Truth in Labeling Campaign Blog
The truth, the whole truth, and nothing but the truth about MSG and manufactured free glutamate
Eating all your fruits and vegetables and still not feeling as chipper as you used to? You’ve probably checked the purity of the water you drink and determined that you don’t live over a toxic waste dump.
But have you checked for excitotoxic – brain damaging – free glutamate in the processed foods you’re eating — even ones considered “healthy”? You’ll find the names of excitotoxic ingredients that are used in food at: https://www.truthinlabeling.org/names.html
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.
What makes a food “ultra-processed?”
Apologists for Big Food are working hard to make us believe that (with a few exceptions) ultra-processed foods are simply the natural evolution of food processing. Bread, they tell us, is likely the very first “processed” food, originally crafted over 30,000 years ago. Then there are cheeses, beer, and fermented foods – all created by humans to advance how we eat.
But along with the introduction of more and more novel ready-to-eat processed foods (such as canned beans and grape jelly in the 1920s and breakfast cereals hitting the market in the 1940s), something odd happened to large categories of these items. No longer did they retain the basic identity of food itself, with some being made entirely of laboratory-created ingredients.
These new creations, later labeled ultra-processed foods, surreptitiously emerged around the 1980s.
Before this sneaky shift in how many “foods” were being manufactured was realized, however, the effects of consuming these items became quite obvious — a growing epidemic of obesity along with a marked rise in chronic diseases.
And despite the increased scrutiny these types of foods have garnered lately you won’t find any kind of FDA-sanctioned labeling or notice that what you’re considering serving for dinner may look like what’s traditionally thought of as food, only it really isn’t.
The ‘Ultra-Processed Food Group’
Investigations by Dr. Carlos Monteiro, a professor of Nutrition and Public Health in Sao Paulo, Brazil, and other researchers at the University of Sao Paulo led to a first-of-its-kind classification of processed foods called Nova in 2010.
Using Nova, Monterio and others published a paper in 2019 that defines what makes up ultra-processed food.
Ingredients characteristic of ultra-processed foods are either food substances of no or rare culinary use, or else classes of additives whose function is to make the final product sellable, palatable and often hyper-palatable.
Classes of additives used only in the manufacture of ultra-processed foods are flavors, flavor enhancers, colors, emulsifiers, emulsifying salts, artificial sweeteners, thickeners, and foaming, anti-foaming, bulking, carbonating, gelling, and glazing agents. All of them, most notably flavors and colors, either disguise unpleasant sensory properties created by ingredients, processes, or packaging used in the manufacture of ultra-processed foods, or give the final product intense sensory properties especially attractive to see, taste, smell and/or touch, or both.
Manufactured flavoring agents, such as MSG and dozens of other additives containing brain-damaging free glutamate are key indicators of these ultra-processed foods. And all of these additives that make a non-food look and taste like real food have been given free rein by the U.S. Food and Drug Administration.
Monterio gives this tip as a way to ID ultra-processed foods:
Generally, the practical way to identify if a product is ultra-processed is to check to see if its list of ingredients contains at least one item characteristic of the ultra-processed food group. These are either food substances never or rarely used in kitchens or classes of additives whose function is to make the final product palatable or more appealing.
The FDA has done its part to help in the proliferation of this “ultra-processed food group” by distracting consumers into reading its mandated and relatively meaningless nutrition facts label and declaring these toxic additives to be either “safe” or GRAS — generally recognized as safe.
Sadly, also making the Nova list of ultra-processed foods are infant formulas and “meal replacement” beverages for the elderly and infirm.
As Dr. Monterio said in an interview in 2023, the “main purpose of ultra-processed food is to make products that can replace real foods (to) amplify profits of the food industry.”
And when the food industry has friends like the FDA to help it along, you can bet the farm that more ultra-processed foods will be replacing real farm-grown foods than ever before.
In case you didn’t know, excitotoxic – brain damaging — free glutamate is an essential ingredient in all ultra-processed food. You may recognize it as the essential ingredient in monosodium glutamate (MSG) – which is itself an ultra-processed food.
Although the typical U.S. supermarket contains a wide variety of packaged foods, that assortment emanates from 10 giant conglomerates.
These multinationals, such as Unilever, Coca-Cola and Mondelez, have their imprints on practically everything you eat. And more and more of these products are “ultra-processed.”
