HOW GABAA RECEPTORS ARE CREATED AND BENZO INDUCED CHANGES

[[Na...]]

Perseverance,

 

Thank you for your kind response.

 

Yes indeed the human brain seems infinitely complex, and that is why taking supplements can be a big risk in delaying one's progression back to normal.

 

In previous posts of yours you have mentioned that steroids are cross reactive or cross suppressive of the HPA axis, with benzos. I am currently on a low dose adrenal cortex supplement once a day. I ve been debating whether I should taper it or not.

 

What are your thoughts? Does low dose in this case bioidentical hydrocortisone ( we are talking maybe 2 mg / day here) be a concern to stop asap if one is making progress?

 

Much thanks.

 

PS Have you considered doing any research on the brain effects of cell phones, wi-fi, smart meters and electromagnetic radiation? I believe this may very well be a very significant "brain health" issue in our ever proliferating wireless world.

 

 

 

[[Kr...]]

I was really interested in this study by John Hopkins University that found that sufferers of restless legs syndrome have high glutamate levels in their brains:  http://www.hopkinsmedicine.org/news/media/releases/restless_legs_syndrome_insomnia_and_brain_chemistry_a_tangled_mystery_solved  The study was small, but it suggests a good reason for the fact that many people experience RLS as a withdrawal symptom from benzos.  I suffer from RLS a great deal and my doctor just prescribed gabapentin enacarbil, which is supposed to reduce glutamate levels in the brain.  While I would rather not start taking another prescription medication, my RLS is so bad, I'm getting very little sleep.  I also wake up frequently feeling very agitated - so, I worry the effects of little sleep and increased stress because of this will prolong my recovery.  I plan to take it only short term in hopes of reining in my glutamate levels.  I hope doing this won't set me back.  Hard to know.

[[ih...]]

Interesting study. I suspect that many of us in bz wdwls have unduly high glutamate levels in the thalamus & perhaps those with RLS also have a dopamine issue.

[[Ca...]]

Is it possible or probable that gluten can cause a glutamate imbalance, and therefore cause the burning skin sensations in the hands and feet, which is now my predominant symptom?  Also difficulty breathing and a burning sensation in the chest.

 

Thank you for your posts!

 

CB

[[Mo...]]

 

hi perse,

i won't be able to join the conversation just now, even though i'd love to.

my benzo-brain wont let me yet.

but i shallk keep on reading it with great interest. thank you

Ig

[[ih...]]

A simple study on the GABA/GLU imbalance:

 

 

"Alteration of glutamate/GABA balance during acute alcohol withdrawal in emergency department: a prospective analysis."

 

 

http://www.ncbi.nlm.nih.gov/pubmed/22791370

[[Pe...]]

ihope- I liked how they called abrupt cessation 'brutal'- IMO that couldn't be more descriptive after my own 'abrupt' experience with BZs.    That was interesting about the neurotransmitter levels.  The part I am zeroing in on happens at the post synaptic area of the dendrites- not the synthesis of the neurotransmitters in the Axon terminal- just goes to show how complex the cascade of events can be, right?

 

From what I have read so far- the LTP that can happen from abrupt benzodiazepine discontinuation (and who knows- may even happen to varying degrees after different types of tapering methods), which consists of an increase in AMPA receptor number and enhanced AMPA conductance, causes increased amplitude of mEPSCs even with normal amount of Glutamate at the synapses.  So I would think that an increase in the neurotransmitter levels would add to this effect.

 

The GABARs that alcohol binds to are extra-synaptic and contain a different subunit configuration that the ones that BZs bind to.  The ones alcohol binds to increase tonic currents of Chloride, while the ones at the synapse that BZs bind to affect phasic currents (cause the ion channel to open more frequently).  So there is a difference there between the two- however both ways will adversely affect the chloride gradient so in this way they are similar.

 

In any case, I do the same thing from time to time- I will pull up studies on alcohol to look at various aspects since both are GABAA allosteric modulators and therefore increase Chloride influx. Alcohol has been studied a lot so sometimes you can find out more information going down that route.  I always enjoy reading the articles you find- really add to our accumulating knowledge- great work! 

