Evidence of MSG toxicity

There are three lines of evidence pointing to the toxic potential of monosodium glutamate

I. The first study to address the possibility that glutamate from exogenous sources (eating for example) might cause brain damage followed by obesity and reproductive dysfunction was published in 1969. At the time, researchers were administering glutamate to laboratory animals subcutaneously using Accent brand MSG because it had been observed that MSG was as effective for inflicting brain damage as more expensive pharmaceutical grade L-glutamate (1).

In the decade that followed, research confirmed that glutamate induces hypothalamic damage when given to immature animals after either subcutaneous or oral doses (2).

II. In the 1980s, researchers focused on identifying and understanding abnormalities associated with glutamate, often for the purpose of finding drugs that would mitigate glutamate’s adverse effects. Researchers had found that glutamate was an excitotoxic amino acid. When consumed in controlled quantities, it is essential to normal body function as neurotransmitters and building blocks of protein. But when accumulated in interstitial tissue in quantities greater than needed for normal body function (in excess) it becomes excitotoxic, firing repeatedly and killing brain cells.

It is well documented that L-glutamate is implicated in kidney and liver disorders, neurodegenerative disease, and more. By 1980, glutamate-associated disorders such as headaches, asthma, diabetes, muscle pain, atrial fibrillation, ischemia, trauma, seizures, stroke, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis, Huntington’s disease, Parkinson’s disease, depression, schizophrenia, obsessive-compulsive disorder (OCD), epilepsy, addiction, attention-deficit/hyperactivity disorder (ADHD), frontotemporal dementia and autism were on the rise, and evidence of the toxic effects of glutamate were generally accepted by the scientific community. A November 15, 2020 search of the National Library of Medicine using PubMed.gov returned 3872 citations for “glutamate-induced.”

By and large, the glutamate in question here was, and still is, glutamate from endogenous sources (glutamate originating within the body). The possible toxicity of glutamate from exogenous sources (sources that originate outside of the body) such as glutamate-containing flavor enhancers or other foods, has generally not been considered. Only Olney and a few others have suggested that ingestion of free glutamate might play a role in producing the excess amounts of glutamate needed for endogenous glutamate to become excitotoxic.

III. The third line of evidence should be studies of the effects of eating MSG, but they are virtually non-existent. Studies of glutamate found in the human body are largely funded by pharmaceutical companies interested in developing drugs with which to fight the effects of glutamate on neurodegenerative disease, obesity, and reproductive disorders for example. Those in the glutamate industry, who know full well that the glutamate in MSG is toxic, are not interested in research on the possible toxicity of ingested MSG. And it would appear that by monetarily rewarding certain activities and discouraging others, researchers are not encouraged to find alternative funding sources to pursue research on the possible toxicity of MSG. Instead, the third line of evidence comes from badly flawed studies produced by the producer of MSG to convince the public that MSG is a harmless food additive. Studies that are flawed to the point of being fraudulent. Thus the third line of evidence of MSG toxicity lies in the flawed studies turned out by glutamate-industry agents in their attempts to deceive the public into believing that MSG is “safe.”

It was possibly to counter data that first demonstrated that L-glutamate and MSG cause brain damage, that researchers pretended to replicate animal toxicity studies but did not do so. But glutamate-industry agents made no attempt to examine MSG-induced brain damage in humans. Rather, in the 1980s human studies of adverse reactions as opposed to brain damage were offered to the FDA as evidence that MSG was a harmless food additive. These weren’t alleged replications like the brain-damage studies were, but were creatively designed, each apparently calculated to produce negative results (i.e., no harm done by MSG). Negative results were ensured when researchers considered the effects of glutamate on irrelevant variables, i.e., variables such as blood pressure and weight loss that have never been shown to be associated with glutamate-induced toxicity. Or if females exhibited MSG-induced reproductive disorders and males did not, males would be studied. A variation used was to study the effects of ingestion of glutamate on plasma glutamate levels. Elevated plasma glutamate is associated with production of brain lesions but has never been shown to be relevant to glutamate-induced adverse reactions. The logical fallacy in these studies comes when it is concluded that finding nothing while studying irrelevant variables proves that glutamate is safe.

