Posted by Larry Hoover on January 1, 2004, at 13:06:40
In reply to Aspartame (Equal, NutraSweet) = POISON, posted by Ame Sans Vie on January 1, 2004, at 12:05:27
> Again, visit http://www.dorway.com or any of the other numerous aspartame truth sites on the web.
>
> ~~MichaelI'm quite ambivalent about the aspartame issue. On the one hand, I never want to be seen to be dismissive of anecdotal accounts of adverse effects arising from ingestion of any substance. On the other hand, I want to try and place those experiences in the context of the population as a whole.
I have no doubt that there are people, like yourself, who are particularly susceptible to aspartame (or MSG, a similar potential excitotoxin). On the other hand, I don't like to see the biased reporting of websites like the one you reference go unchallenged. There is a wealth of evidence showing that there are no measurable adverse effects from acute and chronic aspartame ingestion (just look at the doses used in some of these studies). On the other hand, susceptibility to headache and adverse mood reactions is demonstrable upon aspartame exposure. Also, your experience, vis a vis fibromyalgia, is not unreported in the literature.
I guess what I come down to is the conclusion that we must be responsible for our own food. If MSG or aspartame is a problem, then don't consume them. There are always many alternatives to consider.
I present here a quickly collected blend of aspartame references from Medline, some pro, some con. The first one is available as full-text (pdf format).
http://www.ajcn.org/cgi/reprint/68/3/531
Am J Clin Nutr. 1998 Sep;68(3):531-7.
Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects.Spiers PA, Sabounjian L, Reiner A, Myers DK, Wurtman J, Schomer DL.
Clinical Research Center, Massachusetts Institute of Technology, Cambridge 02139, USA.
BACKGROUND: Neurobehavioral symptoms have been reported anecdotally with aspartame. OBJECTIVE: This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or behavioral functioning in normal individuals. DESIGN: Forty-eight healthy volunteers completed a randomized, double-blind, placebo-controlled, crossover study. The first month was aspartame free. Subjects then consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each. Order was randomized and subjects were assigned to either a high- (45 mg x kg body wt(-1) x d(-1)) or low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group. Neuropsychologic and laboratory testing was done on day 10 of each treatment period to determine possible acute effects and on day 20 for possible chronic effects. RESULTS: Plasma phenylalanine concentrations increased significantly during aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure. CONCLUSION: Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults.
Epilepsia. 1995 Mar;36(3):270-5.Aspartame and seizure susceptibility: results of a clinical study in reportedly sensitive individuals.
Rowan AJ, Shaywitz BA, Tuchman L, French JA, Luciano D, Sullivan CM.
Department of Neurology, Department of Veterans Affairs Medical Center, Bronx, NY 10468, USA.
The high intensity sweetener aspartame has been implicated anecdotally in seizure provocation. This possibility was investigated with a randomized, double-blind, placebo-controlled, cross-over study. After an extensive search, 18 individuals (16 adults and 2 children) who had seizures allegedly related to aspartame consumption were admitted to adult or pediatric epilepsy monitoring units where their EEG was monitored continuously for 5 days. Aspartame (50 mg/kg) or identically enpackaged placebo was administered in divided doses at 0800, 1000, and 1200 h on study days 2 and 4. All meals were uniformly standardized on treatment days. No clinical seizures or other adverse experiences were observed after aspartame ingestion. Mean plasma phenylalanine (Phe) concentrations increased significantly after aspartame ingestion (83.6 microM) as compared with placebo (52.3 microM). Results suggest that aspartame, in acute dosage of approximately 50 mg/kg, is no more likely than placebo to cause seizures in individuals who reported that their seizures were provoked by aspartame consumption.
Pediatrics. 1994 Jan;93(1):70-5.Comment in:
Pediatrics. 1994 Jan;93(1):127-8.
Pediatrics. 1994 Oct;94(4 Pt 1):576.Aspartame, behavior, and cognitive function in children with attention deficit disorder.
Shaywitz BA, Sullivan CM, Anderson GM, Gillespie SM, Sullivan B, Shaywitz SE.
Department of Pediatrics, Yale University School of Medicine, New Haven, CT 06510.
OBJECTIVE. To determine the effects of large doses of aspartame on behavior, cognition, and monoamine metabolism in children with attention deficit disorder. DESIGN. A randomized, double-blind, placebo-controlled crossover study of unmedicated children meeting Diagnostic and Statistical Manual of Mental Disorders (3rd ed) criteria for attention deficit disorder. SETTING. Behavioral assessments were performed in the child's home by their parents and in the classroom by a teacher. Cognitive tests were administered and blood drawing was performed during a 2-day inpatient admission to our Children's Study Center. INTERVENTIONS. Administration of aspartame (single morning dose, 34 mg/kg) or placebo for alternate 2-week periods. MAIN OUTCOME MEASURES. Behavioral and cognitive tests included the Matching Familiar Figures Test (MFFT), Children's Checking Task (CCT), the Airplane Test, the Wisconsin Card Sorting Test (WCST), the Subjects Treatment Emergent Symptom Scale (STESS), the Multigrade Inventory for Teachers (MIT), and the Conners Behavior Rating Scale. Blood was drawn for complete blood cell count and liver function tests, as well as amino acid, methanol, formate, serotonin, and monoamine metabolite analyses, and urine was collected for measurement of catecholamine and monoamine metabolite excretion. RESULTS. No clinically significant differences between aspartame and placebo were found for the STESS, MIT, or Conners ratings, or for the MFFT, CCT, WCST, or Airplane cognition tests. Also, no differences were noted for any of the biochemical measures, except for the expected increase in plasma phenylalanine and tyrosine following aspartame. CONCLUSIONS. The findings indicate that aspartame at greater than 10 times usual consumption has no effect on the cognitive and behavioral status of children with attention deficit disorder. In addition, aspartame does not appear to affect urinary excretion rates of monoamines and metabolites.
