Has Southwest Airlines banned aspartame from the cockpit?

On Sun, 15 Aug 2004 00:33:01 GMT, r5
wrote:

Deirdre Saoirse Moen wrote:
I was hospitalized three times, suffering from near-drowning in my own
saliva, before I put two and two together and realized that it was

And you are 1 data point out of 100,000,000 or so, and you
haven't really documented beyond doubt that it was the
aspartame. This is hardly a reason to ban such a benign

Ask most any GP and they'll tell you there are quite a few people who
react to aspartame, but OTOH I don't think it's a very large percent.

substance from airline cockpits. After all, if aspartame
were such a danger, automobile crash rates would reflect
this problem,

Not unless they were looking for it. It's normally one of those
things they'd never see unless they were looking for it specifically.
Driver got sick, lost control. Only if a regular pattern turned up
would they look for it.

It's a given that some percentage of accidents are ... well... not
accidents, but they are the most difficult of all to prove.

and I'm willing to bet there is **NOT*** a
single case supporting this.

Add one more, although most who are affected by it become readily
aware of it so I see no need to ban it as long as any thing containing
it is labeled. All foods and beverages containing it are so required.
The only thing I really have to worry about are prepared deserts. If
they don't know, I don't eat it. If it has a label that doesn't list
sugar I don't eat it, but I recently purchased one of those pies that
are prepared, but not baked. Sugar was on the label. My wife baked
it, I ate it and two hours later... At any rate I dug the labeled out
of the trash and although it listed sugar in the ingredients, it also
listed aspartame down near the bottom. Now I read the whole label.

Peanuts I can eat. Soybean products do not bother me, but if I drank
or ate something containing Aspartame on a flight, it would get
diverted unless we were close to the destination although it affects
me differently and I do get a warning.

When I'm doing the flying I make certain I do not eat or drink
anything containing the stuff at least two hours prior to flying and
during the flight. Of course I avoid the stuff like the plague
anyway, but I believe the figure is something like 1 out of 100,000
has some kind of reaction to it. There are those on here who should
know the correct figure. That is not to say all have the same
symptoms, or severity. Like any allergy or drug reaction, different
people seem to react differently. For me it's like a very bad case of
flu. Painful, but without the nausea.

Roger Halstead (K8RI & ARRL life member)
(N833R, S# CD-2 Worlds oldest Debonair)
www.rogerhalstead.com

http://groups.yahoo.com/group/aspartameNM/message/1088
Murray, full plain text & critique:
chronic aspartame in rats affects memory, brain cholinergic receptors, and
brain chemistry, Christian B, McConnaughey M et al, 2004 May:
2004.06.05 rmforall

Rich Murray, MA Room For All
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-501-2298

http://groups.yahoo.com/group/aspartameNM/message/1087
chronic aspartame in rats affects memory, brain cholinergic receptors, and
brain chemistry: Christian B, McConnaughey M, et al, 2004 May:
points shared with McMartin KE & Tephly TR (1979), Pall ML (2002):
Murray 2004.06.01 rmforall

[ Comments by Rich Murray are in square brackets. Without removing any
text, I have added much spacing to increase the readability of the typically
dense scientific prose.

http://groups.yahoo.com/group/aspartameNM/message/346
WebMD: Barclay: Barth:
survey shows aspartame hurts memory in students 2000.11.09
http://www.psy.tcu.edu/psy/barth.htm
Timothy M. Barth Department of Psychology
Texas Christian University TCU Box 298920 Fort Worth, TX 76129
Chairman, Physiological Psychology 817-921-7410

Poor memory is one of the main early complaints of aspartame reactors, who
are often people who use over 6 cans ( 2 L) diet soda daily for years.

The 6 experimental rats in this economical, focused study drank a comparable
level for 4 months, about 13% of a 30-month lifespan.

Only after 3 months did the 6 aspartame rats show almost a doubling of time
to run a single-choice maze.

At 4 months, there was almost another doubling of delay: "...two of the
treated rats even went to the wrong side of the T-maze, totally forgetting
where the reward was." I'd like to reveal my bias by calling this '33 %'.

There were highly significant, neurologically relevant changes in certain
brain receptor densities, and changes in brain chemistry.

With 70 citations, the relevant scientific literature is well summarized.
Many other studies, often industry funded, often used single doses or
too short durations of exposure, along with lower doses, thus rarely proving
memory deficits.

The funding source for this extremely valuable study is not given.
It used a team of talented high school students.

The fact that certain brain receptor densitities increased, and that memory
deficit increase took 3 months to be significant, may reflect the paradox of
hormesis, the complex ability of organisms to make themselves stronger in
response to low levels of toxins:

http://groups.yahoo.com/group/aspartameNM/message/1055
hormesis: possible benefits of low-level aspartame (methanol, formaldehyde)
use: Calabrese: Soffritti: Murray 2004.03.11 rmforall

The most toxic part of the fragile aspartame molecule is its 11% methanol
component.

It is an open secret, admitted in a number of published studies for three
decades, that methanol is converted within hours by the liver into
formaldehyde and formic acid, both potent, cumulative toxins that affect all
cell types.

Few know that the classic "morning after" hangover from dark wines and
liquors is due to formaldehyde and formic acid from methanol contamination,
not the ethanol itself.

http://groups.yahoo.com/group/aspartameNM/message/1047
Avoiding Hangover Hell 2003.12.31 Mark Sherman, AP writer:
Robert Swift, MD [ formaldehyde from methanol in aspartame ]:
Murray 2004.01.16 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1048
hangovers from formaldehyde from methanol (aspartame?):
Schwarcz: Linsley: Murray 2004.01.18

The actual disposition of these toxins in the tissues of human aspartame
reactors has never been determined, or, if determined, never publicly
published.

The study should be replicated, using methanol, formaldehyde, and formic
acid to verify if the same results obtain.

If blood and tissue samples have been stored, then the fast, cheap,
automated, highly sensitive Comet assay, often used to prove DNA damage from
formaldehyde, can be used to replicate the results by Yu F. Sakaki (2002)
that showed that a single very high oral dose of aspartame in just 4 mice
produced almost significant levels of DNA damage in five tissues.

This scientific plum is ripe for the plucking.

An intripid and much published team in Japan has found DNA damage
in 8 tissues from single non-lethal doses of aspartame (near-significant
high levels of DNA damage in 5 tissues) and many other additives in groups
of just 4 mice:

Mutat Res 2002 Aug 26; 519(1-2): 103-19
The comet assay with 8 mouse organs: results with 39 currently used food
additives.
Sasaki YF, Kawaguchi S, Kamaya A, Oh****a M, Kabasawa K, Iwama K,
Taniguchi K, Tsuda S.
Laboratory of Genotoxicity, Faculty of Chemical and Biological
Engineering, Hachinohe National College of Technology,
Tamonoki Uwanotai 16-1, Aomori 039-1192, Japan.


We determined the genotoxicity of 39 chemicals currently in use as food
additives.
They fell into six categories-dyes, color fixatives and preservatives,
preservatives, antioxidants, fungicides, and sweeteners.

We tested groups of four male ddY mice once orally with each additive at
up to 0.5xLD(50) or the limit dose (2000 mg/kg) and performed the comet
assay on the glandular stomach, colon, liver, kidney, urinary bladder, lung,
brain, and bone marrow 3 and 24 h after treatment.

Of all the additives, dyes were the most genotoxic.
Amaranth, Allura Red, New Coccine, Tartrazine, Erythrosine, Phloxine, and
Rose Bengal induced dose-related DNA damage in the glandular stomach, colon,
and or urinary bladder.
All seven dyes induced DNA damage in the gastrointestinal organs at a low
dose (10 or 100 mg/kg).

Among them, Amaranth, Allura Red, New Coccine, and Tartrazine induced
DNA damage in the colon at close to the acceptable daily intakes (ADIs).

Two antioxidants (butylated hydroxyanisole (BHA) and butylated
hydroxytoluene (BHT)), three fungicides (biphenyl, sodium
o-phenylphenol, and thiabendazole), and four sweeteners (sodium
cyclamate, saccharin, sodium saccharin, and sucralose) also induced DNA
damage in gastrointestinal organs.

Based on these results, we believe that more extensive assessment of
food additives in current use is warranted. PMID: 12160896

http://groups.yahoo.com/group/aspartameNM/message/934
24 recent formaldehyde toxicity [Comet assay] reports:
Murray 2002.12.31 rmforall

http://groups.yahoo.com/group/aspartameNM/message/935
Comet assay finds DNA damage from sucralose, cyclamate, saccharin in
mice: Sasaki YF & Tsuda S Aug 2002: Murray 2003.01.01 rmforall
[ Also borderline evidence, in this pilot study of 39 food additives,
using test groups of 4 mice, for DNA damage from for stomach, colon,
liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg aspartame--
a very high dose. Methanol is the only component of aspartame that can lead
to DNA damage. ]

http://groups.yahoo.com/group/aspartameNM/message/961
genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor;
sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002:
Murray 2003.01.27 rmforall [A detailed look at the data] ]

J Toxicol Sci. 2002 Dec; 27 Suppl 1: 1-8.
[Genotoxicity studies of stevia extract and steviol by the comet assay]
[Article in Japanese]
Sekihashi K, Saitoh H, Sasaki Y.
Safety Research Institute for Chemical Compounds Co., Ltd., 363-24 Shin-ei,
Kiyota-ku, Sapporo 004-0839, Japan.

The genotoxicity of steviol, a metabolite of stevia extract, was evaluated
for its genotoxic potential using the comet assay.
In an in vitro study, steviol at 62.5, 125, 250, and 500 micrograms/ml did
not damage the nuclear DNA of TK6 and WTK1 cells in the presence and absence
of S9 mix.
In vivo studies of steviol were conducted by two independent organizations.
Mice were sacrificed 3 and 24 hr after one oral administration of steviol at
250, 500, 1000, and 2000 mg/kg.
DNA damage in multiple mouse organs was measured by the comet assay as
modified by us.
After oral treatment, stomach, colon, liver, kidney and testis DNA were not
damaged.
The in vivo genotoxicity of stevia extract was also evaluated for its
genotoxic potential using the comet assay.
Mice were sacrificed 3 and 24 hr after oral administration of stevia extract
at 250, 500, 1000, and 2000 mg/kg.
Stomach, colon and liver DNA were not damaged.
As all studies showed negative responses, stevia extract and steviol are
concluded to not have DNA-damaging activity in cultured cells and mouse
organs. PMID: 12533916 ]
************************************************** ***********

p 121

Brandon Christian, Kenneth McConnaughey, Elena Bethea, Scott Brantley, Amy
Coffey, Leigha Hammond, Shelly Harrell, Kasee Metcalf, Danielle Muehlenbein,
Willie Spruill, Leslie Brinson, Mona McConnaughey*.
Chronic aspartame affects T-maze performance, brain cholinergic
receptors and Na+,K+-ATPase in rats.
Pharmacology, Biochemistry and Behavior. 2004; 78(1): 121-127.
Department of Pharmacology, Brody School of Medicine, East Carolina
University, Greenville, NC 27858, USA
North Carolina School of Science and Mathematics, Durham, NC 27811, USA
Received 21 August 2003; received in revised form 24 February 2004; accepted
28 February 2004; Available online 16 April 2004.

