Seizures and hyponatremia after excessive intake of diet coke, LJ
Mortelmans, M Van Loo, HG De Cauwer, K Merlevede, Klina General
Hospital, Brasschaat, Belgium, EJEM 2008 Feb: Mark D. Gold critique:
Murray 2008.01.10
http://rmforall.blogspot.com/2008_01_01_archive.htm
Thursday, January 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1502
See also:
possible neurologic effects of aspartame, TJ Maher, RJ Wurtman,
Environ. Health Persp. 1987 Nov, full text: other seizure re****ts re
aspartame, methanol, formaldehyde, formic acid: Murray 2008.01.10
http://rmforall.blogspot.com/2008_01_01_archive.htm
Thursday, January 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1501
//////////////////////////////////////////////////////////////////////
Eur J Emerg Med. 2008 Feb; 15(1): 51.
Seizures and hyponatremia after excessive intake of diet coke.
Mortelmans LJ, Luc.mortelmans@[EMAIL PROTECTED]
Loo M,
De Cauwer HG, haralddecauwer@[EMAIL PROTECTED]
K. Karen.Merlevede@[EMAIL PROTECTED]
of
a Emergency Medicine
b Neurology,
Klina General Hospital, Brasschaat, Belgium.
We describe a case of epileptic seizures after a massive intake of
diet coke.
Apart from the hyponatremia due to water intoxication the
convulsions can be potentiated by the high dose of caffeine and
aspartame from the diet coke.
To our knowledge this is the first re****t of seizures due to
excessive diet coke intake. PMID: 18180668
Neurology. 1992 May; 42(5): 1000-3.
Comment in:
Neurology. 1993 Mar; 43(3 Pt 1): 630-1.
Neurology. 1993 Oct; 43(10): 2154-5.
Aspartame exacerbates EEG spike-wave discharge in children with
generalized absence epilepsy: a double-blind controlled study.
Camfield PR, Camfield CS, Dooley JM, Gordon K,
Jollymore S, Weaver DF.
IWK Children's Hospital, Halifax, Nova Scotia, Canada.
There are anecdotal re****ts of increased seizures in humans after
ingestion of aspartame.
We studied 10 children with newly diagnosed but untreated
generalized absence seizures.
Ambulatory cassette recording of EEG allowed quantification of
numbers and length of spike-wave discharges in a double-blind study
on two consecutive days.
On one day the children received 40 mg/kg aspartame and on the other
day, a sucrose-sweetened drink.
Baseline EEG was the same before aspartame and sucrose.
Following aspartame compared with sucrose, the number of spike-wave
discharges per hour and mean length of spike-wave discharges
increased but not to a statistically significant degree.
However, the total duration of spike-wave discharge per hour was
significantly increased after aspartame (p =3D 0.028),
with a 40% =B1 17% (SEM) increase in the number of seconds per hour
of EEG recording that the children spent in spike-wave discharge.
Aspartame appears to exacerbate the amount of EEG spike wave
in children with absence seizures.
Further studies are needed to establish if this effect
occurs at lower doses and in other seizure types. PMID: 1579221
Pharmacology. 1992; 44(1): 48-60.
Plasma concentrations and pharmacokinetics of phenylalanine
in rats and mice administered aspartame.
Hjelle JJ, Dudley RE, Marietta MP, Sanders PG, Dickie BC, Brisson J,
Kotsonis FN.
Preclinical and Clinical Research, NutraSweet Company,
Deerfield, Ill. 60015.
Aspartame (L-aspartyl-L-phenylalanine methyl ester) is an esterified,
dipeptide sweetener that is rapidly and completely metabolized in the
gastrointestinal tract to phenylalanine, aspartic acid and methanol.
The pharmacokinetics of phenylalanine (PHE) and tyrosine (TYR) were
examined following the administration of oral doses of aspartame
(APM) to fasted male Sprague-Dawley rats
(0, 50, 100, 200, 500 and 1,000 mg/kg)
and CD-1 mice (0, 100, 200, 500, 1,000 and 2,000 mg/kg).
Peak plasma PHE/large neutral amino acid (LNAA) ratios
were calculated.
Maximal plasma PHE and TYR concentrations were observed
within 1 h after dosing and returned to baseline
within 4-8 h in both species regardless of the dose of APM.
Mean PHE Cmaxs ranged from 73.6 to 1,161 nmol/ml in the rat,
and from 78.6 to 1,967 nmol/ml in the mouse.
TYR Cmaxs ranged from 91.6 to 502 nmol/ml
and from 89.2 to 792 nmol/ml in the rat and mouse, respectively.
AUCs and Cmaxs were linear with dose in both species.
