Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects

Spiers, Paul A.; Sabounjian, LuAnn; Reiner, A.S.; Myers, D. K.; Wurtman, Judith J.; Schomer, Donald L.

doi:10.1093/ajcn/68.3.531

Cited by 43 publications

(22 citation statements)

References 21 publications

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“…Aspartame also can cause neurochemical changes and affect the levels of neurotransmitters within the brain. In healthy volunteers, plasma phenylalanine (Spiers et al 1998) and aspartate (Møller 1991) concentrations increased significantly after aspartame intake. Møller (1991) has also shown that the intake of aspartame produced a marked and persistent increase of the availability of phenylalanine to the brain, which was not observed after protein intake.…”

Section: Introductionmentioning

confidence: 94%

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

2011

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This study aimed at investigating the effect of the sweetener aspartame on oxidative stress and brain monoamines in normal circumstances and after intraperitoneal (i.p.) administration of lipopolysaccharide (LPS; 100 μg/kg) in mice. Aspartame (0.625-45 mg/kg) was given via subcutaneous route at the time of endotoxin administration. Mice were euthanized 4 h later. Reduced glutathione (GSH), lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), and nitrite concentrations were measured in brain and liver. Tumor necrosis factor-alpha (TNF-α) and glucose were determined in brain. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured in liver. The administration of only aspartame (22.5 and 45 mg/kg) increased brain TBARS by 17.7-32.8%, decreased GSH by 25.6-31.6%, and increased TNF-α by 16.7-44%. Aspartame caused dose-dependent inhibition of brain serotonin, noradrenaline, and dopamine. Aspartame did not alter liver TBARS, nitrite, GSH, AST, ALT, or ALP. The administration of LPS increased nitrite in brain and liver by 26.8 and 37.1%, respectively; decreased GSH in brain and liver by 21.6 and 31.1%, respectively; increased brain TNF-α by 340.4%, and glucose by 39.9%, and caused marked increase in brain monoamines. LPS increased AST, ALT, and ALP in liver tissue by 84.4, 173.7, and 258.9%, respectively. Aspartame given to LPS-treated mice at 11.25 and 22.5 mg/kg increased brain TBARS by 15.5-16.9%, nitrite by 12.6-20.1%, and mitigated the increase in monoamines. Aspartame did not alter liver TBARS, nitrite, GSH, ALT, AST, or ALP. Thus, the administration of aspartame alone or in the presence of mild systemic inflammatory response increases oxidative stress and inflammation in the brain, but not in the liver.

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Section: Introductionmentioning

confidence: 94%

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

2011

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“…We chose aspartame, a sweetener that does not modify plasma insulin and glucose (Spiers et al 1988;Melchior et al 1991) even at doses close to that used in this study (Carlson and Shah 1989). We first performed a single blind, crossover study with 12 healthy participants to identify the aspartame dose that has the same sweetness as glucose.…”

Section: Determination Of a Placebomentioning

confidence: 99%

Effect of glucose on tobacco craving. Is it mediated by tryptophan and serotonin?

et al. 2004

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“…Phenylalanine and aspartic acid are both amino acids which are found in natural proteins and under normal circumstances are beneficial, if not essential, for health (Woodrow, 1984). It has been reported that aspartame consumption was linked with neurological and behavioral disturbances (Humphries et al, 2008), but most of the results yielded negative or inconclusive correlations (Spiers et al, 1998;Magnuson et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Iman¹

2011

Afr. J. Pharm. Pharmacol.

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Aspartame is one of the most widely used artificial sweeteners in over 90 countries worldwide. It is a highly intensity sweetener added to a large variety of food, most commonly found in low calorie beverages, desserts and table top sweeteners added to tea or coffee. The present study examined whether the daily oral administration of ASP (40 mg/kg) for 2, 4 and 6 weeks induce oxidative stress in the liver and kidney of male albino rats. Lipid peroxidation (LPO), glutathione reduced (GSH) levels as well as the activities of superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) enzymes were determined. A significant increase in LPO levels was obtained in the liver tissue after 4 and 6 weeks of ASP administration while there was a significant decrease in LPO level after 2 weeks followed by a significant increase in the renal tissue at the end of the 6 weeks. SOD activity significantly decreased in the liver tissue after 2, 4 and 6 weeks of treatment. Also, there was a significant decrease in SOD activity after 2 and 4 weeks in the renal tissue. CAT activity significantly decreased in the liver tissue after 2 and 4 weeks of ASP administration. Regarding to GSH content, there was a significant decrease in the liver tissue after 2, 4 and 6 weeks which was accompanied by a significant increase in GST activity after 4 and 6 weeks of ASP administration. In conclusion, ASP may induce an oxidative stress in the liver and kidney of male albino rats.

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Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects

Abstract: Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults.

Cited by 43 publications

References 21 publications

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

Effect of glucose on tobacco craving. Is it mediated by tryptophan and serotonin?

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

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