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Processed free glutamic acid

Monosodium glutamate is the common or usual name assigned by the FDA to the ingredient that contains approximately 78 percent free glutamic acid, 22 percent sodium, and a maximum of 1 per cent contaminant.

Glutamic acid-containing ingredients with lesser amounts of free glutamic acid are assigned other common or usual names such as autolyzed yeast, hydrolyzed lecithin, sodium caseinate, and yeast food, for example.

The FDA makes a meaningless distinction between the ingredient called monosodium glutamate and all of the other hydrolyzed protein products. All, by FDA definition, are "natural" or "naturally occurring." All contain processed free glutamic acid that has been freed from protein, or excreted by bacteria, through a manufacturing process. But the industry refers to the processed free glutamic acid in the former as "added," and to the processed free glutamic acid in the latter as "naturally occurring."

Much of the argument for the safety of MSG is based on this meaningless distinction between food additive monosodium glutamate and other hydrolyzed protein products. The distinction is meaningless in a discussion of adverse reactions to processed free glutamic acid because glutamic acid that has been freed from protein or excreted by bacteria through a manufacturing process causes brain lesions, neuroendocrine disorders, and adverse reactions regardless of the method of processing, regardless of the source of the protein, and regardless of the name of the ingredient that contains it.

There is, however, a meaningful distinction to be made between processed free glutamic acid products and truly natural glutamic acid found in or accompanying truly natural, unfermented, unadulterated, unprocessed protein. The processed product contains L-glutamic acid, D-glutamic acid, pyroglutamic acid, and may contain other chemicals/contaminants. The truly natural glutamic acid found in higher organisms contains L-glutamic acid, only. Defenders of the safety of MSG state that processed free glutamic acid is both structurally and functionally identical to truly natural free glutamic acid. That statement simply is not true.


Excerpt from the prepared statement of John W. Olney, M.D.
pertaining to adverse reactions to monosodium glutamate
presented before the Federation of American Societies for Experimental Biology
April, 1993

...When I reported in 1969-70 that glutamate destroys neurons in the hypothalamus when administered either subcutaneously or orally to immature mice (9-12), a U.S. Senate Nutrition Committee was investigating infant nutrition and asked me to comment on the fact that glutamate was being added to baby foods....Under pressure from the Senate committee, FDA arranged for a special ‘scientific' committee to evaluate the safety of glutamate for babies. The committee investigated the matter and concluded that glutamate was safe, but the committee was then investigated and most of its members were found to have close financial ties with the food industry....Of particular note, the committee Chairman, Lloyd J. Filer, was found to be receiving moneys from both the baby food industry and the glutamate industry while he chaired this committee.

When the Filer committee met in 1969-70, I was asked to present my findings to them. Inter alia, I advised the committee that I had demonstrated glutamate-induced brain damage in infant monkeys as well as rodents; the monkey findings were not yet published, but I presented them to the Filer committee. Carefully thereafter, over a period of two years, I completed my monkey study and published the data in the world's leading neuropathology journal (3). Hastily, on behalf of the glutamate and food industries, Filer assembled a group of non-neuroscientists (Reynolds, Filer et al) to study the issue. They hurriedly reported in Science in 1971 that infant monkeys are not susceptible to glutamate neurotoxicity (33) and recommended that my findings be dismissed as fixation artifact. At this time, the glutamate and food industries had also hired several other non-neuroscience groups to study this brain damage issue. At first, they claimed that my findings could not be confirmed in any species, not even rodents (e.g., se 17), but later the industry consortium changed their story with respect to rodents and other subprimate species when numerous legitimate neuroscientists began reporting confirmation of my findings in the inexpensive species. However, the accuracy and authenticity of the industry findings in monkeys were never challenged, except by me, for a simple reason: no one outside of the food/glutamate industry circle had either the motivation or funding to study monkeys.

In the 1970 era, I was alarmed at some apparent flaws in the Reynolds et al. report in Science and began to challenge these authors. For example, they tube-fed very large doses of glutamate to infant monkeys, which led me to suspect that their infant monkeys probably vomited (large doses of glutamate are known to induce vomiting in monkeys). This raised a crucial issue; if their infant monkeys vomited, they obviously lost dose control and this would render their data unreliable for establishing the safety of glutamate. I questioned Dr. Reynolds on this in public at a scientific meeting a few months before their Science paper appeared in print. In front of a large audience, she admitted that their monkeys vomited. When their Science paper appeared in print (33), I was surprised to read the following description: 'Each infant was maintained in an incubator with handling and cuddling at intervals for a 6 hour period. No unusual behavior was exhibited by the infants.' No mention was made at all of vomiting. Therefore, I wrote a letter to Science pointing out that by the author's own acknowledgment at a public meeting, these infants had vomited. The letter was accepted for publication in Science and was sent to Dr. Reynolds for her response. To my astonishment, in a letter signed by Reynolds, she responded with a denial that they had encountered problems with vomiting or with dose control. Therefore, I withdrew my letter and this exchange was never published.

....In the following year, I invited Reynolds et al. to send a member of their group to my laboratory to learn how to find glutamate damage in monkey brain. In May 1972, a member of their group (Dr. N. Lemkey-Johnston) did visit my laboratory and reviewed microscopic slides with me and she told me she was convinced that glutamate neuropathology was present in the hypothalamus of my monkeys. She also thanked me for pointing out specifically where to look in the hypothalamus to find these lesions. Two years later, when Reynolds et al. published their second paper (34), they stated that they had treated a few additional monkeys with glutamate and had serially sectioned the hypothalamus to provide definitive evidence of no damage. To my amazement, the illustration they showed was once again from the wrong region of the brain....

....In summary, the record shows that FDA for two decades has been assuring the public that glutamate is safe, based almost exclusively on certain industry-generated monkey data which appear upon close scrutiny to be seriously flawed, unreliable and spurious. However, even if these data were not flawed, unreliable and spurious, it is obvious from industry's own finding, shown in Fig. 1 above, that the pharmacokinetics of glutamate absorption and/or metabolism are so disparate between monkeys and man that monkeys, despite their phylogenetic closeness to humans, must be regarded as a singularly inappropriate animal model for evaluating oral glutamate safety. The same oral dose of glutamate that causes a dramatic increase in blood glutamate concentrations in humans, causes no increase at all in monkeys. Therefore, it is difficult to understand why so much money and effort was expended on oral glutamate monkey studies, unless the goal was to amass an unchallengeable mountain of negative evidence that could serve as basis for fostering the misleading impression, and fueling the spurious argument, that if monkeys are resistant to glutamate-induced brain damage, other primates, including humans, must be similarly resistant.

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This page was last updated on June 6, 2004.