The opinion of Louis J. Elsas, II, M.D., Director, Division of MedicalGenetics, Professor of Pediatrics, as stated to the Labor and Human ResourcesCommittee, U.S. Senate
EMORY UNIVERSITY SCHOOL OF MEDICINE
DEPARTMENT OF PEDIATRICS
2040 Ridgewood Drive, NE
Atlanta, Georgia 30322
Division of Medical Genetics
Statement for the Labor and Human Resources Committee, U.S. Senate
I have considerable concern forthe increased dissemination and consumption of the sweetener, aspartame(1-methyl N-Laspartyl-L- phenylalanine) in our world food supply. This artificial dipeptide is hydrolyzd by the intestinal tract to productL-phenylalanine which in excess is a known neurotoxin. Normal humansdo not metabolize phenylalanie as efficiently as do lower species suchas rodents, and thus most of the previous studies in Aspartame effectson rats are irrelevant to the question, “does phenylalanine excess occurwith Aspartame ingestion?” and if so “will it adversely affect humanbrain function?”
Preliminary studies in my laboratoryprovide tentative positive answers to both questions. Many studiesof both acute and chronic ingestion of 34 mg Aspartame/kg/day have demonstrateda two to five fold increase in semi-fasting blood phenylalanine concentrations(from approximately 50 5o 250 pM) without concomitant increases in tyrosineor other amino acids. The degree of increase by normal humans dependson several variables including the efficiency of gut transport, liver utilization,and growth rates. It was thought by many scientists and cliniciansthat this degree of blood phenylalanine increases would not affect brainfunction. However, currently available information indicates thatthis is not true.
1) In the developing fetus such a rise inmaternal blood phenylalanine could be magnified four to six fold by theconcentrative efforts of the placenta and fetal blood brain barrier. Thus a maternal phenylalanine of 150 pM could reach 900 pM in the developingfetal brain cell and this concentration kills such cells in tissue culture. The effect of such an increased fetal brain concentrations in vivo wouldprobably be much more subtle and expressed as mental retardation, microcephaly,or potential certain birth defects.
2) In the rapidly growing post-natal brain(children of 9-12 months) irreversible brain damage could occur by thesame mechanism.
3) In the adult we have found that changesin blood phenylalanine in these concentration ranges are associated withslowing of the electroencephalogram, and prolongation of cognitive functiontests. Fortunately, these effects on the mature brain are reversible butprovide clear evidence for a negative effect on sensitive parameters ofbrain function. In view of these new (and confirmation of old) researchfindings, I suggest the following:
1) Immediate quantitative labeling of allaspartame-containing foods, so the consumer will know how much phenylalaninehe/she is ingesting.
2) Declare an immediate moratorium on additionof aspartame to more foods, and remove it from all low-protein beverages,foods, and children’s medications.
3) Provide funds not controlled by industryto:
a) Allow active surveillance for potentialside-effects of aspartame on newborns whose mothers dieted with NutraSweet(aspartame)-containing foods.
b) Allow active evaluation of otherusers whose complaints cannot be adequately studied at present.
c) Clarify the dose relationship andmechanisms by which L- phenylalanine affects human brain function..
Respectfully submitted,
Louis J. Elsas, II, M.D.
Director, Division of Medical Genetics, Professor of Pediatrics