|
|
|
|
|
|
|
|
|
|
|
|
|
|
Dietary intake of glutamate is associated with an increased risk of ALS. [74]
Glutamate is found in monosodium glutamate (MSG) which occurs naturally in many foods. The following foods should be avoided (Source: MSG Facts http://www.msginfo.com): Table1: Monosodium Glutamate Content in Food
Aspartate, another potent neurotoxin, should also be avoided in chronic neurologic disease. Aspartate is found in artificial sweeteners such as Aspartame and NutriSweet.
One cause of brain cell death is glutamate toxicity. Brain cells use glutamate as a neurotransmitter, but unfortunately glutamate is a double-edged sword in that it can also kill aging brain cells. The release of glutamate from the synapses is the usual means by which neurons communicate with each other. Effective communication means controlled release of glutamate at the right time to the right cells. However, when glutamate is released in excessive amounts, intercellular communication ceases. It is like replacing radio signals with x-rays. The flood of glutamate onto the receiving neurons drives them into hyperactivity and the excessive activity leads to cellular degradation.
It may be possible to protect brain cells against glutamate toxicity by taking methylcobalamin (vitamin B12) supplements. In a study published in the European Journal of Pharmacology, it was shown that chronic exposure of rat cortical neurons to methylcobalamin protected against glutamate-, aspartate-, and nitropruside- induced neurotoxicity. This study also showed that S-adenosyl-methionine (SAMe) protected against neurotoxicity. [75]
In a study published in Investigational Ophthalmology Visual Sciences, a combination of methylcobalamin and SAMe was used to protect against retinal brain cell toxicity caused by glutamate and nitroprusside. The mechanism by which methylcobalamin protected against neurotoxicity was postulated by the researchers to be enhancement of brain cell methylation. The scientists who conducted these studies emphasized that chronic exposure of methylcobalamin was necessary to protect against neurotoxicity. [76]
Based on its unique mechanisms of action, methylcobalamin could be effective in slowing the progression of diseases such as ALS. Since methylcobalamin is not a drug, there is little economic incentive to conduct expensive clinical studies. It may be a long time before we know just how effective this vitamin B12 analog is in slowing the progression of ALS. This indicates that for methylcobalamin to be effective in protecting against neurological disease, daily supplementation may be required. An appropriate dose for an ALS patient to take would be 20 to 60 mg a day taken sublingually.
Continue to Part 4 of the ALS Article
© 2002