That eat right/healthy stuff works up to the point one gets sick.

MS folks are really sick - near mutants! They need help! Taking a little extra of some plant extracts and other thingies is a good idea if they have been shown in NIH-NLM studies to help prevent the brain destruction.

This little picture shows what things that need to be lowered for the two stages of MS.

THE BIG PICTURE!!!!!

THE BIG PICTURE - Explanation ---> http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

jackD
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http://home.ix.netcom.com/~jdalton/two%20stage%20MS.jpg
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Hello Jack,

Welcome back stranger! I still take many of the supplements you recommended years ago and I am still hanging on and working full time! Good luck with your sale! Don't stay away so long!

Luteolin

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J Neuroinflammation. 2009 Oct 13;6:29.

Luteolin as a therapeutic option for multiple sclerosis.


Theoharides TC.
SourceMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine and Tufts Medical Center, Boston, MA, USA. theoharis.theoharides@tufts.edu

Abstract
Multiple sclerosis (MS) remains without an effective treatment in spite of intense research efforts. Interferon-beta (IFN-beta) reduces duration and severity of symptoms in many relapsing-remitting MS patients, but its mechanism of action is still not well understood. Moreover, IFN-beta and other available treatments must be given parenterally and have a variety of adverse effects.

Certain naturally occurring flavonoids, such as luteolin, have anti-oxidant and anti-inflammatory effects, including inhibition of activated peripheral blood leukocytes from MS patients.

Luteolin also inhibits mast cells, as well as mast cell-dependent T cell activation, recently implicated in MS pathogenesis.

Moreover, luteolin and structurally similar flavonoids can inhibit experimental allergic allergic encephalomyelitis (EAE), an animal model of MS in rodents. An appropriate luteolin formulation that permits sufficient absorption and reduces its metabolism could be a useful adjuvant to IFN-beta for MS therapy.

PMID: 19825165 [PubMed - indexed for MEDLINE]


J Neuroinflammation. 2009 Oct 13;6:28.

Immunomodulatory responses of peripheral blood mononuclear cells from multiple sclerosis patients upon in vitro incubation with the flavonoid luteolin: additive effects of IFN-beta.

Sternberg Z, Chadha K, Lieberman A, Drake A, Hojnacki D, Weinstock-Guttman B, Munschauer F.

Department of Neurology, Baird MS Center, Jacobs Neurological Institute, Buffalo, NY, USA. zs2@buffalo.edu

The study is aimed to determine the role of luteolin (3',4',5,7-tetrahydroxyflavone), alone and in combination with human interferon-beta (IFN-beta), in modulating the immune response(s) of peripheral blood mononuclear cells (PBMCs) isolated from multiple sclerosis (MS) patients.

PBMC proliferation in the presence or absence of these drugs was determined and the production of pro-inflammatory cytokines (IL-1beta, TNF-alpha), and the ratio of cell migration mediator MMP-9, and its inhibitor, TIMP-1 was assessed in the culture supernatants.

Luteolin reduced, in a dose-dependent manner, the proliferation of PBMCs, and modulated the levels of IL-1beta and TNF-alpha released by PBMCs in the culture supernatants.

Luteolin reduced the MMP-9/TIMP-1 ratio via lowering MMP-9 production. In the majority of cases, luteolin, when combined with IFN-beta, had additive effects in modulating cell proliferation, IL-1beta, TNF-alpha, MMP-9 and TIMP-1.

PMID: 19825164 [PubMed - indexed for MEDLINE]

p.s. MMP-9s do the actual damage to myelin so reducing them a TAD is GREAT!!!

Also getting the ratio of MMP-9s to TIMP-1s to a 1 to 1 ration is GREAT!!!

jackD

Glutamate attacks BOTH axons and myelin cells

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It is interesting to note that Glutamate attacks BOTH axons and myelin cells. The brain in MS folks actually creats this EXCESS GLUTAMATE!!!
Eating things that containe glutamate or breakdown into GLUTAMATE like MSG (monosodium glutamate) is a BAD idea.

jackD


Neural Transm Suppl. 2000;(60):375-85. Related Articles, L

Glutamate excitotoxicity--a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?

Werner P, Pitt D, Raine CS.

Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.


Glutamate excitotoxicity mediated by the AMPA/kainate-type of glutamate receptors is known not only to damage neurons but also the myelin-producing cell of the central nervous system (CNS), the oligodendrocyte.

In Multiple Sclerosis (MS), myelin, oligodendrocytes and axons are lost or damaged as a result of an inflammatory attack on the CNS. Activated immune cells produce glutamate in large quantities by deamidating glutamine via glutaminase.

