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추냥 성분 탐정단 The Ingredient Files 한국어English

Monosodium glutamate (MSG)

CautionHow grades are decided

This is the additive you meet most often on labels. Everything from the old 'Chinese restaurant syndrome' story to claims of liver and nerve damage has been attached to it, and most of that came from high-dose animal work far removed from what people actually eat, or from trials that were not properly blinded. Headache showed no difference when it was given with food, and a Cochrane review found no basis for avoiding it in asthma. One point, however, does not end in reassurance. In its 2017 re-evaluation the European Food Safety Authority set an acceptable daily intake for this group for the first time, at 30 mg/kg, and noted that actual intake in some population groups exceeds not only that figure but also doses at which adverse effects were seen in people. So this is the kind of additive where the amount, not the substance, is the issue.

Claimed harm

Intake above the acceptable daily intake in some population groups
B / Moderate
At high intake (Population groups with high intake)
In 2017 the EFSA Panel on Food Additives and Nutrient Sources re-evaluated glutamic acid and glutamates (E 620-625). No adverse effects were seen in the short-term, subchronic, chronic, reproductive, and developmental studies, and the panel saw no genotoxicity concern. From a neurodevelopmental toxicity study it identified a no observed adverse effect level of 3,200 mg/kg and, applying the default uncertainty factor of 100, derived a group acceptable daily intake of 30 mg/kg expressed as glutamic acid. Effects in humans were identified but the human data lacked dose-response information and so could not be used to derive the guidance value. The panel then noted that exposure in some population groups exceeds not only that intake figure but also doses at which adverse effects were seen in people. Here the exposure level, not any intrinsic toxicity, is what decides the assessment.

PMID: 32625571

Causing headache
C / Minimal
General population
The International Classification of Headache Disorders lists this substance as a cause of headache, yet no literature had comprehensively reviewed that causal relationship, so this study systematically collected human trials. Among five papers covering six studies where it was given with food, none showed a significant difference in headache incidence except the female group in one study. Among five papers covering seven studies where it was given without food, four showed a difference, but many administered it in solution above 2%, a concentration at which its distinctive taste is readily identified. The authors concluded that because the blinding was inadequate and the findings inconsistent, further studies are required to judge whether a causal relationship exists. The key point is that the signal disappears under conditions closer to an actual meal.

PMID: 27189588

Worsening asthma
C / None
Specific group (Adults with chronic asthma)
This Cochrane review examined whether ingesting the substance provokes an asthma response in adults and children with chronic asthma. Searching through May 2012, only two cross-over studies in 24 adults met the eligibility criteria. Challenge doses were 1 g, 5 g, and 25 mg per kg, and there was no statistically significant difference from placebo in the number of subjects whose forced expiratory volume in one second fell by more than 15% or 200 mL. There were also no differences in symptom scores, non-specific bronchial hyper-responsiveness, or blood eosinophil cationic protein and tryptase. The authors stated there is no evidence supporting avoidance in adults with chronic asthma, while making clear that the limited data cannot provide a reliable basis for deciding whether avoidance is worthwhile. They found no studies at all in children.

PMID: 22696342

Liver, nerve, and metabolic damage (claims based on high-dose animal work)
D / None
General population
This review surveyed the long-term safety questions raised about the substance, separating preclinical studies from clinical trials. Preclinical work reported cardiotoxicity, hepatotoxicity, neurotoxicity, low-grade inflammation, metabolic disarray, premalignant alterations, and behavioral changes, along with links to tumorigenesis, increased oxidative stress, apoptosis in thymocytes, and genotoxic effects in lymphocytes. On re-reading that literature, however, the authors found several methodological flaws and concluded that the data have limited relevance for extrapolation to dietary human intake. They closed by stating that many of the reported negative health effects have little relevance for chronic human exposure and are poorly informative because they rest on excessive dosing that does not match levels normally consumed in food.

PMID: 31920467

'Chinese restaurant syndrome' hypersensitivity
D / None
General population
This is the most famous story attached to the substance. The same review examined reports of hypersensitivity, links to increased pain sensitivity, and links to atopic dermatitis, and judged that all three had little supporting evidence. The authors added that further clinical and epidemiological studies with an appropriate design are needed, accounting for both added and naturally occurring dietary amounts. Weak evidence does not mean nothing ever happens, but there is still no body of data matching the strength of the popular story.

