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Can dietary monosodium glutamate intake induce restlestness?

Can dietary monosodium glutamate intake induce restlestness?



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The question is all in the title.

More context:

I like phở soup. I have noticed that I get restless after eating the phở soup at some restaurants. The effects are similar to the ones resulting from caffeine intake. (Ingesting a cup of Turkish coffee or a couple of espressos results in my hands shaking badly.)

The phở soups which I think trigger the reaction appear to be the most savory ones. Given that:

  1. Monosodium glutamate (MSG) is a common ingredient in phở
  2. MSG has flavor enhancing properties
  3. Glutamate is a neurotransmitter

I thought there was possibly a connection. (Or perhaps not. Or perhaps it's the intake of MSG together with the consumption of an herb containing caffeine or another psychoactive drug. Phở contains herbs in large quantities.)

I found this paper which states the effects of caffeine result from an increase of glutamic acid (GA) in the posterior hypothalamus which in turns triggers wakefulness.

Thus I guess what I am asking is: does dietary intake of MSG increase blood serum levels of GA and does an increase of GA blood serum level result in an increase of GA in the brain (or in some parts of the brain)?


There is no strong evidence for MSG having any kind of neurotoxic/neuromodulatory effect.

However, A 2010 article says that, in a double blind trial, it was found that the people who consumed MSG containing soda, reported headache in significantly more numbers compared to the placebo subjects [1]. The concentration of MSG used in this study was 75-150 mg/kg. Assuming that one serving of soda would be 300ml i.e 300g, the amount of MSG consumed would be maximally 45mg, which is much less than glutamate concentration in some natural food stuffs such as tomatoes (~2000mg/kg [2,3]; a tomato that weighs 6oz/~170g contains ~340mg of glutamate). Therefore, I would doubt the findings of this article. The results could have possibly been observed because of some hidden dependent variable (such as the soda formulation).

In general, the USFDA considers MSG as GRAS (generally regarded as safe) [4].

Finally, a 2014 article concludes that dietary MSG would not lead to increase in either blood or brain levels of glutamate [5].

From the Abstract:

The sodium salt of glutamate (monosodium glutamate; MSG) imparts a savory/meaty taste to foods, and has been used as a flavoring agent for millennia. Past research on MSG/glutamate has evaluated its physiologic, metabolic and behavioral actions, and its safety. Ingested MSG has been found to be safe, and to produce no remarkable effects, except on taste. However, some recent epidemiologic and animal studies have associated MSG use with obesity and aberrations in fat metabolism. Reported effects are usually attributed to direct actions of ingested MSG in brain. As these observations conflict with past MSG research findings, a symposium was convened at the 13th International Congress on Amino Acids, Peptides and Proteins to discuss them. The principal conclusions were: (1) the proposed link between MSG intake and weight gain is likely explained by co-varying environmental factors (e.g., diet, physical activity) linked to the "nutrition transition" in developing Asian countries. (2) Controlled intervention studies adding MSG to the diet of animals and humans show no effect on body weight. (3) Hypotheses positing dietary MSG effects on body weight involve results from rodent MSG injection studies that link MSG to actions in brain not applicable to MSG ingestion studies. The fundamental reason is that glutamate is metabolically compartmentalized in the body, and generally does not passively cross biologic membranes. Hence, almost no ingested glutamate/MSG passes from gut into blood, and essentially none transits placenta from maternal to fetal circulation, or crosses the blood-brain barrier. Dietary MSG, therefore, does not gain access to brain. Overall, it appears that normal dietary MSG use is unlikely to influence energy intake, body weight or fat metabolism.


Short answer
Glutamate cannot enter the brain due to the blood-brain-barrier.

Background
You are totally right that glutamate represents the principal excitatory neurotransmitter in the brain (Meldrum, 2000). However, glutamate is a regular amino acid and will be metabolized quickly. More importantly, the blood-brain barrier is extremely effective in keeping polar (hydrophylic) molecules out, and therefore especially ions are not coming through as they are extremely hydrophilic. The blood-brain-barrier is formed by the endothelium lining the blood capillaries in the brain. In the brain, the endothelial cells are coupled through tight-junctions, that effectively keep almost everything out of the brain. The only molecules that can get through are either actively absorbed through specialized channels (glucose transporters for example) or are lipophilic. Glutamate under physiological pH carries two negative charges and a positive charge (Fig. 1), and will hence never make it through the blood-brain-barrier. There are glutamate transporters in the endothelial cells, but these in fact transport glutamate out of the brain, rather than in (Hawkins, 2009).


Fig. 1. Glutamate at physiological pH. Source: WikiWand.

References
- Hawkins, Am J Clin Nutr (2009); 90(3): 867S-4S
- Meldrum, J Nutr (2000) 130(4S Suppl): 1007S-15S


How can I flush MSG out of my system?

Treatment. Most allergic reactions to MSG are mild and go away on their own. More serious symptoms, such as anaphylaxis, require emergency treatment in the form of a shot of epinephrine (adrenaline).

  • Headache.
  • Flushing.
  • Sweating.
  • Facial pressure or tightness.
  • Numbness, tingling or burning in the face, neck and other areas.
  • Rapid, fluttering heartbeats (heart palpitations)
  • Chest pain.
  • Nausea.

One may also ask, can MSG make you sick?

Now renamed MSG symptom complex, it happens when the flavouring causes symptoms like headache, sweating, nausea, tiredness or a rapid heart rate. Scientists have not produced convincing evidence of the negative health effects of eating MSG, and it is considered safe to eat by the US Food and Drug Administration.

How do you test for MSG allergy?

Testing for MSG Allergy Because sensitivity to MSG is not generally accepted as a true allergy, there is no test available to determine whether you are sensitive to it. For example, skin tests and blood tests are not available as they are with other food and environmental allergies.


Abstract

Objectives

Emerging evidence shows that diet is related to asthma. The aim of this analysis was to investigate the association between monosodium glutamate (MSG) intake, overall dietary patterns and asthma.

Methods

Data from 1486 Chinese men and women who participated in the Jiangsu Nutrition Study (JIN) were analyzed. In this study, MSG intake and dietary patterns were quantitatively assessed in 2002. Information on asthma history was collected during followed-up in 2007.