Thus, we hypothesized that during inflammation in MS, glutamate excitotoxicity may contribute to the lesion. This was addressed by treating mice sensitized to develop acute experimental autoimmune encephalomyelitis (EAE) with an AMPA/kainate antagonist, NBQX.

Treatment resulted in substantial amelioration of disease, increased oligodendrocyte survival and reduced axonal damage, as indicated by the levels of dephosphorylated neurofilament-H. Despite the clinical differences, NBQX-treatment had no effect on lesion size and did not reduce the degree of CNS inflammation. In addition, NBQX did not alter the proliferative activity of antigen-primed T cells in vitro, further indicating a lack of effect at the level of the immune system.

In separate studies, infiltrating immune cells present in perivascular cuffs, commonly the site of entry for invading immune cells, were found to express glutaminase in abundance, supporting the production of glutamate in inflammatory lesions.

Thus, glutamate excitotoxicity appears to be an important mechanism in autoimmune demyelination and its prevention with AMPA/kainate antagonists may prove to be an effective therapy for MS.

PMID: 11205156 [PubMed]

LDN was found to counter Glutamate nerve toxicity

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The info that LDN was found to counter Glutamate nerve toxicity was a real surprise to me!!


http://www.suite101.com/content/glut...ariants-a76493
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jackD

L-Theanine neuroprotective

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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]
__________________

Curcumin(tumeric extract) increases the antioxidant glutathione

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The substance the body produces to counter Glutamate is the antioxidant glutathione. Curcumin(tumeric extract) that states that it increases the bodies production of the antioxidant glutathione.

You cannot take glutathione directly as a pill or supplement because it breaks down in the gut, But some supplements will cause the body to increase the natural production of glutathione.

jackD


Popular Botanical Supports Brain Health

A recent study investigated the effects of a popular herb in regards to cognitive deficits and oxidative damage in the brain.

Curcumin is a potent antioxidant and the principle active constituent in turmeric (Curcuma longa). In a new study, rats were treated with a chemical called streptozotocin to induce oxidative damage within the brain, which is used as an experimental model for dementia. The rats then received either 80 mg per kg of curcumin or placebo for 3 weeks.

After 2 weeks of streptozotocin treatment, the rats showed significant cognitive deficits as measured by passive avoidance and water maze tasks. The rats that received curcumin demonstrated significantly improved cognitive performance compared to the rats that did not. In addition, the group supplemented with curcumin also showed a significant decrease in markers for oxidative stress such as 4-hydroxynonenal, malonaldehyde, thiobarbituric reactive substances, hydrogen peroxide, protein carbonyl, and oxidized glutathione. Curcumin also augmented levels of the potent antioxidant glutathione and the enzymes responsible for the regeneration of glutathione in specific areas in the brain, including the hippocampus and cerebral cortex.

Furthermore, curcumin increased the activity of the enzyme called choline acetyltransferase in the hippocampus, which is important in the synthesis of the neurotransmitter acetylcholine. Reduced levels of acetylcholine are believed to play a role in Alzheimer’s disease.

The researchers concluded, “The study suggests that curcumin is effective in preventing cognitive deficits, and might be beneficial for the treatment of sporadic dementia of Alzheimer’s type.”

Reference:

Ishrat T, Hoda MN, Khan MB, Yousuf S, Ahmad M, Khan MM, Ahmad A, Islam F. Amelioration of cognitive deficits and neurodegeneration by curcumin in rat model of sporadic dementia of Alzheimer’s type (SDAT). Eur Neuropsychopharmacol. 2009 Mar 27. Published Online Ahead of Print.

Increase glutathione - reduce glutamate levels

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One of the best ways to counter Glutamate excitotoxicity and resulting neuron deaths is to increase glutathione levels.

Unfortunately, glutathione supplements taken orally are very poorly absorbed and have not raised glutathione levels in the blood. So save your money.

The glutathione precursor, N-acetyl-cystine(commonly just called NAC) provides sufficient sulphur containing amino acid (a duo or dimer of cysteine) to boost glutathione levels.

NAC is readily absorbed and boosts glutathione levels quite well.

Glutathione contains the following 3 amino acids linked together: Glutamate—cysteine--glycine.

There are some foods that that boost glutathione levels. I do not know all of them but a few are Asparagus, avocados, and walnuts which are known to be a rich sources of glutathione.

http://www.nutritionadvisor.com/glutathione_foods.php .. <---- REAL GOOD INFO HERE!!

Also broccoli, brussels sprouts, cabbage and cauliflower all contain cyanohydroxybutene which increases glutathione levels.
Avocados, peaches, bueberries and watermelon are also reported to raise glutathione levels.

Several spices including cinnamon, cardamom and curcumin found in turmeric raise glutathione levels.