Peak plasma PHE/LNAA ratios ranged from 0.112 to 1.117 in rats
and from 0.121 to 1.769 in mice.
Comparison of these ratios with those observed previously in humans
indicates that rodents require a 2-6 times higher dose of APM than
humans to produce similar increases in plasma PHE/LNAA ratios.
PMID: 1553388
Neuropharmacology. 1988 Jan; 27(1): 51-5.
Administration of aspartame potentiates pentylenetetrazole- and
fluorothyl-induced seizures in mice.
Pinto JM, Maher TJ.
Department of Pharmacology, Massachusetts College of Pharmacy,
Boston, MA 02115.
An association has recently been proposed between the incidence of
seizures and prolonged consumption of the phenylalanine-containing
artificial sweetener, aspartame.
Since consumption of aspartame, unlike dietary protein, can elevate
phenylalanine in brain, and thereby inhibit the synthesis and
release of neurotransmitters known to protect against seizure
activity, the effect of oral doses of aspartame on the sensitivity
of mice to the proconvulsant agents, pentylenetetrazole and
fluorothyl was studied.
Doses of aspartame were used which increased phenylalanine more
than tyrosine in brain, as occurs in humans after the consumption
of any dose of aspartame.
Pretreatment with aspartame significantly increased the percentage
of animals convulsing after administration of pentylenetetrazole and
significantly lowered the CD50 for this convulsant.
The average time to onset of seizures induced by fluorothyl
in control mice was 510 sec;
pretreatment with oral doses of 1000, 1500 and 2000 mg/kg
of aspartame 1 hr earlier significantly reduced the time required
to elicit seizures (394, 381 and 339 sec, respectively).
The seizure-promoting effect of aspartame could be demonstrated
30, 60 or 120 min after the 1000 mg/kg dose.
The seizures induced by either convulsant were potentiated
by equimolar amounts of phenylalanine,
a major endogenous metabolite of aspartame,
while the other metabolites, aspartic acid and methanol,
were without effect.
Administration together with aspartame
of the large neutral amino acid valine, which competes with
phenylalanine for entry into the brain, completely abolished the
seizure-promoting effect of aspartame.
(ABSTRACT TRUNCATED AT 250 WORDS) PMID: 3352866
Food Chem Toxicol. 1991 Feb; 29(2): 101-6.
Interspecies and interstrain studies on the increased
susceptibility to metrazol-induced convulsions
in animals given aspartame.
Diomede L, Romano M, Guiso G, Caccia S, Nava S, Salmona M.
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
The ability of aspartame (APM) to increase the susceptibility to
metrazol-induced convulsions was studied in two strains of mice
(CD1 and DBA/2J) and in guinea-pigs.
Rats were included as known positive controls.
Plasma and brain levels of phenylalanine (Phe)
and tyrosine (Tyr) were measured in CD1 mice and guinea-pigs
at various intervals after a dose of 1 g APM/kg body weight
(administered orally to mice and ip to guinea-pigs).
In mice, peak levels of Phe and Tyr were observed in plasma
after 30 min and in brain after 60 min.
In guinea-pigs peak plasma levels of Phe and Tyr
occurred 30 min after treatment.
Phe was at a maximum in guinea-pig brain after 30 min,
while Tyr levels reached a peak at 120 min.
In further experiments Phe and Tyr levels
were measured 1 hr after APM doses of 0.5, 0.75 or 1 g/kg.
In CD1 mice, plasma Phe and Tyr levels were increased significantly
only at the highest dose, whereas in brain, Tyr concentrations were
significantly increased by 0.75 or 1 g APM/kg
and Phe was significantly increased by all three doses.
In the guinea-pig, plasma Phe and Tyr were increased significantly
only by 1 g APM/kg and in brain this dose significantly raised only
the Phe levels.
Monoamine and metabolite levels were determined
in the brain striata of CD1 and DBA/2J mice 1 hr after the oral
administration of 1 or 2 g APM/kg body weight;
no differences from control values were found in either strain.
The studies of potentiation of metrazol-induced convulsions
showed that APM, at doses of up to 2 g/kg body weight,
had no such effect in mice or guinea-pigs.
In contrast, as expected, the potentiation was significant
in the rat at 1 g/kg. PMID: 2010138
http://www.HolisticMed.com/aspartame
mgold@[EMAIL PROTECTED]
Toxicity Information Center Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100
http://www.holisticmed.com/aspartame/abuse/methanol.html
"Scientific Abuse in Aspartame Research"
http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 EU Scientific Committee on Food, a whitewash
http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ):
59 pages, 230 references
http://www.holisticmed.com/aspartame/abuse/seizures.html
Scientific Abuse in Seizure Research Related to Aspartame
Please print and read completely through this do***ent!
