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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 14 of 14. This is the beginning of the thread.
Posted by btnd on September 26, 2003, at 13:20:37
Ok, so does anyone know how much DXM needs to be taken in order to block NDMA receptor and therefore block amphetamine (Adderall,Dexedrine) tolerance?
Are there any studies showing the amounts? (I couldn't find any)I've found site which explains many aspects of DXM's action on NDMA, Ca++ and other factors involved in amphetamine tolerance.
http://free.freespeech.org/ekomstop/subjects/psychoactives/dxm.htm
Posted by linkadge on September 26, 2003, at 13:44:28
In reply to Amphetamine tolerance, DXM, NDMA blocking, posted by btnd on September 26, 2003, at 13:20:37
Why not try Lithium or Magnesium, these both inhibit NDMA receptors and are Ca inhibitors as well.
Linkadge
Posted by jonh kimble on September 26, 2003, at 22:20:18
In reply to Re: Amphetamine tolerance, DXM, NDMA blocking, posted by linkadge on September 26, 2003, at 13:44:28
That has me very interested. If you have the time id appreciate seing some literature on this.
Also, i wonder if dxm can be taken on a daily basis. (like for a year for ex.) You may want to consider memantine, i know it has a reputation for safety (maybe dxm does too, i dont know) email me for more info ;). Thanks
Posted by jonh kimble on September 26, 2003, at 22:26:18
In reply to Re: Lithium's an nmda antagonist?, posted by jonh kimble on September 26, 2003, at 22:20:18
Sorry my email is stopwhining@email.com
Posted by Ame Sans Vie on September 28, 2003, at 8:28:51
In reply to Amphetamine tolerance, DXM, NDMA blocking, posted by btnd on September 26, 2003, at 13:20:37
Near the end of this document are the recommended dosages of the NMDA antagonists methadone, dextromethorphan, and ketamine. Note that the higher end of the suggested daily dose of DXM is 1,000mg!!! That seems a bit... crazy. But it implies that you should begin with 15-30 dextromethorphan polystirex (Delsym -- extended release forumulation) three times daily.
I'm not finding anything specifically addressing the issue of NMDA-antagonists for amphetamine tolerance, but I did come across a lot concerning their use to potentiate and prevent tolerance to opioids as well as the potential for them to have such an impact upon dependence/tolerance in general. The first thing I found interesting is a novel drug called MorphiDex, currently undergoing research, which is a 50/50 combination of morphine and DXM. This study strongly supports its ability to increase analgesic effectiveness of morphine:
http://opioids.com/morphidex/index.html
I'm also inferring from the study that the researchers must consider DXM safe taken long-term. I mean, assuming 80mg morphine qid, we're talking 320mg of DXM daily -- still quite a bit shy of the gram recommended above, but 320mg is (for most people) a very psychoactive dose. I'm only taking 15mg and definitely feel it helps. I can't explain my lack of Ultram tolerance after 400mg/day for several months any other way.
Posted by btnd on September 28, 2003, at 9:18:54
In reply to Here are NMDA antagonist dosages / MorphiDex » btnd, posted by Ame Sans Vie on September 28, 2003, at 8:28:51
Thanks Ame for the info!
> I'm not finding anything specifically addressing the issue of NMDA-antagonists for amphetamine tolerance, but I did come across a lot concerning their use to potentiate and prevent tolerance to opioids as well as the potential for them to have such an impact upon dependence/tolerance in general.
I hope andrewb won't mind if I cut/paste some of his great information on amphetamine tolerance and NDMA antagonism:"For some individuals, amotivation and anergia are only partially resolved by taking selegiline. For these individuals, an amphetamine or related stimulants will, for most, resolve any remaining anergia and amotivation. However, for most, tolerance for these stimulants? motivational and energizing effects develops. Therefore, an agent to prevent tolerance, e.g. an NMDA (partial) antagonist, may also be required, as discussed further on. When the appropriate stimulant at the appropriate dosage, with the proper NMDA antagonist are taken, an individual may achieve normal to robust energy and drive (proper enthusiasm for life) on an ongoing basis"
...
