Scientists Tell Us that Use of MSG Places Humans at Risk

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Scientists Tell Us that Use of MSG Places Humans at Risk

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Sound scientific research tells us that MSG causes brain lesions, is an

endocrine disruptor, can cause retinal degeneration leading to blindness, can

cause behavior problems, crosses the blood brain barrier with much greater

ease than the glutes would have you believe, crosses the placental

barrier, and can be passed on to an infant by a nursing mother who has ingested

MSG.

As early as 1957, Lucas and Newhouse (1) noticed that severe retinal

lesions could be produced in suckling mice (and to some extent in adult mice)

by

a single injection of free glutamic acid. Studies confirming their

findings using neonatal rodents (2-5) and adult rabbits (6) followed shortly

thereafter, with others being reported from time to time.(7-11)

In 2002, Ohguro et al. (11+) 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.(11+) documented the suspicion of many MSG-sensitive people

that there is a cumulative effect to the damage caused by daily ingestion of

MSG.

Studies commencing in 1969 demonstrated that treatment with free glutamic

acid caused brain lesions, particularly acute neuronal necrosis in several

regions of the developing brain of neonatal mice, and acute lesions in the

brains of adult mice given 5 to 7 mg/g of free glutamic acid

subcutaneously.(12)

Research which followed confirmed that free glutamic acid, which is

usually given as the sodium salt, monosodium glutamate, induced hypothalamic

damage when given to immature animals after either subcutaneous (13-34) or oral

(19,25,26,28,35-39) doses.

Studies completed in the 1970's demonstrated that at least 25% of the

population react to free glutamic acid in processed food, a substance popularly

referred to as MSG.(40-43) Today, we recognize that MSG-reactions range

from mild and transitory to debilitating and/or life threatening.(44)

People who are sensitive to MSG react to glutamic acid only in its free

form, and only if it has been created through fermentation or some other

manufacturing process. Manufactured free glutamic acid differs from glutamic

acid bound in protein in that the latter is L-glutamic acid only(45-47),

while the former contains L-glutamic acid, D-glutamic acid (45-46), and

pyroglutamic acid, and may also contain mono and dichloropropanols, and/or

heterocyclic amines.(48-49)

Free glutamic acid ingested as MSG can cross the placenta during

pregnancy,(50-51) can cross the blood brain barrier in an unregulated manner

during

development, and can pass through the five circumventricular organs, which

are " leaky " at best at any stage of life.(52-53) In addition, the blood

brain barrier can be compromised by such things as drugs, seizures, stroke,

trauma to the head, hypoglycemia, hypertension, extreme physical stress, high

fever, and the normal process of aging.(54) It is generally accepted that

the young are particularly at risk from ingestion of MSG.

REFERENCES for the above.

REFERENCES to additional studies that tell us that processed free glutamic

acid (MSG) places humans at risk follow below.

1. Lucas, D.R. and Newhouse, J. P. The toxic effect of sodium-L-glutamate

on the inner layers of the retina. AMA Arch Ophthalmol 58: 193-201, 1957.

2. Potts, A.M., Modrell, R.W., and Kingsbury, C. Permanent fractionation

of the electroretinogram by sodium glutamate. Am J Ophthalmol 50: 900-907,

1960.

3. Freedman, J.K., and Potts, A.M. Repression of glutaminase I in the rat

retina by administration of sodium L-glutamate. Invest Ophthalmol 1:

118-121, 1962.

4. Freedman, J.K., and Potts, A.M. Repression of glutaminase I in rat

retina by administration of sodium L-glutamate. Invest Ophthal 2: 252, 1963.

5. Potts, A.M. Selective action of chemical agents on individual retinal

layers. In: Biochemistry of the retina. Graymore, C.N., Ed. New York:

Academic Press, 1965. pp 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 68: 1621-1636, 1964. (Abstract)

7. Hansson, H.A. Ultrastructure studies on long-term effects of MSG on rat

retina. Virchows Arch [Zellpathol] 6: 1, 1970.