Back to Aspartame Scientific Abuse Main Page
Back to Aspartame Toxicity Information Center
Table of Contents
* Summary of Aspartame-Induced Seizures Issue
* Hopelessly Flawed Double-Blind Studies Funded
by Monsanto/NutraSweet
* FDA Gift to Monsanto
* Aspartame Industry Pumps Out Its Own Animal Research
* References
Summary of Aspartame-Induced Seizures Issue
As of 1995 more than 7% of the aspartame toxicity reactions re****ts
sent to the U.S. Food and Drug Administration (FDA) involve seizures
and convulsions (DHHS 1995).
The FDA stopped accepting aspartame toxicity reaction re****ts in 1995
(Food 1995).
In a study looking at 551 aspartame reactors, Roberts (1988) found
that grand mal, petit mal, and absence seizures occurred in 18%
of the cases.
In 1986, Food and Chemical News re****ted that 80 cases of aspartame-
induced seizures had been re****ted to Dr. Richard Wurtman
at M.I.T. (Food 1986).
Dr. Wurtman re****ted three cases in The Lancet (Wurtman 1985).
Walton (1986, 1988) published re****ts of nine cases of seizures
linked to aspartame use.
Both the U.S. Air Force's magazine "Flying Safety"
and the U.S. Navy's magazine, "Navy Physiology"
published articles warning about the many dangers of aspartame
including that the ingestion of aspartame may make pilots more
susceptible to seizures and vertigo (US Air Force 1992).
In an independent double-blind study of aspartame in children with
generalized absence epilepsy, Camfield showed that a single dose
of 40 mg/kg of aspartame mixed in liquid exacerbated EEG spike-wave
discharge.
The authors stated:
"Aspartame appears to significantly increase the duration of time
that children with absence epilepsy have spike wave on their EEG.
In this study, the children spent 40% more time in spike wave after
aspartame than after sucrose."
The subjects were not on anti-seizure medication during the study.
The authors called for a longer study to be conducted.
I believe that the aspartame-induced seizures are at least partially
caused by the synergistic effects of formaldehyde and excitotoxins
derived from aspartame metabolism.
However, many researchers believe that the adverse neurological
effects of aspartame may be at least partially due to the
phenylalanine derived from aspartame ingestion.
Because the phenylalanine from aspartame is in free-form
(unbound to protein), it is absorbed suddenly
and can spike the blood plasma levels of phenylalanine
(Caballero 1986, Matalon 1988, Stegink 1987).
This sudden "rush" of phenylalanine does not happen when ingesting
food because protein is broken down slowly
and the phenylalanine is gradually absorbed.
Nor does this phenylalanine "rush" occur when ingesting aspartame
in capsules (Stegink 1987).
Maher (1987) points out that increased levels of phenylalanine along
with an increase ratio of phenylalanine to other Large Neutral Amino
Acids (LNAAs) can inhibit enzymes needed to synthesize the
neurotransmitters and diminish the production of brain catecholamines
and s*****onin.
The hypothesis is that this change in brain chemistry will lead to a
lowering of the seizure threshold and persons ingesting aspartame
will become more susceptible to having seizures.
Wurtman (1988) reviews the research to show that a dose of 60 times
more aspartame is needed for rodent studies to simulate the change
in phenylalanine/LNAA ratio change that occurs in humans.
Based on these findings, several research teams have found that
aspartame lowers the seizure threshold in animals (Diomede 1991,
Garrattini 1988, Guiso 1988, Kim 1988, Maher 1987, Pinto 1986, Pinto
1988).
Hopelessly Flawed Double-Blind Studies Funded by Monsanto/NutraSweet
Shaywitz (1994) concludes that "our findings indicate that, in this
group of vulnerable children, APM [aspartame] does not provoke
seizures."
Rowen (1995) concludes that "aspartame, in acute dosage of ~50 mg/kg,
is no more likely than placebo to cause seizures in individuals who
re****ted that their seizures were provoked by aspartame consumption."
Trefz (1994) re****ts that doses of 15 mg/kg and 45 mg/kg of aspartame
in PKU heterozygotes does not change EEG spectral parameters.
(The Trefz (1994) study appears to have been published in summary
form as Benninger (1991), Benninger (1993a) and Benninger (1993b)).
Others have cited these studies as evidence that aspartame does not
cause seizures (Lajtha 1994, Butchko 1994).
These results appear very convincing, but these industry-sponsored
studies are so flawed so as to be nearly worthless.
Below are a selection of major problems with these studies.
