Introduction+and+The+Issue+on+Aspartame

What People Say ?

We had interviewed people who expert in additive-material also to social general human who non-expert in this section. We took as source were student especially in our school, SMAKBO. We interviewed people to stronger and add the report of aspartame as general truth and information. We hope with result of this interview can get basic information whole known by people an as basic and standard about content of this part.


 * Expert's



We had interviewed expert who our Organic Chemistry teacher, Mr. Rusman,S.Si. According to him aspartame is an organic aromatic compound, that contain with amino , and carboxylic group too so can form zwiterr ion in water. The function of aspartame is as sweetener with sweetness level 200 times higher than sucrose. That caused sweet is from hydroxyl group(poly) “Sweetness Theory”. Aspartame has low calori and usually used for people whom has diabetes problem, and also athlete. Aspartame is made of aspartic acid, phenylalanine, and methanol. aspartame is still safety to use because aspartic acid that contain in aspartame is used for human body. Aspartic acid is polar and not disturb blood balanced. whereas phenylalanine and methanol are essential or not digested with body so that can easy to throw away and not disturb healthy. but, if aspartame used too much can change the taste (ex: become bitter), and for long period/time, can caused gen mutation(cell cancer forming) So far research about aspartame is only about rat. If something happen with rat cannot to be reason (aspartame is danger), different with primate that has almost gen likes human. Regulation of aspartame is different in each country because healthy level in each country is different too. If in some country have better technology ,so researches will be better ,also more protect than in country where regulation about aspartame usage will be better. Standard of aspartame in food and drink is same ,but the unit whole used is different ,whereas will appear difference quality that can make people confused at the first time consumer read. Some producers are doubt about aspartame usage. If aspartame not used in industry, so must be naturally(ex: use glucose, sucrose, etc.) And need long time , must use more quantity and high cost, but if aspartame synthesis is more efficient, cheap, and quick. Aware don’t use aspartame too much because is we use too much can caused unwanted things. Socialization from government about aspartame usage, effect, etc. Must be done to remove the frightened and worried about food-additives in the public. Many producers don’t know about aspartame usage and the use aspartame without measuring. Whereas they use aspartame too much and can harm all side.

We also interviewed in educated class. According a student named Suryo Adi Nugroho, Class 12-3. He don’t afraid of aspartame hazard for human health, because bad-effect of aspartame only can release in long time usage. However He is doubt about aspartame, he recognized his ability of aspartame was not enough yet. He suggested to government and producer for more protect people in this country. He also said he will still use the product that contain aspartame. Because he minds the products that exist in market had been observed and matched with standard.

1. History

Aspartame was discovered in 1965 by a chemist working for the American company Searle and an initial marketing authorisation (MA) was granted in the United States by the Food and Drug Administration (FDA) in 1974. This MA was suspended a few months later following an appeal against the authorisation on the grounds that the toxic and carcinogenic effects on the brain of this compound and its metabolites had not been properlyevaluated during the experimental studies. Following a reassessment of the studies on experimental animals and an examination of new data (including a study of carcinogenis in the rat), the FDA granted this product a new MA in 1981 (FDA, FR 1981) for use in solid food. This authorisation was extended to soft drinks in 1983 (FDA, FR 1983) and for its use as a general sweetener in 1996. The safety of aspartame has been assessed and recognised by a number of other national and international organisations including the FAO/WHO Committee of Experts on Food Additives (JECFA) and, at EU level, by the Scientific Committee on Food. It was authorised by Directive 94/35/EC of the European Parliament and of the Council on sweeteners for use in foodstuffs (adopted on 30 June 1994) and its use is permitted in more than 90 countries. In France, aspartame has been permitted since 1988. The Acceptable Daily Intake (ADI) of aspartame for humans was fixed at 40 mg/kg body weight/day by the JECFA (1980).In 1996, an article by J.W. Olney suggesting a link between an increased incidence of brain tumours in the United States and the marketing of aspartame relaunched the debate on the risks to human health posed by its consumption. The debate has been covered by the media, notably on the Internet where several thousand websites are devoted to the effects of aspartame. These contain allegations claiming that this additive is responsible for a large number of adverse effects (more than fifty), some of which are very serious, such as: multiple scloriosis, Gulf War Syndrom, brain tumours, epileptic seizures, complications of diabetes, etc.

