Tag: glutamate

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Everything you need to know about glutamate before your next trip to the supermarket

Glutamic acid (glutamate) is a building block of protein. When present in protein or released from protein in a regulated fashion, glutamate is vital to normal body function. It is the major neurotransmitter in the human body, carrying nerve impulses from glutamate stimuli to glutamate receptors throughout the body. Yet when present outside of protein in amounts that exceed what the healthy human body was designed to accommodate (when present in excess), glutamate takes on excitotoxic properties, becoming an excitotoxic neurotransmitter, firing repeatedly, damaging targeted glutamate-receptors and/or causing neuronal and non-neuronal death by over exciting glutamate receptors until their cells die.

Excitotoxicity of L-glutamic acid (glutamate) was first demonstrated in 1969. On April 3, 2019, a PubMed search for “glutamate” produced 157,021 references. Topics being researched included, but were not limited to, glutamate receptors, transport, excitotoxicity, release, transporter, brain, synthesis, monosodium glutamate, Parkinson’s disease, multiple sclerosis, Alzheimer’s disease, stroke, ALS, autism, schizophrenia, depression, obsessive-compulsive disorder (OCD), epilepsy, ischemic stroke, seizures, Huntington’s disease, addiction, attention-deficit/hyperactivity disorder (ADHD), and autism.

Much, if not all of that research dealt with excitotoxicity caused by glutamate from endogenous1 sources. The contribution of glutamate from exogenous2 sources to endogenous glutamate pools through which excitotoxicity would be triggered, seems never to have been considered.

Overlooked also, is a wealth of knowledge that could be gleaned from the histories of humans who have suffered brain damage, endocrine disorders, and observable adverse reactions following intake of excitotoxic glutamate from exogenous sources.

With the following we present an overview of what we know, or think we know, about the function of glutamate in persons who have experienced reactions to it.  It is our hope that insights generated by this information may be used by researchers probing the mechanisms of glutamate toxicity, and by the medical professionals working with people who react to the excitotoxic effects of Manufactured free Glutamate.

Vulnerability

Everyone is vulnerable to the toxicity of excitotoxins if they get a heavy enough dose of them. There are no exceptions.  To be toxic, an excitotoxin must either target receptors that have become weakened or vulnerable to their attack, or be in such strong concentrations that no glutamate receptor can resist them. 

Vulnerability may be created by:

  • An inadequate BBB — allowing brain cells to be unprotected by a blood-brain barrier (BBB);
  • A damaged BBB;
  • Preexisting brain damage, possibly from a stroke, a blow to the head, or previously consuming a large quantity of Manufactured free glutamate at one sitting, and
  • Preexisting damage done to cells that host glutamate receptors in either the central nervous system or in peripheral tissue.

We know very little about the actions of excitotoxins. Glutamate loads on (triggers) glutamate receptors both in the central nervous system and in peripheral tissue (heart, lungs, and intestines, for example). When loading on (stimulating) a glutamate receptor, glutamate may simply stimulate receptors and then fade, so to speak; may damage the cells that those receptors cling to; or may stimulate those receptors (over-excite those receptors) until the cells that host them die.

There’s another possibility. There are a great many glutamate receptors in the brain. It is possible that if a few are damaged or wiped out following ingestion of Manufactured free glutamate, their loss may not be noticed because there would be many undamaged glutamate receptors remaining. It is also possible that individuals differ in the numbers of glutamate receptors that they have to begin with; that people with more glutamate receptors are less likely to demonstrate brain damage following ingestion of Manufactured free glutamate because even after some cells are killed or damaged, there are still sufficient undamaged cells to carry out normal functions.

Saying it another way, people with fewer receptors to begin with might be more likely to demonstrate brain damage following ingestion of MSG or MfG because they have fewer glutamate receptors remaining after excitotoxic insult than individuals who had more glutamate receptors to begin with. That might account for some people being more sensitive to Manufactured free glutamate than others.

Less is known about glutamate receptors outside the brain – in the heart, stomach, and lungs, for example. But it would be anticipated that in each location there would be fewer glutamate receptors siting on host cells than found in the brain; and for some individuals, there might be so few cells with glutamate receptors to begin with, that ingestion of even small amounts of Manufactured free glutamate might trigger asthma, atrial fibrillation, or irritable bowel, for example; while individuals with more cells hosting glutamate receptors to begin with, would not notice the loss of a relatively few cells.

Short-term effects of excitotoxic glutamate (effects like asthma and migraine headache) have long been obvious to all who are not swayed by the rhetoric of the glutamate industry and their friends, including friends at the U.S. Food and Drug Administration (FDA). Researchers may only now begin to correlate the adverse effects of glutamate ingestion with endocrine disturbances such as reproductive disorders and gross obesity, with some psychological disorders, and with neurodegenerative disease. And a few have begun to realize the importance of glutamate’s access to the human body through the mouth, through the nose, and through the skin.  

Excess

Glutamate is a non-essential amino acid, meaning that there is no need for a human to ingest glutamate as the body will produce what it needs from other available amino acids.

A reaction to glutamate, is a reaction to excess free glutamate. Because of differences in vulnerability, what is an excess for one will not necessarily be excess for another. While excess might ordinarily be defined as “more than is needed for normal body function,” that doesn’t seem to be the case with glutamate-sensitivity. Rather, excess seems to be related to the amount of glutamate that will damage or kill a given subject’s glutamate receptors.

Excess may be created by:

  • Eating enough Manufactured free glutamate at one sitting to trigger glutamate receptors on vulnerable cells;
  • Eating enough Manufactured free glutamate to trigger glutamate receptors on cells that had not previously been damaged or made vulnerable, and
  • Adding ingested Manufactured free glutamate to stores of glutamate in the body.

Manufactured free glutamate will be found in infant formula, protein powders, protein drinks, processed food, enteral care products, cosmetics, pharmaceuticals, and dietary supplements. There is more than sufficient Manufactured free glutamate in processed foods to cause reactions in people who choose not to limit their access to Manufactured free glutamate. 

Data on availability will be found in grocery stores. Access a list of ingredients that contain Manufactured free glutamate (https://www.truthinlabeling.org/names.html), then look for products that don’t contain them. You won’t find 10 products that don’t contain at least one of the ingredients on that list, and every one of them contains Manufactured free glutamate. Consider how many of those Manufactured free glutamate containing products are in the meals and snacks enjoyed by people everywhere. Include restaurant foods in that tally.