"It is normal for tolerance to develop over time for many or all of amphetamines effects. Tolerance may occurs slowly over a period of months, with all the positive effects fading away over times except those associated with features of apathy. Alternatively, tolerance may develop quickly, within a period of, say, 3 to 6 days. When the ?crash? comes, the individual is left irritable and dysphoric. However, if the amphetamines are stopped for 1 or 2 days, the full effect of the amphetamine is restored. In ADD, these breaks from taking amphetamine to restore effect are termed ?drug holidays?.
Amphetamine tolerance is caused by excess Ca++ influx through the NMDA receptor gated calcium channels on the outer membranes of the dopamine cells bodies in the ventral tegental area, one of two areas in the brain with concentrations of dopamine producing neurons.
As alluded to above, taking an appropriate NMDA antagonist will prevent the development of a tolerance for the effects of an amphetamine or amphetamine-like stimulant. Also by preventing excess Ca++ influx into the neuron, an NMDA antagonist will prevent associated brain alterations and damage (excitotoxicity).
Many studies have indicated that amphetamine tolerance is prevented by exogenous or endogenous agents that are able to inhibit excess Ca+ influx into the neuron through the gated calcium channels on the neuronal membrane that have NMDA subtype glutamate receptors. Glutamate, the body?s major excitatory neurotransmitter, opens the gated calcium ion channels upon attaching to the NMDA receptor. A number of other receptors are also expressed on these calcium channels, which, when stimulated, either facilitate or inhibit glutamate?s action.
Excess Ca++ influx has been implicated in a number of neurodegenerative disorders and depressive processes. That being said, calcium channel activity is essential for brain function. Without it, neurotransmission would not occur. Furthermore, deficient calcium channel activity is also associated with neurodegeneration and the development of certain neurological pathologies.
Therefore it is important that agents that inhibit calcium channel activity not also cause deficient Ca++ influx. For example, ketamine is a NMDA receptor full antagonist that prevents excess Ca++ influx and amphetamine tolerance. But, being a full NMDA antagonist, ketamine in excessive doses results in deficient Ca++ influx. Besides being damaging to the brain, it causes severe memory loss and states of disassociation. Perhaps you?ve heard of ketamine by its street names; PCP, angel dust.
Two agents with minimal or no side effects have been identified as preventing amphetamine tolerance, memantine and acamprosate."
Posted by jparsell82 on September 28, 2003, at 9:52:32
In reply to Re: Amphetamines and NDMA antagonism » Ame Sans Vie, posted by btnd on September 28, 2003, at 9:18:54
I've took Dexedrine before and started to develope a tolerance. As a replacement I've just started taking Selegilene w/Phenylalanine(sometimes Tyrosine instead) and I have to say I really get the stimulant effect. These 2 synergize together pretty well.
Posted by Larry Hoover on September 29, 2003, at 8:11:55
In reply to Here are NMDA antagonist dosages / MorphiDex » btnd, posted by Ame Sans Vie on September 28, 2003, at 8:28:51
> Near the end of this document are the recommended dosages of the NMDA antagonists methadone, dextromethorphan, and ketamine. Note that the higher end of the suggested daily dose of DXM is 1,000mg!!! That seems a bit... crazy.
Uh-huh! Olny's lesions....
> But it implies that you should begin with 15-30 dextromethorphan polystirex (Delsym -- extended release forumulation) three times daily.
What is polystirex? Is that a plastic bead vehicle?
> http://216.239.39.104/search?q=cache:7vJZCHDAF4AJ:www.aacpi.wisc.edu/meeting/Strouse-CSMCCPMS2003.ppt+%22amphetamine%22+%22nmda%22+%22dextromethorphan%22&hl=en&start=12&ie=UTF-8&client=REAL-tb
>
> I'm not finding anything specifically addressing the issue of NMDA-antagonists for amphetamine tolerance, but I did come across a lot concerning their use to potentiate and prevent tolerance to opioids as well as the potential for them to have such an impact upon dependence/tolerance in general. The first thing I found interesting is a novel drug called MorphiDex, currently undergoing research, which is a 50/50 combination of morphine and DXM. This study strongly supports its ability to increase analgesic effectiveness of morphine:
>
> http://opioids.com/morphidex/index.html
>
> I'm also inferring from the study that the researchers must consider DXM safe taken long-term. I mean, assuming 80mg morphine qid, we're talking 320mg of DXM daily -- still quite a bit shy of the gram recommended above, but 320mg is (for most people) a very psychoactive dose.Maybe not, in interaction with the morphine.
