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What is the evidence from human subjects research that aspartame consumption is associated with adverse effects in the general population?

Conclusion Statement

Aspartame consumption is not associated with adverse effects in the general population. Studies have found no evidence of a wide range of adverse effects of aspartame including hypersensitivity reactions, elevated blood methanol or formate levels, and hematopoietic or brain cancers. Neurological changes tested included cognitive functions, seizures, headaches and changes in memory or mood.

The 2009 update did not find new studies meeting the inclusion criteria for this question and the N&NNS workgroup (2009) concurs with the conclusion above formulated by the Aspartame workgroup (2008).

Evidence Summary

The American Dietetic Association (ADA) uses only human studies published in peer-reviewed journals for its Evidence Analysis Library (EAL®). Many studies have been done in animal models and thus do not meet criteria for inclusion in the Library.

The Food and Drug Administration (FDA) has approved the use of aspartame and it is considered to be safe. Aspartame has also been approved for use in more than 90 other countries, including Canada, the European Union, Japan, Australia and New Zealand. Given the wide distribution of use of aspartame, continued post-marketing surveillance for possible adverse effects and additional research on the safety of aspartame has been conducted.
Sixteen peer-reviewed, human-subject research studies were considered for this evidence analysis question. Subjects were mostly young and middle-aged adults, including both men and women.

There were 11 randomized controlled trials (RCTs):

In a positive research quality study, Garriga et al, 1991 investigated potential hypersensitivity reactions in 20 subjects ages 15 to 51 years (40% male) who had reported suspected aspartame hypersensitivity reactions that included urticaria, GI distress, rhinitis or wheezing. A single-blind aspartame challenge of increasing dosage (zero, 10, 100, 500, 1,000 and 2,000mg at 30-minute intervals) was administered to the subjects and 11 control subjects (27% male of whom five were normal and six were considered “atopic”). Hives developed in only one patient during the single-blind challenge, but two subsequent double-blind challenges were negative. The authors concluded it was difficult to recruit subjects with a history of hypersensitivity reactions, and that those who believed themselves to be allergic did not have reproducible reactions.

In a study of positive research quality designed to test whether aspartame was causative of urticaria, Geha, 1993 tested 21 subjects (19% male) by administering three doses of aspartame (50mg at 8 A.M., followed by 300mg at 10 A.M., followed by 600mg aspartame plus 7.5mg B-aspartame plus 15mg diketopiperazine at 12 P.M.). 17 of the 21 who completed the study had no positive reactions. Of the four who had urticaria, two each had the reaction after either aspartame or placebo. Thus, there was no significant difference in incidence of positive reactions between placebo and aspartame (P=1.0). In addition, 10 subjects reported a total of 17 other adverse events, including throat tightness, light-headedness, feeling warm, dyspnea, nausea, headache, small hives, pruritis, periorbital swelling, nasal congestion and slight tingling of the tongue. However, there were no significant differences between aspartame and placebo challenges for these reported side effects (P=0.289).

In a study of positive research quality, Knopp et al, 1976 tested the use of aspartame during weight reduction. In this toxicity study of chronic aspartame ingestion, particular attention was given to possible long-term effects of aspartame on the fuel hormonal alterations characteristically caused by weight reduction. As a group, mean age was 19.3 years. Mean body weight and height were 164 pounds and 65.4 inches, respectively. Subjects were an average of 33% in excess of ideal body weight. The aspartame dose was 2.7g per day and was compared on a double-blind randomized basis with a lactose placebo. Both materials were given in gelatin capsules and subjects followed a calculated 1,000-calorie diet for 13 weeks. Subjects who received aspartame lost 6.9±1.5 pounds while the placebo group lost 4.5±1.2 pounds (no significant difference between the two groups). After an overnight fast, glucose and immunoreactive insulin decreased in both groups. Rising trends in immunoreactive glucagon were observed. These changes are all characteristic of calorie restriction. In no instance was there a detectable effect of the ingested aspartame. No meaningful effect of weight reduction or aspartame was seen on plasma triglyceride and cholesterol, nor on any other parameter of hematologic, hepatic or renal function that was measured. Similarly, side effects were equally distributed between aspartame and placebo.