Glutamate receptors

Glutamate receptors receive the glutamate sent to them by glutamate neurotransmitters. Although glutamate is essential to normal body function, when present in excess outside of intact protein it becomes excitotoxic, firing repeatedly and causing cell death and/or damage to targeted cells.

If cells are protected from excess glutamate, as the brain may be protected at least in part by a robust BBB, a little excess glutamate sent their way may not harm them. But if the BBB is ineffective, targeted cells die. Outside of the brain and central nervous system, glutamate-receptors may have no protective shield from excitotoxins at all.

Relatively recently, researchers discovered glutamate-receptors beyond the brain and central nervous system.  These include, but are not limited to peripheral receptors in the stomach, heart, lungs, kidney, liver, immune system, spleen, and testis. And cells associated with each may be damaged or killed if glutamate sent from glutamate neurotransmitters reaches them. It’s possible that these peripheral receptors may have some type of protection system, but if so, scientists have not yet identified it.

Years ago, it was thought to be remarkable that glutamate-toxicity worked through the brain, since glutamate could produce an immediate migraine headache. Glutamate eaten – brain triggered – headache happened within seconds. Today it is understood that glutamate can move directly to peripheral receptors without traveling through the brain.

It appears that cells that host glutamate receptors can be damaged if exposed to a little glutamate, but not enough to kill them outright. There might be times when one ingests enough Manufactured free glutamate to damage a cell, but not enough to kill it, or damage some of the cells in a group that control a particular function but not enough to knock out all of them. Ingest more glutamate on a second occasion, however, and those cells may die. Some Manufactured free glutamate sensitive people report that they can knowingly ingest Manufactured free glutamate in a favorite food on one occasion without noticing a reaction, but visibly react when that same food is consumed several days in a row.

What would increase glutamate receptor vulnerability?

Damage to the BBB would be the most obvious factor.  It is known that lack of blood-brain barrier development in the fetus and infant make them extremely vulnerable to exposure to Manufactured free glutamate passed through their mothers’ diets.

Damage done to the BBBs of mature humans through use of drugs, from seizures, stroke, head trauma, hypoglycemia, hypertension, extreme physical stress, high fever, and the normal process of aging, can render them more vulnerable than others.

Individual sensitivity may also be related to the integrity of cells or groups of cells that control a particular function. A person who has experienced heart problems might very well be predisposed to experiencing cardiac-related reactions by virtue of having glutamate receptors in the heart vulnerable to insult by glutamate. A person with asthma, is likely predisposed to having an asthma attack after consuming free glutamate.

Reports from consumers tell us that intensity or severity of reactions appear to be affected by alcohol ingestion and/or exercise just prior to, or immediately following MSG ingestion, and some women report variations in their reactions at different times in their menstrual cycles. 

Summary/conclusion

We have presented an overview of glutamate excitotoxicity gleaned in large part from persons who have experienced reactions to it.  This is information not generally considered by those researching abnormalities associate with glutamate.  Hopefully, insights generated by this information will be used by researchers probing the mechanisms of glutamate toxicity and by medical professionals working with people who react to the excitotoxic effects of Manufactured free glutamate.

1 growing or originating from within an organism.
2 originating from outside an organism.

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Who’s suppressing information about MSG toxicity?

Research has demonstrated that excess glutamate accumulated in the human body is implicated in brain damage, kidney and liver disorders, obesity, reproductive disorders, neurodegenerative disease, and additional disorders such as headaches, asthma, diabetes, muscle pain, atrial fibrillation, ischemia, trauma, seizures, stroke, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), Huntington’s disease, Parkinson’s disease, depression, multiple sclerosis, schizophrenia, obsessive-compulsive disorder (OCD), epilepsy, addiction, attention-deficit/hyperactivity disorder (ADHD), frontotemporal dementia and autism. A November 15, 2020 search of the National Library of Medicine using PubMed.gov returned 3872 citations for “glutamate-induced.

It has also been demonstrated that glutamate from exogenous (external) sources, often from ingestion of monosodium glutamate (MSG), produces brain lesions, reproductive disorders, gross obesity, and behavior disorders. A review of the literature has also demonstrated that studies concluding MSG is harmless, or finding no evidence that MSG is harmful, are seriously flawed, with double-blind studies using placebos containing excitotoxic amino acids that cause reactions identical to those caused by MSG.

So why aren’t researchers exploring the relationship between ingestion of glutamate-containing ingredients such as MSG and disease and disability?

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There’s good glutamate and bad glutamate

It’s really tricky to talk about glutamate.  It’s one of a bundle of amino acids – molecules used by all living things to make proteins. Humans have always created glutamate in their bodies in carefully controlled amounts. And up until the time industry discovered how to make unlimited supplies of glutamate, you could generally get all the essential amino acids your body needed by eating a healthy balanced diet on top of the amino acids that you made in your body.

Then in 1957, what had been true wasn’t true anymore. In 1957 one of industry’s finest began to produce free glutamate in unlimited quantities. Now, humans were no longer dealing with carefully controlled amounts of free glutamate in their food. Instead, they were dealing with adverse reactions such as skin rashes, asthma, migraine headache and fibromyalgia. And although it only became evident years later, many also suffered brain damage followed by obesity and infertility.

Think about it. Ingesting the quantities of free glutamate that became available in 1957 means there is more glutamate flooding the human body than the cells of the body can use.  And the excesses accumulate in what’s called interstitial tissue (areas between cells), where they join with other excitotoxic neurotransmitters, firing repeatedly until their targeted glutamate receptors die – causing brain damage. 

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It’s never too late to set the record straight. Glutamate: The weapon we used against ourselves in the Gulf War

Introduction

In the well-researched article, “Emerging role of glutamate in the pathophysiology and therapeutics of Gulf War illness (GWI),” substantial evidence is presented demonstrating that Gulf War-related agents and traumatic stress (Gulf War-related exposures) affect glutamate transmission in the brain (1).

Named as examples of Gulf War-related chemical agents were pyridostigmine bromide (given to soldiers as an anti-nerve agent pretreatment), sarin nerve agent, pesticides, and smoke from burning oil wells.

