Aspartame and Multiple Sclerosis
Note: the paper below gives a viable theory for why an
MS-like syndrome is seen in diet pop drinkers (and other aspartame
consumers). Vaccines use a type of mercury for a preservative - some
are higher in this neurotoxin than others. Flu vaccine rates one of the
highest in mercury content. Obviously taking it yearly might well cause
neurological side effects. Anyone who has lived several decades has
noticed that the incidence of neurologic disorder has greatly increased in
the last decade or two. In 1978, the incidence of MS was 200,000.
Now it's up to 350,000 cases. Some can be explained by the baby
boomers coming of age but can all the cases be explained thusly? Dr
Blaylock feels not. Read his theory below.
Connection between MS
Recently, much controversy has surrounded a claim that aspartame may produce an MS-like syndrome. A current review of recent peer-reviewed scientific studies have 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 are 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 breakdown 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 covert 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 occurs with MS) greatly magnifies 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.
TREATMENT FOR MS: It is now known the cause for the destruction of the myelin in the lesions is overactivation of the microglia in the region of the myelin. An enzyme that converts glutamine to glutamate called glutaminase increases tremendously, thereby greatly increasing excitotoxicity. Mercury also activates microglia, even in subtoxic doses.
Any dietary excitotoxin can activate the microglia, thereby greatly aggravating the injury. This includes the aspartate in aspartame. The methanol adds to this toxicity as well. Now, the secret to treatment appears to be shutting down, or at least calming down, the microglia. It has been found the antibiotic minocycline powerfully shuts down the microglia. I tried this treatment on a friend of mine who just came down with fulmanant MS. He was confined to a wheelchair. I had him placed on minocycline and now, just a few weeks later, he is walking.
The good news is that other things also calm the microglia-the most potent are: silymarin, curcumin and Advil. Phosphatidylcholine helps re-myelinate the nerve sheaths that are damaged, as does B12, B6, B1, vitamin D, folate, vitamin C, Natural vitamin E and L-carnitine. DHA plays a major role in repairing the myelin sheath. Vitamin D may even prevent MS, but it acts as an immune modulator, preventing further damage - the dose is 2000 IU a day. Magnesium, as magnesium malate is needed in a dose of 500 mg 2X a day. They must avoid all excitotoxins, even natural ones in foods-such as soy, red meats, nuts, mushrooms and tomatoes. Avoid all fluoride and especially all vaccinations. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Dr. Blaylock is a recently retired board-certified neurosurgeon with more than twenty six years experience. He is a recently retired Clinical Assistant Professor of Neurosurgery at the Medical University of Mississippi. Author of thirty scientific papers on various medical subjects, chapters in three medical textbooks and a booklet on multiple sclerosis, he serves on the editorial staff of The Journal of American Physicians and Surgeons, the Journal of the American Nutraceutical Association, and acts as a medical advisor to the American Nutraceutical Association. Those interested can subscribe to his newsletter (monthly magazine mailed) at www.blaylockreport.com He lives in Ridgeland, Mississippi.