> I'm only taking 15mg and definitely feel it helps. I can't explain my lack of Ultram tolerance after 400mg/day for several months any other way.
>Ah-hah! I don't recall your mentioning using DXM when you first reported lack of tolerance to the tramadol. You know what? I didn't do that when I tried tramadol, and I developed tolerance in mere days.
Lar
Posted by Larry Hoover on September 29, 2003, at 8:19:25
In reply to Re: Amphetamines and NDMA antagonism » Ame Sans Vie, posted by btnd on September 28, 2003, at 9:18:54
> I hope andrewb won't mind if I cut/paste some of his great information on amphetamine tolerance and NDMA antagonism:
"Perhaps you?ve heard of ketamine by its street names; PCP, angel dust."
Just a correction, here. Ketamine is Special K. PCP and angel dust are phencyclidine. NOT the same thing. Not.
Lar
Posted by Ramon Paz on October 1, 2003, at 2:04:54
In reply to Re: Amphetamines and NDMA antagonism » btnd, posted by Larry Hoover on September 29, 2003, at 8:19:25
There is a lot of NMDA antagonists directly or indirectly. Other opiods are not good, taking opiates to lower tolerance of others? dont work!
The one I take and is glutamate antagonists receptor(being NMDA the more important)is the "lamotrigine", and works directly in the Key. The Ca++ channel blocker "nimodipine" that works most in brain taking in 20-60mg/day will put more antagonist. But one I never used and is the most potent is Riluzole(expensive and dont have proprieties in limbic system as lamictal and nimodipine). Jist an resume.
Posted by Ame Sans Vie on October 1, 2003, at 10:00:12
In reply to Re: Amphetamines and NDMA antagonism, posted by Ramon Paz on October 1, 2003, at 2:04:54
According to one study I have below, Rilutek is certainly neuroprotective, but does not act via NMDA receptors: "The results indicate that when given alone, riluzole has a behavioral profile resembling that of competitive NMDA receptor antagonists. However, coadministration of riluzole with NMDA/AMPA receptor ligands suggests that this assumption is incorrect, and that riluzole affects glutamatergic transmission by a more indirect mechanism."
I have however been wondering about Rilutek as GABA-enhancing med for some time now. A lot of very interesting things I've come across below... the first thing that really strikes me as interesting is this line in the second abstract: "... riluzole-induced potentiation was inhibited by the lactone antagonist alpha-isopropyl-alpha-methyl-gamma-butyrolactone (alpha-IMGBL)." So if its effects were attenuated by a lactone inhibitor (gamma butyrolactone, no less), then I have to wonder whether part of its M.O.A. is through GHB (or similar) receptors... I may be totally wrong about this, but it sounds possible. After all, it's said to possess anxiolytic, sedative, and anaesthetic qualities... remind you of anything? :-)
1. Beneficial effects of the antiglutamatergic agent riluzole in a patient diagnosed with obsessive-compulsive disorder and major depressive disorder.
Coric V, Milanovic S, Wasylink S, Patel P, Malison R, Krystal JH.
Clinical Neuroscience Research Unit, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, CT 06519, New Haven, USA.
2. Neuroprotective agent riluzole potentiates postsynaptic GABA(A) receptor function.
He Y, Benz A, Fu T, Wang M, Covey DF, Zorumski CF, Mennerick S.
Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA.
The antiepileptic drug riluzole is a use-dependent blocker of voltage-gated Na(+) channels and selectively depresses action potential-driven glutamate over gamma-aminobutyric acid (GABA) release. Here we report that in addition to its presynaptic effect, riluzole at higher concentrations also strongly potentiates postsynaptic GABA(A) responses both in cultured hippocampal neurons and in Xenopus oocytes expressing recombinant receptors. Although peak inhibitory postsynaptic currents (IPSCs) of autaptic hippocampal neurons were inhibited, 20-100 microM riluzole significantly prolonged the decay of IPSCs, resulting in little change in total charge transfer. The effect was dose-dependent and reversible. Riluzole selectively increased miniature IPSC fast and slow decay time constants, without affecting their relative proportions. Miniature IPSC peak amplitude, rise time and frequency were unaffected, indicating a postsynaptic mechanism. In the Xenopus oocyte expression system, riluzole potentiated GABA responses by lowering the EC(50) for GABA activation. Riluzole directly gated a GABA(A) current that was partially blocked by bicuculline and gabazine. Pharmacological experiments suggest that the action of riluzole did not involve a benzodiazepine, barbiturate, or neurosteroid site. Instead, riluzole-induced potentiation was inhibited by the lactone antagonist alpha-isopropyl-alpha-methyl-gamma-butyrolactone (alpha-IMGBL). While most anticonvulsants either block voltage-gated Na(+) channels or potentiate GABA(A) receptors, our results suggest that riluzole may define an advantageous class of anticonvulsants with both effects.