 

Carebear16- Being that I do not know the exactly the precise causal factors behind the burning skin sensations it would be difficult to address it.  However, these types of sxs can be neurological in origin and are typical of BW.  I personally am not a fan of eliminating foods during recovery that might decrease nutrition.  I would venture to say that a well balanced diet that included whole grains, as long as you do not have a condition that would prohibit this such as celiac disease or certain types of epilepsy for example, would probably be ok based on the fact that Ashton did not prohibit grains when she discussed diet in her manual.

 

I too had burning skin for periods of time that eventually went away.  I would start a thread on it and ask others here about their experiences.  Sometimes groups of people experiencing the same sxs will notice an aggravating factor that they all seem to have in common.

 

Morreweg- No problem, I have been where you are myself.  Just keep reading and do your best to understand what you are reading.  As you recover you will able to understand more and more.

[[Br...]]

In any case, I do the same thing from time to time- I will pull up studies on alcohol to look at various aspects since both are GABAA allosteric modulators and therefore increase Chloride influx. Alcohol has been studied a lot so sometimes you can find out more information going down that route.

 

Hiya Perseverance.  I do the same and occasionally look at papers to do with alcohol.  The research into alcohol tolerance and dependency sometimes contains remarkable similarities with what we know about benzos.

 

I can't believe that researchers haven't already studied the similarities.  I suspect there are some interesting research papers to be found.

[[Br...]]

Hi again Pers.  Here are a couple of papers which touch upon the role of glutamate (and more) in benzo dependency.  I'm still getting brain fogged and do not get enough clarity to read through this material at the moment.  However you may find it useful.

 

"Glutamic Acid Decarboxylase and Glutamate Receptor Changes During Tolerance and Dependence to Benzodiazepines"  http://www.pnas.org/content/98/6/3483.full

 

"Abuse and Dependence Liability of Benzodiazepine-Type Drugs: GABAA Receptor Modulation and Beyond" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453238/

[[Be...]]

If I'm understanding this GAD and Glutamate Receptor Changes research correctly, it's saying that GABAA downregulation is not responsible for w/d s/x's, but that glutamate receptor changes and increase in density cause excess glutamate and the w/d s/x's?  So, is this why my anxiety is getting worse the longer I've been off these pills?  This is a very interesting research paper about what is going on the mice brains from benzo use.  I guess I need to be looking for a glutamate antagonist to prune off all these glutamate receptors that are spitting out too much glutamate.  It said they looked at slices of these mice brains and found increased density of Glu receptors in the the frontal cortex, responsible for reasoning, problem solving, behavior (i.e. cog fog), occipital cortex, responsible for visual stuff (hallucinations), my depth perception is off and DP/DR.  The article said that the glutamate receptor density increases comes on the heals of, or coincides with the GABAA receptor upregulation.  It seems that might explain why my anxiety is worse now than it was in the beginning of w/d.  I need a glutamate antagonist.  Which drugs are out there or natural supplement to stop the glutamate surge?       

[[Pe...]]

Hey guys-

 

I ended up calling the PhD I had sent an email to who had done a ton of research into the Glutamate Hypothesis.  Her name was Dr. Tietz and she worked at the University of Toledo.  The secretary who answered the phone informed me that she is retired.  She asked me why I was calling and after I explained the reason she put me on hold and called some of the other researchers who knew her.  when she came back she informed me that they told her that no one was carrying on her work--which was a real blow as I think she could have answered so many questions for us.  Here is a link to her old University of Toledo web page that discusses the type of research she was doing:

 

http://www.utoledo.edu/med/depts/physpharm/faculty/tietz.html

 

 

Here are links to some of the research she was involved with which are also the papers I am currently mulling over:

 

http://www.nature.com/npp/journal/v29/n11/full/1300531a.html#fig5

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904841/

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014299/#!po=2.00000

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399473/

 

 

I think there is another group in the Netherlands looking into this.  I will try to see if I can contact them through Skype.  Let's hope that another group will carry on the work she started.

 

 

 

 

[[Pe...]]

Hi again Pers.  Here are a couple of papers which touch upon the role of glutamate (and more) in benzo dependency.  I'm still getting brain fogged and do not get enough clarity to read through this material at the moment.  However you may find it useful.

