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At least 19 recordsLinked to original sources
PubMed1995

Postingestive inhibition of food intake by aspartame: importance of interval between aspartame administration and subsequent eating.

Aspartame administered in capsules (i.e., without tasting) 1 h before a meal significantly reduces the amount eaten in that meal. In the present study 36 young men and women were divided into 3 groups of 12 to receive aspartame (400 mg) or placebo (400 mg starch) on separate occasions either 5 min (Group A), 30 min (Group B) or 60 min (Group C) before beginning an ad lib test meal. Compared with placebo, aspartame reduced food intake in Group C (by 18.5%, p < 0.01), but did not reliably affect intake in Groups A or B. There were, in contrast, no significant effects of aspartame on premeal ratings of hunger, desire to eat or fullness for any of the groups. These results confirm a postingestive inhibitory action of aspartame on appetite, which may involve the amplification of the satiating effects of food. The lack of effect of aspartame administered at the shorter intervals before eating suggests a postgastric or even postabsorptive mechanism of action. This observation is also important in its implications for the possible therapeutic exploitation of the anorexic effect of capsulated aspartame.

Adolescent↗
PubMed1988

Administration of aspartame potentiates pentylenetetrazole- and fluorothyl-induced seizures in mice.

An association has recently been proposed between the incidence of seizures and prolonged consumption of the phenylalanine-containing artificial sweetener, aspartame. Since consumption of aspartame, unlike dietary protein, can elevate phenylalanine in brain, and thereby inhibit the synthesis and release of neurotransmitters known to protect against seizure activity, the effect of oral doses of aspartame on the sensitivity of mice to the proconvulsant agents, pentylenetetrazole and fluorothyl was studied. Doses of aspartame were used which increased phenylalanine more than tyrosine in brain, as occurs in humans after the consumption of any dose of aspartame. Pretreatment with aspartame significantly increased the percentage of animals convulsing after administration of pentylenetetrazole and significantly lowered the CD50 for this convulsant. The average time to onset of seizures induced by fluorothyl in control mice was 510 sec; pretreatment with oral doses of 1000, 1500 and 2000 mg/kg of aspartame 1 hr earlier significantly reduced the time required to elicit seizures (394, 381 and 339 sec, respectively). The seizure-promoting effect of aspartame could be demonstrated 30, 60 or 120 min after the 1000 mg/kg dose. The seizures induced by either convulsant were potentiated by equimolar amounts of phenylalanine, a major endogenous metabolite of aspartame, while the other metabolites, aspartic acid and methanol, were without effect. Administration together with aspartame of the large neutral amino acid valine, which competes with phenylalanine for entry into the brain, completely abolished the seizure-promoting effect of aspartame.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Behavioral assessment of the toxicity of aspartame.

Six experiments with rats assessed the toxicity of aspartame with behavioral measures. The first three experiments used a conditioned taste aversion procedure since taste aversions are typically observed after a taste is followed by a toxin. Thirty min after thirsty rats drank a sweet solution they were intraperitoneally injected (Experiment 1) or intragastrically intubated (Experiment 2) with saline or 176, 352, or 704 mg/kg of aspartame. Relative to rats given saline, rats injected with 704 and 352 mg/kg aspartame showed strong and mild aversions, respectively. Rats injected with 176 mg/kg of aspartame or intubated with any dose of aspartame did not show taste aversions. In Experiment 3, rats voluntarily consumed an aspartame solution sweetened with saccharin for 7 hr each day. Consumption of the taste paired with aspartame was not reduced. When 352 mg/kg aspartame was injected (Experiment 4), but not when intubated (Experiment 5), 5 min prior to access to a running wheel, running was reduced. Wheel running was not affected by the voluntary consumption of aspartame (Experiment 6). The route of administration effect (intraperitoneal vs. intragastric) on behavior corresponded with the amino acid levels in blood plasma (Experiment 7). Aspartate, phenylalanine, tyrosine and glutamate levels increased more after the injection, than the intubation, of aspartame (176 mg/kg). Overall, the results suggest that aspartame may have adverse effects when intraperitoneally injected but not when the route of administration is oral.

Amino Acids↗
PubMed1993

Aspartame is no more likely than placebo to cause urticaria/angioedema: results of a multicenter, randomized, double-blind, placebo-controlled, crossover study.

