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The Use of Lithium to alter glutamate reception


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Ok Buddies,

 

This is part of a thread that came from the "Protracted" area, where we were discussing ideas to actively reverse the damage benzos has caused us.  This was one of the ideas, and we will move the best of the posts on that topic here.

 

If you were not part of the original thread, give us a day to move the topics.  It is now 12:30 pm Eastern US time on Tuesday Nov. 6.  Please wait until Midnight Thursday Nov 8 wherever you live to make any comments on this topic.

 

Thank you all for your cooperation.

 

Ramcon1

Your personal neuroscientist, reminding you to hang in there, and if you are going thru hell, keep going!

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Dear Buddies,

 

The idea that most of our pain is due to glutamate reception is not an original idea I had.  Other buddies have had it, and there is research to support it.  I will bring the discussion of how this could be done with Lithium from the protracated area where someone first brought it up.  But I want to start these two threads centered on glutamate with this opening:

 

My thesis statement is:

 

Although every case of Protracted Benzodiazepine Withdrawal Syndrome (PBWS) is unique, a cure that applies to almost every case is still possible.

 

Mutuuaria has posted:

“I believe the reason there is no collective consensus about what "works" is because we don't share the exact same pathologies. There can be no collective "treatment" that works for everyone, only individual treatments that work for individuals.”

 

I respect mutuu, and her opinion(s).  The part of that statement with which I firmly agree is “we don’t share the exact same pathologies.”  In fact I think the pathologies of those who suffer PBWS vary wildly from individual to individual.  But I still believe a cure that works for nearly everyone is possible because benzos can do only one thing: open an ionotropic GABA-A receptor to release negatively charged chloride anions (Cl-). Period.  That is all they do.  The dozens (hundreds?) of different things that happen to us all result from that one thing.

 

The reason there are so many different issues, and that each case is unique is that GABAergic nerves enervate every organ and body system and our CNS, and everyone’s genetics and epigenetics of those systems is different, which means literally almost anything is possible.

 

The very next thing that happens downstream is the Cl- anions immediately remove the positive charged (usually calcium, Ca+2) cations from the synapse.  If this happens once or a dozen times, no big deal.  But do this on a continuous basis, and the body responds by upregulating the number of glutamate receptors to receive the fewer cations, and probably also lowers their firing potential and duration the stay open, aka Long Term Potentiation (LTP) as well.  While this is the secondary effect, I think it is the longer lasting effect and the reason some of us are sick for so long.

 

Could I be wrong?  Yes, but I do not think so.  Ionotropic glutamate receptor upregulation is required for learning and so the mechanisms are well established.  But downregulation not normally required in nature, so why would it happen on its own?  Very, very, slowly to the painful, regular, presence of what is perceived as excess cations?  This might happen, and this would explain protracted success stories.

 

I have found a common term across a variety of disorders that have nothing to do with PBWS; “hypervigilance.” This is associated with the neurological conditions of Irritable Bowel Syndrome (IBS, which has “visceral” hypervigilance) Temporal Lobe Epilepsy (TLE), and Autism Spectrum Disorder (ASD), and the psychiatric conditions Generalized Anxiety Disorder (GAD) and Obsessive Compulsive Disorder (OCD), and those are just the main ones for which there is a tangible research consensus.  One only has to google any of those terms with “hypervigilance” and look at the plethora of articles that pop up.  Better still, google them with “glutamate,” and/or “NMDA, and AMPA.” and you will quickly see from where my thesis comes.  (I would add “prostatitis,” “chronic Lyme’s Disease,” and others, but those are speculative on my part and I have found no correlating research.)

 

Examples:

IBS

https://www.ncbi.nlm.nih.gov/pubmed/27356126

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817711/

TLE

http://www.biomed.cas.cz/physiolres/pdf/62%20Suppl%201/62_S21.pdf

ASD (autism)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134390/

PTSD

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482215/

OCD

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3205262/

 

And I have already posted but to bring this full circle:

PBWS (US!)

https://www.jstage.jst.go.jp/article/jjp/81/1/81_1_1/_pdf/-char/en

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321276/

 

Pain, stiffness, bloating/distention, anxiety, disruption of the HPA axis and everything that flows downstream from there, dozens if not hundreds of possible health issues, all stemming from upregulated ionotropic glutamate receptors.

 

Consequently, since it was upregulation that caused our issues, I postulate that if one could coax downregulation, in a relatively short period of time, the majority of downstream issues should also be corrected.