Rowen (1995) Flaws
* 16 of the 18 subjects were taking anti-seizure medication during
the study.
* The aspartame was given in capsules so that instead of spiking
the plasma phenylalanine level and significantly changing the
phenylalanine/LNAA ratio the phenylalanine was absorbed
very slowly -- more like what happens when ingesting food
(Stegink 1987).
These researchers discussed in detail the issue of plasma
phenylalanine and LNAA levels.
It was particularly absurd is that they gave the aspartame
in capsules even though they cited industry research (Burns 1990)
which proves capsule administration of aspartame eliminates
the spike in plasma phenylalanine levels!
Simply stated, the researchers were pretending
to test the hypothesis that phenyalalnine/LNAA ratio changes
would cause seizures, but they knowingly administered aspartame
in a way that eliminated the possibility of a large change
in plasma phenylalanine levels and phenylalanine/LNAA ratios.
Capsule administration of aspartame slows the absorption
of methanol and may reduce its toxicity somewhat similar
to the way ingestion of food with methanol may slightly reduce
its toxicity (Posner 1975).
Capsule administration of aspartame also eliminates the
quick absorption of the excitotoxin, aspartic acid (Stegink 1987).
When aspartic acid is absorbed quickly, it can be excitotoxic
(Blaylock 1994, Olney 1980), especially in conjunction with
formaldehyde derived from methanol
as discussed in the Methanol article.
* The study consisted of only single dose of aspartame ingestion!
This results of this study only apply to people
who ingest a single dose of encapsulated aspartame
while taking anti-seizure medication.
Not only is this study worthless,
but key information was not put in the abstract,
namely, the fact that the subjects were on anti-seizure medication
and that the aspartame was given in capsules.
Shaywitz (1994) Flaws
* Nine out of 10 children were taking anti-seizure medication
during the study.
* Again the aspartame was given in capsules
at a dose of 34 mg/kg per day.
This makes the experiment worthless since they were testing the
hypothesis of changes in plasma phenylalanine to LNAA ratios as
described above.
It also reduces the toxicity of other aspartame breakdown products
as described above.
* The experiment lasted only two weeks.
The Rowen (1995) study used individuals who had experienced aspartame-
induced seizures and it was only one day long
(with other flaws described above).
This short study used epileptic children who had not re****ted
aspartame-induced seizures.
A cynic might wonder if the researchers were able
to make this study slightly longer than the Rowen (1995) study
because the subjects had not re****ted aspartame-induced seizures.
Trefz (1994) Flaws
* Like the other studies, aspartame was given in slow-dissolving
capsules despite the fact that the researchers were claiming
to test the effects of the spike in phenylalanine levels
and the change in phenylalanine to LNAA ratios.
* The aspartame was given with meals which would further slow the
absorption of aspartame breakdown products.
* This study was longer than the others, ~ 3 months.
However, an analysis of seizure cases
by the U.S. Centers for Disease Control (CDC 1984)
shows that most seizures linked to aspartame
do not begin to appear until after 3 or more months
of real-world (i.e., non-encapsulated) aspartame.
What did industry scientists know or should have known?
1. These researchers must have known
that administering the aspartame in capsules
would mean that they were not testing
the phenylalanine and LNAA changes as they claimed.
2. The researchers should have known
that given encapsulated aspartame
would reduced the toxicity of the methanol
and the excitotoxic amino acid.
3. These researchers must have known
that allowing the subjects
to take anti-seizure medication during the study
would drastically reduce the likelihood of seizures.
FDA Gift to Monsanto
In 1992, the FDA published an analysis of re****ts
of seizures associated with consumption of aspartame
(Tollefson 1992). The re****t concludes:
"In most cases, information obtained from the
complaintants' medical records
as well as data on consumption patterns,
tem****al relation****ps, and challenge tests
did not sup****t the claim that the occurrences
of the seizures were linked to consumption of aspartame."
Monsanto scientists repeated the FDA conclusion
in their postmarketing surveillance re****t published in 1994
(Butchko 1994).
Shaywitz (1994) also used this FDA re****t
to bolster their conclusion.
What they do not mention
is that this FDA analysis has major flaws
and is provably biased, rendering it useless.
A short summary is in order for those
who have not yet read the
History of Aspartame Frequently Asked Questions (FAQs) re****t.
During the FDA approval process,
a number of government officials
were rewarded with jobs connected to the aspartame industry
(GAO 1986).
This included two US Attorneys investigating the manufacturer for pre-
approval research fraud,
who were hired by the manufacturer's law firm
(one during the investigation itself).
The Director of the FDA's Bureau of Foods
was given a job as the Vice President
of the National Soft Drink Associaton (GAO 1986).