Biol Psychiatry. 1993 Jul 1-15;34(1-2):13-7.Adverse reactions to aspartame: double-blind challenge in patients from a vulnerable population.
Walton RG, Hudak R, Green-Waite RJ.
Department of Psychiatry, Northeastern Ohio Universities College of Medicine, Youngstown.
This study was designed to ascertain whether individuals with mood disorders are particularly vulnerable to adverse effects of aspartame. Although the protocol required the recruitment of 40 patients with unipolar depression and a similar number of individuals without a psychiatric history, the project was halted by the Institutional Review Board after a total of 13 individuals had completed the study because of the severity of reactions within the group of patients with a history of depression. In a crossover design, subjects received aspartame 30 mg/kg/day or placebo for 7 days. Despite the small n, there was a significant difference between aspartame and placebo in number and severity of symptoms for patients with a history of depression, whereas for individuals without such a history there was not. We conclude that individuals with mood disorders are particularly sensitive to this artificial sweetener and its use in this population should be discouraged.
J Allergy Clin Immunol. 1991 Apr;87(4):821-7.A combined single-blind, double-blind, placebo-controlled study to determine the reproducibility of hypersensitivity reactions to aspartame.
Garriga MM, Berkebile C, Metcalfe DD.
Mast Cell Physiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md.
Aspartame is an O-methyl ester composed of phenylalanine and aspartic acid. After its final approval as a sweetener in 1981, a number of reports of adverse reactions to aspartame appeared in the literature. To explore the pathogenesis of such reactions, we initiated a study in July 1986 to identify subjects with hypersensitivity reactions to aspartame with blinded challenge procedures. The study was closed after 32 months. During that time, we advertised in local newspapers and worked closely with the local community of allergists and dermatologists in an attempt to recruit subjects with hypersensitivity reactions to aspartame. A total of 61 self-referrals and physician referrals were screened, with 20 referrals evaluated in clinic. After this evaluation, 12 patients underwent single- and double-blind challenge with up to 2000 mg of aspartame. No subject with a clearly reproducible adverse reaction to aspartame was identified. In summary, we found that it is difficult to recruit study subjects with a history of hypersensitivity reactions to aspartame and that subjects who believed themselves allergic to aspartame did not have reproducible reactions.
Neurology. 1994 Oct;44(10):1787-93.Comment in:
Neurology. 1995 Aug;45(8):1631-2; author reply 1632-3.
Neurology. 1995 Aug;45(8):1631; author reply 1632-3.
Neurology. 1995 Aug;45(8):1632; author reply 1632-3.Aspartame ingestion and headaches: a randomized crossover trial.
Van den Eeden SK, Koepsell TD, Longstreth WT Jr, van Belle G, Daling JR, McKnight B.
Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle 98195.
To examine whether ingestion of aspartame is associated with headaches, we conducted a double-blind crossover study using volunteers with self-identified headaches after using aspartame. Of the 32 subjects randomized to receive aspartame (approximately 30 mg/kg/d) and placebo in a two-treatment, four-period crossover design, 18 completed the full protocol, seven completed part of the protocol before withdrawing due to adverse effects, three withdrew for other reasons, two were lost to follow-up, one was withdrawn due to noncompliance, and one withdrew and gave no reason. Each experimental period was 7 days long. Subjects reported headaches on 33% of the days during aspartame treatment, compared with 24% on placebo treatment (p = 0.04). Subjects who were "very sure" prior to the study that aspartame triggered some of their headaches reported larger treatment differences (aspartame = 0.37 headache-days, placebo = 0.18 headache-days; p < 0.001) than subjects who were "somewhat sure" (aspartame = 0.29 headache-days, placebo = 0.22 headache-days; p = 0.51) or "not sure" (aspartame = 0.33 headache-days, placebo = 0.39 headache-days; p = 0.51). There was no significant treatment difference in the length or intensity of headaches or in the occurrence of side effects associated with the headaches. This experiment provides evidence that, among individuals with self-reported headaches after ingestion of aspartame, a subset of this group report more headaches when tested under controlled conditions. It appears that some people are particularly susceptible to headaches caused by aspartame and may want to limit their consumption.
Ann Pharmacother. 2001 Jun;35(6):702-6.
Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins.Smith JD, Terpening CM, Schmidt SO, Gums JG.
Malcolm Randall Veterans Affairs Medical Center, Gainesville, FL, USA.
BACKGROUND: Fibromyalgia is a common rheumatologic disorder that is often difficult to treat effectively. CASE SUMMARY: Four patients diagnosed with fibromyalgia syndrome for two to 17 years are described. All had undergone multiple treatment modalities with limited success. All had complete, or nearly complete, resolution of their symptoms within months after eliminating monosodium glutamate (MSG) or MSG plus aspartame from their diet. All patients were women with multiple comorbidities prior to elimination of MSG. All have had recurrence of symptoms whenever MSG is ingested. DISCUSSION: Excitotoxins are molecules, such as MSG and aspartate, that act as excitatory neurotransmitters, and can lead to neurotoxicity when used in excess. We propose that these four patients may represent a subset of fibromyalgia syndrome that is induced or exacerbated by excitotoxins or, alternatively, may comprise an excitotoxin syndrome that is similar to fibromyalgia. We suggest that identification of similar patients and research with larger numbers of patients must be performed before definitive conclusions can be made. CONCLUSIONS: The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.
poster:Larry Hoover
thread:295365
URL: http://www.dr-bob.org/babble/alter/20031218/msgs/295379.html