Aspartame

294.30300

294.30

616-062-2

Z0H242BBR1

758953

DTXSID0020107

Colorless needles from water|White crystalline powder from water or alcohol

2924299090

118.72000

-2.7

White powder or flake

1.28 g/cm3

246-247 °C

535.8ºC at 760 mmHg

277.8ºC

14.5 ° (C=4, 15mol/L Formic Acid)

The solubility of aspartame in water is dependent on pH and temperature, the maximum solubility is reached at pH 2.2 (20 mg/mL at 25 °C) and the minimum solubility at pH 5.2 (pHi) is 13.5 mg/mL at 25 °C.

Ventilated low temperature drying

2.6E-12mmHg at 25°C

TDLo orl-wmn: 3710 mg/kg:SKN AIMEAS 104,207,86

[α]D/20: + 14,5° to + 16,5°; Determine in a 4 in 100/15 N formic acid solution within 30 minutes after preparation of the sample solution

Odorless

Sweet

Between 4,5 and 6,0 (1 in 125 solution)

Henry's Law constant = 2.53X10-18 atm-cu m/mol at 25 °C (est)

pKa1 = 2.96 (carboxyl); pKa2 = 7.30 (amine) (est)

169.6 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|166.71 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|167.6 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|126.6 Ų [M-H]-

Dipeptide ester about 160 times sweeter than sucrose in aqueous solution

NONH for all modes of transport

2

S22-S24/25

WM3407000

Stable. Incompatible with strong oxidizing agents.

P260, P261, P264, P270, P271, P280, P302+P352, P304+P312, P304+P340, P312, P314, P322, P363, P501

H312

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Aspartame is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient.

WHO Food Additives Series 15. Aspartame. This monograph contains summaries of data on aspartame examined by JECFA in 1975, 1976, 1977 and 1980.[Available from, as of August 3, 2010; http://www.inchem.org/documents/jecfa/jecmono/v15je03.htm]|WHO Food Additives Series 16. Aspartame. In 1980 JECFA evaluated additional animal studies and several human studies and an ADI of 0-40 mg/kg bw for aspertame and an ADI of 0-7.5 mg/kg bw for its breakdown product, diketopiperazine, were established. Additional studies that have since become available are summarized and discussed in this monograph addendum.[Available from, as of August 3, 2010; http://www.inchem.org/documents/jecfa/jecmono/v16je03.htm]|European Food Safety Authority; Report of the Meetings on Aspartame with National Experts. Question Number. This report summarizes the deliberations of a group of National Experts that met in 2009 to review existing published and unpublished information on aspartame, identify possible data gaps and discrepancies in the information, and consider options to address any outstanding issues.[Available from, as of August 3, 2010: http://www.efsa.europa.eu/en/scdocs/doc/af100423.pdf]

Not Classified

Eye protection is recommended.

Mild gastrointestinal side effects including diarrhea have been reported.

