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HOT TOPICS is a review of the medical literature on a topic of
current interest. The articles are taken from the MEDLINE online database
produced by the National Library of Medicine, as well as many other
online sources of information.
This listing is NOT a complete review, but represents a selection.
Further information may be obtained from campus libraries (including the
Biomedical Library), or from your local library. Many of the articles will
be available in the Biomedical Library. We will be happy to assist you in
locating them during our regular hours. If you have any questions please
leave a message. I welcome any suggestions for further HOT TOPICS, and will
be happy to answer any questions regarding this section. -- Steve Clancy,
Biomedical Library, UCI.
*******************************************************************************
KEY TO HOT TOPICS REFERENCES
3. France C; Ditto B. <AUTHOR(S)>
Cardiovascular responses to occupational stress and caffeine in
telemarketing employees. <ARTICLE TITLE>
Psychosomatic Medicine, 1989 Mar-Apr, 51(2):145-51. <JOURNAL TITLE>
More <[Y],N,C,A>!
Abstract: Cardiovascular responses to the combination of caffeine and a
challenging occupational activity were examined using a within-subject,
double-blind design. Seventeen female and 11 male telemarketing employees
received drinks that did and did not contain 250 mg of caffeine on two
***************************************************************************
NUTRASWEET: ADVERSE EFFECTS
1. Dailey JW; Lasley SM; Mishra PK; Bettendorf AF; Burger RL; Jobe PC.
Aspartame fails to facilitate pentylenetetrazol-induced convulsions in
CD-1 mice.
Toxicology and Applied Pharmacology, 1989 May, 98(3):475-86.
Abstract: Concentrations of plasma amino acids and brain monoamines as well as
pentylenetetrazol-induced seizures were monitored in CD-1 mice treated with
aspartame in acute oral doses from 0 to 2500 mg/kg. One hour after
administration aspartame produced increases in plasma concentrations of
phenylalanine and tyrosine and modest reductions in concentrations of brain
serotonin and 5-hydroxyindole acetic acid. However, these effects of the
sweetener had no influence on the convulsive dose fifty (CD50) of
pentylenetetrazol. Moreover, aspartame failed to alter the percentage of
mice exhibiting seizures when exposed to an approximate CD50 of
More <[Y],N,C,A>! pentylenetetrazol. Finally, aspartame had no effect on brain norepinephrine
or dopamine concentrations. In sharp contrast to previously reported
studies, these observations suggest that aspartame, given in heroic doses,
does not alter the propensity to seizure activity in CD-1 mice. We conclude
that changes in plasma amino acids and brain serotonin produced by large
oral bolus doses of aspartame are insufficient to result in functional
deficits which might have the capacity to facilitate
pentylenetetrazol-induced seizures.
2. Lipton RB; Newman LC; Cohen JS; Solomon S.
Aspartame as a dietary trigger of headache.
Headache, 1989 Feb, 29(2):90-2.
Abstract: Many dietary factors have been implicated as possible precipitants of
headache. There have been recent differences of opinion with regard to the
effect of the artificial sweetener aspartame as a precipitant of headache.
To assess the importance of aspartame as a dietary factor in headache, 190
consecutive patients of the Montefiore Medical Center Headache Unit were
questioned about the effect of alcohol, carbohydrates and aspartame in
triggering their headaches. Of the 171 patients who fully completed the
survey, 49.7 percent reported alcohol as a precipitating factor, compared
to 8.2 percent reporting aspartame and 2.3 percent reporting carbohydrates.
Patients with migraine were significantly more likely to report alcohol as
a triggering factor and also reported aspartame as a precipitant three
More <[Y],N,C,A>! times more often than those having other types of headache. The conflicting
results of two recent placebo-control studies of aspartame and headache are
discussed. We conclude that aspartame may be an important dietary trigger
of headache in some people.
3. Yost DA.
Clinical safety of aspartame.
American Family Physician, 1989 Feb, 39(2):201-6.
Abstract: Aspartame is a synthetic sweetener commonly used in soft drinks and
many foods. Even with high doses, the metabolites of this sweetener do not
accumulate in toxic amounts. To date, no definite symptom complex has been
connected with aspartame, and it is considered safe for use in all
populations, including diabetics, phenylketonuric heterozygotes and
pregnant women.
4. Tollefson L.
Monitoring adverse reactions to food additives in the U.S. Food and Drug
Administration.
Regulatory Toxicology and Pharmacology, 1988 Dec, 8(4):438-46.