 

"Glutamic Acid Decarboxylase and Glutamate Receptor Changes During Tolerance and Dependence to Benzodiazepines"  http://www.pnas.org/content/98/6/3483.full

 

"Abuse and Dependence Liability of Benzodiazepine-Type Drugs: GABAA Receptor Modulation and Beyond" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453238/

 

Thanks for the links Braben.

[[Pe...]]

If I'm understanding this GAD and Glutamate Receptor Changes research correctly, it's saying that GABAA downregulation is not responsible for w/d s/x's, but that glutamate receptor changes and increase in density cause excess glutamate and the w/d s/x's?  So, is this why my anxiety is getting worse the longer I've been off these pills?

 

A depolarization of the neuron happens which in turn causes the NMDA receptors to release their extra-cellular Mg2+.  The Mg2+ normally prevents Ca2+ from entering the neuron.  Ca2+ activates a lot of processes when it enters the neuron such as kinases and transcription pathways.

 

As a result the AMPARs are phosphorylated and go into autophosphorylation mode- plus they are upregulated.  The studies I have read observed this in pyramidal neurons in the CA1 region of the hippocampus.  This then causes hyperexcitability in these neurons which are involved in brain anxiety circuits- and the result in WD anxiety.

 

Administration of AMPA or NMDA antagonists at different stages of WD have been able to prevent or reduce WD sxs in several studies.  That is as far as I have gotten---still have a lot more to learn about it all before I can put together information about it for the forum.

 

  This is a very interesting research paper about what is going on the mice brains from benzo use.  I guess I need to be looking for a glutamate antagonist to prune off all these glutamate receptors that are spitting out too much glutamate.

 

Well...sort of---Glutamate is a neurotransmitter released from the pre-synaptic terminal (on the Axon) through exocytosis.  It then travels across the synapse to the Glutamate receptors located on the post-synaptic terminal (on the dendrite of the next neuron).  Researchers showed that Glutamate receptor antagonists stopped the casacade of events leading to the commencement of the Wd syndrome.  Here is the first studie that showed this- the first article Braben gave links to also referenced it- and the articles by Dr. Tietz built upon this research:

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC47038/pdf/pnas01471-0520.pdf

 

 

 

  It said they looked at slices of these mice brains and found increased density of Glu receptors in the the frontal cortex, responsible for reasoning, problem solving, behavior (i.e. cog fog), occipital cortex, responsible for visual stuff (hallucinations), my depth perception is off and DP/DR.  The article said that the glutamate receptor density increases comes on the heals of, or coincides with the GABAA receptor upregulation.  It seems that might explain why my anxiety is worse now than it was in the beginning of w/d.

 

I assume you were referring to the articles Braban gave links to?  I glanced throught them- I plan to read them thoroughly---However the articles I have read thus far did mention other areas of the brain as well--not surprising really as the GABAARs that benzos bind to are all over the place in the brain.  In the first article Braban posted it said something to the effect that the GABAARs upregulate rather quickly and therefore the problem lies in Glutamate receptor changes- which would coincide with what I have read on Long-Term Potentials (LTPs) being set up from the phosphorylation and upregulation of the AMPA receptors- which essentially creates an LTP situation.

 

  I need a glutamate antagonist.  Which drugs are out there or natural supplement to stop the glutamate surge?     

 

Researchers did not reach that point yet.  They made these observations in mice and rats--not even close to human trials.  Plus it is more complicated than that-- e.g. AMPA antagonists did nothing once the active phase began.  NMDA antagonists did not work during the silent period-- so you have to know when and which kind--  Also there were no long term studies to see what happened later on down the road after these drugs were administered so that leaves a big question mark.

 

Glutamate is used by areas of your brain that are not affected too---so you could inadvertently cause something else to go awry by trying to cut back your Glutamate production by taking a supplement.  This is why researchers study on animals first.  At this point the research is no where near that yet, unfortunately.  This is why I was not happy to learn that Dr. Tietz retired---she was working toward a remedy and was getting there- but still had a ways to go before she retired.

 

 

 

 

Corrected information regarding polarization of the neurons.

[[ih...]]

As Pers says, NMDA antagonists are challenging to chemists as they tend to have unwanted side fx due to the importance & prevalence of NMDA receptors in cognition. A coomon side fx is dissociation which would not be a plus for some in wdwl.

