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

The substance the body produces to counter Glutamate is the antioxidant glutathione. Here is an extract from the current newsletter from VRP Vitamin Research Products on curcumin(tumeric extract) that states that it increases the bodies production of the antioxidant glutathione.

JackD

http://www.vrp.com/newsletter.aspx


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.

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."

I highly reccommend this ACE inhibitor - CAPTOPRIL. It is generic and cheap BUT you must take it twice a day. I am stilll researching this also.

jackD

p.s. This elevation of the ACE stuff may explain some of our(MS floks) high BP.


"Immunopharmacol Immunotoxicol. 1995 Aug;17(3):471-91.

Effects of the angiotensin converting enzyme inhibitor captopril on experimental autoimmune encephalomyelitis.

• Constantinescu CS,
• Ventura E,
• Hilliard B,
• Rostami A.

Department of Neurology, University of Pennsylvania, Philadelphia 19104, USA.
Angiotensin converting enzyme (ACE)1 mediates inflammation, participates in T cell stimulation by certain antigenic peptides, and influences the permeability of the blood brain barrier (BBB).

ACE is elevated in multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), characterized by increased BBB permeability.

ACE inhibitor captopril suppresses certain immune functions and inhibits inflammatory or autoimmune diseases.

We studied the effect of captopril on Lewis rat EAE, an animal model of MS. Fourteen rats with EAE were treated with captopril 30 mg/kg daily from immunization to day 21 post-immunization, and compared with 14 untreated rats. Severity scores and lymphocyte reactivity to myelin basic protein and mitogen were measured.

There was a statistically significant (p < 0.05) difference between the mean and cumulative clinical scores of captopril-treated and untreated animals. Lymphocytes from captopril treated EAE rats at the peak of disease severity had diminished responses to MBP and concanavalin A.

The data suggest a significant beneficial effect of captopril in Lewis rat EAE. Further studies including other inhibitors of ACE or of other peptidases with immune, inflammatory or BBB role, may identify potentially valuable immunopharmacologic agents.

PMID: 8576541 [PubMed - indexed for MEDLINE]"

I must point out that the other oral B12 - Cyanocobalamin - does NOT share this nice attribute, however it is a great way to get some Cyanide in your liver.

jackD

ps. I get mine at http://www.lifeextensionvitamins.com/metcob1.html


Protection via Methylcobalamin (Oral B12)

Protective effects of a vitamin B12 analogue, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons.

Akaike A Tamura Y Sato Y Yokota T, Eur J Pharmacol (1993 Sep 7) 241(1):1-6

The effects of methylcobalamin, a vitamin B12 analogue, on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free medium for 1 h. Glutamate cytotoxicity was prevented when the cultures were maintained in methylcobalamin-containing medium. Glutamate cytotoxicity was also prevented by chronic exposure to S-adenosylmethionine, which is formed in the metabolic pathway of methylcobalamin.

Chronic exposure to methylcobalamin and S- adenosylmethionine also inhibited the cytotoxicity induced by methyl-D-aspartate or sodium nitroprusside that releases nitric oxide. In cultures maintained in a standard medium, glutamate cytotoxicity was not affected by adding methylcobalamin to the glutamate-containing medium.

In contrast, acute exposure to MK-801, a NMDA receptor antagonist, prevented glutamate cytotoxicity. These results indicate that chronic exposure to methylcobalamin protects cortical neurons against NMDA receptor-mediated glutamate cytotoxicity.