Abstract: Technological advances in food science have resulted in the
development of numerous food additives, most of which require premarket
approval by the Food and Drug Administration (FDA). Concomitant with the
More <[Y],N,C,A>! benefits of these additives, such as extending the shelf life of certain
food commodities, is the potential for various risks. These potential risks
include the possibility of the consumer experiencing an adverse reaction to
the additive. In order to ascertain the character and the gravity of
alleged adverse reactions to food products which it regulates, the FDA's
Center for Food Safety and Applied Nutrition has developed the Adverse
Reaction Monitoring System (ARMS). This postmarketing surveillance system
for food additives is designed to analyze consumer reports of adverse
reactions in order to alert FDA officials about any potential public health
hazard associated with an approved food additive, and to delineate specific
syndromes which may lead to focused clinical investigations. To date, among
the products routinely monitored in the ARMS, sulfiting agents and the
artificial sweetener aspartame have generated the largest volume of
consumer reports describing adverse reactions. An overview of the analyses
of the sulfite and aspartame adverse reaction reports is presented, along
with a description of the mechanics of the postmarketing surveillance
system, and a detailed discussion of its limitations.
5. Fountain SB; Hennes SK; Teyler TJ.
Aspartame exposure and in vitro hippocampal slice excitability and
plasticity.
Fundamental and Applied Toxicology, 1988 Aug, 11(2):221-8.
Abstract: Aspartame (APM) is a low-calorie sweetener recently approved and
More <[Y],N,C,A>! released for widespread use in the United States. However, concerns still
exist that APM consumption may be responsible for adverse neurological and
psychological effects in some people. In addition, recent reports indicate
that APM exposure may alter regional brain neurotransmitter levels. The
present study assessed the effects of APM and its amino acid moieties on
rat hippocampal slice excitability and plasticity. Specifically, tests of
excitatory systems, inhibitory systems, and synaptic plasticity (induction
of long-term potentiation--LTP) were administered postexposure. Exposures
of 0.01, 0.1, 1, and 10 mM APM potentiated the response of hippocampal CA1
pyramidal cells, but had no apparent effect on local inhibitory systems.
APM exposure did not block the establishment of LTP at any dose despite the
potentiation of pyramidal cell response observed postexposure. In addition,
0.1 mM phenylalanine (PHE) produced a greater increase in excitability than
that produced by an equivalent dose of APM, 0.1 mM aspartic acid (ASP) and
0.1 mM phenylalanine methyl ester (PM) produced effects comparable to those
produced a smaller, but reliable, change in hippocampal CA1 excitability
relative to baseline. Like APM, none of the amino acids produced detectable
changes in inhibitory systems or neuronal plasticity.
6. Stegink LD; Filer LJ Jr; Baker GL; Bell EF; Ziegler EE; Brummel MC; Krause
WL.
Repeated ingestion of aspartame-sweetened beverage: effect on plasma amino
acid concentrations in individuals heterozygous for phenylketonuria.
Metabolism: Clinical and Experimental, 1989 Jan, 38(1):78-84.
More <[Y],N,C,A>!
Abstract: It has been suggested that excessive use of aspartame (APM)
(N-L-alpha-aspartyl-L-phenylalanine methyl ester) might grossly elevate
plasma aspartate and phenylalanine concentrations in individuals
heterozygous for phenylketonuria (PKUH). In study 1 six adult PKUH (three
males; three females) ingested three successive 12-oz servings of beverage
at 2-h intervals. The study was carried out in two parts in a randomized
crossover design. In one arm the beverage was not sweetened. In the other
the beverage provided 10 mg APM/kg body weight per serving. The addition of
APM to the beverage did not significantly increase plasma aspartate
concentration but did increase plasma phenylalanine levels 2.3 to 4.1
mumol/dL above baseline values 30 to 45 min after each dose. The high mean
plasma phenylalanine level after repeated APM dosing (13.9 +/- 2.15
mumol/dL) was slightly, but not significantly, above the normal
postprandial range for PKUH (12.6 +/- 2.11 mumol/dL). In study 2 six
different adult PKUH ingested beverage providing 30 mg APM/kg body weight
as a single bolus. The high mean plasma phenylalanine concentration and the
phenylalanine to large neutral amino acid ratio were significantly higher
when APM was ingested as a single bolus than when ingested as a divided
dose.
7. Garriga MM; Metcalfe DD.
Aspartame intolerance.