3. Riluzole, a novel antiglutamate, blocks GABA uptake by striatal synaptosomes.
Mantz J, Laudenbach V, Lecharny JB, Henzel D, Desmonts JM.
Department of Anesthesiology, Hospital Bichat, Paris, France.
The effect of riluzole (2-amino-6-trifluoro-methoxybenzothiazole, a novel antiglutamate agent) on the uptake of [3H]GABA (gamma-aminobutyric acid) by striatal synaptosomes was investigated in rats. Both nipecotic acid (a classical blocker of GABA uptake) and riluzole were found to inhibit [3H]GABA uptake in a dose-related fashion (IC50 = 3.6 x 10(-6) M and 4.3 x 10(-5) M for nipecotic acid and riluzole, respectively). These results indicate that, in addition to its antiglutamate properties, riluzole probably also promotes synaptic GABA accumulation, which might contribute to the anticonvulsant and/or anesthetic properties of this pharmacological agent.
4. Riluzole antagonizes the anxiogenic properties of the beta-carboline FG 7142 in rats.
Stutzmann JM, Cintrat P, Laduron PM, Blanchard JC.
Rhone-Poulenc Sante, Centre de Recherches de Vitry, France.
The possible anxiolytic activity of riluzole, a drug which interferes with glutamic acid neurotransmission, was studied in rats using operant conflict procedures. In both "anxiolytic" and "anxiogenic" procedures, riluzole alone did not possess any anticonflict or proconflict effect at doses of 2 and 4 mg/kg PO. Riluzole over the same dose-range was able to antagonize the well known proconflict effect of the beta-carboline derivative FG 7142, an inverse agonist at the GABA-benzodiazepine-chloride ionophore receptor complex. This effect could be related to the possible interaction of riluzole with glutamic acid neurotransmission, since it has been demonstrated previously that beta-carbolines such as DMCM and beta-CCM were able to deplete the levels of aspartic and glutamic acids in rodent cortex, perhaps by enhancing release of amino acid neurotransmitters. If one subscribes to the hypothesis that the anxiety induced by beta-carboline derivatives is related to depression, riluzole might be of value in the treatment of anxiety related to depression.
5. The pharmacology and mechanism of action of riluzole.
Doble A.
Vitry-Alfortville Research Centre, Rhone-Poulenc Rorer SA, Vitry-sur-Seine, France.
The excitotoxic hypothesis of neurodegeneration has stimulated much interest in the possibility of using compounds that will block excitotoxic processes to treat neurologic disorders. Riluzole is a neuroprotective drug that blocks glutamatergic neurotransmission in the CNS. Riluzole inhibits the release of glutamic acid from cultured neurons, from brain slices, and from corticostriatal neurons in vivo. It is thought these effects may be partly due to inactivation of voltage-dependent sodium channels on glutamatergic nerve terminals, as well as activation of a G-protein-dependent signal transduction process. Riluzole also blocks some of the postsynaptic effects of glutamic acid by noncompetitive blockade of N-methyl-D-aspartate (NMDA) receptors. In vivo, riluzole has neuroprotective, anticonvulsant, and sedative properties. In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemia-evoked surge in glutamic acid release has been observed. In vitro, riluzole protects cultured neurons from anoxic damage, from the toxic effects of glutamic-acid-uptake inhibitors, and from the toxic factor in the CSF of patients with amyotrophic lateral sclerosis.
6. Protective effects of riluzole on dopamine neurons: involvement of oxidative stress and cellular energy metabolism.
Storch A, Burkhardt K, Ludolph AC, Schwarz J.
