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Betreff: autism/aspartame/Blaylock |
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Von: Dorothee Krien |
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Datum: Sat, 23 Jun 2007 22:23:12 +0100 |
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The two
articles on the link between autism and aspartame are the last in the list of
references below.
Aspartame permeates the blood-brain barrier, allowing toxins to seep into the
brain.
D
http://www.truthinlabeling.org/Blaylock-AspartameAndMultipleSclerosis-Neurosurgeon'sWarning.html
WWW.truthinlabeling.org -- Home page
Return to the Table of Contents
The Connection Between
Multiple Sclerosis (MS) and Aspartame
From
the Truth in Labeling Campaign
Aspartame is a low calorie
sweetener. Called a potent neurotoxin by some researchers. While making
no claim to be effective in weight control, it is being sold as a sugar
substitute for those on low calorie diets and for diabetics.
Trade names for Aspartame
are NutraSweet, Equal, Spoonful, Canderel, Benevia, Misura. In Europe Aspartame
hides under the seemingly innocuous "E 951" label. World-wide,
warning labels that say "contains a source of phenylalanine" or
"phenylketonurics should not consume this product," signal the
presence of aspartame.
Dr. Russell Blaylock, a
recently retired neurosurgeon, has been warning about the hazards of ingesting
aspartame for years. In his book, "Excitotoxins: The Taste that
Kills," Blaylock says that Aspartame and Multiple Sclerosis (MS) are
closely related. The Multiple Sclerosis society, however, denies there is any
connection between MS and Aspartame. It may be that the Society has chosen to
hang on to industry funding rather than to warn its members of the toxic
potential of Aspartame. Blaylock explains the biological mechanism by which
Aspartame circumvents the blood-brain-barrier and gets at vital nervous
tissues.
The aspartic acid in
aspartame and the glutamic acid in MSG-containing products are structural
analogs. They load on the same receptors in the brain, cause the same
brain lesions and neuroendocrine disorders, and act in an additive fashion,
i.e., 2 parts aspartic acid and 3 parts glutamic acid equal 5 parts neurotoxin.
The Truth in Labeling Campaign
has every reason to believe that anyone who is adversely affected by aspartame
will be adversely affected by MSG, too. We have been repeatedly informed
by people diagnosed with MS that their conditions appear to be worsened by
ingestion of MSG.
__________________________
The Connection Between MS and
Aspartame
By
Russell L. Blaylock, MD
Neurosurgeon
6-7-4
(Originally published on Rense.com )
Recently, much controversy has surrounded a claim that aspartame may produce an
MS-like syndrome. A current review of recent peer-reviewed scientific studies
has disclosed a pathophysiological mechanism to explain this connection. As far
back as 1996 it was shown that the lesions produced in the myelin sheath of axons
in cases of multiple sclerosis were related to excitatory receptors on the
primary cells involved called oligodendroglia. Recent studies have now
confirmed what was suspected back then. The loss of myelin sheath on the nerve
fibers characteristic of the disease is due to the death of these
oligodendroglial cells at the site of the lesions (called plaques). Further,
these studies have shown that the death of these important cells is as a result
of excessive exposure to excitotoxins at the site of the lesions.
Normally, most of these
excitotoxins are secreted from microglial immune cells in the central nervous
system. This not only destroys these myelin-producing cells it also breaks down
the blood-brain barrier (BBB), allowing excitotoxins in the blood stream to
enter the site of damage. Aspartame contains the excitotoxin aspartate as 40%
of its molecular structure. Numerous studies have shown that consuming
aspartame can significantly elevate the excitotoxin level in the blood. There
is a common situation during which the excitotoxin exposure is even greater. When
aspartate (as aspartame) is combined in the diet with monosodium glutamate
(MSG) blood levels are several fold higher than normal. With the BBB damaged,
as in MS, these excitotoxins can freely enter the site of injury, greatly
magnifying the damage. So, we see that dietary excitotoxins, such as aspartame
and MSG, can greatly magnify the damage produced in multiple sclerosis. Likewise,
excitotoxins have been shown to break down the BBB as well.
Of equal concern is
observation that we know that about 10% of the population (based on autopsy
studies of elderly) have MS lesions without ever developing the full blown
disease, a condition called benign MS. A diet high in excitotoxins, such as
aspartame, can convert this benign, subclinical condition into full-blown
clinical MS. The amount of excitotoxins consumed in the average American diet
is considerable, as shown by several studies. In addition, the toxin methanol
is also in the aspartame molecule. Methanol is a axon poison. Combined toxicity
of the aspartate and the methanol adds up to considerable brain toxicity and
can convert benign, subclinical MS into full-blown MS. Once the MS becomes
full-blown, further consumption of excitotoxins magnifies the toxicity,
increasing disability and death.
Recent studies have also
shown that even single exposures to these food-based excitotoxins can produce
prolonged worsening of neurological lesions. In addition, it has been
demonstrated that autoimmune reactions (as occur with MS) greatly magnify the
toxicity of aspartate and glutamate (the excitotoxins). We also know liquid
forms of excitotoxins are significantly more toxic because of rapid absorption
and higher blood levels. In the face of this connection between excitotoxicity
and the pathophysiology of MS, it would be ludicrous to allow further use of
this excitotoxin containing sweetener.
References:
1. Sannchez-Gomez MV,
Malute C. AMPA and kainate receptors each mediate excitotoxicity in oligodendroglial
cultures. Neurobiology of Disease 6:475-485, 1999
2. Yoshika A, et al.
Pathophysiology of oligodendroglial excitotoxicity, J Neuroscience
Research 46: 427-437, 1996.
3. Singh P, et al.
Prolonged glutamate excitotoxicity: effects on mitochondrial antioxidants and
antioxidant enzymes. Molecular Cell Biochemistry 243: 139-145,
2003.
4. Leuchtmann EA, et al.
AMPA receptors are the major mediators of excitotoxin death in mature
oligodendrocytes. Neurobiology of Disease 14:336-348, 2003.
5. Takahashi JL, et al. Interleukin1 beta promotes
oligodendrocyte death through glutamate excitotoxicity. Annal Neurology
53: 588-595, 2003.
6. Pitt D, et al Glutamate
uptake by oligodendrocytes: implications for excitotoxicity in multiple
sclerosis. Neurology 61: 1113-1120, 2003.
7. Soto A, et al.
Excitotoxic insults to the optic nerve alter visual evoked potentials. Neuroscience
123: 441-449, 2004.
8. Blaylock RL.
Interactions of cytokines, excitotoxins and reactive nitrogen and oxygen
species in autism spectrum disorders. Journal of American Nutraceutical
Association 6: 21-35, 2003.
9. Blaylock RL. Chronic
microglial activation and excitotoxicity secondary to excessive immune
stimulation: possible factors in Gulf War Syndrome and autism. Journal
American Physicians and Surgeons, Summer, 2004.
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IF
MSG ISN'T HARMFUL, WHY IS IT HIDDEN? |