BACKGROUND: Anecdotes and single case reports have suggested that the high-intensity sweetener, aspartame, may be associated with allergic/hypersensitivity-type reactions. METHODS: We conducted a multicenter, placebo-controlled clinical study to evaluate individuals who had experienced urticaria and/or angioedema allegedly associated with ingestion of an aspartame-containing product. Despite extensive recruiting efforts over 4 years, only 21 subjects could be enrolled. After admission to clinical research units, subjects were given aspartame and placebo in a randomized, double-blind, crossover fashion. Subjects received, on different days, increasing doses (50, 300, 600 mg) of aspartame and placebo at 8:00 AM, 10:00 AM, and noon. Subjects who weighed less than 40 kg received one half of these doses. Conversion products of aspartame, aspartyl-phenylalanine diketopiperazine and beta-aspartame, were also included in the aspartame arm of the study. Positive reactions were defined as urticaria (hives with wheals 4 mm or more in diameter with a collective diameter of at least 15 mm or one or more hives with a wheal of 4 mm or greater with a flare of 8 mm or greater) or as angioedema. RESULTS: According to these criteria, four reactions were observed; two followed aspartame ingestion and two followed placebo ingestion (p = 1.00). The incidence of other adverse experiences was no different after aspartame versus placebo ingestion (p = 0.289). CONCLUSION: These results indicate that aspartame and its conversion products are no more likely than placebo to cause urticaria and/or angioedema reactions in subjects with a history consistent with hypersensitivity to aspartame.

Administration, Oral↗
PubMed1988

Aspartame: review of recent experimental and observational data.

In this report the neurotoxicity of aspartame and its constituent amino acids aspartic acid and phenylalanine is reviewed. The adverse reactions ascribed to the consumption of aspartame-containing products, as reported in the U.S.A., are discussed and placed in perspective with the results of recent behavioural studies in humans and animals. The issue of common intake levels associated with proposed uses of aspartame is addressed. In brief, the following conclusions can be drawn: When aspartame is consumed at levels within the ADI-limit of 40 mg/kg body wt, there is no significant risk for an aspartate-induced neurotoxic effect in the brain. When aspartame is consumed at levels within the ADI-limit by normal subjects or persons heterozygous for phenylketonuria (PKU) the resultant plasma phenylalanine concentrations are practically always within the normal postprandial range; elevation to plasma concentrations commonly associated with adverse effects has not been observed. Persons suffering from phenylketonuria (PKU-homozygotes) on a phenylalanine-restricted diet should avoid consumption of aspartame. PKU-homozygotes on the (less strict) phenylalanine-liberalized diet should be made aware of the phenylalanine content of aspartame. In the available behavioural studies in humans with acute dosing, no adverse effects were observed. Long-term studies on behaviour and cognitive function in (sensitive) humans are lacking. Analyses of adverse reaction reports made by consumers in the U.S.A. have not yielded a specific constellation of symptoms clearly related to aspartame that would suggest a widespread public health hazard associated with aspartame use. Focussed clinical studies are now being carried out in the U.S.A.; the results should provide additional evidence concerning the interpretation of the reports on adverse reactions ascribed to aspartame. In the regulation of admitted uses for aspartame the possibility of intake levels exceeding the ADI-limit in some groups of consumers should be a point of attention.

Animals↗
PubMed1998

Aspartame ingestion increases urinary calcium, but not oxalate excretion, in healthy subjects.

Aspartame is the artificial sweetener most extensively used as a substitute for glucose or sucrose in the food industry, particularly in soft drinks. As glucose ingestion increases calciuria and oxaluria, the two main determinants of urinary calcium-oxalate saturation, we considered it worthwhile to determine whether aspartame ingestion also affects calcium-oxalate metabolism. Our study compares the effects of the ingestion of similarly sweet doses of aspartame (250 mg) and glucose (75 g) on calcium and oxalate metabolisms of seven healthy subjects. Urinary calcium excretion increased after the intake of both aspartame (+86%; P < 0.01) and glucose (+124%; P < 0.01). This may be due to the rise in calcemia observed after both aspartame (+2.2%; P < 0.05) and glucose ingestion (+1.8%; P < 0.05). The increased calcemia may be linked to the decrease in phosphatemia that occurred after both aspartame (P < 0.01) and glucose (P < 0.01) load. Aspartame did not alter glycemia or insulinemia, whereas glucose intake caused striking increases in both glycemia (+59%; P < 0.001) and insulinemia (+869%; P < 0.01). Although insulin was considered the main calciuria-induced factor after glucose load, it is unlikely that this mechanism played a role with aspartame. Urinary oxalate excretion did not change after aspartame, whereas it increased (+27%; P < 0.05) after glucose load. Thus, as aspartame induced a similar increase in calciuria as did glucose but, conversely, no change in oxaluria, substituting glucose by aspartame in soft drinks may appear to be of some potential benefit.

