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Revisiting the Safety of Aspartame

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Revisiting the Safety of Aspartame Special Article Revisiting the safety of aspartame Arbind Kumar Choudhary and Etheresia Pretorius Aspartame is a synthetic dipeptide artificial sweetener, frequently used in foods, medications, and beverages, notably carbonated and powdered soft drinks. Since 1981, when aspartame was first approved by the US Food and Drug Administration, researchers have debated both its recommended safe dosage (40 mg/kg/d) and its general safety to organ systems. This review examines papers published between 2000 and 2016 on both the safe dosage and higher-than- recommended dosages and presents a concise synthesis of current trends. Data on the safe aspartame dosage are controversial, and the literature suggests there are potential side effects associated with aspartame consumption. Since aspartame consumption is on the rise, the safety of this sweetener should be revisited. Most of the literature available on the safety of aspartame is included in this review. Safety studies are based primarily on animal models, as data from human studies are lim- ited. The existing animal studies and the limited human studies suggest that aspar- tame and its metabolites, whether consumed in quantities significantly higher than the recommended safe dosage or within recommended safe levels, may disrupt the oxidant/antioxidant balance, induce oxidative stress, and damage cell membrane integrity, potentially affecting a variety of cells and tissues and causing a deregula- tion of cellular function, ultimately leading to systemic inflammation. INTRODUCTION ester.5 It was first marketed as NutraSweet and Equal and is now freely available in supermarkets. Aspartame Non-nutritive sweeteners are high-intensity sweeteners is incorporated into more than 6000 products, includ- that are used in small amounts to reduce the caloric and ing soft drinks, dessert mixes, frozen desserts and yo- sugar content of food and beverages.1 The controversial in- gurt, chewable multivitamins, and breakfast cereals. It is creased use of non-nutritive sweeteners in so-called healthy also contained in about 600 pharmaceutical products6–9 food and beverages has recently come under the spotlight. and is, therefore, consumed by millions of people In particular, aspartame, which was accidentally discovered worldwide.10 Aspartame metabolites may reduce or po- in 1969,2 has received much attention because of its potent tentiate drug action through various mechanisms.11 sweetness, which is 200 to 300 times greater than that of Metabolites amino acids, and proteins may (1) alter sucrose.3 Aspartame has a clean sugar-like taste, with no blood proteins to which drugs attach; (2) alter drug undesirable metallic or bitter taste. It is far cheaper than receptors on cell membranes; (3) change the sites at sugar and is an attractive option for manufacturers.4 which impulses are transmitted along nerves to muscle; Aspartame is a synthetic dipeptide formed by the (4) cause metabolic abnormalities in elderly people that reaction of L-aspartic acid with L-phenylalanine methyl may enhance the vulnerability of this population to Affiliation: A.K. Choudhary is with the Department of Physiology, School of Medicine, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa. E. Pretorius is with the Department of Physiological Sciences, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa. Correspondence: E. Pretorius, Department of Physiological Sciences, Faculty of Health Sciences, Stellenbosch University, Private Bag X1 Maiteland, 7602, South Africa. Email: [email protected]. Key words: aspartame, aspartic acid, methanol, phenylalanine. VC The Author(s) 2017. Published by Oxford University Press on behalf of the International Life Sciences Institute. All rights reserved. For Permissions, please e-mail: [email protected]. doi: 10.1093/nutrit/nux035 718 Nutrition ReviewsVR Vol. 75(9):718–730 drug reactions; or (5) interfere with drug action. Safety issues associated with the use of aspartame include po- tential toxicity from aspartame metabolites, including methanol and/or its metabolite, formaldehyde.12,13 This review examines the existing literature (pub- lished 2000–2016) describing the effects of aspartame on cells and organ systems when used within the safe dosage range. The interactions between aspartame and cells and organ systems are examined, and extensive references for current recommended safe dosages are provided. Finally, literature that considers the effects of aspartame on different cells in the body is reviewed. Figure 1 Structure of aspartame (L-aspartyl-L-phenylalanine Biochemistry of aspartame methyl ester). Aspartame is an L-aspartyl-L-phenylalanine methyl es- further metabolized in the liver into L-tyrosine by the en- 14 ter (Figure 1) and is very stable under dry conditions zyme phenylalanine hydroxylase. L-Tyrosine in turn, is when stored at temperatures ranging from 30 Cto converted into L-dopa (L-3,4-dihydroxyphenylalanine) by 15 23 80 C. It degrades at high temperatures and in aqueous the enzyme tyrosine hydroxylase. L-Dopa