In a double-blind randomized crossover trial of neutral research quality, Lapierre et al, 1990 tested 10 healthy volunteers (six men, four women, ages 21 to 36 years) to evaluate the effect of a single dose of aspartame (15mg per kg body weight) or placebo capsules on mood, cognitive function and reaction time. No effect was observed on hunger, headache, memory, reaction time or cognition during the study despite elevation of plasma phenylalanine levels after consumption of aspartame (data values not reported). The percentage of tryptophan to total LNAA (leucine, isoleucine, valine, tyrosine and phenylalanine) was increased from approximately 11% to a peak of approximately 18% at the two-hour time point after dosing, but dropped to normal after eight hours.

In a study of positive research quality, Leon et al, 1989, examined the effects of chronic aspartame consumption in 108 healthy adult volunteers, ages 18 to 62 years. This was a randomized, double-blind, placebo-controlled, parallel-group design. Participants included 57 women and 51 men, randomly assigned to either the aspartame (N=53) or placebo (N=55) groups. Exclusion criteria were well-defined and included body weight more than 20% above normal range. Subjects consumed three capsules per day containing either 300mg aspartame or 300mg microcrystalline cellulose plus 0.9mg silicon dioxide for 24 weeks. Compliance was monitored. The approximate dose of aspartame was 75mg per kg body weight per day. Extensive clinical laboratory measurements were conducted at baseline and after three, six, nine, 12, 18 and 24 weeks. Measurements included body weight, vital signs, complete blood cell count, serum chemistry of 18 standard parameters, and plasma lipids after a 12-hour fast. In addition, metabolic studies evaluated levels of plasma amino acids, blood methanol and formate, and urinary formate and creatinine. The results indicated no differences between groups in body weight, vital signs, blood lipid levels, urinalysis results or incidence of complaints. No difference was found in fasting plasma levels of 22 amino acids, including aspartic acid and phenylalanine, or the ratio of phenylalanine to large neutral amino acids. Plasma tyrosine levels were higher in the aspartame group during weeks three and 24 than in the control group, but were still within the normal values range. Blood methanol concentrations were usually below detection limits (0.31mmol per L); however, one individual in the aspartame group had a methanol concentration of 1.0mmol per L and one in the control group had a level of 0.84mmol per L. These levels are well below the concentration of blood methanol associated with methanol toxicity, which is greater than 100mmol per L. Serum folate, urinary and blood formic acid and urinary calcium levels were unchanged in both groups.

In a study of positive research design, Rowan et al, 1995 designed a randomized, double-blind, placebo-controlled, crossover study to assess seizure induction after aspartame ingestion in self-reported aspartame-sensitive individuals. Targeted recruitment was conducted of individuals who had complained of experiencing a seizure in response to aspartame to government officials or the manufacturer and through nearly 9,000 neurologists. After four years of recruitment, only 16 adults and two children participated in the study. Continued recruitment for another five years did not locate additional subjects despite reports of large numbers of individuals experiencing seizures. In this study, subjects received 50mg per kg body weight aspartame or an identical placebo in three divided doses throughout the day on days two and four. EEG recordings were performed for five consecutive days. All meals were uniformly standardized on treatment days. No clinical seizures were observed in subjects during the study. Electrographic seizures were recorded in two subjects on days consuming the placebo. Sleep variables were also measured, but no effect of aspartame was observed. Plasma phenylalanine levels, and the ratio of phenylalanine to large neutral amino acids, were increased on the day of aspartame dosing, but returned to normal on the following day. The major limitation of this study was the small number of participants.

In an RCT of positive research quality, Ryan-Harshman et al, 1987 did two experiments. In the first, 13 subjects received multiple doses of aspartame (zero, 0.84, 2.54 or 5.04g). Food intake at lunch was not significantly different (mean energy consumed, percentage of carbohydrate, percentage of protein, percentage of fat were relatively constant) between placebo or aspartame. There were no differences in mood or arousal in the healthy males ages 20 to 35 years. Results were similar when 13 subjects were given five or 10g aspartame in a second experiment.

