Someone found something, Jordan Peterson's family

[[wo...]]

Hi guys,

I've caught up on this thread and wanted to make a few points it spilled over into what i spoke with pacenik with the last few days, i will tell you guys what i told him, since this thread should be renamed glutamate vs gaba. I read the article on Xenon blocking receptors. We have medication that does exactly the same thing (it blocks AMPA, NMDA, and kainate and more!) all of you can get it right now (either over the counter in serbia  or from your doctor with a good explanation in low dose), its called topirimate, here's excerpt from an article and rationale in benzo withdrawal:

 

Topiramate: Topiramate (TPM) is a sulfamate-substituted analog of fructose-1,6-diphosphate, whose efficacy in the treatment of SUD is thought to be through three mechanisms of action. Firstly, TPM facilitates Gamma-Aminobutyric Acid (GABA) transmission by binding to a non-BZD site on GABA-A receptors [75] and inhibits glutamatergic transmission at ionotropic Alpha-amino-3-hydroxi-5-Methilisoxazole-Propionic Acid (AMPA) and kainite glutamate receptors [76], which mediate voltage-dependent sodium [77] and L-type calcium currents [78]. Secondarily to these actions, TPM neuro-stabilizes and downstream reduces DA release in the corticomesolimbic system, which is involved in the mechanism of reward and reinforcement. In addition, TPM's blockade of AMPA-type GLU receptors in the nucleus paragigantocellularis appears to inhibit noradrenergic neuron in the locus coeruleus, the activation of which plays an essential role in producing autonomic symptoms of withdrawal states. Finally, because of its weak inhibition of carbonic anhydrase, it could contribute to an anticonvulsant effect, a potentially important property in the treatment of withdrawal syndromes [79]. It has a specific pharmacokinetic profile, which is characterized by: 1) a biovariability of at least 80%; 2) it reaches its maximum concentration between 1.3-1.7 hours post-ingestion; 3) it has a half-life of 19-23 hours; 4) it reaches steady-state plasma concentration in about 4 days; 5) it has low binding potential to proteins; 6) less than 20% of it undergoes metabolism to inactive metabolites; 7) up to 80% unchanged excretion in the urine; and 9) has little drug-to-drug interactions [32].

 

from: http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

In the article it further describes two cases (a shocking one where some kid was snorting 90mg of midazolam a day over 7 years and was took 500mg of topirimate and tapered off over 3 days (sounds like a miracle to me).

 

I took topirimate 2 years ago, its an interesting medication (for my mood disorder), you can rapidly stop it (although i dont recommend it), anticonvulsants (other than gabapentoids) are nothing like antidepressants/antipsychotics. In higher doses, its called dopamax (because it causes cognitive impairment). Its the best psychiatric med for losing weight for all those interested, they combine it with phen phen for all those who remember than fiasco in the 1990s. I slept better on it for sure

 

Anyway if you want proven glutamate reduction/gaba increase, then why is nobody mentioning lamictal/depakote/topirimate etc? Its very possible (pacenik's idea) that i had a more positive reaction to flumazenil is because i am currently taking 1250mg of depakote every day (which is also an excellent medication!). Anyway something to chew the fat on.

[[Ma...]]

Hi guys,

I've caught up on this thread and wanted to make a few points it spilled over into what i spoke with pacenik with the last few days, i will tell you guys what i told him, since this thread should be renamed glutamate vs gaba. I read the article on Xenon blocking receptors. We have medication that does exactly the same thing (it blocks AMPA, NMDA, and kainate and more!) all of you can get it right now (either over the counter in serbia  or from your doctor with a good explanation in low dose), its called topirimate, here's excerpt from an article and rationale in benzo withdrawal:

 