Also named were the commonly reported symptoms of veterans identified as suffering with GWI, which include mood problems, cognitive impairment, muscle and joint pain, migraine headache, chronic fatigue, gastrointestinal complaints, skin rashes, and respiratory problems. 

Encouraged by growing evidence indicating that abnormal glutamate neurotransmission may contribute to the GWI symptoms, the authors summarized the potential roles of glutamate dyshomeostasis and dysfunction of the glutamatergic system in linking the initial cause to the multi-symptomatic outcomes in GWI and suggested the glutamatergic system as a therapeutic target for GWI.  

Their research did not, however, take into account the fact that those deployed to the Gulf War were consuming excitotoxic chemicals in their food on a daily basis. The authors failed to realize that food being fed to those deployed to the Gulf War contained neurotoxic chemical agents just as the Gulf War environment did, and that review of relevant literature would demonstrate that the excitotoxic manufactured free glutamate (MfG), present in quantity in processed food could cause and/or exacerbate GWI.

A May 2021 search of PubMed for Gulf War Illness returned 730 articles, 622 of which made no mention of glutamate. Of the eight others, only one came close to associating glutamate with food consumed by service men and women in the combat zone, but even that study focused on the value of a low-glutamate diet as treatment for the injured, not as a possible means of prevention (2). No study of GWI cited on PubMed considered the possibility that those on the front lines were consuming excitotoxic chemicals in processed foods on a daily basis.

Glutamate as an excitotoxic amino acid

Evidence that glutamate is an excitotoxic amino acid is well understood by neuroscientists.  In 1969, Olney published results of the first study that demonstrated that glutamate administered to laboratory animals caused brain lesions in the arcuate nucleus of the hypothalamus as well as other areas of the brain, with brain damage followed by obesity, behavioral abnormalities and reproductive dysfunction (3). And Olney coined the term “excitotoxin” to explain the phenomenon.  At the time, researchers were administering glutamate to laboratory animals subcutaneously using Accent brand MSG because it had been observed that the product was as effective for inflicting brain damage as more expensive pharmaceutical grade L-glutamate (3).  The glutamate administered would have been made up of both L-glutamate (the glutamate enantiomer with flavor-enhancing potential) and D-glutamate (an unwanted by-product accompanying the manufacture of the L-glutamate manufactured for use in MSG).

L-glutamate is the L enantiomer of glutamic acid (glutamate), an acidic amino acid which when present in protein or released from protein in a regulated fashion (through routine digestion) is vital for normal body function. It is the principal neurotransmitter in humans, carrying nerve impulses from glutamate stimuli to glutamate receptors throughout the body. Yet, when present outside of protein in amounts that exceed what the healthy human body was designed to accommodate (which can vary widely from person to person), glutamate becomes an excitotoxic neurotransmitter, firing repeatedly, damaging targeted glutamate-receptors and/or causing neuronal and non-neuronal death by over exciting those glutamate receptors until their host cells die (4-9).

Throughout the 1970s, researchers confirmed that glutamate induces hypothalamic damage when given to immature animals after either subcutaneous or oral doses (10).

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.  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), Huntington’s disease, Parkinson’s disease, depression, multiple sclerosis, 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 was, and still is, glutamate from endogenous sources. The possible toxicity of glutamate from exogenous sources such as glutamate-containing protein substitutes and glutamate-containing flavor enhancers 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 (11).

Additional evidence of the toxicity of glutamate from exogenous sources such as eating, comes from studies undertaken by the producer of MSG to convince the public that MSG is a harmless food additive. Detail of how studies were systematically designed to produce negative results (no harm found) is elaborated in supplemental files at the end: 1 (The Toxicity/Safety of Processed Free Glutamic Acid (MSG): A Study in Suppression of Information), 2 (Designed for Deception), and 3 (The Alleged Safety of Monosodium Glutamate (MSG).

The success of glutamate-industry double-blind studies that always produced negative results (no MSG-induced damage demonstrated) can be attributed, at least in part, to use of “placebos” containing undisclosed excitotoxic amino acids that cause reactions identical to those caused by MSG test material.

The single greatest obstacle to transparency of the dangers of MSG has been the FDA’s 50-year allegiance to Ajinomoto, the U.S. manufacturer of MSG, with the FDA maintaining that MSG, a product never tested for safety, is generally recognized as safe (GRAS) while simultaneously parroting Ajinomoto’s misleading statements and downright lies. During the 1990s, that relationship was harmonized by the FDA’s Center for Food Safety and Applied Nutrition (SFSAN), Fred Shank (deceased) being CFSAN director at the time. As Director of CFSAN, Shank led the development of policies and programs focused on consumer protection, including the implementation of the Nutrition Labeling and Education Act of 1990, the most comprehensive food labeling legislation in U.S. History. And he refused to include consideration of the toxicity of MSG in that legislation. Also notably influential at that time on behalf of the alleged safety of MSG was Linda Tollefson, Associate Commissioner for Foods and Veterinary Medicine (retired).

Those familiar with adverse reactions following ingestion of MSG, whose essential component is excitotoxic – brain damaging — free glutamic acid (MfG), understand that MfG affects each individual differently, with multiple organ systems involved including the nervous system, digestive system, and respiratory system. Similar to reports of GWI symptoms, symptoms reported by MSG-sensitive people include fatigue, joint pain, memory loss, sleep difficulties, headaches, concentration loss, depression and anxiety, skin rashes, gastrointestinal problems, and breathing problems, chronic fatigue syndrome, fibromyalgia, and irritable bowel syndrome.

Table 2 lists reactions reported following ingestion of MSG and the other ingredients that contain MfG.  For a short time, the FDA also maintained a list of adverse reactions to MSG in their Adverse Reactions Monitoring System. These were unsolicited reports kept before the FDA decided that “there was no point to keeping such records because the FDA knew that virtually no one was sensitive to MSG (12).”

The wide variety in GWI symptomatology provides the clue to identifying at least one cause of GWI. 

Pharmaceuticals come with package inserts that list the side effects known to occur in some people following administration. The reactions listed in those package inserts are as varied as reactions known to occur following ingestion of MfG. (Different pharmaceuticals produce different side effects in different people.  MSG produces different side effects, a.k.a. adverse reactions, in different people.)  No surprise here, for when used in food, glutamate is called a food and when used in pharmaceuticals, the same glutamate is called a drug.  The symptoms expressed individually by GWI veterans are all symptoms that occur to some consumers following ingestion of MfG.