Annals of Allergy, 1988 Dec, 61(6 Pt 2):63-9.
More <[Y],N,C,A>!
Abstract: Aspartame is a food additive marketed under the brand name
Nutrasweet. Aspartame is a white, odorless, crystalline powder and consists
of two amino acids, L-aspartic acid and L-phenylalanine. It is 180 times as
sweet as sugar. The Food and Drug Administration (FDA) first allowed its
use in dry foods in July 1981 and then approved its use in carbonated
beverages in July 1983. It has subsequently been approved for use in a
number of materials including multivitamins, fruit juices, stick-type
confections, breath mints, and iced tea. The FDA requires the statement
"phenylketonurics: contains phenylalanine" on labels of food products
containing aspartame because individuals with phenylketonuria (PKU) must
restrict their intake of phenylalanine. Aspartame is judged to be free of
long-term cancer risks. Aspartame is not stable under certain conditions
including baking and cooking, and prolonged exposure to acid conditions. In
such situations it loses its sweetness. Products formed from aspartame
include its component amino acids (phenylalanine and aspartic acid),
methanol, and diketopiperazine (DKP). Animal studies show DKP to be
nontoxic. Methanol occurs in small amounts and does not exceed that formed
during consumption of many foods including fresh fruits and vegetables.
FDA's Center for Food Safety and Applied Nutrition (CFSAN) monitors
aspartame's safety in part through reports of adverse reactions. After
aspartame was approved for use in carbonated beverages, the FDA received an
increased number of reports concerning adverse reactions related to
aspartame. The Centers for Disease Control (CDC) reviewed these reports,
More <[Y],N,C,A>! which included complaints of neurologic, gastrointestinal, andallergic
reactions.(ABSTRACT TRUNCATED AT 250 WORDS)
8. Guiso G; Caccia S; Vezzani A; Stasi MA; Salmona M; Romano M; Garattini S.
Effect of aspartame on seizures in various models of experimental
epilepsy.
Toxicology and Applied Pharmacology, 1988 Dec, 96(3):485-93.
Abstract: We investigated in rats whether aspartame intake affected the
susceptibility to seizures induced chemically (metrazol, quinolinic acid)
or electrically (electroshock). Aspartame (0.75-1.0 g/kg), given orally as
a single bolus to 16-hr fasted animals 60 min before metrazol,
significantly increased the number of animals showing clonic-tonic
seizures. At 1.0 g/kg the ED50 for clonic-tonic convulsions was lowered by
23%. A similar increase in seizure susceptibility was observed with
0.25-0.5 g/kg of the aspartame's metabolite phenylalanine. When aspartame
was administered to fasted rats in three divided doses (0.33 g/kg) over 120
min or to fed animals after a meal, or overnight with the diet, no
significant changes in the incidence of animals showing seizures was
observed. One gram per kilogram aspartame and 0.5 g/kg phenylalanine did
not modify the CC50 (mA) for tonic hindlimb extension induced by
electroshock and the electroencephalographic seizures caused by
intrahippocampal injection of 120 nmol quinolinic acid. Plasma and brain
levels of phenylalanine and tyrosine significantly raised after both 1 g/kg
More <[Y],N,C,A>! aspartame as a single bolus (plasma: Phe 285%, Tyr 288%; brain: Phe 146%,
Tyr 192%; above controls) or in three divided doses (plasma: Phe 207%, Tyr
315%; brain Phe 103%, Tyr 211%; above controls) and 0.5 g/kg phenylalanine
(plasma: Phe 339%, Tyr 410%; brain: Phe 219%, Tyr 192%; above controls),
but the ratio Phe/Tyr was not modified. Our data indicate that aspartame
cannot be regarded as a general proconvulsant agent. The mechanisms of
potentiation of seizures induced by metrazol after the administration of
the sweetner in a single rapid intake will be discussed.
9. Nabors LO.
Saccharin and aspartame: are they safe to consume during pregnancy?
[latter].
Journal of Reproductive Medicine, 1988 Aug, 33(8):102.
10. Copestake P.
Aspartame--a bit of a headache?
Food and Chemical Toxicology, 1988 Jun, 26(6):571.
11. Janssen PJ; van der Heijden CA.
Aspartame: review of recent experimental and observational data.
Toxicology, 1988 Jun, 50(1):1-26.