Negative results were also reliably produced by a series of double-blind studies conducted by a variety of researchers from various universities and medical schools who were given study protocols that would guarantee negative results, all supervised by Andrew G. Ebert, Ph.D., Ajinomoto’s agent in charge of research at the time (without the involvement of Ajinomoto being disclosed). Although these studies had common elements, no two studies were identical. There was, however, one feature shared by all – use of placebos that contained excitotoxic amino acids that would trigger reactions identical to those caused by the MSG test material. According to a letter from Ebert to Sue Ann Anderson, Senior Staff Scientist with the Life Sciences Research Office at FASEB, this practice began in 1978 (3).

In a double-blind study, test material is given to a subject on one occasion, and on another occasion the subject is given a placebo. The placebo, if it’s a true placebo, looks, tastes and smells like the test material, but it will not cause a reaction. If the subject reacts to the inert placebo, the researchers could conclude that the subject is not reacting to the test material, but is responding to the thought of consuming MSG. In other words, the subject would be portrayed as some kind of nut case who might react to anything, and reactions to MSG test material would be discounted.

To make sure that it appeared to be appropriate for researchers to conclude that MSG is harmless, glutamate-industry researchers guaranteed that subjects would react to placebos by using aspartame in their placebos, for the aspartic acid in aspartame and the glutamic acid in MSG cause virtually identical reactions as well as identical brain damage (4,5).

Having set that up, glutamate-industry researchers (and those who quote them) will say “These people aren’t sensitive to MSG, they reacted to the ‘placebo’ too” (6).

Conclusions drawn from these industry-sponsored studies were based on negative results. The inferential statistics used ask the question of whether a difference between two groups of subjects or two sets of measurements could have occurred by chance. If statistical analysis determines that observed differences rarely would have occurred by chance, an investigator would describe those differences as statistically significant and would specify the probability with which differences of that magnitude would be expected to be reproduced if the experiment were replicated at another time. In statistical parlance, the investigator had tested the hypothesis that there would be no difference between two groups — the null hypothesis — and had rejected that hypothesis when he found that there was indeed a significant difference. The statistical model on which these statistics are based allows the investigator to conclude that it is highly likely — the probability used usually being 95 percent or 99 percent — that differences found were not due to chance. The statistical model does not allow the investigator to conclude that no difference exists between the two groups when a statistically significant difference is not found. The industry-sponsored studies invariably violated the assumptions of the statistics used.

There is a certain sameness to these studies. They are generally methodologically inadequate, statistically unsound, and/or irrelevant to the safety/toxicity of MSG.

Researchers have gone so far as to use aspartame, which contains excitotoxic aspartic acid, and/or excitotoxic manufactured free glutamate (MfG) in placebos to cause subjects to respond to placebos just as they would respond to monosodium glutamate test material (7).

References

  1. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science. 1969;164(880):719-721. https://pubmed.ncbi.nlm.nih.gov/5778021/
  2. Studies demonstrating both glutamate and MSG-induced brain damage https://www.truthinlabeling.org/Data%20from%20the%201960s%20and%201970s%20demonstrate_2.html
  3. The Ebert/Anderson letter: Andrew Ebert’s letter to FASEB acknowledging that from 1978 forward, placebos used in International Glutamate Technical Committee (IGTC) studies of the safety of monosodium glutamate were laced with aspartame. https://www.truthinlabeling.org/assets/ebert_letter.pdf
  4. FDA Adverse Reactions Monitoring System (ARMS) – Collected Reports of Adverse reactions to monosodium glutamate. https://www.truthinlabeling.org/assets/arms_msg.pdf
  5. FDA Adverse Reactions Monitoring System (ARMS) – Collected Reports of Adverse reactions to Aspartame. https://www.truthinlabeling.org/assets/arms_aspartame.pdf
  6. Studies demonstrating both glutamate and MSG-induced brain damage https://www.truthinlabeling.org/Data%20from%20the%201960s%20and%201970s%20demonstrate_2.html
  7. Discussion of glutamate-industry-study protocols https://www.truthinlabeling.org/flawed.html


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