[ minor typos and unclear sentences have been edited, and links added
by Rich Murray, Moderator.
I will post critical responses, pro and con,
that are specific, relevant, informed, referenced, and civil. See also:
http://groups.yahoo.com/group/aspartameNM/message/1032
Tagatose and diabetes: James D. Bowen, MD 10.8.3
http://groups.yahoo.com/group/aspartameNM/message/1030
tagatose (Naturlose), a "natural" sweetener: wired.com Ratliff:
Murray 10.24.3 rmforall
http://www.bowendrjim.com
http://www.bowendrjim.com/index.cfm#46 ]
http://www.aspartame.ca/Brain%20Cell%20Damage.pdf
Brain Cell Damage from Amino Acid Isolates:
A Primary Concern about Aspartame-based Products and Artificial
Sweetening Agents NutraSweet ~ Equal ~ "Sugar Free" ~ Neotame
May 6, 2002
James D. Bowen, M.D., specializing in the applied biochemistry of
aspartame
Arthur M. Evangelista, former FDA investigator
Forward
This article is a review of long-standing intensive research into the
brain chemistry effects of aspartame, a toxic artificial sweetener
consumed daily by hundreds of millions of unsuspecting individuals.
We acknowledge the uncounted and unnecessary suffering, illness, and
death, associated with the marketing of a trio of neurotoxic
ingredients,
collectively known as aspartame,
[ L- aspartyl - L - phenylalanine methyl ester ], also called:
NutraSweet, Equal, "Sugar Free", and Neotame, et al. [Canderel,
Spoonful, E951], a food additive in over 8,000+ food products
worldwide.
The three toxic ingredients of Aspartame are methanol (wood alcohol),
phenylalanine and aspartic acid; both the latter are amino acid
isolates.
Moreover. we hold accountable the U.S. Food and Drug Administration;
G.D.
Searle, the original maker of aspartame; Monsanto; and the numerous
corrupted politicians, government officials, physicians, and health care
organizations that have literally sold themselves for greed of wealth
and
power. This was done knowingly, at the expense of the health of millions
of infants, children, and adults, who needlessly suffer the debilitating
effects of this known neurotoxin.
This article is for the education of the public at large, and for the
physicians and health specialists who have the integrity and intellect
to
understand the implications of aspartame's ingredients and their
biochemical and pathological effects upon brain nerve cells and tissues,
which result in serious neuro-endocrine disorders and other
symptomologies.
We hope that all people will cease consumption of this deadly product
and
become self-educated in order to protect their own health against an
array of marketed food and environmental toxins. It is our hope that
all people will live healthier and more fruitful lives, and maintain the
freedom and wisdom to choose what they put in their mouths and feed
their children.
Protein and Amino Acids
Proteins are nature's building blocks of life. Proteins are used for
producing and maintaining muscle, tissue, blood, hormones, and enzymes,
including the body's organs, skin, and healing processes.
Proteins are large, complex organic compounds made up of many groups of
amino acids linked together. There have been twenty-two (22) amino acids
identified as necessary for normal human growth and development.
The body can make fourteen (14) of these amino acids, which are named
non-essential amino acids. The other eight (8) amino acids must be
received through outside sources, as in the foods we eat. These amino
acids are called essential amino acids.
Proteins are broken down during the process of digestion into their
component amino acids or into very small groups. The amino acids are
then
used by the body for maintaining health.
Amino acids also play a key role in--
neurotransmission,
solute concentration and balance (especially in areas of the brain),
calcium pump (gate) effectors in cells,
production and expenditure of ATP (the cell's energy stores),
overall body nerve cell conduction systems.
The amino acids that are released into the blood stream are competitive.
This means that the various types of amino acids compete for attachment
sites on enzymes and cell structures. It is this competition, which
restricts any one type of amino acid from becoming too dominant and
causing an inbalance in the normal ratio of the different circulating or
cellular amino acids.
The enzymes, which are located throughout the body, including the brain
and nerve cells, are responsible for ensuring that the amino acids get
to their proper end destination to be utilized by body tissues.
Many key factors, including food additive excitotoxins and environmental
poisons, play a role in nervous system degeneration. Collected evidence
and accumulated non-industry funded research leaves no doubt that the
powerful excitotoxin, aspartame, and its breakdown products, have a
central or predominant role in creating or exacerbating
neurodegenerative or neurocarcinogenic diseases.
Amino Acid Isolates
The focus of our report is an overview of excitotoxic effects upon brain
chemistry due to aspartame's amino acid isolates.
Amino acid isolates have been artificially separated from the rest of
their protein chains. Two are part of the aspartame compound. Aspartame
is then added to foods during the manufacturing process.
Thus, these amino acids exist by themselves (isolated), as single or
dipeptide molecules.
This is very different than the long 80-300 amino acid chains that form
from natural proteins from dietary sources.
Some examples of genetically modified (rDNA) or manufactured amino acid
isolates are glutamic acid or glutamate (i.e., monosodium glutamate,
MSG), aspartic acid or aspartate, and phenylalanine, among others.