Aside from a pair of studies that demonstrated a low-glutamate diet reduced multiple symptoms of GWI (13,14) there has not been even a hint in the medical literature that ingestion of MfG in the food available to Gulf War forces might have contributed to GWI.

It comes as no surprise to those of us who have dealt on a daily basis with the adverse reactions caused by MfG, that the military would be unaware of its relevance to GWI, for beginning in 1969 with the first evidence of glutamate excitotoxicity, information pertaining to glutamate toxicity has been systematically suppressed.  Since 1991, no major U.S. media have carried so much as a hint that MSG, the best-known of the ingredients that contain MfG, might be anything more than controversial.  And few researchers in the U.S. broached the subject of glutamate-toxicity prior to the relatively new research cited here that has suggested or demonstrated a link between glutamate and GWI (1,13-18). 

Since 1988, when George Schwartz, M.D. published “In Bad Taste: the MSG Syndrome,” (19) the U.S. manufacturer of MSG has been engaged in dissemination of deceptive and misleading information that hypes the safety of their product.

That includes the MSG-is-safe research double-blind studies systematically designed to produce negative studies (no MSG-inflicted harm found) which always included, among other things, the use of placebos containing excitotoxic amino acids known to cause reactions identical to those caused by MSG.

In discussing the suppression of information about the excitotoxicity of free glutamate, we would be remiss in not addressing the subject of “authoritative bodies” who have said that MSG and the glutamate in it are safe for human consumption. Recently mentioned in glutamate-industry material as organizations on record as having reviewed the safety of MSG and found it to be a harmless food additive were Food Standards Australia New Zealand (FSANZ), the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives (JECFA), the Federation of American Societies for Experimental Biology (FASEB), the New South Wales Government Food Authority in Australia, the American Medical Association and the Food and Drug Administration (FDA).

Those organizations did no research of their own, either in the laboratory or the library, but reviewed material brought to them by the U.S. manufacture of MSG, the FDA, or others such as Andrew Ebert, Ph.D. the “scientist” in charge of MSG-is-safe research prior to the time he was exposed for overseeing use of excitotoxic amino acids in double-blind study placebos. Ebert distributed both test materials and material that he called placebos (allegedly inert substances that could not possibly cause a physical reaction in a person who ingested them) for use in double-blind studies designed to demonstrate that MSG is safe.

The only question about the role that glutamate plays in cause or exacerbation of GWI that remains to be addressed here has to do with availability of sufficient free glutamate to cause the free glutamate present to express excitotoxicity. At one time it would have been meaningful to note that the amount of excitotoxic material in a particular ingredient would not be sufficient to cause brain damage or adverse reactions. But since the 1957 change in method of MSG production, there are so many products that contain manufactured free glutamate and other excitotoxins that it is easy for a consumer to ingest an excess of excitotoxic material during the course of a day (20-24).

Prior to 1957, the amount of free glutamate or other excitotoxic additives in the average U.S. diet had been unremarkable. During that year, however, the method of producing the free glutamate that makes up the excitotoxic portion of MSG changed from extraction of glutamate from a protein source, a slow and costly method, to a process of bacterial fermentation (25). This allowed virtually unlimited production of free glutamate and MSG.

It didn’t take long for industry to add dozens more excitotoxic food additives to the American diet. Following MSG’s surge in production and aggressive advertising, it was realized that profits could be significantly increased if companies produced their own flavor-enhancing additives. Since that time, the market has been flooded with flavor enhancers and protein substitutes that contain MfG such as hydrolyzed proteins, yeast extracts, maltodextrin and soy protein isolate, as well as MSG. (See table 3). To that has been added the toxic load contributed by excitotoxic aspartic acid, approved by the FDA for use in aspartame, equal, and related products starting in 1974.  The excitotoxins in aspartic acid and glutamic acid act in an additive fashion.

Soon after use of genetically modified bacteria in the production of MSG began, availability of MSG and other MfG-containing products increased to the point where there was more than sufficient MfG to become excitotoxic if a number of processed and ultra-processed foods were consumed during the course of a day. And an environment full of war-related toxic chemical agents would be likely to enhance a soldier’s vulnerability.

Summary

There was sufficient manufactured free glutamate in processed foods served to Gulf War service members to serve as an excitotoxic – brain damaging – chemical, causing or exacerbating GWI.

References          

1. Wang X, Ali N, Lin C.  Emerging role of glutamate in the pathophysiology and therapeutics of Gulf War illness.  Life Sci.  2021 May 12: 119609.

2. Joyce MR, Holton KF.  Neurotoxicity in Gulf War Illness and the potential role of glutamate.  Neurotoxicology. 2020;80:60-70.

3. 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/

4. Excitotoxicity and cell damage https://www.sciencedaily.com/terms/excitotoxicity.htm

5. Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells https://www.frontiersin.org/articles/10.3389/fncel.2020.00051/full

6. Hernández DE et al. Axonal degeneration induced by glutamate excitotoxicity is mediated by necroptosis. J. Cell Sci. 2018 Nov 19;131(22):jcs214684.

7. Garzón F et al. NeuroEPO preserves neurons from glutamate-induced excitotoxicity J. Alzheimers Dis. 2018;65(4):1469-1483.

8. Zárate SC, Traetta ME, Codagnone MG,  Seilicovich A  Reinés AG.

Humanin, a mitochondrial-derived peptide released by astrocytes, prevents synapse loss in hippocampal neurons. Front Aging Neurosci. 2019 May 31;11:123.

9. Plitman E et al. Glutamate-mediated excitotoxicity in schizophrenia: a review. Eur Neuropsychopharmacol. 2014;24:1591-1605.

10. Studies demonstrating both glutamate and MSG-induced brain damage https://www.truthinlabeling.org/Data%20from%20the%201960s%20and%201970s%20demonstrate_2.html

11. Alerts from independent researchers outside of the United States, warning of the dangers posed by ingesting MSG https://www.truthinlabeling.org/assets/researchers_warnings.pdf

12. Summary of adverse reactions attributed to MSG https://www.truthinlabeling.org/assets/arms_msg.pdf

13. Joyce MR, Holton KF. Neurotoxicity in Gulf War Illness and the potential role of glutamate. Neurotoxicology. 2020 Sep;80:60-70.