8. Cohen, A.I. An electron microscopic study of the modification by

monosodium glutamate of the retinas of normal and " rodless " mice. Am J Anat

120:

319-356, 1967.

9. Olney, J.W. Glutamate-induced retinal degeneration in neonatal mice.

Electron-microscopy of the acutely evolving lesion. J Neuropathol Exp Neurol

28: 455-474, 1969.

10. Hansson, H.A. Scanning electron microscopic studies on the long term

effects of sodium glutamate on the rat retina. Virchows Arch ABT B

(Zellpathol) 4: 357-367, 1970.

11. Arees, E., Sandrew, B., and Mayer, J. MSG-induced optic pathway

lesions in infant mice following subcutaneous injection. Fed Proc 30: 521,

1971.

11+. Ohguro, H., Katsushima, H., Maruyama, I., Maeda, T., Yanagihashi, S.

Metoki, T., Nakazawa, M. A high dietary intake of sodium glutamate as

flavoring (Ajinomoto) causes gross changes in retinal morphology and function.

Experimental Eye Research 75:(3),2002.

12. Olney, J.W. Brain lesions, obesity, and other disturbances in mice

treated with monosodium glutamate. Science 164: 719-721, 1969.

13. Olney, J.W. Ho, O.L., and Rhee, V. Cytotoxic effects of acidic and

sulphur containing amino acids on the infant mouse central nervous system. Exp

Brain Res 14: 61-76, 1971.

14. Olney, J.W., and Sharpe, L.G. Brain lesions in an infant rhesus monkey

treated with monosodium glutamate. Science 166: 386-388, 1969.

15. Snapir, N., Robinzon, B., and Perek, M. Brain damage in the male

domestic fowl treated with monosodium glutamate. Poult Sci 50: 1511-1514, 1971.

16. Perez, V.J. and Olney, J.W. Accumulation of glutamic acid in the

arcuate nucleus of the hypothalamus of the infant mouse following subcutaneous

administration of monosodium glutamate. J Neurochem 19: 1777-1782, 1972.

17. Arees, E.A., and Mayer, J. Monosodium glutamate-induced brain lesions:

electron microscopic examination. Science 170: 549-550, 1970.

18. Arees, E.A., and Mayer, J. Monosodium glutamate-induced brain lesions

in mice. Presented at the 47th Annual Meeting of American Association of

Neuropathologists, Puerto Rico, June 25-27, 1971. J Neuropath Exp Neurol 31:

181, 1972. (Abstract)

19. Everly, J.L. Light microscopy examination of monosodium glutamate

induced lesions in the brain of fetal and neonatal rats. Anat Rec 169: 312,

1971.

20. Olney, J.W. Glutamate-induced neuronal necrosis in the infant mouse

hypothalamus. J Neuropathol Exp Neurol 30: 75-90, 1971.

21. Lamperti, A., and Blaha, G. The effects of neonatally-administered

monosodium glutamate on the reproductive system of adult hamsters. Biol Reprod

14: 362-369, 1976.

22. Takasaki, Y. Studies on brain lesion by administration of monosodium

L-glutamate to mice. I. Brain lesions in infant mice caused by

administration of monosodium L-glutamate. Toxicology 9: 293-305, 1978.

23. Holzwarth-McBride, M.A., Hurst, E.M., and Knigge, K.M. Monosodium

glutamate induced lesions of the arcuate nucleus. I. Endocrine deficiency and

ultrastructure of the median eminence. Anat Rec 186: 185-196, 1976.

24. Holzwarth-McBride, M.A., Sladek, J.R., and Knigge, K.M. Monosodium

glutamate induced lesions of the arcuate nucleus. II Fluorescence

histochemistry of catecholamines. Anat Rec 186: 197-205, 1976.

25. Paull, W.K., and Lechan, R. The median eminence of mice with a MSG

induced arcuate lesion. Anat Rec 180: 436, 1974.