Abstract: In this report the neurotoxicity of aspartame and its constituent
amino acids aspartic acid and phenylalanine is reviewed. The adverse
More <[Y],N,C,A>! reactions ascribed to the consumption of aspartame-containing products, as
reported in the U.S.A., are discussed and placed in perspective with the
results of recent behavioural studies in humans and animals. The issue of
common intake levels associated with proposed uses of aspartame is
addressed. In brief, the following conclusions can be drawn: When aspartame
is consumed at levels within the ADI-limit of 40 mg/kg body wt, there is no
significant risk for an aspartate-induced neurotoxic effect in the brain.
When aspartame is consumed at levels within the ADI-limit by normal
subjects or persons heterozygous for phenylketonuria (PKU) the resultant
plasma phenylalanine concentrations are practically always within the
normal postprandial range; elevation to plasma concentrations commonly
associated with adverse effects has not been observed. Persons suffering
from phenylketonuria (PKU-homozygotes) on a phenylalanine-restricted diet
should avoid consumption of aspartame. PKU-homozygotes on the (less strict)
phenylalanine-liberalized diet should be made aware of the phenylalanine
content of aspartame. In the available behavioural studies in humans with
acute dosing, no adverse effects were observed. Long-term studies on
behaviour and cognitive function in (sensitive) humans are lacking.
Analyses of adverse reaction reports made by consumers in the U.S.A. have
not yielded a specific constellation of symptoms clearly related to
aspartame that would suggest a widespread public health hazard associated
with aspartame use. Focussed clinical studies are now being carried out in
the U.S.A.; the results should provide additional evidence concerning the
interpretation of the reports on adverse reactions ascribed to aspartame.
More <[Y],N,C,A>! In the regulation of admitted uses for aspartame the possibility of intake
levels exceeding the ADI-limit in some groups of consumers should be a
point of attention.
12. Schiffman SS.
Aspartame and headache [letter].
Headache, 1988 Jun, 28(5):370-2.
13. Aspartame and headache [letter].
New England Journal of Medicine, 1988 May 5, 318(18):1200-2.
14. Koehler SM; Glaros A.
The effect of aspartame on migraine headache.
Headache, 1988 Feb, 28(1):10-4.
15. Edmeads J.
Aspartame and headache.
Headache, 1988 Feb, 28(1):64-5.
16. London RS.
Saccharin and aspartame. Are they safe to consume during pregnancy?
Journal of Reproductive Medicine, 1988 Jan, 33(1):17-21.
Abstract: Saccharin and aspartame are commonly used artificial sweeteners. Some
More <[Y],N,C,A>! of the currently available information on their safety in pregnancy was
reviewed, with recommendations formulated on their use in the
periconceptional period and pregnancy.
17. Pinto JM; Maher TJ.
Administration of aspartame potentiates pentylenetetrazole- and
fluorothyl-induced seizures in mice.
Neuropharmacology, 1988 Jan, 27(1):51-5.
Abstract: An association has recently been proposed between the incidence of
seizures and prolonged consumption of the phenylalanine-containing
artificial sweetener, aspartame. Since consumption of aspartame, unlike
dietary protein, can elevate phenylalanine in brain, and thereby inhibit
the synthesis and release of neurotransmitters known to protect against
seizure activity, the effect of oral doses of aspartame on the sensitivity
of mice to the proconvulsant agents, pentylenetetrazole and fluorothyl was
studied. Doses of aspartame were used which increased phenylalanine more
than tyrosine in brain, as occurs in humans after the consumption of any
dose of aspartame. Pretreatment with aspartame significantly increased the
percentage of animals convulsing after administration of pentylenetetrazole
and significantly lowered the CD50 for this convulsant. The average time to
onset of seizures induced by fluorothyl in control mice was 510 sec;
pretreatment with oral doses of 1000, 1500 and 2000 mg/kg of aspartame 1 hr
earlier significantly reduced the time required to elicit seizures (394,
More <[Y],N,C,A>! 381 and 339 sec, respectively). The seizure-promoting effect of aspartame
could be demonstrated 30, 60 or 120 min after the 1000 mg/kg dose. The
seizures induced by either convulsant were potentiated by equimolar amounts
of phenylalanine, a major endogenous metabolite of aspartame, while the
other metabolites, aspartic acid and methanol, were without effect.
Administration together with aspartame of the large neutral amino acid
valine, which competes with phenylalanine for entry into the brain,
completely abolished the seizure-promoting effect of aspartame.(ABSTRACT
TRUNCATED AT 250 WORDS)
18. Lout RK; Messer LB; Soberay A; Kajander K; Rudney J.
Cariogenicity of frequent aspartame and sorbitol rinsing in laboratory
rats.