The isolates differ from dietary amino acids from foods, because dietary
amino acids are absorbed from the gut. The body's digestive action
breaks down the long amino acid chains in proteins and then absorbs
them. Thus, through the body's natural regulation of its metabolism,
proteins from foods are broken down slowly, and always into a nutritious
mix of other amino acids in the proper enzyme-regulated proportion for
use by the body.
Following digestion of normal food proteins, the broken amino acid
chains
are slowly released into the body. Since they are in competition with
one
another for the enzyme sites, as earlier discussed, the body ensures
that no one amino acid dominates the others. However, it has been noted
that
phenylalanine is the strongest competitor for many of these enzyme
sites.
Moreover, the effect of a dosed amino acid isolate cannot be used in
synthesis of proteins in the same manner as food amino acids, because
the
body requires the "variety of the mix" to prepare and manufacture
proteins, including the availability of many different enzymes and
intermediary structures.
The excitotoxic effects of glutamic acid isolates are well studied and
widely known. Some beneficial uses of amino acid isolates, such as
L-lysine for use against oral herpes virus (SI) are also well known.
It is important to recognize the difference between natural, dietary
amino acids from foods, and pharmaceutically produced (including rDNA)
amino acid isolates.
It is also important to recognize that the isolates of aspartame are
incorporated into a compound containing free methanol, a dangerous
carcinogen and mutagen, which readily breaks down into formaldehyde and
formates inside the human body.
The hazards of ignoring the pharmacological nature of amino acid
isolates
are best illustrated by the phenylalanine isolate, 50% by weight of
aspartame. A can of soda pop yields about as much phenylalanine as a
large helping of beans.
NOTE: One 12 oz. can of diet soda contains 200 mg of aspartame.
Phenylalanine = 100 mg 50%
Aspartic Acid = 80 mg 40%
Methanol = 20 mg 10%
It should also be noted that the pharmaceutical isolates of amino acids
in aspartame are produced from genetically modified bacteria (E.coli).
About Phenylalanine
The dietary phenylalanine from the beans would only be harmful to the
person with PKU (phenylketonuria), an inherited genetic condition caused
by one of several enzyme deficiencies. This creates/allows increased
plasma levels of phenylalanine (overload), leading to the formation of
destructive neurotoxic effects.
In healthy individuals, the fact that dietary phenylalanine is in
competition with the other amino acids and is absorbed slowly over ten
to
twenty hours from the digestive tract, makes it helpful rather than
harmful for them.
In contrast, the phenylalanine (isolate) from the can of aspartame-laced
soda pop is absorbed in about five minutes. This goes to the portal vein
in the liver, with virtually no other competitive amino acids. Amino
acid
release from the liver is through an enzyme-linked channel. Without any
competition from any other amino acids, this phenylalanine is released
into the blood stream as an overwhelming bolus, or flood.
Even when ingested with foods, aspartame substantially increases the
plasma phenylalanine (and aspartic acid) levels, due to their
pharmaceutical make-up as isolates, and due to phenylalanine's strong
competitive affinity for the enzyme mediators and transmitter catalysts.
Synergistic damage also results from the absorption-metabolism sequence
of methanol, turned into formaldehyde and then formic acid. Methanol
and
formaldehyde are carcinogenic and mutagenic. As a metabolic poisons,
formaldehyde alters both mitochondrial DNA and nucleic DNA by binding as
adducts. This may be a strong initiator of disease states, because DNA,
damaged by formaldehyde adducts, may not allow cells to function
properly or maintain homeostasis.
Excitotoxic Amino Acids' Pathway to the Brain
Background: THE BRAIN
The brain, on an anatomical level, is an integrated network of nerve
cells and support cells (astrocytes, oligodendrocytes, et al), and is
the
controller for nerve-endocrine coordinating functions and their feedback
networks.
The brain controls the body's endocrine system through nerve
transmission, which centers on the functionality of the hypothalamus and
pituitary gland.
This includes the nerve-endocrine coordination of the pancreas and
secretions of the adrenals, thyroid, and gonads. This, in turn, acts
upon
the brain and pituitary and on the tissues throughout the body. This
tightly controlled system produces a wide range of effects for proper
functioning of the human organism.
Some hormone effects are used for development of the organism, from
conception through birth. Some are long lasting. Many are a permanent
element for life. Hormones can be initiated during maturity. Some
hormones act later in adult life, can signify changes in brain function,
or are associated with disease states or aging.
Nerve-endocrine functions can also act upon aspects of human behavior.
This integrated system signals when one are hungry or upset. The overall
health of this system affects learning and cognitive reasoning, controls
temperature, allows one to smell fresh-baked chocolate chip cookies,
stimulates growth, oversees ones heart rate, and is necessary for all
the
life functions enjoyed and needed. The brain, in effect, is the "Chief
Operating Officer" of the physical body.
There are two avenues or pathways to furnish nutrients, oxygen, and
other
selective chemicals to the brain. These are via the Blood Brain Barrier
(BBB) and/or the Cerebral Spinal Fluid (CSF).
The blood brain barrier is similar, in some ways, to the blood vascular
network in the other parts of the body. The blood brain barrier
resembles
normal capillaries, with a few exceptions.
The body's capillaries, outside of the brain, are more permeable
(porous) to fluids, ions, and other molecular structures, because there
are very minute spaces between the cells making up the capillary walls.
