1. Monosodium Glutamate in the Diet Does Not Raise Brain Glutamate Concentrations or Disrupt Brain Functions
John D Fernstrom Ann Nutr Metab. 2018;73 Suppl 5:43-52. doi: 10.1159/000494782. Epub 2018 Dec 3.
The non-essential amino acid glutamate participates in numerous metabolic pathways in the body. It also performs important physiologic functions, which include a sensory role as one of the basic tastes (as monosodium glutamate [MSG]), and a role in neuronal function as the dominant excitatory neurotransmitter in the central nervous system. Its pleasant taste (as MSG) has led to its inclusion as a flavoring agent in foods for centuries. Glutamate's neurotransmitter role was discovered only in the last 60 years. Its inclusion in foods has necessitated its safety evaluation, which has raised concerns about its transfer into the blood ultimately increasing brain glutamate levels, thereby causing functional disruptions because it is a neurotransmitter. This concern, originally raised almost 50 years ago, has led to an extensive series of scientific studies to examine this issue, conducted primarily in rodents, non-human primates, and humans. The key findings have been that (a) the ingestion of MSG in the diet does not produce appreciable increases in glutamate concentrations in blood, except when given experimentally in amounts vastly in excess of normal intake levels; and (b) the blood-brain barrier effectively restricts the passage of glutamate from the blood into the brain, such that brain glutamate levels only rise when blood glutamate concentrations are raised experimentally via non-physiologic means. These and related discoveries explain why the ingestion of MSG in the diet does not lead to an increase in brain glutamate concentrations, and thus does not produce functional disruptions in brain. This article briefly summarizes key experimental findings that evaluate whether MSG in the diet poses a threat to brain function.
2. Patho-physiological and toxicological aspects of monosodium glutamate
Subhankari Prasad Chakraborty Toxicol Mech Methods. 2019 Jul;29(6):389-396. doi: 10.1080/15376516.2018.1528649. Epub 2019 May 6.
Nowadays, the life-line of urban population has been formed by commercial foods due to industrialization, urbanization, and rapid increase in working class. Commercial foods are time and energy saving foods but it compromising the nutritional value of foods. The term adulteration refers to the deliberate addition of compound which is usually not present in food. These compounds are known as food additives or food adulterant. Monosodium Glutamate (MSG) is one of the most common food additives. Several studies revealed that MSG has toxic effect on fetal development/fetus, children's, adolescent, and adults. Physiological complication associated with MSG toxicity are hypertension, obesity, gastrointestinal tract troubles, and impairment of function of brain, nervous system, reproductive, and endocrine system. The effect of MSG depends upon its dose, route of administration and exposure time. Public awareness may play a major role in controlling the food adulteration by working in collaboration with National testing facilities to scrutinize each commercial food article from time to time. The aim of this review article is to highlight the deleterious impact of MSG on human health.
3. Does monosodium glutamate really cause headache? : a systematic review of human studies
Yoko Obayashi, Yoichi Nagamura J Headache Pain. 2016;17:54. doi: 10.1186/s10194-016-0639-4. Epub 2016 May 17.
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.