 

One could argue that if my hypothesis were true, there would be a cure for those other things too.  My answer to that is: there will be.*

 

There are published ways to make those ionotropic (and metabotropic too) downregulate with intervention, and that is the focus of my research.  I have been a human guinea pig, but even the baby steps involved in these methods have, to put it in the most technical terms, revved the B’Jesus out of me.  But I have posted and will state again, that in my own personal case, I think Florida is right.  I may be banging my head up against a wall until I log a few months clean of benzos.  If only because I cannot coerce downregulation by one mechanism while coercing upregulation by another.

 

So that is it in a nutshell, my buddies.  If you agree, chime in.  If you can find a hole in this logic PLEASE chime in.  I want to find where I might be making a mistake.  But if you find a hole, please make it a logical one, and post a link for supporting evidence that this logic is flawed.

 

Thank you all in advance for your input.

 

Be well and good luck,

 

Ramcon1

 

 

*I did not want to interrupt the flow of the post, but this works as a foot note.  I remember about 4 years ago I read an article in which a woman found a doctor who had discovered a treatment for multiple myeloma.  His “cure” involved taking a person’s own “killer” T cells and “programming” them by a process called CAR T-cell therapy to attack multiple myeloma cells.  Her mom was in the final stages of the disease.  She approached him and begged him to treat her mom who was going to die soon anyway. Unbelievably, he did and she made a full recovery.  I remember thinking at the time, “Well I guess that is that.  Cancer, or at the very least blood cancer is cured.”  It was not yet perfected and they are still tweaking it, and medicine has as usual been slow, but they are getting there:

https://www.cancer.gov/publications/dictionaries/cancer-terms/def/car-t-cell-therapy

 

My point is it had never been done before, and it all started with one guy looking to treat one disease.  Somebody had to be first.

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Well ramcon, I think you hit the nail right on the head. It's not just the downregulation of the GABA receptors. The upregulation of the glutamate system is probably responsible for half our problems. So I'm interested in what you mean by "the cure". I suppose everyone is different in some ways, but the differences are nothing compared to the similarities - or what would be the point of even having this forum? We all have GABA, we all have glutamates, we all have receptors for both and systems that are activated by them, we all have brains - or at least most of us. We're not so different after all. So go for it.

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Ramcon,

 

Good thoughts & research !

 

A cursory search reveals a LOT of research has been done regarding the "GABAA System Hypotheses"

and very little regarding the Glutamate System Hypotheses with regard to withdrawal symptoms after benzodiazepine discontinuation.  No doubt Glutamate is equally as important as Gabaa in the other half of the equation.  Could it be our preoccupation with GABAA is a case of "can't see the forest for the trees"?

 

 

Mechanisms Underlying Tolerance after Long-Term Benzodiazepine Use: A Future for Subtype-Selective GABAA Receptor Modulators?

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321276/#B107

 

 

4.3. Glutamate System Hypotheses

 

4.3.1. General

 

".....From the previous sections, we conclude that compensatory changes solely arising from the GABA system may at most partially explain the tolerance arising following chronic treatment with benzodiazepines. Glutamate is an excitatory neurotransmitter acting on glutamate receptors. Together with the GABA system, they constitute the two fast-acting and opposing neurotransmitter systems that can modulate synaptic plasticity. In support, close neuroanatomical connections exist between GABAergic and glutamatergic neurons [108, 109]. With a presence in at least 30–50% of all synapses in the CNS, inhibitory GABA and excitatory glutamate together coordinate the balance in the brain's excitability. Therefore, it is not surprising that as these two opposing and fast-acting neurotransmitter systems form a delicate balance,

chronic (increased) activation of the GABAergic system during benzodiazepine treatment may pertubate glutamatergic transmission. The basis of benzodiazepine tolerance could then lie in sensitization of the glutamatergic system—a putative process that could account for the withdrawal symptoms after chronic benzodiazepine discontinuation
[5, 110]. Such sensitization is reminiscent to adaptive glutamatergic processes as seen in kindling experiments, although it should be noted that kindling only occurs with intermittent and not after continuous treatment [111]. Glutamatergic sensitization could thus play a role in the development of tolerance as well as withdrawal symptoms upon cessation of treatment. Glutamatergic changes after benzodiazepine withdrawal will not be discussed here, but there are indications that the glutamatergic system plays a role in withdrawal states with accompanying increases in anxiety and seizure activity (for review see [5]). However, glutamate receptor mRNA and protein changes may be dynamic during withdrawal, with unchanged levels during the early phase of withdrawal but changes occurring several days later [112]. This consequently complicates the interpretation of withdrawal studies and their significance for our understanding of benzodiazepine tolerance.

