Aspartame Symptoms list
Aspartame： The bitter-sweet truth behind this poison. STOP NOW !
DONALD RUMSFELD AND ASPARTAME
１９８５．５．７付け；Congressional Record （連邦議会議事録） 中のアスパルテームの有害性についての記述（米国ソフトドリンク協会の抗議！）
Ajinomoto, Aspartame & Brain Tumors: Recipe for Death
Aspartame Disease: An Ignored Epidemic H. J. Roberts (ペーパーバック - 2001/5/1)
New Study - LOW DOSES Of Aspartame Cause CANCER
From Dr. Betty Martini, D.Hum.
Journal of Orthomolecular Medicine - Aspartame Induces Lymphomas and Leukaemias in Rats
Eur. J. Oncol., vol.10, n.2, pp.00-00, 2005
Morando Soffritti, Fiorella Belpoggi, Davide Degli Esposti, Luca Lambertini
Cancer Research Centre, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy
AWARD PRESENTED TO DR. MORANDO SOFFRITTI
Award presented to Dr. Morando Soffritti of The Romazzini Institute (Italy) by Mission Possible International for his scientific work in exposing the dangers of aspartame.
Environ Health Perspect. 2007 Sep;115(9):1293-7.
Life-Span Exposure to Low Doses of Aspartame Beginning during Prenatal Life Increases Cancer Effects in Rats. Soffritti M, Belpoggi F, Tibaldi E, Esposti DD, Lauriola M.Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy.
BACKGROUND: In a previous study conducted at the Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation (CMCRC/ERF), we demonstrated for the first time that aspartame (APM) is a multipotent carcinogenic agent when various doses are administered with feed to Sprague-Dawley rats from 8 weeks of age throughout the life span. OBJECTIVE: The aim of this second study is to better quantify the carcinogenic risk of APM, beginning treatment during fetal life. METHODS: We studied groups of 70-95 male and female Sprague-Dawley rats administered APM (2,000, 400, or 0 ppm) with feed from the 12th day of fetal life until natural death. RESULTS: Our results show a) a significant dose-related increase of malignant tumor-bearing animals in males (p < 0.01), particularly in the group treated with 2,000 ppm APM (p < 0.01); b) a significant increase in incidence of lymphomas/leukemias in males treated with 2,000 ppm (p < 0.05) and a significant dose-related increase in incidence of lymphomas/leukemias in females (p < 0.01), particularly in the 2,000-ppm group (p < 0.01); and c) a significant dose-related increase in incidence of mammary cancer in females (p < 0.05), particularly in the 2,000-ppm group (p < 0.05). CONCLUSIONS: The results of this carcinogenicity bioassay confirm and reinforce the first experimental demonstration of APM's multipotential carcinogenicity at a dose level close to the acceptable daily intake for humans. Furthermore, the study demonstrates that when life-span exposure to APM begins during fetal life, its carcinogenic effects are increased.
PMID: 17805418 [PubMed - in process]
Ann N Y Acad Sci. 2006 Sep;1076:559-77.
Results of long-term carcinogenicity bioassay on Sprague-Dawley rats exposed to aspartame administered in feed. Belpoggi F, Soffritti M, Padovani M, Degli Esposti D, Lauriola M, Minardi F.
Cesare Maltoni Cancer Research Center, European Foundation of Oncology and Environmental Sciences B. Ramazzini, 40010 Bentivoglio, Bologna, Italy.
Aspartame (APM) is one of the most widely used artificial sweeteners in the world. Its ever-growing use in more than 6000 products, such as soft drinks, chewing gum, candy, desserts, etc., has been accompanied by rising consumer concerns regarding its safety, in particular its potential long-term carcinogenic effects. In light of the inadequacy of the carcinogenicity bioassays performed in the 1970s and 1980s, a long-term mega-experiment on APM was undertaken at the Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation on groups of male and female Sprague-Dawley rats (100-150/sex/group), 8 weeks old at the start of the experiment. APM was administered in feed at concentrations of 100,000, 50,000, 10,000, 2,000, 400, 80, or 0 ppm. Treatment lasted until spontaneous death of the animals. The results of the study demonstrate that APM causes: (a) an increased incidence of malignant tumor-bearing animals, with a positive significant trend in both sexes, and in particular in females treated at 50,000 ppm (P < or = 0.01) when compared to controls; (b) an increase in lymphomas-leukemias, with a positive significant trend in both sexes, and in particular in females treated at doses of 100,000 (P < or = 0.01), 50,000 (P < or = 0.01), 10,000 (P < or = 0.05), 2000 (P < or = 0.05), and 400 ppm (P < or = 0.01); (c) a statistically significant increased incidence, with a positive significant trend, of transitional cell carcinomas of the renal pelvis and ureter in females and particularly in those treated at 100,000 ppm (P < or = 0.05); and (d) an increased incidence of malignant schwannomas of the peripheral nerves, with a positive trend in males (P < or = 0.05). The results of this mega-experiment indicate that APM, in the tested experimental conditions, is a multipotential carcinogenic agent.
PMID: 17119233 [PubMed - indexed for MEDLINE]
Environ Health Perspect. 2006 Mar;114(3):379-85.
Environ Health Perspect. 2006 Mar;114(3):A176.
Environ Health Perspect. 2006 Sep;114(9):A516; author reply A516-7.
Environ Health Perspect. 2007 Jan;115(1):A16-7; author reply A17.