... If mice are given aspartame in doses that elevate plasma phenylalanine levels more than those of tyrosine ... , 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...|Antimutagenic effects of combination of aspartame (0.4 and 4 mg/kg) and beta-carotene (0.15-15 mg/kg) were studied by estimation of chromosome aberrations in bone marrow cells of C57Bl/6 mice. Single and 5-day treatment with this combination decreased the clastogenic effects of dioxidine and cyclophosphamide and produced a more potent and universal antimutagenic effect than its constituents.|The purpose of the present study was to investigate analgesic and anti-inflammatory properties of aspartame, an artificial sweetener and its combination with various opioids and NSAIDs for a possible synergistic response. The oral administration of aspartame (2-16 mg/kg, po) significantly increased the pain threshold against acetic acid-induced writhes in mice. Co-administration of aspartame (2mg/kg, po) with nimesulide (2 mg/kg, po) and naproxen (5 mg/kg, po) significantly reduced acetic acid-induced writhes as compared to effects per se of individual drugs. Similarly when morphine (1 mg/kg, po) or pentazocine (1 mg/kg, po) was co-administered with aspartame it reduced the number of writhes as compared to their effects per se. Aspartame (4,8,16 mg/kg, po) significantly decreased carrageenan-induced increase in paw volume and also reversed the hyperalgesic effects in rats in combination with nimesulide (2 mg/kg, po). The study indicated that aspartame exerted analgesic and anti-inflammatory effects on its own and have a synergistic analgesic response with conventional analgesics of opioid and non-opioid type, respectively.|Ochratoxin A (OTA) is a mycotoxin produced by Aspergillus ochraceus as well as other molds. This mycotoxin contaminates animal feed and food. OTA is immunosuppressive, genotoxic, teratogenic, carcinogenic and is nephrotoxic in all animal species studied so far. OTA inhibits protein synthesis and induces lipid peroxidation. Since it seems impossible to avoid completely contamination of foodstuffs by toxigenic fungi, it is necessary to investigate the possible ways of limiting such toxicity. An attempt to prevent OTA-induced nephrotoxic and genotoxic effects, mainly the karyomegaly, has been made in vivo using aspartame (L-aspartyl-L-phenylalanine methyl ester), a structural analogue of both OTA and phenylalanine. Aspartame (25 mg/kg bw) prevented most of the nephrotoxic effects induced by OTA (289 ug/kg bw). It also showed some utility in preventing morphological and histological damage, mainly the karyomegaly.|For more Interactions (Complete) data for Aspartame (9 total), please visit the HSDB record page.

Conventional 2 year rodent cancer studies of aspartame are considered negative, although a small number of neoplasms of the brain were observed in a rat study. The NTP has explored the use of genetically altered mouse models as adjuncts to the 2 year rodent cancer assay. These models may prove to be more rapid, use fewer animals, and provide some mechanistic insights into neoplastic responses. As part of the evaluation of new mouse cancer screening models, aspartame was tested for potential toxicity and carcinogenicity in two relatively well-studied models, the Tg.AC hemizygous strain and the p53 haploinsufficient strain, and an uncharacterized model, the Cdkn2a deficient strain. Male and female Tg.AC hemizygous, p53 haploinsufficient, and Cdkn2a deficient mice were given feed containing aspartame (greater than 98% pure) for 9 months. Genetic toxicology studies were conducted in Salmonella typhimurium, rat bone marrow cells, and mouse peripheral blood erythrocytes. Groups of 15 male and 15 female Tg.AC hemizygous mice were fed diets containing 0, 3,125, 6,250, 12,500, 25,000, or 50,000 ppm aspartame (equivalent to average daily doses of approximately 490, 980, 1,960, 3,960, or 7,660 mg aspartame/kg body weight to males and 550, 1,100, 2,260, 4,420, or 8,180 mg/kg to females) for 40 weeks. Exposure to aspartame had no effect on survival. The mean body weights of 50,000 ppm females were greater than those of the controls from week 15 until the end of the study. Feed consumption by the exposed groups was similar to that by the control groups throughout the study. There were no neoplasms or nonneoplastic lesions that were attributed to exposure to aspartame. Groups of 15 male and 15 female p53 haploinsufficient mice were fed diets containing 0, 3,125, 6,250, 12,500, 25,000, or 50,000 ppm aspartame (equivalent to average daily doses of approximately 490, 970, 1,860, 3,800, or 7,280 mg/kg to males and 630, 1,210, 2,490, 5,020, or 9,620 mg/kg to females) for 40 weeks. Exposure to aspartame had no effect on survival or mean body weights. Feed consumption by the exposed groups was similar to that by the control groups throughout the study. No neoplasms or nonneoplastic lesions were attributed to exposure to aspartame. Groups of 15 male and 15 female Cdkn2a deficient mice were fed diets containing 0, 3,125, 6,250, 12,500, 25,000, or 50,000 ppm aspartame for 40 weeks (equivalent to average daily doses of approximately of approximately 490, 960, 1,900, 3,700, and 7,400 mg/kg to males and 610, 1,200, 2,390, 4,850, and 9,560 mg/kg to females). Survival of all exposed groups was similar to that of the control groups. Mean body weights of 3,125 and 6,250 ppm males were less than those of the controls after weeks 29 and 16, respectively. Mean body weights of female mice were similar to those of the controls throughout the study. The incidences of minimal to mild cytoplasmic vacuolization of periportal hepatocytes were significantly greater than controls in males exposed to 6,250, 25,000, or 50,000 ppm aspartame. Aspartame was tested for induction of gene mutations in Salmonella typhimurium. No mutagenicity was detected in strains TA98, TA100, or TA1535 with or without exogenous metabolic activation (S9). In addition, a single test in TA1537 with 30% rat liver S9 gave negative results. In TA97 with 30% rat liver S9, however, a reproducible small increase in mutant colonies was observed, and this response was judged to be equivocal. No mutagenicity was detected in TA97 without S9 or with hamster liver S9. An acute bone marrow micronucleus test was conducted with aspartame administered by gavage to male F344/N rats. No increase in micronucleated polychromatic erythrocytes was observed at any dose level. Peripheral blood micronucleus tests were conducted after 9 months exposure of Tg.AC hemizygous, p53 haploinsufficient, and Cdkn2a deficient mice to aspartame in dosed feed. Negative results were obtained in male and female Tg.AC hemizygous and Cdkn2a deficient mice. Negative results were also obtained with male p53 haploinsufficient mice. In female p53 haploinsufficient mice, the results of the micronucleus test were judged to be positive, based on a significant trend test and a small but statistically significant increased frequency of micronucleated erythrocytes in the 50,000 ppm group. Under the conditions of this 9-month feed study, there was no evidence of carcinogenic activity of aspartame in male or female p53 haploinsufficient mice exposed to 3,125, 6,250, 12,500, 25,000, or 50,000 ppm. Because this is a new model, there is uncertainty whether the study possessed sufficient sensitivity to detect a carcinogenic effect.

