horvath G, et al. Early postnatal enriched environment decreases retinal degeneration induced by monosodium glutamate treatment in rats. Brain Res. 2009;1259(March):107-12.
The glutamate industry, led by Ajinomoto Co., Inc., the world’s largest producer of monosodium glutamate, responded. Their researchers claimed to replicate the studies that demonstrated MSG-induced neurotoxicity, but did not do so. Delay in examination of potentially damaged tissue beyond the time that damage could be observed, and delay in administering or feeding monosodium glutamate to test animals beyond the age that brain damage would most readily be inflicted, were common to these studies. Researchers also used entirely different (and inappropriate) methods of preservation and staining brain tissue in analysis of results.
As evidence of MSG-induced neurotoxicity became undeniable, the glutamate industry gave up producing its badly flawed animal studies and turned to designing, producing, and publishing human studies that seem to have been carefully designed to guarantee that no difference would be found between subjects given MSG test material and control subjects or between subjects given MSG and subjects given placebos. It was from these studies that they would argue that ingestion of MSG poses no risk to humans.
Today, despite scientific evidence to the contrary, the people who produce and sell products that contain MSG, and their friends at the U.S. Food and Drug Administration (FDA), claim that here are a few people, but only a few people, who will suffer adverse reactions following ingestion of MSG; and that their reactions will be mild and transitory. Similarly, industry claims that it will take a fairly substantial dose of MSG to cause an adverse reaction--a claim that cannot be substantiated because it is literally untrue.
As you read through the studies in this post and in posts that follow, please note that evidence of MSG-induced toxicity rarely comes from researchers in the United States any more. In the United States, researchers who might criticise the safety of MSG are generally not funded, and research done independent of outside funding is generally not published.
MSG Induced Retinal Degeneration
In 1957, Lucas and Newhouse(1) first noticed that severe retinal lesions could be produced in suckling mice (and to some extent in adult mice) by a single injection of glutamate. Studies confirming their findings using neonatal rodents (2-5) and adult rabbits(6) followed shortly, with others being reported from time to time(7-11). These studies concerned themselves not only with the confirmation of monosodium glutamate induced retinal lesions, but with the formulation and testing of hypotheses to explain the phenomenon.
Between 1971 (the date of the last study referenced above) and 2002, there were studies discussing the role of glutamate in diseases of the retina, but no feeding studies. Most, if not all of this research, was done with an eye toward developing pharmaceuticals with which to counter glutamate toxicity related to vision. A number of these studies are cited here as examples of ongoing research(12-18).
In 2002, Ohguro et al.(19) found that rats fed 10 grams of sodium glutamate (97.5% sodium glutamate and 2.5% sodium ribonucleotide) added to a 100 gram daily diet for as little as 3 months had a significant increase in amount of glutamic acid in vitreous, had damage to the retina, and had deficits in retinal function. Ohguro et al. also documented the cumulative effect of damage caused by daily ingestion of MSG.
Subsequently, reports of toxic effects of monosodium glutamate on the retina have come from studies at the University of Pecs, Hungary, where the neuroprotective effects of PACAP in the retina have been studied(20-21).
REFERENCES
________________________________________
1. Lucas DR, Newhouse JP. The toxic effect of sodium-L-glutamate on the inner layers of the retina. AMA Arch Ophthalmol. 1957;58(2):193-201.
2. Potts AM, Modrell RW, Kingsbury C. Permanent fractionation of the electroretinogram by sodium glutamate. Am J Ophthalmol. 1960;50(Nov): 900-907.
3. Freedman JK, Potts AM. Repression of glutaminase I in the rat retina by administration of sodium-L-glutamate. Invest Ophthalmol Vis Sci. 1962;1(Feb):118-121.
4. Freedman JK, Potts AM. Repression of glutaminase I in the rat retina by administration of sodium-L-glutamate II. Invest Ophthal Vis Sci. 1963;2(June):252-258.
5. Potts AM. Selective action of chemical agents on individual retinal layers. In: Graymore CN, ed. Biochemistry of the retina. New York: Academic Press; 1965:155-161.
6. Hamatsu T. Experimental studies on the effect of sodium iodate and sodium L-glutamate on ERG and histological structure of retina in adult rabbits. Acta Soc Ophthalmol Jpn. 1964;68(11):1621-1636. (Abstract)
7. Hansson HA. Ultrastructure studies on long-term effects of MSG on rat retina. Virchows Arch [Zellpathol]. 1970;6(1):1-11.
8. Cohen AI. An electron microscopic study of the modification by monosodium glutamate of the retinas of normal and "rodless" mice. Am J Anat. 1967;120(2): 319-356.
9. Olney JW. Glutamate-induced retinal degeneration in neonatal mice. Electron-microscopy of the acutely evolving lesion. J Neuropathol Exp Neurol 1969;28(3):455-474.
10. Hansson HA. Scanning electron microscopic studies on the long term effects of sodium glutamate on the rat retina. Virchows Arch ABT B (Zellpathol). 1970; 4(4): 357-367.
11. Arees E, Sandrew B, Mayer J. MSG-induced optic pathway lesions in infant mice following subcutaneous injection. Fed Proc. 1971;30(2):287Abs (Abstract # 521).
12.Casper DS, Trelstad RL, Reif-Lehrer L. Glutamate-induced cellular injury in isolated chick embryo retina: Müller cell localization of initial effects. J Comp Neurol. 1982 Jul 20;209(1):79-90.
13. Katz A, Kruger EF, Minko G, Liu CH, Rosen RB, Alfano RR. Detection of glutamate in the eye by Raman spectroscopy. J Biomed Opt. 2003 Apr;8(2):167-72.
14. Van Rijn CM, Marani E, Rietveld WJ. The neurotoxic effect of monosodium glutamate (MSG) on the retinal ganglion cells of the albino rat. Histol Histopathol. 1986 Jul;1(3):291-5.
15. Azuma N, Kawamura M, Kohsaka S. [Morphological and immunohistochemical studies on degenerative changes of the retina and the optic nerve in neonatal rats injected with monosodium-L-glutamate]. Nippon Ganka Gakkai Zasshi. 1989 Jan;93(1):72-9. [Article in Japanese]
16. Bellhorn RW, Lipman DA, Confino J, Burns MS. Effect of monosodium glutamate on retinal vessel development and permeability in rats. Invest Ophthalmol Vis Sci. 1981 Aug;21(2):237-47.
17. Fang JH, Wang XH, Xu ZR, Jiang FG. Neuroprotective effects of bis(7)-tacrine against glutamate-induced retinal ganglion cells damage. BMC Neurosci. 2010 Mar 3;11:31.
18. Varga B, Szabadfi K, Kiss P, Fabian E, Tamas A, Griecs M, Gabriel R, Reglodi D, Kemeny-Beke A, Pamer Z, Biro Z, Tosaki A, Atlasz T, Juhasz B. PACAP improves functional outcome in excitotoxic retinal lesion: an electroretinographic study. J Mol Neurosci. 2011 Jan;43(1):44-50. Epub 2010 Jun 22.
19. 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.
20. Babai N, Atlasz T, Tamas A, et al. Search for the optimal monosodium glutamate treatment schedule to study the neuroprotective effects of PACAP in the retina. Ann N Y Acad Sci. 2006;1070(July):149-155.
21. Szabadfi K, Atlasz T, Horvath G, et al. Early postnatal enriched environment decreases retinal degeneration induced by monosodium glutamate treatment in rats. Brain Res. 2009;1259(March):107-12.