Caries Research, 1988, 22(4):237-41.
Abstract: The cariogenicity of frequent rinsings with aspartame and sorbitol
was studied in the rat caries model with animals randomly assigned to four
oral rinse groups (16 rats/group): 0.05% aspartame, 20% sorbitol, deionized
distilled water, and 20% sucrose; all solutions at pH 3.0. After rinsing
five times daily for 21 days, mandibular molars were scored for caries.
Smooth surface, proximal and morsal caries scores did not differ
significantly between groups. Moderate dentinal sulcal caries for the
sucrose group was significantly greater than in the aspartame, sorbitol,
and water groups (p less than 0.05). Rinsing with 0.05% aspartame (similar
in pH and concentration to that found in carbonated beverages) or sorbitol
did not potentiate caries activity.
19. Position of the American Dietetic Association: appropriate use of nutritive
and non-nutritive sweeteners.
Journal of the American Dietetic Association, 1987 Dec, 87(12):1689-94.
Abstract: Moderation in the consumption of nutritive and non-nutritive
sweeteners appears to be prudent advice for persons who choose to use
sweeteners. The major benefit from use of sweeteners is a perceived
More <[Y],N,C,A>! c improvement in the quality of life. Some nutritive sweeteners also provide
important textural properties to many foods. Sweeteners should be used in
the context of an otherwise nutritious and well-balanced diet. Excessive
intake of any sweetener requires nutrition counseling for basic nutrition
reasons. An individual can minimize potential risks from any one sweetener
by using a variety of available sweeteners, thus ingesting less of any
specific sweetener. Research into possible risks of long-term uses of
non-nutritive sweeteners, either alone or in combination, should continue.
It is important that the public have a choice of various non-nutritive
sweeteners, with safe and reasonable guidelines on how to use each. As new
sweeteners become available, they must receive the same rigorous testing to
which previously approved sweeteners have been subjected.
20. Schiffman SS; Buckley CE 3d; Sampson HA; Massey EW; Baraniuk JN; Follett
JV; Warwick ZS.
Aspartame and susceptibility to headache.
New England Journal of Medicine, 1987 Nov 5, 317(19):1181-5.
Abstract: We performed a double-blind crossover trial of challenges with 30 mg
of aspartame per kilogram of body weight or placebo in 40 subjects who
reported having headaches repeatedly after consuming products containing
aspartame. The incidence rate of headache after aspartame (35 percent) was
not significantly different from that after placebo (45 percent) (P less
than 0.50). No serious reactions were observed, and the incidence of
symptoms other than headache following aspartame was also equivalent to
that after placebo. No treatment-related effects were detected in vital
signs, blood pressure, or plasma concentrations of cortisol, insulin,
glucagon, histamine, epinephrine, or norepinephrine. Most of the subjects
were well educated and overweight and had a family or personal history of
allergic reactions. The subjects who had headaches had lower plasma
concentrations of norepinephrine (P less than 0.0002) and epinephrine (P
less than 0.02) just before the development of headache. We conclude that
in this population, aspartame is no more likely to produce headache than
placebo.
21. Maher TJ; Wurtman RJ.
Possible neurologic effects of aspartame, a widely used food additive.
Environmental Health Perspectives, 1987 Nov, 75:53-7.
Abstract: The artificial sweetener aspartame (L-aspartyl-L-phenylalanyl-methyl
ester), is consumed, primarily in beverages, by a very large number of
Americans, causing significant elevations in plasma and, probably, brain
phenylalanine levels. Anecdotal reports suggest that some people suffer
neurologic or behavioral reactions in association with aspartame
consumption. Since phenylalanine can be neurotoxic and can affect the
synthesis of inhibitory monoamine neurotransmitters, the phenylalanine in
aspartame could conceiveably mediate neurologic effects. If mice are given
aspartame in doses that elevate plasma phenylalanine levels more than those
of tyrosine (which probably occurs after any aspartame dose in humans), the
frequency of seizures following the administration of an epileptogenic
drug, pentylenetetrazole, is enhanced. This effect is simulated by
equimolar phenylalanine and blocked by concurrent administration of valine,
which blocks phenylalanine's entry into the brain. Aspartame also
potentiates the induction of seizures by inhaled fluorothyl or by
electroconvulsive shock. Perhaps regulations concerning the sale of food
additives should be modified to require the reporting of adverse reactions
and the continuing conduct of mandated safety research.