 

 

 

 

 

A glutamatergic hypothesis of drug dependence: extrapolations from benzodiazepine receptor ligands.

https://www.ncbi.nlm.nih.gov/pubmed/11224351

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Buddies,

 

For better or worse, I have studied what you brought up so long and hard it is in my bones, and I can "discuss" it without thought.  I prefer "opinions are like elbows," because everyone has a couple, they do not all stink, but "they can accidentally poke someone leaving them bruised and annoyed." ;-)  I was preoccupied with GAD for a while and the GABA-Glutamine-Glutamate cycle.  But upon further study, while GAD makes sure there is enough GABA to be used as needed, and if we the sensitive eat too much free glutamine, that cycle turns it into glutamate via GAD's opposite glutaminase.  But the presence of glutamate in the synapse is not controlled by GAD or glutaminase, but buy the Excitory Amino Acid Transporters (EAAT).

 

EAAT suck glutamate out of the synapse where it is causing a flow of cations from the postsynaptic neuron, and transport the glutamate into adjacent glial cells where it is inactive.  This is actually how one can be kindled on a long course of antibiotics, specifically beta lactam antibiotics.  They boost the heck out of EAAT.  I did that by accident.  Twice. And boy did I feel the rebound!  So we must be careful with glutamate modulators, like alcohol, tobacco, (and firearms ;-) ) and antibiotics. It is the presence of glutamate in the synapse controlled by EAAT, and for our specific case, the lack of cations caused by the excess anions from benzos that have resulted in the upregulation of our ionotropic glutamate receptors.

 

LTP is the result of upregulation.  The mechanism is complicated and it involves first the creation of more AMPA receptors which fire at a lower potential and then more NMDA receptors which let more cations thru.  How this happens is well studied.  It is related to kindling because the more AMPA receptors you have the more primed your nerves are to give you more powerful NMDA receptors on a dime.

 

And "the cure" is not designed to scare or provide false hope.  I am not telling anyone that I have a method to cure anyone.  This is a discussion only that it is possible.  I know in my mind and in my bones there are ways to permanently remove ionotropic glutamate receptors.  Stop LTP and kindling and reverse our damage in months rather than years, or more importantly, at all in the case of the veterans still suffering after such a long time.  But I have also stated that everything I have tried has revved the B'Jesus out of me.  So I put this here looking for holes and ideas as to why it should succeed or fail.

 

PS.  The non linear recovery of waves and windows is our body's ability to deal with glutamate and cations.  Eat some (free glutamate or calcium), or have some triggered in you by circumstances and you get a wave.  As your body downregulates on its own, as most do, you deal with the glutamate and cations better.  Have a period where you have low glutamate, for whatever reason, and you have a window.

 

I am very cloudy headed today, so that is all I have for now.

 

Thanks again for your replies.

 

Ramcon1

 

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Buddies,

 

If you are on this thread, you have at least a passing interest in glutamate reception.  I have asked this twice before, but so far no one has volunteered.

 

This is an experiment that will provide definitive proof that you personally have too many NMDA receptors that are letting too much current through.

 

Take a period when you have nothing to do for 4 days.  Go out and get yourself a box of your favorite flavor of sugar free jello sweetened with nutrasweet/aspartame.  Follow the directions with the slow prep (no ice cubes) method and make yourself a really big bowl of two large packets.  As your last meal of the day eat the whole bowl, or as much as you can.

 

The boiling water will liberate the aspartic acid from the aspartame.  The only receptor in your body that can receive aspartic acid is NMDA, and if you are NMDA upregulated it will hit you . . .

 

LIKE A MACK TRUCK.

 

You will have pain, stiffness, and anxiety like you have never felt in your life.  It does no permanent damage and wears off completely in 3-4 days.

 

I have done that experiment on myself, twice just to be sure, and I am sure.  I have posted twice for guinea pigs, and so far no one has volunteered.

 

Do I have any takers here?  Anyone?

 

Be well and good luck,

 

ramcon1

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Ramcon1, Have you ever tried Lithium Orotate to down regulate NMDA receptors? I take lithium orotate 5 times a week and it does wipe out my anxiety. So maybe the NMDA receptors are the problem.

 

Also. I just ordered some Sesamin. There's a study that says sesamin down regulates the NMDA receptors in the amygdala. We shall see.