is further solutions. The rate of degradation in aqueous solutions, converted into the catecholamines—dopamine, norepi- 16 however, depends on pH as well as temperature. At nephrine (noradrenaline), and epinephrine (adrena- room temperature, aspartame is most stable at pH 4.3, line)—by the amino acid decarboxylase enzyme. with a half-life of 300 days. Degradation is minimal Phenylalanine can cross the blood–brain barrier.24,25 when pH ranges between 4.0 and 5.0 and reaches a maxi- Furthermore, elevations in plasma concentrations of phe- mum when heated under conditions of high humidity at nylalanine and aspartic acid result in increased transport 16 a pH greater than 6.0. Under strongly acidic of these amino acids into the brain, modifying the brain’s (pH < 4.0) or alkaline conditions (pH > 6.0), aspartame neurochemical composition.26 Neuroendocrine changes, may generate methanol by hydrolysis. Under more se- particularly increased concentrations of catecholamine vere conditions, such as elevated temperature or high 17 resulting from phenylalanine and its hydroxylation prod- pH, the peptide bonds are also hydrolyzed. This results uct, tyrosine, have been observed in the brain.26 in the release of free amino acids (particularly phenylala- Phenylalanine is a large neutral amino acid that nine and aspartic acid). It should also be noted that the competes with other important large neutral amino pH of diet sodas—a major vehicle for aspartame acids for binding on the large neutral amino acid trans- consumption—tends to be somewhere between 3.0 and porter.26 However, excess phenylalanine concentrations 4.0. Interestingly, following breakdown in the gut or ex- are associated with decreased concentrations of cate- posure to temperature changes, aspartame and its metab- cholamine, serotonin, and dopamine.26 Aspartic acid is olites lose their sweetness.18,19 Conditions during storage metabolized in the liver into L-lysine and L-methionine vs during ingestion are thus different and may determine 20 by the enzyme aspartate kinase. At high concentrations, the formation of aspartame metabolites. aspartic acid may cross the blood–brain barrier and bind to the N-methyl-D-aspartate receptor (also known Aspartame during storage. Aspartame can be stored in a 27 dry or an aqueous form. In the dry form, stability as the NMDA receptor or NMDAR) or to other gluta- depends mainly on temperature, and stability decreases mate binding sites, causing an influx of calcium ions at temperatures < 30oCor> 80oC. In the aqueous into cells (Figure 2). Increased firing of action potentials form, stability is greatest at a pH of 4.3; beyond this pH, and higher rates of neuron depolarization can potentiate 26 aspartame degrades into its 3 known metabolites (phe- neurodegeneration. The enzyme responsible for me- 28 nylalanine, aspartic acid, and methanol) and loses some tabolism of methanol (Ch3OH) is species dependant. of its sweetness. The aqueous form also becomes In primates, methanol is metabolized into formaldehyde 29 sweeter with increased temperature.21 (HCHO) in the liver by alcohol dehydrogenase. In rodents, on the other hand, methanol is mainly metabo- Aspartame during ingestion. Upon ingestion, aspartame lized by alcohol catalase and differences in the embry- is metabolized by gut enzymes (esterase and peptidase) onic metabolism of CH3OH may determine species into 3 amino acid isolates, phenylalanine (50%), aspartic sensitivity, in which mouse embryos were more sensitive acid (40%), and methanol (10%).22 Phenylalanine is than the rat.30 Formaldehyde is oxidized into formic Nutrition ReviewsVR Vol. 75(9):718–730 719 Table 1 Phenylalanine and aspartic acid content of as- partame-sweetened beverages and other common foods and beverages Food or beverage Phenylalanine (g) Aspartic acid (g) Aspartame-sweetened 1.186 0.983 beverages (per 100 g) Fat-free or skim milk 0.175 0.288 (per 100 g) Apple juice (per 100 g) – – Tomato juice (per 100 g) 0.026 0.130 Orange juice (per 100 g) 0.043 0.437 Banana (raw) 0.049 0.124 Egg white (raw) 0.686 1.220 metabolism. The so-called free forms of amino acids found in aspartame-sweetened beverages are released Figure 2 Binding of aspartate to NMDA (N-methyl-D-aspartate) receptor structures. The NMDA receptor has 3 binding sites: a rapidly and in greater concentrations. For example, the glutamate binding site, a glycine binding site, and an allosteric methanol released during aspartame metabolism is a binding site. When aspartate binds to the glutamate-binding site, free form and is thus released directly into the blood- it results in the opening of the Ca21 ion channel and allows Ca21 stream.45 It was also recently shown that, after an ac- into cells, leading to a higher rate of neuron depolarization. ceptable daily intake (ADI) of 40 mg per kilogram of body weight, blood methanol concentrations increased acid (HCOOH) by formaldehyde dehydrogenase in both 3- to 6-fold over individual baseline values.46 primates and rodents. Formic acid is metabolized more The daily consumption of chemically produced as- rapidly into carbon dioxide and water in rodents,31 as partame is increasing.
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