[ 0091-3057/$ - see front matter D 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.pbb.2004.02.017 [ $30.00 to purchase online. ]
* Corresponding author. Tel.: +1-252-744-3301;
fax: +1-252-744-3203. (M. McConnaughey).
www.elsevier.com/locate/pharmbiochembeh ]

Abstract
This study demonstrated that chronic aspartame consumption in rats can lead
to altered T-maze performance
and increased muscarinic cholinergic receptor densities in certain brain
regions.
Control and treated rats were trained in a T-maze to a particular side and
then periodically tested to see how well they retained the learned response.
Rats that had received aspartame (250 mg/kg/day) in the drinking water
for 3 or 4 months showed a significant increase in time to reach the reward
in the T-maze,
suggesting a possible effect on memory due to the artificial sweetener.
Using [3H]quinuclidinyl benzilate (QNB) (1 nM) to label muscarinic
cholinergic receptors and
atropine (10E-6 M) to determine nonspecific binding in whole-brain
preparations,
aspartame-treated rats showed a 31% increase in receptor numbers when
compared to controls.
In aspartame-treated rats, there was a significant increase in muscarinic
receptor densities in
the frontal cortex, midcortex, posterior cortex, hippocampus, hypothalamus
and cerebellum of 80%, 60%, 61%, 65%, 66% and 60%, respectively.
The midbrain was the only area where preparations from aspartame-treated
rats showed a significant increase in Na+,K+-ATPase activity.
It can be concluded from these data that long-term consumption of aspartame
can affect T-maze performance in rats
and alter receptor densities or
enzymes in brain. D 2004 Elsevier Inc. All rights reserved.
Keywords: Aspartame; Cholinergic receptors; Chronic; T-maze; Memory; ATPase

1. Introduction
Anecdotal reports on the toxic effects of aspartame (NutraSweet) are
numerous, and various issues continue to be raised today, more than 20 years
after aspartame approval by the FDA.

Concern relating to possible adverse effects has been raised due to the
metabolic components, phenylalanine, aspartic acid, diketopiperazine (DKP)
and methanol as well as the compound itself (Trocho et al., 1998).

There are many accounts of situations in which aspartame is believed
to have caused negative effects on specific human functions.
These include brain tumors, memory loss, seizures, headaches, confusion,
personality disorders, visual difficulty and dizziness (Tollefson and
Barnard, 1992).

There is very little scientific evidence in the literature to prove an
aspartame connection in these instances.

Shortly after aspartame was marketed, the FDA began to receive an increased
number of reports concerning adverse reactions related to aspartame
(Garriga and Metcalfe, 1988).

However, conclusive evidence was not found
(Aspartame, 1985; Butchko and Stargel, 2001; Butchko et al., 2002; Stegink,
1987; Stegink et al., 1981; Yost, 1989).

Numerous short-term studies have been conducted and none of these have
suggested any relationship between aspartame consumption and memory loss
(Moser, 1994).

Very few long-term studies have been done.

Most short-term studies consisted of either giving one large dose of
aspartame or treating for a short time (a few days or weeks) and then
assessing aspartame's effects on learning or memory.
Whether done in either humans or animals, these studies have shown no
adverse effects of aspartame on memory (Lapierre et al., 1990; Mullenix et
al., 1991; Saravis et al., 1990; Shaywitz et al., 1994; Spiers et al., 1998;
Stokes et al., 1994; Tilson et al., 1991; Wolraich et al., 1994).

p 122

In a longer study, Holder (1989) showed that 50 days of NutraSweet had no
effect on reflex or spatial memory development.

Another study (Leon et al., 1989) showed no persistent changes in vital
signs, body weight or standard laboratory tests in subjects receiving
aspartame for 24 weeks; however, extensive memory testing was not done.

A few chronic studies have implicated aspartame consumption in learning
or memory.

Potts et al. (1980) showed that administration of aspartame as 9% of the
diet for 13 weeks altered learning behavior in male rats.

Using a much lower daily dose of aspartame, Dow-Edwards et al. (1989)
treated pregnant guinea pigs throughout gestation and demonstrated the
aspartame-treated pups showed a disruption of odor-associative learning.

Various neurochemical effects due to aspartame consumption have been
reported (Coulombe and Sharma, 1986; Goerss et al., 2000; Pan-Hou et al.,
1990).

Neuropeptide Y concentrations have been shown to be lower in
arcuate nucleus in rats treated with aspartame for 14 weeks
(Beck et al., 2002).

Certain brain amino acid levels have been shown to be increased after
aspartame consumption (Dailey et al., 1991; Diomede et al., 1991; Yokogoshi
et al., 1984).

Neurochemical changes following high-dose aspartame with dietary
carbohydrates have also been reported (Wurtman, 1983).

Taken collectively, these studies suggest that aspartame might affect brain
neurotransmitters and receptors,
and these effects may become more prominent with long-term consumption.

Numerous studies have implicated muscarinic cholinergic receptors in
learning and memory (Bartus et al., 1982; Granon et al., 1995; Kadar et al.,
1990; Mezey et al., 1999; Rose et al., 1980; Russell, 1996; Uchida et al.,
1991; Van der Zee and Luiten, 1999; Vogt et al., 1991).

In the rabbit, elevated muscarinic binding has been shown in the
anterodorsal nucleus early in the learning process, and
this increase was maintained throughout subsequent training (Vogt et al.,
1991).

The density of muscarinic receptors in the CNS has been correlated with
cognitive performance in aging Wistar rats (Kadar et al., 1990).

Two or more muscarinic receptor states have been suggested to be
associated with age-related memory deficits in laboratory animals (Lippa et
al., 1985).

Muscarinic receptor binding has been shown to be altered in forebrain and
midbrain regions of chicks during passive avoidance learning (Longstaff
and Rose, 1981).

It has been suggested that nicotinic transmission may be important in
delayed response tasks,
while the muscarinic system may be involved in general working memory
processes (Granon et al., 1995).

These studies lead us to hypothesize that if memory impairment were seen
with chronic aspartame consumption in the rat,
then we might see an alteration in brain muscarinic cholinergic receptor
densities.

Ionic involvement has been suggested to be involved in memory formation and
the Na+,K+-ATPase enzyme is crucial for maintaining ionic gradients in
neurons and tissues (Conrad and Roy, 1993; Ng et al., 1992).

Na+,K+-ATPase activity has been found to change in young chicks after taste
stimulation using a chemical aversant (Hajek et al., 1994).

Bourre et al. (1989) have found that a diet rich in sunflower oil can
affect Na+,K+-ATPase activity in rat brain cells and
alter learning tasks measured with the shuttle box test.

Because these studies suggest that Na+,K+-ATPase activity could potentially
be involved with memory, we also wanted to investigate the possibility that
chronic aspartame treatment might affect the levels of this enzyme in the
brain.

The specific aim of this study was to determine if longterm aspartame
administration (4 months) would lead to memory loss using rats trained in a
T-maze and if so,
to explore a possible biochemical explanation by measuring
muscarinic cholinergic receptor densities and
Na+,K+-ATPase activity in nine brain areas.

We chose the aspartame dose of approximately 250 mg/kg/day because this dose
is consistent with other values in the literature and could be easily within
the limits of human consumption after species factor correction.

Dose comparisons between humans and rats have usually been corrected by a
factor of 5 since rats metabolize aspartame faster than humans (Fernstrom,
1989);
however, a factor of 60 has also been suggested as a better value to use
(Wurtman and Meher, 1987).

The everyday consumption of NutraSweet by people is increasing and it is
important to know if this substance has longterm adverse effects under
certain conditions.
Such studies are necessary to prove or disprove existing fears concerning
aspartame.

2. Methods
2.1. T-maze
The T-maze was brown and had a start arm and a left and right arm
(80X7X30 cm, Fig. 1).
A dark screen covered the top of the entire maze.
At the extremity of each arm, there was an opening to a 1215-cm room.
In the middle of the right room,
a 1-g piece of chocolate was placed as the reward.

Latency to find the reward was recorded as the seconds from the time the
animals entered the maze until they found the chocolate.

[ Replications should use single-blind designs, in which those handling the
rats and observing their runs are not aware which are on aspartame. Also,
rats are capable of simply following the scent trail that would soon be left
by most previous rats going to the right. The strong decline in performance
after 3 and 4 months might be due to other brain and sensory deficits than
just memory impairment. To prevent this effect, the two sides of the maze
could simply be made movable, and switched to serve equally as left and
right paths.

Chocolate contains a high level of phenylalanine, a 50% component of
aspartame. There conceivably might be subtle interactions for the aspartame
rats performance in their response to the phynylalanine in chocolate. This
might be studied in a replication, using other food targets. ]

2.2. Animals
Male Sprague-Dawley rats (225 g) were housed two per cage with unlimited
access to laboratory chow. [ 12 rats used ]
Control rats received regular tap water and
treated rats received aspartame in the drinking water (250 mg/kg/day).
[ Tap water can also contain neurotoxins, such as heavy metals and
fluoride. ]
Body weight as well as food and water consumption was recorded throughout
the 4 months.
Drinking solutions of aspartame were prepared to provide the appropriate
dose of aspartame in the expected volume consumed.

p 123

The gain in body weight and the amount of water consumed during the 4 months
of treatment were not affected by aspartame.

Rats were trained three times/day in the T-maze for 2 weeks.
At the end of this time all animals would consistently find the reward
(piece of chocolate) at the end of the maze within 12 s.