In a study of positive research quality, Schiffman et al, 1987 conducted a well-controlled, double-blind crossover study. The investigators housed 40 inpatients (12 males, 28 females; ages 19 to 69 years) who had reported having headaches each time they consumed aspartame. Participants were monitored for two days, and then challenged with capsules of aspartame (30mg per kg body weight) or placebo (microcrystalline cellulose) on days three and five, with day four being a washout day. Diet and extraneous variables were controlled. There was no evidence of an effect of aspartame, as incidence of headache after consumption of aspartame (35%) was similar to after the placebo (45%).

Spiers et al, 1988 investigated cognitive, neurophysiologic and behavioral effects of consuming aspartame for 20 days in a study of positive research quality. A group of 48 healthy volunteers (24 males, 24 females, ages 18 to 34 years) participated in a three-way crossover double-blind study with treatments consisting of aspartame, sucrose and placebo. 24 participants received a high dose of aspartame (45mg per kg body weight per day) and the remaining received 15mg per kg body weight per day. Acute effects were evaluated on day 10 of each treatment arm, with testing starting 90 minutes after consumption of test material. Chronic effects were evaluated on day 20. Plasma phenylalanine levels increased dose-dependently with aspartame consumption, but no other effects were observed.

In a study of positive research quality, Stokes et al, 1991 investigated the effect of aspartame on cognitive performance. 12 healthy certified pilots (four females and eight males) were tested five times, with at least one week between treatments given in random order among the 12 participants. Participants were pre-tested for baseline values, then given either placebo capsules (dextrose), aspartame (50mg per kg body weight), or ethyl alcohol (positive control, estimated dose to raise blood alcohol 0.1%), followed by a post-test with no treatment. Cognitive performance was tested using the SPARTANS cognitive test battery, which is a sensitive test to detect changes in performance of complex tasks required for aircraft operations. All participants consumed a small carbohydrate meal prior to treatments. Consumption of other foods, aspartame and alcohol was controlled prior to testing. Blood levels of amino acids were not measured. Cognitive impairment was detected in several tasks following consumption of the low dose of alcohol but not with aspartame or placebo treatments.

In a follow-up study of positive research quality, Stokes et al, 1994 employed a more complex battery of tests (SPARTANS Version 2) to test the effect of chronic exposure to aspartame on cognitive performance and blood phenylalanine levels. 12 subjects (college students, gender not defined) received aspartame capsules (50mg per kg body weight per day) for nine days, placebo capsules as a negative control (dextrose), and an acute dose of ethyl alcohol to achieve 0.1% blood ethanol levels. All participants received the placebo and ethanol treatments once and the aspartame treatment twice within a seven-day interval. Blood phenylalanine and breath alcohol levels were measured. On the last day of treatment periods, when subjects completed the cognitive testing, blood alcohol levels were 0.0% during all treatments except following the alcohol treatment when it averaged 0.09%. Plasma phenylalanine levels averaged 59.08μmol following placebo treatments and 121.5μmol following aspartame consumption. 47 task variables were measured and significant differences between pre- and post-test results and aspartame treatment were detected for three tasks. For those tasks, there was an improvement, rather than impairment, of function in participants following the aspartame treatments. The authors attribute the finding of enhanced performance after aspartame treatment to chance, and conclude that although aspartame given at high doses (50mg per kg body weight per day) approximately doubled plasma phenylalanine levels, there is no evidence of impaired cognitive performance. Following ethanol treatments, participants scored lower on 14 tasks.

One cohort study was reviewed.

Lim et al 2006, in a prospective cohort study (quality rating positive), investigated the association between self-reported consumption of aspartame-containing beverages and incident hematopoietic and brain cancers in the prospective NIH-AARP Diet and Health study. During 1995 and 1996, 3.5 million baseline questionnaires were mailed to members of the American Association of Retired Persons (AARP), ages 50 to 71 years old, living in eight study areas. 473,984 questionnaires met inclusion criteria for the study (285,079 men, 188,905 women). All participants included in the study had been free of cancer for five years prior to submitting the questionnaire. Daily aspartame intake was estimated from results of a self-administered food frequency questionnaire included as part of the baseline questionnaire, and calibrated against two 24-hour recalls. Aspartame intake was reported as consumption of soda, fruit drinks, sweetened ice tea and aspartame added to tea or coffee during the past year. Participants were stratified to one of six aspartame intake levels: (none, more than zero to less than 100mg per day, 100 to less than 200mg per day, 200 to less than 400mg per day, 400 to less than 600mg per day, 600mg or more per day.