The brain's capillary system (blood brain barrier), on the other hand,
are composed of tightly packed cells or "junctions", which reduce their
permeability and eliminate the bulk flow of solutes through them.
Because of the tight junctions between the blood brain barrier's
capillary cells, there are two specialized ways that nutrients and other
molecules can gain access to brain cell components and neurons. These
pathways are:
1) lipid mediation or
2) catalyzed (active carrier)) transport.
The lipid transport system is confined to the transfer of small
molecules to the brain tissue, generally proportional to their lipid
solubility.
The catalyzed transport system includes both receptor and carrier
mediating enzyme processes in order to provide the brain with nutrients
(glucose, amino acids, and nucleosides, etc.)
Diag. # 1. The Blood Brain Barrier - capillary structure and adjacent
nerve cell structures.
Brain Capillary Wall
Another function of the blood brain barrier is to isolate the brain from
toxic products and certain chemicals that could disrupt the delicate
balance of ions, nutrients, and neurotransmitter substances that are
used by the brain's nerve cells.
When aspartame is ingested and enters the blood stream, the three toxins
of aspartame are "launched" throughout the body very rapidly.
Following consumption of aspartame-laced products, the phenylalanine
flood overpowers the enzyme systems of the brain, setting off an induced
PKU effect.
This induced PKU affect occurs by grossly overwhelming those enzymes
required to reduce the circulating phenylalanine for use in other
metabolic reactions.
This "overdose" of the competitive phenylalanine isolate (and also
aspartic acid) incapacitates the enzyme actions which control several
types of neurotransmitters (and their precursor amino acids), reducing
dopamine and serotonin production.
The excitotoxins' effects create secondary components, which are also
destructive in nature to the sensitive, surrounding neural tissues,
including a breakdown by-product of phenylalanine, called
diketopiperazine
(DKP), which instigates tumor generation, especially that of aggressive
glioblastoma.
Further neuron insult is added due to the destruction and mutation of
nucleic and mitochondrial DNA from the known carcinogenic properties of
formaldehyde, from the methanol component of aspartame.
The other avenue of delivering nutrients and other necessary molecules
to the brain's cell structures is by way of the Cerebral Spinal Fluid
(CSF).
There is a structure called the 'Choroid Plexus" which is a specialized
arterio-venous capillary bed, located within the lateral ventricles of
the cerebral hemispheres, that secretes the cerebral spinal fluid.
(See Diag. # 2 and # 3)
The cerebral spinal fluid is a clear, colorless liquid that circulates
around the brain and spinal cord, bathing the tissues with needed
nutrients and other constituent molecules.
Diag. # 2 Cerebral Hemisphere Lateral ventricles
Diag. # 3 Close-Up of Choroid Plexus
The brain is seen to contain four cavities within it. The cerebrum holds
two large Lateral Ventricles that connect at the midline. From here, the
CSF follows the Interventricular Foramina into the Third Ventricle.
Here, at the Third Ventricle, another Choroid Plexus adds additional
CSF.
The CSF then passes through the Aqueduct of Sylvius, continuing into the
Fourth Ventricle, located between the cerebellum and brainstem. Here,
still another Choroid Plexus, at the roof of the Fourth Ventricle,
contributes additional CSF fluid.
After leaving the Fourth Ventricle, the CSF essentially flows backward
and downward around the midbrain, exiting the ventricular network below
the cerebellum.
Some of the CSF passes downward into the Spinal Subarachnoid Space
(circulating around the spinal cord), and a portion rises upward,
through
the Tentorial Notch, spreading over the hemispheres of the brain.
Reabsorption of CSF is predominantly assumed through the lymph and blood
capillary network, in the subarachnoid space covering the cerebral
hemispheres and spinal canal.
Ventricle Network
Diag. # 4
The lateral ventricles are the large, parallel structures denoted by the
letter L, that wrap around like ram's horns, also moving laterally into
the two cerebral hemispheres.
The third ventricle is a medial structure indicated by the number 3.
The fourth ventricle is difficult to see in this diagram. You can just
see it starting to open up where the number 4 is, but it is largely
obscured by the cerebellum. Like the third ventricle, it lies along the
midline of the brain.
Cerebellum Aqueduct of Sylvius
The nutrients supplied by the CSF are delivered by diffusion into those
structures adjacent to the CSF. This leads to some specialized
circumstances.
First, as the CSF diffuses nutrients (or toxins) to these adjacent
structures, as it continues along its track, the concentrations of the
nutrient molecules remaining within the CSF becomes lower and lower.
If toxins are present within the CSF, those structures first contacted
are far more severely attacked by these toxins (or excitotoxins), than
those bathed in CSF farther away from the ventricular system and choroid
plexus.
Second, diffusion of chemicals is greatly increased by increases in
hydrostatic pressures or flow rates.
Third, inflammation of the Aqueduct of Sylvius, from repeated insults of
neurotoxic chemicals contained within the CSF, can cause narrowing of
this duct, resulting in obstruction and the onset of adult
hydrocephalus.
It is in the CSF that the phenylalanine and dicarboxylic aspartic acid
diffuse, setting off a chain reaction of repeated excitatory stimuli of
the surrounding nerve cells and neuronal structures adjacent to the flow
route of the CSF. This eventually leads to nerve cell necrosis (cell
death) in those areas.