 

The problems with NMDA anatagonists & some alternatives which have been trialled are set out here:

 

http://www.dana.org/news/cerebrum/detail.aspx?id=7376

 

Bird has been on one or more Ca++ channel blockers so you could ask about her experience which I think has been somewhat helpful.

 

 

[[Mo...]]

 

hi pers and all,

sorry , i know i am in a outsider position in this valuable discussion at the moment.

but simply said, did i get it right, that gabaars which benzos bind to are all over the whole body.

so thats the reason for all the physical sxs we get ?

thanks

[[ih...]]

More, the purpose of this thread, (from my perspective anyway), is for us to learn from one another so there are no outsiders.

 

It's correct that there are GABAARs throughout the body & the change in receptor function also has downstream effects on the HPA which in turn means that our hormones & other neurotransmitters can get also thrown into disarray.

[[Be...]]

I guess that was my big question then..... What happens to these upregulated AMPAR receptors and the other alterations down the road?  It seems  to me that they will downregulate and be destroyed and/or neuroadapt now that we don't need them anymore.  I read these research articles and I wish they would have followed some of these mice down the road in time to see how these new and changed receptors and other alterations adapted.  I guess we keep going back to the anecdotal information for a hint of what happens to our neurochemistry then.  These studies were disturbing for me, because it makes sense now why I'm feeling different, not really relaxed after these months.  I'm feeling better very slowly and the anxiety is not as bad now most days, but can be amped up in short notice by any event.  I want to get to the truth about what these benzo's have done to me, so I don't have to wake up every morning saying, "What's happened to me?"  I pray that my chemistry balances itself out soon.

Pers, I did stumble on that research article from 1993 about the use of CPP to stop w/d s/x's from starting.  Wish I had had some of that before the big AMPA receptors came on the scene.  I'm not a big detail person, but I get the gist of what I've been reading. 

[[Br...]]

Hey guys-

 

I ended up calling the PhD I had sent an email to who had done a ton of research into the Glutamate Hypothesis. Her name was Dr. Tietz and she worked at the University of Toledo. The secretary who answered the phone informed me that she is retired. She asked me why I was calling and after I explained the reason she put me on hold and called some of the other researchers who knew her. when she came back she informed me that they told her that no one was carrying on her work--which was a real blow as I think she could have answered so many questions for us. Here is a link to her old University of Toledo web page that discusses the type of research she was doing:

 

http://www.utoledo.edu/med/depts/physpharm/faculty/tietz.html

 

Hiya Pers.  Elizabeth Tietz is a really outstanding find!! Her research interests look very relevant. What a pity she has retired. I wonder if it's worth contacting her direct? I found it quite easy to locate her in the White Pages. She's also in LinkedIn. She may be pleased to speak to people interested in her research.

 

I think there is another group in the Netherlands looking into this. I will try to see if I can contact them through Skype. Let's hope that another group will carry on the work she started.

 

Are you referring to Christiaan Vinkers at Utrecht University who wrote an interesting paper on benzos with Prof Berend Olivier? http://downloads.hindawi.com/journals/aps/2012/416864.pdf  He's listed at http://www.uu.nl/staff/CHVinkers/0 and is also on LinkedIn.

 

 

 

 

[[Pe...]]

Becksblue- I think many of us have questions and concerns similar to yours.

 

Braban-

 

While reading through the article you linked:

 

"Glutamic Acid Decarboxylase and Glutamate Receptor Changes During Tolerance and Dependence to Benzodiazepines"  http://www.pnas.org/content/98/6/3483.full

 

I thought this was an interesting observation-

 

"...the levels of GluR1 mRNA were significantly increased in frontal cortex (48%), occipital cortex (38%), and hippocampus (56%), but failed to change in the cerebellum of 96-hr diazepam-withdrawn rats when compared with 96-hr vehicle-withdrawn rats. Notably, the increase in GluR1 mRNA expression detected in the frontal cortex and hippocampus of 96-hr diazepam-withdrawn rats was either not detectable or not statistically significant after 12 or 48 h of diazepam withdrawal."