14. Holton KF, Kirkland AE, Baron M, Ramachandra SS, Langan MT, Brandley ET, Baraniuk JN. The Low Glutamate Diet Effectively Improves Pain and Other Symptoms of Gulf War Illness. Nutrients. 2020 Aug 26;12(9):2593.

15. Wang X, Xu Z, Zhao F, Lin KJ, Foster JB, Xiao T, Kung N, Askwith CC, Bruno JP, Valentini V, Hodgetts KJ, Lin CG.  Restoring tripartite glutamatergic synapses: A potential therapy for mood and cognitive deficits in Gulf War illness. Neurobiol Stress. 2020 Jul 13;13:100240.

16. Macht VA, Woodruff JL, Burzynski HE, Grillo CA, Reagan LP, Fadel JR. Interactions between pyridostigmine bromide and stress on glutamatergic neurochemistry: Insights from a rat model of Gulf War Illness. Neurobiol Stress. 2019 Dec 31;12:100210.

17. Gargas NM, Ethridge VT, Miklasevich MK, Rohan JG. Altered hippocampal function and cytokine levels in a rat model of Gulf Warillness. Life Sci. 2021 Jun 1;274:119333.

18. Torres-Altoro MI, Mathur BN, Drerup JM, Thomas R, Lovinger DM, O’Callaghan JP, Bibb JA. Organophosphates dysregulate dopamine signaling, glutamatergic neurotransmission, and induce neuronal injury markers in striatum. J Neurochem. 2011 Oct;119(2):303-13.

19. Schwartz GR. In Bad Taste: the MSG Syndrome. Santa Fe: Health Press, 1988.

20. Hashimoto S. Discovery and History of Amino Acid Fermentation.  Adv Biochem Eng Biotechnol. 2017;159:15-34. https://pubmed.ncbi.nlm.nih.gov/27909736/

21. Sano C. History of glutamate production. Am J Clin Nutr. 2009;90(3):728S-732S. https://pubmed.ncbi.nlm.nih.gov/19640955/

22. Market Research Store. Global Monosodium Glutamate Market Poised to Surge from USD 4,500.0 Million in 2014 to USD 5,850.0 Million by 2020. https://www.globenewswire.com/news-release/2016/03/17/820804/0/en/Global-Monosodium-Glutamate-Market-Poised-to-Surge-from-USD-4-500-0-Million-in-2014-to-USD-5-850-0-Million-by-2020-MarketResearchStore-Com.html   (Accessed 5/29/2020)

23. Open PR Worldwide Public Relations for Verified Market. Global Flavor Enhancers Market. https://www.bccresearch.com/partners/verified-market-research/global-flavor-enhancers-market.html   (Accessed 5/29/2020)

24. Dataintelo. Global Food Flavor Enhancer Market Report, History and Forecast 2014-2025, Breakdown Data by Manufacturers, Key Regions, Types and Application.  https://dataintelo.com/report/food-flavor-enhancer-market    (Accessed 5/29/2020)

25. Khan IA, Abourashed EA. Leung’s Encyclopedia of common natural ingredients used in food, drugs, and cosmetics (Third Edition). New Jersey: Wily, 2010. Pp 452-455. https://naturalingredient.org/wp/wp-content/uploads/leungs-encyclopedia-of-common-natural-ingredients-3rd-edition.pdf

Tables      

Table 2: Adverse reactions known to be caused from time to time by MSG and the other ingredients that contain MfG

https://www.truthinlabeling.org/assets/reactions_list2.pdf

Table 3: Names of ingredients that contain Manufactured free Glutamate (MfG)  (Updated May 2021)

https://www.truthinlabeling.org/assets/ingredient_names.pdf

Supplemental material

File 1. The Toxicity/Safety of Processed Free Glutamic Acid (MSG): A Study in Suppression of Information

https://www.truthinlabeling.org/assets/manuscript2.pdf

File 2. The Alleged Safety of Monosodium Glutamate (MSG)

https://www.truthinlabeling.org/assets/review_studies.pdf

File 3. Designed for Deception: The fail-safe way to ensure that their studies would conclude MSG is harmless

https://www.truthinlabeling.org/assets/designed_for_deception_short.pdf

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If MSG was so bad for you, why doesn’t everyone in Asia have a headache?

Listen up Jeffrey Steingarten. Twenty-four years ago you were one of a handful of food writers coming to the defense of the safety of MSG.  It was the “in” thing to do.  And your “If MSG was so bad for you, why doesn’t everyone in Asia have a headache?”  was so well written and so provocative, it’s still referred to today.

It’s been 24 years since you wrote those words for Vogue Magazine. It’s long been obvious to those of us who can differentiate fact (produced by honest scientists) from glutamate industry rigged research and paid-for-propaganda, that the defining component of MSG is its brain damaging excitotoxic free glutamate.  To be brain-damaging, there has to be more glutamate floating free in the body than is used for normal body functions.  And it wasn’t until 1957 that Ajinomoto began mass-producing free glutamate in amounts needed to produce brain damage.  Before 1957, there wasn’t enough free glutamate to cause brain damage.

To be brain damaging, large quantities of free glutamate have to be floating free in the body. Before 1957, there wasn’t enough free glutamate available in processed foods and drinks to cause brain damage.

It’s a mouthful to say, and not easy to understand, but prior to 1957, the amino acid known as glutamic acid (or glutamate) would only have been found in the healthy human body under well-defined and tightly controlled circumstance — when all glutamate was used to support normal healthy functions.

That’s how it was.  That’s how it had always been.  But in 1957, the major U.S. producer of MSG began mass-producing MSG in the U.S. using genetically modified bacteria that would secrete free glutamate through their cell walls. That was followed by aggressive marketing.

In The Perfect Poison there’s a section that describes the thought process that went into becoming certain that the placebos used in the Glutes double-blind studies of the safety of MSG were not really placebos, but were concoctions that would cause reactions identical to reactions caused by MSG test material.

That’s the kind of thinking that I found myself doing when I happened upon a market report published in the Taiwan News written by Report Ocean, a renowned market research firm that had recently released an insightful report focusing on the MSG market in China.  What caught my eye was this simple statement, “Monosodium glutamate (MSG) is a manufactured (emphasis added) flavor enhancer that has a place with the class of mixtures on the whole known as glutamates.”  And I found myself intrigued more by words left unsaid than by anything else, because in the United States with that simple statement, there would have been an extensive barrage of “MSG is safe” propaganda, with the repeated assertion that MSG is natural or naturally occurring.

