Additional reports attempted to look at this.In 1986, FDAs Advisory Committee on Hypersensitivity to Food Constituents concluded that monosodium glutamate poses no threat to the general public but that reactions of brief duration might occur in some people. Other reports have given the following findings:

The 1987 Joint Expert Committee on Food Additives of the United Nations Food and Agriculture Organization and the World Health Organization placed monosodium glutamate in the safest category of food ingredients. A 1991 report by the European Communitys (EC) Scientific Committee for Foods reaffirmed monosodium glutamates safety and classified its "acceptable daily intake" as "not specified", the most favorable designation for a food ingredient. In addition, the EC Committee said, "Infants, including prematures, have been shown to metabolize glutamate as efficiently as adults and therefore do not display any special susceptibility to elevated oral intakes of glutamate." Legislation in effect since June 2013 classifies glutamic acid and glutamates as salt substitutes, seasonings, and condiments with a maximum level of consumption of 10g/kg expressed as glutamic acid. European Union
Following the compulsory EU-food labeling law the use of glutamic acid and its salts has to be declared, and the name or E number of the salt has to be listed. Glutamic acid and its salts as food additives have the following E numbers: glutamic acid: E620, monosodium glutamate: E621, monopotassium glutamate: E622, calcium diglutamate: E623, monoammonium glutamate: E624, and magnesium diglutamate: E625.
Genetics
Neu-Laxova syndrome is a heterogeneous metabolic disorder caused by homozygous or compound heterozygous mutations in one of three genes: PHGDH, PSAT1 and PSPH These genes are involved in the serine biosynthesis pathway and are essential for cell proliferation. Mutations in all three genes had been previously identified as the cause of serine-deficiency syndromes. Although there is some clinical overlap between NLS and these neurometabolic disorders, the phenotype in other serine-deficiency disorders is milder. Diagnosis
The diagnosis is usually based on clinical features present at birth. Ultrasound in the second trimester may show abnormalities associates with NLS, including polyhydramnios, intrauterine growth restriction, microcephaly, proptosis and decreased fetal motility. Treatment
Serine and glycine supplementation has shown tentative benefits in those with related serine biosynthesis defects and milder forms of NLS. Prognosis
The prognosis is poor; affected individuals are either stillborn or die shortly after birth. The longest survival reported in literature is of 134 days. This syndrome is transmitted as an autosomal recessive disorder and there is a risk for recurrence of 25% in future pregnancies. References


== External links ==