The animals were then periodically tested in the same T-maze at the same
time each day (4:00 p.m.) for the next 4 months and
the seconds [ of time ] to reach the reward recorded.
[ How many staff handled the rats in these runs? ]

At the end of the 4 months, the animals were anesthetized with pentobarbital
(60 mg/kg), sacrificed by decapitation and brains quickly removed and frozen
at -70 degrees C until time of assay.

The experimental protocol was approved by the East Carolina University
Institutional Review Committee for the Use of Human or Animal Subjects.

2.3. Membrane preparations
For whole-brain preparations, the frozen brains were thawed and homogenized
for 15 s with a Brinkmann Polytron PT-10 in 10 ml of ice-cold homogenization
buffer (50 mM Tris base, 150 mM sucrose, 5 mM MgCl2, pH 7.4 with HCl).

The homogenate was then centrifuged at 500g, the pellet discarded, and the
supernatant centrifuged at 10,000g for 20 min.
The pellet was resuspended in cold homogenization buffer to a concentration
of 8-10 mg/ml.

For individual brain areas, the brains were thawed and the nine areas
dissected. These sections were then homogenized in 3-5 ml of ice-cold buffer
(50 mM Tris base, 150 mM sucrose, 5 mM MgCl2, pH 7.4 with HCl) for 10 s with
a Brinkmann Polytron PT-10.
The homogenate was centrifuged for 15 min at 10,000g.
The pellet was resuspended in 1.5-2 ml of ice-cold homogenization buffer and
immediately assayed.

Excess membrane preparations were frozen at -70 degrees C and were stable up
to 4 months when stored in this manner.
Protein was determined by the method of Lowry et al. (1951).

2.4. Radioligand binding assay
Maximal binding capacity (Bmax) was determined by the use of [3H]
[ radioactive tritium ] quinuclidinyl benzilate (QNB, Perkin-Elmer) to label
the receptors.
Briefly, 1 nM [3H]QNB was incubated with 40-50 Ag membrane protein in 200
microl total volume (buffer: 50 mM Tris, 5 mM MgCl2, pH 7.4) for 30 min at
27 degrees C.
At the end of the incubation period the tubes were placed on ice for 10 min,
rapidly filtered through Whatman GF/C glass fiber filters and washed with 12
ml of ice-cold incubation buffer.
Nonspecific binding was determined in the presence of 10E-6 M atropine.
Radioactivity remaining on the filters was quantified using a
Beckman scintillation counter.

2.5. Na+,K+-ATPase assay
Na+,K+-ATPase activity was measured at 37 degrees C by monitoring the
release of inorganic phosphorus from 3 mM Tris ATP (Blumenthal et al., 1982;
McConnaughey et al., 1979).
Total Na+,K+-ATPase activity was unmasked in membrane preparations by
pretreating the membranes with sodium dodecyl sulfate (SDS) (Besch et al.,
1976).
Briefly, freshly thawed preparations (approximately 1 mg/ml) were
diluted 1:2 in 30 mM imidazole-HCl buffer (pH 7.1) containing 3.8 mM SDS.
After preincubation for 20 min at room temperature, 20 microl of the diluted
suspension was added to previously prepared reaction tubes containing 1
ml incubation medium (50 mM histidine, 3 mM MgCl2, 100 mM NaCl, 10 mM KCl,
pH 7.4).
Na+,K+-ATPase activity was defined by the activity inhibited by 8 mM
ouabain.

Fig. 1. T-maze dimensions are depicted as described in Methods. Reward
was always placed on the right side at the end of the maze.

Fig. 2. Aspartame effects on latency to find reward in the T-maze. Seconds
were measured from time of T-maze entry to when the reward (chocolate)
was found for control and aspartame-treated rats. At 90 days of aspartame
treatment and at 120 days of treatment the treated animals took
significantly longer to find the reward than the controls. *P.05 (n=12).

p 124

2.6. Statistics
Data are expressed as the mean +-S.E.M.
All values were compared with a Student's t test.
The level of statistical significance for these experiments was P.05.

3. Results
The results of this study demonstrated that rats consuming aspartame in the
drinking water for 3-4 months took longer to find the reward in a T-maze
(Fig. 2).

After 90 days of treatment, rats that had received aspartame showed a
significant increase (P.05) in time to reach the reward,
with controls taking 10+-1.4 s and
aspartame-treated rats taking 18+-4 s.

After 120 days of treatment,
control rats took 14+-2 s to reach the reward and
aspartame-treated rats took 34+-5 s (P.05).

The aspartame-treated animals did not show any differences in the amount of
food or water consumed when compared to controls,
and at the end of the 4 months
both groups had gained a similar amount of weight (data not shown).

Aspartame-treated rats learned at the same rate as control rats initially
when maze training took place during the first 2 weeks.

Fig. 3. [3H] [ radioactive tritium ] QNB binding for control and
aspartame-treated rats (4 months) was performed as described in Methods.

Brain tissue from aspartame-treated rats had significantly more apparent
muscarinic cholinergic receptors when compared to controls. *P.05 (n=6).

Fig. 4. Aspartame effects on muscarinic receptor binding in various brain
regions. [3H] [ radioactive tritium ] QNB binding for control and
aspartame-treated rats (4 months) was performed as described in Methods.
Areas included:
frontal cortex (FC),*
midcortex (MC),*
posterior cortex (PC),*
hypothalamus (HYP),*
hippocampus (HIP),*
pons (PON),
medulla (MED),
cerebellum (CER)*
and midbrain (MID).

FC, MC, PC, HYP, HIP and CER tissue from aspartame-treated rats had
significantly more apparent muscarinic cholinergic receptors when compared
to controls. *P.05
(determinations were on three to five separate pooled preparations each
containing two to six brain areas each).

Table 1
Na+,K+-ATPase in control and aspartame-treated rats (micromol Pi/mg
protein/h)
Tissue Control Aspartame-treated

Frontal cortex 3.86+-0.05 3.98+-0.40

Midcortex 3.74+-0.05 3.88+-0.09

Posterior cortex 3.41+-0.06 3.47+-0.06

Hypothalamus 4.55+-0.08 4.67+-0.09

Hippocampus 2.99+-0.08 2.83+-0.09

Pons 2.59+-0.02 2.45+-0.07

Medulla 2.53+-0.08 2.41+-0.10

Cerebellum 3.42+-0.16 3.04+-0.19

Midbrain 3.58+-0.05 4.39+-0.04*

Na+,K+-ATPase activities were assessed as described in Methods.

The midbrain area was the only one that showed a difference between control
and aspartame-treated animals.
* Significantly different from control ( P.05). Determinations were on
four to five separate pooled preparations each containing two to six brain
areas each.

p 125

As shown in Fig. 3,
muscarinic cholinergic receptor densities were found to be significantly
higher (P.05) in whole-brain preparations from
aspartame-treated rats (161+-16 fmol/mg protein) when compared to
controls (122+-8 fmol/mg protein).

When particular brain areas were investigated, it was found that apparent
muscarinic receptor numbers were significantly higher (P.05) in all three
areas of the cortex as well as the hypothalamus, hippocampus and cerebellum
(Fig. 4).

No significant differences were observed in the pons, medulla or midbrain.

Affinities of the muscarinic receptor for the agonist methacholine were not
different between control and treated animals (data not shown).

Na+,K+-ATPase activities were similar in all areas of brain tested (Table 1)
with the exception of the midbrain where the activities were significantly
increased in the aspartame-treated animals (P.05).

4. Discussion
This study produced the novel findings that chronic aspartame consumption
lengthened the time it took rats to find the reward in a T-maze and
increased muscarinic receptor numbers in specific brain areas.

We postulate this first finding to represent impaired long-term memory
retention.

This effect was seen only after prolonged aspartame administration [ thus ]
supporting short-term studies finding no effects.

The impairment was seen only after 90 days of aspartame consumption and
increased with longer exposure to up to the 120-day conclusion of the study.

At this final endpoint, not only did the aspartame-treated rats take longer
to find the reward, but two of the treated rats even went to the wrong side
of the T-maze, totally forgetting where the reward was.

These results indicate the aspartame-treated animals did not retain the
learned behavior as well as the control rats.

Other explanations for these results might include a decrease in smell to
locate the reward or a decreased desire for the chocolate reward;
however, once the rats did locate the reward, they devoured it immediately.

Other physiological markers including weight gain and water and food
consumption appeared stable throughout the study, making it less likely that
an impaired sensory or metabolic effect of the chemical could be the cause
of the impaired maze performance.

Aspartame did not affect learning early in the course of the experiment when
the animals were being trained in the maze.
We found the aspartame-treated rats learned at the same rate as the control
rats.

This study did not address which stage or stages of memory could possibly be
affected by aspartame.
The rats seemed more vulnerable to forgetting the learned T-maze
task after 4 months, and
it is certainly possible that various memory stages including short-term,
long-term, semantic, recognition, implicit or memory consolidation could be
affected (Brunelli et al., 1997, Murre et al., 2001).

If longterm memory or memory recall involves synthesis of proteins and gene
expression, then it is certainly possible that chronic exposure to high
amounts of aspartame could affect these processes.
Since hormonal as well as neural influences can regulate memory
consolidation (McGaugh, 2000), then long-term exposure to aspartame
may also play a part in impairing this consolidation.

Three distinct stages of memory were recently described by Walker et al.
(2003) involving initial, sleep dependent and recall phases.
The recall phase allows a previously stabilized memory to be
modified, and
it is certainly possible that chronic aspartame could influence this phase.

We hypothesized that if long-term aspartame consumption appeared to affect
memory retention in the rats, then brain muscarinic cholinergic receptor
densities might also be altered by the chronic aspartame.
The second major finding of this study demonstrated that after 4 months of
aspartame treatment, muscarinic receptor densities were increased in
numerous brain areas.

If we relate these increases to decreased memory retention, then our data
are contradictory to the results of others who show a correlation between
muscarinic blockers or a decreased number of brain muscarinic receptors and
impaired memory (Granon et al., 1995; Okuma et al., 2000; Power et al.,
2000; Uchida et al., 1991).

Considerable evidence supports an increase in cholinergic receptor binding
being associated with learning and memory (Gill and Gallagher, 1998; Loullis
et al., 1983; Vogt et al., 1991);
however, other studies have suggested a decrease in muscarinic receptors may
be involved with improved memory.

Anagnostaras et al. (2003) showed that M1-deficient mutant mice showed
enhanced memory for tasks that involve matching-to-sample problems.