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All,

 

I am definitely going to dig deeper into lithium, but here is just something I have picked up along the way.  Lithium orotate is a supplement, and lithium carbonate is the psyche med "mood stabilizer" often used for bipolar disorder.  There is no "real" difference between the two.  They are both salts of lithium.  The difference is mostly in the dose.

 

Here is the best chart I have been able to find showing the equivalent doses of elemental lithium ion in orotate, carbonate, and naturally occurring in diet and water:

 

https://psycheducation.org/treatment/mood-stabilizers/the-big-three-for-bipolar-depression/lithium/lithium-orotate/#Microdosing_how_much_actual_lithium_in_each_form

 

The study you posted only discusses the lithium ion, not the dose or the source.  It maybe be that we need the lowest psyche med dose of 150 mg (28 mg lithium ion from the chart) or that a few 120 mg orotate tablets (5 mg each from the chart) are sufficient or even better.  It is hypothesized that orotate is more bioavaliable because it occurs in nature.  This author showed no difference at all, but the study is old:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1666891/pdf/brjpharm00512-0006.pdf

 

I think when I try it (6 mos?) I will try orotate, if for no other reason than I can start slower.  If it ends up that I need 5 pills, then the drug will probably be a lot cheaper.

 

I hope that was useful.

 

ramcon1

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Well, before everyone goes running out to dose themselves with lithium, take a look at this Wikipedia article:

 

Lithium toxicity

 

It's one thing to discuss all the theories and possibilities. That's interesting and useful.

It's quite a different thing to encourage people to experiment on themselves with these untested "cures".

I think we should knock it off.

 

A REALLY good point from redevan.  We are talking about LOW DOSE lithium ions, topping out at 28 mg.  People who take the doses of lithium required to treat bipolar disorder are always in danger of toxicity.  We do not want to get any where near those doses to effect glutamate receptor change.

 

Ramcon1

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Ok,

 

The "Illustrated guide," simply states that lithium will down regulate NMDA (N-methyl-D-Aspartate, a specific, powerful type of glutamate receptor)  One of the references in that guide, "Potential Mechanisms of Action" states:

 

https://sci-hub.tw/https://www.ncbi.nlm.nih.gov/pubmed/23371914

(If you want to read the paper, but get Russian letters, thE letters are saying "solve the captcha" so just type in what you see in the window, click on the "button," and you will get the whole paper.)

 

THIS IS THE REASON I PERSONALLY THINK THIS COULD BE HELPFUL:

 

"Lithium competes with magnesium at this binding site, and acutely stimulates the NMDA receptor, which in turn increases the availability of glutamate in the post-synaptic neuron [107]. However, with chronic lithium administration, glutamate neurotransmission stabilizes as the NMDA receptor is downregulated, and  this increases glutamate re-uptake, which restores glutamate transmission. This is one possible mechanism through which lithium achieves its long-term mood-stabilizing effect as  well as its anti-manic properties [108–110]."

 

Remember, it works on 1/2 dozen other things too, so that is why it might be less painful to some, and more painful to others.  I still have to think about it for a long time, but maybe it can be applied "homeopathically."  You take 1/4 of an orotate pill.  It revvs you, then you downregulate, and take 1/2?  Hmmm.

 

Ramcon1

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Took,

 

I am convinced that after a few months to a year off tops, all of our issues are glutamate.  I would not preoccupy my thought process with antagonizing GABA or what will affect GABA, think instead, what will reduce the number and potential of glutamate receptors?  That is why I like lithium so much.  It SHOULD do what we want it to do, make glutamate hang out in the synapse just a little longer, and have the receptors respond by reducing.  Will it happen for us?:  Who the heck knows, but I think it is worth a shot for that reason alone.

 

I stand behind what I said about 50-50, I think some will be calmed, others revved, but that is just my "gut feeling."

 

Ramcon1

YPNS. RYTHIT, AWYAGTH, KG!

 

Ram,  just for clarification let's lay out your thesis here.  So you believe that the Glutamate receptors are stuck in upregulation due to the initial downregulation of the GABAA receptors.  And you also believe that, regardless of the current state of the GABAA receptors, that finding a way to suppress and even reduce the numbers of Glutamate receptors will bring a reduction in our symptoms.  Have I got that right?

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Took,

 

Almost.  My thesis is that taking benzos floods the synapse with Chloride ions (Cl-) released from the GABA-A ligand gated ion channel.  These Cl- ions halt many cascades, many of which by neutralizing the Ca+2 ions in the synapse.  All of that part is actually not theory.  That is 100% proven fact.

