Evaluation of the Dietary Additive Aspartame (‘Nutrasweet’) as a risk factor for central nervous system tumours (Dr Peter Nunn)
3 year project with grant funding of £187,074.00.
A substantial sum from The Community Fund (National Lotteries) of £147,624 has been awarded towards this project.
Dec 1999 - Dec 2002
Tsed to various concentrations of native aspartame and various breakdown products of aspartame (the here has been an increase in both the incidence of, and mortality from, intrinsic brain tumours of some 35% over the past three decades and especially since 1985. This increase may be due, at least in part, to improved diagnostic practice, since the introduction of neuro-imaging in the mid 1980’s made the detection of brain tumours at an early stage more reliable. This factor alone does not explain, however, the significant increase in the reported incidence of brain tumours and a variety of environmental chemicals have been considered as potential neuro-carcinogens. Attention has focused on aspartame, an artificial sweetener, which has been consumed world wide since its commercial introduction in 1981; the market for this product was worth £607 million in 1995. Although the amount of the chemical produced is not known, relatively large amounts are used to artificially sweeten soft drinks (‘diet Pepsi’ about 480 mg per litre bottle) and many other food products such as yoghurt (41 mg per 100g), coffee sweeteners and confectionery (100 mg per 100g).
The objective of this work is to establish experimental systems in which the carcinogenicity of aspartame can be studied in tissue culture. Because recent reports indicate that the chemical modification of aspartame (‘nitrosation’ – which can occur during intestinal absorption of the compound) increases the carcinogenic potential of aspartame to induce specific mutations in oncogenes and so-called ‘tumour’ suppressor’ genes will be addressed.
Various mature cell types and their precursors were separated and expo
sweetener is broken down in the body to a variety of metabolic derivatives and its form may change according to storage conditions). Moreover, these metabolic/breakdown products such as DKP, an agent whose chemical structure was suggestive of possible carcinogenic properties, were artificially nitrosated (nitrosation occurs naturally in the human body and can render agents toxic or carcinogenic) prior to treatment of brain cells.
MTT and SRB viability assays and enzyme biochemistry studies were used to test different concentrations of the agents for toxicity on various cell types derived from the brain. DNA damage (Comet assays) studies were then used to determine the possible influence of the agents causing changes in the nuclei of cells which would be likely to result in malignant transformation. Finally, the P53 gene which controls cell division and it frequently mutated in cancer cells was examined in untreated cells by PCR-based techniques. Conclusion:
Evaluation of the dietary additive Aspartame (NutraSweet) as a risk factor for central nervous system tumours King's College, London, professor G. Pilkington, Dr. P. Nunn The purpose of this three year project was to investigate the possible neurocarcinogenicity of aspartame and its metabolites, the project finished in November 2002.
This study found that Aspartame and its derivatives
• I. Do not appear to interact with cellular macromolecules
• II. Do not cause biochemical changes characteristic of reactive molecules
• III. Lack the activity normally associated with direct carcinogens
• IV. Do not cause DNA damage as defined by comet assay.
In summary, taken together with the data from the literature, it is concluded that Aspartame and the breakdown products studied are not carcinogenic.
A full report on this is due later in the year when a number of papers will be submitted for publication in scientific journals.
In view of the public interest in this study, we feel it is only right we publish the main findings of the study rather than wait until early next year. It is, however, only through important studies such as this that we can start to isolate the environmental factors that play a part in causing malignant brain tumours.
This three year project amounted to £187,074 over three years. £147,624 was sponsored by The Community Fund.
Neither DNA damage nor P53 alterations were detected in any “normal” brain cells at any age studied when treated with aspartame or its breakdown products studied, in either nitrosated or non-nitrosated forms. Moreover, none of these agents elicited any changes in cell proliferation rate or cell motility. This would suggest that, in itself, aspartame does not directly cause tumours of the brain.
It should be noted, however, that while we were able to extensively study various fully developed, mature brain cell types, due to low yield of immature (or precursor) cells from the tissues available, we were unable to fully examine the potential of the agents on these, possibly sensitive, cells.
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