It used to be that food technologists designed processed foods. Those would be whole foods that were canned, freeze-dried, or fermented, for example. But in the 1980s ultra-processed food — products manufactured with substances extracted from foods or synthesized in laboratories — started to line supermarket shelves.
Ultra-processed foods are fractionated-recombined foods consisting of an extensive number of additives and ingredients, but little actual whole food. They can be identified by the remarkably long list of ingredients – including many unpronounceable ones — found on their labels. According to a recent study, Canadians are taking in practically half of their daily calories from ultra-processed foods.
Not mentioned in any study of ultra-processed foods, however, are the toxic ingredients added for color, flavor, shelf life (preservatives), and protein, along with low-calorie sweeteners. Free glutamate, the toxic component of monosodium glutamate, and all of the ingredients in the following list are found in both flavor enhancers and protein enhancers. And some say because they mask the taste of old or rancid food, free glutamate is used as a preservative as well.
Names of ingredients that always contain free glutamate:
Names of ingredients that often contain or produce free glutamate during processing:
The following are ingredients suspected of containing or creating sufficient processed free glutamate to serve as reaction triggers in HIGHLY SENSITIVE people:
Convenient, relatively inexpensive and heavily advertised, the future of ultra-processed foods seems to be assured (1). And why not? The FDA lets the people who manufacture ultra-processed foods declare that they are GRAS (generally recognized as safe), and the general public seems unaware that the fox is guarding the hen house.
Reference
1. Open PR Worldwide Public Relations. Press release. 7/3/2019. “What’s driving the Flavor Enhancers Market Growth? Cargill, Synergy Flavors, Tate & Lyle, Associated British Foods pic, Corbion …” https://www.openpr.com/news/1794737/what-s-driving-the-flavor-enhancers-market-growth-cargill. Accessed 7/31/2019.
Say “no” to brain damage caused by manufactured free glutamate. Check out the names of ingredients that contain it: https://www.truthinlabeling.org/names.html
Reactions to MSG and other sources of manufactured free glutamate are reactions to poison. They’re not allergic reactions, and the rules for allergies don’t apply.
You may hear people refer to an “MSG allergy,” but that’s incorrect. And allergists aren’t the ones to ask about your reactions to MSG.
Long before 1969, when Olney first demonstrated the toxic effects of free glutamic acid, it was observed that on occasion glutamic acid would accumulate in the space between neurons referred to as interstitial tissue, and that would be followed by brain damage.
It has long been understood that acute increases in extracellular glutamate levels can lead to over-stimulation of glutamate receptors, resulting in a cascade of excitotoxic-related mechanisms culminating in neuronal damage.
Recognition of the significance of the role played by glutamic acid was slow in coming. Indeed, for a long time, it was not realized that glutamate was a neurotransmitter. The presence of glutamate in every part of the body as a building block for protein made its special role in the nervous system difficult to recognize. Its function as a neurotransmitter was not generally accepted until the 1970s, decades after the identification of acetylcholine, norepinephrine, and serotonin as neurotransmitters. 1.
Glutamate is an excitatory neurotransmitter with several types of receptors found throughout the central nervous system, and its metabolism is important to maintaining optimal levels within the extracellular space.
“Over the past three decades, researchers have learned that glutamate is the major excitatory neurotransmitter of the healthy mammalian brain, as the most profuse free amino acid that happens to sit at the intersection between several metabolic pathways (Watkins and Jane, 2006; Zhou and Danbolt, 2014). Glutamate is stored in synaptic vesicles of nerve terminals until it is released by exocytosis into the extracellular fluid, where it can quickly become highly concentrated (Zhou and Danbolt, 2014). Additionally, micromolar concentrations of basal extracellular glutamate, originating from non-vesicular release from the cystine-glutamate antiporter, continue to circulate in the space outside the synaptic cleft (Baker et al., 2002). Maintaining optimal levels in this space is essential, as low levels can deplete energy whereas excess levels can lead to cell death (Zhou and Danbolt, 2014). Glutamate transporters located on the outside of astrocytes and neurons quickly act to remove excess glutamate (Zhou and Danbolt, 2014). Receptor proteins at the surface of cells detect glutamate in the extracellular fluid and receive it (Zhou and Danbolt, 2014).” 2.
In the meantime, the incidence of neurodegenerative disease and disease states such as autism was growing, and myriads of studies of “glutamate-induced” abnormalities were published and chronicled in PubMed.gov. It is well documented that glutamic acid is implicated in kidney and liver disorders, neurodegenerative diseases, 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 the scientific community generally accepted evidence of the toxic effects of glutamate.