Participants were followed-up for five years (1995 to 2000, up to 5.2 years) to determine the incidence of hematopoietic cancers and gliomas and their subtypes. 1,888 cases of hematopoietic cancers and 315 malignant gliomas were ascertained from Cancer Registry data. There was no association between increased intake of aspartame and hematopoietic cancers (RR≥600mg per day 0.98, 95% CI: 0.76 to 1.27) or malignant gliomas (RR≥400mg per day 0.73, 95% CI: 0.46 to 1.15).

The investigators concluded that their findings do not support the hypothesis that increased use of aspartame increases hematopoietic or brain cancer risk. The authors stated that their study had many strengths, including a large sample size. They said that their study was limited by use of self-reported food frequency questionnaire data, which may be subject to a substantial amount of measurement error. The study was also limited by a small number of subjects (less than 1%) in the high-intake group (greater than 1,200mg per day).

One non-randomized clinical trial was reviewed.

In a positive research quality study designed to investigate sleepiness and mood changes in 120 young college women ages 18 to 30, Pivonka and Grunewald, 1990 compared the effect of water and aspartame- and sugar-containing beverages on mood in 120 young women and found no effect on self-reported surveys of mood.

Link to explanation of the relationship of aspartame, methanol and formaldehyde.

Three review articles were included:

One review article examined the role of non-nutritive sweeteners in the development of cancer.
  • Weihrauch and Diel, 2004 (neutral quality) found no evidence that aspartame presents a carcinogenic risk in humans in a review of literature.
One review article examined general toxicity data:
  • Butchko and Stargel, 2001 (neutral quality), reviewed post-marketing surveillance studies and the results of focused clinical studies of potential health issues related to aspartame. There was no evidence of adverse effects related to aspartame consumption.
One review article reported on the use of non-nutritive sweeteners in pregnancy. The authors reported that the use of non-nutritive sweeteners during pregnancy is safe unless the woman is homozygous for PKU.
  • London, 1988 (negative quality), in a review article, addressed the issue of the safety of using both saccharin and aspartame in pregnancy. PKU and abnormality in the body's ability to convert phenylalanine into tyrosine is of concern for the developing fetus. The author concluded that foods and beverages sweetened with aspartame pose no hazard to the mother or fetus unless she is homozygous for PKU.

View full table in new window
Author, Year,
Study Design,
Number of Subjects Age Population Dose of Aspartame Side Effect Tested Results
Butchko HH et al, 2001 

Study Design: Narrative Review

Class: R 

Rating: Neutral







Varied among studies.


Review of research on safety since regulatory approval of aspartame.

1984-1992; detailed menu census surveys, from more than 2,000 households per year, were monitored for a 14-day survey.


The results of the intake studies, despite differences in methodology, demonstrated consistent intakes in various countries that were well below the ADI.

The totality of scientific evidence clearly demonstrates that even in amounts many times what people typically consume, aspartame is safe.

Garriga MM, Berkebile C et al, 1991 

Study Design: Randomized Controlled Trial

Class: A 

Rating: Neutral

Control N=11 (three males, eight females); suspected aspartame-sensitive group: N=20 (eight males, 12 females).


Age range 15 to 51 years; no age reported for 12 patients confirmed with sensitivity.


Cases: Individuals who reported sensitivity to aspartame; controls (atopic individuals).


Aspartame challenge: Food-grade aspartame administered each 30 minutes with increasing doses (zero, 10, 100, 500, 1,000 and 2,000mg).


Hypersensitivity reactions (urticaria, GI distress, rhinitis, wheezing).


No patient complaints during double-blind challenge; one patient developed hives during single-blind challenge; two subsequent double-blind challenges negative; one patient's complaint of throat tightness during single-blind challenge.