Administration, Oral↗
PubMed1991

Further analysis of the short-term inhibition of food intake in humans by the dipeptide L-aspartyl-L-phenylalanine methyl ester (aspartame).

It was reported previously that the dipeptide sweetener aspartame suppresses food intake in humans by a postingestive action. The present study examined the hypothesis that this is due to an effect of phenylalanine, one of the primary breakdown products of aspartame (phenylalanine is a potent releaser of the so-called satiety hormone cholecystokinin, CCK). Capsulated aspartame (400 mg) administered to human volunteers reduced food intake by 15% (253 kcal) in a lunchtime test meal begun 1 hour later. However, neither phenylalanine (200 mg) nor the other constituent amino acid of aspartame, aspartic acid (200 mg), altered intake compared with placebo. Despite the large effect on food intake there were no treatment differences in pre- or postmeal ratings of motivation to eat. This suggests that aspartame may act to intensify the satiating effects of ingested food. Although high doses of phenylalanine reduce food intake, an individual action of phenylalanine cannot account for the potent anorexic effect of aspartame. In discussing alternative mechanisms it is noted that the amino acid sequence of aspartame (Asp-Phe) is the same as the C-terminal dipeptide of CCK. A direct action of aspartame at CCK receptors appears to be unlikely; however, aspartame might act as CCK releaser. Further studies are required to elucidate the mechanism of aspartame's anorexic action and perhaps to evaluate its therapeutic potential as an antiobesity agent.

Adult↗
PubMed2001

Aspartame effect in sickle cell anemia.

OBJECTIVE: To examine the in vitro and in vivo attributes of aspartame and to determine its efficacy for treating sickle cell anemia. RATIONALE: Aspartame (l-aspartyl-l-phenylalanine methyl ester) binds with 2 human Bence Jones proteins. The proteins (Mcg and Sea) showed phenylalanine penetrating into hydrophobic binding sites. This aspartame property suggested a potential to interfere with sickle hemoglobin fibril formation. METHODS: For the in vitro studies, blood from 20 subjects monitored for sickle cell anemia was collected in heparinized tubes. Specimens were divided in thirds and aspartame was added to 2 tubes to yield a 1 mg/mL or 2 mg/mL concentration. Sickled cells that were present after a drop from each aliquot was added to a fresh 2% metabisulfite solution were counted 3 times. For the in vivo studies, 23 subjects from the Sickle Cell Clinic (University of Oklahoma Health Sciences Center, Oklahoma City, Okla) consented to participate in a randomized single-dose administration of 1.5, 3.0, or 6 mg/kg aspartame. Heparinized blood was obtained at 0, 30, 60, 120, 240, 480, and 1440 minutes after aspartame administration. Specimens were counted in a blinded manner by means of the technique used for the in vitro method, but a photomicrograph of 1 field from each triplicate count was made. The pictures were marked and were computer counted. RESULTS: For the in vitro studies, sickled cells decreased from 28% to < 14% when 1 mg/mL aspartame was added and decreased further with 2 mg/mL. For the in vivo studies, a decreased number of sickled cells in homozygous blood (HbSS) were observed after oral administration of aspartame. Sickling was inhibited by 6 mg/kg aspartame for at least 6 hours in 15 subjects with HbSS anemia. CONCLUSIONS: Further evaluations of the efficacy of aspartame for sickle crisis and crisis prevention appears to be warranted.

Administration, Oral↗
PubMed1990

Effect of sucrose on the metabolic disposition of aspartame.

Twelve normal adult subjects ingested a beverage providing 0.136 mmol aspartame/kg body wt on 2 different days. On 1 study day the beverage provided only aspartame, on the other the beverage provided both aspartame and 3.51 mmol sucrose/kg body wt. The high mean plasma phenylalanine concentrations were similar after administration of aspartame alone (158 +/- 28.9 mumol/L, mean +/- SD) and administration of aspartame plus sucrose (134 +/- 44.1 mumol/L). Evaluation of the area under the plasma concentration-time curve (AUC) for phenylalanine also showed no significant difference between groups (197 +/- 49.1 vs 182 +/- 28.3 mumol.L-1.h for aspartame alone and aspartame plus sucrose, respectively). Similarly, the high mean ratio of phenylalanine to large neutral amino acids (Phe:LNAA) in plasma did not differ significantly (0.265 +/- 0.046 for aspartame alone, 0.275 +/- 0.107 for aspartame plus sucrose). However, there was a small but significant difference between groups for the 4-h AUC values for plasma Phe:LNAA. The simultaneous ingestion of sucrose with aspartame had only minor effects on aspartame's metabolic disposition.