A January 15, 2023 search of the National Library of Medicine using PubMed.gov returned 4276 citations for “glutamate-induced.”
In 1969 and the decade that followed, it was demonstrated that ingestion of free glutamate of various dosages and routes of administration would produce excess amounts of free glutamate in such quantity as to cause brain damage in every laboratory animal available. In 1969, Olney coined the term “excitotoxin” to describe the brain-damaging actions of glutamic acid. 3.
Olney was a neuroscientist interested in such things as amino acids and brain function and had no interest in food science.
In the late 1960s, he became suspicious that obesity in mice, which was observed after neonatal mice were treated with monosodium glutamate for purposes of inducing and studying retinal pathology, might be associated with hypothalamic lesions caused by monosodium glutamate treatment; and in 1969 he first reported that monosodium glutamate treatment did indeed cause 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 glutamate subcutaneously.
Research that followed confirmed that monosodium glutamate, which was routinely given as the sodium salt, monosodium glutamate (brand name Accent), induces hypothalamic damage when given to immature animals after either subcutaneous or oral doses.
At the time, Olney and others were using inexpensive, off-the-supermarket shelf Accent brand monosodium glutamate for their studies instead of using more expensive pharmaceutical grade glutamic acid.
Those who manufactured and profited from the sale of MSG had a different agenda. They knew that their product, monosodium glutamate, had been used as the source of free glutamate that caused brain damage in laboratory animals. And they made it their mission to do whatever it might take to convince the public that MSG was a harmless, or even beneficial, food additive.
After Olney’s 1969 discovery, the existence of free excitotoxic amino acids present in food became the best-guarded secret of the food and drug industries. The U.S. producer of monosodium glutamate established an organization, hired researchers and PR firms that produced non-stop propaganda, and successfully censored anything that suggested that MSG might be harmful. This is how it was and how it continues to be done.
1) Start with a well-funded organization
In 1969, the International Glutamate Technical Committee (IGTC) was founded. Andrew G. Ebert, Ph.D. took credit as its founder. Ajinomoto’s role was not publicly disclosed.
The IGTC sponsored, gathered, and disseminated research on the use and safety of monosodium glutamate; designed and implemented research protocols and provided financial assistance to researchers; promoted acceptance of monosodium glutamate as a food ingredient; and represented members’ collective interests. Those collective interests were to sell monosodium glutamate. Ajinomoto was its principal sponsor. There is every indication that its financial resources were unlimited.
2) Identify and employ MDs and PhDs to conduct research designed and supervised by your organization – research from which readers will conclude that monosodium glutamate is a harmless food additive.
By and large, those who have represented the glutamate industry have produced research relative to the safety of monosodium glutamate only in response to encouragement (payment of some sort) from the glutamate industry.
3) Identify and employ prestigious universities and medical schools to host your research. Universities and medical schools profit from hosting research.
4) Identify and befriend FDA, USDA, EPA, and NIH staff who will work actively to support the position that monosodium glutamate should be accepted as generally recognized as safe (GRAS). It is well understood that those who work for government agencies and do nothing to challenge the industries that they are employed to regulate will be rewarded with industry jobs from time to time (the revolving door policy) or with government retirement.
5) Use a variety of strategies.
Vary the details of the individual research studies so the studies give the appearance of being independent of one another. (When asked for the details of their studies, IGTC-sponsored researchers know little or nothing of the details.)
Suppress unfavorable information.
Disseminate seemingly unlimited amounts of deceptive and/or misleading information.
6) Disrupt the activities of those who oppose you.
7) Convince both appointed and elected officials to endorse monosodium glutamate as a harmless food additive.
They’re called lobbyists. They do most of Ajinomoto’s work in this area.
8) Legitimize the need for the existence of monosodium glutamate.
After years of funding studies aimed at renaming glutamate receptors in the mouth and on the tongue – calling them taste receptors — Ajinomoto had some of those studies published and reported on by the media. From that point, the concept of “umami” as a fifth taste was picked up by the food industry, and its friends at the FDA. That was how Ajinomoto moved the concept of “umami” into the vernacular.
What is “umami?” It’s a hypothetical construct invented by Ajinomoto to legitimize and promote the use of MSG in food. Think about it. MSG is a neurotoxic flavor enhancer. By referring to MSG as umami and promoting its new name, Ajinomoto is working to sell MSG to the public as a way to provide an ‘exciting’ fifth taste.