Geha R, Buckley CE et al, 1993 

Study Design: Randomized Crossover Trial

Class: A 

Rating: Positive

21 (17 female, four male).


10 to 55 years (mean 34±12 years). 


History of urticaria or angioedema within 12 hours of ingestion of an aspartame-containing product during the previous three years; history of chronic urticaria, which resolved without medication on cessation of aspartame consumption and recurred when consumption was resumed; positive histamine skin test result.


Capsule with 50mg aspartame at 8:00 A.M., followed by capsule with 300mg aspartame at 10:00 A.M., followed by capsule with 600mg aspartame at 12:00 P.M. This last dose was accompanied by 7.5mg aspartame + 15mg DKP (diketopiperazine). Both of these compounds are present in aspartame-containing products and were included to evaluate the possibility that allergic/hypersensitivity-type reactions could be caused by them, rather than by the parent compound.




17 of the 21 who completed the study had no positive reactions during study; four subjects had urticaria during the study; two of four with urticaria had urticaria after placebo but not aspartame. No statistically significant difference in incidence of positive reactions (P=1.000) between aspartame and placebo challenges. Ten subjects had total of 17 other adverse events (throat tightness, light-headed, warm feeling, dyspnea, nausea, headache, small hives, pruritis, periorbital swelling, nasal congestion, slight tingling of tongue). No statistically significant differences (P=0.289) between aspartame and placebo challenges for adverse experiences.

Knopp 1976 

Study Design: Randomized Controlled Trial

Class: A 

Rating: Positive

59 (55 completed study).


Mean age 19.3 years.


Healthy young people, primarily nursing students (Note: Age range was from 10 to 21; however, since mean age was 19.3 years, this study was included in adult question).


Three 300mg aspartame capsules administered three times per day for a total of 2.7g of aspartame per day for 13 weeks; 2.7g approximately four times the anticipated daily intake of ordinary use during weight loss.


Toxicity of chronic aspartame ingestion in overweight children.


Aspartame is without detectable effect in this setting.

Lapierre KA, Greenblatt DJ et al, 1990 

Study Design: Randomized Crossover Trial

Class: A 

Rating: Neutral

14 subjects. Final N=10 (six males, four females), for dropout rate of 29%.


21 to 36 years, mean 26.3 years.


Healthy volunteers.


Aspartame (15mg per kg of body weight) or placebo capsules were taken with orange juice after an overnight fast; subjects refrained from drugs, alcohol and aspartame for 72 hours.


Hunger, sedation, changes in cognitive function, memory and reaction time.


No significant differences between aspartame and placebo were found in measures of sedation, hunger, headache, mood, reaction time, cognition or memory at any time during the study. Plasma phenylalanine levels were significantly higher after aspartame (P<0.01) than with placebo between one and six hours post-dosage, reaching a maximum difference of +3.36 mmol per dL at two hours. Plasma glucose concentrations were not significantly different between aspartame and placebo.

Leon AS, Hunninghake DB et al, 1989 

Study Design: Randomized Crossover Trial

Class: A 

Rating: Positive

108 (57 females).


31.4±1.3 years for aspartame group; 29.5±1.4 for placebo group.


Students, faculty and staff at a midwestern university.


300mg aspartame or placebo three times per day with meals for 24 weeks (approximately 75mg per kg per day or 1.5 times the FDA's acceptable intake).


Blood methanol levels, serum folate levels, physical side effects.


There was no consistent pattern of occurrence of reported physical symptoms and no significant differences between control and study group in total number of symptoms, number of symptoms per subject, laboratory abnormalities or changes from baseline laboratory values and measures. Most blood methanol concentrations were less than detectable level of 0.31mmol per L. Two individuals who had the highest levels, one from the aspartame group and one from the control group, were both well below toxic levels. Serum folate levels during the study were unchanged in both groups.

Lim U, Subar AF et al, 2006 

Study Design: Retrospective Cohort Study

Class: B 

Rating: Positive

3.5 million questionnaires mailed by authors.


50 to 71 years.


AARP (American Association of Retired Persons) members.