The hypothalamus sits adjacent on either side of the Third Ventricle,
where there is a high diffusion rate of any toxins from the CSF, leading
to sustained and potentially extreme damage to this neuro-endocrine
structure, one of the most vital neural systems in the body.
Diag. # 5
Lateral Ventricles Third Ventricle Hypothalamus
Parts of the hypothalamus that are visible in basal and mid-sagittal
views of the gross brain include the mammillary body and the
infundibulum (tuber cinereum).
Fourth Ventricle
A (simplistic) sequence of events would be the following:
The transport of excitotoxins across the blood brain barrier and within
the CSF causes several reactions to occur.
1) The excitotoxins stimulate the nerves to fire excessively.
2) The normal enzyme actions required to offset the induced, repeated
firing of these neurons are negated by the phenylalanine and aspartic
acid.
Furthermore, 3) the energy system for the required enzyme reactions
becomes compromised from:
4) depleted intracellular ATP stores,
5) the presence of formaldehyde,
6) altered intracellular Ca+ uptake,
7) damage to cellular mitochondria,
8) destruction of the cellular wall,
and 9) the subsequent release of free radicals.
This potentiates 10) oxidative stress and neurodegeneration. These toxic
by-products initiate secondary damage, which increases capillary
permeability, continuing to destroy the surrounding nerve and glial
cells. This further impedes enzyme reactions, and 11) promotes DNA
structural defects.
Cellular death occurs over the next 1 to 12 hours. This does not include
the long-term or cumulative effects of formaldehyde adducts and other
metabolites. The dead cells leave behind lesions, or holes, as Dr. Olney
discovered with the tests he conducted.
Evidence indicates that the following disease states can be clinically
identified by the corresponding damage to their anatomic nerve fibers,
or
nerve bundles:
a) Aqueduct of Sylvius = Hydrocephalus
b) White matter bundles = Multiple Sclerosis (MS)
c) Pyramids/Basal Ganglia = Parkinson's Disease
d) Lateral corticospinal tracts of spinal cord and bulbar nuclei =
Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease), ALS
e) Destruction of hypothalamic regions = Neuro-endocrine disorders,
obesity, psychogenic disorders (behavior, anger), malfunction of
autonomic nervous system, immune suppression, et al. (See Diag. # 5,
previous page)
Above the Fourth Ventricle, lie the pyramids, and slightly forward are
the basal ganglia. Powerful insults from excitotoxic stimulations
develop clinical manifestations of Parkinson's disease (See Diag. # 6).
This is further complicated by the depletion of the neurotransmitter,
dopamine, caused by the obliteration of enzyme sites by the flood of
these excitotoxins.
Parkinson's Disease, itself, is a complex chronic brain disorder
resulting primarily from progressive death of a specific group of nerve
cells in a layer of a region of the substantia nigra (basal ganglia) in
the midbrain.
Diag. # 6 Lateral Ventricles Fourth Ventricle
These nerve cells produce a chemical neurotransmitter called dopamine
(which is inhibited by the phenylalanine/aspartic acid isolates of
aspartame). The dopamine enables communication with receptors on neurons
in a region of the brain called the striatum. Additional dopamine
pathways run from the midbrain to the limbic area and to the cerebral
cortex.
The striatum includes three structures: globus pallidus, putamen and
caudate nucleus. (See Diag. 7, below)
The striatum is a part of the brain involved with regulating the
intensity of coordinated muscle activity such as movement, balance and
walking. Insufficient levels of dopamine from the neurons of the
substantia nigra synapsing on neurons in the striatum is believed to be
responsible for the primary symptoms of Parkinson's.
View of Brain structures affected by Parkinson's (and surrounding
structures)
Diag. # 7
Compromised nerve pathways caused by depletion of dopamine
As with Parkinsonian, Amyotrophic Lateral Sclerosis (ALS), commonly
called Lou Gehrig's Disease, clearly represents a connection between
nerve damage and the presence of excitotoxic amino acids.
Amyotrophic lateral sclerosis, or ALS, is a progressive, degenerative
disease resulting from damage or destruction of motor neurons within the
brain and spinal cord. Nerve cell destruction impairs or prevents muscle
movement that corresponds to the affected neurons.
The various types of ALS include "bulbar", which affects the cranial
nerves, creating complications with speech and swallowing, et al.
When the damaged neurons extend from the spinal cord to muscle fibers,
this is often termed motor neuron disease.
There can also be various combinations of these degenerative states.
Effects of the excitatory amino acid, glutamate, have been observed in
the brain and spinal cord. There is an increase of this excitotoxin
within the CSF. Additionally, the damaged areas of the cerebral cortex
and spinal cord fail to "uptake" this neurotransmitter substance,
leaving higher amounts in the extracellular space, causing notable
cellular damage due to its excitatory properties.
NOTE: Aspartate (aspartic acid) is similar to glutamate and reacts with
many of the same enzyme structures.