By and large, the IGTCs human studies commenced in 1980 with research that “failed to produce any evidence that monosodium glutamate causes asthma or Chinese restaurant syndrome.” And coming to that conclusion was a slam dunk. All they had to do was look at the wrong thing, at the wrong time, in people who were not sensitive to MSG. For good measure, they laced their placebos with excitotoxic aspartame and/or ingredients other than monosodium glutamate that contained excitotoxic processed free glutamic acid. Then the propaganda people would spin the story that monosodium glutamate is safe.
The Glutes don’t plagiarize, fabricate (make up) data, or falsify data by manipulating research materials, equipment, or processes, or changing or omitting data or results such that the research is not accurately represented in the research record. Instead, the Glutes design and implement studies guaranteed to fail to find evidence of MSG toxicity.
Leaving nothing to chance, Andrew Ebert supplied all industry researchers with placebos that caused reactions identical to those caused by MSG test material. That practice started in 1978 and remained in operation until it was made public.
Adverse reactions
Despite the fact that the Glutes are in control of mainstream media and social media, individuals continue to share information about their adverse reactions following eating things that contain free glutamate.
The growing literature on control of glutamate release testifies to this increasing awareness — awareness of glutamate-induced brain damage, but without focus on the benefits of reducing the availability of free glutamate. This growing literature on control of glutamate release focuses on the development of drugs with which to treat glutamate-induced brain damage, giving little attention to actually reducing free glutamate.
At last search, there were 5778 articles listed on PubMed on the subject of “control of glutamate release,” with titles such as “Influence of glutamate and GABA transport on brain excitatory/inhibitory balance” 4. and “Astrocytes Maintain Glutamate Homeostasis in the CNS by Controlling the Balance between Glutamate Uptake and Release.” 5.
Each studied the subject through the review of potential remedies (drugs) that might reduce whatever abnormality was being studied.
In contrast, I have found only one article that suggests the way to prevent adverse reactions following ingestion of foods that contain free glutamate might be to stop eating things that contain it.
Today, excitotoxins present in food remain largely ignored or unknown, mostly because the rich and powerful food and pharmaceutical industries want it that way. A great deal of food industry profit depends on using excitotoxins to “enhance” the taste of cheaply made food. And a great deal of pharmaceutical industry profit depends on selling drugs to “cure” the diseases and disabilities caused by the excitotoxins in the food supply.
It may be that industry’s ability to censor anything that might suggest that MSG might be harmful continues to be effective, for no one has yet come out and said, “The way to prevent adverse reactions following ingestion of foods that contain free glutamate might be to stop eating things that contain it.”
Adrienne Samuels
References
1. Watkins JC. l-glutamate as a central neurotransmitter: looking back. Biochem Soc Trans. 2000;28(4):297-309. PMID: 10961913.
2. Pal MM. Glutamate: The Master Neurotransmitter and Its Implications in Chronic Stress and Mood Disorders. Front Hum Neurosci. 2021 Oct 29;15:722323. doi: 10.3389/fnhum.2021.722323. PMID: 34776901; PMCID: PMC8586693.
3. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science. 1969 May 9;164(3880):719-21. doi: 10.1126/science.164.3880.719. PMID: 5778021.
4. Sears SM, Hewett SJ. Influence of glutamate and GABA transport on brain excitatory/inhibitory balance. Exp Biol Med (Maywood). 2021 May;246(9):1069-1083. doi: 10.1177/1535370221989263. Epub 2021 Feb 7. PMID: 33554649; PMCID: PMC8113735.
5. Mahmoud S, Gharagozloo M, Simard C, Gris D. Astrocytes Maintain Glutamate Homeostasis in the CNS by Controlling the Balance between Glutamate Uptake and Release. Cells. 2019 Feb 20;8(2):184. doi: 10.3390/cells8020184. PMID: 30791579; PMCID: PMC6406900.
Trouble avoiding MSG? That’s because it’s not MSG per se that’s causing your reactions. it’s the Manufactured free Glutamate in it. And MfG is found in snacks, processed foods, protein drinks, protein powders, dietary supplements, infant formula and pharmaceuticals.
Download our list of ingredient names here.
Adrienne Samuels, Ph.D., March, 2022
NOTE: Studies confirming that the free glutamate in MSG causes brain damage, intractable obesity, infertility and more were done before it was understood that excitotoxic free glutamate would be found in ingredients other than MSG.