Results

Of the sample, 1.4% reported ever having asthma. MSG intake was not positively associated with asthma. There was a significant positive association between ‘traditional’ (high loadings on rice, wheat flour, and vegetable) food pattern and asthma. No association between ’macho’ (rich in meat and alcohol), ‘sweet tooth’ (high loadings on cake, milk, and yoghurt) ‘vegetable rich’ (high loadings on whole grain, fruit, and vegetable) food patterns and asthma was found. Smoking and overweight were not associated with asthma in the sample.

Conclusion

While a ‘Traditional’ food pattern was positively associated with asthma among Chinese adults, there was no significant association between MSG intake and asthma.

Citation: Shi Z, Yuan B, Wittert GA, Pan X, Dai Y, Adams R, et al. (2012) Monosodium Glutamate Intake, Dietary Patterns and Asthma in Chinese Adults. PLoS ONE 7(12): e51567. https://doi.org/10.1371/journal.pone.0051567

Editor: D. William Cameron, University of Ottawa, Canada

Received: August 7, 2012 Accepted: November 2, 2012 Published: December 11, 2012

Copyright: © 2012 Shi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The study was funded by Jiangsu Provincial Natural Science Foundation BK2008464 and Jiangsu Provincial Health Bureau, China. The data analysis was supported a research grant from International Glutamate Technical Committee. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have read the journal's policy and have the following conflicts. The data analysis was supported a research grant from International Glutamate Technical Committee. There are no patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.


What is Monosodium Glutamate (MSG)?

Monosodium glutamate (MSG) is a food additive derived from glutamate, used to enhance the flavor of food.

MSG was developed in 1908 by Japanese biochemist Kikunae Ikeda, who wanted to identify the source of the rich taste of kombu, a type of seaweed. He managed to isolate glutamic acid and name its distinct taste “umami,” which essentially translates to “delicious.”

This umami taste (one of the five basic tastes along with sweet, sour, salty and bitter) helps balance and intensify flavors, just like naturally occurring glutamate found in foods like meats, cheeses, stews and bone broths.

MSG is a salt, a combination of sodium and glutamate. It’s produced by fermentation of starch or sugar.

It’s popular in Asian cooking and found in many packaged and processed foods, including stock (Bouillon) cubes, soups, ramen, condiments, dressings, salty snacks, frozen dinners and more.

The chemical structure of MSG is the same as the glutamate found naturally in most whole foods. However, the big distinction is that glutamate in MSG is “free,” or not bound to other amino acids.

That said, some foods naturally contain a form of MSG, or free glutamate, including tomatoes, potatoes, grapes and Parmesan cheese.

Without being bound within protein molecules, free glutamate may be absorbed much more rapidly, potentially leading to high concentrations in the blood.

Summary: MSG is a food additive derived from glutamate, used to enhance the flavor of food with its umami taste. It’s popular in Asian cooking and found in many packaged and processed foods. Glutamate in MSG is “free,” or not bound to other amino acids, so it may be absorbed more rapidly in the body.


Contents

Pure MSG is reported to not have a highly pleasant taste until it is combined with a savory aroma. [12] The basic sensory function of MSG is attributed to its ability to enhance savory taste-active compounds when added in the proper concentration. [6] The optimum concentration varies by food in clear soup, the "pleasure score" rapidly falls with the addition of more than one gram of MSG per 100 mL. [13]

The sodium content (in mass percent) of MSG, 12%, is about one-third of that in sodium chloride (39%), due to the greater mass of the glutamate counterion. [14] Although other salts of glutamate have been used in low-salt soups, they are less palatable than MSG. [15] "MSG might even promote healthy eating, [food scientist Steve Witherly] hypothesizes, by not only making kale more delicious but also letting you get away with using less salt." [16]

The ribonucleotide food additives disodium inosinate (E631) and disodium guanylate (E627), as well as conventional salt are usually used with monosodium glutamate-containing ingredients as they seem to have a synergistic effect. "Super salt" is a mixture of 9 parts salt, to one part MSG and 0.1 parts disodium inosinate and disodium guanylate. [17]

MSG is generally recognized as safe to eat. [2] [18] [19] A popular belief is that MSG can cause headaches and other feelings of discomfort but blinded tests have found no good evidence to support this. [9] International and national bodies governing food additives currently consider MSG safe for human consumption as a flavor enhancer. [20] Under normal conditions, humans can metabolize relatively large quantities of glutamate, which is naturally produced in the gut in the course of protein hydrolysis. The median lethal dose (LD50) is between 15 and 18 g/kg body weight in rats and mice, respectively, five times the LD50 of sodium chloride (3 g/kg in rats). The use of MSG as a food additive and the natural levels of glutamic acid in foods are not of toxic concern in humans. [20] Specifically MSG in the diet does not increase glutamate in the brain or affect brain function. [21]

A 1995 report from the Federation of American Societies for Experimental Biology (FASEB) for the United States Food and Drug Administration (FDA) concluded that MSG is safe when "eaten at customary levels" and, although a subgroup of otherwise-healthy individuals develop an MSG symptom complex when exposed to 3 g of MSG in the absence of food, MSG as a cause has not been established because the symptom reports are anecdotal. [22]

According to the report, no data supports the role of glutamate in chronic disease. High quality evidence has failed to demonstrate a relationship between the MSG symptom complex and actual MSG consumption. No association has been demonstrated, and the few responses were inconsistent. No symptoms were observed when MSG was used in food. [23] [24] [25] [26]

Adequately controlling for experimental bias includes a blinded, placebo-controlled experimental design and administration by capsule, because of the unique aftertaste of glutamates. [25] In a 1993 study, 71 fasting participants were given 5 g of MSG and then a standard breakfast. One reaction (to the placebo, in a self-identified MSG-sensitive individual) occurred. [23] A 2000 study tested the reaction of 130 subjects with a reported sensitivity to MSG. Multiple trials were performed, with subjects exhibiting at least two symptoms continuing. Two people out of the 130 responded to all four challenges. Because of the low prevalence, the researchers concluded that a response to MSG was not reproducible. [27]

Studies exploring MSG's role in obesity have yielded mixed results. [28] [29]

Although several studies have investigated anecdotal links between MSG and asthma, current evidence does not support a causal association. [30] Since glutamates are important neurotransmitters in the human brain, playing a key role in learning and memory, ongoing neurological studies indicate a need for further research. [31]