Topiramate: Topiramate (TPM) is a sulfamate-substituted analog of fructose-1,6-diphosphate, whose efficacy in the treatment of SUD is thought to be through three mechanisms of action. Firstly, TPM facilitates Gamma-Aminobutyric Acid (GABA) transmission by binding to a non-BZD site on GABA-A receptors [75] and inhibits glutamatergic transmission at ionotropic Alpha-amino-3-hydroxi-5-Methilisoxazole-Propionic Acid (AMPA) and kainite glutamate receptors [76], which mediate voltage-dependent sodium [77] and L-type calcium currents [78]. Secondarily to these actions, TPM neuro-stabilizes and downstream reduces DA release in the corticomesolimbic system, which is involved in the mechanism of reward and reinforcement. In addition, TPM's blockade of AMPA-type GLU receptors in the nucleus paragigantocellularis appears to inhibit noradrenergic neuron in the locus coeruleus, the activation of which plays an essential role in producing autonomic symptoms of withdrawal states. Finally, because of its weak inhibition of carbonic anhydrase, it could contribute to an anticonvulsant effect, a potentially important property in the treatment of withdrawal syndromes [79]. It has a specific pharmacokinetic profile, which is characterized by: 1) a biovariability of at least 80%; 2) it reaches its maximum concentration between 1.3-1.7 hours post-ingestion; 3) it has a half-life of 19-23 hours; 4) it reaches steady-state plasma concentration in about 4 days; 5) it has low binding potential to proteins; 6) less than 20% of it undergoes metabolism to inactive metabolites; 7) up to 80% unchanged excretion in the urine; and 9) has little drug-to-drug interactions [32].

 

from: http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

In the article it further describes two cases (a shocking one where some kid was snorting 90mg of midazolam a day over 7 years and was took 500mg of topirimate and tapered off over 3 days (sounds like a miracle to me).

 

I took topirimate 2 years ago, its an interesting medication (for my mood disorder), you can rapidly stop it (although i dont recommend it), anticonvulsants (other than gabapentoids) are nothing like antidepressants/antipsychotics. In higher doses, its called dopamax (because it causes cognitive impairment). Its the best psychiatric med for losing weight for all those interested, they combine it with phen phen for all those who remember than fiasco in the 1990s. I slept better on it for sure

 

Anyway if you want proven glutamate reduction/gaba increase, then why is nobody mentioning lamictal/depakote/topirimate etc? Its very possible (pacenik's idea) that i had a more positive reaction to flumazenil is because i am currently taking 1250mg of depakote every day (which is also an excellent medication!). Anyway something to chew the fat on.

 

Good that you brought this up. Topiramate in clinical studies failed to alleviate symptoms of benzo withdrawal highlighting that this approach is not feasible.

[[Ko...]]

You know in Tasmania old people with Parkinson’s have been wearing buckets on their head lined with Near infrared LED lights to treat their Parkinson’s.  I’m sure if you were on a Parkinson’s forum you would have been calling them all foolish as well.  Yet the research on photobiomodulation continues to pile up for treating everything from Parkinson’s to Alzheimer’s to TBI’s. I for one have a pbm helmet I use on myself and my father who has Parkinson’s. 

 

https://www.abc.net.au/news/2019-02-24/clinical-trials-for-wearing-led-helmets-treatment-parkinsons/10836906

 

LOL, just today, I ran across this YouTube video:  "My Absolute #1 Tip To Promote Benzo Withdrawal Healing!"

 

He provides links in support of photobiomodulation (some of which are listed below), as well as links to equipment recommendations. 

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066074/

https://www.research.va.gov/currents/spring2015/spring2015-7.cfm

https://trialsjournal.biomedcentral.com/articles/10.1186/s13063-018-2632-5

https://www.laserfocusworld.com/lasers-sources/article/16558020/nearir-light-penetrates-skull-to-aid-traumatic-brain-injury

 

I have no idea if this works, but for $30-$35, it's an inexpensive experiment. 

 

 

[[ra...]]

Wolfie,

 

I am glad you brought up topiramate.  "Blocking" as achieved by topiramate and modulating reception as done by xenon are as different as blocking by an NMDA agonist like for example ketamine, and modulating reception of glutamate, by for example benzos.  As those who have tried glutamate antagonists have found out, they are not generally helpful to us.  It is my hope that an agent like xenon will modulate glutamate reception permanently, in a way that will counter the reception modulation (damage) done by benzos.   

 

We really will not know until we try, and I hope those interested in xenon will not be dissuaded.

 

ramcon1

[[Ma...]]