Obesity is the excessive or abnormal accumulation of fat or adipose tissue in the body that impairs health through its association with numerous serious diseases and health conditions. It is a public health epidemic with an economic burden estimated to be about $100 billion annually in the United States alone (1).
According to the Centers for Disease Control and Prevention (CDC), those who are obese, compared to those with a healthy weight, are at increased risk for many serious diseases and health conditions, including the following:
There are countless factors that contribute to obesity, but only one that by itself can explain the ongoing obesity epidemic:the fact that excitotoxic amino acids (EAA) ingested by pregnant women are passed via the placenta to their fetuses where they cause brain lesions in the arcuate nucleus – brain damage that is followed by gross obesity as these children approach maturity.
A series of studies from 1969 and the decade that followed demonstrated that three conditions had to be met in order to produce food-induced neurotoxicity:
Damage caused by manufactured free glutamate delivered by pregnant women to the vulnerable brains of their fetuses meets all three of these conditions. A sufficient quantity of excitotoxic material became available and accessible in 1957 when vast amounts of free glutamate began to appear in processed food.
Undisputed is the fact that there are high concentrations of glutamate in the brain. When present in protein or released from protein in a regulated fashion (through routine digestion) glutamate is vital for normal body function. Glutamate is the principal neurotransmitter in humans, carrying nerve impulses from glutamate stimuli to glutamate receptors throughout the body.
Disputed by some producers of free glutamate is the assertion that glutamate is an excitotoxic amino acid. This Jekyll and Hyde amino acid becomes toxic when present in greater quantity than a healthy human needs for normal body function. Then, as an excitotoxic neurotransmitter, it fires repeatedly, damaging targeted glutamate receptors and/or causing neuronal and non-neuronal death by over exciting those glutamate receptors until their host cells die (3-8).
The first study to address the possibility that glutamate from exogenous sources (from eating, for example) might cause brain damage was published in 1969. At the time, it was demonstrated that glutamate-induced brain damage to the arcuate nucleus of the hypothalamus of neonatal animals was followed by obesity, reproductive dysfunction, behavioral disturbances and more (9). 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 after either subcutaneous (10-31) or oral (17,23,24,26,32-36) doses.
Developmental dysfunction or abnormalities in growth and behavior were also noted in a number of studies. Animals treated with glutamate as neonates or in the first 12 days of life suffer neuroendocrine disturbances including obesity and stunting, abnormalities of the reproductive system, and underdevelopment of certain endocrine glands (9,18,20,36,37-54) and possible learning deficits either immediately or in later life (40,43,44,55-61).
In addition, Bhagavan and others reported behavioral reactions including somnolence and seizures (62-69; tail automutilation; (42,56) and learned taste aversion (58). Irritability to touch was interpreted as conspicuous emotional change by Nemeroff (42). Lynch (70) reported hyperglycemia along with growth suppression. He noted that hyperglycemia did not occur when subjects were given intact protein that contained a large amount of glutamate.
Since the 1980s, researchers have focused on identifying and understanding human abnormalities associated with free glutamate, often for the purpose of finding drugs that would mitigate glutamate’s adverse effects. Invariably, those have been studies of the glutamate from endogenous sources. The possibility that glutamate from exogenous sources might contribute to those abnormalities and/or might cause brain damage in humans leading to gross obesity, was not considered.
Brain lesions
In the 1960s and 1970s, research done by people not employed by the glutamate industry demonstrated that monosodium glutamate fed to laboratory animals causes brain lesions, endocrine disorders, and observable adverse reactions.
In response, glutamate-industry researchers pretended to replicate those animal studies; but changed the methodology enough to make certain that there would be nothing negative to report.
These investigators made no attempt to replicate the methods of the independent scientists, and used entirely different (and inappropriate) methods for preservation and staining brain tissue in the analysis of results.
On occasion, I had the privilege of visiting with John W. Olney, MD, the man who coined the term “excitotoxin” to describe the effects he had seen free glutamate have on neonatal animals. And while he didn’t dwell on criticizing the research of others, he was generous in answering my questions. He told me that when he first found that glutamate (given as MSG) caused brain damage in infant mice, he searched out or was put in touch with Dr. W. Ann Reynolds, and either Reynolds or someone sent by Reynolds spent a great deal of time in Olney’s laboratory, learning the detail of how his experiments had been conducted. By and large, it was Reynolds and coworkers Filer, Stegink, and Lemkey Johnson who failed to replicate Olney’s findings. Other industry scientists producing similar results using similar methodology were affiliated with laboratories that did contract work for the glutamate industry.