2. What are the uses and properties of aspartame ?
The E number of aspartame in France and Europe is E 951. It was first marketed by NutraSweet AG and more recently by Ajinomoto and Holland Sweetener Company. This sweetener is incorporated into a number of foodstuffs (drinks, desserts, sweets, etc.) and in table sweeteners, under the name Canderel, Pouss-suc and into some 600 medicines; this report does not consider the possible intake (very limited compared with dietary intake) of aspartame from this later source. Its sweetening power is 180 to 200 times greater than that of saccharose. Aspartame is a dipeptide methyl ester of L-aspartyl-L-phenylalanine. It is a white, odourless, crystalline powder. Its molecular weight is 294.3 Daltons and its rotatory power [a]D22 = 2.3° in 1M HCl. > > Its main impurity (approximately 2%) is diketopiperazine, a degradation product of aspartame which has no sweetening properties. > The solubility of aspartame in water is dependent on pH and temperature, the maximum solubility is reached at pH 2.2 (20 mg/ml at 25°C) and the minimum solubility at pH 5.2 (pHi) is 13.5 mg/ml at 25°C. > The stability of aspartame is dependent on time, temperature, pH and water activity (Dziezak, 1986; Bell et al., 1991; Tsoubeli et al., 1991; Homler, 1984; Graves et al., 1987; Huang et al., 1987; Neiderauer, 1998). > Aspartame is very stable in the dry state: at 105°C a loss of approximately 5% (formation of diketopiperazine) is observed after 100 hours of treatment. At 120°C, a 50% loss is obtained after 80 hours of treatment. > In solution, when stored at temperatures ranging from 30 to 80°C, aspartame is progressively degraded into diketopiperazine (Pattanaargson et al., 2000). It is therefore not usable in foods heated at higher temperature (cooking, sterilisation, etc.). At room temperature its stability is good at pH values of between 3.4 and 5 and it is maximum at pH 4.3. At pH below 3.4 the dipeptide is hydrolysed and at a pH greater than 5, cyclisation occurs with the formation of diketopiperazine. In both cases, this transformation results in the loss of sweetness. > > In foods with a low or moderate water content (water activities between 0.34 and 0.66), the maximum stability is observed at pH 5.0. > Aspartame has good stability in deep frozen products.

=THE ISSUE = In industries aspartame usage is the most artificial sweetener that used. Look graphic below ! 

__A. Genotoxicity and carcinogenicity__
The available mutagenicity and long-term carcinogenicity studies on aspartame were recently reviewed by AFSSA (2002). AFSSA noted that: "Aspartame is not genotoxic in a reverse mutation test on S. typhimurium, in two chromosome aberration tests in vivo on somatic cells and in Rodent dominant lethal test on germ cells (JECFA, 1980). Recently, two studies have confirmed the absence of clastogenic potential (Durnev et al., 1995; Mukhopadhyay et al., 2000) of the compound." The AFSSA report also noted: "Trocho et al., (1998) demonstrated that aspartame, radio-labelled on the methanol, induced in the liver stable DNA and protein adducts. According to these authors, the accumulation of these adducts after repeated administration of aspartame could pose problems of toxicity and carcinogenicity in the long term. Besides the fact that aspartame at high doses has never induced liver cancer in rats, Trocho's studies did not identify the radioactivity found in the proteins and DNA. Consequently, the formation of adducts of formaldehyde on the proteins and nucleic acids from aspartame, in vivo, remains to be proved (Tephly, 1999)." As regards the long-term studies, the AFSSA report noted that: "In a carcinogenicity study on CD-1 mice (FDA, FR 1981), aspartame administered in feed at doses of 1, 2 and 4 g/kg bw/day for 110 weeks, showed no carcinogenic potential."

__B. Toxicity of diketopiperazine in terms of effects on the nervous system__
The toxicity of diketopiperazine, a degradation product of aspartame, has been studied in laboratory animals. This substance is neither genoyoxic nor carcinogenic in rats and mice. The Acceptable Daily Intake of diketopiperazine for humans has been established at 7.5 mg/kg body weight (JECFA, 1980) based on the no observed effect level of 750 mg/kg bw./day obtained in a long term toxicity study on rats, divided by a safety factor of 100

1.2 Epidemiological data
Concerning the epidemiological data on brain tumours, the AFSSA (2002) report noted that: "In 1996, Olney et al. published an article on a possible link between the increase in the frequency of brain tumours in humans and the consumption of aspartame in the United States. Based on the data from the NCI (10% of the population) from 1975-1992, the authors concluded that there was a significant increase in the frequency of brain tumours in the mid- 1980s, that is to say the period following aspartame came onto the market. The conclusions of this have been criticised by a number of scientists who questioned the methodology, the use of the data and their interpretation (Levy et al., 1996; Linet et al., 1999; Ross, 1998; Seife, 1999; Smith et al., 1998). One of the major criticism is that the authors only took into account the frequency of brain tumours during a selected period (1975-1992). When all the epidemiocal data are used (1973-1992) a different conclusion is reached, as the frequency of brain cancers began to increase in 1973 and stabilised from the mid-1980s (Levy et al., 1996). Furthermore, Olney et al. did not provide any quantitative or qualitative relationship between the exposure of the population to aspartame and the observed frequency of brain tumours. Finally, an increase in the incidece of the tumours can have many causes including, among others, improvements in diagnostic methods (Modan et al., 1992)."