Adult↗
PubMed1994

Aspartame ingestion and headaches: a randomized crossover trial.

To examine whether ingestion of aspartame is associated with headaches, we conducted a double-blind crossover study using volunteers with self-identified headaches after using aspartame. Of the 32 subjects randomized to receive aspartame (approximately 30 mg/kg/d) and placebo in a two-treatment, four-period crossover design, 18 completed the full protocol, seven completed part of the protocol before withdrawing due to adverse effects, three withdrew for other reasons, two were lost to follow-up, one was withdrawn due to noncompliance, and one withdrew and gave no reason. Each experimental period was 7 days long. Subjects reported headaches on 33% of the days during aspartame treatment, compared with 24% on placebo treatment (p = 0.04). Subjects who were "very sure" prior to the study that aspartame triggered some of their headaches reported larger treatment differences (aspartame = 0.37 headache-days, placebo = 0.18 headache-days; p < 0.001) than subjects who were "somewhat sure" (aspartame = 0.29 headache-days, placebo = 0.22 headache-days; p = 0.51) or "not sure" (aspartame = 0.33 headache-days, placebo = 0.39 headache-days; p = 0.51). There was no significant treatment difference in the length or intensity of headaches or in the occurrence of side effects associated with the headaches. This experiment provides evidence that, among individuals with self-reported headaches after ingestion of aspartame, a subset of this group report more headaches when tested under controlled conditions. It appears that some people are particularly susceptible to headaches caused by aspartame and may want to limit their consumption.

Adult↗
PubMed1994

Neuropsychological and biochemical investigations in heterozygotes for phenylketonuria during ingestion of high dose aspartame (a sweetener containing phenylalanine).

Aspartame, a high intensity sweetener, is used extensively worldwide in over 5,000 products. Upon ingestion, aspartame is completely metabolized to two amino acids and methanol (approximately 50% phenylalanine, 40% aspartic acid, and 10% methanol). The effects of aspartame on cognitive function, electroencephalograms (EEGs) and biochemical parameters were evaluated in 48 adult (21 men, 27 women) heterozygotes for phenylketonuria (PKUH), PKUH subjects whose carrier status had been proven by DNA analysis ingested aspartame (either 15 or 45 mg/kg/day) and placebo for 12 weeks on each treatment using a randomized, double-blind, placebo-controlled, crossover study. A computerized battery of neuropsychological tests was administered at baseline weeks -2 and -1, and during treatment at weeks 6, 12, 18, and 24. Samples for plasma amino acids and urinary organic acids were also collected during these visits. EEGs were evaluated by conventional and spectral analysis at baseline week -1 and treatment weeks 12 and 24. The results of the neuropsychological tests demonstrated that aspartame had no effect on cognitive function. Plasma phenylalanine significantly increased, within the normal range for PKUH, at 1 and 3 h following the morning dose of aspartame in the group receiving the 45 mg/kg per day dose only. There were no significant differences in the conventional or spectral EEG analyses, urinary organic acid concentrations, and adverse experiences when aspartame was compared with placebo. This study reaffirms the safety of aspartame in PKUH and refutes the speculation that aspartame affects cognitive performance, EEGs, and urinary organic acids.

Adolescent↗
PubMed1990

Aspartame ingested without tasting inhibits hunger and food intake.

The effects on motivation to eat and food intake of administering small amounts of aspartame (234 to 470 mg: lower dose equivalent to the amount of aspartame contained in 1-2 cans of some soft drinks) in capsules to human volunteers were examined in two separate experiments (the second was a replication of the first). The results provided clear evidence of a prominent postingestive inhibitory action of aspartame on appetite: consumed in capsules, aspartame reduced subsequent food intake and, to a lesser extent, motivation to eat. The mechanism underlying this effect has yet to be elucidated. A possibility is that the release of cholecystokinin by phenylalanine, a constituent of aspartame, is involved. A further result was that drinking aspartame-sweetened water did not reliably reduce motivational ratings or food intake (in the first experiment aspartame ingested in capsules significantly reduced food intake compared with the same amount ingested as a sweet drink). One interpretation of these together with previous findings is that the response to consuming aspartame is determined by at least two interacting influences: an inhibitory postingestive effect and a stimulatory effect of its sweet taste. In turn, the relative potency of these influences may be modified by certain other features of the aspartame-sweetened food or drink (e.g., its nutrient content). Another implication of these results is that it cannot be assumed that intense sweeteners will all have equivalent effects on appetite.