"There is no convincing evidence that MSG is a significant factor in causing systemic reactions resulting in severe illness or mortality. The studies conducted to date on Chinese restaurant syndrome (CRS) have largely failed to demonstrate a causal association with MSG. Symptoms resembling those of CRS may be provoked in a clinical setting in small numbers of individuals by the administration of large doses of MSG without food. However, such effects are neither persistent nor serious and are likely to be attenuated when MSG is consumed with food. In terms of more serious adverse effects such as the triggering of bronchospasm in asthmatic individuals, the evidence does not indicate that MSG is a significant trigger factor." [32] [33]

However, the FSANZ MSG report says that although no data is available on average MSG consumption in Australia and New Zealand, "data from the United Kingdom indicates an average intake of 590 mg/day, with extreme users (97.5th percentile consumers) consuming 2330 mg/day" (Rhodes et al. 1991). In a highly seasoned restaurant meal, intakes as high as 5000 mg or more may be possible (Yang et al. 1997). When very large doses of MSG (>5 g MSG in a bolus dose) are ingested, plasma glutamate concentration will significantly increase. However, the concentration typically returns to normal within two hours. In general, foods providing metabolizable carbohydrate significantly attenuate peak plasma glutamate levels at doses up to 150 mg/kg body weight. Two earlier studies – the 1987 Joint FAO/WHO Expert Committee on Food Additives (JECFA) and the 1995 Federation of American Societies for Experimental Biology (FASEB) – concluded, "there may be a small number of unstable asthmatics who respond to doses of 1.5–2.5 g of MSG in the absence of food". The FASEB evaluation concluded, "sufficient evidence exists to indicate some individuals may experience manifestations of CRS when exposed to a ≥3 g bolus dose of MSG in the absence of food". [32]

MSG has been produced by three methods: hydrolysis of vegetable proteins with hydrochloric acid to disrupt peptide bonds (1909–1962) direct chemical synthesis with acrylonitrile (1962–1973), and bacterial fermentation (the current method). [34] Wheat gluten was originally used for hydrolysis because it contains more than 30 g of glutamate and glutamine in 100 g of protein. As demand for MSG increased, chemical synthesis and fermentation were studied. The polyacrylic fiber industry began in Japan during the mid-1950s, and acrylonitrile was adopted as a base material to synthesize MSG. [35]

Currently (2016), most global MSG is produced by bacterial fermentation in a process similar to making vinegar or yogurt. Sodium is added later, for neutralization. During fermentation, Corynebacterium species, cultured with ammonia and carbohydrates from sugar beets, sugarcane, tapioca or molasses, excrete amino acids into a culture broth from which L-glutamate is isolated. The Kyowa Hakko Kogyo Company developed industrial fermentation to produce L-glutamate. [36]

The conversion yield and production rate (from sugars to glutamate) continues to improve in the industrial production of MSG, keeping up with demand. [34] The product, after filtration, concentration, acidification, and crystallization, is glutamate, sodium, and water.

The compound is usually available as the monohydrate, a white, odorless, crystalline powder. The solid contains separate sodium cations Na +
and glutamate anions in zwitterionic form, − OOC-CH( NH +
3 )-( CH
2 )2-COO − . [37] In solution it dissociates into glutamate and sodium ions.

MSG is freely soluble in water, but it is not hygroscopic and is insoluble in common organic solvents (such as ether). [38] It is generally stable under food-processing conditions. MSG does not break down during cooking and, like other amino acids, will exhibit a Maillard reaction (browning) in the presence of sugars at very high temperatures. [39]

MSG has been used for more than 100 years to season food. Consumption and manufacture of high-salt and high-glutamate foods, which contain both sodium and glutamate, stretch back far longer, with evidence of cheese manufacture as early as 5,500 BCE. [40]

Glutamic acid was discovered and identified in 1866 by the German chemist Karl Heinrich Ritthausen, who treated wheat gluten (for which it was named) with sulfuric acid. [41] Kikunae Ikeda of Tokyo Imperial University isolated glutamic acid as a taste substance in 1908 from the seaweed Laminaria japonica (kombu) by aqueous extraction and crystallization, calling its taste umami ("pleasant savory taste"). [42] [43] Ikeda noticed that dashi, the Japanese broth of katsuobushi and kombu, had a unique taste not yet scientifically described (not sweet, salty, sour, or bitter). [42] To verify that ionized glutamate was responsible for umami, he studied the taste properties of glutamate salts: calcium, potassium, ammonium, and magnesium glutamate. All these salts elicited umami and a metallic taste due to the other minerals. Of them, sodium glutamate was the most soluble, most palatable, and easiest to crystallize. [ citation needed ] Ikeda called his product "monosodium glutamate", and submitted a patent to produce MSG [44] the Suzuki brothers began commercial production of MSG in 1909 as Ajinomoto ("essence of taste"). [34] [39] [45]

Regulations Edit

United States Edit

MSG is one of several forms of glutamic acid found in foods, in large part because glutamic acid (an amino acid) is pervasive in nature. Glutamic acid and its salts may be present in a variety of other additives, including hydrolyzed vegetable protein, autolyzed yeast, hydrolyzed yeast, yeast extract, soy extracts, and protein isolate, which must be specifically labeled. Since 1998, MSG cannot be included in the term "spices and flavorings". However, the term "natural flavor" is used by the food industry for glutamic acid (chemically similar to MSG, lacking only the sodium ion). The Food and Drug Administration (FDA) does not require disclosure of components and amounts of "natural flavor." [46]

The FDA considers labels such as "no MSG" or "no added MSG" misleading if the food has ingredients which are sources of free glutamate, such as hydrolyzed protein. In 1993, it proposed adding "contains glutamate" to the common names of certain hydrolyzed proteins with substantial amounts of glutamate. [ citation needed ]

Australia and New Zealand Edit

Standard 1.2.4 of the Australia and New Zealand Food Standards Code requires MSG to be labeled in packaged foods. The label must have the food-additive class name (e.g. "flavour enhancer"), followed by the name of the additive ("MSG") or its International Numbering System (INS) number, 621. [47]

Pakistan Edit

The Punjab Food Authority banned Ajinomoto, commonly known as Chinese salt, which contains MSG, from being used in food products in the Punjab Province of Pakistan in January 2018. [48]

Names Edit

The following are alternative names for MSG: [1] [49] [50]