Also noted, are pathologies related to cellular calcium (Ca+) channels,
which are altered by the presence of glutamate or aspartate. Calcium
changes may cause further deterioration by triggering secondary antibody
effects that react to this damage. Cellular damage will cause the
release of oxidizing agents, resulting in high, free radical exposure
that even further damages the nerve cells. Mitochondrial damage is
compounded from this surge in free radical generation.
Cerebrum Diag. # 8
NEURONS AFFECTED BY AMYOTROPHIC LATERAL SCLEROSIS
Multiple Sclerosis (MS) is a disease that affects the myelin (myelin
sheath), which is the insulation or coating of some of the nerves of the
brain, spinal cord, and of the periphery. Damage has also been
identified
that affects a part of the nerve fibers called the axons.
Oligodendrocyte
damage and cell loss also occurs.
Nerve cell damage takes place within the "white matter" of the brain,
where the neurons have myelin sheaths, giving this part of the brain its
color.
Demyelination of the central nervous system (white matter) are hallmarks
of this disease. This is normally (but not always) accompanied by optic
neuritis, asymmetrical muscle weakness, or fatigue.
Evidence seems to point to an immunological disorder, as a response to
an
inflammatory process in the brain (and/or spinal cord).
Although scientists have not identified a definitive cause of Multiple
Sclerosis, many hypothesize that MS may be of a triggered immunological
origin. Bowen and Evangelista's investigative research into known
scientific endeavors, biochemical facts, and available data, leads to
the
following proposed deduction. Hopefully, this will prompt further
investigation into the etiology of MS by non-industry funded
researchers.
IF MS is an "immunological" response, then the following need be
considered:
1) A reduction in glutathione synthesis will impair antioxidant
defenses.
2) Glutathione is virtually eradicated (not available) following the
ingestion of aspartame and its resulting metabolic reactions.
3) T-Cells (immune response cells) are dependant upon intracellular
glutathione.
4) Functionality of the T-cells is impaired during this period.
5) Toxicity by formaldehyde and formic acid from methanol results in
deamination, and can also be highly mutagenic for nucleotides, DNA, and
RNA transcription processes.
6) Pharmaceutically manufactured isolates (alone or in concert with
additional excitotoxic food additives/environmental toxins) create
excitotoxic responses, including:
* increased cell damage from oxidation,
* mitochondrial damage (incuding a reduction in available ATP),
* imbalance of inter/extracellular amino acids and their precursors,
* increased intracellular Ca+ or disruption of gated processes,
* release of damaging free radicals,
* excessive nitric oxide (NO) production,
* displacement/release of free iron within the brain,
* mutagenic effects from formaldehyde or generalized cellular DNA
mutations,
* subsequent inflammatory response as a result of this cellular damage
7) Evidence reveals that methanol has long been the agent most well
know to cause auto-immune antibodies to "attack" the pancreas and myelin
sheaths of neurons.
8) The structures damaged in MS are the white fibers of the CNS. These
structures are in intimate contact with the cerebral spinal fluid
immediately after the fluid is formed by the Choroid Plexus. Therefore,
the white matter receives massive doses of dicarboxylic amino acid
neuro-excitotoxins which are delivered to the brain from the CSF.
It is proposed that, regarding MS diagnosis (and possibly other
potential
auto-immune diseases of the central nervous system), this sequence of
damage from aspartame would elicit an inflammatory reaction. This leads
to a generalized (and possibly defective) immune response against the
neurons that have sustained damage, alteration, or exhibit other
"non-familiar" DNA changes.
In some cases, the immune system itself may have been damaged by the
formaldehyde's mutagenic effects or affected by brain chemistry/enzyme
changes, creating a flawed system. This could cause the body to attack
and catabolize its own nerve (or other) cells. Destroyed neurons will
eventually be absorbed, leaving lesions or holes where they once had
been.
Abstinence from aspartame appears to relieve the clinical presentation
of
excitotoxic-induced MS.
This immune process defect may (in part) also explain the rise in
cross-chemical sensitivity syndrome.
Furthermore, during maternal aspartame consumption, development of the
fetal nervous system is damaged or impaired via excitotoxic-saturated
placental blood flow that can cause or contribute to cerebral palsy and
pervasive developmental disorders, such as discussed here.
This is due to an incompetent blood brain barrier and neuronal (brain)
damage produced by excitotoxins circulating in the fetal brain areas.
This is especially true for those areas adjacent to the brain's
ventricular system. There is no doubt that destruction or damage of the
hypothalamus and corresponding neuro-endocrine organs leads to potential
developmental complications (physical and mental).
Additionally, fetal alcohol syndrome can be mimicked through the
methanol
components of aspartame, and so is a direct result from the maternal
ingestion of aspartame.
Other disorders of fetal neurotoxin exposure will show up after birth,
in
the form of patho-physiologically induced learning and behavior
disorders, attention deficit disorders, and the potential of DNA
structural mutagenisis from formaldahyde concentrations, adducts, and
the accompanying excitotoxic damage.
Of Special Note:
During the production of aspartame, none of the animal studies conducted
revealed the true neurotoxic nature of this poison in humans. That means
that the studies were design-flawed from day one. A successful
pharmaceutical firm and seasoned intelligence or research personnel do
not overlook this type of testing application by accident.
It is evidenced that, even with the relatively lower doses used during
initial testing, many of these test animals still became sick or died as
a result of ingesting aspartame.
