MSG: The Chemical and Biological Reactions

Monosodium glutamate (MSG) is a flavorless chemical added to a variety of foods. While there is no 100 percent conclusive study that shows MSG as harmful, it is widely linked to seizures, chest pain, and other adverse side effects in adults and children. In this paper, I will show how the chemistry of MSG causes a negative biological reaction.
N. Peica, C. Lehene, N. Leopold, S. Schlucker, and W. Kiefer (2007) wrote, “MSG or E621, the sodium salt of glutamic acid, is probably the most common food additive used in many packaged and prepared foods” (p. 604). Because of this, it is easy for MSG to hide. This is especially problematic for people who have a sensitivity to MSG. Reporter Sandra Blakeslee (1990) wrote, “Several months ago Jack Samuels, a Chicago businessman, carefully read the label on a box of breakfast cereal and decided it was safe to eat.
An hour later, however, Mr. Samuels collapsed in his physician’s office after a treadmill test. ‘As I started to lose consciousness, I knew it was an MSG attack,’ he said” (p. C3). The article went on to report that the FDA allows several different names for MSG; sometimes the pseudonyms make it difficult for consumers to realize they are ingesting MSG.

In its monohydrate form, the “two carboxy groups of MSG twist to an equal but opposite extent with respect to the carbon chain (Peica et al. 2006, p. 606). In its anhydrous form, “Anhydrous MSG is arched and two hydrogen bond interactions are possible” (Peica et al. 2006, p. 607). Either way, the result is the formation of white crystals. The crystals don’t have any flavor; however, its chemical make-up allows it to enhance the flavor of other foods. MSG concentrations can be as low as 10-5, or much higher.
Michelle Meadows (2003) expressed that the 1995 FASEB report confirmed that MSG is safe if consumed moderately. She added that there is a group of people who is sensitive to MSG if more than 3 grams are consumed at a meal (a typical serving is 0.5 grams). She wrote that some severe and poorly controlled asthmatics also have trouble with MSG consumption. For them, the lack of labeling is problematic because labels only have to reflect foods that have MSG added to them, not foods that contain it naturally, like tomatoes, cheeses, soy sauce, and some meats.
Chris Kilham (2006) pointed out that a vast number of foods contain MSG, although there are plenty of studies that prove its harmful effects. He wrote, “Studies have shown that mice fed large amounts of MSG suffer destruction of brain cells … Several years ago, baby food manufacturers stopped using MSG under intense public pressure. However, MSG remains in popular use” (p. 25). He added that the risk of using MSG is unnecessary, since it has absolutely no nutritional value.
Angelica Soares, Joao Paulo Ferreira Schoffen, Elsa Maria De Gouveia, and Maria Raquel Marcal Natali (2006) also looked at the disturbing effect MSG had on rats. They studied infant rats and found that the bay rats that ingested MSG showed high levels of NADH-diaphorase. The NADH caused nerve damage, as well as caused the baby rats to retain more adipose tissue that the ones not given MSG. The conclusion of the study was that not only did MSG contribute to obesity; it also caused a deterioration in the intestinal lining.
M. Hermanussen, A.P. Garcia, M. Sunder, M. Voigt, V. Salazar, and J.A.F. Tresguerres (2006) agreed with Soares et al (2006), but added some interesting findings of their own. They looked at glutamic acid (GLU), since it is a major component in glutamine. The study started with administering MSG to pregnant rats, then to the offspring of the rats. Obviously, there was a control group not receiving MSG, except what was normally found in the regular feed.
The conclusion was that male rats showed a lot more damage from the MSG than female rats did. Obesity was the obvious result, but, in part, because the MSG-fed rats ate more. This indicated that GLU significantly increased appetite. The group noted, too, that the MSG-fed rats retained much more adipose tissue that the rats that weren’t fed MSG. As well, it was noted that the same nerve damage found in the study by Soares et al. (2006) was consistent with the findings by Hermanussen et al. (2006). Hermanussen et al. clearly discovered impaired glucose tolerance and insulin resistance in their rats, as a result of “GH burst frequency” (p. 30).
Despite statements that there is no definite evidence that MSG causes negative reactions, very recent studies prove the contrary. Since MSG does not add any nutritional value to food, it might be wise to avoid it, especially in large quantities. The studies show that MSG is linked to nerve damage, obesity, voracity, and diabetes. We also know that chemical make-up of the product is more likely to affect men and asthmatics – meaning that a significant number of Americans may suffer adverse reaction s from MSG, and some of them don’t even know why.
References

Blakeslee, S. (1990, March 6). With MSG sensitivity still at issue in studies, label rules tighten.
New York Times, p. C3. Retrieved Thursday, March 29, 2007 from the ProQuest database.
Hermanussen, M., Garcia, A.P., Sunder, M., Voigt, M., Salazar, V., & Tresguerres, J.A.F.
(2006). Obesity, voracity, and short stature: The impact of glutamate on the regulation of appetite. European Journal of Clinical Nutrition, 60, 25-31. Retrieved Thursday, March 29, 2007, from the Academic Search Premier database.
Kilham, C. (2006, March/April). The dangers of chemical food additives. Share Guide, p. 25.
Meadows, M. (2003, January/February). A common flavor enhancer. FDA Consumer, p. 35.
Pieca, N., Lehene, C., Leopold, N., Schlucker, S., & Kiefer, W. (2006). Monosodium glutamate
in its anhydrous and monohydrate form: Differentiation by Raman spectroscopies and density functional calculations. Spectrochimica Acta Part A, 604-615. Retrieved Thursday, March 29, 2007, from the ScienceDirect database.
Soares, A., Schoffen, J.P.F., De Gouveia, E.M., & Natali, M.R.M. (2006). Effects of the neonatal
treatment with monosodium glutamate on myenteric neurons and the intestinal wall in the ileum of rats. Journal of Gastroenterology, 41, 674-680. Retrieved Thursday, March 29, 2007, from the Academic Search Premier database.