  • Chemical names and identifiers
    • Monosodium glutamate or sodium glutamate
    • Sodium 2-aminopentanedioate
    • Glutamic acid, monosodium salt, monohydrate
    • L-Glutamic acid, monosodium salt, monohydrate
    • L-Monosodium glutamate monohydrate
    • Monosodium L-glutamate monohydrate
    • MSG monohydrate
    • Sodium glutamate monohydrate
    • UNII-W81N5U6R6U
    • Flavour enhancer E621
    • Accent, produced by B&G Foods Inc., Parsippany, New Jersey, US [51][52]
    • Aji-No-Moto, produced by Ajinomoto, 26 countries, head office Japan [53][54]
    • Tasting Powder
    • Ve-Tsin by Tien Chu Ve-Tsin
    • Sazón, distributed by Goya Foods, Jersey City, NJ [55]

    Controversy Edit

    Origin Edit

    A controversy surrounding the safety of MSG began on 4 April 1968, when Dr. Robert Ho Man Kwok wrote a letter to the New England Journal of Medicine, coining the term "Chinese restaurant syndrome". [56] [57] In his letter, Kwok suggested several possible causes before he nominated MSG for his symptoms. [58] [23] This letter was initially met with insider satirical responses, some using race as prop for humorous effect, within the medical community. [56] Some claimed that during the discursive uptake in media, the conversations were recontextualized as legitimate while the supposed race-based motivations of the humor were not parsed. [56]

    In January 2018, Dr. Howard Steel claimed that the letter was actually a prank submission by him under the pseudonym, Ho Man Kwok. [57] [59] However, there was a Dr. Robert Ho Man Kwok who worked at the National Biomedical Research Foundation, both names Steel claimed to have invented. [59] Kwok's children, his colleague at the research foundation, and the son of his boss there confirmed that Dr. Robert Ho Man Kwok, who had died in 2014, wrote this letter. [59] After hearing about Kwok's family, Steel's daughter Anna came to believe this claim itself was one of the last pranks by her late father. [59]

    Reactions Edit

    The controversy about MSG has been tied by some to alleged racial stereotypes about East Asians, [60] [61] [62] saying that East Asian cuisine is being targeted while the widespread use of MSG in other processed food hasn't been stigmatized. [63] These activists have claimed that the perpetuation of the negative image of MSG through the Chinese restaurant syndrome was caused by "xenophobic" or "racist" biases. [64] [65]

    In 2016, Anthony Bourdain stated in Parts Unknown that "I think MSG is good stuff . You know what causes Chinese restaurant syndrome? Racism". [66]

    In 2020, Ajinomoto, the corporation founded by the inventor of MSG and today its leading manufacturer, launched the #RedefineCRS campaign to combat what it said was the myth that MSG is harmful to people's health, saying it intended to highlight the xenophobic bias against East Asian cuisine and the scientific evidence. [67]

    In 2021, Chinese Michelin 3-star chef Kwong Wai-keung said, "I tell my chefs if you know ingredients are not good, don't use them, because they can affect the customers' health. [. ] We [at T'ang Court] use chicken powder, not MSG. If you wouldn’t eat it, then don’t serve it to the guests." [68]


    Causes of Excess Glutamate

    Brain tissue readily accumulates glutamate and normally there are safeguards to keep excess glutamate from building up to dangerous levels. (23)

    As the authors of one study explain, “neurons eat glutamate to stay alive” which usually keeps glutamate from reaching toxic levels. (24)

    Numerous protein transporter molecules can bind to glutamate and move it out of the brain. (25)

    Also, the blood-brain barrier keeps glutamate that’s circulating in the bloodstream from entering the brain.

    And finally, when all works right, excess glutamate is “supposed” to get turned into GABA.

    But, even with all these checks and balances, there are still times the glutamate system goes awry.

    Here are some of the things that can go wrong:

    GAD Autoimmunity

    Glutamic acid decarboxylase (GAD) is the enzyme used to turn glutamate into its calming counterpart, GABA.

    But it’s possible to develop an autoimmune reaction to the GAD enzyme, leading to poor conversion into GABA. (26)

    Gluten intolerance, celiac disease, Hashimoto’s disease, type 1 diabetes, and other autoimmune diseases are linked to GAD autoimmunity.

    Vitamin B6 Deficiency

    Vitamin B6 (pyridoxine) is an essential cofactor in the conversion of glutamate to GABA.

    Lack of this vitamin results in diminished GABA synthesis and a buildup of glutamate. (27)

    Other Causes of Excess Glutamate

    It’s also possible to have a genetic tendency for glutamate oversensitivity and imbalances between glutamate and GABA. (28)

    Traumatic stress can elevate glutamate to abnormally high levels. (29)

    Many mood-altering substances disrupt the glutamate-GABA balance. (30)

    Caffeine, the most widely used stimulant, increases glutamate activity at the expense of GABA.

    A brain injury or stroke causes glutamate to flood the injured area.

    This can be counterproductive, causing brain damage by overexciting damaged neurons to death. (31)


    Dietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memory

    Recent evidence suggests that intake of excessive dietary fat, particularly saturated fat and trans-hydrogenated oils (trans-fatty acids: TFA) can impair learning and memory. Central obesity, which can be induced by neonatal injections of monosodium Glutamate (MSG), also impairs learning and memory. To further clarify the effects of dietary fat and MSG, we treated C57BL/6 J mice with either a TFA-enriched diet, dietary MSG, or a combination of both and examined serum lipid profile and spatial memory compared to mice fed standard chow. Spatial learning was assessed at 6, 16 and 32 weeks of age in a Morris Water Maze (MWM). The subjects were given four days of training to find a hidden platform and a fifth day of reversal learning, in which the platform was moved to a new location.

    Results

    The TFA + MSG combination caused a central adiposity that was accompanied by impairment in locating the hidden platform in the MWM. Females in the TFA + MSG group showed a greater impairment compared to the other diet groups, and also showed elevated levels of fasting serum LDL-C and T-CHOL:HDL-C ratio, together with the lowest levels of HDL-C. Similarly, males in the TFA + MSG diet group were less successful than control mice at locating the hidden platform and had the highest level of abdominal adiposity and elevated levels of fasting serum LDL-C.

    Conclusion

    Dietary trans-fat combined with MSG increased central adiposity, promoted dyslipidemia and impaired spatial learning.


    Monosodium Glutamate, or MSG for short, is one of those food additives that appears to be very safe when in fact it’s quite dangerous. There is a great deal of confusion about MSG. Because it is not regulated, and because it can be found in many forms and called so many different names, many of which sound very healthy, it is difficult for those in the know, and impossible for the uninformed, to avoid it. Adding to the confusion, is the fact that it can be harmless in some forms, while being extremely harmful in other forms.