Adverse reactions
Glutamate-induced adverse reactions may or may not involve the brain. There has been no study of that issue. But since the subject of this paper is glutamate-induced obesity second to brain damage caused by glutamate ingested in quantity by pregnant women and passed to fetuses through the placenta, the subject of glutamate-induced adverse reactions has not been considered.
It is necessary for a substantial amount of free glutamate to be ingested for that free glutamate to become excitotoxic. For glutamate to be excitotoxic, there must be an accumulation of free glutamate greater than needed for normal body function.
In 1957, bacterial fermentation was introduced as a new and improved method for production of free glutamate for use in food. From that point forward, with genetically modified bacteria secreting free glutamic acid through their cell walls, unlimited production of free glutamic acid was virtually assured (71).
It wasn’t long before competing manufacturers added dozens more excitotoxic food additives to the American diet. Following MSG’s surge in production and its manufacturer’s aggressive advertising, there was broad recognition that profits could be increased if a company produced its own flavor-enhancing additives. Since that time, the market has been flooded with flavor enhancers and protein substitutes that contain manufactured free glutamate such as hydrolyzed pea protein, yeast extracts, maltodextrin and soy protein isolate, as well as MSG.
Although there have been studies that mention the fact that there are substantial amounts of free glutamic acid in processed food (72-80) there has been no systematic study. There are, however, numerous market reports with promotional materials that speak of manufactured glutamate history and forecast. Market reports for monosodium glutamate focus on that commodity. Market reports for glutamic acid generally take into account all flavor enhancers (81-87).
You only have to compare the ingredients listed on the labels of processed and ultra-processed foods to a list of the hidden sources of manufactured free glutamate to realize just how much manufactured free glutamate there is in the food supply. Table 1 lists the food ingredients that contain free glutamate as an ingredient or a constituent of an ingredient. By virtue of the fact that ultra-processed foods are typically made with inferior foods and/or chemicals, every ultra-processed food contains flavor-enhancers, which will contain manufactured free glutamate regardless of the ingredient names on the labels describing those ingredients.
Today, there is sufficient excitotoxic free glutamate in processed foods, dietary supplements, snacks, protein powders and protein drinks, protein substitutes, fake meat, enteral care products, and pharmaceuticals for a person to consume in a day’s time the quantity necessary for that free glutamate to become excitotoxic. Only a portion of that comes in an ingredient called monosodium glutamate or E621.
Since the 1957 change in method of MSG and manufactured free glutamate production, there are so many products that contain excitotoxic ingredients that it is easy for a consumer to ingest an excess of excitotoxic material during the course of a day.
Effective delivery of excitotoxic free glutamate would depend in large part on the integrity/health of the brain to which it is being delivered.
In children and adults with mature brains, delivery can be accomplished by providing the subject with free glutamate to ingest in sufficient quantity to cause it to be excitotoxic.
Delivery of excitotoxic free glutamate to a fetus and/or neonate will be accomplished when a pregnant or lactating female passes excess free glutamate to a fetus or neonate through the placenta or in mothers’ milk.
Nourishment (and not so nourishing material) is delivered to the fetus in the form of material ingested by a pregnant woman and passed to the fetus through the placenta. MSG can cross the placenta during pregnancy (88-90), can cross the blood brain barrier (BBB) in an unregulated manner during development (91-94), and can pass through the five circumventricular organs which are leaky at best at any stage of life (92,95). Glutamate is an ingredient that passes to the fetus. The placenta does not filter out glutamate (88). Moreover, the BBB is easily damaged by fever, stroke, trauma to the head, seizures, ingestion of MSG, and the normal process of aging (66,96).
And the fetus will be more vulnerable to glutamate-insult than the newborn.
Similar to drugs and alcohol, free glutamate can also be passed to infants through mothers’ milk. Newborn humans will receive glutamate through mothers’ milk or through infant formula, both of which routinely contain free glutamate (97).
The glutamate in mothers’ milk, however, will not be excitotoxic unless lactating mothers ingest excessive quantities of free glutamate – quantities sufficient to cause free glutamate to become excitotoxic.
According to the Surgeon General’s “Vision for a Healthy and Fit Nation,” the prevalence of obesity changed relatively little during the 1960s and 1970s, but increased sharply over the ensuing decades (98).
