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