The FDA Commissioner was rewarded
with a high-paying consulting position
with the public relations company
of the manufacturer (Burston Marsteller)
not long after approving aspartame (GAO 1986).
After these and other employees were given jobs
related to the aspartame industry,
the FDA sup****ted the manufacturer unconditionally.
The FDA redirected aspartame reaction re****ts to the AIDS Hotline
(Turner 1987).
In addition, the FDA told its regional offices
to not re****t aspartame toxicity reactions
to the Wa****ngton, D.C. headquarters (CNI 1984).
The extreme FDA bias continues to this day,
leading some people to refer to the FDA as a Monsanto subsidiary.
Tollefson (1992) Flaws
* Tollefson inappropriately classified seizures
as "Group D -- highly unlikely" related to aspartame
if the subjects refused to release their medical records.
This shows extreme bias as such cases would obviously be more
appropriately categorized in a
"possible aspartame reaction" category
since the cases may or may not be caused by aspartame -- more
information was needed.
* Tollefson inapropriately classified seizures
as "Group D -- highly unlikely" related to aspartame
if there was any possible factor in the patient's life
that could have caused or contributed to those seizures.
This is akin as categorizing smoking or stress
as "highly unlikely" for contributing to heart disease
if the patient eats a diet which could contribute to heart disease!
Clearly, these patients should have been classified
in a "possible aspartame reaction" category.
* The authors inappropriately declared ineligable,
35% of the non-Group D seizure victims
because the seizures occured more than 13 hours
after ingestion of aspartame.
This is absurd because
1) it is thought that aspartame may lower the seizure threshold
and therefore, aspartame-caused seizures could occur long after
phenylalanine levels return to normal;
2) an animal study has shown that excitotoxins can ac***ulate
in areas of the brain not protected by the blood brain barrier
and remain there for as much as 24 hours (Inouye 1976);
3) formaldehyde adducts appear to ac***ulate from aspartame
ingestion (Trocho 1998); and
4) a journal article immediately following this biased analysis,
Carroll (1992), points out that food reactions
can be delayed up to 48 hours after ingestion!
* The authors claim that only 251 cases of seizures due to aspartame
ingestion have been re****ted to the FDA.
In reality, the FDA splits the categories into:
"Seizures and Convulsions,"
"Grand Mal,"
"Petit Mal,"
"Complex Partial Seizures,"
and "Simple Partial Seizures."
The 251 cases quoted by the authors referred only to the
"Seizures and Convulsions" category as of 1995.
There have been over 500 seizures re****ted to the FDA (DHHS 1995) at
probably a re****ting rate of far less 1% (Gold 1996), leading to well
over 50,000 cases of seizures which have already been linked to
aspartame consumption.
* Even with the major flaws in classifying adverse reaction re****ts,
76 of 251 cases were still categorized as Group A and Group B,
meaning that a rechallenge with aspartame lead to furthur seizures.
Clearly, one cannot possibly conclude that this analysis
shows no link between aspartame and seizures
as implied in the abstract.
What is particularly disturbing about this analysis -- aside
from its major flaws -- is that independent research
was totally ignored in favor of aspartame industry-sponsored
research.
For example, the one-day industry study of aspartame and headache
(Schiffman 1987) was listed,
but not the much longer independent study (Koehler 1988).
An aspartame industry-sponsored International Workshop was cited
Dews 1987), but the authors completely ignored an
International Conference which invited both independent
and industry researchers and which focused largely
on the aspartame and seizure issue (Wurtman 1988).
Most of the rest of the citations are from publications of aspartame
industry-funded scientists.
Aspartame Industry Pumps Out Its Own Animal Research
Not surprisingly, the aspartame industry
has its own selection animals studies
which claim that aspartame does not lower the seizure threshhold
(Cain 1989, Dailey 1987, Dailey 1988, Dailey 1989, Dailey 1991,
Jobe 1988, Lasley 1988, Meldrum 1988, Nevins 1986, Thai 1988,
Tilson 1989).
The discussion sections of some of these studies
and the review by Sze (1989) points to the huge doses of aspartame
in rodents needed to lower the seizure threshold
in many of the independent studies.
The implication is that normal doses of aspartame ingested
by humans could not possibly cause lower the seizure threshold.
What these researchers fail to mention is that Wurtman (1988)
showed that it takes approximately 60 times more phenylalanine
given to rodents to cause the changes in phenylalanine/LNAA ratio
seen in humans.
Therefore, the aspartame doses given to the rodents in these
experiments are really not very high after adjusting
for differences between rodent and human metabolism.
