Monosodium Glutamate (MSG) is a flavor enhancer commonly used to enhance the flavor of umami, which is savory or meaty flavors. Persons with a preference for dietary protein or with repeated exposure to MSG also appear to be more receptive (taste-wise) to the addition of MSG, while MSG increases subjective rating scores of 'meatiness' of a meal.
It is thought to contribute to the obesity epidemic due to its association with obese persons, although this data has been called into question, and due to injections of MSG into newborn rats being able to induce obesity later in life due to disrupting caloric regulation.
Causes food to possess a meaty/meatier taste, associated with obese persons (causation not established) and thought to contribute to obesity due to MSG being used in a research model to induce obesity in newborn rats (via injection)
MSG appears to be one of the more potent (yet not necessarily adverse) stimulators of salivation; citric acid can outperform MSG on a weight basis but may not be consumed in as high doses. The mechanism of enhanced sensation of meat, however, may be due to MSG acting on similar receptors as some peptides (which are components of meat) suggesting the mGlu4a receptor may induce the sense of umami.
It may raise plasma glutamate levels, and in adult men consuming 75mg/kg and 150mg/kg this has been recorded to be elevated by 375% or 556%, respectively. Another study using 150mg/kg bodyweight MSG noted increased plasma glutamate measured at 18-fold when ingested and compared to resting subjects, but this difference was attenuated during exercise; exercise normally increases glutamate (in this study, to 470+/-52uM) while the increase seen in MSG combined with exercise was 630+/-63uM (134% of placebo). MSG also appeared to increase circulating levels of Taurine, alanine, and aspartate which paralleled the circulating levels of glutamate, and a slow but steady increase in Glutamine thought to be from conversion from glutamate.
May stimulate glutamate receptors where MSG reaches (such as the tongue) and may also increase circulating glutamate levels after oral ingestion, although other amino acids are increased
A few blinded interventions have been conducted with MSG. It should be noted that blinding is both desired due to the social perception of MSG being 'bad', yet difficult due to the unique sensory properties of MSG; many studies attempt to mimic the taste of MSG with NaCl or inosine monophosphate-5, another umami flavoring.
As pertaining to issues with body weight, MSG (1.2g) appears to reduce appetite and hunger for up to 210 minutes after consumption when added to chicken broth (double-blind study) yet did not reduce subsequent food intake; did not increase either. This study also noted that the addition of added fats was successful in reducing subsequent food intake, but conferred added calories. Another study in 22 persons pairing MSG with a high protein meal also noted that the addition of MSG did not further suppress appetite or measured biomarkers (insulin, GLP-1) any more than the high protein meal itself, but increased food intake slightly (0.64+/-0.2 MJ, which is 152.8 calories).
Other studies measuring food intake as a secondary outcome may also note increased food intake associated with MSG, even when blinded. However, these are countered with other studies failing to note increases in energy intake overall.
At least one study looking at food preferences noted a shift towards starch products, and less yogurt and lemon juice; suggesting food availability may play a role.
Does not appear to significantly influence appetite or hunger in any way, but it has been reported to increase food intake when blinded although this is inconsistent. Neither the possibility of nutrient partitioning (eating more starches) or the possibility of making food more delicious cannot be refuted at this time due to lack of evidence
Limited studies are conducted on MSG for a prolonged period of time, but this study over 16 weeks in a nursing home (where food intake is easily measured) noted that the addition of 300mg MSG daily was not associated with an increase in food intake or weight at the end of the study.
In regards to headaches, a study with 14 health men consuming 75mg/kg or 150mg/kg bodyweight MSG that was blinded was able to find a significant increase in headache frequency in the MSG group, which may have been due to the increase in systolic blood pressure observed (diastolic and heart rate unaffected) during 2 hours after consumption or the increase in plasma glutamate. Although no men reported headaches when they consumed the drink laced with salt (NaCl), four reported headaches at 75mg/kg (the lower dose) and and only one at 150mg/kg. On a subjective scale of 1-10, the headaches were rated 1, 1, 4, and 4 for the lower dose and 3.5 for the higher dose. A later study (with a larger sample of 130) noted that there was indeed an association (of 'general symptoms' of which headache/cerebral blood pressure was a major one) that held when blinded, where people who self-reported as being sensitive to MSG were more likely to report side effects with 5g of MSG relative to placebo and these results have been replicated elsewhere. The former study did note, however, that there was inconsistency with repeated trials, and no significant side-effects were seen. The symptoms reported appear to be related mostly to fatigue, muscle tightness or cramping, and headaches.
Limited evidence exists, but it supports the existence of the 'MSG symptom complex' (also known as the Chinese Restaurant Syndrome) and supports the association between people who self-report sensitivity to MSG and actually experiencing the effects
One study that induced intestinal lesions in rats with the use NSAID drug overdose noted that giving the rats MSG in their food supply (at 5%) after the lesion was induced prevented the NSAID drug from impairing recovery rate. These protective effects have been replicated in vitro (outside of a living body) and an improved intestinal defense against acids (from inducing secretion of sodium bicarbonate) was noted.
The currently hypothesized mechanism is that MSG is negating the enterobacterium invasion that precedes NSAID-induced ulcers and lesions, thus hindering the pro-inflammatory actions of the bacteria to almost the level of control.
Moderate to high doses may exert protective effects against NSAID-induced intestinal damage
The MSG-Obese rat model (sometimes also called glutamate-obese) is an animal model where neonatal mice or rats are injected with MSG into their brains. This technique damages monoamine metabolism in the brain acutely which prolongs until the adult life and may cause increased food intake in rats. Even independent of food intake, impairment to the thyroid gland and its hormones also occur in adult rats to a small degree and impair growth hormone fluctuations as well. These effects are due to injections of MSG into the brain inducing a excitotoxic reaction, and destroying the ventromedial nucleus and arcuate nucleus in the hypothalamus and permanent hormonal and nerve damage.
This is a rat model mainly used to study obesity as it pertains to catecholamines (dopamine, adrenaline) or deficiencies in other monoamines (serotonin); deficiencies of which are sometimes seen in humans who are obese.
There is no evidence currently that oral administration of MSG can induce these effects in adult animals, despite the reliability of intracerebral injections to neonatal rats in doing so.
Injecting MSG is unsafe. Especially when injected directly into the brain.
While it would be incorrect to state MSG as being proven safe, it would be equally incorrect to state that MSG is unsafe. Provided you do not feel any side-effects, MSG consumption is likely safe for you.
(Common phrases used by users for this page include msg obesity induced mice, monosodium glutamate and thyroid, how does monosodium glutamate affect obesity mechanism, glutamate site:examine.com, articles related to msg and rat liver, 2)