Lerer et al. (1984) showed that diisopropyl fluorophosphate administration
caused a decreased number of muscarinic receptors and
that this was associated with enhanced performance on memory tasks.

These studies are consistent with the idea that if muscarinic receptors are
down-regulated, then certain memory functions may be enhanced.

Our results indicate that an increase in muscarinic receptors may be related
to memory-retention problems and that chronic consumption of aspartame may
be partially responsible.

Our study investigated total number of muscarinic receptors but did not
evaluate specific receptor subtypes.
It is possible that aspartame may selectively affect both numbers and
affinities of muscarinic receptor subtypes in the different brain regions.
Various studies have implicated muscarinic subtypes to be involved in memory
formation (Ortega et al., 1996; Patterson et al., 1990).
By decreasing M2 receptors with antisense oligonucleotides, Galli et al.
(2000) showed that scopolamine-induced memory impairment in the Morris water
maze was reversed; thus learning and memory improved.
These authors postulated that there might be an increase in acetylcholine to
compensate for the decrease in receptors and that this increase could
possibly be related to the improved memory.

p. 126

The up-regulation of muscarinic receptors that we observed after 4 months of
aspartame consumption could be related to a compensatory decrease in
acetylcholine levels or be due to other compensatory mechanisms such as
sprouting.

Although Na+,K+-ATPase has not attracted as much attention dealing with
memory and learning as muscarinic receptors, this enzyme has been implicated
in memory function (Brunelli et al., 1997; Klink and Alonso, 1997;
dos Reis et al., 2002; Nakazato et al., 2002).

It is interesting that the only area of brain where we showed Na+,K+-ATPase
activity to be altered was the midbrain area.
This may be an effect unrelated to memory retention, but may be specific for
chronic aspartame consumption.

It is certainly possible that the increases we observed in muscarinic
receptor densities are unrelated to the memory deficits observed after 4
months of aspartame consumption.

In addition, aspartame may be producing nonspecific increases in cholinergic
receptor densities since these increases are similar in brain areas known to
involve memory formation such as the hippocampus, as well as areas not
associated with memory formation such as the hypothalamus.

Our data support the idea that the inability to remember where the reward is
in the T-maze could be related to an increased density of brain muscarinic
receptors;
however, it is certainly possible that other receptors, enzymes or
transmitters are altered with long-term aspartame treatment and contribute
to this decreased maze performance.

Conflicting data exist concerning aspartame's effects on various receptors
and transmitters.

Pan-Hou et al. (1990) demonstrated that aspartame caused a significant
change in affinity of L-[3H]glutamate binding, whereas

Reilly et al. (1989) found no changes in receptor binding for six amine
neurotransmitter receptors after 30 days of aspartame treatment.

Others have reported various neurochemical alterations due to aspartame
consumption (Beck et al., 2002; Fernstrom et al., 1986; Goerss
et al., 2000; Melchior et al., 1991).

These data taken collectively suggest that the possibility is there for
other receptors or transmitters to be altered by chronic aspartame treatment
in addition to the increased density of muscarinic receptors that we have
shown.

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************************************************** ***********

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Mona M. McConnaughey, Ph.D. Research Assistant Professor

Our major interests lie in receptor isolation and characterization in a
variety of tissues and disease states. It is very possible that many
diseases cause or are caused by receptor changes. By characterizing these
alterations, we may learn more about the disease at the biochemical level
and possibly be able to develop drugs specifically designed to affect the
altered receptors.

Publications
McConnaughey, M.M., Wong, S.C. and Ingenito, A.J.
Dynorphin receptor changes in hippocampus of the spontaneously hypertensive
rats.
Pharmacology, 45: 52-57, 1992.

McConnaughey, M.M. and Iams, S.G.
Sex hormones change adrenoceptors in blood vessels of the spontaneously
hypertensive rats.
Clin. Exper. Hypertensive, 15: 153-170, 1993.

McConnaughey, M.M., Zhai, Q.Z. and Ingenito, A.J.
Effects on rat brain K1- and K2-opioid receptors after chronic treatment
with non-peptide K-agonists. J. Pharmacy and Pharmacology, 50(10):
1121-1125, 1998.

Student Name: Kenneth L McConnaughey Birthdate: 05/17 Userid: KLM0517
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Metabolism. 2004 Feb; 53(2): 247-51.
Differences in beta-adrenergic receptor densities in omental and
subcutaneous adipose tissue from obese African American and Caucasian women.
McConnaughey MM, Sheets KA, Davis J, Privette J, Hickner R, Christian B,
Barakat H.
Department of Medicine, Brody School of Medicine, East Carolina University,
Greenville, NC, USA.

African American women lose less weight and at a slower rate than Caucasian
women under the same weight loss conditions.
This is likely due to decreased mobilization of fat, possibly involving
differences in the responsiveness of adipose tissue to adrenergic
stimulation.
To better understand the causes behind the decreased lipolysis in African
American women, this study was initiated to determine if there were
differences in the numbers and affinities of beta adrenoreceptors in omental
and subcutaneous adipose tissue of obese African American and Caucasian
women.
We determined the number of beta receptors using a nonselective antagonist
and found the total number of receptors in both omental and subcutaneous
adipose tissue preparations were higher in African American than Caucasian
women. beta(1)(,) beta(2), and beta(3) densities were higher in omental
adipose tissue (P .05), but not different in the subcutaneous tissue of the
African American women.
No racial differences in kd values for adrenergic agents (agonists and
antagonists) were found with regard to beta(1), beta(2), or beta(3)
receptors in either the omental or the subcutaneous preparations. beta(1)
and beta(2) receptor protein (mass) was significantly increased in African
American omental tissue preparations, but not subcutaneous.
Our in vitro data demonstrating increased beta receptor numbers in omental
tissue from obese African Americans suggest that the potential for lipolysis
would be higher in these women.
Future studies should determine the biologic significance of the differences
in the beta adrenergic receptors in vivo. Publication Types: Clinical
Trial PMID: 14767879
************************************************** ***********

http://groups.yahoo.com/group/aspartameNM/message/1071
research on aspartame (methanol, formaldehyde, formic acid) toxicity:
Murray 2004.06.04 rmforall

Rich Murray, MA Room For All
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-501-2298

[ NutraSweet, Equal, Canderel, Benevia, E951 ]

http://groups.yahoo.com/group/aspartameNM/message/927
Donald Rumsfeld, 1977 head of Searle Corp., got aspartame FDA approval:
Turner: Murray 2002.12.23 rmforall

http://www.dorway.com/upipart1.txt
http://groups.yahoo.com/group/aspartameNM/message/262
aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon, UPI reporter:
Murray 2000.07.10 rmforall

http://www.dorway.com/enclosur.html
http://groups.yahoo.com/group/aspartameNM/message/53
aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06 rmforall

http://groups.yahoo.com/group/aspartameNM/message/928
revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23 rmforall

http://groups.yahoo.com/group/aspartameNM/message/841
RTM: Merisant Co., MSD Capital, Dell Computer Corp., NutraSweet Co.,
JW Childs Assc.: aspartame-neotame toxicity 2002.07.10 rmforall
************************************************** ***********

C. Trocho (1998):
"In all, the rats retained, 6 hours after administration, about 5% of the
label, half of it in the liver."

They used a very low level of aspartame ingestion, 10 mg/kg, for rats, which
have a much greater tolerance for aspartame than humans.
So, the corresponding level for humans would be about 1 or 2 mg/kg.
Many headache studies in humans used doses of about 30 mg/kg daily.

http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 1998.06.26: Murray 2002.12.22 rmforall

http://ww.presidiotex.com/barcelona/index.html full text
Formaldehyde derived from dietary aspartame binds to tissue components in
vivo.
Life Sci June 26 1998; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular,
Facultat de Biologia, Universitat de Barcelona, Spain.
http://www.bq.ub.es/cindex.html Línies de Recerca: Toxicitat de
l'aspartame http://www.bq.ub.es/grupno/grup-no.html
Sra. Carme Trocho, Sra. Rosario Pardo, Dra. Immaculada Rafecas,
Sr. Jordi Virgili, Dr. Xavier Remesar, Dr. Jose Antonio
Fernandez-Lopez, Dr. Marià Alemany [male]
Fac. Biologia Tel.: (93)4021521, FAX: (93)4021559
Sra. Carme Trocho "Trok-ho" Fac. Biologia Tel.: (93)4021544,
FAX: (93)4021559



Abstract:
Adult male rats were given an oral dose of 10 mg/kg aspartame,
14C-labeled in the methanol carbon.
At timed intervals of up to 6 hours, the radioactivity in plasma and several
organs was investigated.
Most of the radioactivity found (98% in plasma, 75% in liver) was bound to
protein.
Label present in liver, plasma and kidney was in the range of 1-2% of total
radioactivity administered per g or mL, changing little with time.
Other organs (brown and white adipose tissues, muscle, brain, cornea and
retina) contained levels of label in the range of 1/12th to 1/10th of that
of liver.
In all, the rats retained, 6 hours after administration, about 5% of the
label, half of it in the liver.

The specific radioactivity of tissue protein, RNA and DNA was quite uniform.
The protein label was concentrated in amino acids, different from
methionine, and largely coincident with the result of protein exposure to
labeled formaldehyde.
DNA radioactivity was essentially in a single different adduct base,
different from the normal bases present in DNA.
The nature of the tissue label accumulated was, thus, a direct consequence
of formaldehyde binding to tissue structures.

The administration of labeled aspartame to a group of cirrhotic rats
resulted in comparable label retention by tissue components, which suggests
that liver function (or its defect) has little effect on formaldehyde
formation from aspartame and binding to biological components.

The chronic treatment of a series of rats with 200 mg/kg of non-labeled
aspartame during 10 days results in the accumulation of even more label when
given the radioactive bolus, suggesting that the amount of formaldehyde
adducts coming from aspartame in tissue proteins and nucleic acids may be
cumulative.

It is concluded that aspartame consumption may constitute a hazard because
of its contribution to the formation of formaldehyde adducts. PMID: 9714421

[ Extracts ]
"The high label presence in plasma and liver is in agreement with the
carriage of the label from the intestine to the liver via the portal vein.
The high label levels in kidney and, to a minor extent, in brown adipose
tissue and brain are probably a consequence of their high blood flows (45).
Even in white adipose tissue, the levels of radioactivity found 6 hours
after oral administration were 1/25th those of liver.
Cornea and retina, both tissues known to metabolize actively methanol
(21,28) showed low levels of retained label.
In any case, the binding of methanol-derived carbon to tissue proteins was
widespread, affecting all systems, fully reaching even sensitive targets
such as the brain and retina....