Consumption of aspartame (divided into cohorts based on aspartame content per 100g beverage, determined by self-administered baseline questionnaire including a food frequency questionnaire (FFQ) calibrated against two 24-hour recalls).


Hematopoietic and brain cancers.


Findings did not support the hypothesis that aspartame increases hematopoietic or brain cancer risk.

London RS, 1988 

Study Design: Narrative Review

Class: R 

Rating: Negative







Varied among studies.


A review of some currently available information on the safety in pregnancy with recommendations formulated on their use in the periconceptional period and pregnancy.


Primarily animal studies: saccharine and aspartame are generally safe to consume during pregnancy (unless mother is homozygous for PKU, when aspartame is unsafe).

Pivonka EEA, Grunewald KK, 1990 

Study Design: Non-Randomized Controlled Trial

Class: C 

Rating: Positive

120 females.


18 to 30 years of age.


Young college women.


12 ounces of water, aspartame-sweetened beverage (180mg to 280mg aspartame) or sugar-sweetened beverage (50g sucrose).


Sleepiness, mood changes.


Sleepiness was induced in young women after ingestion of a sucrose-containing beverage in the afternoon hours. The aspartame-sweetened beverage did not affect any of the mood states tested in our study.

Rowan AJ et al, 1995 

Study Design: Randomized controlled trial

Class: A 

Rating: Positive

18 subjects: 16 adults and two children.


Two children, age 10 and 15 years; 16 adults, age 20 to 70 years (mean 35 years).


159 recruitment letters were sent to individuals who had become known to the FDA, CDC or the NutraSweet Company and who claimed to have experienced seizures after consuming aspartame or who had come to our attention as a result of canvassing of 8,760 adult and pediatric neurologists by letter.


50mg per kg dose. The total dose was divided into three equal doses administered at 8:00 A.M., 10:00 A.M. and 12:00 P.M.




No clinical seizures or adverse experiences were seen during the course of the study.

Ryan-Harshman et al 1987 

Study Design:

Class: A 

Rating: Positive

13 males.


20 to 35 years.


Healthy men.


Multiple doses of aspartame (zero, 0.84, 2.54 or 5.04g).


Mean energy consumed, percentage of carbohydrate, percentage of protein, percentage of fat, mood, arousal after consuming varying amounts of aspartame.


No significant differences among any endpoints tested.

Schiffman SS, Buckley CE et al, 1987 

Study Design: Randomized Crossover Trial

Class: A 

Rating: Positive

N=40 (70% female).


18.8 to 68.9 years (range), mean 33.5±1.90.


Individuals who had reported headache (to FDA or manufacturer) after aspartame use.


10mg per kg of 98% pure aspartame given three times during one of two challenge days.




Incidence rate of headache after aspartame (35%) was not significantly different from that after placebo (45%), P<0.50. 

Spiers PA et al, 1998 

Study Design: Randomized Crossover Trial

Class: A 

Rating: Positive

48 (24 males, 24 females).


18 to 35 years.


Healthy graduate or undergraduate college students.


High (45mg per kg of body weight) or low (15mg per kg of body weight) doses of aspartame.


Cognitive, neurophysiologic or behavioral functioning.


No effect on neuropsychologic, neurophysiologic or behavioral functioning in healthy young adults.

Stokes AF, Belger A et al, 1991 

Study Design: Randomized Controlled Trial

Class: A 

Rating: Neutral

12 certified pilots, 4 female/8 male.




Airline pilots.


Placebo capsules (dextrose), aspartame (50mg per kg body weight), or ethyl alcohol (positive control, estimated dose to raise blood alcohol 0.1%).


Effect of aspartame on cognitive performance.


Cognitive impairment was detected in several tasks after consumption of the low dose of alcohol, but not with aspartame or placebo treatments.

Stokes et al 1994 

Study Design: Randomized Controlled Trial

Class: A 

Rating: Positive

12 (gender not defined).


College students.


Young adults.


Aspartame capsules (50mg per kg body weight per day) for nine days, placebo capsules (dextrose) as a negative control, and an acute dose of ethyl alcohol to achieve 0.1% blood ethanol levels

All participants received the placebo and ethanol treatments once and the aspartame treatment twice within a seven-day interval.