... There is some concern that phenylalanine released during the course of normal metabolism /of aspartame/ or generated during externally induced hydrolysis reactions may affect persons with phenylketonuria (PKU). About 1 in 10000 humans is afflicted with this genetically induced metabolic defect. As a result, they cannot metabolize phenylalanine and must restrict intake of this amino acid.|Aspartame is the methylester of a dipeptide composed of two amino acids, phenylalanine and aspartic acid. Persons with phenylketonuria, who must restrict carefully their phenylalanine intake, must be alerted to the presence of phenylalanine in the drug product and the amount of the ingredient in each dosage unit.|Persons suffering from phenylketonuria (phenylketonuria-homozygotes) on a phenylalanine restricted diet should avoid consumption of aspartame. Phenylketonuria homozygotes on the (less strict) phenylalanine liberalized diet should be made aware of the phenylalanine content of aspartame.|This study was designed to ascertain whether individuals with mood disorders are particularly vulnerable to adverse effects of aspartame. Although the protocol required the recruitment of 40 patients with unipolar depression and a similar number of individuals without a psychiatric history, the project was halted by the Institutional Review Board after a total of 13 individuals had completed the study because of the severity of reactions within the group of patients with a history of depression. In a crossover design, subjects received aspartame 30 mg/kg/day or placebo for 7 days. Despite the small n, there was a significant difference between aspartame and placebo in number and severity of symptoms for patients with a history of depression, whereas for individuals without such a history there was not. /It was/ concluded that individuals with mood disorders are particularly sensitive to this artificial sweetener, and its use in this population should be discouraged.

Aspartame's production and use as a non-nutritive sweetener(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 25(SRC), determined from a structure estimation method(2), indicates that aspartame is expected to have very high mobility in soil(SRC). Volatilization of aspartame from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.5X10-18 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Aspartame is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.8X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2010).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 25(SRC), determined from a structure estimation method(2), indicates that aspartame is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.5X10-18 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3.2(SRC), from an estimated log Kow of 0.07(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). The hydrolysis half-life of aspartame in water is about 1 day at 25 °C and pH 7(7). Biodegradation data were not available(SRC, 2010).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), aspartame, which has an estimated vapor pressure of 2.8X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase aspartame may be removed from the air by wet or dry deposition(SRC). Aspartame does not contain chromophores that absorb at wavelengths >290 nm(3), and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