The amount of label recovered in tissue components was quite high in all the
groups, but especially in the NA rats.
In them, the liver alone retained, for a long time, more than 2 % of the
methanol carbon given in a single oral dose of aspartame, and the rest of
the body stored an additional 2 % or more.
These are indeed extremely high levels for adducts of formaldehyde, a
substance responsible of chronic deleterious effects (33), that has also
been considered carcinogenic (34,47).
The repeated occurrence of claims that aspartame produces headache and other
neurological and psychological secondary effects-- more often than not
challenged by careful analysis-- (5, 9, 10, 15, 48) may eventually find at
least a partial explanation in the permanence of the formaldehyde label,
since formaldehyde intoxication can induce similar effects (49).

The cumulative effects derived from the incorporation of label in the
chronic administration model suggests that regular intake of aspartame may
result in the progressive accumulation of formaldehyde adducts.
It may be further speculated that the formation of adducts can help to
explain the chronic effects aspartame consumption may induce on sensitive
tissues such as brain (6, 9, 19, 50).
In any case, the possible negative effects that the accumulation of
formaldehyde adducts can induce is, obviously, long-term.
The alteration of protein integrity and function may needs some time to
induce substantial effects.
The damage to nucleic acids, mainly to DNA, may eventually induce cell death
and/or mutations.
The results presented suggest that the conversion of aspartame methanol into
formaldehyde adducts in significant amounts in vivo should to be taken into
account because of the widespread utilization of this sweetener.
Further epidemiological and long-term studies are needed to determine the
extent of the hazard that aspartame consumption poses for humans."

http://groups.yahoo.com/group/aspartameNM/message/864
Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats: Murray 2002.09.08 rmforall
Prof. Alemany vigorously affirms the validity of the Trocho study
against criticism:
Butchko, HH et al [24 authors], Aspartame: review of safety.
Regul. Toxicol. Pharmacol. 2002 April 1; 35 (2 Pt 2): S1-93, review
available for $35, [an industry paid organ]. Butchko:
"When all the research on aspartame, including evaluations in both the
premarketing and postmarketing periods, is examined as a whole, it is
clear that aspartame is safe, and there are no unresolved questions
regarding its safety under conditions of intended use."
[ They repeatedly pass on the ageless industry deceit that the methanol
in fruits and vegetables is as as biochemically available as that in
aspartame-- see the 1984 rebuttal by W.C. Monte. ]
In the same report, Schiffman concludes on page S49, not citing any
research after 1997, "Thus, the weight of the scientific evidence
indicates that aspartame does not cause headache."
Dr. Susan S. Schiffman, Dept. of Psychiatry, Duke University
919-684-3303, 660-5657

http://groups.yahoo.com/group/aspartameNM/message/911
RTP ties to industry criticized by CSPI: Murray: 2002.12.09 rmforall

http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16 rmforall

Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center, New York, NY
Department of Neurology
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research
http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches Nov 1997:
Murray 2002.07.28 rmforall

Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov-Dec; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of Medicine,
Tulsa, USA.
Aspartame, a popular dietetic sweetener, may provoke headache in some
susceptible individuals. Herein, we describe three cases of young women
with migraine who reported their headaches could be provoked by chewing
gum sweetened with aspartame. [ 6-8 mg aspartame per stick chewing gum ]

Subject: Murray: Butchko:

Tephly: critique of Trocho report Apr 2002 8.29.2
Date: Fri, 30 Aug 2002 09:49:56 +0200
From: Marià Alemany
To: "Rich Murray"
References: 1

Dear Rich,

Thank you for the opportunity to say something about the "paper" by Tephly
that followed our study on the incorporation of aspartame-derived methanol
label into DNA and protein of rats.
I don't know if responding to that publication is worth the effort.

Surprisingly, a serious journal, such as Life Sciences published a rebuttal
of our previous paper as a normal "research paper", but including no new
information neither experimental work.
This is only a sample of the "scientific" power of the advocates of
aspartame.

Anybody can extract conclusions from this anomaly, but it seems to me that
there was nothing new in that pamphlet that may add information to what we
already explained in our paper.
The responses to the questions raised by Tephly are already in our paper,
which means that either that it was not read or, worst, it was misread.

The presence of aspartame-derived label in DNA and protein adducts is
unquestionable and unquestioned, and agrees with previous studies.
Then, what importance has the mechanism of incorporation?
There were adducts, and they represent loss of function and mutation.
That was our thesis.

The reference to previous studies showing very low levels of formaldehyde in
blood do not refute our data.
First of all, measuring formaldehyde is tricky,
and in any case, the circulating levels would be below the current limit of
detection for most of the methods used.
That is the current explanation for the low levels of methanol in plasma
after aspartame loading: they are zero, using most of the methods available
for methanol, since the expected levels are currently below the limit of
detection...

In addition, it is not logical to expect to find measurable levels of
formaldehyde in a medium (blood) containing a huge amount of protein.
Formaldehyde reacts immediately with proteins because it is highly reactive:
that is the reason why we have found it in cell protein and DNA.
It is absurd to expect it to forfeit binding with cell proteins and go all
the way into the bloodstream!
Remember that formaldehyde is used to preserve corpses precisely because it
binds protein (including those of putrefactive bacteria) and prevents its
degradation.

The "alternative" point expressed by Tephly, suggesting that aspartame
methanol-label goes all the way into formic acid and the C1 pathway was
thoroughly refuted by us, using experimental data.
There was no labelled methionine nor thymine in protein and DNA respectively
in the rat protein we recovered from rats treated with aspartame.
This means--unequivocally-- that the label present in DNA and protein
adducts was NOT incorporated into amino acids or nucleic acid bases.

The only explanation for our data was that the label was in the form of
formaldehyde adducts.

If this explanation does not satisfy other scientists, they are free to
repeat the experiment and show where we went wrong, or to probe and prove
experimentally their hypotheses. Otherwise, our results stand unchecked
and, consequently, should be deemed true.

I hope that this information will help any attentive reader understand why
we have left for good this field of study.

Best regards.
------------------------------
Prof.Dr. Marià Alemany
Grup de Recerca Nitrogen-Obesitat
Departament de Nutrició i Bromatologia
Facultat de Biologia, Universitat de Barcelona
Av. Diagonal, 645; 08028 Barcelona Espanya/España/Spain
tel. +34 93 403 4606; fax: +34 93 403 7064; E-mail:

Life Sci 1999; 65(13): PL157-60. [ letter, usually not peer reviewed ]
Comments on the purported generation of formaldehyde and adduct
formation from the sweetener aspartame.

Tephly TR Thomas R. Tephly 319-335-7979
Department of Pharmacology
The University of Iowa, Iowa City 52242, USA.

A recent paper by Trocho et al. (1) describes experiments meant to show that
formaldehyde adducts are formed when rats are administered the sweetener
aspartame.
These authors assume that the methanol carbon of aspartame generates
formaldehyde which then forms adducts with protein, DNA, and RNA.
Doses employed range widely.
In this letter, studies which have been published previously and which were
not cited by these authors are reviewed in order to put into perspective the
disposition of methanol and formaldehyde in monkeys and humans, species
relevant to the toxicity of methanol and its toxic metabolite, formic acid.
PMID: 10503962, UI: 99431287

[ A number of pro-aspartame studies by Tephly and associates, invariably
funded by the aspartame industry (Monsanto, NutraSweet) are criticized in
detail at:

http://www.HolisticMed.com/aspartame
Aspartame Toxicity Information Center Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100
http://www.holisticmed.com/aspartame.../methanol.html
"Scientific Abuse in Aspartame Research"

Gold points out that industry methanol assays were too insensitive to
properly measure blood methanol levels. ]

http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity: Ramazzini Foundation
carcinogenicity results Dec 2002: Soffritti: Murray 2003.08.03 rmforall

p. 88 "The sweetening agent aspartame hydrolyzes in the gastrointestinal
tract to become free methyl alcohol, which is metabolized in the liver
to formaldehyde, formic acid, and CO2. (11)"
Medinsky MA & Dorman DC. 1994; Assessing risks of low-level
methanol exposure. CIIT Act. 14: 1-7.

Ann N Y Acad Sci. 2002 Dec; 982: 87-105.
Results of long-term experimental studies on the carcinogenicity of
formaldehyde and acetaldehyde in rats.
Soffritti M, Belpoggi F, Lambertin L, Lauriola M, Padovani M, Maltoni C.
Cancer Research Center, European Ramazzini Foundation for Oncology and
Environmental Sciences, Bologna, Italy.

Formaldehyde was administered for 104 weeks in drinking water supplied
ad libitum at concentrations of 1500, 1000, 500, 100, 50, 10, or 0 mg/L
to groups of 50 male and 50 female Sprague-Dawley rats beginning at
seven weeks of age.
Control animals (100 males and 100 females) received tap water only.
Acetaldehyde was administered to 50 male and 50 female Sprague-Dawley
rats beginning at six weeks of age at concentrations of 2,500, 1,500,
500, 250, 50, or 0 mg/L.
Animals were kept under observation until spontaneous death.
Formaldehyde and acetaldehyde were found to produce an increase in total
malignant tumors in the treated groups and showed specific carcinogenic
effects on various organs and tissues. PMID: 12562630

Ann N Y Acad Sci. 2002 Dec; 982: 46-69.
Results of long-term experimental studies on the carcinogenicity of methyl
alcohol and ethyl alcohol in rats.
Soffritti M, Belpoggi F, Cevolani D, Guarino M, Padovani M, Maltoni C.
Cancer Research Center, European Ramazzini Foundation for Oncology and
Environmental Sciences, Bologna, Italy.

Methyl alcohol was administered in drinking water supplied ad libitum at
doses of 20,000, 5,000, 500, or 0 ppm to groups of male and female
Sprague-Dawley rats 8 weeks old at the start of the experiment.
Animals were kept under observation until spontaneous death.
Ethyl alcohol was administered by ingestion in drinking water at a
concentration of 10% or 0% supplied ad libitum to groups of male and
female Sprague-Dawley rats; breeders and offspring were included in the
experiment.
Treatment started at 39 weeks of age (breeders), 7 days before mating,
or from embryo life (offspring) and lasted until their spontaneous death.
Under tested experimental conditions, methyl alcohol and ethyl alcohol
were demonstrated to be carcinogenic for various organs and tissues.
They must also be considered multipotential carcinogenic agents.
In addition to causing other tumors, ethyl alcohol induced malignant
tumors of the oral cavity, tongue, and lips.
These sites have been shown to be target organs in man by epidemiologic
studies. Publication Types: Review Review, Tutorial PMID: 12562628

Surely the authors deliberately emphasized that aspartame is well-known
to be a source of formaldehyde, which is an extremely potent, cumulative
toxin, with complex, multiple effects on all tissues and organs.