    In this article we will provide a comprehensive list of the names used, definitions that clarify which forms are dangerous and which are not and tips on how to avoid MSG.

    Safe Forms of MSG:

    • Unprocessed and Unbound Glutamic Acid. Monosodium Glutamate, which is unbound, or free, can be found naturally in very small amounts in foods such as cheese, ripe tomatoes, fermented soy products, and yeast extracts. For those who are allergic to MSG in it’s natural form, they must avoid these foods. For everyone else, naturally occurring MSG is not a problem.
    • Bound and Unprocessed Glutamic Acid. In addition to the small amounts of unprocessed free glutamic acid, we also have bound glutamic acid, which is not only harmless, but like most of the amino acids, a building block for muscle and many other important functions. Bound (unprocessed) glutamic acid is found in proteins in much higher concentrations than the unbound naturally occurring MSG. The bottom line is that neither the unprocessed unbound or the unprocessed bound glutamate cause adverse reactions in the vast majority of people and one is a building block for muscle.

    Unsafe L-Glutamate

    • Processed Unbound (free) Glutamic Acidaka MSG. Monosodium Glutamate becomes an excitotoxin when it is processed by converting bound glutamic acid into free glutamic acid, which is then manufactured as a food additive. In this state, it is a neurotoxin and a stimulant that is toxic and highly addictive. That is a double whammy. Now instead of a little jolt of excitement, we get a relentless firing of neurons that cause cravings, food addictions, obesity and it’s complications, inflammation, autoimmune disorders and various cancers. In this state it is referred to as L-Glutamine.

    The Dangers of Ingesting MSG

    Excitotoxins are not only dangerous, they are also difficult to detect until they have done considerable damage. Retired neurosurgeon Russell Blaylock, MD (author of Excitotoxins: The Taste That Kills) claims there is growing evidence that excitotoxins are a major cause of degenerative brain diseases in adults including Alzheimer’s, Parkinson’s, Huntington’s, ALS and MS diseases. He has also stated that once ingested (or injected) excitotoxins interact with one another and increase the toxicity of each chemical a hundred-fold. He points out that one of the most pervasive and destructive excitotoxins is Monosodium Glutamate or processed free MSG.

    The following is a simplification of how L-Glutamine causes disease:

    1. Foods containing L-Glutamine, aka MSG, are eaten and attack the body. The cells in the hypothalamus that regulate appetite are a target and are destroyed over time. They are literally stimulated to death by L-Glutamine, which is why it is referred to as an excitatory neurotoxin. It is a mechanism similar to that which takes place when we get high from any drug. The brain can be “fried” by one bad LSD trip or more slowly from repeated use of cocaine. Processed L-Glutamine, or MSG, behaves in the same way. The difference is we know when we are abusing drugs, we do not know that we are being poisoned by foods that we eat every day.

    One of the mechanisms making this possible is that L-Glutamine damages Leptin receptors. Leptin is the hormone that regulates appetite and fat storage. It is found in fat tissue. It turns out that fat is an organ, or at least it behaves like other organs, in as much as it has it’s own hormone.

    Leptin’s job is to send a message to the Hypothalamus to stop eating and stop storing fat when the body has enough fat stored. Unfortunately, L-Glutamine excites Leptin receptors to death so that the hypothalamus no longer receives these messages. This is called leptin-resistance.

    2. In the obese individual, Leptin is high, due to excess body fat, but it may not be functional because of damage from MSG. In other words, if the individual is eating foods containing L-Glutamine, (and highly palatable foods are loaded with MSG) the Leptin receptors become too damaged over time to receive the message that there is enough fat on board. When this happens, it does not send the do not eat, do not store fat message. Thus the individual feels hungry despite having eaten, and stores fat despite having an abundance of fat already on board. That’s not good, right?

    3. Glutamate also activates AMPK, which is an enzyme responsible for conserving energy. AMPK slows metabolism and reduces our need for physical activity. In the lab, it creates “lazy mice” that are fat and tend to sleep a lot. Under normal circumstances when Leptin levels rise, due to higher levels of fat storage, the production of AMPK stops, allowing us to resume burning calories and feeling energetic.

    The exception is when a food contains L-Glutamine. (Have I mentioned that almost all processed foods, even many of the organic ones, contain MSG?) The reason for this is that glutamate, which is needed for learning and the formation of short-term memories, must have access to the hypothalamus. Since the brain doesn’t differentiate between natural glutamate and L-Glutamine, it allows both to pass through the blood-brain barrier.

    That bears repeating: The hypothalamus cannot tell the difference between Glutamate, which is an amino acid, and L-Glutamine, which is a neurotoxic denatured protein in the form of MSG. Under normal circumstances, Glutamate overrides Leptin, which is what it is supposed to do. Unfortunately, so does L-Glutamine. So the brain ignores signals from Leptin to stop conserving energy by slowing our metabolism and stop storing fat. In other words, the Leptin levels are not registering, so there is nothing to stop the production of AMPK, which causes more fat storage.

    What ends up happening is:

    • Appetite stays high – so calorie intake goes up
    • Activity is depressed – so calories burned go down
    • Metabolism slows down
    • Weight goes up

    A plethora of disorders result from L-Glutamate. This is because L-Glutamine enters the bloodstream up to 10 times faster than bound glutamates. Because there are glutamate receptors in many parts of the body, including the brain, heart, lungs and pancreas, consuming large amounts of it “overwhelms” many of the body’s systems by over-stimulating receptor neurons. However, until very recently, the medical establishment seems to have missed this epidemic.

    This is likely because so many of the body’s systems are involved with conditions driven by MSG. The most common ones today are autoimmune disorders, which, when combined, are currently the third cause of death in the US, surpassing cancer and heart disease. The result is that the patient presents with a variety of symptoms, each of which is treated by a different specialist. When specialists get involved, treatment focuses upon their area of specialty, i.e. patients suffering from joint problems, like rheumatoid arthritis and lupus, see a rheumatologist and are treated with medications that focus on those symptoms, whereas those with skin issues, like psoriasis, are treated by dermatologists and usually with something topical or with a steroid, and so on. No one is tasked with looking at the cause or source of the problem, because the treatment is symptom focused, so the problem just keeps getting worse. In many cases, the treatment becomes part of the problem.

