Betreff: autism/aspartame/Blaylock

Von: Dorothee Krien

Datum: Sat, 23 Jun 2007 22:23:12 +0100



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.

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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

(Originally published on )

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.


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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