Alpha Lipoic Acid (ALA) promotes the synthesis of glutathione in the body. Food sources of ALA include spinach, broccoli, tomatoes, peas, Brussels sprouts, and rice bran. Real Hellman’s Mayonnaise also provides 660 mg of ALA per 1 tablespoon.

jackD

-lipoic acid reduces glutamate neuronal damage

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I take some R-Dihydro-Lipoic Acid 150 mg because it lower MMP-9s (stage 1 of MS) and now I know that it helps in Stage 2 of MS by lowering Glutamate neuron damage.

jackD

P.S. If anyone knows of other "thingies" that lower/counters Glutamate excitotoxic neuronal damage please fell free to add it to this thread.

J Cereb Blood Flow Metab. 1995 Jul;15(4):624-30.

Prolonged pretreatment with alpha-lipoic acid protects cultured neurons against hypoxic, glutamate-, or iron-induced injury.

Müller U, Krieglstein J.

Institut für Pharmakologie und Toxikologie, Philipps-Universität, Marburg, Germany.

Abstract
The antioxidant dihydrolipoic acid has been shown to reduce hypoxic and excitotoxic neuronal damage in vitro. In the present study, we tested whether pretreatment with alpha-lipoic acid, which presumably allows endogenous formation of dihydrolipoic acid, can protect cultured neurons against injury caused by cyanide, glutamate, or iron ions, using the trypan blue exclusion method to determine neuronal damage.

One hour of preincubation with dihydrolipoic acid (1 microM), but not with alpha-lipoic acid, reduced damage of neurons from chick embryo telencephalon caused by 1 mM sodium cyanide or iron ions. alpha-Lipoic acid (1 microM) reduced cyanide-induced neuronal damage when added 24 h before hypoxia, and pretreatment with alpha-lipoic acid for > 24 h enhanced this neuroprotective effect.

Both the R- and the S-enantiomer of alpha-lipoic acid exerted a similar neuroprotective effect. Pretreatment with alpha-lipoic acid (1 microM) from the day of plating onward prevented the degeneration of chick embryo telencephalic neurons that had been exposed to Fe2+/Fe3+. alpha-Lipoic acid (1 microM) added to the culture medium the day of plating also reduced neuronal injury induced by 1 mM L-glutamate in rat hippocampal cultures, whereas 30 min of preincubation with alpha-lipoic acid failed to attenuate glutamate-induced neuronal damage.

Our results indicate that neuroprotection by prolonged pretreatment with alpha-lipoic acid is probably due to the radical scavenger properties of endogenously formed dihydrolipoic acid.

PMID: 7790411 [PubMed - indexed for MEDLINE]

I'm grateful for this information. I've already been doing some of these supplements because I find they curtail leg and back jerking and spasticity. Because of you, Jack, I switched to D3 from D2 years ago, and upped my dose of D3. The doctor did find D3 deficiency--my pcp's have tested almost all of their patients for d3 deficiency.

I have taken Vitamin E complex with Tocotrinols for years, as well. I found that taking a higher dose of tocotrinols caused increase of spasticity and anxiety, so I went back to the more modest dose. I am a poster child for what Erika brought up, that there can be too much of a good thing, as far as SOME supplements go.

Of course I am one of the absolutely sold out fans of Magnesium. I might be in a nursing home with severed nerves leading to my legs if I did not have Magnesium. I have taken it over 25 years on the advise of a neuro at Scripps, when it was found I could not tolerate any Baclofen or Zanaflex, even very minor doses. The fact that I cannot tolerate B or Z may be related to the fact that I have Porphyria. My Porph interacts with my MS in a subtle way and makes diagnosis almost impossible...neuros disagreed on whether I had MS or Porph, and I gave up l5 or more years ago even trying to figure out that tangle, just doing what I can with supplements and foods to help both MS and Porph. I probably have both, but somehow have not succumbed to either, just go on fighting and defying the Whatevers.

I know my grandson aged 9 will need some help with the Whatevers, but it is hard to deal with parents who insist on going to the more typical pediatricians and will not take the opportunity to go to one who understands more about chemical pathways. I will insinuate D3 into his diet through his mom, who "believes" in vitamins, unlike my son.

I also have Polycythemia Vera and produce too many platelets and red cells, so I have to be careful taking large doses of new things. Not all substances affect PV, so I am usually pretty safe, but must be cautious.

I know that the Swank Diet helps me, has done so for over 25 years. I am beginning to forget when I was dx'd with MS because it was a gradual process, and I had symptoms for decades prior to dx.

I don't think I can take LDN. Demerol is the only pain killer I can take. I can take aspirin but only through the skin. I can take some pain killers, but very selectively--for instance, can take Marcaine but not Lidocaine.

Thanks again!