In “The curious history of MSG in China, and a tour of an MSG Factory,” Christopher St. Cavish tells the reader that in China, there is no such thing as Chinese Restaurant Syndrome, which reinforced my growing suspicion that the MSG produced in the U.S. and MSG produced in China are actually different things — an idea reinforced by St. Cavish’s statement, “long fascinated by the contrast between their cultural baggage and supposed medical ill-effects in the U.S. and their unconditional acceptance in Asia. In China, which consumes 55% of the world’s MSG, there is no such thing as Chinese Restaurant Syndrome.”  Moreover, St. Cavish makes no mention of adverse reactions following ingestion of MSG; he repeatedly asserts that all MSG is exactly the same thing; and he describes how Chinese MSG is made, with no mention of bacteria that excrete glutamate through their cell walls.

I have studied the few English language papers I could find relevant to the procedures used outside of the United States for producing monosodium glutamate prior to 1957 and have come to the conclusion that the monosodium glutamate manufactured in the United States after 1957 contained excitotoxic free glutamate complete with its impurities while monosodium glutamate manufactured elsewhere did not.

So, there it is Mr. Steingarten.  It was the MSG produced in the United States (not in Asia) after mass production of MSG was introduced in 1957 that caused headaches, other adverse reactions, brain damage and all the various abnormalities of the nervous system like obesity, infertility, behavior disorders and neurodegenerative disease. And it still does.

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Everything you need to know about glutamate before your next trip to the supermarket

Glutamic acid (glutamate) is a building block of protein. When present in protein or released from protein in a regulated fashion, glutamate is vital to normal body function. It is the major neurotransmitter in the human body, carrying nerve impulses from glutamate stimuli to glutamate receptors throughout the body. Yet when present outside of protein in amounts that exceed what the healthy human body was designed to accommodate (when present in excess), glutamate takes on excitotoxic properties, becoming an excitotoxic neurotransmitter, firing repeatedly, damaging targeted glutamate-receptors and/or causing neuronal and non-neuronal death by over exciting glutamate receptors until their cells die.

Excitotoxicity of L-glutamic acid (glutamate) was first demonstrated in 1969. On April 3, 2019, a PubMed search for “glutamate” produced 157,021 references. Topics being researched included, but were not limited to, glutamate receptors, transport, excitotoxicity, release, transporter, brain, synthesis, monosodium glutamate, Parkinson’s disease, multiple sclerosis, Alzheimer’s disease, stroke, ALS, autism, schizophrenia, depression, obsessive-compulsive disorder (OCD), epilepsy, ischemic stroke, seizures, Huntington’s disease, addiction, attention-deficit/hyperactivity disorder (ADHD), and autism.

Much, if not all of that research dealt with excitotoxicity caused by glutamate from endogenous1 sources. The contribution of glutamate from exogenous2 sources to endogenous glutamate pools through which excitotoxicity would be triggered, seems never to have been considered.

Overlooked also, is a wealth of knowledge that could be gleaned from the histories of humans who have suffered brain damage, endocrine disorders, and observable adverse reactions following intake of excitotoxic glutamate from exogenous sources.

With the following we present an overview of what we know, or think we know, about the function of glutamate in persons who have experienced reactions to it.  It is our hope that insights generated by this information may be used by researchers probing the mechanisms of glutamate toxicity, and by the medical professionals working with people who react to the excitotoxic effects of Manufactured free Glutamate.

Vulnerability

Everyone is vulnerable to the toxicity of excitotoxins if they get a heavy enough dose of them. There are no exceptions.  To be toxic, an excitotoxin must either target receptors that have become weakened or vulnerable to their attack, or be in such strong concentrations that no glutamate receptor can resist them. 

Vulnerability may be created by:

  • An inadequate BBB — allowing brain cells to be unprotected by a blood-brain barrier (BBB);
  • A damaged BBB;
  • Preexisting brain damage, possibly from a stroke, a blow to the head, or previously consuming a large quantity of Manufactured free glutamate at one sitting, and
  • Preexisting damage done to cells that host glutamate receptors in either the central nervous system or in peripheral tissue.

We know very little about the actions of excitotoxins. Glutamate loads on (triggers) glutamate receptors both in the central nervous system and in peripheral tissue (heart, lungs, and intestines, for example). When loading on (stimulating) a glutamate receptor, glutamate may simply stimulate receptors and then fade, so to speak; may damage the cells that those receptors cling to; or may stimulate those receptors (over-excite those receptors) until the cells that host them die.

There’s another possibility. There are a great many glutamate receptors in the brain. It is possible that if a few are damaged or wiped out following ingestion of Manufactured free glutamate, their loss may not be noticed because there would be many undamaged glutamate receptors remaining. It is also possible that individuals differ in the numbers of glutamate receptors that they have to begin with; that people with more glutamate receptors are less likely to demonstrate brain damage following ingestion of Manufactured free glutamate because even after some cells are killed or damaged, there are still sufficient undamaged cells to carry out normal functions.

Saying it another way, people with fewer receptors to begin with might be more likely to demonstrate brain damage following ingestion of MSG or MfG because they have fewer glutamate receptors remaining after excitotoxic insult than individuals who had more glutamate receptors to begin with. That might account for some people being more sensitive to Manufactured free glutamate than others.

Less is known about glutamate receptors outside the brain – in the heart, stomach, and lungs, for example. But it would be anticipated that in each location there would be fewer glutamate receptors siting on host cells than found in the brain; and for some individuals, there might be so few cells with glutamate receptors to begin with, that ingestion of even small amounts of Manufactured free glutamate might trigger asthma, atrial fibrillation, or irritable bowel, for example; while individuals with more cells hosting glutamate receptors to begin with, would not notice the loss of a relatively few cells.

Short-term effects of excitotoxic glutamate (effects like asthma and migraine headache) have long been obvious to all who are not swayed by the rhetoric of the glutamate industry and their friends, including friends at the U.S. Food and Drug Administration (FDA). Researchers may only now begin to correlate the adverse effects of glutamate ingestion with endocrine disturbances such as reproductive disorders and gross obesity, with some psychological disorders, and with neurodegenerative disease. And a few have begun to realize the importance of glutamate’s access to the human body through the mouth, through the nose, and through the skin.  

