Hate to point this out ...

BUT it is our own MS lesions that produce the Glutamate that causes all the axon/neuron damage.

Taking in more Glutamate from our diet is obviously not a good idea.

Here is how the Glutamate does the dastardly deed.

THE BELOW LINK IS VERY, VERY CRITICAL TO UNDERSTANDING HOW NEURONS DIE ie the Calcium connection!!!!


http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)


The Second Stage of MS is "The Degererative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage".

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

jackD

http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)


http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

There are "THINGIES" that counter Glutamate neuron toxicity.

It does not take too much effort to do some simple searches to locate some of them.

I have found several supplements that I take each day however I have no human research data to show it makes a difference or is worth the expense.

I will do a quick post of some of the abstracts.

jackD

Here is one GOOD protector of neurons.

JackD

1: Ann N Y Acad Sci. 2004 Dec;1031:127-42.

Tocotrienol: the natural vitamin E to defend the nervous system?

Sen CK, Khanna S, Roy S.

Davis Heart & Lung Research Institute, 473 West 12th Avenue, The Ohio State
University Medical Center, Columbus, Ohio 43210, USA. sen-1@medctr.osu.edu

Vitamin E is essential for normal neurological function. It is the major
lipid-soluble, chain-breaking antioxidant in the body, protecting the integrity
of membranes by inhibiting lipid peroxidation. Mostly on the basis of symptoms
of primary vitamin E deficiency, it has been demonstrated that vitamin E has a
central role in maintaining neurological structure and function. Orally
supplemented vitamin E reaches the cerebrospinal fluid and brain. Vitamin E is a
generic term for all tocopherols and their derivatives having the biological
activity of RRR-alpha-tocopherol, the naturally occurring stereoisomer compounds
with vitamin E activity. In nature, eight substances have been found to have
vitamin E activity: alpha-, beta-, gamma- and delta-tocopherol; and alpha-,
beta-, gamma- and delta-tocotrienol. Often, the term vitamin E is synonymously
used with alpha-tocopherol. Tocotrienols, formerly known as zeta, , or
eta-tocopherols, are similar to tocopherols except that they have an isoprenoid
tail with three unsaturation points instead of a saturated phytyl tail. Although
tocopherols are predominantly found in corn, soybean, and olive oils,
tocotrienols are particularly rich in palm, rice bran, and barley oils.
Tocotrienols possess powerful antioxidant, anticancer, and cholesterol-lowering
properties. Recently, we have observed that alpha-tocotrienol is multi-fold more
potent than alpha-tocopherol in protecting HT4 and primary neuronal cells
against toxicity induced by glutamate as well as by a number of other toxins. At
nanomolar concentration, tocotrienol, but not tocopherol, completely protected
neurons by an antioxidant-independent mechanism. Our current work identifies two
major targets of tocotrienol in the neuron: c-Src kinase and 12-lipoxygenase.
Dietary supplementation studies have established that tocotrienol, fed orally,
does reach the brain. The current findings point towards tocotrienol as a potent
neuroprotective form of natural vitamin E.

PMID: 15753140 [PubMed - indexed for MEDLINE]


1: Neuropharmacology. 2004 Nov;47(6):904-15.

Alpha-tocotrienol provides the most potent neuroprotection among vitamin E
analogs on cultured striatal neurons.

Osakada F, Hashino A, Kume T, Katsuki H, Kaneko S, Akaike A.

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto
University, 46-29 Yoshida-shimoadachi-cho, Sakyo-ku, Kyoto 606-8501, Japan.

Oxidative stress and apoptosis play pivotal roles in the pathogenesis of
neurodegenerative diseases. We investigated the effects of vitamin E analogs on
oxidative stress and apoptosis using primary neuronal cultures of rat striatum.
A tocotrienol-rich fraction of edible oil derived from palm oil (Tocomin 50%),
which contains alpha-tocopherol, and alpha-, gamma- and delta-tocotrienols,
significantly inhibited hydrogen peroxide (H2O2)-induced neuronal death. Each of
the tocotrienols, purified from Tocomin 50% by high-performance liquid
chromatography, significantly attenuated H2O2-induced neurotoxicity, whereas
alpha-tocopherol did not. alpha-, gamma- and delta-Tocotrienols also provided
significant protection against the cytotoxicity of a superoxide donor, paraquat,
and nitric oxide donors, S-nitrosocysteine and 3-morpholinosydnonimine.
Moreover, tocotrienols blocked oxidative stress-mediated cell death with
apoptotic DNA fragmentation caused by an inhibitor of glutathione synthesis,
L-buthionine-[S,R]-sulfoximine. In addition, alpha-tocotrienol, but not gamma-
or delta-tocotrienol, prevented oxidative stress-independent apoptotic cell
death, DNA cleavage and nuclear morphological changes induced by a non-specific
protein kinase inhibitor, staurosporine. These findings suggest that
alpha-tocotrienol can exert anti-apoptotic neuroprotective action independently
of its antioxidant property. Among the vitamin E analogs examined,
alpha-tocotrienol exhibited the most potent neuroprotective actions in rat
striatal cultures.