Administration, Oral↗
PubMedDate not supplied

Effects of perinatal exposure to aspartame on rat pups.

Possible effects of perinatal exposure to L-aspartyl-L-phenylalanine methyl ester (aspartame) on rat pups were investigated. Adult female rats, and later their pups, were exposed, via their drinking water, to aspartame (0.007%, 0.036%, 0.18% or 0.9% w/v) or phenylalanine (0.45% w/v) for 12 days prior to conception until the pups were 38 days old. Control rats were given plain water. The adults exposed to aspartame consumed an average of 14, 68, 347 and 1614 mg/kg/day of aspartame and those exposed to phenylalanine consumed an average of 835 mg/kg/day of phenylalanine. After weaning the pups given aspartame consumed an average of 32, 154, 836, and 3566 mg/kg/day of aspartame and those given phenylalanine consumed an average of 1795 mg/kg/day of phenylalanine. No effect of aspartame or phenylalanine was detected on either two measures of morphological development (i.e., latencies to pinnae detachment and eye opening) or two tests of reflex development (i.e., latencies for surface righting at 7 days of age and negative geotaxis at 8 days of age). All groups were similar in spatial memory as assessed with two different mazes with pups 30-36 days old. The number of arms before reentry in an 8-arm radial-arm maze and the acquisition curves from a milk maze did not differ between groups. Furthermore, the latencies of mothers to retrieve their litters was also unaffected by the aspartame and phenylalanine. These results indicate that perinatal exposure to aspartame, when voluntarily consumed by mothers (14-1614 mg/kg/day) and later directly by the rat pups (32 to 3566 mg/kg/day) does not affect reflex development, morphological development or spatial memory.

Animals↗
PubMed1998

Treatment of osteoarthritis with aspartame.

OBJECTIVE: The binding of sweet-tasting compounds in a human (Mcg) Bence-Jones dimer has been characterized by x-ray crystallography. Aspartame binding in this immunoglobulin fragment is remarkable. Unexpected pain relief noted by A.B.E., a crystallographer with diagnosed osteoarthritis, suggested that the accommodation of aspartame in the active site of the dimer may represent surrogate binding by other proteins, with analgesia as the outcome. METHODS: X-ray analysis of the complex of aspartame and the Bence-Jones dimer was conducted with crystalline Mcg protein and pure aspartame. A single-blind (n = 1) study to confirm analgesia was completed by administration of aspartame to A.B.E. A controlled double-blind trial was performed in patients with x-ray-documented osteoarthritis. Pain and performance changes were evaluated with use of two doses of placebo and two doses of aspartame. Effects on bleeding time were then evaluated by determination of template bleeding times in 34 normal volunteers. Finally, antipyretic effects were studied in Sprague-Dawley rats given intramuscular turpentine injections. RESULTS: Aspartame binding in the Bence-Jones dimer was verified by x-ray crystallography. Improvements in performance and pain relief were observed in A.B.E. at p < 0.001. Decreased pain and improved performance were also observed in patients with osteoarthritis (p < 0.001). Mild antihemostatic responses were observed in bleeding times after aspartame treatment. Modified template bleeding times increased at p < 0.01. Aspartame blocked the turpentine-mediated febrile responses in the treated rats (p < 0.01). CONCLUSIONS: L-Aspartyl-L-phenylalanine methyl ester is biologically active and appears to relieve pain, induce mild antithrombotic effects in humans, and decrease fever in animals.

Animals↗
PubMed1998

Determination of aspartame and its degradation and epimerization products by capillary electrophoresis.