    Damaged Proteins

    In general, separating a protein or freeing it, which occurs when we heat it, results in L-Glutamine. The best, and most common example, is pasteurizing milk. Even if the cows are grass-fed, pasteurization denatures the otherwise perfect proteins, causing them to behave like L-Glutamine. This is why the raw milk movement is so popular. In Ohio, where I reside, one must buy into a herd share to obtain raw milk and dairy, but it is worth it. This is not to say that pasteurized milk is not beneficial. If you buy milk, go for the lightly pasteurized, not ultra pasteurized milk, if you cannot find or afford raw milk.

    According to the Truth in Labeling Organization When It Comes to Protein that Contain MSG: [1]

    1. Low fat and no fat milk products often contain milk solids that contain MSG and many dairy products contain carrageenan, guar gum, and/or locust bean gum, all of which are forms of MSG.
    2. Protein powders contain glutamic acid, which, invariably, will be processed free glutamic acid (MSG). Individual amino acids are not always listed on labels of protein powders.
    3. Hydrolyzed protein is the main problem. At present there is an FDA requirement to include the protein source when listing hydrolyzed protein products on labels of processed foods. Examples are hydrolyzed soy protein, hydrolyzed wheat protein, hydrolyzed pea protein, hydrolyzed whey protein, hydrolyzed corn protein. If a tomato, for example, were whole, it would be identified as a tomato. Calling an ingredient tomato protein indicates that the tomato has been hydrolyzed, at least in part, and that processed free glutamic acid (MSG) is then present.
    4. Disodium guanylate and disodium inosinate are relatively expensive food additives that work synergistically with inexpensive MSG. When you see either of them, it suggests that the product has MSG in it. They would probably not be used as food additives if there were no MSG present.
    5. MSG reactions have been reported from soaps, shampoos, hair conditioners, and cosmetics, where MSG is hidden in ingredients with names that include the words “hydrolyzed,” “amino acids,” and/or “protein.” Most sun block creams and insect repellents also contain MSG.
    6. Drinks, candy, and chewing gum are potential sources of hidden MSG.
    7. Binders and fillers for medications, nutrients, and supplements, both prescription and non-prescription, enteral feeding materials, and some fluids administered intravenously in hospitals, may contain MSG.
    8. According to the manufacturer, Varivax–Merck chicken pox vaccine (Varicella Virus Live), contains L-monosodium glutamate and hydrolyzed gelatin, both of which contain processed free glutamic acid (MSG) which causes brain lesions in young laboratory animals, and causes endocrine disturbances like OBESITY and REPRODUCTIVE disorders later in life. It would appear that most, if not all, live virus vaccines contain some ingredient(s) that contains MSG.
    9. Reactions to MSG are dose related, i.e., some people react to even very small amounts. MSG-induced reactions may occur immediately after ingestion or after as much as 48 hours. The time lapse between ingestion and reaction is typically the same each time for a particular individual who ingests an amount of MSG that exceeds his or her individual tolerance level.
    10. Remember: By food industry definition, all MSG is “naturally occurring.” “Natural” on the label doesn’t mean safe or MSG free. “Natural” only means that the ingredient started out in nature, like arsenic and hydrochloric acid, both or which are poisonous.

    Case History

    My favorite story is one in which a patient came to me extremely depressed because her fiancé had dumped her when he discovered that she had Multiple Sclerosis. Her doctor told her that she would be in a wheel-chair and disabled for the rest of her life and that the MS would continue to worsen. She was a VP at a fortune 10 company.

    During our intake it became apparent that she lived on processed foods, which are loaded with MSG, but also on artificial sweeteners that have the same impact as the MSG. Prior to working with me, this young woman rarely ate real food. She was a road warrior and ate most of her foods in airports and hotels from a bag or a can. Really terrible diet. She kept her energy up with sugar free gums that are loaded with aspartame and other dangerous sweeteners.

    I explained that if she did not want to spend the rest of her life in a wheelchair, she would have to embrace clean eating. She is the best example of a convert that I have ever treated. She is the only patient I have that may eat “cleaner” than I do. No more processed anything, everything organic, whole and no more food additives like MSG or aspartame/acesulfame.

    Within the first year, she went from the worst form of MS to the best. After 2 years, I discovered Low Dose Naltrexone and recommended that she try it and within a year of trying it, she tested negative for MS. Technically, she is not cured, but practically she is. She and her new husband (her former internist) now reside in sunny California where she can absorb Vitamin D3 as recommended. They have a two-year-old.

    This is because aspartic acid (from aspartame) and glutamic acid (from MSG) can both stimulate a receptor in the brain called the NMDA receptor (n methyl d aspartate). Chronic overstimulation of the NMDA receptor over time is neurotoxic! As Dr. Russell Blaylock explains in his book, Excitotoxins: The Taste that Kills , aspartame and MSG excite brain cells to the point that they die.

    Other Legal Mechanisms For Dosing Us With L-Glutamine (MSG)

    The manufacturers of L-Glutamine are relentless in finding ways of getting us to ingest MSG.Here are the most common methods:

    • As a By-Product – Though previous reports have disallowed MSG in foods for infants or those under one year of age, as we saw above, many infants and children still ingest MSG that is a by-product of the processing of protein, such as hydrolization or autolyzation, and therefore listed under another name such as brewers yeast or citric acid.
    • As Part Of Another Ingredient – It may also be part of an ingredient such as Sucralose, aka Splenda, which is partly L-Glutamine.
    • In Infant and Childhood Vaccinations – Many infants and children in the US also receive doses of MSG in their vaccinations, which also include MSG:
      • MMR – Measles-Mumps-Rubella
      • M-R-Vax – Measles-Rubella, Merck & Co., Inc.
      • Attenuvax – Measles, Merck & Co., Inc.
      • Biavax – Rubella, Merck & Co., Inc.
      • Prevnar Pneumococcal – 7-Valent Conjugate Vaccine, Wyeth Lederle
      • Varivax – Chickenpox, Merck & Co., Inc.
      • YF-VAX – Yellow Fever, Aventis Pasteur USA[1]

      From corn-fields to hospitals, school cafeterias, and nursing homes MSG is added to mass-produced food with no restrictions and no notice. MSG awareness activists call it nicotine for food. The problem with this analogy is that we know when we are smoking a cigarette that it contains nicotine. But how many young women today know that they are being exposed to a major toxin causing irreparable damage to their child even before they discover they are pregnant?

