PREGNANCY, LACTATING MOTHERS, INFANTS AND ASPARTAME
 

The opinion of Louis J. Elsas, II, M.D., Director, Division of Medical Genetics, Professor of Pediatrics, as stated to the Labor and Human Resources Committee, 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 for the 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 product L-phenylalanine which in excess is a known neurotoxin.  Normal humans do not metabolize phenylalanie as efficiently as do lower species such as rodents, and thus most of the previous studies in Aspartame effects on rats are irrelevant to the question, “does phenylalanine excess occur with Aspartame ingestion?�?and if so “will it adversely  affect human brain function?�?
       Preliminary studies in my laboratory provide tentative positive answers to both questions.  Many studies of both acute and chronic ingestion of 34 mg Aspartame/kg/day have demonstrated a two to five fold increase in semi-fasting blood phenylalanine concentrations (from approximately 50 5o 250 pM) without concomitant increases in tyrosine or other amino acids.  The degree of increase by normal humans depends on several variables including the efficiency of gut transport, liver utilization, and growth rates.  It was thought by many scientists and clinicians that this degree of blood phenylalanine increases would not affect brain function.  However, currently available information indicates that this is not true.
     1) In the developing fetus such a rise in maternal blood phenylalanine could be magnified four to six fold by the concentrative efforts of the placenta and fetal blood brain barrier.  Thus a maternal phenylalanine of 150 pM could reach 900 pM in the developing fetal brain cell and this concentration kills such cells in tissue culture.  The effect of such an increased fetal brain concentrations in vivo would probably 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 the same mechanism.
     3) In the adult we have found that changes in blood phenylalanine in these concentration ranges are associated with slowing of the electroencephalogram, and prolongation of cognitive function tests. Fortunately, these effects on the mature brain are reversible but provide clear evidence for a negative effect on sensitive parameters of brain function. In view of these new (and confirmation of old) research findings, I suggest the following:
     1) Immediate quantitative labeling of all aspartame-containing foods, so the consumer will know how much phenylalanine he/she is ingesting.
     2) Declare an immediate moratorium on addition of aspartame to more foods, and remove it from all low-protein beverages, foods, and children’s medications.
     3)  Provide funds not controlled by industry to:
      a) Allow active surveillance for potential side-effects of aspartame on newborns whose mothers dieted with NutraSweet (aspartame)-containing foods.
      b) Allow active evaluation of other users whose complaints cannot be adequately studied at present.
      c) Clarify the dose relationship and mechanisms by which L- phenylalanine affects human brain function..
Respectfully submitted,
Louis J. Elsas, II, M.D.
Director, Division of Medical Genetics, Professor of Pediatrics