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generation and declining energy production with ageing. Several disease. For example, there is evidence that dopamine deficiency factors of ageing have been shown to magnify this process. For causes a disinhibition (overactivity) of the subthalamic nucleus example, as the brain ages, its iron content increases, making it and that this may result in excitotoxic injury to the substantia more susceptible to free radical generation. Also, ageing changes nigra. By blocking the glutamatergic neurons in this nucleus, in the blood-brain barrier, microvascular changes leading to one may be able to reduce this damage. There is also evidence impaired blood flow, free radical mitochondrial injury to energy- that several nutrients can significantly reduce excitotoxicity. For generating enzymes, DNA adduct formation, alterations in example, combinations of coenzyme Q10 and niacinamide have glucose and glutamate transporters, and free radical and lipid been shown to protect against striatal excitotoxic lesions. peroxidation induced alterations in the neuronal membranes all Methylcobolamin, phosphotidylserine, pycnogenol and acety]l-L- act to make the ageing brain carnitine all protect against excito- increasingly susceptible to toxicity as well. excitotoxic injury. H Of particular concern are the Over a lifetime of free radical Other hypothalamic syndromes toxic otfects of these excitotoxic injury due to chronic stress, infec- associated with early excitotoxic compounds on the developing tions, trauma, impaired blood flow, lesions include immune alterations brain. It is well recognised that hypoglycaemia, hypoxia and poor . the immature brain is four times antioxidant defences secondary to and violence dyscontrol. more sensitive to the toxic effects poor nutritional intake, the nervous of the excitatory amino acids as is system is significantl akened ATH A the mature brain. and ‘made more susceptible to fur- Over 100 million Americans now This means that excitotoxic ther excitotoxic injury. We know consume aspartame products, and a injury is of special concern from that a loss of neuronal energy gen- the foetal stage to adolescence. eration is one of the early changes greater number consume products There is evidence that the placenta seen with the neurodegenerative containing one or more excitotoxins. concentrates several of these toxic diseases. This occurs long before amino acids on the foetal side of clinical disease develops. But, the placenta. Consumption of even earlier is a loss of neuronal aspartame- and MSG-containing glutathione functional levels. products by pregnant women during this critical period of brain I included the material about the special function of ascorbic formation is of special concern and should be discouraged. acid because few are aware of the importance of adequate ascor- Many of the effects, such as endocrine dysfunction and com- bate levels for CNS function and neural protection against excito- plex learning difficulties, are subtle and may not appear until the toxicity. As we have seen, it plays a vital role in neurobehaviour- child is older. Other hypothalamic syndromes associated with al regulation and the dopaminergic system as well, which may early excitotoxic lesions include immune alterations and violence link ascorbate supplementation to improvements in schizophrenia. dyscontrol. Our knowledge of this process opens up new avenues for treat- Over 100 million Americans now consume aspartame products, ment as well as prevention of excitotoxic injury to the nervous and a greater number consume products containing one or more system. For example, there are many nutritional ways to improve excitotoxins. CNS antioxidant defences and boost neuronal energy generation, There is sufficient medical literature documenting serious as well as improve membrane fluidity and receptor integrity. By injury by these additives in the concentrations presently in our using selective glutamate-blocking drugs or nutrients, one may be food supply to justify warning the public of these dangers. The able to alter some of the more devastating effects of Parkinson's _ case against aspartame is especially strong. oo Other hypothalamic syndromes associated with early excitotoxic en: a: oe an eae Benen = Pee 83. Fisher, G.H., D'Aniello, A.D. et al., Biomed. Biochem. ACTA 46:705-711, 1987. Endocrinology 128:1100-1106, 1991. "Quantification of D-asparate in normal and 89. Freider, B. and Grimm, V.E., "Prenatal 94. Lipton, S.A. and Rosenberg, P.A., Alzheimer brains", Neurosci. Lett. 143:215-218, monosodium glutamate (MSG) treatment given "Excitatory amino acids as a final common path- 1992. through the mother's diet causes behavioral way for neurologic disorders", New Eng. J. Med. 84. Suzuki, K. and Martin, P.M., deficits in rat offspring", Intern. J. Neurosci. 330:613-622, 1994. "Neurotoxicants and the Developing Brain", in 23:117-126, 1984. 95. Rodriguez, M.C., Obeso, J.A. and Olanow, Harry, G.T. (ed.), Developmental 90. Frieder, B. and Grimm, V.E., "Prenatal C.W., "Subthalamic nucleus-mediated excitotox- Neurotoxicology, ibid. monosodium glutamate causes long-lasting icity in Parkinson's disease: a target for neuro- 85. Olney, J.W., "Excitotoxic food additives: cholinergic and adrenergic changes in various protection", Ann. Neurol. 44:(Supp 1)S175- functional teratological aspects", Progress. Brain _ brain regions", J. Neurochem. 48:1359-1365, S188, 1998. Res. 73:283-294, 1988. 1987. 86. Brody, J.R. et al., "Effect of micro-injections 91. Kubo, T., Kohira, R. et al., "Neonatal gluta- Editor's Note: of L-glutamate into the hypothalamus on attack mate can destroy the hippocampal CAI structure This article is reproduced courtesy of Dr and flight behaviour in cats", Nature 224:1330, and impair discrimination learning in rats", Russell Blaylock and was first published 1969. _ Brain Res. 616:311-314, 1993. in Medical Sentinel (vol. 4, no. 6, Nov- 87. Wong, P.T., Neo, L.H. et al., "Deficits in 92. Bakke, J.L., Lawrence, J. et al., "Late Dec 1999), the bimonthly peer-reviewed water escape performance and alterations in hip- endocrine effects of administering monosodium journal of the Association of American pocampal cholinergic mechanisms associated glutamate to neonatal rats", Neuwroendocrinology Physici ds AAPS): with neonatal monosodium glutamate treatment 26:220-228, 1978. ysicians an yo urgeons ( )i in mice", Pharmacol. Biochem. Behav. 57:383- 93. Maiter, D., Underwood, LE. et al., Hacienda Publishing, Inc., PO Box 388, 1997. “Neonatal treatment with monosodium gluta- 13648, Macon, GA 31208-3648, USA, tel 88. Klingberg, H., Brankack, J. and Klingberg, mate: effects of prolonged growth hormone (912) 757 9873, fax (912) 757 9725, F., "Long-term effects on behavior after post- (GH)-releasing hormone deficiency on pulsatile €-mail hfaria@mindspring.com, website natal treatment with monosodium L-glutamate", GH secretion and growth in female rats", www.haciendapub.com. 46 - NEXUS lesions include immune alterations and violence dyscontrol. Over 100 million Americans now AUGUST - SEPTEMBER 2000