MSG and neurodegenerative disease
There is a relatively new area of research for which the food industry, to date, has had no comment, contradiction or excuse. These are studies which link MSG to neurodegenerative disease.
Discovery that MSG caused lesions in specific areas of the brains of laboratory animals and concomitant proliferation of neuroendocrine dysfunction came through interest in the brain. It was brain research that identified glutamic acid as a possible, probable, and now certain neurotransmitter, transmitting nerve impulses. Likewise, it was study of the brain that suggested that a group of these neurotransmitters, specifically the excitatory amino acids (EAA), possess properties that very likely play an important role in the development of certain neurodegenerative diseases(172, 229-236). Glutamic acid and aspartic acid are among the EAA that have great potential for involvement in neuro-degenerative disease.
At the present time, significant headway in the study of neurodegenerative disease is being made. "Three EAA receptor subtypes that mediate excitotoxicity have been identified, drugs with anti-excitotoxic actions have been discovered, and evidence for the complicity of both exogenous and endogenous excitotoxins in neurodegenerative disorders has begun to unfold. There now is substantial evidence for the involvement of each EAA receptor subtype in one or more human neurodegenerative syndrome, and recent findings suggest that EAA receptors are sensitive mediators of excitotoxicity at both ends of the age spectrum."(231)
All forms of MSG are exogenous sources of glutamic acid, i.e., coming from outside of the body. There are over 40 ingredients that contain MSG without giving consumers a clue to its presence. In addition, MSG can be produced when protease enzymes or reaction flavors are used in the manufacture of processed food. Processed free glutamic acid (MSG) always contains free glutamic acid, an EAA.
It has been suggested, and there is evidence to support the suggestion, that the EAA might well play a role in the following neurodegenerative conditions: sulfite oxidase deficiency; epileptic, hypoglycemic and hypoxic/ischemic brain damage; central nervous system trauma; dementia pugilistica; domoate dementia; olivopontocerebellar degeneration; neurolathyrism; amyotrophic lateral sclerosis, parkinsonism, Alzheimer's dementia; Huntington's disease; and Wernicke/Korsakoff syndrome(231). These conditions are referred to as part of the glutamate cascade.
The following excerpt from the March 15, 2004 American Family Physician illustrates the relationship between glutamate and Alzheimer’s disease.
Memantine (Namenda) for Moderate to Severe Alzheimer's Disease
Adrienne Z. Ables, Pharn.D., Spartanburg, South Carolina
Synopsis: Memantine (Namenda) is an N-methyl-d-aspartate (NMDA) receptor blocker indicated for the treatment of moderate to severe Alzheimer's disease (AD). The NMDA receptor is activated by glutamate, the primary excitatory neurotransmitter in the brain. Overstimulation by glutamate may result in neuronal damage and has been implicated in neurodegenerative disorders such as AD. Memantine is the first pharmacologic agent approved by the U.S. Food and Drug Administration for the treatment of moderate to severe AD.
172. Olney, J.W. Excitatory neurotoxins as food additives: an evaluation of risk. Neurotoxicology 2: 163-192, 1980.
229. Olney, J.W. Excitatory amino acids and neuropsychiatric disorders. Biol Psychiatry 26: 505-525, 1989.
230. Choi, D.W., and Rothman. S.M. The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death. Annu Rev Neurosci 13: 171-182, 1990.
231. Olney, J.W. Excitotoxic amino acids and neuropsychiatric disorders. Annu Rev Pharmacol Toxicol 30: 47-71, 1990.
232. Olney, J.W. Excitotoxicity: an overview. Biol Psychiatry 27: 90A, 1990. (Abstract)
233. Coyle, J.T. Glutamate receptors and age-related neurodegenerative disorders. Biol Psychiatry 27: 91A, 1990.
234. Pomara, N., Deptula, D., Singh, R., LeWitt, P.A., and Banay-Schwartz, M. Excitatory amino acid concentrations in CSF of patients with Alzheimer's disease. Biol Psychiatry 27: 91A, 1990.
235. Zukin, S.R., and Javitt, D.C. The NMDA-PCP theory of schizophrenia: implications of receptor interactions. Biol Psychiatry 27: 91A, 1990.
236. Olney, J.W. Excitotoxins and neurological diseases. Proceedings
of the 11th International Congress of Neuropathology, Kyoto, Japan, September