Aspartame is expected to undergo hydrolysis in the environment. It is unstable in water and decomposes to diketopiperazine; the rate of decomposition is temperature and pH dependent(1). At 25 °C and a pH of 5 the half-life of decomposition is 245 days, but the value is 120 days at pH 6(1). At 25 °C and a pH of 7 and above, the decomposition of aspartame is about 1 day(1). Therefore, aspartame will be unstable in natural waters having pH 7 or higher(SRC). Aspartame does not contain chromophores that absorb at wavelengths >290 nm(2), and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3.2 was calculated in fish for aspartame(SRC), using an estimated log Kow of 0.07(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of aspartame can be estimated to be 25(SRC). According to a classification scheme(2), this estimated Koc value suggests that aspartame is expected to have very high mobility in soil.

The Henry's Law constant for aspartame is estimated as 2.5X10-18 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that aspartame is expected to be essentially nonvolatile from water surfaces(2). Aspartame is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.8X10-11 mm Hg(SRC), determined from a fragment constant method(3).

Occupational exposure to aspartame may occur through inhalation of dusts and dermal contact with this compound at workplaces where aspartame is produced or used(SRC). Use data indicate that the general population may be exposed to aspartame through the ingestion of food and beverages containing aspartame, and dermal contact with this compound(SRC). Aspartame is approved for use in carbonated beverages and as a packaged food additive(1).

Used as a diet supplement and sugar substitute.

Aspartame is used as an intense sweetening agent ... in pharmaceutical preparations including tablets, powder mixes, and vitamin preparations. It enhances flavor systems and can be used to mask some unpleasant taste characteristics; the approximate sweetening power is 80-200 times that of sucrose.

Aspartame is the methylester of a dipeptide composed of two amino acids, phenylalanine and aspartic acid. ... Persons with phenylketonuria, who must restrict carefully their phenylalanine intake, must be alerted to the presence of phenylalanine in the drug product and the amount of the ingredient in each dosage unit.|Excessive use of aspartame should be avoided by patients with phenylketonuria.|Aspartic acid and sodium glutamate were both neuroexcitatory amino acids which had an additive toxic effect on hypothalamic neurones. As this might be specially damaging to young children, who already receive sodium glutamate in gram quantities in their diet, aspartame should not generally be added to children's food.|Reported adverse effects include: headaches; grand mal seizure; memory loss; gastrointestinal symptoms; and dermatological symptoms. However, scientifically controlled peer-reviewed studies have consistently failed to produce evidence of a causal effect between aspartame consumption and adverse health events ...|For more Drug Warnings (Complete) data for Aspartame (8 total), please visit the HSDB record page.

Aspartame (L-alpha-aspartyl-L-phenylalanine methyl ester) is a low-calorie sweetener used to sweeten a wide variety of low- and reduced-calorie foods and beverages, including low-calorie tabletop sweeteners. Aspartame is composed of two amino acids, aspartic acid and phenylalanine, as the methyl ester. Aspartic acid and phenylalanine are also found naturally in protein containing foods, including meats, grains and dairy products. Methyl esters are also found naturally in many foods such as fruits and vegetable and their juices. Upon digestion, aspartame breaks down into three components (aspartic acid, phenylalanine and methanol), which are then absorbed into the blood and used in normal body processes. Neither aspartame nor its components accumulates in the body. These components are used in the body in the same ways as when they are derived from common foods.

Substances that sweeten food, beverages, medications, etc., such as sugar, saccharine or other low-calorie synthetic products. (From Random House Unabridged Dictionary, 2d ed) (See all compounds classified as Sweetening Agents.)

Absorbed in the small intestine, aspartame is metabolized and absorbed very quickly.