2. Can aspartame affect reproduction and development ?
__Reproduction and Developmental toxicity__

The derivation of an ADI for aspartame by JECFA (1980) and the EEA (1985) included assessment of single- and multi-generation studies in animals that were specifically designed to examine the possible effects of aspartame and its metabolic conversion products on reproduction, and development, including neuro-development.

3. Can aspartame produce neurological disorders ?
Much of the recent interest in the safety of aspartame has explored whether its consumption is linked with neurological effects. Therefore this end point has been given special consideration in this review. Shortly after the widespread marketing of aspartame, there were a number of anecdotal reports of health effects, which some consumers related to their consumption of aspartame-containing products (Hull, 1999). Most of the earlier complaints and reports of aspartame-related adverse reactions were analysed by experts at the Centres for Disease Control (CDC) in Atlanta on behalf of the FDA, who concluded that there was no symptom complex that could be assigned to the ingestion of aspartame (Janssen and Van der Heijden, 1988; Tollefson, 1988). A number of complaints were of a neurologica or behavioural type (Tollefson, 1988) and these received special consideration, in part because experiments in animals have shown that high doses (1000mg/kg bw and above in rats) can alter the concentrations of neurotransmitters and their precursors within the central nervous system (Lajtha et al., 1994).

4. Can aspartame affect behaviour, cognition or mood ?
Some years ago, it was hypothesised that aspartame, primarily due to its content of Phe, could have an effect on human behaviour, cognition, and possibly on measures of physiological function (Wurtman, 1985). However, no consistent and reproducible effects were observed in a number of older animal studies investigating the effects of aspartame on neurotransmitter levels. Only a limited number of studies on behavioural aspects in animals have been published in the last ten years. A proportion of these focused on seizure activity but a causal link with aspartame could not be established; no adverse effects on other aspects of behaviour and cognition were reported in experimental animals when aspartame was given at oral dose levels of up to 2000 mg/kg bw/day (Yirmiya et al., 1989; Tilson et al., 1991; Mullenix et al., 1991; Vitulli et al., 1996; LaBuda and Hale, 2000; Goerss et al., 2000). A number of anecdotal reports in humans were received by the manufacturers of aspartame in early to mid 1980's relating to a variety of symptoms following the marketing of aspartame in the USA. About two-thirds of these symptoms fell into the neurobehavioural category (Butchko and Stargel, 2001). These consisted mostly of headaches (see below), mood alterations, insomnia, and dizziness. More than 500 reports were received by CDC, and almost half underwent follow-up and evaluation. A post-marketing surveillance system was developed by the NutraSweet company (Butchko and Kotsonis, 1994; Butchko et al., 1996), which was followed by scientific research on these neurological symptoms (see below). A number of scientific studies were carried out in healthy and potentially sensitive individuals, including children, to test whether the consumption of aspartame was associated with behavioural and cognitive changes. The potentially sensitive individuals studied were, heterozygotes for PKU individuals suffering from depression, Attention Deficit Disorder (ADD), Parkinson’s Disease, epilepsy or other suspected seizures. They included double-blind studies in children (Saravis et al., 1990; Shaywitz et al., 1994) in which no effects were observed on behaviour, mood or learning when aspartame was given as a drink at single and multiple doses of 34 mg/kg bw/day for up to two weeks. The longer term study of Shaywitz et al. (1994) examined the effect of aspartame in children with ADD and included an assessment of liver function as well as measurement of plasma levels of amino acids, serotonin and monoamine metabolites. Treatment-related effects were also absent in a study of pre- school children who were given aspartame at 32 mg/kg bw/day and described as sugar sensitive by their parents (Wolraich et al., 1994).

5. Does aspartame cause headaches ?
Headache was one of the more common symptoms that was reported to the FDA and evaluated by the CDC (Janssen and Van der Heijden, 1988; Tollefson, 1988). Several studies were carried out to test the potential association between aspartame intake and the onset of headaches. Although the results of a questionnaire-based study (Lipton et al., 1989) and two double-blind out-patient investigations (Koehler and Glaros, 1988; Van Den Eeden et al., 1994) employing daily doses of up to 30 mg/kg bw/day indicated a potential association between aspartame intakes and headache, it was not possible to deduce causality as the effect of diet had not been adequately controlled for and the interpretation of the data was complicated by a high drop out rate and a limited experimental design.

6. Does aspartame trigger epileptic seizures ?
The AFSSA (2002) report noted that: "Among the possible adverse effects of aspartame, researchers have paid particular attention to seizures. Several studies have suggested a relationship between the consumption of large amounts of aspartame and the triggering of epileptic seizures. In an old study (1972), on new-born monkeys (2-3 animals per group) treated with doses of aspartame of 1, 3 and 4g/kg bw/day for 52 weeks, epileptic seizures were recorded at the highest doses, after 218 days of treatment. Thereafter, sporadic convulsions were observed during handling of the animals. These symptoms were identical with those observed in young monkeys treated with phenylalanine."