 

Then my thesis is that the body responds by looking to maintain homeostasis.  So in response to, "oh, we have too many Cl- ions," your GABA-A receptors "respond," by downregulating.  This is standard benzo healing thinking.  But also in response to, "where did all of those Ca+2 ions go?" your NMDA (and potential other types of glutamate receptors) upregulate.

 

And my thesis continues that the body is designed to upregulate.  We "learn" anything in our mind and nerves by upregulating NMDA, and in general we are designed to build and rebuild.

 

But why should something we "rebuilt" dissipate? The answer is, I don't think it will, and that is the story of protracted withdrawal.  That is the part of my thesis that is not proven, but I can feel it.  In my mind and in my nerves and in my bones, like 2+2 is 4 I believe that to be true, and my neurologist agrees with me. 

 

And to be clear, I do not think we need to "suppress" glutamate.  We need to give those NMDA receptors a damn good reason to disappear.  I think if we could be put in a medically induced coma given an IV with glutamate to the point just below going into a seizure we would be cured in a month. 

 

In the absence of that, there is a lot of good research that an increase in serotonin at the synapse would do it.  I have been hesitant to discuss that at length because in general most people here would not be open to taking an SSRI after having such a bad experience with at least one psyche med, and I do not blame them.  And you can increase serotonin with supps, but that method is so fraught with peril that until I can get clean and try it on myself, I am not posting that method at all!  I just bought a higher level biochem book to help me work out the bugs.

 

The Lithium idea shows promise because it seems that is will simultaneously reduce Ca+2 gated reactions, AND slow glutamate transport out of the synapse.  By having glutamate in the synapse but reducing the downstream reactions, it could "trick" the body into downregulating NMDA.  It is postulated but not proven, that kidney damage not withstanding, that is the reason biopolar patients who respond well to Lithium often get better the longer they are on Lithium while other meds tend to "peter out."

 

And finally, when we achieve this, we will not have reduced our symptoms, we will be cured, and by cured I mean "restored to neurotypical."  We will be able to eat what we want when we want, and do what we want when we want.

 

At least that is the thesis.

 

Ramcon1

YPNS, RYTHIT, AWYAGTH, KG!

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All,

 

Think about it this way: Benzos do one thing.  They attach onto your GABA receptors causing them release GABA and open a channel and let negatively charged Chloride anions through (Cl-)  That is it.  Everything that happens from there is how our bodies adapt to that unnatural activation and outpouring of Cl-.  GABA receptors are everywhere, most notably near other receptors so the Cl- anions can say "stop."  Stop transmitting other things.  Stop whatever you are doing. 

 

Previous thinking had us believe we are sick because our GABA receptors start to disappear as we trigger those Cl- anions with benzos, and that may be a part of it, especially in the "tolerance" phase.  But I am not in tolerance, the same little dose of Valium calms me, and a little bit more makes me sleepy.  Certainly anyone here in the protracted section is no longer dealing with "tolerance," so what is going on?

 

Because of the excessive GABA and Cl- anions, our glutamate receptors respond by increasing in number, and by a long elaborate mechanism, those that open ion channels open easier, and as FnF mentioned LTP, or Long Term Potentiation, means they let more Calcium cations (Ca2+) thru.  The glutamate receptors are also everywhere, and glutamate and its Ca2+ cations tell everything to "go go go," and are the source of ALL of our protracted pain.

 

So to get well, to find an active cure, we need to find something that will reduce the number of glutamate receptors and the Ca+2 cations they let thru.  Of the glutamate receptors, those called NMDA are the most powerful.  Some of the studies I have read talk about methods that reduce NMDA "receptor count" and "EPSC" and "EPSV," Excitory Post Synaptic Current / Voltage.  That is the Ca+2 cations.  Reducing those things is "scrubbing away the receptors."

 

Then the papers talk about RNA activity.  RNA is how our DNA tells our nerves what to do.  When you reduce RNA activity for the transcription (signaling) to nerves to make NMDA proteins, you have "scrubbed away the memory" of those NMDA receptors at the genetic level. Then we are truly cured.

 

Upregulating GABA receptors is relatively easy.  The body is designed to grow.  Downregulating glutamate receptors is much harder, and that is why some people are sick for a long time. Slowing RNA activity is harder still, and that is why NMDA are "kindled," as in some one who is "well" does something that pokes his NMDA receptors like alcohol, an antibiotic, a flu shot, whatever, and his NMDA receptors go back to the sick state.  They do not grow back "wrong," they just "remember" the state of having too many, and letting too much current thru, and we kindle.