26. Burde, R.M., Schainker, B., and Kayes, J. Acute effect of oral and

subcutaneous administration of monosodium glutamate on the arcuate nucleus of

the hypothalamus in mice and rats. Nature (Lond) 233: 58-60, 1971.

27. Olney, J.W. Sharpe, L.G., Feigin, R.D. Glutamate-induced brain damage

in infant primates. J Neuropathol Exp Neurol 31: 464-488, 1972.

28. Abraham, R., Doughtery, W., Goldberg, L., and Coulston, F. The

response of the hypothalamus to high doses of monosodium glutamate in mice and

monkeys: cytochemistry and ultrastructural study of lysosomal changes. Exp Mol

Pathol 15: 43-60, 1971.

29. Burde, R.M., Schainker, B., and Kayes, J. Monosodium glutamate:

necrosis of hypothalamic neurons in infant rats and mice following either oral

or

subcutaneous administration. J Neuropathol Exp Neurol 31: 181, 1972.

30. Robinzon, B., Snapir, N., and Perek, M. Age dependent sensitivity to

monosodium glutamate inducing brain damage in the chicken. Poult Sci 53:

1539-1942, 1974.

31. Tafelski, T.J. Effects of monosodium glutamate on the neuroendocrine

axis of the hamster. Anat Rec 184: 543-544, 1976.

32. Coulston, F. In: Report of NAS,NRC, Food Protection Subcommittee on

Monosodium Glutamate. July, 1970. pp 24-25.

33. Inouye, M. and Murakami, U. Brain lesions and obesity in mouse

offspring caused by maternal administration of monosodium glutamate during

pregnancy. Congenital Anomalies 14: 77-83, 1974.

34. Olney, J.W., Rhee, V. and DeGubareff, T. Neurotoxic effects of

glutamate on mouse area postrema. Brain Research 120: 151-157, 1977.

35. Olney, J.W., Ho, O.L. Brain damage in infant mice following oral

intake of glutamate, aspartate or cystine. Nature (Lond) 227: 609-611, 1970.

36. Lemkey-Johnston, N., and Reynolds, W.A. Incidence and extent of brain

lesions in mice following ingestion of monosodium glutamate (MSG). Anat Rec

172: 354, 1972.

37. Takasaki, Y. Protective effect of mono- and disaccharides on

glutamate-induced brain damage in mice. Toxicol Lett 4: 205-210, 1979.

38. Takasaki, Y. Protective effect of arginine, leucine, and preinjection

of insulin on glutamate neurotoxicity in mice. Toxicol Lett 5: 39-44, 1980.

 

39. Lemkey-Johnston, N., and Reynolds, W.A. Nature and extent of brain

lesions in mice related to ingestion of monosodium glutamate: a light and

electron microscope study. J Neuropath Exp Neurol 33: 74-97, 1974.

40. Kenney, RA and Tidball, CS Human susceptibility to oral monosodium

L-glutamate. Am J Clin Nutr. 25:140-146, 1972.

41. Reif-Lehrer, L. Prevalence of Chinese restaurant syndrome. Federation

Proceedings 35:1617-1623,1977.

42. Kerr, GR, Wu-Lee, M, El-Lozy, M, McGandy, R, and Stare, F.

Food-symptomatology questionnaires: risks of demand-bias questions and

population-biased surveys. In: Glutamic Acid: Advances in Biochemistry and

Physiology

Filer, LJ, et al., eds. New York: Raven Press, 1979.

43. Schaumburg, HH, Byck, R, Gerstl, R, and Mashman, JH. Monosodium

L-glutamate: its pharmacology and role in the Chinese restaurant syndrome.

Science 163:826-828,1969.

44. Analysis of Adverse Reactions to Monosodium Glutamate (MSG). Prepared

for the Center for Food Safety and Applied Nutrition, Food and Drug

Administration. Raiten, DJ, Talbot, JM, and Fisher, KD, eds. Bethesda, Maryland:

Life Sciences Research Office of the Federation of American Societies for

Experimental Biology, July, 1995.