Excess

Glutamate is a non-essential amino acid, meaning that there is no need for a human to ingest glutamate as the body will produce what it needs from other available amino acids.

A reaction to glutamate, is a reaction to excess free glutamate. Because of differences in vulnerability, what is an excess for one will not necessarily be excess for another. While excess might ordinarily be defined as “more than is needed for normal body function,” that doesn’t seem to be the case with glutamate-sensitivity. Rather, excess seems to be related to the amount of glutamate that will damage or kill a given subject’s glutamate receptors.

Excess may be created by:

  • Eating enough Manufactured free glutamate at one sitting to trigger glutamate receptors on vulnerable cells;
  • Eating enough Manufactured free glutamate to trigger glutamate receptors on cells that had not previously been damaged or made vulnerable, and
  • Adding ingested Manufactured free glutamate to stores of glutamate in the body.

Manufactured free glutamate will be found in infant formula, protein powders, protein drinks, processed food, enteral care products, cosmetics, pharmaceuticals, and dietary supplements. There is more than sufficient Manufactured free glutamate in processed foods to cause reactions in people who choose not to limit their access to Manufactured free glutamate. 

Data on availability will be found in grocery stores. Access a list of ingredients that contain Manufactured free glutamate (https://www.truthinlabeling.org/names.html), then look for products that don’t contain them. You won’t find 10 products that don’t contain at least one of the ingredients on that list, and every one of them contains Manufactured free glutamate. Consider how many of those Manufactured free glutamate containing products are in the meals and snacks enjoyed by people everywhere. Include restaurant foods in that tally.

Glutamate receptors

Glutamate receptors receive the glutamate sent to them by glutamate neurotransmitters. Although glutamate is essential to normal body function, when present in excess outside of intact protein it becomes excitotoxic, firing repeatedly and causing cell death and/or damage to targeted cells.

If cells are protected from excess glutamate, as the brain may be protected at least in part by a robust BBB, a little excess glutamate sent their way may not harm them. But if the BBB is ineffective, targeted cells die. Outside of the brain and central nervous system, glutamate-receptors may have no protective shield from excitotoxins at all.

Relatively recently, researchers discovered glutamate-receptors beyond the brain and central nervous system.  These include, but are not limited to peripheral receptors in the stomach, heart, lungs, kidney, liver, immune system, spleen, and testis. And cells associated with each may be damaged or killed if glutamate sent from glutamate neurotransmitters reaches them. It’s possible that these peripheral receptors may have some type of protection system, but if so, scientists have not yet identified it.

Years ago, it was thought to be remarkable that glutamate-toxicity worked through the brain, since glutamate could produce an immediate migraine headache. Glutamate eaten – brain triggered – headache happened within seconds. Today it is understood that glutamate can move directly to peripheral receptors without traveling through the brain.

It appears that cells that host glutamate receptors can be damaged if exposed to a little glutamate, but not enough to kill them outright. There might be times when one ingests enough Manufactured free glutamate to damage a cell, but not enough to kill it, or damage some of the cells in a group that control a particular function but not enough to knock out all of them. Ingest more glutamate on a second occasion, however, and those cells may die. Some Manufactured free glutamate sensitive people report that they can knowingly ingest Manufactured free glutamate in a favorite food on one occasion without noticing a reaction, but visibly react when that same food is consumed several days in a row.

What would increase glutamate receptor vulnerability?

Damage to the BBB would be the most obvious factor.  It is known that lack of blood-brain barrier development in the fetus and infant make them extremely vulnerable to exposure to Manufactured free glutamate passed through their mothers’ diets.

Damage done to the BBBs of mature humans through use of drugs, from seizures, stroke, head trauma, hypoglycemia, hypertension, extreme physical stress, high fever, and the normal process of aging, can render them more vulnerable than others.

Individual sensitivity may also be related to the integrity of cells or groups of cells that control a particular function. A person who has experienced heart problems might very well be predisposed to experiencing cardiac-related reactions by virtue of having glutamate receptors in the heart vulnerable to insult by glutamate. A person with asthma, is likely predisposed to having an asthma attack after consuming free glutamate.

Reports from consumers tell us that intensity or severity of reactions appear to be affected by alcohol ingestion and/or exercise just prior to, or immediately following MSG ingestion, and some women report variations in their reactions at different times in their menstrual cycles. 

Summary/conclusion

We have presented an overview of glutamate excitotoxicity gleaned in large part from persons who have experienced reactions to it.  This is information not generally considered by those researching abnormalities associate with glutamate.  Hopefully, insights generated by this information will be used by researchers probing the mechanisms of glutamate toxicity and by medical professionals working with people who react to the excitotoxic effects of Manufactured free glutamate.

1 growing or originating from within an organism.
2 originating from outside an organism.

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A short explanation of the obesity epidemic

I know something you don’t know.  I know that man-made free glutamic acid (free glutamate), the active ingredient in monosodium glutamate (MSG), caused and maintains the obesity epidemic.

Evidence? Some things are easy to understand.

1. Anyone who was reading medical journals in 1969 and the 1970s knew that monosodium glutamate (which contains manufactured free glutamate) fed in large amounts to newborn animals causes brain damage in a particular area of the hypothalamus — brain damage that is aways followed by gross obesity, infertility, behavior disorders and other abnormalities (1).

2. The obesity epidemic materialized in the 1960s.  Prior to 1957, there were people who had problems with obesity, but not in numbers so significant that they couldn’t be explained (2,3).

3. In 1957 the major U.S. producer of MSG and the free glutamate contained in it started producing free glutamate in sufficient amounts to cause that free glutamate to be excitotoxic – brain damaging (4).

Studies done over the years leave no question that there are three requirements for glutamate-induced brain damage, and that humans can meet them all:

A vulnerable brain –

The vulnerable brain in humans is the immature brain of a fetus or newborn, never protected by a blood-brain barrier. 

Sufficient free glutamate to cause the free glutamate to become excitotoxic –

Virtually unlimited amounts of free glutamate became available in 1957 when production of free glutamate for use in food changed from extraction of glutamate from protein to production of free glutamate by bacterial fermentation (4).

