The Connection Between MS and Aspartame

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The Connection Between MS and Aspartame

By Russell L. Blaylock, MD Neurosurgeon

6-7-4

(Originally published on Rense.com )

_http://www.truthinlabeling.org/Blaylock-AspartameAndMultipleSclerosis-Neuro

surgeon'sWarning.html_

(http://www.truthinlabeling.org/Blaylock-AspartameAndMultipleSclerosis-Neurosurg\

eon'sWarning.html)

 

 

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.