First experimental demonstration of the multipotential carcinogenic effects of aspartame administered in the feed to Sprague-Dawley rats. Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L, Tibaldi E, Rigano A.Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy. email@example.com
The Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation has conducted a long-term bioassay on aspartame (APM), a widely used artificial sweetener. APM was administered with feed to 8-week-old Sprague-Dawley rats (100-150/sex/group), at concentrations of 100,000, 50,000, 10,000, 2,000, 400, 80, or 0 ppm. The treatment lasted until natural death, at which time all deceased animals underwent complete necropsy. Histopathologic evaluation of all pathologic lesions and of all organs and tissues collected was routinely performed on each animal of all experimental groups. The results of the study show for the first time that APM, in our experimental conditions, causes a) an increased incidence of malignant-tumor-bearing animals with a positive significant trend in males (p < or = 0.05) and in females (p < or = 0.01), in particular those females treated at 50,000 ppm (p < or = 0.01); b) an increase in lymphomas and leukemias with a positive significant trend in both males (p < or = 0.05) and females (p < or = 0.01), in particular in females treated at doses of 100,000 (p < or = 0.01), 50,000 (p < or = 0.01), 10,000 (p < or = 0.05), 2,000 (p < or = 0.05), or 400 ppm (p < or = 0.01); c) a statistically significant increased incidence, with a positive significant trend (p < or = 0.01), of transitional cell carcinomas of the renal pelvis and ureter and their precursors (dysplasias) in females treated at 100,000 (p < or = 0.01), 50,000 (p < or = 0.01), 10,000 (p < or = 0.01), 2,000 (p < or = 0.05), or 400 ppm (p < or = 0.05); and d) an increased incidence of malignant schwannomas of peripheral nerves with a positive trend (p < or = 0.05) in males. The results of this mega-experiment indicate that APM is a multipotential carcinogenic agent, even at a daily dose of 20 mg/kg body weight, much less than the current acceptable daily intake. On the basis of these results, a reevaluation of the present guidelines on the use and consumption of APM is urgent and cannot be delayed.
PMID: 16507461 [PubMed - indexed for MEDLINE]
In Vivo. 2007 Jan-Feb;21(1):89-92.Links
The effect of aspartame administration on oncogene and suppressor gene expressions.Gombos K, Varjas T, Orsós Z, Polyák E, Peredi J, Varga Z, Nowrasteh G, Tettinger A, Mucsi G, Ember I.
Faculty of Medicine, Institute of Public Health University of Pécs, Pécs, Hungary. firstname.lastname@example.org
BACKGROUND: Aspartame (L-phenylalanine N-L-alpha-aspartyl-1-methyl ester) is an artificial sweetener with widespread applications. Previously published results have shown that among rats receiving aspartame a significant increase of lymphoreticular neoplasms, brain tumours and transitional cell tumours occurred. The aim of our short-term experiment was to investigate the biological effect of aspartame consumption by determining the expressions of key oncogenes and a tumour suppressor gene. MATERIALS AND METHODS: After one week per os administration of various doses of aspartame to CBA/CA female mice, p53, c-myc, Ha-ras gene expression alterations were determined in individual organs. RESULTS: The results showed an increase in gene expressions concerning all the investigated genes especially in organs with a high proliferation rate: lymphoreticular organs, bone-marrow and kidney. CONCLUSION: Aspartame has a biological effect even at the recommended daily maximum dose.
PMID: 17354619 [PubMed - indexed for MEDLINE]
Toxicol Sci. 2006 Mar;90(1):178-87. Epub 2005 Dec 13. Links
Synergistic interactions between commonly used food additives in a developmental neurotoxicity test.Lau K, McLean WG, Williams DP, Howard CV.Developmental Toxicopathology Unit, Department of Human Anatomy & Cell Biology, University of Liverpool, Sherrington Buildings, Liverpool L69 3GE, UK. email@example.com
Exposure to non-nutritional food additives during the critical development window has been implicated in the induction and severity of behavioral disorders such as attention deficit hyperactivity disorder (ADHD). Although the use of single food additives at their regulated concentrations is believed to be relatively safe in terms of neuronal development, their combined effects remain unclear. We therefore examined the neurotoxic effects of four common food additives in combinations of two (Brilliant Blue and L-glutamic acid, Quinoline Yellow and aspartame) to assess potential interactions. Mouse NB2a neuroblastoma cells were induced to differentiate and grow neurites in the presence of additives. After 24 h, cells were fixed and stained and neurite length measured by light microscopy with computerized image analysis. Neurotoxicity was measured as an inhibition of neurite outgrowth. Two independent models were used to analyze combination effects: effect additivity and dose additivity. Significant synergy was observed between combinations of Brilliant Blue with L-glutamic acid, and Quinoline Yellow with aspartame, in both models. Involvement of N-methyl-D-aspartate (NMDA) receptors in food additive-induced neurite inhibition was assessed with a NMDA antagonist, CNS-1102. L-glutamic acid- and aspartame-induced neurotoxicity was reduced in the presence of CNS-1102; however, the antagonist did not prevent food color-induced neurotoxicity. Theoretical exposure to additives was calculated based on analysis of content in foodstuff, and estimated percentage absorption from the gut. Inhibition of neurite outgrowth was found at concentrations of additives theoretically achievable in plasma by ingestion of a typical snack and drink. In addition, Trypan Blue dye exclusion was used to evaluate the cellular toxicity of food additives on cell viability of NB2a cells; both combinations had a straightforward additive effect on cytotoxicity. These data have implications for the cellular effects of common chemical entities ingested individually and in combination.
PMID: 16352620 [PubMed - indexed for MEDLINE]