Two capillary zone electrophoretic assays using run buffers of pH 9.35 and pH 2.70 have been developed for the determination of aspartame (alpha-L-Asp-L-PheOMe) and its potential degradation products including Phe, PheOMe, 5-benzyl-3,6-dioxo-2-piperazineacetic acid (DKP), the dipeptides Asp-Phe and Phe-Asp, as well as the isomeric beta-aspartame (beta-L-Asp-L-PheOMe). As an uncharged species at pH 2.7 DKP could not be determined. Between pH 2.0 and 3.5 the resolution of the diastereomers of aspartame and beta-aspartame was investigated. While the resolution of the epimeric beta-isomers exhibited a plateau between pH 2.3 and 2.7, resolution of the aspartame diastereomers peaked at pH 3.0. Using salicylic acid and Phe-Gly as internal standards at pH 9.35 and 2.70, respectively, linear calibration curves were obtained for a concentration range between 5 micrograms ml-1 and 1 mg ml-1. The R.S.D. for intraday and interday analysis ranged from 1.0 to 3.6% and 1.5% to 9.1%, respectively. The capillary electrophoresis assays were applied to analyze aspartame solutions heated to 70 degrees C. In agreement with the literature data aspartame was found to be less stable at pH 7 compared to pH 3. In contrast to aspartame itself, an approximate 20% epimerization of beta-aspartame was observed in the incubation mixtures.

Aspartame↗
PubMed1984

Effects of aspartame and glucose administration on brain and plasma levels of large neutral amino acids and brain 5-hydroxyindoles.

Administration of the artificial sweetener aspartame (L-aspartylphenylalanylmethyl ester; 200 mg/kg) by gavage to rats caused large increments in brain and plasma levels of phenylalanine and its product tyrosine. Glucose administration (3 g/kg, by gavage, a dose sufficient to cause insulin-mediated reductions in plasma levels of the large neutral amino acids leucine, isoleucine, and valine) also elevated brain phenylalanine and tyrosine, and enhanced the increments caused by the aspartame, nearly doubling the rise in brain phenylalanine. Each animal's brain phenylalanine or tyrosine levels were highly correlated (r = 0.97 and 0.99, respectively) with its plasma phenylalanine or tyrosine ratios, affirming that aspartame's effects on the brain amino acids result from the changes it produces in plasma composition. As described previously, glucose consumption increased brain tryptophan levels, and consequently, brain levels of the 5-hydroxyindoles serotonin and 5-hydroxyindoleacetic acid. Aspartame alone had no effect on these compounds but completely blocked the changes in 5-hydroxyindoles caused by glucose. Each animal's brain level of tryptophan (r = 0.89) and 5-hydroxyindoles (r = 0.74) was also significantly correlated with its plasma tryptophan ratio, affirming that the effects of glucose or aspartame on these brain constituents also result from the changes they produce in plasma composition. The aspartame-glucose combination also reduced brain levels of leucine, isoleucine, and valine to a significantly greater extent than aspartame or glucose alone. These observations indicate that high aspartame doses can generate major neurochemical changes in rats, especially when consumed along with carbohydrate-containing foods. However, they should not in any way be interpreted as demonstrating that aspartame significantly affects the human brain.

Amino Acids↗
PubMed1997

The effect of aspartame as part of a multidisciplinary weight-control program on short- and long-term control of body weight.

This study investigated whether the addition of the high-intensity sweetener aspartame to a multidisciplinary weight-control program would improve weight loss and long-term control of body weight. One hundred sixty-three obese women were randomly assigned to consume or to abstain from aspartame-sweetened foods and beverages during 16 wk of a 19-wk weight-reduction program (active weight loss), a 1-y maintenance program, and a 2-y follow-up period. Women in both treatment groups lost approximately 10% of initial body weight (10 kg) during active weight loss. Among women assigned to the aspartame-treatment group, aspartame intake was positively correlated with percentage weight loss during active weight loss (r = 0.32, P < 0.01). During maintenance and follow-up, participants in the aspartame group experienced a 2.6% (2.6 kg) and 4.6% (4.6 kg) regain of initial body weight after 71 and 175 wk, respectively, whereas those in the no-aspartame group gained an average of 5.4% (5.4 kg) and 9.4% (9.4 kg), respectively. The aspartame group lost significantly more weight overall (P = 0.028) and regained significantly less weight during maintenance and follow-up (P = 0.046) than did the no-aspartame group. Percentage weight losses at 71 and 175 wk were also positively correlated with exercise (r = 0.32, P < 0.001; and r = 0.34, P < 0.01, respectively) and self-reported eating control (r = 0.37, P < 0.001; and r = 0.33, P < 0.01, respectively). These data suggest that participation in a multidisciplinary weight-control program that includes aspartame may facilitate the long-term maintenance of reduced body weight.

Adult↗