Department of Neurology, University of Ulm Medical School, Ulm, Germany. alexander.storch@medizin.uni-ulm.de
Riluzole is neuroprotective in patients with amyotrophic lateral sclerosis and may also protect dopamine (DA) neurons in Parkinson's disease. We examined the neuroprotective potential of riluzole on DA neurons using primary rat mesencephalic cultures and human dopaminergic neuroblastoma SH-SY5Y cells. Riluzole (up to 10 microM:) alone affected neither the survival of DA neurons in primary cultures nor the growth of SH-SY5Y cells after up to 72 h. Riluzole (1-10 microM:) dose-dependently reduced DA cell loss caused by exposure to MPP(+) in both types of cultures. These protective effects were accompanied by a dose-dependent decrease of intracellular ATP depletion caused by MPP(+) (30-300 microM:) in SH-SY5Y cells without affecting intracellular net NADH content, suggesting a reduction of cellular ATP consumption rather than normalization of mitochondrial ATP production. Riluzole (1-10 microM:) also attenuated oxidative injury in both cell types induced by exposure to L-DOPA and 6-hydroxydopamine, respectively. Consistent with its antioxidative effects, riluzole reduced lipid peroxidation induced by Fe(3+) and L-DOPA in primary mesencephalic cultures. Riluzole (10 microM) did not alter high-affinity uptake of either DA or MPP(+). However, in the same cell systems, riluzole induced neuronal and glial cell death with concentrations higher than those needed for maximal protective effects (> or =100 microM:). These data demonstrate that riluzole has protective effects on DA neurons in vitro against neuronal injuries induced by (a) impairment of cellular energy metabolism and/or (b) oxidative stress. These results provide further impetus to explore the neuroprotective potential of riluzole in Parkinson's disease.
7. Riluzole, a glutamate release inhibitor, and motor behavior.
Kretschmer BD, Kratzer U, Schmidt WJ
Naunyn-Schmiedeberg's Archives of Pharmacology 358(2), 181-190.Riluzole (2-amino-6-trigluoromethoxy benzothiazole) has neuroprotective, anticonvulsant, anxiolytic and anesthetic qualities. These effects are mediated by blockade of glutamate transmission, stabilizing of sodium channels and blockade of gamma-aminobutyric acid (GABA) reuptake. The action profile of riluzole is dominated by its effects on glutamate transmission which are predominately mediated by N-methyl-D-aspartate (NMDA) receptor-linked processes in vitro. In vivo studies show that blockade and stimulation of the different NMDA receptor complex binding sites or AMPA receptors modulate motor behavior in a characteristic manner. It was therefore interesting to examine if blockade of glutamatergic transmission by riluzole induced similar behavioral effects as direct NMDA/AMPA receptor antagonists and if these effects are mediated by a specific receptor. The effects of riluzole alone and in combination with several other neuroactive compounds on the central nervous system was assessed by behavioral paradigms to evaluate sniffing behavior, locomotion, ataxia and rigidity. Accompanying compounds included the NMDA receptor agonist NMDA, the partial glycine site agonist D-cycloserine (DCS), and the alpha-amino-3-hydroxy-5-phenyl-4-isoxazolepropionic acid (AMPA) receptor antagonist GYKI 52466 [1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzo-diazepine HCl]. Riluzole influenced neither stereotyped sniffing behavior nor locomotion but impaired motor coordination and attenuated rigidity induced by blockade of dopamine D1 and D2 receptor antagonists when given alone. At higher doses spontaneous behavioral activity decreased and motor coordination was more impaired. Augmentation of the riluzole effects were observed when NMDA, but not GYKI 52466, was coadministered. The glycine site agonist DCS increased the anticataleptic properties of riluzole. The results indicate that when given alone, riluzole has a behavioral profile resembling that of competitive NMDA receptor antagonists. However, coadministration of riluzole with NMDA/AMPA receptor ligands suggests that this assumption is incorrect, and that riluzole affects glutamatergic transmission by a more indirect mechanism. Nevertheless, the profile of riluzole together with its pre- and postsynaptic blockade of glutamatergic transmission implies beneficial properties in diseases where an overactive glutamate system induces chronic neurotoxicity and/or acute behavioral effects.
8. Interaction of the neuroprotective drug riluzole with GABA(A) and glycine receptor channels.
Mohammadi B, Krampfl K, Moschref H, Dengler R, Bufler J.
