Review of findings since regulatory approval over 20 years ago.
MRCA Information Services began monitoring aspartame in the U.S.
- 1984-1992: Detailed menu census surveys from over 2,000 households per year were monitored for a 14-day survey. Data were by age groups: zero to 23 months, two to five years, six to 12 years, 13 to 17 years and 18 years and over, as well as all age groups together. Intake of children was of concern due to their smaller body weights, as they may consume more of an additive on a milligram-per-kilogram basis than adults.
Aspartame Intake (Mg per Kg of Body Weight per Day) in the U.S. 90th Percentile, 14-Day Average for Eaters from 1984 to 1992 (Butcko et al, 1994)
Dates of Survey
Two to Five Years
Individuals on a Reducing Diet
Women of Child-Bearing Age
- Average daily intake over the 14-day period for the general population of aspartame eaters in the 90th percentile ranged from 1.6 to 3.0mg per kg of body weight per day from 1984 to 1992
- Children, diabetics, people on weight reduction and females of child-bearing age consumed about 5% to 10% of the ADI in the U.S. (50mg per kg of body weight)
- Other data from the USDA on CSFII have found similar results.
Intake: European Countries
Virtanen et al, 1988: Almost three quarters of the diabetic children surveyed in Finland consume aspartame-containing products. Mean intake was 1.15mg per kg of body weight per day, less than 3% of the ADI in Europe (40mg per kg of body weight).
Chambolle et al, 1994: Reported that from 1991 to 1992, intake was 0.6mg and 1.0mg per kg of body weight per day at the 90th and 95th percentiles. Study was limited due to no data for food consumed outside the home and some categories were missing.
Garnier-Sagne et al, 2001: Insulin-dependent diabetic children from two years to 20 years old were evaluated with a five-day dietary questionnaire. Intakes were mean, 2.4, 97.5th percentile, 7.8 and a maximum 15.6mg per kg of body weight per day. All sugar-free products were assumed to contain only one sweetener at its maximum level, whereas many products are blends of several sweeteners.
Bar, Biermann, 1992: Survey conducted in 1988 and 1989 found the 90th percentile of average daily intake was 2.75mg per kg of body weight per day for aspartame.
Leclercq et al, 1999: Teenagers who were known to be users of diet products had estimated average intakes of aspartame intakes of 0.03mg per kg of body weight per day. Maximum intake was 0.39mg per kg of body weight per day.
Hulshof, Bouman, 1995: A food frequency questionnaire showed mean estimated intake was 2.4mg per kg of body weight per day. Intake at the 95th percentile was 7.5mg per kg of body weight per day. Food intake records showed the mean and 95th percentile intakes were 1.9mg and 7.5mg per kg of body weight per day, respectively.
Bergsten 1993: Average estimated intake varied from 0.9mg to 3.4mg per kg of body weight per day among males and females of various age groups.
Hinson, Nicol, 1992: Survey from 1988 found aspartame consumption at the 90th percentile was 4% of the ADI (40mg per kg of body weight per day). Children and diabetics ingested about 7% and 6%, respectively.
MAFF, 1995: In 1994, the 97.5th percentile of asparatame consumption in diabetics who would likely be frequent consumers of aspartame was about 10.1mg per kg of body weight per day, only 25% of the ADI.
Intake: Other Countries
Australia National Food Authority, 1995: Mean consumption was about 6% to 7% of the ADI for a seven-day survey.
Toledo and Ioshi 1995: Aspartame intake at the median by users of intense sweeteners was 2.9% of the ADI. Intakes at the median by diabetics and individuals on weight control diets were 1.02mg per kg of body weight per day (2.6% of the ADI and 1.28mg per kg of body weight per day (3.2% of the ADI).
Heybach, Ross, 1989: General population of aspartame eaters consumed 5.5mg per kg of body weight per day during cold weather months and 5.9mg during warm weather months in 1987. Children and special populations consumed from 5.5mg to 11.4mg per kg of body weight per day.
The safety of aspartame was evaluated through extensive monitoring of intake, post-marketing surveillance of anecdotal reports of alleged health effects and additional research to evaluate these anecdotal reports.
Actual intake levels of aspartame were monitored from 1984 to 1992.
Through dietary surveys in the U.S., average daily aspartame intake at the 90th percentile (eaters only) in the general population ranged from about two mg to three mg per kg of body weight. Consumption by two- to five-year-old children in these surveys ranged from about 2.5mg to 5.0mg per kg of body weight per day. Aspartame intake has also been estimated in other countries. Although survey methodologies differed among these evaluations, aspartame intake is remarkably consistent across studies and is well below the ADI.
The post-marketing surveillance of reports of adverse health effects allegedly associated with aspartame was the first such evaluation for a food additive. Extensive monitoring and evaluation of these reports over many years led to the conclusion that the reported symptoms generally were mild and common in the general population. There was no evidence to suggest a causal relationship with aspartame.
Leon et al, 1989: A long-term clinical study using high doses of aspartame (75mg per kg per day for 24 weeks or about 25 to 30 times current consumption levels at the 90th percentile) resulted in no significant differences in clinical or biochemical parameters or adverse experiences, compared with a placebo.
Koehler, Glaros, 1988: Reported the results of an outpatient study to evaluate the effect of aspartame on the occurrence of migraine headaches in migraineurs and concluded that aspartame caused a significant increase in the frequency of headaches, but not the intensity or duration of headaches.
Van Den Eeden et al, 1994: Reported that subjects had more days with headaches, but there was no difference in the length or intensity of headaches.
Schiffman et al, 1987: When individuals who were convinced that aspartame had caused their headaches were evaluated in a randomized double-blind, placebo-controlled study in the controlled environment of the Clinical Research Unit at Duke University, aspartame (at a dose about 10 times the 90th percentile consumption) was no more likely than a placebo to elicit headache.