If the seizures from aspartame are caused by the combination of
methanol/formaldehyde and the excitotoxic amino acid
from aspartame as I believe may be the case,
it is im****tant to note that methanol is 10 times
more acutely toxic in humans than in rodents (Roe 1982),
and it takes five times more excitotoxins given to rodents
to simulate human ingestion (Olney 1988, Stegink 1979, page 90).
It is also not surprising that Monsanto/NutraSweet attempted
to challenge the Wurtman (1988) conclusion
that it takes 60 times the dose of phenyalanine given to rodents
to change the phenylalanine to LNAA ratio
similar to what happens in humans (Hjelle 1992).
The results in this study are ridiculous,
and do not even come close to matching the results
of other, independent research
(Perego 1988, Pinto 1988, Wurtman 1983, Yokogo**** 1984).
The numerous studies that Hjelle (1992)
claims their results are similar to
actually have results far different.
This will be discussed in more detail
when the research abuses related to aspartame and phenylalanine
are looked at.
References
Benninger, C., P. Matthis, L.M.J. de Sonneville, et al. 1991.
"High Dose Aspartame Has No Effect on EEG Spectral Parameters in
Phenylketonuric Heterozygotes (PKUH),"
Society for Neuroscience Abstracts, Volume 17, page 504.
Benninger, C., P. Matthis, L.M.J. de Sonneville, et al. 1993a.
"Chronic High-Dose Aspartame Ingestion Does Not Affect Electro-
Encephalogram (EEG) Spectral Parameters in Phenylketonuric
Heterozygotes,"
Journal of Clinical and Experimental Neuropsychology,
Volume 15, page 407.
Benninger, C., et al., 1993b.
"Electroencephalographic Evaluation of Chronic Aspartame Ingestion in
Phenylketonuric Heterozygoes (PKUH),"
Electroencephalography and Clinical Neurolophysiology,
Volume 87, page S58.
Blaylock, Russell L., 1994.
"Excitotoxins: The Taste That Kills,"
Health Press, Santa Fe, New Mexico, c1994.
Butchko, Harriet, Frank Kotsonis, 1994.
"Postmarketing Surveillance in the Food Industry:
The Aspartame Case Study,"
Nutritional Toxicology,
edited by Frank Kotsonis, Maureen Mackey, and Jerry Hjelle,
Raven Press, Ltd., New York, pages 235-249.
Cain, D.P., et al., 1989.
"Failure of Aspartame to Affect Seizure Susceptibility
in Kindled Rats,"
Neuropharmacology, Volume 28, No. 4, pages 433-435.
Caballero, Benjamin, et al., 1986.
"Plasma Amino Acid Levels After Single-Dose Aspartame
Consumption in Phenylketonuria, Milk
Hyperphenylalaninemai, and
Heterozygous State for Phenylketonuria,"
Journal of Pediatrics, Volume 190, No. 4, page 668-671.
Camfield, PR, et al., 1992.
"Aspartame exacerbates EEG spike-wave discharge
in children with generalized absence epilepsy:
a double-blind controlled study."
Neurology, Volume 42, page 1000-1003.
Carroll, Polly, Kelsy Caplinger, Gene France, 1992.
"Guidelines for Counseling Parents of Young Children
with Food Sensitivities,"
Journal of the American Dietetic Association,
Volume 92, No. 5, page 602-603.
CDC 1984.
"Evaluation of Consumer Complaints Related to Aspartame Use,"
Division of Nutrition, Center for Health Promotion and Education,
Centers for Disease Control, Atlanta, GA 30333, November 1984.
CNI 1984.
Letter from Rodney E. Leonard and James S. Turner
of Community Nutrition Institute (CNI)
to Dr. Frank E. Young, Commissioner,
Food and Drug Administration,
Reprinted in Congressional Record 1985b, page S10841.
Congressional Record 1985b.
"Aspartame Safety Act,"
Congressional Record,
Volume 131, No. 106, August 1, 1985, page S10820-10847.
Dailey, J.W., S.M. Lasley, J. Frasca, P.C. Jobe, 1987.
"Aspartame (APM) is Not Proconvulsant
in the Genetically Epilepsy-Prone Rat (GERP),"
Pharmacologist, Volume 29, page 142.
Dailey, J.W., S.M. Lasley, A.F. Bettendorf,
R.L. Burder, P.C. Jobe, 1988.
"Aspartame Does Not Facilitate
Pentylenetetrazol Induced Seizures
in Genetically Epilepsy Prone Rats,"
Epilepsia, Volume 29, page 651.
Dailey, J.W., S.M. Lasley, P.K. Mishra, A.F. Bettendorf, R.L. Burger,
P.C. Jobe, 1989.
