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The Sugar Trehalose is a Healthful Replacement for MSG

Comments by J. C. Spencer

A small amount of the sugar trehalose can be used to enhance the flavor of foods in a healthful way. MSG is widely used to make foods more flavorful but MSG has serious side effects including possible inflammation, obesity, diabetes, autoimmune diseases and liver disease. MSG can induce neuronal death. MSG may have contributed more damage to neurodegenerative diseases than we previously thought. But now, a pinch of trehalose is not only a fabulous replacement for MSG but appears to be one of the best brain foods available.

Here are three Abstracts from recently published papers on monosodium glutamate (MSG).

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Int J Dev Neurosci. 2008 Aug;26(5):487-95. Epub 2008 Mar 4.

Role of p38 MAPK and pro-inflammatory cytokines expression in glutamate-induced neuronal death of neonatal rats.
Chaparro-Huerta V, Flores-Soto ME, Gudiño-Cabrera G, Rivera-Cervantes MC, Bitzer-Quintero OK, Beas-Zárate C.

Laboratorio de Neurobiología Molecular, División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Guadalajara, Mexico.

Pro-inflammatory cytokines TNF-alpha, IL-1beta and IL-6 rises significantly during neuronal damage and activate the signaling p38 MAPK pathway, which is involved in the apoptotic (AP) neuronal death. Systemic administration of glutamate as monosodium salt (MSG) to newborn animals induces neuronal death, however whether neurons die by AP or necrosis through MAPK p38 pathway activation it is unknown. In this study, TNF-alpha, IL-1beta and IL-6 expression levels, AP neuronal death and cellular type that produces TNF-alpha was also identified in the cerebral cortex (CC) and striatum (St) of rats at 8, 10, and 14 days of age after neonatal exposure to MSG. TNF-alpha production and AP neuronal death was significantly increased in the CC at PD8-10, and in the St in all ages studied by excitotoxicity effect induced with MSG. This effect was completely inhibited by SB203580 (p38 inhibitor) in both regions studied. TNF-alpha, IL-1beta and IL-6 RNAm increased after MSG administration, whereas SB203580 did not modify their expression. These data indicates that neuronal death induced by excitotoxicity appears to be mediated through p38 signaling pathway activated by TNF-alpha and their inhibition may have an important neuroprotective role as part of anti-inflammatory therapeutic strategy.

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Indian J Physiol Pharmacol. 2007 Jul-Sep;51(3):216-34.

Understanding safety of glutamate in food and brain.
Mallick HN.

Department of Physiology, All India Institute of Medical Sciences, New Delhi.

Glutamate is ubiquitous in nature and is present in all living organisms. It is the principal excitatory neurotransmitter in central nervous system. Glutamate is being used as food additive for enhancing flavour for over last 1200 years imparting a unique taste known as "umami" in Japanese. It is being marketed for about last 100 years. The taste of umami is now recognized as the fifth basic taste. Many of the foods used in cooking for enhancing flavour contain high amount of glutamate. Breast milk has the highest concentration of glutamate amongst all amino acids. Glutamate in high doses as gavage or parenteral injection have been reported to produce neurodegeneration in infant rodents. The neurodegeneration was not produced when gluamate was given with food. The Joint FAO/WHO Expert Committee on Food Additives, based on enumerable scientific evidence, has declared that, "glutamate as an additive in food" is not an health hazard to human being. Glutamate is used as signaling molecule not only in neuronal but also in non-neuronal tissues. Excessive accumulation of glutamate in the synaptic cleft has been associated with excitotoxicty and glutamate is implicated in number of neurological disorders. Excessive accumulation could be attributed to increase release, failure of transport system for uptake mechanism, neuronal injury due to hypoxia-ischemia, trauma and associated metabolic failures. The role blood brain barrier, vesicular glutamate and sodium dependent excitatory amino acid transporters in glutamate homeostasis are emphasized in the review.

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J Autoimmun. 2008 Feb-Mar;30(1-2):42-50.

Monosodium glutamate (MSG): a villain and promoter of liver inflammation and dysplasia.
Nakanishi Y, Tsuneyama K, Fujimoto M, Salunga TL, Nomoto K, An JL, Takano Y, Iizuka S, Nagata M, Suzuki W, Shimada T, Aburada M, Nakano M, Selmi C, Gershwin ME.
Department of Diagnostic Pathology, Graduate School of Medicine and
Pharmaceutical Sciences, University of Toyama, Toyama, Japan.

Chronic inflammation is a common theme in a variety of disease pathways, including autoimmune diseases. The pathways of chronic inflammation are well illustrated by nonalcoholic steatohepatitis (NASH), which is of a serious concern due to its increasing prevalence in the westernized world and its direct correlation with lifestyle factors, particularly diet. Importantly, NASH may ultimately lead to the development of hepatocellular carcinoma. We previously reported that injection of monosodium glutamate (MSG) in ICR mice leads to the development of significant inflammation, central obesity, and type 2 diabetes. To directly address the long-term consequences of MSG on inflammation, we have performed serial analysis of MSG-injected mice and focused in particular on liver pathology. By 6 and 12 months of age, all MSG-treated mice developed NAFLD and NASH-like histology, respectively. In particular, the murine steatohepatitis at 12 months was virtually undistinguishable from human NASH. Further, dysplastic nodular lesions were detected in some cases within the fibrotic liver parenchyma. We submit that MSG treatment of mice induces obesity and diabetes with steatosis and steatohepatitis resembling human NAFLD and NASH with pre-neoplastic lesions. These results take on considerable significance in light of the widespread usage of dietary MSG and we suggest that MSG should have its safety profile re-examined and be potentially withdrawn from the food chain.

Last Updated ( Oct 25, 2008 at 03:12 PM )