- 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 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 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
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