"Aspartame Fails to Facilitate
Pentylenetetrazol-Induced Convulsions in CD-1 Mice,"
Toxicology and Applied Pharmacology, Volume 98, pages 475-486.
Dailey, J.W., S.M. Lasley, R. L. Burger, A.F. Bettendorf, P.K. Mishra,
P.C. Jobe, 1991.
"Aspartame Failes to Facilitate
Pentylenetetrazol-Induced Convulsions in CD-1 Mice,"
Toxicology and Applied Pharmacology,
Volume 98, pages 475-486.
Dews, P.B., 1987.
"Summary Re****t of an International Aspartame Workshop,"
Food and Chemical Toxicology, Volume 25, No. 7, pages 549-552.
DHHS 1995. Department of Health and Human Services.
"Re****t on All Adverse Reactions
in the Adverse Reaction Monitoring System." (April 20, 1995).
Dietary Phenylalanine and Brain Function, 1987.
Proceedings of the First International Meeting
on Dietary Phenylalanine and Brain Function,
Wa****ngton, D.C., May 8-10, 1987.
Center for Brain Sciences
and Metabolism Charitable Trust,
P.O. Box 64, Kendall Square, Cambridge, MA 02142.
Reprinted in "Dietary Phenyalalnine and Brain Function,"
c1988, Birkhauser, Boston, MA USA.
Diomede, L., et al., 1991.
"Interspecies and Interstrain Studies
on the Increased Susceptibility
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Food and Chemical Toxicology, Volume 29, pages 101-106.
Food 1986.
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Food 1995.
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in 1994 From 1985 Peak: FDA,"
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GAO 1986.
"Six Former HHS Employees'
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United States General Accounting Office,
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Garrattini, Silvo, et al., 1988.
"Studies on the Susceptibility
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Presented at "Dietary Phenylalanine and Brain Function."
Proceedings of the First International Meeting
on Dietary Phenylalanine and Brain Function,
Wa****ngton, D.C., May 8-10, 1987.
Center for Brain Sciences
and Metabolism Charitable Trust,
P.O. Box 64, Kendall Square, Cambridge, MA 02142.
Reprinted in "Dietary Phenyalalnine and Brain Function," c1988,
Birkhauser, Boston, MA USA, page 131-143.
Gold, Mark, 1996.
"Re****ted Aspartame Toxicity Effects"
(Referenced Analysis of Re****ted Toxicity From Aspartame
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Aspartame (NutraSweet) Toxicity Information Center Web Page,
http://www.holisticmed.com/aspartame/suffer.faq
Gordon, Gregory, 1987.
"NutraSweet: Questions Swirl," UPI Investigative Re****t, 10/12/87.
Reprinted in US Senate (1987, page 483-510), page 497.
Guiso, G., et al. 1988.
"Effect of Aspartame on Seizures
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"Selective Distribution of Radioactivity
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Toxicologist, Volume 8, page 85.
Kim, K.C., M.D. Tasch, S.H. Kim, 1988.
"The Effect of Aspartame on 50% Convulsion Doses of Lidocaine,"
Presented at "Dietary Phenylalanine and Brain Function."
Proceedings of the First International Meeting
on Dietary Phenylalanine and Brain Function,
Wa****ngton, D.C., May 8-10, 1987.
Center for Brain Sciences
and Metabolism Charitable Trust,
P.O. Box 64, Kendall Square, Cambridge, MA 02142.
Reprinted in "Dietary Phenyalalnine and Brain Function," c1988,
Birkhauser, Boston, MA USA, page 127-130.
Koehler, SM, A. Glaros, 1988.
"The Effect of Aspartame on Migraine Headache,"
Headache, Volume 28, page 10-14.
Lajtha, Abel, Margaret Reilly, David Dunlop, 1994.
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Journal of Nutritional Biochemistry, Volume 5, page 266-283.
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Environmental Health Perspectives, Volume 75, page 53-57.
Matalon, Reuben, et al., 1988.
"Aspartame Consumption in Normal Individuals
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Presented at "Dietary Phenylalanine and Brain Function."
Proceedings of the First International Meeting
on Dietary Phenylalanine and Brain Function,
Wa****ngton, D.C., May 8-10, 1987.
Center for Brain Sciences
and Metabolism Charitable Trust,
P.O. Box 64, Kendall Square, Cambridge, MA 02142.
Reprinted in "Dietary Phenyalalnine and Brain Function," c1988,
Birkhauser, Boston, MA USA, page 41-52.
Meldrum, B.S., N. Nanji, 1988.
"Lack of Effect of Large Doses of Aspartame
on Photically-Induced Seizures in the Baboon (Papio papio),"
FASEB Journal, Volume 2, page A434.