PMID: 15527824 [PubMed - indexed for MEDLINE]

L-Theanine - Stuff in Green Tea is available as a supplement. I add an extra 200 mg to my mug of green/white tea that I drink twice each day.

jackD

Theanine is an amino acid found in green tea that produces
tranquilizing effects in the brain. In Japan, soft drinks and
chewing gum are spiked with theanine for the purpose of
inducing relaxation.

Although theanine creates a feeling of
relaxation, it doesn't shut down the brain. Studies on rodents
show that theanine enhances the ability to learn and remember.
By shutting off worry central, theanine appears to increase
concentration and focus thought.

Theanine is different than kava-kava in that it doesn't cause
drowsiness, just relaxation. Theanine increases GABA, while
caffeine decreases it. GABA doesn't just relax, it also
creates a sense of well-being. Theanine's ability to increase
this brain chemical can literally put you in a better mood.
Theanine also increases levels of dopamine, another brain
chemical with mood-enhancing effects.

Protecting neurons
In studies on neurons in cell culture, theanine significantly
reverses glutamate-induced toxicity. In vivo studies show the
same effect in rodents. Glutamate-induced neuro-toxicity is a
major cause of degenerative brain disease.

Many Americans suffer from slightly elevated blood pressure,
but don't know they have it. Chronic high blood pressure
inflicts damage on the delicate cerebral vascular network and
increases the risk of stroke. Theanine has been shown to help
lower blood pressure.

Theanine readily crosses the blood-brain barrier and changes
brain chemistry in a way that has been compared to
aromatherapy. Studies show that theanine is a non-toxic,
highly desirable mood modulator.


1: Biol Pharm Bull. 2002 Dec;25(12):1513-8.

Neuroprotective effects of the green tea components theanine and catechins.

Kakuda T.

Central Research Institute, Itoen, Ltd, Shuzuoka, Japan.

The neuroprotective effects of theanine and catechins contained in green tea are
discussed. Although the death of cultured rat cortical neurons was induced by
the application of glutamic acid, this neuronal death was suppressed with
exposure to theanine. The death of hippocampal CA1 pyramidal neurons caused by
transient forebrain ischemia in the gerbil was inhibited with the ventricular
preadministration of theanine. The neuronal death of the hippocampal CA3 region
by kainate was also prevented by the administration of theanine. Theanine has a
higher binding capacity for the AMPA/kainate receptors than for NMDA receptors,
although the binding capacity in all cases is markedly less than that of
glutamic acid.

The results of the present study suggest that the mechanism of
the neuroprotective effect of theanine is related not only to the glutamate
receptor but also to other mechanisms such as the glutamate transporter,
although further studies are needed. One of the onset mechanisms for
arteriosclerosis, a major factor in ischemic cerebrovascular disease, is
probably the oxidative alteration of low-density lipoprotein (LDL) by active
oxygen species. The oxidative alterations of LDL were shown to be prevented by
tea catechins. Scavenging of *O(2)(-) was also exhibited by tea catechins.
The
neuroprotective effects of theanine and catechins contained in green tea are a
focus of considerable attention, and further studies are warranted.

Publication Types:
Review
Review, Tutorial

PMID: 12499631 [PubMed - indexed for MEDLINE]

Good (and easy to understand) article on L-Theanine:

http://intelegen.com/nutrients/L-Theanine.htm

Jack,

Have you found a type of green tea that has more of the theanine than others?

gmi

I have not come across any info of varying levels of theanine in teas.

The BEST most therapeutic tea is "WHITE TEA". I know thore are many dirfferent kinds of WHITE TEA. It has a very high level of EGCG - a flavonoid that does many wonderful things.

Theanine is also called l-Theanine and is available in most all health food stores and the internet.

I get mine from http://www.biosynergy.com/theanine.htm

I get the 200 mg caps and I just poured it out of the capsule into my tea mug.

To get a true therapeutic effect you would need to drink 8 to 10 cups of tea per day. My bladder could not survive this every day so I have only two mugs of mostly green and white tea with one 200 L-theanine added.

I also have two Mega Green Tea extract caps each day. The AM one lightly caffeinated and the PM one is Decaffeinated. I like to get HIGH in the morning.

http://www.lef.org/Vitamins-Suppleme...ffeinated.html (decaffeinated)

http://www.lef.org/Vitamins-Suppleme...ffeinated.html (lightly-caffeinated)

A recreational cup of green tea each day is nice but ...there is no treatment effect to be expected.

jackD

Below in quotes extracted from above links.

"Can a neuron be excited to death? Some interesting new findings about glutamate suggest that this excitatory neurotransmitter not only talks to neurons, but can also scream at them, strangle their dendrites, and even assassinate them.