Eur J Pharmacol 2001 Mar 16;415(2-3):135-40
Neurological Department, Medical School Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany
Riluzole is used as therapeutic agent in amyotrophic lateral slerosis. We investigated the interaction of riluzole with recombinant GABA (gamma-aminobutyric acid)(A) receptor channels (alpha(1)beta(2)gamma(2)-subunits) and glycine receptor channels (alpha(1)beta-subunits) transiently expressed in HEK293 cells. For electrophysiological experiments, the patch-clamp technique in combination with tools for ultrafast solution exchange was used. Saturating concentrations of GABA or glycine were applied with different concentrations of riluzole to outside-out patches containing alpha(1)beta(2)gamma(2) GABA(A) receptor channels or alpha(1)beta-glycine receptor channels on their surface, respectively. The current declined after application of GABA or glycine with three time constants of desensitization to a steady-state current amplitude. Application of riluzole resulted in a shift to fast desensitized states at both receptors. The proportion of the time constants of fast desensitization increased and the time constants of slow desensitization and the steady-state current decreased whereas the maximal current amplitudes were not affected by riluzole. The data of the study demonstrate for the first time interaction of GABAergic and glycinergic currents with riluzole under physiological conditions.
Posted by SLS on October 1, 2003, at 22:51:00
In reply to Re: Riluzole (long -- lots of abstracts) » Ramon Paz, posted by Ame Sans Vie on October 1, 2003, at 10:00:12
Thanks for the links. The NIMH is investigating the use of riluzole (Rilutek) in the treatment of bipolar depression.
http://www.clinicaltrials.gov/show/NCT00054704
- Scott
Posted by Ramon Paz on October 2, 2003, at 5:08:05
In reply to Re: Riluzole (long -- lots of abstracts) » Ramon Paz, posted by Ame Sans Vie on October 1, 2003, at 10:00:12
well, I just wrote one phrase about riluzole so few things... but the abstracts are very good and I got things that I didnt knew.
Now, what about LAMOTRIGINE? I ask it cause a very worthy Psychiatry said that lamotrigine doesnt work for nothing, a trash. But I dont agree with him. Put some words to us ok? tanks...
Posted by btnd on October 3, 2003, at 17:39:40
In reply to Re: Amphetamines and NDMA antagonism, posted by Ramon Paz on October 1, 2003, at 2:04:54
Maybe L-Theanine would be cheap and effective way to prevent amphetamine tolerance? Here is some info I've found:
A natural glutamate antagonist is the structurally similar amino acid L-theanine. The similarity enables L-theanine (L-Glutamic acid-?-monoethylamide) to physically block glutamate, thus preventing calcium ion induced hyperexcitability. Although researchers aren't positive how theanine works yet, they theorize that theanine blocks the NMDA receptor which is the doorway that glutamate uses to enter cells. Theanine is known to increase GABA (Gamma-Amino-Butyric Acid), an important inhibitory neurotransmitter. Because of the similar structure, theanine can also fit in this doorway, blocking access to glutamate. But, although it can fit in the doorway, theanine does not have the same effect on the cell as glutamate does. Rather than causing damage, theanine acts like a shield against damage. Theanine is the active ingredient in green tea. The Japanese have used enormous amounts of MSG for many years to improve taste of poor quality food, but they offset its toxic effects with green tea. In 1964, Japan approved theanine?s use in all food, except baby food. In Japan, you can buy over 50 different food items that contain theanine. Japanese soft drinks are spiked with the relaxant, and it has been put into chewing gum. The tranquilizing effects of theanine definitely are not imaginary. Theanine readily crosses the blood-brain barrier of humans and exerts subtle changes in biochemistry. An increase in brain alpha waves (resulting in an increase in wakeful relaxation) has been documented, and the effect has been compared to getting a massage or taking a hot bath. And, unlike tranquilizing drugs (including kava-kava, valerian and St. John's wort), it doesn't interfere with the ability to either think or exercise good judgement. It does not sedate, as demonstrated by no change in brain theta waves upon administration. It does not help one doze or fall asleep, unless the person is excited or hyper. By shutting down the "worry" mode, L-theanine increases concentration and focuses thought. This is the concept behind the Japanese tea ceremony which causes a person to focus on the moment. Dosage is reported to be 100 mg 1 to 4 times per day.
This is the end of the thread.
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