This is even more significant, considering that they have already tested
aspartame, but not yet released the results:

p. 29-32 Table 1: The Ramazzinni Foundation Cancer Program
Project of [200] Long-Term Carcinogenicity Bioassays: Agents Studied

No. No. of Bioassays Species No. Route of Exposure
108. "Coca-Cola" 4 Rat 1,999 Ingestion, Transplantal Route

109. "Pepsi-Cola" 1 Rat 400 Ingestion
110. Sucrose 1 Rat 400 Ingestion
111. Caffeine 1 Rat 800 Ingestion
112. Aspartame 1 Rat 1,800 Ingestion

http://members.nyas.org/events/confe...f_02_0429.html
Soffritti said that Coca-Cola showed no carcinogenicity.

It may be time to disclose these important aspartame results.

http://groups.yahoo.com/group/aspartameNM/message/1018
aspartame toxicity coverup increases danger of corporate meltdown:
Michael C. Carakostas of Coca-Cola: Murray 2003.08.11 rmforall
http://www.isrtp.org/new_members/members1.htm
The International Society of Regulatory Toxicology and Pharmacology
Carakostas, Michael C., DVM, PhD Director/Scientific & Regulatory
Affairs The Coca-Cola Company PO Drawer 1734 Atlanta, GA 30301
T. 404/676-4234 F. 404/676-7166 E-mail:
http://www2.coca-cola.com/ourcompany...aspartame.html [photo]
Aspartame: The world agrees it's safe By Michael Carakostas, DVM, PhD
Director, Scientific and Regulatory Affairs, Coca-Cola

It is commendable that Carakostas mentions the core problem, albeit
disparagingly, and overlaid with multiple untruths: "During digestion,
aspartame yields a very small amount of methanol-- as do many other food
substances. The body converts this methanol to formaldehyde, which is
instantly converted to formate. Formate is quickly eliminated as carbon
dioxide and water."

Carakostas deceptively make claims, unsupported by research, that the amount
of methanol from aspartame is "very small", that many foods release as much,
and that little of the inevitable formaldehyde or formic acid toxic products
accumulate in body tissues. This executive, with a PhD in veterinary
science, is deceiving people about very serious multiple toxicities.

Thus, there is evidence here cited from 1973 to 2004 that research and
reviews by immense vested interests about aspartame must be scrutinized with
the greatest skepticism. The greatest Internet myth about aspartame is
this: "Aspartame is the most thoroughly tested food additive in history."

http://groups.yahoo.com/group/aspartameNM/message/857
www.dorway.com: original documents and long reviews of flaws in
aspartame toxicity research: Murray 2002.07.31 rmforall

http://groups.yahoo.com/group/aspartameNM/message/858
Samuels: Strong: Roberts: Gold: flaws in double-blind studies re
aspartame and MSG toxicity: Murray 2002.08.01 rmforall

"Survey of aspartame studies: correlation of outcome and funding
sources," 1998, unpublished: http://www.dorway.com/peerrev.html
Walton found 166 separate published studies in the peer reviewed
medical literature, which had relevance for questions of human safety.
The 74 studies funded by industry all (100%) attested to aspartame's
safety, whereas of the 92 non-industry funded studies, 84 (91%)
identified a problem. Six of the seven non-industry funded studies
that were favorable to aspartame safety were from the FDA, which
has a public record that shows a strong pro-industry bias.
Ralph G. Walton, MD, Prof. of Clinical Psychology, Northeastern Ohio
Universities, College of Medicine, Dept. of Psychiatry, Youngstown,
OH 44501, Chairman, The Center for Behavioral Medicine,
Northside Medical Center, 500 Gypsy Lane, P.O. Box 240 Youngstown,
OH 44501 330-740-3621
http://www.neoucom.edu/DEPTS/Psychiatry/walton.htm

http://groups.yahoo.com/group/aspartameNM/message/622
Gold: Koehler: Walton: Van Den Eeden: Leon:
aspartame toxicity: Murray 2001.06.04 rmforall four double-blind studies

Headache 1988 Feb; 28(1): 10-4
The effect of aspartame on migraine headache.
Koehler SM, Glaros A PMID: 3277925, UI: 88138777
Shirley M. Koehler, PhD 904-858-7651
http://www.med.umich.edu/abcn/alpha/...K.html#Koehler
Alan Glaros 816-235-2074

They conducted a double-blind study of patients, ages 18-55, who had
a medical diagnosis of classical migraines (normally having 1-3
migraines in 4-weeks), who were not on medications (other than
analgesics), and who suspected that aspartame had a negative effect on
their migraine headaches. The subjects were given 1200 mg daily,
aspartame or placebo, for four weeks, about 17 mg/kg. The placebo
group had no increase in headaches. Approximately half of the subjects
(5 of 11) who took aspartame had a large, statistically significant
(p = 0.02), increase in migraine headache frequency, but not in
intensity or duration, compared to baseline or placebo. Only 11 of
25 subjects completed the program: 8 dropped out, 4 began new
medications, 2 had incomplete records. They were at home.
Since 1/3 of the subjects dropped out, they may have been choosing
to avoid headaches-- were they unpaid? To achieve statistical
signifance with only 11 subjects hints that the incidence rate from
aspartame is very high, about 1/2, for migraine cases who believe
that they are hurt by aspartame.

http://groups.yahoo.com/group/aspartameNM/message/1077
eight depressed people react strongly to aspartame, Prof. Ralph G. Walton,
MD, 1993 double-blind study, full text: Murray 2004.04.26 rmforall

Walton, RG, "Adverse reactions to aspartame: double-blind challenge in
patients from a vulnerable population," 1993, with Robert Hudak and
Ruth J. Green-Waite, Biological Psychiatry, 34 (1), 13-17.
Ralph G. Walton, MD, Prof. of Clinical Psychology, Northeastern Ohio
Universities, College of Medicine, Dept. of Psychiatry, Youngstown,
OH 44501, Chairman, The Center for Behavioral Medicine,
Northside Medical Center, 500 Gypsy Lane, P.O. Box 240 Youngstown,
OH 44501 330-740-3621
http://www.neoucom.edu/DEPTS/Psychiatry/walton.htm

Eight depressed patients, ages 24-60, and five non-depressed controls,
ages 24-56, employed at the hospital, were given for 7 days either
aspartame or a placebo, and then after a 3 day break, given the
opposite. Each got 2100 mg aspartame daily, 30 mg/kg bodyweight,
equal to 10-12 cans of diet soda daily, about a gallon. Despite the
very small number of subjects, the results were dramatic and
statistically significant. The eight depressed patients reported with
aspartame, compared to placebo, much higher levels of nervousness,
trouble remembering, nausea, depression, temper, and malaise. (For each
symptom, p0.01) The five normals did not report strong enough
differences between aspartame and placebo to be significant.
Initially, the study was to be on a group of 40, but was halted by the
Institutional Review Board because of severe reactions among 3 of the
depressed patients.

Again, statistical significance with only 8 depressed patients:
"In this study, patients most often began to report significant
symptoms after day 2 or 3." The incidence rate is very high,
indeed, about 1/3. The most common symptoms are entirely typical
of thousands of case histories.

Stephen K. Van Den Eeden, T.D. Koepsell, W.T. Longstreth, Jr,
G. van Belle, J.R. Daling, B. McKnight, "Aspartame ingestion and
headaches: a randomized crossover trial," 1994, Neurology, 44, 1787-93
Steven K. Van Den Eeden,PhD 550-450-2202
Division of Research, Kaiser Permanente Medical Care Program
3505 Broadway, Oakland, CA 94611-5714
http://www.dor.kaiser.org/dorhtml/in...Den_Eeden.html

In their introduction, they comment:

"In addition, the FDA had received over 5,000 complaints as of July,
1991 in a passive surveillance system to monitor adverse side effects.
(17) Neurologic problems constitute the primary complaints in these
and several other case series, with headaches accounting for
18 to 45 %,depending on the case series reported. (17-19)"

Subjects, ages 18-57, were recruited who believed they got headaches
from aspartame, but were otherwise mentally and physically healthy.
They were paid $ 15 total, and were at home. Of the 44 subjects, 32
contributed data to the 38-day trials: a week of inert placebo, a week
of either aspartame or placebo, followed by a week of the opposite, and
then this two-week cycle repeated. The daily dose was about 30 mg/kg.
"The proportion of days subjects reported having a headache was
higher during aspartame treatment compared with placebo treatment
(aspartame = 0.33, placebo = 0.24; p = 0.04) (table 5)".
Of the 12 subjects not included in the data, 7 reported adverse
symptoms before withdrawing.

Again, statistical significance with a moderate number of healthy
subjects, willing to be recruited by a newspaper ad, who believed
aspartame hurt them. The number of headaches for each subject
for each treatment week are given: it appears that 4 subjects
had the strongest increase in headaches from the run-in week
or placebo week to their first week on aspartame, jumping from 0 to 5,
1 to 6, 1 to 4, 0 to 5 headaches per week. So, about 4 of the 44
healthy people recruited for the study, who believed aspartame hurt
them, had a stong increase in headaches from the first week of daily
asparame exposure, while 7 reported adverse symptoms before leaving,
a total of 11 out of 44, an incidence ratio of 1/4.