 

That is the entire depth of my knowledge at this point, except for the methods we are discussing like serotonin, glutamate itself, and lithium.  Those are discussed in this thread.  Right now those SEEM to be the best shots for the protracted.  Will they work?  I have no idea.  Exactly how does all of this happen?  I had to take a break from studying neuroscience to refocus on biochem because I do not know enough biochem to take my understanding deeper.  But that is my job right now, and I am on it. 

 

I hope that explanation was helpful to anyone trying to understand our goals.

 

Ramcon1

(YPN, RYTHIT, AIYGTH, KG!)

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Colley and All,

 

I have tried a few NMDA antagonists and inverse agonists, and so have other buddies.  For reasons I cannot explain, in me they revved me up, and others had no benefit.

 

Inhibitors are a different story.  If you have ever been in a wave and taken a drink of alcohol and had the wave "magically vanish," that is the alcohol inhibiting the current flow through your NMDA.  The problem with that of course is the rebound, which happens in neurotypical people too, but can be quite severe in the sensitive among us.  Plus, alcohol abuse isn't going to help us heal. But the fact that it DOES make us feel better in that instant just proves that lowering the current long term is a big part of the key to the cure.

 

Ramcon1

(YPN, RYTHIT, AIYGTH, KG!)

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Dear Buddies,

 

This is my "guide to trying lithium." I wrote up this protocol for a buddy struggling at 18 months who wants to see if lithium will help.  Maybe some of you will find this useful.  Note to moderators, This is VERY prescriptive because this is what a specific buddy asked me to do.  For the record, I state below that this is what I intend to do once I have logged a few months off valium:

 

I found a good clean source of lithium orotate with as little else in it as possible.  This brand is pure.  It goes out of its way to say that it does not contain any of the “other things” that normal people would not feel, but we might find a trigger, like ascorbyl palmitate (Vitamin C) or calcium or magnesium in any form, etc.  When I do this, this is what I will get.  It is also a capsule which means it is powder so you can empty the capsules and weigh the powder:

https://www.amazon.com/Relentless-Improvement-High-Purity-Excipient-Formulation/dp/B07BSMQPDW/ref=sr_1_2_sspa?crid=3UV8G7W5IXAZI&keywords=lithium+orotate&qid=1571852532&sprefix=lithium%2Caps%2C139&sr=8-2-spons&psc=1&spLa=ZW5jcnlwdGVkUXVhbGlmaWVyPUEzS01VM1FUVEQwR05RJmVuY3J5cHRlZElkPUEwMTM1NjU5MzZNS0VNTEowNVdGSCZlbmNyeXB0ZWRBZElkPUEwNjQyNDc5Mk9VSjBCNTZWSTMzJndpZGdldE5hbWU9c3BfYXRmJmFjdGlvbj1jbGlja1JlZGlyZWN0JmRvTm90TG9nQ2xpY2s9dHJ1ZQ==

 

You will need large, empty capsules to fill:

https://www.amazon.com/PurecapsUSA-Clear-Vegetarian-Capsules-Joined/dp/B00I7DVEJS/ref=sr_1_2_sspa?keywords=empty+vegetarian+capsules&qid=1571850888&sr=8-2-spons&psc=1&spLa=ZW5jcnlwdGVkUXVhbGlmaWVyPUFDUEpGUFRJTVlINzYmZW5jcnlwdGVkSWQ9QTA2NDcxMjYzOE5CQkNIOVc2MTQ4JmVuY3J5cHRlZEFkSWQ9QTAwMDAwNDAyOFpDS1JVMzFSTFRUJndpZGdldE5hbWU9c3BfYXRmJmFjdGlvbj1jbGlja1JlZGlyZWN0JmRvTm90TG9nQ2xpY2s9dHJ1ZQ==

 

Tiny spoons for measuring and filling:

https://www.amazon.com/Norpro-Stainless-Measuring-Spoons-smidgen/dp/B0009X1P9S/ref=sr_1_4?crid=27YSLSSIXL2UO&keywords=measuring+spoons+smidgen+pinch+dash&qid=1571850673&sprefix=measuring+spoons+smid%2Caps%2C134&sr=8-4

 