Prior to the development of aspartame, it was a well known fact that
phenylalanine interferes with human brain chemistry and had once been
considered as a chemical warfare agent due to its neurotoxic
capabilities.
Physiologically, human beings are approximately 60 times more sensitive
to phenylalanine toxicity than any of the animals tested.
Furthermore, humans are 10-20 times more sensitive to methanol poisoning
both as a subchronic and chronic toxin/carcinogen. On the contrary, the
animals studied are more sensitive to the more common ethanol found in
alcoholic beverages, due to differences in enzyme concentrations among
species.
Humans are also about 8-10 times more sensitive to the affects of
aspartic acid and glutamates than the test animals being used.
NOTE:
A new sweetener known as Neotame has chemical properties of known
toxicity to man.
Neotame appears to be a chemically altered "aspartame", possessing
similar proportionate neurotoxic qualities.
I suspect the new name was formed to superficially distance this product
from aspartame, due to the symptoms generated and because of the
publicity this poison has received. Additionally, we should note that
our public health agencies, as well as our regulatory policies, are in
severe need of reorganization, to put it mildly.
[ http://groups.yahoo.com/group/aspartameNM/message/860
RTM: FDA: objections to neotame approval 8.4.2 rmforall ]
All evidence substantiates that aspartame is a powerful neurotoxin.
Further investigation is absolutely warranted.
James D. Bowen, MD bowen...@yahoo.com
P.O. Box 177 Walla Walla, Washington 99362
Arthur M. Evangelista orw...@msn.com
P.O. Box 474
Barnardsville, N.Carolina 28709
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Bressler Report. 1977: U.S. Food and Drug Administration, EIR: G.D.
Searle, Searle Laboratories. Summary of Findings (FDA). 1977 Aug.
[ http://groups.yahoo.com/group/aspartameNM/message/857
RTM: www.dorway.com: original documents and long reviews of flaws in
aspartame toxicity research 7.31.2 rmforall ]
Brown, Scott. Free Radicals Appear to Fuel Lou Gehrig's Disease . At
an
international conference at George Washington University Medical
Center, it was noted amyotrophic lateral sclerosis (ALS) is probably
caused by free radicals.
Family Practice News, 12230 Wilkins Ave., Rockville, MD 20852.
Camu W, M Billiard, M Baldy-Moulinier. Fasting plasma and CSF amino
acid
levels in amyotrophic lateral sclerosis: A subtype analysis. Service de
Neurologie B, Hopital Gui-de-Chauliac, 2 Avenue Bertin-Sans, 34059
Montpellier Cedex France.
Acta Neurol. Scand. (Denmark). 1993; 88 (1): 51-55.
Chiueh, CC, RM Wu, KP Mohanakumar, LM Sternberger, G Krishna, T Obata,
DL Murphy. In vivo generation of hydroxyl radicals and
MPTP-induced dopaminergic toxicity in the basal ganglia.
Unit on Neurotoxicology and Neuroprotection, National Institute of
Mental
Health, National Institutes of Health, Bethesda, Maryland 20892.
Ann N Y Acad Sci (United States). 1994 Nov 17; 738: 25-36.
Eisen A, H Stewart, M Schulzer, D Cameron. Anti-glutamate therapy in
amyotrophic lateral sclerosis: a trial using lamotrigine.
Neuromuscular Diseases Unit, Vancouver General Hospital, British
Columbia, Canada.
Can J Neurol Sci. 1993 Nov; 20 (4): 297-301.
Gordon, Gregory. NutraSweet. WASHINGTON (UPI), UPI Investigative Report.
1987. http://www.dorway.com/upipart1.txt
http://groups.yahoo.com/group/aspartameNM/message/262
Gredal O, SE Moller. Effects of branched-chain amino acids on plasma
amino acids in amyotrophic lateral sclerosis. Department of
Biochemistry, Res. Institute Biological Psychiatry, St Hans Hospital,
DK-4000 Roskilde Denmark
Amino Acids (Austria). 1996; 11 (1): 37-42.
King, Michael W, Ph.D /IU School of Medicine. Neurotransmitter
Receptors.
mk...@medicine.indstate.edu
Lennon VA, TJ Kryzer, GE Griesmann, PE O'Suilleabhain, et al.
Calcium-channel antibodies in the Lambert-Eaton syndrome and other
paraneoplastic syndromes.
N Engl J Med. 1995; 332: 1467-1474.
Maher, Timothy J, Judith MB Pinto. Administration of Aspartame
Potentiates Pentylenetetrazole- and Fluorothyl-Induced Seizures in Mice.
Neuropharmacology. 1998; 27 (1): 51-55.
Maher, Timothy J, Judith MB Pinto; Aspartame and the Rat Brain
Monoaminergic System.
Toxicology Letters. 1986 or 1988; 44: 331-339.
Metzenbaum, Howard M, United States Senator, Letter from Senator Howard
Metzenbaum on United States Senate Stationary (Committee on the Budget),
dated February 3, 1986: to Orrin Hatch, Utah ,who was the Chairman of
the
Labor and Human Resources Committee: (Metzenbaum was a member of this
committee, along with Ted Kennedy, Strom Thurmond, Lowell Weicker,
Christopher Dodd, Dan Quale, et al.). U.S. Congress 1986.
http://www.dorway.com
Millstone, Erik. Increasing Brain Tumor Rates: Is There a Link to
Aspartame. 1996; Science Policy Research Unit, Mantell Building,
University of Sussex Brighton, England.