 

I wonder if there was an increase in GluR1 homomeric receptors.  In the hippocampus, most synaptic AMPARs are heteromeric because they are composed of combinations of different subunits, e.g. GluR1/2 or GluR2/3, with the GluR2 subunit preventing Ca2+ influx. However, a small number of Ca2+-permeable GluR1 homomeric receptors (meaning they contain only one type of subunit- GluR1) reside in extrasynaptic locations where they can be rapidly recruited to synapses during synaptic plasticity through lateral diffusion.

 

I also found it interesting that the pattern matched the temporal fashion of the silent and active phases.

 

About Dr. Tietz-- the secretary I spoke with told me that she thought she continued to check her emails but she now travels a lot since retiring so that might be why I haven't heard from her.  I am a little leery about contacting people in retirement as they may or may not want to stay connected to their work.  I will probably just wait to see if she replies to my email- you never know--I received replies sometimes months after I had written emails in the past.

 

I have a lot of Vinkers work in my data base under the GABAR PDFs- he did cite others work on the Glutamate Hypothesis in the article you linked- but I thought his work focused mainly on the GABA side.  I have to look through various PDFs I was reviewing- I may have been thinking of his team- I am having a hard time remembering now.

 

You did a good job tracking down people.  I encourage everyone to contact researchers if you have questions regarding their work.  I have done this numerous times and have always found them to be willing and eager to discuss their work.  I would make sure that you are well versed with the subject matter before speaking with them because they tend to speak in scientific terms and will assume that you understand the basic principles.

 

You can explain to them that you are a layman and the reason you are interested in their work.  They have sent me freebies via email (articles that I normally would have had to purchase copies of).  You also might want to wait for a window or semi-window day to make the call. 

[[Pe...]]

I was surprised to find out that the reason for the GABAAR mediated depolarization may be entirely different than I first thought.  I just read the second reference in the sentence below:

 

"A GABAR-mediated depolarizing potential, which is present in 2-day FZP-withdrawn CA1 neurons (Zeng et al, 1995), has been shown to activate NMDARs (Staley et al, 1995) and may contribute to increased postsynaptic Ca2+-mediated signal transduction."

 

http://www.nature.com/npp/journal/v29/n11/full/1300531a.html

 

Here is what the abstract said:

 

"Gamma-aminobutyric acid A (GABAA) receptors are the principal mediators of synaptic inhibition, and yet when intensely activated, dendritic GABAA receptors excite rather than inhibit neurons. The membrane depolarization mediated by GABAA receptors is a result of the differential, activity-dependent collapse of the opposing concentration gradients of chloride and bicarbonate, the anions that permeate the GABAA ionophore. Because this depolarization diminishes the voltage-dependent block of the N-methyl-D-aspartate (NMDA) receptor by magnesium, the activity-dependent depolarization mediated by GABA is sufficient to account for frequency modulation of synaptic NMDA receptor activation. Anionic gradient shifts may represent a mechanism whereby the rate and coherence of synaptic activity determine whether dendritic GABAA receptor activation is excitatory or inhibitory."

 

http://www.ncbi.nlm.nih.gov/pubmed/7638623?dopt=Abstract&holding=npg

 

This blew me away...I never expected this.  Just goes to show there is so much more to learn about the Glutamate Hypothesis. I would really like to read the full text of this article if anyone can help out like Bak233 did before.

[[Br...]]

I would really like to read the full text of this article if anyone can help out like Bak233 did before.

 

"Ionic Mechanisms of Neuronal Excitation by Inhibitory GABA, Receptors"  http://worldtracker.org/media/library/Science/Science%20Magazine/science%20magazine%201995-1996/root/data/Science%201995-1996/pdf/1995_v269_n5226/p5226_0977.pdf

[[Pe...]]

Wow- that was quick!

 

Thanks Braban!

[[he...]]