And a REASONABLY accurate milligram scale

https://www.amazon.com/Smart-Weigh-GEM20-Precision-Milligram/dp/B00ESHDGOI/ref=sr_1_1_sspa?crid=1BW30LCGBPR31&keywords=gemini+milligram+scale&qid=1571851012&sprefix=gemini+mill%2Caps%2C131&sr=8-1-spons&psc=1&spLa=ZW5jcnlwdGVkUXVhbGlmaWVyPUEzRFRYSVVLSVMyNlo0JmVuY3J5cHRlZElkPUEwNjU1NzUyMVhZSk4zQVdEWERBRCZlbmNyeXB0ZWRBZElkPUEwNzMxNDUxTTNGSTYzNk1TVjNBJndpZGdldE5hbWU9c3BfYXRmJmFjdGlvbj1jbGlja1JlZGlyZWN0JmRvTm90TG9nQ2xpY2s9dHJ1ZQ==

 

Not sure about shipping, but all of that will cost about $60 without shipping.

 

Each capsule contains a certain amount of powder, but the important thing is that the powder contains 5 mg lithium.  If you get a different brand that is a tablet instead of a capsule, that is ok, but it could contain stuff we do not want, and you will need to cut the tablet into quarters.  I like capsules, so I can weigh powders, but if all you can get is tablets, then buy the scale, but do not buy the empty capsules.

 

If you get the lithium orotate capsules, empty 1 capsule onto the scale and see what it weighs.  If you get tabs, weigh the tabs. Do a few to get an average weight.  Then either weigh out a bunch of powder until you are get 1/4 of a capsule, and fill the empties, or cut tablets until you get a bunch of good quarter tabs.

 

The scale is accurate to about +/- 0.003g (+/- 3 mg), so do not worry about its being exact.  For example if the capsule content weighs about 0.200 g (200 mg) you will find it will vary from 0.180 g to 0.220 g.  That is accounting for manufacturing variation and scale accuracy. So in this example, you weigh out about 0.050 g (50 mg).  So anywhere from 0.045 to 0.055 g is acceptable.  If you have powder from capsules, you can use the tiny spoons to put that amount in the capsule.  Remember that 0.050 g or whatever a quarter capsule of POWDER (or tablet) weighs = 1.25 mg lithium.

 

Once you have prepared a few days wait for a day when you have nothing to do, and take one in the morning.  It might make you calm.  It might rev you up.  It might do nothing.  I want you to take it in the morning so you are awake and can feel what it does.

 

If it makes you calm, move the dose to night. 

If it revs you up, keep it in the morning. 

If it revs you up A LOT, halve the dose. 

If it does nothing, double the dose.

 

Once you feel it do SOMETHING, hold there.  Take that dose until you no longer feel it do anything.  That might be a week. That might be a month.  If it still makes you calm after a month, increase the dose until you feel just a little drowsy during the day.  Just barely.  Hold there until you no longer feel drowsy during the day.

 

Ideally, you don’t feel it until you get to a few milligrams of LITHIUM.  Then you keep building lithium orotate until you can take about 25 mg lithium or 5 pills.  At that point you see a psychiatrist, and get a scrip for 150 mg lithium carbonate, the lowest available dose, which equals 28 mg lithium. You never take more than that.  When you can stay on that dose for several months, you might notice significant improvement.

 

That is the theory.    Now here is the catch.  It looks very good, and I mean VERY good on paper.  That DOES NOT MEAN IT WILL ACTUALLY WORK AT ALL.  If I had a dollar for everything that I thought would work on paper, I would have a lot of dollars.

 

If anyone actually does this, please let the rest of us know.

 

Good luck,

 

Ramcon1

(YPNRYTHIT, AIYAGTH, KG!)

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Hey, ramcon.

Just wanted to throw my experience into this thread in case it could help.

 

Last year, I took a stack of supplements for about 6 months or so with the goal of boosting BDNF.

Lithium was one of said supplements. I took it in the orotate form daily for those 6 months.

I felt pretty decent while on the stack, seemed to be more alert with more energy, etc. Basic nootropic type of effects.

 

But it didn't cure me by any means. I had a 'setback' a few months after I stopped taking the stack and am worse than I ever have been. So... it may have helped a little while on it, but 6 months taking it was definitely not enough to repair whatever neurological damage or issue I have.

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Maybe it’s not necessarily about time but about finding the right “medicine “. My background is in Osteopathic manual therapy. We were taught the general principle that the body has self regulating and self healing mechanisms. In cases where illness presented itself, as Osteopaths we would work through structure trying to find tissues or bones that were lacking physiological range of motion and bring motion to that structure. This would then effectively take the barrier away from healing and the body would then resume its self regulating/healing mechanism. It’s not effective and even detrimental to just throw everything at the body hoping that something sticks. The key lesion would have to be found and corrected and then miracles could occur. I understand that the brain is much more complicated than physical structure but in principle the approach and outcome should be the same.
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Nov,

 

Thank you for sharing.  I do think one would have to get beyond a few milligrams found in orotate to have permanent change.  I do hope it did not contribute to your setback.  Do you have any thoughts on that?