Kulczycki, 1986: Reported a single case report of an individual who believed he was allergenic to asparatame.
Geha et al, 1993: Reported the results of a multi-center randomized double-blind placebo-controlled crossover study done with individuals who were convinced they were allergenic to aspartame. Concluded that aspartame and its conversion products are no more likely than a placebo to cause allergic-type reactions.
Garriga et al, 1991: Study demonstrated that alleged allergic-type reactions to aspartame were not reproducible under blinded conditions.
Human studies have demonstrated that even massive doses of aspartame, many times those typically consumed, have no effect on cognitive performance, mood or behavior, when compared with a placebo. These include the following: Wolraich et al, 1985, 1994; Ferguson et al, 1986; Goldman et al, 1986; Milich, Pelham, 1986; Kruesi et al, 1987; Ryan-Harshman et al, 1987; Lieberman et al, 1988; Dodge et al, 1990; Lapierre et al, 1990; Saravis et al, 1990; Stokes et al, 1991, 1994; Shawywitz et al, 1994; Trefz et al, 1994; Spiers et al, 1988.
Camfield and co-workers, 1992: A study of children with absence seizures reported that aspartame, compared with sugar, may increase the amount of EEG spike-wave activity.
Shaywitz et al, 1994b: Reported the results of a four-week study in children with seizure disorders, including absence seizures. After a dose about 10 times the 90th percentile intake levels, aspartame neither provoked nor exacerbated seizures nor altered EEG activity, compared to placebo.
Stegink et al, 1977, 1979, 1980: Consumption of aspartame-sweetened foods does not increase plasma phenylalanine concentrations beyond those which normally occur post-prandially.
Butchko, Kotsonis, 1989, 1991: Aspartame yields about 10% methanol by weight. The amount of methanol released from aspartame is well below normal dietary exposure to methanol from fruits, vegetables and juices.
Stegink et al, 1981, 1983: Aspartame in amounts many times those consumed from products does not significantly change baseline blood concentrations of methanol or formate.
FDA, 1996: Has established acceptable levels of exposure to methanol at 7.1mg to 8.4mg per kg per day for 60kg adults. Thus, acceptable dietary exposure to methanol is about 25 times potential exposure to methanol, following a 90th percentile consumption of aspartame.
Olney et al, 1996: Claimed that the reported increase rate of brain tumors in the U.S. may be associated with the marketing of aspartame. The allegations by Olney and co-workers regarding brain tumors and aspartame have been evaluated by scientists at government and regulatory agencies in the U.S., United Kingdom, the European Union, Australia and Brazil and concluded that aspartame does not cause brain tumors.
Gurney et al, 1997: A case-control study (subjects 19 years of age or older, who were diagnosed with a primary brain tumor between 1984 and 1991), which evaluated aspartame consumption and the risk of childhood brain tumors, found that children with brain tumors were no more likely to have consumed aspartame than control children nor was there any elevated risk from maternal consumption of aspartame during pregnancy.
The results of these studies confirm that aspartame is safe and not associated with adverse health effects.
In the post-marketing period, the safety of aspartame was further confirmed through extensive monitoring of intake vs. the ADI, post-marketing surveillance of anecdoctal reports of adverse health effects and post-marketing research to evaluate these allegations and other scientific issues in controlled scientific studies.
The results of the intake studies, despite differences in methodology, demonstrated consistent intakes in various countries that were well below the ADI. Analysis of the post-marketing surveillance consumer reports of adverse health effects revealed no consisitent pattern of symptoms that could be causally related to consumption of aspartame as well as the results of scientific studies.
The totality of scientific evidence clearly demonstrates that even in amounts many times what people typically consume, aspartame is safe: Stegink, Filer, 1984; American Medical Association, 1985; Stegink, 1987; Janssen, van der Heijden, 1988; Butchko, Kotsonis, 1989; Fischer, 1989; Sze, 1989; Fernstrom, 1991; Jobe, Dailey, 1993; Lajtha et al, 1994; Tschanz et al, 1996.
Quality Criteria Checklist: Review Articles
|1.||Will the answer if true, have a direct bearing on the health of patients?||Yes|
|2.||Is the outcome or topic something that patients/clients/population groups would care about?||Yes|
|3.||Is the problem addressed in the review one that is relevant to dietetics practice?||Yes|
|4.||Will the information, if true, require a change in practice?||Yes|
|1.||Was the question for the review clearly focused and appropriate?||Yes|
|2.||Was the search strategy used to locate relevant studies comprehensive? Were the databases searched and the search termsused described?||No|
|3.||Were explicit methods used to select studies to include in the review? Were inclusion/exclusion criteria specified andappropriate? Wereselectionmethods unbiased?||No|
|4.||Was there an appraisal of the quality and validity of studies included in the review? Were appraisal methodsspecified,appropriate, andreproducible?||No|
|5.||Were specific treatments/interventions/exposures described? Were treatments similar enough to be combined?||Yes|
|6.||Was the outcome of interest clearly indicated? Were other potential harms and benefits considered?||Yes|
|7.||Were processes for data abstraction, synthesis, and analysis described? Were they applied consistently acrossstudies and groups? Was thereappropriate use of qualitative and/or quantitative synthesis? Was variation in findings among studies analyzed? Were heterogeneity issued considered? If data from studies were aggregated for meta-analysis, was the procedure described?||No|
|8.||Are the results clearly presented in narrative and/or quantitative terms? If summary statistics are used, are levels ofsignificance and/or confidence intervals included?||Yes|
|9.||Are conclusions supported by results with biases and limitations taken into consideration? Are limitations ofthe review identified anddiscussed?||No|
|10.||Was bias due to the review's funding or sponsorship unlikely?||Yes|