The effect of chronic aspartame exposure on cognitive performance and blood phenylalanine levels.


Although aspartame given at high doses (50mg per kg body weight per day) approximately doubled plasma phenylalanine levels, there is no evidence of impaired cognitive performance.

Following ethanol treatments, participants scored lower on 14 tasks.

Weihrauch MR, Diehl V, 2004 

Study Design: Narrative Review

Class: R 

Rating: Neutral







Varied among studies.


Compared animal and human studies for cancer.


There is no evidence that the artificial sweetener aspartame bears a carcinogenic risk.


Quality Rating Summary
For a summary of the Quality Rating results, click here.
Butchko HH, Stargel WW. Aspartame: scientific evaluation in the postmarketing period. Regul Toxicol Pharmacol. 2001 Dec; 34 (3): 221-233. PMID: 11754527.

Garriga MM, Berkebile C, Metcalfe DD. A combined single-blind, double-blind, placebo-controlled study to determine the reproducibility of hypersensitivity reactions to aspartame. J Allergy Clin Immunol. 1991 Apr; 87 (4): 821-827.

Geha R, Buckley CE, Greenberger P, Patterson R, Polmar S, Saxon A, Rohr A, Yang W, Drouin M. Aspartame is no more likely than placebo to cause urticaria/angioedema: Results of a multicenter, randomized, double-blind, placebo-controlled, crossover study. J Allergy Clin Immunol. 1993 Oct; 92 (4): 513-520.

Knopp RH, Brandt K, Arky RA. Effects of aspartame in young persons during weight reduction. J Toxicol Environ Health. 1976 Nov; 2 (2): 417-428.

Lapierre KA, Greenblatt DJ, Goddard JE, Harmatz JS, Shader RI. The neuropsychiatric effects of aspartame in normal volunteers. J Clin Pharmacol. 1990; 30 (5): 454-460.

Leon AS, Hunninghake DB, Bell C, Rassin DK, Tephly TR. Safety of long-term large doses of aspartame. Arch Intern Med. 1989 Oct; 149 (10): 2,318-2,324.

Lim U, Subar AF, Mouw T, Hartge P, Morton LM, Stolzenberg-Solomon R, Campbell D, Hollenbeck AR, Schatzkin A. Consumption of aspartame-containing beverages and incidence of hematopoietic and brain malignancies. Cancer Epidemiol Biomarkers Prev. 2006 Sep; 15 (9): 1,654-1,659.

London RS. Saccharin and aspartame. Are they safe to consume during pregnancy? J Reprod Med. 1988 Jan; 33 (1): 17-21.

Pivonka EEA, Grunewald KK. Aspartame- or sugar-sweetened beverages: effects on mood in young women. J Am Diet Assoc. 1990; 90: 250-254.

Rowan AJ et al. Aspartame and seizure susceptibility: results of a clinical study in reportedly sensitive individuals. Epilepsia. 1995 Mar; 36 (3): 270-275.

Ryan-Harshman M, Leiter LA, Anderson H. Phenylalanine and aspartame fail to alter feeding behavior, mood and arousal in men. Physiology and Behavior. 1987; 39(2): 247-253.

Schiffman SS, Buckley CE III, Sampson HA, Massey EW, Baraniuk JN, Follett JV, Warwick ZS. Aspartame and susceptibility to headache. N Engl J Med. 1987 Nov 5; 317(19): 1,181-1,185.

Spiers PA et al, Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects. Am J Clin Nutr. 1998 Sep; 68 (3): 531-537.

Stokes AF, Belger A, Banich MT, Taylor H. Effects of acute aspartame and acute alcohol ingestion upon the cognitive performance of pilots. Aviat Space Environ Med. 1991; 62: 648-653.

Stokes AF, Belger A, Banich MT, Bernadine E. Effects of alcohol and chronic aspartame consumption upon performance in aviation relevant cognitive tasks. Aviation, Space and Environmental Medicine. 1994; 65(1): 7-15.

Weihrauch MR, Diehl V. Artificial sweeteners-do they bear a carcinogenic risk? Annals of Oncology, 2004, 15: 1,460-1,465.

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