That information is consistent with information that comes from the National Health and Nutrition Examination Surveys (NHANES) which periodically collect measured height and weights in representative samples of the population. The first records of weight came from the CDC’s 1960-1962 report with subsequent reports confirming that the prevalence of obesity among adults more than doubled between 1976-1980 and 2007-2008 (99).
We have briefly discussed excitotoxicity, the phenomenon underlying the obesity epidemic, drawing attention to the fact that a possible role for excitotoxins from exogenous sources has not previously been considered.
We have reviewed the studies that present evidence of glutamate excitotoxicity. Underscoring the recognition that glutamate-induced brain damage leads to obesity, is the fact that since 1980, it has been common practice to use monosodium glutamate or glutamic acid to produce brain-damaged obese animals for use in studies of various glutamate-related abnormalities.
We have described the way in which excitotoxic free glutamate can be delivered by pregnant women to fetuses and neonates, causing brain damage and subsequent obesity.
The single challenge to the assertion that the brains of the fetus and neonate are vulnerable to the toxic effects of glutamic acid from exogenous sources has been mounted by the International Glutamate Committee (IGTC) based on a paper Richard Hawkins presented in September 2008 at the IGTC’s 100th Anniversary Symposium of Umami Discovery: “The Roles of Glutamate in Taste, Gastrointestinal Function.”
In 1969, the IGTC was organized to represent the interests of Ajinomoto, the U.S. producer of MSG and manufactured free glutamate. Hawkins received both travel expenses and an honorarium from the IGTC, and acknowledged the sharing of ideas and advice from Andrew Ebert, Ajinomoto’s agent in charge of providing test and placebo materials to their researchers doing double-blind studies on the safety of MSG. It was Ebert who provided his researchers with placebos containing aspartic acid, an excitotoxic amino acid known to cause adverse reactions and brain damage identical to that caused by the excitotoxic glutamic acid in MSG test material.
Without taking into consideration the unique properties of an immature brain, Hawkins asserted that the human brain is impervious to glutamate damage.
It has been demonstrated that following the 1957 modernization of glutamate production, there has been sufficient free glutamate available and accessible in processed and ultra-processed foods to cause accumulated glutamate to become excitotoxic.
From National Health and Nutrition Examination Surveys (NHANES) documenting the prevalence of overweight, obesity, and extreme obesity, we have observed increased incidence of obesity dating from 1960, as well as the demonstration of racial disparities. In the 2012 article “The Nation’s childhood obesity epidemic: Health disparities in the making,” Suzanne Johnson makes a case for the obesity epidemic being, in part, a product of an environment that promotes overeating — over time having changed the type and quantity of food we eat. She cites less time for in home food preparation, the consumption of a plethora of fast food and convenience food, and the fact that fast-food restaurants are more common in ethnic minority neighborhoods (100).
The reader has only to connect the dots between 1) the vulnerable brain of the fetus and neonate receiving excitotoxic amino acids in processed and ultra-processed food, and 2) the fact that prior to the surge in production of glutamic acid triggered by the modernization of manufacture of the glutamic acid in MSG, there was no obesity epidemic. Then trace the unfolding of the obesity epidemic from reformulation of free glutamate in 1957 to the early 1970s when those made obese by the influx of free glutamate began to become noticeable.
Thus, it has been demonstrated that obesity can be caused by excitotoxic amino acids ingested by pregnant and/or nursing women and delivered to fetuses and neonates who exhibit obesity as they reach maturity.
No discussion would be complete without considering why this information has not been discussed previously by others. With the first suggestion that MSG might have toxic potential, those with financial interest in promoting MSG as a valuable flavor-enhancer launched well-funded, well-articulated campaigns to promote their product and deny its toxicity. That included rigging studies to come to the foredrawn conclusion that MSG is a harmless food additive and securing the active cooperation of regulators as well as the help of medical professionals (101).
That might account for the fact that to date, the roles of MSG and manufactured free glutamate in the obesity epidemic have been overlooked.
Recognition of the fact that glutamate-induced brain damage in fetuses and neonates lies at the root of the obesity epidemic should serve as a valid starting point for new ground-breaking research. It should put an end to the shame and blame that have long been associated with obesity, and facilitate appropriate counseling and medical interventions for those who are afflicted.
Excitotoxic amino acids delivered to fetuses and neonates by pregnant and nursing women should be included as recognized risk factors for obesity.