Muller T, SB Peterson, U Sonnewald, G Unsgard. Effects of aspartame
on Ca+ influx and LDH leakage from nerve cells in culture.
Neuropharmacology and Neurotoxicology Rapid Communications of Oxford
Ltd.
1995; Vol. 6 (PP318-320) MR-Centre, SINTEF UNIMED, N-7034 Trondheim,
University of Trondheim, Dept. of Neurosurgery, University Hospital
N-7006 Trondheim; Norwegian Institute of Tecnology, Drpt. of
Biotecnology, N-7034 Trondheim, Norway
[ http://groups.yahoo.com/group/aspartameNM/message/938
aspartame harms mice brain cells: Hetle & Eltervaag: 2001 thesis
abstract: Sonnewald 1995 study, full text: Murray 1.5.3 rmforall ]
Muller WE, FJ Romero, S Perovic, G Pergande, P Pialoglou. Protection
of flupirtine on beta-amyloid-induced apoptosis in neuronal cells in
vitro: prevention of amyloid-induced glutathione depletion.
Institut fur Physiologische Chemie, Abteilung Angewandte
Molekularbiologie, Universitat, Mainz, Germany.
J Neurochem (United States). 1997 Jun; 68 (6): 2371-7.
Mundy WR, TM Freudenrich. Aluminum potentiates glutamate-induced
calcium accumulation and iron- induced oxygen free radical formation in
primary neuronal cultures. Kodavanti PRS, WR Mundy. Neurotoxicology
Division, Natl. Hlth./Envtl. Effects Res. Lab., US Environmental
Protection Agency, Research Triangle Park, NC 27711 United States.
Molecular and Chemical Neuropathology (United States). 1997; 32 (1-3):
41-57.
Natarajan M and M Wilkinson. Recovery of hypothalamic NMDA-induced c-fos
expression following neonatal glutamate (MSG) lesions.
Department of Obstetrics and Gynecology, IWK-Grace Health Centre,
Halifax, NS, Canada.
Brain Res Dev Brain Res. 1997 Aug 18; 102 (1): 97-104.
Nijmegen, GL. Amino Acid Information Centre for Molecular and
Biomolecular Informatics. University of Nijmegen, Toernooiveld 1, P.O.
Box 9010, 6500.
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Aspects. In Progress in Brain Research, 1988. Vol. 73.
Olney, John W. Researchers call for further studies after identifying a
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Washington University School of Medicine, St. Louis.
Roberts, HJ. Reactions Attributed to Aspartame-Containing Products:
551 Cases.
Journal of Applied Nutrition, 1988; 40: 85-94.
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Methanol Poisoning.
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block in vitro the neurotoxicity of CSF from patients with amyotrophic
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of
Medicine, Limoges, France.
Neuroreport (England). 1996 Aug 12; 7 (12): 1970-2.
Testa D, T Caraceni, V Fetoni. Branched-chain amino acids in the
treatment of amyotrophic latera sclerosis. Istituto Neurologico
'C.Besta', I-20133 Milan Italy
J Neurol. (Germany, Federal Republic of). 1989; 236 (8): 445-447.
Vyth A, JG Timmer, PM Bossuyt, ES Louwerse, JM de Jong.
Survival in patients with amyotrophic lateral sclerosis, treated with an
array of antioxidants. Department of Pharmacy E-0,
University of Amsterdam, UK.
J Neurol Sci (Netherlands). 1996 Aug; 139 Suppl: 99-103.
Walton, Ralph G. The Possible Role of Aspartame in Seizure
Induction. Presented at "Dietary Phenylalanine and Brain Function."
Proceedings of the First International Meeting on Dietary Phenylalanine
and Brain Function, Washington, D.C., May 8-10, 1987. Center for Brain
Sciences and Metabolism Charitable Trust, P.O. Box 64, Kendall Square,
Cambridge, MA 02142. Reprinted in "Dietary Phenyalalnine and Brain
Function," c1988; Birkhauser, Boston, MA USA: 159-162.
Welty DF, GP Schielke, JD Rothstein. Potential treatment of
amyotrophic lateral sclerosis with gabapentin: A hypothesis.
Parke-Davis
Pharmaceutical Res. Div., Pharmacokinetic/Drug Metabol. Dept.,
Warner-Lambert, 2800 Plymouth Rd, Ann Arbor, MI 48105 USA .
Annals of Pharmacotherapy (USA). 1995; 29 (11): 1164-1167.
Woodrow C Monte, Director, Food Science and Nutrition Laboratory,
Arizona State University. Aspartame: Methanol and the Public Health.