One of the key glutamate receptors is called NMDA, named after its selective ligand N-methyl-d-aspartate. Once glutamate binds to its NMDA receptor, this opens an ion channel in the neuronal membrane so the nerve can drink calcium. Sipping calcium is exciting to a neuron and a normal reaction when glutamate is speaking pleasantly.

Too much glutamate can behazardous to your health

When glutamate screams at a neuron, it reacts by drinking more calcium. Imbibing too much calcium can anger intracellular enzymes, which then generate nasty chemicals called free radicals. A small commune of free radicals can crash the chemical party in the postsynaptic dendrite and strangle it.

Why would the neuron allow this to happen? It is possible that the brain needs this excitotoxic mechanism so that glutamate can act as a gardener in the brain, pruning worn out branches from dendrite trees so that healthy new sprouts might prosper. However, this also equips glutamate with a powerful weapon that can be misused to cause various pathologic states.

When glutamate decides to act as an abusive bully, neurons may seize, panic, become manic, or become psychotic. Furthermore, such symptoms of calcium intoxication may be followed by an unfortunate glutamate hangover in the form of destroyed dendrites that can never be excited again.

Glutamate as endogenous assassin.

At the far end of the excitotoxic spectrum, glutamate's molecular mischief can run rampant and actually murder entire neurons by overwhelming calcium poisoning and free-radical mayhem. Certain illnesses such as Alzheimer's disease, Parkinson's disease, Lou Gehrig's disease (amyotrophic lateral sclerosis), and even schizophrenia may hire glutamate as a methodical assassin, eliminating a whole subpopulation of pre-designated neurons. This is a systematic process consistent with the pace of such neurodegenerative disorders. In the case of stroke, glutamate may form an army of hit-men, and then massacre an entire region of distressed ischemic neurons in the midst of a catastrophic molecular mess.

In summary, glutamate's actions can range across a vast spectrum. It can be a friendly neuronal conversationalist or a screaming hypothetical mediator of symptoms of mental illness. After an abusive tirade, glutamate may even strangle the dendrite it excited. As excitotoxicity escalates, glutamate can become a serial murderer of neurons, wiping them out in a devastating cumulative process over months and years. At an extreme, glutamate is a mass murderer, wreaking the destruction of localized neurons during the chaos of stroke.


Can the brain be rescued or protected?

One approach to protect the neuron from drinking too much calcium is by blocking NMDA receptors with antagonists. Thus, neurons are allowed to quench their thirst in normal excitatory neurotransmission, but not guzzle so much calcium that they become excitotoxically inebriated. Numerous NMDA antagonists are able to mitigate neuronal death, including ischemic stroke. Clinical testing of such compounds will be rapidly accelerating in the near future. Such approaches are deemed neuroprotective since they arrest glutamate before it can assassinate any more neurons."



I have found some Callcium Channel Blockers which is a class of blood pressure drugs which seems to block this "death to the neurons by Callicum" process. I am now taking one of these drugs for my high BP. It has been tested as a MS treatment and I will post that later.

jackD

A concern of mine is whether we should take calcium supplements due to this murderous effect described in your post. What channel blocker are you taking? I have also been on BP meds for several years.

Just checked my meds and found that one is a calcium channel blocker.


gmi

"A concern of mine is whether we should take calcium supplements due to this murderous effect described in your post. What channel blocker are you taking? I have also been on BP meds for several years." gonnamakeit

I would say you should take vit D3, magnesium AND calcium supplements as they work well together and help the MS condition.

It is HOW the cells USE Calcium that needs regulating.

I take Nifedia CC which a timed release form of Nitrendipine mentioned below. I am still researching this.

jackD


"Document title
Calcium channel blockers ameliorate disease in a mouse model of multiple sclerosis

Author(s)
BRAND-SCHIEBER Elimor (1) ; WERNER Peter (1 2) ;
Author(s) Affiliation(s)
(1) Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461,
(2) Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461


Abstract
Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS, are inflammatory demyelinating diseases of the central nervous system. The inflammatory attacks lead to glial dysfunction and death, axonal damage, and neurological deficits.

Numerous studies in rat suggest that extracellular calcium influx, via voltage-gated calcium channels (VGCC), contributes to white matter damage in acute spinal cord injury and stroke. Our immunohistochemical finding that mouse spinal cord axons display subunits of L-type VGCC also supports this hypothesis.

Furthermore, we hypothesized that VGCC also play a role in EAE, and possibly, MS.

In our study, administration of the calcium channel blockers (CCB) bepridil and nitrendipine significantly ameliorated EAE in mice, compared with vehicle-treated controls.

Spinal cord samples showed reduced inflammation and axonal pathology in bepridil-treated animals.

Our data support the hypothesis that calcium influx via VGCC plays a significant role in the development of neurological disability and white matter damage in EAE and MS."