This question is for perseverance , please and thank you, Is it possible that chemicals in our body can flow throughout from our Brain so much that we can feel it not by only pain but by sensation, as well as taste it. I had a test down for glutamate , it was off the charts , the test was done through urine, I wonder if that's what's flowing , or is other toxins in my body??? what are  symptoms of neuro toxicity of glutamate? any one know this? I just recently had a test done by my family Dr for Dopamine, Norepinephrine, and epinephrine, my 24 urine creatinine levels showed in Volume was high , but the normal counts were normal . I am dng a hair analysis test for metal and it tests for any lack of minerals , I had a Live blood count test done it was normal , white blood cells and red blood cells were normal . My muscles in my throat feel like they are actually compressing and squeezing the nerves , I am not sure if that's possible ? is it? The nerve pain I endure is actually effecting and cusing nerve damage although I can still use my muscles. My mouth gets a severe pain as if its being compressed of the nerves . My Entire body feels this throughout. I started Glutathione by immunacal , its seems to help some, I had a test done by Genovations , it indicated that I am absent of Gluthione from the Liver/Gut , I will send an article on it.  bUT WHE I HAD A TEST DONE BY 23ANDME DNA it showed I had no issues of Detoxing. IDK so confusing .

 

http://discoverglutathione.blogspot.com/feeds/posts/default

 

http://discoverglutathione.blogspot.ca/

 

 

Discover Glutathione

 

 

 

It's the most important molecule you need to stay healthy and prevent disease -- yet you've probably never heard of it. It's the secret to prevent aging, cancer, heart disease, dementia and more, and necessary to treat everything from autism to Alzheimer's disease. There are more than 89,000 medical articles about it -- but your doctor doesn't know how address the epidemic deficiency of this critical life-giving molecule ...

 

What is it? I'm talking about the mother of all antioxidants, the master detoxifier and maestro of the immune system: GLUTATHIONE (pronounced "gloota-thigh-own").

 

The good news is that your body produces its own glutathione. The bad news is that poor diet, pollution, toxins, medications, stress, trauma, aging, infections and radiation all deplete your glutathione.

 

This leaves you susceptible to unrestrained cell disintegration from oxidative stress, free radicals, infections and cancer. And your liver gets overloaded and damaged, making it unable to do its job of detoxification.

What is Glutathione?

 

Glutathione is a very simple molecule that is produced naturally all the time in your body. It is a combination of three simple building blocks of protein or amino acids -- cysteine, glycine and glutamine.

 

The secret of its power is the sulfur (SH) chemical groups it contains. Sulfur is a sticky, smelly molecule. It acts like fly paper and all the bad things in the body stick onto it, including free radicals and toxins like mercury and other heavy metals.

 

Normally glutathione is recycled in the body -- except when the toxic load becomes too great. And that explains why we are in such trouble.

 

 

Posted by  Randall Payne  at  3:29 PM    No comments:       

 

 

 

 

 

 

 

 

How do Toxins Damage our Cells

 

 

 

We humans were created in a time before the 80,000 toxic industrial chemicals found in our environment today were introduced into our world, before electromagnetic radiation was everywhere and before we polluted our skies, lakes, rivers, oceans and teeth with mercury and lead.

 

That is why most people survived with the basic version of the genetic detoxification software encoded in our DNA, which is mediocre at ridding the body of toxins. At the time of our creation we just didn't need more. Who knew we would be poisoning ourselves and eating a processed, nutrient-depleted diet thousands of years later?

 

Because most of us didn't require additional detoxification software, almost of half of the population now has a limited capacity to get rid of toxins. These people are missing GSTM1 function -- one of the most important genes needed in the process of creating and recycling glutathione in the body.

 

The Importance of Glutathione in Protecting Against Chronic Illness

Glutathione is critical for one simple reason: It recycles antioxidants. You see, dealing with free radicals is like handing off a hot potato. They get passed around from vitamin C to vitamin E to lipoic acid and then finally to glutathione which cools off the free radicals and recycles other antioxidants. After this happens, the body can "reduce" or regenerate another protective glutathione molecule and we are back in business.

 

However, problems occur when we are overwhelmed with too much oxidative stress or too many toxins. Then the glutathione becomes depleted and we can no longer protect ourselves against free radicals, infections, or cancer and we can't get rid of toxins. This leads to further sickness and soon we are in the downward spiral of chronic illness.

 

But that's not all. Glutathione is also critical in helping your immune system do its job of fighting infections and preventing cancer. That's why studies show that it can help in the treatment of AIDS.

 

Glutathione is also the most critical and integral part of your detoxification system. All the toxins stick onto glutathione, which then carries them into the bile and the stool -- and out of your body.