PMID: 31920467

Acceptable Daily Intake (ADI): 30 mg/kg 체중/일 (글루탐산으로 환산, E 620-625 그룹 ADI)

Set for the first time in EFSA's 2017 re-evaluation, by applying an uncertainty factor of 100 to the no observed adverse effect level of 3,200 mg/kg from a neurodevelopmental toxicity study. Before that there was no numerical limit.

Journal quotations are checked character by character against the original. Quotations from Korean MFDS documents are outside that automated check and were verified by hand.

Sources

Each source shows its one-line summary and key summary up front. Expand the collapsed section to read the original abstract. Every citation is verified by re-resolving through the API.

PMID 32625571 Re-evaluation of glutamic acid (E 620), sodium glutamate (E 621), potassium glutamate (E 622), calcium glutamate (E 623), ammonium glutamate (E 624) and magnesium glutamate (E 625) as food additives Agency re-evaluation opinion · EFSA Journal, 2017 Group ADI of 30 mg/kg newly derived (NOAEL 3,200 mg/kg with a factor of 100). Exposure in some population groups exceeds both the ADI and doses linked to adverse effects.

Key summary

Show original abstract
The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re-evaluating the safety of glutamic acid-glutamates (E 620-625) when used as food additives. Glutamate is absorbed in the intestine and it is presystemically metabolised in the gut wall. No adverse effects were observed in the available short-term, subchronic, chronic, reproductive and developmental studies. The only effect observed was increased kidney weight and increased spleen weight; however, the increase in organ weight was not accompanied by adverse histopathological findings and, therefore, the increase in organ weight was not considered as an adverse effect. The Panel considered that glutamic acid-glutamates (E 620-625) did not raise concern with regards to genotoxicity. From a neurodevelopmental toxicity study, a no observed adverse effect level (NOAEL) of 3,200 mg monosodium glutamate/kg body weight (bw) per day could be identified. The Panel assessed the suitability of human data to be used for the derivation of a health-based guidance value. Although effects on humans were identified human data were not suitable due to the lack of dose-response data from which a dose without effect could be identified. Based on the NOAEL of 3,200 mg monosodium glutamate/kg bw per day from the neurodevelopmental toxicity study and applying the default uncertainty factor of 100, the Panel derived a group acceptable daily intake (ADI) of 30 mg/kg bw per day, expressed as glutamic acid, for glutamic acid and glutamates (E 620-625). The Panel noted that the exposure to glutamic acid and glutamates (E 620-625) exceeded not only the proposed ADI, but also doses associated with adverse effects in humans for some population groups. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.
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PMID 27189588 Does monosodium glutamate really cause headache? : a systematic review of human studies Systematic review · J Headache Pain, 2016 Essentially no difference across six studies giving it with food. The without-food studies used concentrations high enough to break blinding.

Key summary

Show original abstract
Although monosodium glutamate (MSG) is classified as a causative substance of headache in the International Classification of Headache Disorders 3rd edition (ICHD-III beta), there is no literature in which causal relationship between MSG and headache was comprehensively reviewed. We performed systematic review of human studies which include the incidence of headache after an oral administration of MSG. An analysis was made by separating the human studies with MSG administration with or without food, because of the significant difference of kinetics of glutamate between those conditions (Am J Clin Nutr 37:194-200, 1983; J Nutr 130:1002S-1004S, 2000) and there are some papers which report the difference of the manifestation of symptoms after MSG ingestion with or without food (Food Chem Toxicol 31:1019-1035, 1993; J Nutr 125:2891S-2906S, 1995). Of five papers including six studies with food, none showed a significant difference in the incidence of headache except for the female group in one study. Of five papers including seven studies without food, four studies showed a significant difference. Many of the studies involved administration of MSG in solution at high concentrations (>2 %). Since the distinctive MSG is readily identified at such concentrations, these studies were thought not to be properly blinded. Because of the absence of proper blinding, and the inconsistency of the findings, we conclude that further studies are required to evaluate whether or not a causal relationship exists between MSG ingestion and headache. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.
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PMID 22696342 Monosodium glutamate avoidance for chronic asthma in adults and children Cochrane review · Cochrane Database Syst Rev, 2012 Only two cross-over studies in 24 adults qualified. No difference from placeboAn inert dummy treatment used as the comparison baseline.. No studies in children at all.

