- Glutamate receptors, neurotoxicity and neurodegeneration, Lau & Tymianski 2010.
full text ||| Get password>
* excitotoxicity, MSG, Lau, Tymianski." Glutamate excitotoxicity is a hypothesis that states excessive glutamate causes neuronal dysfunction and degeneration. . . Despite the continued research into the mechanisms of excitotoxicity, there are currently no pharmacological interventions capable of providing significant neuroprotection in the clinical setting of brain ischaemia or injury. This review addresses the current state of excitotoxic research, focusing on the structure and physiology of glutamate receptors; molecular mechanisms underlying excitotoxic cell death pathways and their interactions with each other; the evidence for glutamate excitotoxicity in acute neurologic diseases; laboratory and clinical attempts at modulating excitotoxicity; and emerging targets for excitotoxicity research. "
- Possible pathomechanism of autoimmune hepatitis (AI-H). Prandota J, Am J Ther. 2003 Jan-Feb;10(1):51-7." . . . In addition, some food additives, such as monosodium glutamate (MSG) and/or aspartame regularly consumed in excessive amounts, may eventually disturb the delicate balance between a positively charged amino acid residue at position DRbeta71 (lysine or arginine) and a negatively charged amino acid residue at position P4 on the antigenic peptide (glutamic acid or aspartic acid). This may favor formation of a salt bridge between these amino acid residues . . . MSG and aspartate may also depress serum concentrations of growth hormone, which downregulate the activity of several cytochrome P-450 hepatic and other drug-metabolizing enzymes, thus increasing sensitivity to some environmental agents and possibly influencing efficacy of treatment regimens and final outcome of patients with type 1 AI-H. "
- A high dietary intake of sodium glutamate as flavoring (ajinomoto) causes gross changes in retinal morphology and function. Ohguro H et al., Exp Eye Res. 2002 Sep;75(3):307-15." . . .Significant accumulation of glutamate in vitreous was observed in rats following addition of sodium glutamate to the diet as compared to levels with a regular diet. In the retinal morphology, thickness of retinal neuronal layers was remarkably thinner in rats fed on sodium glutamate diets than in those on a regular diet. . . The present study suggests that a diet with excess sodium glutamate over a period of several years may increase glutamate concentrations in vitreous and may cause retinal cell destruction. "
Note: There were two groups who received MSG. One received a "moderate excess" and the other received a "large excess" of MSG in their diet. Both these diets showed retinal cell destruction.
- Effects of oral monosodium (L)-glutamate on insulin secretion and glucose tolerance in healthy volunteers.Chevassus H, et al, Br J Clin Pharmacol. 2002 Jun;53(6):641-3." . . . Oral (L)-glutamate enhances glucose-induced insulin secretion in healthy volunteers in a concentration-dependent manner. "
- Locomotor and learning deficits in adult rats exposed to monosodium-L-glutamate during early life. Ali MM, Bawari M, Misra UK, Babu GN., Neurosci Lett. 2000 Apr 21;284(1-2):57-60." . . . The results indicate that exposure to MSG in early life in rats could lead to subtle behavioral aberrations in late adulthood. "
- Why do some dietary migraine patients claim they get headaches from placebos? Strong FC 3rd. Clin Exp Allergy. 2000 May;30(5):739-43." . . . Quantities giving moderate headaches were: 1 gelatin capsule, 400 mg MSG, 118 mg PHVP, 4.0 mg aspartame . . . Capsules may give headaches to dietary migraine patients that are similar to those from foods. This would explain some of the headaches of patients from placebos. . . "
- The monosodium glutamate symptom complex: assessment in a double-blind, placebo-controlled, randomized study. Yang WH, Drouin MA, Herbert M, Mao Y, Karsh J., J Allergy Clin Immunol. 1997 Jun;99(6 Pt 1):757-62" . . . We conducted oral challenge studies in self-identified MSG-sensitive subjects to determine whether they had a statistically significant difference in the incidence of their specific symptoms after ingestion of MSG compared with placebo. . . . Total and average severity of symptoms after ingestion of MSG (374 and 80) were greater than respective values after placebo ingestion . . . Rechallenge revealed an apparent threshold dose for reactivity of 2.5 gm MSG. Headache (p < 0.023), muscle tightness (p < 0.004), numbness/tingling (p < 0.007), general weakness (p < 0.040), and flushing (p < 0.016) occurred more frequently after MSG than placebo ingestion. . . . "
- Chronobiological variations in the convulsive effect of monosodium L-glutamate when administered to adult rats, Feria-Velasco A, Feria-Cuevas Y, Gutierrez-Padilla R, Arch Med Res 1995;26 Spec No:S127-32" Monosodium L-glutamate (MSG) when administered intraperitoneally (i.p.) to rodents induces convulsions and has been used as a model . . .The aim of this work was to learn whether the convulsive effect of MSG in rats would vary when the drug is given at different times of the day. . . .. . . Nearly 70% of animals injected at 07:00 h died in status epilepticus, [seizure] whereas no deaths were recorded in animals injected at 15:00 and 23:00 h. Results could be explained in terms of variations of physiological processes . . . related to circadian rhythms."
- Monosodium L-glutamate: a double-blind study and review. Tarasoff L, Kelly MF. Food Chem Toxicol. 1993 Dec;31(12):1019-35." 71 healthy subjects were treated with placebos and monosodium L-glutamate (MSG) doses of 1.5, 3.0 and 3.15 g/person, . . . The present study led to the conclusion that 'Chinese Restaurant Syndrome' is an anecdote applied to a variety of postprandial (following a meal) illnesses; rigorous and realistic scientific evidence linking the syndrome to MSG could not be found. "
- Neonatal exposure to monosodium glutamate alters the neurobehavioral performance of adult rats. Squibb RE, Tilson HA, Meyer OA, Lamartiniere CA, Neurotoxicology 1981 Nov;2(3):471-84"... body weights of MSG exposed males were less than the 13% exposed isosmotic controls. MSG exposed females, however, appeared to be obese compared to their controls at 102 days and exhibited a 50% incidence of tail-automutilation. ...results indicate that postnatal exposure to MSG produced measurable, long-term behavioral and somatic alterations in female and, to a lesser degree, male rats."
- Monosodium glutamate exposure in the neonate alters hypothalamic and pituitary neuropeptide levels in the adult. Hong JS, Lowe C, Squibb RE, Lamartiniere CA, Regul Pept. 1981 Nov;2(6):347-52." Administration of monosodium glutamate (MSG) during the neonatal period in rats produced differential effects on the contents of various neuropeptides in the hypothalamus: . . .MSG treatment reduced the pituitary content of beta-ELI and abolished the sex difference in beta-ELI level seen in the control rats. . . . "