This is sky high, if we consider that, if the incidence ratio for the
about two hundred million users in the USA is 1 of 100, that is 2
million cases. It is plausible that the incidence ratio lies between 1
and 10 out of 100 for continuous daily exposure. These three flames
should have set off alarm bells, with extensive follow-up studies and
much more careful study of thousands of case histories. But these
little flares were adroitly smothered by thick blankets of industry
funded fluff:

http://groups.yahoo.com/group/aspartameNM/message/623
Simmons: Gold: Schiffman: Spiers:
aspartame toxicity: Murray 2001.06.04 rmforall two double-blind studies

http://www.truthinlabeling.org/ Truth in Labeling Campaign [MSG]
Adrienne Samuels, PhD The toxicity/safety of processed
free glutamic acid (MSG): a study in suppression of information.
Accountability in Research 1999; 6: 259-310. 52-page review
P.O. Box 2532 Darien, Illinois 60561
858-481-9333

http://groups.yahoo.com/group/aspartameNM/message/1067
eyelid contact dermatitis by formaldehyde from aspartame, AM Hill & DV
Belsito, Nov 2003: Murray 2004.03.30 rmforall [ 150 KB ]

http://groups.yahoo.com/group/aspartameNM/message/1070
critique of aspartame review, French Food Safety Agency AFSSA 2002.05.07
aspartamgb.pdf (18 pages, in English), Martin Hirsch:
Murray 2004.04.13

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 rmforall EU Scientific Committee on Food, a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame...2-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ): 59 pages, 230 references

http://groups.yahoo.com/group/aspartameNM/message/989 On 2003.04.10
the European Union Parliament voted 440 to 20 to approve sucralose,
limit cyclamates & reevaluate aspartame & stevia: Murray 2003.04.12 rmforall
There is an astonishing amount of positive research about stevia, banned in
the EU, and not allowed to be claimed as a sweetener in the USA:

http://groups.yahoo.com/group/aspartameNM/message/1084
26 stevia safety abstracts since 1993: aspartame vs stevia debate on
alt.support.diabetes, George Schmidt, OD: Murray 2004.05.17

http://www.eatright.org/Nutritive(1).pdf
J Am Diet Assoc. 2004 Feb; 104(2): 255-75.
Position of the American Dietetic Association: use of nutritive and
nonnutritive sweeteners. American Dietetic Association.

http://groups.yahoo.com/group/aspartameNM/message/1068
critique of aspartame review by American Dietetic Association Feb 2004,
Valerie B. Duffy & Madeleine J. Sigman-Grant: Murray 2004.05.14 rmforall

It is certain that high levels of aspartame use, above 2 liters daily for
months and years, must lead to chronic formaldehyde-formic acid toxicity.

Fully 11% of aspartame is methanol-- 1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).
The methanol is immediately released into the body after drinking--
unlike the large levels of methanol locked up in complex molecules inside
many fruits and vegetables.
Within hours, the liver turns much of the methanol into formaldehyde, and
then much of that into formic acid, both of which in time are partially
eliminated as carbon dioxide and water.

However, about 30% of the methanol remains in the body as cumulative
durable toxic metabolites of formaldehyde and formic acid-- 37 mg daily,
a gram every month, accumulating in and affecting every tissue.

If only 10% of the methanol is retained daily as formaldehyde, that would
give 12 mg daily formaldehyde accumulation-- about 60 times more than the
0.2 mg from 10% retention of the 2 mg EPA daily limit for formaldehyde in
drinking water.

Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.

http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30 rmforall

This long-term low-level chronic toxic exposure leads to typical patterns of
increasingly severe complex symptoms, starting with headache, fatigue, joint
pain, irritability, memory loss, rashes, and leading to vision and eye
problems, and even seizures. In many cases there is addiction. Probably
there are immune system disorders, with a hypersensitivity to these toxins
and other chemicals.

J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70% of the radioactive methanol in aspartame put into
the stomachs of 3 to 7 kg monkeys was eliminated within 8 hours, with little
additional elimination, as carbon dioxide in exhaled air and as water in
the urine.
They did not mention that this meant that about 30% of the methanol must
transform into formaldehyde and then into formic acid, both of which must
remain as toxic products in all parts of the body.
They did not report any studies on the distribution of radioactivity in body
tissues, except that blood plasma proteins after 4 days held 4% of the
initial methanol.
This study did not monitor long-term use of aspartame.

The low oral dose of aspartame and for methanol was 0.068 mmol/kg, about 1
part per million [ppm] of the acute toxicity level of 2,000 mg/kg, 67,000
mmol/kg, used by McMartin (1979).
Two L daily use of diet soda provides 123 mg methanol, 2 mg/kg for a 60 kg
person, a dose of 67 mmole/kg, a thousand times more than the dose in this
study.
By eight hours excretion of the dose in air and urine had leveled off at
67.1 +-2.1% as CO2 in the exhaled air and 1.57+-0.32% in the urine, so 68.7
% was excreted, and 31.3% was retained.
This data is the average of 4 monkeys.
"...the 14C in the feces was negligible."

"That fraction not so excreted (about 31%) was converted to body
constituents through the one-carbon metabolic pool."
"All radioactivity measurements were counted to +-1% accuracy..."
This indicates that the results could not be claimed to have a precision of
a tenth of a percent. OK, so this is a nit-pick-- but I believe espousing
spurious accuracy is a sign of scientific insecurity.

The abstract ends, "It was concluded that aspartame was digested to its
three constituents that were then absorbed as natural constituents of the
diet."
Thus, the concept is very subtly insinuated that methanol, as a
constituent of aspartame, is absorbed as a natural constituent of the diet.
"Dietary methanol is derived in large part from fresh fruits and
vegetables."
This is a serious error, since the large amounts of methanol in fresh fruits
and vegetables are not readily released by human digestion. (W. C. Monte,
1984)
Nowhere in this report are mentioned the dread words, "formaldehyde" and
"formic acid".

Of course, methanol and formaldehyde toxicity studies are highly relevant to
the issue of aspartame toxicity. [ Aspartame has to be turned into its
toxic products, formaldehyde and formic acid, in the body, before it is
toxic, so some pro-aspartame reseach studies test aspartame outside the
body, and then proclaim that they have proved that it is not toxic. ]

http://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold:
Wilson: CIIN: Murray 2002.12.12 rmforall

Thrasher (2001): "The major difference is that the Japanese demonstrated
the incorporation of FA and its metabolites into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9% of the administered dose." [ Ref. 14-16 ]

Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH.
Sam-1 Trust, Alto, New Mexico, USA.
http://www.drthrasher.org/formaldehy..._toxicity.html full text

http://www.drthrasher.org/formaldehyde_1990.html full text Jack Dwayne
Thrasher, Alan Broughton, Roberta Madison. Immune activation and
autoantibodies in humans with long-term inhalation exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223. "Immune activation,
autoantibodies, and anti-HCHO-HSA antibodies are associated with long-term
formaldehyde inhalation." PMID: 2400243

Confirming evidence and a general theory are given by Pall (2002):
http://groups.yahoo.com/group/aspartameNM/message/909
testable theory of MCS type diseases, vicious cycle of nitric oxide &
peroxynitrite: MSG: formaldehyde-methanol-aspartame:
Martin L. Pall: Murray: 2002.12.09 rmforall

Environ Health Perspect. 2003 Sep; 111(12): 1461-4.
Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity:
central role of N-methyl-D-aspartate receptors in the sensitivity mechanism.
Pall ML.
School of Molecular Biosciences, 301 Abelson Hall, Washington State
University, Pullman, WA 99164, USA.

The elevated nitric oxide/peroxynitrite and the neural sensitization
theories of multiple chemical sensitivity (MCS) are extended here to propose
a central mechanism for the exquisite sensitivity to organic solvents
apparently induced by previous chemical exposure in MCS.
This mechanism is centered on the activation of N-methyl-D-aspartate (NMDA)
receptors by organic solvents producing elevated nitric oxide and
peroxynitrite, leading in turn to increased stimulating of and
hypersensitivity of NMDA receptors.
In this way, organic solvent exposure may produce progressive sensitivity to
organic solvents.
Pesticides such as organophosphates and carbamates may act via muscarinic
stimulation to produce a similar biochemical and sensitivity response.

Accessory mechanisms of sensitivity may involve both increased blood-brain
barrier permeability, induced by peroxynitrite, and cytochrome P450
inhibition by nitric oxide.
The NMDA hyperactivity/hypersensitivity and excessive nitric
oxide/peroxynitrite view of MCS provides answers to many of the most
puzzling aspects of MCS while building on previous studies and views of this
condition. PMID: 12948884

Prof. Pall describes processes by which an initial trigger exposure, such as
carbon monoxide or formaldehyde, can generate hypersensitivity to many
substances. He himself had recovered from a sudden, debilitating attack of
multiple chemical sensitity in June/July 1997.

http://groups.yahoo.com/group/aspartameNM/message/1055
hormesis: possible benefits of low-level aspartame (methanol, formaldehyde)
use: Calabrese: Soffritti: Murray 2004.03.11 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1056
disorders of NMDA glutamate receptors in brain range from high activity
(MCS, CF, PTSD, FM, from carbon monoxide or formaldehyde (methanol,
aspartame)-- Pall)
to low activity (schizophrenia-- Coyle, Goff, Javitts):
Murray 2004.03.13 rmforall

http://groups.yahoo.com/group/aspartameNM/message/946
Functional Therapeutics in Neurodegenerative Disease Part 1/2:
Perlmutter 1999.07.15: Murray 2003.01.10 rmforall

http://groups.yahoo.com/group/aspartameNM/message/97
Lancet website aspartame letter 1999.07.29:
Excitotoxins 1999 Part 1/3 Blaylock: Murray 2000.01.14 rmforall
The Medical Sentinel Journal 1999 Fall; (95 references)
http://www.dorway.com/blayenn.html

http://groups.yahoo.com/group/aspartameNM/message/1034
Brain cell damage from amino acid isolates (aspartame releases
phenylalanine, aspartate, methanol [formaldehyde, formic acid] Bowen &
Evangelista May 6 2002: Murray 2003.11.10 rmforall

http://www.aspartame.ca/Brain%20Cell%20Damage.pdf
Brain cell damage from amino acid isolates 5.6.2 41 references
detailed 22 page review by James D. Bowen, MD and Arthur M. Evangelista,
former FDA Investigator

http://groups.yahoo.com/group/aspartameNM/message/628
Professional House Doctors: Singer: EPA: CPSC:
formaldehyde toxicity: Murray 2001.06.10 rmforall
************************************************** ***********

Many scientific studies and case histories report: * headaches * many body
and joint pains (or burning, tingling, tremors, twitching, spasms, cramps,
stiffness, numbness, difficulty swallowing) * fever, fatigue, swollen
glands * "mind fog", "feel unreal", poor memory, confusion, anxiety,
irritability, depression, mania, insomnia, dizziness, slurred speech, sexual
problems, poor vision, hearing (deafness, tinnitus), or taste * red face,
itching, rashes, allergic dermatitis, hair loss, burning eyes or throat, dry
eyes or mouth, mouth sores, burning tongue * obesity, bloating, edema,
anorexia, poor appetite or excessive hunger or thirst * breathing
problems, shortness of breath * nausea, diarrhea or constipation * coldness
* sweating * racing heart, low or high blood pressure, erratic blood sugar
levels * hypothryroidism or hyperthyroidism * seizures * birth defects
* brain cancers * addiction * aggrivates diabetes, autism, allergies,
lupus, ADHD, fibromyalgia, chronic fatigue syndrome, multiple chemical
sensitivity, multiple sclerosis, pseudotumor cerebri and interstitial
cystitis (bladder pain).
************************************************** ***********

http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984: Monte:
Murray 2002.09.23 rmforall

Dr. Woodrow C. Monte Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science [retired 1992]
Arizona State University, Tempe, Arizona 85287
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the aspartame.
The EPA limit for water is 7.8 mg daily for methanol (wood alcohol), a
deadly cumulative poison.
Many users drink 1-2 L daily.
The reported symptoms are entirely consistent with chronic methanol
toxicity. (Fresh orange juice has 34 mg/L, but, like all juices, has 16
times more ethanol, which strongly protects against methanol.)