And lastly, it also helps us reach peak mental and physical function. Research has shown that raised glutathione levels decrease muscle damage, reduce recovery time, increase strength and endurance and shift metabolism from fat production to muscle development.

 

If you are sick or old or are just not in peak shape, you likely have glutathione deficiency.

 

In fact, the top British medical journal, the Lancet, found the highest glutathione levels in healthy young people, lower levels in healthy elderly, lower still in sick elderly and the lowest of all in the hospitalized elderly.

 

Keeping yourself healthy, boosting your performance, preventing disease and aging well depends on keeping your glutathione levels high. I'll say it again ... Glutathione is so important because it is responsible for keeping so many of the keys to UltraWellness optimized.

 

It is critical for immune function and controlling inflammation. It is the master detoxifier and the body's main antioxidant, protecting our cells and making our energy metabolism run well.

 

 

Posted by  Randall Payne  at  3:25 PM    No comments:       

 

 

 

 

 

 

 

 

9 Tips to Optimize Gluathione

 

 

 

9 Tips to Optimize your Glutathione Levels

 

These 9 tips will help you improve your glutathione levels, improve your health, optimize your performance and live a long, healthy life.

Eat Foods that Support Glutathione Production

 

1. Consume sulfur-rich foods. The main ones in the diet are garlic, onions and the cruciferous vegetables (broccoli, kale, collards, cabbage, cauliflower, watercress, etc.).

 

2. Try bioactive whey protein. This is great source of cysteine and the amino acid building blocks for glutathione synthesis. As you know, I am not a big fan of dairy. But this is an exception -- with a few warnings. The whey protein MUST be bioactive and made from non-denatured proteins ("denaturing" refers to the breakdown of the normal protein structure). Choose non-pasteurized and non-industrially produced milk that contains no pesticides, hormones, or antibiotics. Immunocal is a prescription bioactive non-denatured whey protein that is even listed in the Physician's Desk Reference.

 

Exercise for Your Way to More Glutathione

 

3. Exercise boosts your glutathione levels and thereby helps boost your immune system, improve detoxification and enhance your body's own antioxidant defenses. Start slow and build up to 30 minutes a day of vigorous aerobic exercise like walking or jogging, or play various sports. Strength training for 20 minutes 3 times a week is also helpful.

 

Take Glutathione Supporting Supplements

 

One would think it would be easy just to take glutathione as a pill, but the body digests protein -- so you wouldn't get the benefits if you did it this way. However, the production and recycling of glutathione in the body requires many different nutrients and you CAN take these. Here are the main supplements that need to be taken consistently to boost glutathione. Besides taking a multivitamin and fish oil, supporting my glutathione levels with these supplements is the most important thing I do every day for my personal health.

 

4. N-acetyl-cysteine. This has been used for years to help treat asthma and lung disease and to treat people with life-threatening liver failure from Tylenol overdose. In fact, I first learned about it in medical school while working in the emergency room. It is even given to prevent kidney damage from dyes used during x-ray studies.

 

5. Alpha lipoic acid. This is a close second to glutathione in importance in our cells and is involved in energy production, blood sugar control, brain health and detoxification. The body usually makes it, but given all the stresses we are under, we often become depleted.

 

6. Methylation nutrients (folate and vitamins B6 and B12). These are perhaps the most critical to keep the body producing glutathione. Methylation and the production and recycling of glutathione are the two most important biochemical functions in your body. Take folate (especially in the active form of 5 methyltetrahydrofolate), B

 

6 (in active form of P5P) and B12 (in the active form of methylcobalamin).

 

7. Selenium. This important mineral helps the body recycle and produce more glutathione.

 

8. A family of antioxidants including vitamins C and E (in the form of mixed tocopherols), work together to recycle glutathione.

 

9. Milk thistle (silymarin) has long been used in liver disease and helps boost glutathione levels.

[[Be...]]

helpme123,  it's interesting that your urine glutamate test was high.  This area of the thread is revealing research into the glutamate problem with benzo w/d.  I also had a borderline high glutamate test a few years ago when I was in tolerance w/d.  I had other neurotransmitters done and my GABA was normal, though I was still on benzo's and taking a GABA supplement. 

[[Mo...]]

 

thank you helpme and pers

this is sooooooooo interesting.

Ig