Key summary

Show original abstract
BACKGROUND: Monosodium glutamate (MSG) is the sodium salt of the non-essential amino acid, glutamic acid, and is used as a flavour enhancer. It has been implicated in causing adverse reactions, which have been referred to as "Chinese restaurant syndrome". Over the last two decades there have been a number of studies investigating whether MSG ingestion induces an asthmatic response, and several reviews have been published (ILSI 1991; Stevenson 2000; Woods 2001), but no meta-analysis or Cochrane systematic review has been performed. OBJECTIVES: The objectives of this review are to: 1) identify randomised controlled trials (RCTs) of MSG ingestion and asthma response in adults and children older than two years of age with asthma; 2) assess the methodological quality of these trials; and 3) determine the effect of MSG ingestion on asthma outcomes. SEARCH METHODS: We searched the Cochrane Airways group's Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), and bibliographies of existing trials. Searches were current up to May 2012. SELECTION CRITERIA: We included RCTs that investigated the effect of MSG on chronic asthma in adults and children. DATA COLLECTION AND ANALYSIS: Two authors independently extracted, entered and analysed data from included studies. We contacted study authors for additional information. MAIN RESULTS: Only two cross-over studies involving 24 adults met the eligibility criteria; the challenge dosages of MSG were 1 g, 5 g and 25 mg/kg. They reported the number of subjects who had a maximum fall in forced expiratory volume in the first second (FEV(1)) greater than 15% or 200 mL after MSG or the control challenge. The pooled data found no statistically significant difference between MSG and placebo. One trial reported the mean change at four hours and maximum fall in FEV(1) over four hours after MSG or the placebo challenge, but found no statistically significant difference between interventions. There were no differences in symptom scores, non-specific bronchial hyper-responsiveness (BHR), eosinophil cationic protein (ECP) or tryptase levels in peripheral blood between MSG and control, although we were unable to perform meta-analyses. AUTHORS' CONCLUSIONS: The limited evidence available (n = 24) found no significant difference between MSG or the control challenge for the number of subjects who had a maximum fall in FEV(1) greater than 15% or 200 mL. There is no evidence to support the avoidance of MSG in adults with chronic asthma, but as data were limited, this review cannot provide a reliable evidence base for determining whether MSG avoidance is a worthwhile strategy. We could not find any studies conducted on the effect of MSG in children with chronic asthma. There is therefore, a need for further RCTs to investigate any relationship between MSG and asthma, especially in children. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.
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PMID 31920467 A review of the alleged health hazards of monosodium glutamate Review · Compr Rev Food Sci Food Saf, 2019 Many preclinical toxicity reports carry methodological flaws and excessive dosing, making extrapolation to human dietary intake unsound.

Key summary

Show original abstract
Monosodium glutamate (MSG) is an umami substance widely used as flavor enhancer. Although it is generally recognized as being safe by food safety regulatory agencies, several studies have questioned its long-term safety. The purpose of this review was to survey the available literature on preclinical studies and clinical trials regarding the alleged adverse effects of MSG. Here, we aim to provide a comprehensive overview of the reported possible risks that may potentially arise following chronic exposure. Furthermore, we intend to critically evaluate the relevance of this data for dietary human intake. Preclinical studies have associated MSG administration with cardiotoxicity, hepatotoxicity, neurotoxicity, low-grade inflammation, metabolic disarray and premalignant alterations, along with behavioral changes. Moreover, links between MSG consumption and tumorigenesis, increased oxidative stress and apoptosis in thymocytes, as well as genotoxic effects in lymphocytes have been reported. However, in reviewing the available literature, we detected several methodological flaws, which led us to conclude that these studies have limited relevance for extrapolation to dietary human intakes of MSG risk exposure. Clinical trials have focused mainly on the effects of MSG on food intake and energy expenditure. Besides its well-known impact on food palatability, MSG enhances salivary secretion and interferes with carbohydrate metabolism, while the impact on satiety and post-meal recovery of hunger varied in relation to meal composition. Reports on MSG hypersensitivity, also known as 'Chinese restaurant syndrome', or links of its use to increased pain sensitivity and atopic dermatitis were found to have little supporting evidence. Based on the available literature, we conclude that further clinical and epidemiological studies are needed, with an appropriate design, accounting for both added and naturally occurring dietary MSG. Critical analysis of existing literature, establishes that many of the reported negative health effects of MSG have little relevance for chronic human exposure and are poorly informative as they are based on excessive dosing that does not meet with levels normally consumed in food products. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.
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Revision history

The full history of when and how this ingredient's evidence changed (git commits = proof of trust).