Approximately 10% of aspartame (by weight) is broken down into methanol in the small intestine. Most of the methanol is absorbed and quickly converted into formaldehyde. Approximately 50% of aspartame (by weight) is broken down into phenylalanine. Approximately 40% of aspartame (by mass) is broken down into aspartic acid.|Unlike some other intense sweeteners, aspartame is metabolized in the body and consequently has some nutritive value: 1 g provides approx 17 kJ (4 kcal). However, in practice, the small quantity of aspartame consumed provides a minimal nutritive effect.|The use of aspartame has been of some concern owing to the formation of the potentially toxic metabolites methanol, aspartic acid, and phenylalanine. Of these materials, only phenylalanine is produced in sufficient quantities, at normal aspartame intake levels, to cause concern.|Aspartame [SC-18862; 3-amino-N-(alpha-carboxyphenethyl) succinamic acid, methyl ester, the methyl ester of aspartylphenylalanine] is a sweetening agent that organoleptically has about 180 times the sweetness of sugar. The metabolism of aspartame has been studied in mice, rats, rabbits, dogs, monkeys, and humans. The compound was digested in all species in the same way as are natural constituents of the diet. Hydrolysis of the methyl group by intestinal esterases yielded methanol, which was oxidized in the one-carbon metabolic pool to CO2. The resultant dipeptide was split at the mucosal surface by dipeptidases and the free amino acids were absorbed. The aspartic acid moiety was transformed in large part to CO2 through its entry into the tricarboxylic acid cycle. Phenylalanine was primarily incorporated into body protein either unchanged or as its major metabolite, tyrosine.|Although aspartame was hydrolyzed in the gut of the monkey to its constituent moieties, methanol, aspartic acid, and phenylalanine, the ingestion of 15 or 60 mg/kg doses for 10 days did not modify phenylalanine metabolism. Aspartame had little effect on the disappearance of iv admin (14)C-phenylalanine from the plasma, it did not substantially affect the conversion of phenylalanine into tyrosine or carbon dioxide, and it did not alter the rate of incorporation of label into protein. The majority of phenylalanine derived from aspartame was incorporated into body protein, with only 20-25% of the compound being excreted. 60-80% of the derived methanol and aspartic acid was oxidized to carbon dioxide.|For more Metabolism/Metabolites (Complete) data for Aspartame (7 total), please visit the HSDB record page.

At room temperature, aspartame is most stable at pH 4.3, where its half-life is nearly 300 days. At pH 7, its half-life is shortened to only a few days.

180 to 200 times sweeter than sucrose, it is metabolized as a protein and its subsequent amino-acids used up in there respective mechanisms.