Nevins, M.E., S.M. Arnolde, H.J. Haigler, 1986.
"Aspartame: Lack of Effect
on Convulsant Thresholds in Mice,"
Federal Proceedings, Volume 45, page 1096.
Olney, John W., et al., 1980.
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Neurobehavioral Toxicology and Teratology,
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Perego, C., et al., 1988.
"Aspartame and the Rat Brain Monoaminergic System,"
Toxicology Letters, Volume 44, page 331-339.
Pinto, Judith M.B., Timothy J. Maher, 1986.
"High Dose Aspartame Lowers the Seizure Threshold
to Subcutaneous Pentylenetetrazol in Mice,"
The Pharmacologist, Volume 28, page 155.
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"Administration of Aspartame Potentiates
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Neuropharmacology, Volume 27, No. 1, page 51-55.
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Journal of Applied Nutrition, Volume 40, page 85-94.
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CRC Critical Reviews In Toxicology, October 1982, page 275-286.
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The New England Journal of Medicine,
Volume 317, No. 19, page 1181-1185.
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Society of Neuroscience Abstracts, Volume 14, page 866.
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Do***ent # Y 4.L 11/4:S.HR6.100, page 316.
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Proceedings of the First International Meeting
on Dietary Phenylalanine and Brain Function,
Wa****ngton, D.C., May 8-10, 1987.
Center for Brain Sciences
and Metabolism Charitable Trust,
P.O. Box 64, Kendall Square, Cambridge, MA 02142.
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"Effects of Aspartame and Glucose
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Wa****ngton, D.C., May 8-10, 1987.
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recent aspartame (methanol, formaldehyde, formic acid) toxicity
research: Rich Murray 2008.01.10
Methyl alcohol ingestion as a model etiologic agent in multiple
sclerosis, WC Monte, D Glanzman, C Johnston; Methanol induced
neuropathology in the mammalian central nervous system, Woodrow C.
Monte, Renee Ann Zeising, both re****ts 1989.12.04: Murray 2007.12.28
http://rmforall.blogspot.com/2007_12_01_archive.htm
Friday, December 28 2007
http://groups.yahoo.com/group/aspartameNM/message/1499
[ These seminal 1989 studies by Prof. Woodrow C. Monte are also given
in this previous post, along his two recent comprehensive reviews:
role of formaldehyde, made by body from methanol from foods and
aspartame, in steep increases in fetal alcohol syndrome, autism,
multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition
Prof. Woodrow C. Monte, retired, Arizona State U., two reviews, 190
references supplied, Fitness Life, New Zealand 2007 Nov, Dec: Murray
2007.12.26
http://rmforall.blogspot.com/2007_12_01_archive.htm
Wednesday, December 26 2007
http://groups.yahoo.com/group/aspartameNM/message/1498
]
folic acid prevents neurotoxicity from formic acid, made by body from
methanol impurity in alcohol drinks [ also 11 % of aspartame ], BM
Kapur, PL Carlen, DC Lehotay, AC Vandenbroucke, Y Adamchik, U. of
Toronto, 2007 Dec., Alcoholism Cl. Exp. Res.: Murray 2007.11.27
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 27, 2007
http://groups.yahoo.com/group/aspartameNM/message/1495
"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and environment."
Rich Murray, MA Room For All rmforall@[EMAIL PROTECTED]
1943 Otowi Road, Santa Fe, New Mexico 87505
http://RMForAll.blogspot.com
new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 115 members, 1,502 posts in a public archive
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies on
aspartame toxicity since summer 2005: Murray 2007.11.27
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490
http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books: updated research review of 2004.07.16:
Murray 2006.05.11
http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation
cancer studies 2007.06.25: Murray 2007.07.18
http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring
agents will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12
http://groups.yahoo.com/group/aspartameNM/message/1487
Sainsbury's supermarket chain in UK details its bans of aspartame,
sodium benzoate, and artificial flavourings and colours: Carol Key,
Customer Manager: Murray 2007.11.09
http://groups.yahoo.com/group/aspartameNM/message/1427
more from The Independent, UK, Martin Hickman, re ASDA
(unit of Wal-Mart Stores) and Marks & Spencer ban of
aspartame, MSG, artificial chemical additives and dyes
to prevent ADHD in kids: Murray 2007.05.16
http://news.independent.co.uk/uk/health_medical/article2548747.ece
http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit
aspartame, MSG, artificial flavors dyes preservatives additives,
trans fats, salt "nasties" to protect kids from ADHD:
leading UK media: Murray 2007.05.15
http://en.wikipedia.org/wiki/Aspartame_controversy
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