22. Kruesi MJ; Rapoport JL; Cummings EM; Berg CJ; Ismond DR; Flament M; Yarrow
M; Zahn-Waxler C.
Effects of sugar and aspartame on aggression and activity in children.
American Journal of Psychiatry, 1987 Nov, 144(11):1487-90.
Abstract: Habitual sugar consumption and behavior following challenge by sugar
and aspartame were studied in 30 preschool boys. The 18 subjects whose
parents considered them sugar reactive had more disruptive behavior
problems at baseline than the other 12 subjects. Habitual sugar consumption
correlated only with duration of aggression against property in alleged
responders. Double-blind crossover challenges with aspartame, saccharin,
sucrose, and glucose produced no significant effect on aggression or
observers' ratings of behavior. Lower actometer counts followed the trials
of aspartame, but the difference was not apparent to observers. It is
unlikely that sugar and aspartame are clinically significant causes of
disruptive behavior.
23. Alfin-Slater RB; Pi-Sunyer FX.
Sugar and sugar substitutes. Comparisons and indications.
Postgraduate Medicine, 1987 Aug, 82(2):46-50, 53-6.
Abstract: Public confusion and concern about the use of sugar and sugar
substitutes are widespread. Physicians must be prepared to answer patients'
inquiries about these substances. Some population groups should avoid
certain sugar substitutes. In particular, pregnant women and young children
should avoid saccharin, and phenylketonuric homozygous persons should avoid
aspartame. In a varied, balanced diet, the use of aspartame and saccharin
is one safe way for the general population to enjoy sweet foods with fewer
calories and less cariogenic potential. Sugar substitutes may be helpful in
dietary compliance for overweight and diabetic patients.
24. The safety of aspartame [letter].
Jama, 1987 Jul 10, 258(2):205-6.
25. Stegink LD.
The aspartame story: a model for the clinical testing of a food additive.
American Journal of Clinical Nutrition, 1987 Jul, 46(1 Suppl):204-15.
Abstract: Toxicology is based on the premise that all compounds are toxic at
some dose. Thus, it is not surprising that very large doses of aspartame
(or its components--aspartate, phenylalanine, and methanol) produce
deleterious effects in sensitive animal species. The critical question is
whether aspartame ingestion is potentially harmful to humans at normal use
and potential abuse levels. This paper reviews clinical studies testing the
effects of various doses of aspartame upon blood levels of aspartate,
phenylalanine, and methanol. These studies demonstrate that blood levels of
these compounds are well below levels associated with adverse effects in
sensitive animal species.
26. Dews PB.
Summary report of an International Aspartame Workshop.
Food and Chemical Toxicology, 1987 Jul, 25(7):549-52.
27. Zametkin AJ; Karoum F; Rapoport JL.
Treatment of hyperactive children with D-phenylalanine.
American Journal of Psychiatry, 1987 Jun, 144(6):792-4.
Abstract: Eleven hyperactive boys were treated for 2 weeks with D-phenylalanine
(20 mg/kg per day) and for 2 weeks with placebo in a double-blind crossover
study. Tests included parent and teacher behavior ratings, cognitive
measures, and blood and urine measures of norepinephrine, amino acids, and
trace amines. No significant improvement or deterioration in behavior and
no side effects were noted, and only serum phenylalanine was increased by
the active treatment phase. This provides reassurance about the toxicity of
aspartame, a food additive that contains phenylalanine, but argues against
precursor loading treatment of hyperactivity.
28. Freedman M.
Consumption of aspartame by heterozygotes for phenylketonuria [letter].
Journal of Pediatrics, 1987 Apr, 110(4):662-3.
29. Maher TJ.
Natural food constituents and food additives: the pharmacologic
connection.
Journal of Allergy and Clinical Immunology, 1987 Mar, 79(3):413-22.
itory monoamine neurotransmitters, the phenylalanine in
aspartame could conceiveably mediate neurologic effects. If mice are given
aspartame in doses that elevate plasma phenylalanine levels more than those
of tyrosine (which probably occurs after any aspartame dose in humans), the
frequency of seizures following the administration of an epileptogenic
drug, pentylenetetrazole, is enhanced. This effect is simulated by
equimolar phenylalanine and blocked by concurrent administration of valine,
which blocks phenylalanine's entry int

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