Diketopiperazine

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ Although aspartame has been reported to cause hyperactivity and behavioral problems in children, a double-blind controlled trial of 48 preschool-age children fed diets containing a daily intake of 38 +/- 13 mg/kg bw of aspartame for 3 weeks showed no adverse effects attributable to aspartame, or dietary sucrose, on children's behavior or cognitive function.|/HUMAN EXPOSURE STUDIES/ Neurobehavioral symptoms have been reported anecdotally with aspartame. This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or behavioral functioning in normal individuals. Forty-eight healthy volunteers completed a randomized, double-blind, placebo-controlled, crossover study. The first month was aspartame free. Subjects then consumed sodas and capsules with placebo, aspartame, or sucrose for 20 days each. Order was randomized and subjects were assigned to either a high- (45 mg/kg bw/day) or low- (15 mg/kg bw/day) dose aspartame group. Neuropsychologic and laboratory testing was done on day 10 of each treatment period to determine possible acute effects and on day 20 for possible chronic effects. Plasma phenylalanine concentrations increased significantly during aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure. Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults.|/HUMAN EXPOSURE STUDIES/ OBJECTIVE: To determine the effects of large doses of aspartame on behavior, cognition, and monoamine metabolism in children with attention deficit disorder. DESIGN: A randomized, double-blind, placebo-controlled crossover study of unmedicated children meeting Diagnostic and Statistical Manual of Mental Disorders (3rd ed) criteria for attention deficit disorder. SETTING: Behavioral assessments were performed in the child's home by their parents and in the classroom by a teacher. Cognitive tests were administered and blood drawing was performed during a 2-day inpatient admission to our Children's Study Center. INTERVENTIONS: Administration of aspartame (single morning dose, 34 mg/kg) or placebo for alternate 2-week periods. MAIN OUTCOME MEASURES: Behavioral and cognitive tests included the Matching Familiar Figures Test (MFFT), Children's Checking Task (CCT), the Airplane Test, the Wisconsin Card Sorting Test (WCST), the Subjects Treatment Emergent Symptom Scale (STESS), the Multigrade Inventory for Teachers (MIT), and the Conners Behavior Rating Scale. Blood was drawn for complete blood cell count and liver function tests, as well as amino acid, methanol, formate, serotonin, and monoamine metabolite analyses, and urine was collected for measurement of catecholamine and monoamine metabolite excretion. RESULTS: No clinically significant differences between aspartame and placebo were found for the STESS, MIT, or Conners ratings, or for the MFFT, CCT, WCST, or Airplane cognition tests. Also, no differences were noted for any of the biochemical measures, except for the expected increase in plasma phenylalanine and tyrosine following aspartame. CONCLUSIONS: The findings indicate that aspartame at greater than 10 times usual consumption has no effect on the cognitive and behavioral status of children with attention deficit disorder. In addition, aspartame does not appear to affect urinary excretion rates of monoamines and metabolites.|/HUMAN EXPOSURE STUDIES/ The effect of aspartame on the learning, behavior, and mood of children was evaluated in two experiments. After an overnight fast and a standard breakfast, 20 healthy 9- to 10-year-old children were given the treatments in a double-blind crossover design at 10:30 AM. Lunch was served at 12:00 noon. In experiment 1, the treatment consisted of an ice slurry of strawberry Kool-Aid containing 1.75 g/kg of carbohydrate (polycose) plus either aspartame (34 mg/kg) or the equivalent sweetness as sodium cyclamate and amino acids as alanine. In experiment 2, the treatment consisted of a drink of cold unsweetened strawberry Kool-Aid, containing either 1.75 g/kg of sucrose or 9.7 mg/kg of aspartame. Measures of associative learning, arithmetic calculation, activity level, social interaction, and mood were unaffected by treatment in experiment 1. In experiment 2, the only significant treatment effect was that on the frequency of minor and gross motor behaviors, which were less frequent after the consumption of sucrose than after aspartame. Thus, the effect of aspartame on the short-term behavior of healthy 9- to 10-year-old children appears to be related to its absence of metabolic consequences rather than to its amino acid composition and putative neurochemical impact.|For more Human Toxicity Excerpts (Complete) data for Aspartame (32 total), please visit the HSDB record page.

Aspartame

(1992) 8,040 tons in US

As a table-top sweetener ... /aspartame/ is spray-dried with partially hydrolyzed corn starch.|Canderel /Formulation name/|Equal /Formulation name/|NatraTaste /Formulation name/|For more Formulations/Preparations (Complete) data for Aspartame (9 total), please visit the HSDB record page.

food additive - sweetener|L-Phenylalanine, L-.alpha.-aspartyl-, 2-methyl ester: ACTIVE|Aspartame is the methylester of a dipeptide composed of two amino acids, phenylalanine and aspartic acid. When these two amino acids are so combined to form aspartame (1-methyl N -L-a-aspartyl-L-phenylalanine), they produce an intensely sweet-tasting substance, approximately 180 times as sweet as sucrose.|A combination of aspartame with either granular or fused mannitol in a 1:9 ratio can provide a suitable base for chewable tablets with respect to sweetness, mouth feel, absence of unpleasant aftertaste, and low caloric value. Both compounds are compatible with leucine.|... In the July 26, 1974, decision by the FDA to approve the use of aspartame, labeling provisions were made in which foods not containing protein or intended for admixture to protein sweetened with aspartame should bear the statement "contains protein."

PURITY OF ASPARTAME WAS DETERMINED USING THIN LAYER CHROMATOGRAPHY, LIQ CHROMATOGRAPHY, AND OPTICAL ROTATION.|ASPARTAME WAS ANALYZED BY LIQUID CHROMATOGRAPHY.

Food additives|Food Additives -> SWEETENER; -> JECFA Functional Classes|Cosmetics -> Masking

Food Additives -> SWEETENER;