J Applied Nutrition. 1984; 36 (1): 42-54. (62 references)
http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984:
Monte: Murray 9.23.2 rmforall woody...@xtra.co.nz
************************************************************
Rich Murray, MA Room For All rmfo...@att.net
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-986-9103
http://groups.yahoo.com/group/aspartameNM/message/1026
brief aspartame review: formaldehyde toxicity: Murray 9.11.3 rmforall
http://google.com gives 221,000 websites for "aspartame" , with the top
9 of 10 listings being anti-aspartame, while
http://groups.google.com finds on 700 MB of posts from 20 years of
Usenet groups, 83,800 posts, the top 10 being anti-aspartame.
http://news.google.com 28 recent aspartame items from 4500 sources.
http://www.AllTheWeb.com gives 291,700, the top 7 of 10 being
leading and very well informed volunteer anti-aspartame sites.
http://teoma.com/index.asp gives 85,700 websites, top 8 of 10 anti.
http://www.ncbi.nlm.nih.gov/PubMed lists 742 aspartame items.
http://groups.yahoo.com/group/aspartameNM/message/989
EU votes 440 to 20 to approve sucralose, limit cyclamates & reevaluate
aspartame & stevia: Murray 4.12.3 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1025
aspartame & formaldehyde toxicity: Murray 9.9.3 rmforall
http://groups.yahoo.com/group/aspartameNM/messages
for 1034 posts in a public searchable archive
http://groups.yahoo.com/group/aspartame/messages 730 members
http://groups.yahoo.com/group/aspartameNM/message/1024
aspartame review: methanol, formaldehyde, formic acid toxicity:
Murray 9.5.3 rmforall
http://groups.yahoo.com/group/aspartameNM/message/910
formaldehyde & formic acid from methanol in aspartame:
Murray: 12.9.2 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, since 11% of aspartame (1,120 mg in 2L diet soda, 5.6 12-oz
cans) is 123 mg methanol (wood alcohol), immediately released into the
body after drinking (unlike the large levels of methanol locked up in
molecules inside many fruits), then quickly transformed into
formaldehyde, which in turn becomes 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. [Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
J. Nutrition 1973 Oct; 103(10): 1454-1459.]
If 10% of the methanol is retained 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
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
RTM: ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999
5.30.2 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, 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.
http://groups.yahoo.com/group/aspartameNM/message/872
immune system reactions due to formaldehyde from the 11% methanol in
aspartame: Thrasher: Tephly: Monte: Murray 9.27.2 rmforall
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.]
http://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold: Murray:
Wilson: CIIN: 12.12.2 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/formaldehyde_embryo_toxicity.html full text
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: 12.9.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/946
Functional Therapeutics in Neurodegenerative Disease Part 1/2:
Perlmutter 7.15.99: Murray 1.10.3 rmforall
http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall
http://ww.presidiotex.com/barcelona/index.html
Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, Alemany M ["Trok-ho"]
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo. Life Sci 1998 Jun 26; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular, Facultat de Biologia,
Universitat de Barcelona, Spain.
http://www.presidiotex.com/barcelona/index.html
Maria Alemany, PhD (male) ale...@porthos.bio.ub.es
http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 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 Monte, below.
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
s...@acpub.duke.edu 919-684-3303, 660-5657
http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall ]
http://groups.yahoo.com/group/aspartameNM/message/911
RTP ties to industry criticized by CSPI: Murray: 12.9.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/782
RTM: Smith, Terpening, Schmidt, Gums:
full text: aspartame, MSG, fibromyalgia 1.17.2 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.
http://groups.yahoo.com/group/aspartameNM/message/939
aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 1.5.3 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and
its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr gkok...@atlas.uoa.gr
"K.H. Schulpis" <inch...@otenet.gr> "G.J. Reclos" <rek...@otenet.gr>
http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity: Ramazzini Foundation
carcinogenicity results Dec 2002: Soffritti: Murray 8.3.3 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. cr...@tin.it
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
http://groups.yahoo.com/group/aspartameNM/message/934
24 recent formaldehyde toxicity [Comet assay] reports:
Murray 12.31.2 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 1.1.3 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.]
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 1.27.3 rmforall [A detailed look at the data]
http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRob...@aol.com
http://www.sunsentpress.com/ sunsen...@aol.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://www.dorway.com/enclosur.html
http://groups.yahoo.com/group/aspartameNM/message/53
aspartame history Part 1/4 1964-1976: Gold: Murray 11.6.9: rmforall
http://groups.yahoo.com/group/aspartameNM/message/927
Rumsfeld, 1977 head of Searle Corp., got aspartame FDA approval:
Turner: Murray 12.23.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/928
revolving door, Monsanto, FDA, EPA: NGIN: Murray 12.23.2 rmforall
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame (12.4.2): 59 pages, 230 references
http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 1.12.3 rmforall EU Scientific Committee on Food, a whitewash
http://groups.yahoo.com/group/aspartameNM/message/841
RTM: Merisant Co., MSD Capital, Dell Computer Corp., NutraSweet Co.,
JW Childs Assc.: aspartame-neotame toxicity 7.10.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/876
hyperthyroidism (Graves disease) in George and Barbara Bush, 1991--
aspartame toxicity? Roberts 1997: Murray 10.9.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/874
re "dry drunk": Bisbort: danger to President Bush from aspartame
toxicity: Murray: 2.24.2 9.29.2 rmforall
************************************************************
Rich Murray <rmfo...@att.net> wrote in message news:<3FB1CDC5...@att.net>...