Therefore, Williams and Woessner (2009, pp. 640-646) state that the Federation of American Societies for Experimental Biology published a report of a comprehensive analysis of the safety of MSG and established a list of symptoms that constitutes the syndrome as shown in table 1. The less pejorative and more inclusive term Monosodium glutamate symptom complex (MSGSC) was also proposed. Additionally, these studies suggest that there may be a small number of people at risk for developing symptoms consistent with the MSGSC when consuming large amounts of MSG on an empty stomach without accompanying food. However, Geha et al. (2000, pp. 1058–1062) argue that approximately 20% of consumers may have at least one disease from MSGSC. On the other hand, Williams and Woessner (2009, pp. 640-646) contradict that the overall incidence of MSGSC appears to be low, even in self-identified MSG-sensitive patients. Thus, current evidence does not suggest that this entity is associated with persistent or serious effects, but numerous experiments show that MSG is not safe for some individuals with …show more content…
Therefore, Olney, Adamo and Ratner (1971, p. 294) estimate that larger numbers of adult rats after multiple MSG treatments in infancy and have consistently found that average weights of the adenohypophysis (the glandular, anterior lobe of the pituitary gland) are about one-half those of control animals. In addition, Young and Ajami (2000, pp. 892-900) argue that in infant retina and hypothalamus (a neural control centre at the base of the brain), susceptible nerve cells undergo rapid necrosis (the death of most or all of the cells in an organ) and are phagocytized (the cellular process of engulfing solid particles), degraded, and evacuated from affected areas within 24 to 48 hours after MSG treatment. Consequently, it is clearly shown that MSG may have several hostile effects on brain work possibilities. Although Arees, Mayer, Burde, Shainker and Kayes, J. (1970, p. 549) have found both the rat and mouse susceptible to MSG-induced brain damage, Olney’s at al. (1971, p. 294) study was the first report to suggest the possibility that a single subcutaneous injection of MSG may not produce neuronal necrosis in the arcuate nucleus of infant rats. Additionally, Sampson (2003, pp. 701-706) reported failure to detect brain damage in infant rats injected subcutaneously with monosodium glutamate (MSG). However, Hanon (2007) states that normal neural components can