Dietary Phenylalanine and Brain Function 1988
DOI: 10.1007/978-1-4615-9821-3_4
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Aspartame Consumption in Normal Individuals and Carriers for Phenylketonuria

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Cited by 4 publications
(3 citation statements)
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“…In contrast, patients with PKU according to the quality of their dietary treatment clearly show differences from controls. Also, there was no evidence from our study that an additional aspartame load of 45 mg/kg in PKUH resulted in urine aromatic acids derived from phe and tyrosine that approached levels found in the classic untreated PKU (Matalon et al 1988). In our study no difference between aromatic acid excretion in urine following placebo and aspartame was found.…”
Section: Discussionmentioning
confidence: 57%
See 1 more Smart Citation
“…In contrast, patients with PKU according to the quality of their dietary treatment clearly show differences from controls. Also, there was no evidence from our study that an additional aspartame load of 45 mg/kg in PKUH resulted in urine aromatic acids derived from phe and tyrosine that approached levels found in the classic untreated PKU (Matalon et al 1988). In our study no difference between aromatic acid excretion in urine following placebo and aspartame was found.…”
Section: Discussionmentioning
confidence: 57%
“…This potential competitive advantage for phe to enter the brain following aspartame consumption has been suggested to affect brain function, i.e., behavior, cognition, and the EEG, by altering brain neurotransmitter concentrations (Elsas et al 1988). Matalon et al (1988) claimed that PKUH receiving high doses of aspartame (100 mg/kg of body weight per day) may have plasma phe levels and urinary metabolites in the same Aspartame is currently being consumed by over 200 million consumers worldwide, approximately 2% of whom are PKUH. This prompted us to conduct our study.…”
Section: Introductionmentioning
confidence: 99%
“…This enhanced biological stability of FC-APM and FCaMe-APM may make these compounds attractive as alternatives to APM in certain applications. One such possibility is as an artificial sweetener for phenylketonuriacs, those heterozygous for phenylketonuria and other individuals susceptible to symptoms due to ingestion of APM (Novick, 1985;Pardridge, 1986), in whom the hydrolysis of APM can cause increased plasma levels of Phe which may then have deleterious effects (Caballero et al, 1986;Matalón et al, 1988;Stegink et al, 1988). ABBREVIATIONS USED APM, aspartame; C-APM, N-carbamoyl aspartame; F-APM, /V-formylaspartame; FC-APM, N-formylcarbamoylaspartame; aMe-APM, aMe-aspartame; CaMe-APM, Ñ-carbamoyl aMe-aspartame; FCaMe-APM, TV-formylcarbamoyl-aMe-aspartame.…”
Section: Discussionmentioning
confidence: 99%