      1. The Slow Poisoning of Mankind. By John Erb www.TruthinLabeling.org.
      2. Lifestyle Choices…Up to YOU! Biblical and Health Guidelines for More Abundant Living. By Ginger Woods O’Shea. See “MSG Is Being Sprayed On Fruits, Veggies, Nuts, Grains And Seeds As They Are Growing…Even Those Used In Baby Food. “
      3. Prepared by the Truth in Labeling Campaign Web page: www.truthinlabeling.org

      Dr. Renae Norton specializes in the treatment of eating disorders. Located in Cincinnati, Ohio. Call 513-205-6543 to schedule an appointment or fill out our online contact form for someone to call you to discuss your concerns. Tele-therapy sessions available. Individual and family sessions also available.

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      Central nervous system

      General aspects

      In cases of an impaired blood/brain barrier (BBB) GLU from blood might cross the barrier and might cause toxic effects even at physiological plasma levels.

      As the gastrointestinal tract has a very high capacity for using GLU, dietary intake (free and bound GLU) has a minor impact on plasma levels. Only high concentrations (as bolus) (e.g. 550 μmol/l) may lead to a transient increase of plasma level. Consequently food-derived GLU (including added GLU as food additive in normal amounts of <1 g/day) does not further increase the risk for toxic effects in cases of an impairment of BBB because plasma levels do not rise.

      Does the BBB control the GLU transfer under normal conditions?

      Consensus

      As long as BBB is intact there is no risk for GLU transfer across BBB.

      Background

      The BBB restricts and regulates the flux of substrates between the circulation and the central nervous system. To cross the barrier substances must either cross the lipoid cellular membranes or be transported by selected BBB carriers. GLU is a polar solute, thus the passive influx is limited to <1% of that occurring at the blood vessels of other tissues (Smith, 2000).

      Are there conditions where this barrier function regarding GLU might be impaired?

      Consensus

      Several common brain pathologies are known to be associated with BBB disruption. There is no assured research data available whether augmented plasma levels in this situation influence synaptic GLU concentrations.

      Background

      There is evidence that a doubling of plasma GLU, for example after infusion of GLU containing parenteral nutrition augments brain edema in conditions with a lesioned BBB (Stover and Kempski, 1999). Elevated plasma GLU may also occur during anesthesia with isoflurane (Stover et al., 2004 Stover and Kempski, 2005).

      Do we have data that might promote a relationship or role of added GLU in the development of neurological degenerative diseases under in vivo conditions?

      Consensus

      At present there is no scientific data available supporting the presumption of an involvement of added GLU in the development of human neurological disease.

      Background

      GLU functions in the CNS as excitatoric transmitter. Therefore, high intracellular GLU concentrations concurrently with low extracellular concentrations have to be maintained. This will be reached on the one hand by a fast elimination of the released GLU by surrounding astrocytes and on the other hand by an active transport mechanism provided at the BBB which ensures that the spinal fluid (CSF)-GLU level is kept lower than the concentration in blood.

      In the brain, GLU binds to the NMDA-receptor and controls the intra- and extracellular (synaptic) calcium levels. In times of overactivation there is a reinforced calcium influx into the cell leading finally to apoptosis. After ischemia in definite brain sections neurons will be destroyed. Out of these damaged cells GLU will be released and the CSF GLU level will increase. Therefore, primarily not infarcted brain sections will probably also be affected.

      Basal synaptic concentrations of GLU are estimated to be in the 2–5 μmol/l range, and rise to 50–100 μmol/l following release (Daikhin and Yudkoff, 2000 Meldrum, 2000). Plasma GLU concentrations are typically 50–100 μmol/l under normal conditions (Tsai and Huang, 1999 Fernstrom et al., 1996) and do not rise significantly even in the presence of sizable oral doses of MSG (Tsai and Huang, 1999). Plasma GLU concentrations appear to rise only when pharmacologic doses of MSG are administered. Hence, if the BBB were to become permeable (for review see Ballabh et al., 2004 Neuwelt, 2004), or BBB GLU transporters were to become compromised (they normally function to transport GLU out of the brain (O'Kane et al., 1999), one might imagine that synaptic GLU concentrations could rise, which would be sufficient to stimulate GLU receptors.

      Few studies to date have searched for changes in BBB GLU transport in physiologic and pathophysiologic settings. However, a growing body of evidence addresses alterations in BBB permeability (typically to large molecules). For example, increases in BBB permeability have been reported to accompany aging (Shah and Mooradian, 1997), Alzheimers dementia (Skoog et al., 1998 Ujiie et al., 2003), type II diabetes (Starr et al., 2003), and hypertension (Mooradian, 1988 Mayhan, 1990 Ueno et al., 2004). BBB permeability also increases with increasing plasma osmolarity (Tamaki et al., 1984), and after the administration of certain drugs (Boertje et al., 1992). Presumably, increases in BBB permeability would permit increased entry of all molecules from the plasma, including molecules such as GLU. However, most studies that have specifically examined GLU transport (penetration) into the brain, deal with aging, in which GLU transport appears to be not different in adult and aged animals (Shah and Mooradian, 1997), and with hypertension, in which GLU uptake into brain may be increased (Tang et al., 1993 Al-Sarraf and Philip, 2003).

      However, there is evidence that a doubling of plasma GLU, e.g. after infusion of GLU-containing parenteral nutrition augments brain edema in conditions with a lesioned blood brain barrier (Kempski et al., 1990). In those experiments the BBB of rats was focally destroyed by a freezing lesion, and water content of the brain was measured a day later. In animals that had received a continuous infusion of GLU water content (edema) was significantly higher than in rats without GLU infusion. A doubling of plasma GLU concentrations was sufficient to cause this effect, and brain edema only worsened in those animals, which had elevated plasma GLU concentrations. GLU increases brain water content most likely as a consequence of glial GLU uptake systems, which eliminate extracellular GLU together with sodium ions and – osmotically obliged – water. The deterioration of brain edema hence was a direct consequence of homeostatic mechanisms that prevent interaction of extracellular GLU with neuronal receptor sites.

      However, several caveats should be noted: (1) The GLU transporters at the BBB appear to be on the abluminal membrane, and function to transport GLU out of the brain (O'Kane et al., 1999). These transporters presumably would still function in situations in which BBB permeability has increased (2) Glial and neuronal GLU transporters (Goldsmith, 2000 Meldrum, 2000) would also presumably remain functional under conditions of increased BBB permeability (except if the brain is ischemic, and thus oxygen deprived, such as during a stroke/vascular occlusion or under conditions of increased intracranial pressure), and help to keep brain ECF and basal synaptic GLU concentrations low and (3) Dietary GLU and MSG, even at a very high dose in the daily diet (Tsai and Huang, 1999), do not raise plasma GLU concentrations (MSG intake is self-limiting, since it is not palatable at high concentrations in foods (Yamaguchi, 1987)) hence, dietary GLU or MSG should not influence synaptic GLU concentrations, per se, if BBB permeability were to be increased.