45. Rundlett, KL, and Armstrong, DW. Evaluation of Free D-Glutamate in

Processed Foods. Chirality 6:277-282, 1994.

46. Man, EH, and Bada, JL. Dietary D-Amino Acids. Ann. Rev. Nutr.

7:209-25,1987.

47. Analysis of Adverse Reactions to Monosodium Glutamate (MSG). Prepared

for the Center for Food Safety and Applied Nutrition, Food and Drug

Administration. Raiten, DJ, Talbot, JM, and Fisher, KD, eds. Bethesda, Maryland:

Life Sciences Research Office of the Federation of American Societies for

Experimental Biology, July, 1995. Page 9.

48. Pommer, K. (Novo Nordisk BioChem Inc., Franklinton, NC) Cereal Foods W

orld. October, 1995 Vol 40. No 10. Page 745.

49. Analysis of Adverse Reactions to Monosodium Glutamate (MSG). Prepared

for the Center for Food Safety and Applied Nutrition, Food and Drug

Administration. Raiten, DJ, Talbot, JM, and Fisher, KD, eds. Bethesda, Maryland:

Life Sciences Research Office of the Federation of American Societies for

Experimental Biology, July, 1995. Page 32.

50. Frieder, B, and Grimm, VE. Prenatal monosodium glutamate (MSG)

treatment given through the mother's diet causes behavioral deficits in rat

offspring. Intern J Neurosci. 23:117-126,1984.

51. Gao, J, Wu, J, Zhao, XN, Zhang, WN, Zhang, YY, Zhang, ZX.

[Transplacental neurotoxic effects of monosodium glutamate on structures and

functions

of specific brain areas of filial mice.] Sheng Li Hsueh Pao Acta

Physiologica Sinica. 46:44-51,1994.

52. Price MT, Olney JW, Lowry OH, Buchsbaum S. Uptake of exogenous

glutamate and aspartate by circumventricular organs but not other regions of

brain. J. Neurochem. 36:1774-1780,1981.

53. Broadwell RD, Sofroniew MV. Serum proteins bypass the blood-brain

fluid barriers for extracellular entry to the central nervous system. Exp

Neurol. 120:245-263,1993.

54. Blaylock, RL. Excitotoxins: The Taste That Kills. Santa Fe, NM: Health

Press; 1994.

REFERENCES - to additional studies that tell us that processed free

glutamic acid (MSG) places humans at risk:

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Broadwell, R.D., and Sofroniew, M.V. Serum proteins bypass the blood-brain

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Neurol. 120: 245-263, 1993.

Choi, D.W., and Rothman. S.M. The role of glutamate neurotoxicity in

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Cochran, J.W., and Cochran A.H. Monosodium glutamania: the Chinese

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Colman, A.D. Possible psychiatric reactions to monosodium glutamate. N

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During, M.J., and Spencer, D.D. Extracellular hippocampal glutamate and

spontaneous seizure in the conscious human brain. Lancet 341: 1607-1610,

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Elman, R. The intravenous use of protein and protein hydrolysates. Ann New

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Fisher, K.N., Turner, R.A., Pineault, G., Kleim, J., and Saari, M.J. The

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Freed, D.L.J. and Carter, R. Neuropathy due to monosodium glutamate

intolerance. Annals of Allergy. 48: 96-97, 1982.

Frieder, B. and Grimm, V.E. Prenatal monosodium glutamate (MSG) treatment

given through the mother's diet causes behavioral deficits in rat

offspring. Intern J Neurosci. 23: 117-126, 1984.

Frieder, B. and Grimm, V.E. Prenatal monosodium glutamate. Neurochem. 48:

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Gann, D. Ventricular tachycardia in a patient with the " Chinese restaurant

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Gao, J., Wu, J., Zhao, X.N., Zhang, W.N., Zhang, Y.Y., and Zhang, Z.X.

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York:

Oxford University Press, 1973.

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