"The greater toxicity of methanol to man is deeply rooted in the limited
biochemical pathways available to humans
for detoxification. The loss of uricase (EC 1.7.3.3.),
formyl-tetrahydrofolate synthetase (EC 6.3.4.3.) (42)
and other enzymes (18) during evolution sets man apart from all
laboratory animals including the monkey (42).

There is no generally accepted
animal model for methanol toxicity (42, 59).

Humans suffer "toxic syndrome" (54) at a minimum lethal dose
of 1 gm/kg, much less than that of monkeys, 3-6 g/kg (42, 59).

The minimum lethal dose of methanol
in the rat, rabbit, and dog is 9, 5, 7, and 8 g/kg, respectively (43);
ethyl alcohol is more toxic than methanol to these test animals (43)."

"Fruit and vegetables contain pectin with variable methyl ester content.
However, the human has no digestive enzymes for pectin (6, 25) particularly
the pectin esterase required for its hydrolysis to methanol (26).

Fermentation in the gut may cause disappearance of pectin (6) but the
production of free methanol is not guaranteed by fermentation (3).
In fact, bacteria in the colon probably reduce methanol directly to formic
acid or carbon dioxide (6) (aspartame is completely absorbed before
reaching the colon).
Heating of pectins has been shown to cause virtually no demethoxylation;
even temperatures of 120 deg C produced only traces of methanol (3).
Methanol evolved during cooking of high pectin foods (7) has been accounted
for in the volatile fraction during boiling and is quickly lost to the
atmosphere (49).
Entrapment of these volatiles probably accounts for the elevation in
methanol levels of certain fruits and vegetable products during canning (31,
33)."

Recent research supports his focus on the
methanol to formaldehyde toxic process:

"The United States Environmental Protection Agency in their Multimedia
Environmental Goals for Environmental Assessment recommends a minimum
acute toxicity concentration of methanol in drinking water at 3.9 parts
per million, with a recommended limit of consumption below 7.8 mg/day (8).
This report clearly indicates that methanol:

"...is considered a cumulative poison due to the low rate of excretion
once it is absorbed. In the body, methanol is oxidized to formaldehyde
and formic acid; both of these metabolites are toxic." (8)...

Recently the toxic role of formaldehyde (in methanol toxicity) has been
questioned (34).
No skeptic can overlook the fact that, metabolically, formaldehyde must be
formed as an intermediate to formic acid production (54).

Formaldehyde has a high reactivity which may be why it has not been found in
humans or other primates during methanol posisioning (59)....

If formaldehyde is produced from methanol and does have a reasonable half
life within certain cells in the poisoned organism the chronic toxicological
ramifications could be grave.

Formaldehyde is a known carcinogen (57) producing squanous-cell carcinomas
by inhalation exposure in experimental animals (22).
The available epidemiological studies do not provide adequate data for
assessing the carcinogenicity of formaldehyde in man (22, 24, 57).

However, reaction of formaldehyde with deoxyribonucleic acid (DNA) has
resulted in irreversible denaturation that could interfere with DNA
replication and result in mutation (37)..."
************************************************** ***********

http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan;
http://www.sunsentpress.com/
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

http://groups.yahoo.com/group/aspartameNM/message/790
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07 rmforall

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780

http://groups.yahoo.com/group/aspartameNM/message/859
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02 rmforall
************************************************** ***********

http://groups.yahoo.com/group/aspartameNM/message/782
RTM: Smith, Terpening, Schmidt, Gums:
full text: aspartame, MSG, fibromyalgia 2002.01.17 rmforall
Jerry D Smith, Chris M Terpening, Siegfried OF Schmidt, and John G Gums
Relief of Fibromyalgia Symptoms Following
Discontinuation of Dietary Excitotoxins.
The Annals of Pharmacotherapy 2001; 35(6): 702-706.
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.

Siegfried O. Schmidt, MD Asst. Clinical Prof.
Community Health and Family Medicine, U. Florida, Gainesville, FL
Shands Hospital West Oak Clinic Gainesville, FL 32608-3629
352-376-5071

http://www.perque.org/Fibromyalgia.pdf
A Novel Treatment for Fibromyalgia Imrpoves Clinical Outcomes in a
Community-Based Study.
Patricia A. Deuster, Russell M. Jaffe.
Journal of Musculoskeletal Pain. 1998; Vol. 6(2): 133-149.

http://www.perque.com/ 800-525-7372

Using blood tests, the researchers ran a panel of 350 antigens including
environmental chemicals, food additives and preservatives, crustaceans,
diary products, fish, fruits, grains, meats, mollusks, and oils.

Normal, healthy people react to only two or less of this panel. The greatest
offenders we

MSG 42.5 % (17 out of 40 patients)
Candida albicans 37.5
Caffeine 37
Chocolate/cocoa 37
Food colorings 37
Cola beverages 37
Cow Dairy Products 25
Sulfite/metabisulfite 22.5
Xylene 22.5
Yogurt 22.5
Aspartame 20
BHA 20
Cadmium 20
Lead 20
Tylenol 20
Yeast 20
Sodium benzoate 20
Orange 20
************************************************** ***********

http://groups.yahoo.com/group/aspartameNM/messages 2004.08.01
130 members, 1,107 posts in a public searchable archive

http://groups.yahoo.com/group/aspartame/messages 2004.08.01
829 members, 17,208 posts in a public, searchable archive
************************************************** ***********

Nothing like junk food science.

Bottom line: aspertame contains small amounts of methanol, a compound that
is found in naturally and in much higher concentrations in many other foods.
If you are worried about methanol in your food, then you need to give up a
lot more than aspertame. The fact that the ninnies that are so worried about
aspertame will not do this tells you far more about them than it does about
aspertame.

Nothing like junk food science.

Bottom line: aspertame contains small amounts of methanol,

Another bottom line: if you have a serious allergy to aspartame, you know it
before you grow up, go all the way through pilot training, and become an
airline transport pilot.

Why not ban peanuts too, in case you've grown up in another galaxy till the
minute Northwest hired you and offered you a bag of snacks that'll turn out to
kill you?

Honestly. A pilot reckless enough to take control and slam a diet Coke knowing
he has a disabling allergy to the sweetener will have disqualified himself from
professional employment a long time before he slugs down a beverage that'll
knock him out in the cockpit.

On 22 Aug 2004 03:34:01 GMT, (StellaStar) wrote:

Nothing like junk food science.

Bottom line: aspertame contains small amounts of methanol,

Another bottom line: if you have a serious allergy to aspartame, you know it
before you grow up, go all the way through pilot training, and become an
airline transport pilot.

Typically it doesn't work that way for most people and most people
don't understand allergies.

My allergist tells me: People develop allergies. They may have them as
youngsters and out grow them and people who have never been allergic
to anything may develop them later in life.

Allergies can just suddenly appear without warning or they may slowly
develop. Like lightening they are unpredictable.

I'm allergic to mold, a number of pollens, dust, eggs and aspartame.
Eggs are probably the worst. That makes getting a flu shot time
consuming and expensive.

I used to eat two stacks of pancakes, 4 eggs, 4 slices of toast, plus
enough jam to cover what toast wasn't needed to soak up the eggs for
breakfast.

Why not ban peanuts too, in case you've grown up in another galaxy till the
minute Northwest hired you and offered you a bag of snacks that'll turn out to
kill you?

Honestly. A pilot reckless enough to take control and slam a diet Coke knowing
he has a disabling allergy to the sweetener will have disqualified himself from
professional employment a long time before he slugs down a beverage that'll
knock him out in the cockpit.

When it comes to allergies he/she may have never had an allergy
reaction before. Be that as it may, I see no reason to ban aspartame,
peanuts, Soy products, or eggs...course I've never found an airline
serving eggs.

I guess they'll just have to serve every one a concentrated capsule of
Metamucile(sp?) and a glass of water. At least you'd be full. :-))

Roger Halstead (K8RI & ARRL life member)
(N833R, S# CD-2 Worlds oldest Debonair)
www.rogerhalstead.com

I have to agree. During the summer time where I live, I gets hot enough
that
I consume incredble quantities of soda, mostly diet, and I do not suffer any
ill effects.


"Dylan Smith" wrote in message
...
In article , Paul G
wrote:
Let's keep out of the debate over aspartame's safety. This is an
exercise in getting some primary source evidence. I just want to find
out if SWA does indeed have such a policy. Are there any crew out
there who can confirm or deny?

It sounds pretty silly on the face of it. Aspartame is consumed in vast
quantities - if it was dangerous, it'd have shown up by now.

--
Dylan Smith, Castletown, Isle of Man
Flying: http://www.dylansmith.net
Frontier Elite Universe: http://www.alioth.net
"Maintain thine airspeed, lest the ground come up and smite thee"

Dylan Smith wrote:
In article , Paul G wrote:

Let's keep out of the debate over aspartame's safety. This is an
exercise in getting some primary source evidence. I just want to find
out if SWA does indeed have such a policy. Are there any crew out
there who can confirm or deny?


It sounds pretty silly on the face of it. Aspartame is consumed in vast
quantities - if it was dangerous, it'd have shown up by now.

I agree.

And, further, why do we contribute to, and support, the irrational
"concerns" people with too much spare time on their hands conjure up?

They're everywhere. Let 'em stew in their own juices.