A way to deliver the toxin to the vulnerable brain –

You couldn’t feed glutamate-containing ingredients to a newborn with a fork or a spoon.  But if a pregnant woman consumes enough glutamate during the course of a day (which she will do if she is eating processed and ultra-processed foods), she will pass that glutamate through the placenta to her fetus, damaging the fetuses’ vulnerable brain.

It’s the timing that tells the story of the obesity epidemic.

Prior to 1957, there was obesity, but not in such amounts that it would be called an epidemic.  During that time, glutamate was produced using a slow and costly method.

After 1957, there was sufficient production of glutamate to cause it to be excitotoxic – brain damaging.  And sales of products containing free glutamate, not just MSG, were vigorously promoted.

Increases in the incidence of obesity began to be noticed in the early 1970s, when the first glutamate-induced brain damaged fetuses reached maturity as obese adults.

NOTES

1. The first study to address the possibility that glutamate from outside the body (from 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 (7).

In the decade that followed, research confirmed that glutamate given as monosodium glutamate administered or fed to neonatal animals causes hypothalamic damage, endocrine disruption, and behavior disorders when given to immature animals after either subcutaneous (8-29) or oral (15,21,22,24,30-34) doses. 

15. Olney, J.W. Glutamate-induced neuronal necrosis in the infant mouse hypothalamus. J Neuropathol Exp Neurol 30: 75-90, 1971.

21. 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.

22. Olney, J.W. Sharpe, L.G., Feigin, R.D. Glutamate-induced brain damage in infant primates. J Neuropathol Exp Neurol 31: 464-488, 1972.

24. 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. 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.

31. 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.

32. Takasaki, Y. Protective effect of mono- and disaccharides on glutamate-induced brain damage in mice. Toxicol Lett 4: 205-210, 1979.

33. Takasaki, Y. Protective effect of arginine, leucine, and preinjection of insulin on glutamate neurotoxicity in mice.Toxicol Lett 5: 39-44, 1980.

34. 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 Neurol33: 74-97, 1974.

2. Monitoring Human Tissues for Toxic Substances (https://www.ncbi.nlm.nih.gov/books/NBK234172/)

3. Overweight and Obesity in the United States, 1960–2000 https://www.infoplease.com/math-science/health/fitness-nutrition/overweight-and-obesity-in-the-united-states-1960-2000

4. Sano C. History of glutamate production. Am J Clin Nutr. 2009 Sep;90(3):728S-732S. doi: 10.3945/ajcn.2009.27462F. Epub 2009 Jul 29. PMID: 19640955.

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Not all glutamate is created equal

There are two types of glutamate. One is bound glutamate, glutamate tied or “bound” to other amino acids in protein.

Bound glutamate causes no damage in the brain or peripheral tissue. It triggers no adverse reactions.

Then there is free glutamate.  Free glutamate does three things simultaneously, it:

1. Triggers glutamate receptors in the mouth and on the tongue causing them to swell, so to speak, giving the food with which they were ingested a more robust taste.

2. Triggers glutamate receptors in the brain. In well-regulated amounts, glutamate enables the brain to function properly. However, in excess amounts such as those presently available in processed food, glutamate becomes an excitotoxic neurotransmitter firing repeatedly until its targeted glutamate receptors die.

3. Triggers glutamate receptors in peripheral tissue.

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Who are the ‘Glutes’?

For years, the Truth in Labeling Campaign has been calling them the “Glutes,” a name that many now recognize as being those who make money selling their poisons hidden in food. We gave them a name because we want you to know them and start talking about them, and it’s hard to talk about someone or something if it doesn’t have a name.

The founder and chief operating officer of this loosely knit operation is Ajinomoto, the world’s largest producer of monosodium glutamate. Ajinomoto designs and bankrolls its research, bragging of the millions it’s spending on public relations to “clear MSG’s bad name.” Their goal is to counter the fact that every day more and more people are suffering reactions to MSG and other flavor enhancers that contain MSG’s toxic manufactured free glutamate (MfG) by plastering the world with propaganda that MSG has gotten a bad rap.

Without the researchers who execute their double-blind studies using excitotoxic, brain damaging placebos, without the food technologists who incorporate MfG into thousands of processed foods, without the manufacturers that use MSG in their products so they can skimp on quality — aided by the grocery outlets that sell their products — and without the “public servants” at the FDA who for 50 years have turned their backs on research that clearly demonstrates MSG has toxic potential while endorsing the out and out lie that MSG is safe for use in food, MSG would have long ago been banned. And it can be done. As recently as 2018 the FDA acted to no longer allow the use of seven flavoring substances and flavor enhancers deemed dangerous.

Those are the Glutes: the people who work to keep MSG flowing without mentioning that they work for the producer of MSG when signing off on their work.

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There is no controversy!

Like everything else the “Glutes” put out to deceive you into believing that MSG is “safe,” claiming that the safety of MSG is controversial is part of their basic con.

The only “controversy” here is that the Glutes continue to say MSG is “safe” despite clear and copious data demonstrating MSG is toxic.

There really is nothing to debate.  But being that selling MSG is their business, they work very hard on twisting the truth. Here are the facts of the matter: 

1. The opinion that free glutamic acid (the active component in MSG) causes brain damage, is based on data amassed between 1969 and 2021 by neuroscientists studying the brain.

2. No data demonstrating anything to the contrary exist.  Those who manufacture and sell MSG say that MSG is harmless or “safe” by pointing to studies that failed to find toxicity. That’s a big difference.

Here’s how it works:

  • They claimed to have replicated studies of glutamate induced toxicity from the 1970s without finding toxicity, but they were not true replications.  Rather, the methods and materials used in setting up studies and analyzing results prevented identifying evidence of MSG toxicity.
  • From the 1980s until it was made public that they were using placebos in their double-blind studies that caused reactions identical to those caused by MSG test material, their claims of “safety” were based on studies that were rigged to exclude the possibility that MSG was anything but “safe.”
  • Since being exposed, claims of safety now come from what’s called consensus meetings. These are meetings organized and paid for by the U.S. manufacturer of MSG or their agents where participants discuss the safety of MSG and publish the conclusion that they find it to be “safe.”

MSG is a toxic ingredient.  There should be no question about the truth of the matter.  In that sense, there really is no controversy.