      Are toxicological data derived from animal experiments (dose–effect-relations) directly transferable to humans?

      Consensus

      Comparative functional and metabolic studies in a variety of animals including primates and human studies provide a rational safety evaluation for human beings.

      Background

      Relevant literature has already been summarized and listed (Biesalski et al., 1997 Walker and Lupien, 2000). Briefly, the toxicologic database available for review includes acute, subchronic and chronic toxicity studies as well as studies on reproductive toxicity and teratology in rats, mice and dogs. GLU has a very low acute toxicity under normal circumstances the oral dose that is lethal to 50% of subjects (LD50) in rats and mice is 15000–18000 mg/kg bw, respectively. Subchronic and chronic toxicity studies of up to 2 years duration in mice and rats, including a reproductive phase, did not reveal any specific adverse effects at dietary levels of up to 4%. Reproduction and teratology studies using the oral route of administration have been uneventful indicating that the fetus and suckling neonate was not exposed to toxic GLU levels from the maternal diet through transplacental transfer. Based on these results from mammals authoritative organizations have affirmed the safety of added GLU at levels normally consumed by the general population.

      Large doses of dietary GLU: do they have an impact on endocrine parameters?

      Consensus

      Very high doses of GLU influence the insulin reaction induced by an unphysiologically high glucose load.

      Background

      Recently, Chevassus et al. (2002) gave 10 g MSG or placebo in capsules orally to fasted human subjects at the time they received a 75 g glucose load, and followed the plasma insulin changes over time. There was a significant positive correlation between plasma insulin area-under-the-curve and peak plasma GLU concentrations, suggesting to the authors that GLU enhanced glucose-induced insulin secretion, consistent with the existence of stimulatory GLU receptors on pancreatic beta cells (Hinoi et al., 2004). In this study, peak plasma GLU concentrations were about doubled over baseline and placebo values. Studies of similar design have also been conducted by Graham and associates, but administering MSG (or a placebo) by itself to fasting subjects with this design, significant increases in plasma insulin concentrations are clearly evident (Graham et al., 2000 Mourtzakis and Graham, 2002).

      Are there any effects of GLU on neonatal development?

      Consensus

      Even in unphysiologically high doses GLU will not trespass in fetal circulation. Therefore, orally applied GLU is not expected to influence neonatal development.

      Background

      There is a single study on this topic by Anantharaman (1979), who conducted a multi-generation study in male and female mice exposed to MSG in a standard diet (at 1 or 4%). The average daily MSG intake at the higher dose was calculated to be 6000 mg/kg/day in males and 7200 mg/kg/day in females, extremely high doses. Animals were exposed to MSG at all ages and at all stages of development. No developmental or reproductive effects were noted. No histological incidences of brain lesions or brain abnormalities were noted.

      Do babies fed with breast milk consume free GLU?

      Consensus

      Breast milk contains measurable amounts of free GLU with great individual variations. Babies, thus, consume higher amount of free GLU per kg body weight than during their later life.

      Background

      Free amino acids are constituents of the so-called nonprotein nitrogen fraction of human milk (Rudloff and Kunz, 1997 Agostoni et al., 2000). The total amount of free amino acids is around 3 mmol/l plasma with great variations (association with the nutritional behavior of the mother). GLU, glutamine and taurine are the prevalent amino acids accounting for around 50% of total free amino acids (Agostoni et al., 2000 Ramirez et al., 2001). Actual analyses of free GLU in milk samples of mothers delivered on time revealed 827±342 μmol/l for transitional milk and 868±462 μmol/l for mature milk (Meinardus et al., 2004 Jochum et al., 2006). Considering a daily feeding of 600 ml, a 4-kg-infant would ingest around 130 μmol/kg (19 mg/kg) free GLU. Moreover, the intake of bound GLU would reach ca. 1.3–1.5 g/day depending of the protein content of the milk. The role of free amino acids in breast milk is still under debate. It is, however, speculated that especially free GLU and glutamine might have a double role of protecting the intestinal growth while supplying functional substrates to the nervous tissue (Agostoni et al., 2000 Jochum et al., 2006). Consequently, the intake of free GLU in suckling babies is seen as a useful physiological support of growth and metabolic development. In addition, GLU is seen as a rapidly available nitrogen donor in growing mammals due to its central role in transamination processes.


      CONCLUSIONS

      l -Glutamate is an important biomolecule. Its roles in taste (umami) perception, intermediary metabolism, and excitatory neurotransmission have been well documented. In addition, evidence from recent studies suggests new functions for dietary l -glutamate. In particular, dietary l -glutamate is now known to stimulate l -glutamate receptors in the stomach and intestines, which produces local actions on gut function, and also, through the release of signaling molecules (nitric oxide and 5-HT), activates the afferent vagus nerve and consequently a number of areas in the brain. One current hypothesis is that this signaling cascade informs the brain of the amount of protein ingested ( 20). In the other study, the chronic intake of a palatable solution of MSG has been found to slow the development of obesity, fat deposition, and plasma leptin concentrations in growing rats, most likely through an enhancement of energy expenditure ( 22). Altogether, these findings indicate that dietary l -glutamate influences numerous physiologic functions, which suggests a broad, integrative role for dietary l -glutamate in body homeostasis. (Other articles in this supplement to the Journal include references 54– 82.)

      We thank John D. Fernstrom (University of Pittsburgh School of Medicine, Pittsburgh, PA) for his valuable comments on the manuscript.

      The authors’ responsibilities were as follows—TK: contributed to the study concept, design, and data acquisition and analysis and was responsible for the drafting of the manuscript HNM: contributed to the interpretation of the data and the critical revision of the manuscript and KT: supervised the study. The authors are employees of the Ajinomoto Company. Ajinomoto is a manufacturer of food and amino acids including glutamate.


      Watch the video: അജനമടട ഭകഷണതതൽ ചർകകമപൾ സഭവകകനനതനത? അജനമടട വലലനകനനത എപപൾ? (August 2022).