 

Greek,

 

I could not agree more.  I think we need time to heal, but also that first identifying the question, "what is wrong?" and then identifying the "right medicine" to coax what is wrong back to healthy neurotypical functioning.  This thread is exploring the possibility that the main thing wrong in benzo wd damage is glutamate receptor count and function, and if lithium can lower the count and reduce the synaptic current.  Is that "the" answer?  I don't know, but it is a good place to start. and I am investigating further.

 

Ramcon1

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Another question I have is since benzo withdrawal Mimicks symptoms of depression and anxiety. Why would the body increase glutamate receptors as a result of emotional trauma to somebody not withdrawing from anything? For example, you have an injury and the body responds with an inflammatory response to precipitate healing. This response is not pleasant but needed for the body to do its work. Does glutamate act in a similar way as a necessary evil to healing? I don’t really know where I’m going with this. I guess I’m just trying to think on the basis that the body is wise and it’s responses are calculated.
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Why go as far as Lithium?

 

Lithium should be taken under the advice of a psychiatrist specifically because of kidney problems.

 

Lithium is interesting in the bipolar group because it DOES work. Funny enough, it will also EVENTUALLY

do kidney damage.

 

 

The whole reason I floated the idea of using Theanine in this thread - http://www.benzobuddies.org/forum/index.php?topic=232260.0

 

Is because I was looking at Glutamate receptor antagonists that showed strong anxiolytic potential. I ran across the pharmacodynamics of

Theanine and thought "I don't remember it having all these effects. This might be interesting to try in a larger dose."

 

https://en.wikipedia.org/wiki/Theanine#Pharmacodynamics

 

It has a bunch of interesting effects but unfortunately it's not highly selective. It's a grab bag of stuff you want. Not having something

hyper selective makes it hard to say "This specific receptor antagonist is definitely one solution." Which leads you on a path of finding

similar compounds.

 

The plus side is theanine is easy to acquire, has no terrible side effects, and has very limited evidence of withdrawal. It also tastes like not

much and readily dissolves in water.

 

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Why go as far as Lithium?

 

Lithium should be taken under the advice of a psychiatrist specifically because of kidney problems.

 

Lithium is interesting in the bipolar group because it DOES work. Funny enough, it will also EVENTUALLY

do kidney damage.

 

 

The whole reason I floated the idea of using Theanine in this thread - http://www.benzobuddies.org/forum/index.php?topic=232260.0

 

Is because I was looking at Glutamate receptor antagonists that showed strong anxiolytic potential. I ran across the pharmacodynamics of

Theanine and thought "I don't remember it having all these effects. This might be interesting to try in a larger dose."

 

https://en.wikipedia.org/wiki/Theanine#Pharmacodynamics

 

It has a bunch of interesting effects but unfortunately it's not highly selective. It's a grab bag of stuff you want. Not having something

hyper selective makes it hard to say "This specific receptor antagonist is definitely one solution." Which leads you on a path of finding

similar compounds.

 

The plus side is theanine is easy to acquire, has no terrible side effects, and has very limited evidence of withdrawal. It also tastes like not

much and readily dissolves in water.

 

I believe we're talking about Lithium Orotate in much smaller dosages than Lithium Carbonate which is prescribed in very high doses for Bipolar disorder. I'm not sure if the potential of Kidney damage would be as profound by taking the Orotate supplement that's available OTC. Lot's of information on both available from a variety of reputable sites.

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Well put Colley.  We are talking about working up to a dose a bipolar person would not even feel.

 

And Why Lithium?  Because lithium has one very specific trait that makes it unique, it slows cations (positive ions) thru ion gated channels, which makes us calm, while simultaneously holding glutamate in the synapse longer.  If we can hold glutamate in the synapse longer, increasing slowly and repeatedly for 6 months to a year, we juuuuuuuuuuuust might coax some of those receptors away, and reduce current flow on a more permanent basis.  If we coax some glutamate receptors away and reduce their current, we might reverse some benzo damage.

 

Maybe.  That is the question.

 

Ramcon1

YPN,RYTHIT, AIYAGTH, KG!

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