Wolfie,

 

I am glad you brought up topiramate.  "Blocking" as achieved by topiramate and modulating reception as done by xenon are as different as blocking by an NMDA agonist like for example ketamine, and modulating reception of glutamate, by for example benzos.  As those who have tried glutamate antagonists have found out, they are not generally helpful to us.  It is my hope that an agent like xenon will modulate glutamate reception permanently, in a way that will counter the reception modulation (damage) done by benzos.   

 

We really will not know until we try, and I hope those interested in xenon will not be dissuaded.

 

ramcon1

 

I do not want to dissuade you if you want to do it. Just one correction, which is not meant to put you down, OK? Also it's not because anybody made me the Pope of science. So my correction is that ketamine is not really an NMDA agonist but antagonist, which also blocks/inhibits/antagonizes the NMDA receptor. Also, ketamine (which I use in my laboratory regularly), which similar to xenon is a short term antagonist of the NMDA receptors does not seem to improve benzo issues.

[[wo...]]

Wolfie,

 

I am glad you brought up topiramate.  "Blocking" as achieved by topiramate and modulating reception as done by xenon are as different as blocking by an NMDA agonist like for example ketamine, and modulating reception of glutamate, by for example benzos.  As those who have tried glutamate antagonists have found out, they are not generally helpful to us.  It is my hope that an agent like xenon will modulate glutamate reception permanently, in a way that will counter the reception modulation (damage) done by benzos.   

 

We really will not know until we try, and I hope those interested in xenon will not be dissuaded.

 

ramcon1

 

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

[[Fo...]]

Light therapy for Parkinson's started because a scientist/physician had an idea that it might work based on light therapy in other conditions and that scientist/physician tried it. There were no forums involved.

 

Xenon therapy didn’t originate on forums either. It’s being used in multiple clinics for drug and medication detox and happens to be used in clinics in Belgrade where Jordan Peterson was treated.  A relative of Jordan Peterson specifically referred me to a clinic that happens to use xenon therapy.  There’s also enough studies showing neuroprotective mechanisms that could theoretically apply to benzodiazepine damage.  It’s simply being discussed on a forum.  Which for some bizarre reason really seems to irritate you.  Yet based on your posting habits, you seem to be irritated by lots of things. 

 

Have you considered going back on the benzos?  There’s countless people, myself included, in the throws of horrific withdrawals.  Yet somehow we are able to maintain some level of positivity, curiosity, and respect. 

[Guest [pa...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

[[Ch...]]

Does anyone have any idea so as to how one would acquire xenon gas in UK? To do an at home treatment.

 

Any ideas welcome

[[Ma...]]

Light therapy for Parkinson's started because a scientist/physician had an idea that it might work based on light therapy in other conditions and that scientist/physician tried it. There were no forums involved.

 

Xenon therapy didn’t originate on forums either. It’s being used in multiple clinics for drug and medication detox and happens to be used in clinics in Belgrade where Jordan Peterson was treated.  A relative of Jordan Peterson specifically referred me to a clinic that happens to use xenon therapy.  There’s also enough studies showing neuroprotective mechanisms that could theoretically apply to benzodiazepine damage.  It’s simply being discussed on a forum.  Which for some bizarre reason really seems to irritate you.  Yet based on your posting habits, you seem to be irritated by lots of things. 

 

Have you considered going back on the benzos?  There’s countless people, myself included, in the throws of horrific withdrawals.  Yet somehow we are able to maintain some level of positivity, curiosity, and respect.

 

Let's not be personal here. I state what I think is scientifically right. Some may agree, some don't. I don't remember ever having any emotions about the discussions here. I just say whether it's in my view right or wrong. Everything can work "theoretically". What you mentioned about a relative of Jordan Peterson is a so-called anecdotal experience. Anecdotal means that we don't know if it's going to work for other people. If it works, fine. If it doesn't, you waste a lot of money and hope. I never said that xenon should not be discussed on the forum. Discuss it, by all means. But I will voice my opinion. People who don't like it can skip reading my comments.

 

I also disagree with you on using the term "neuroprotective" with regard to benzo dependence. In my view neuroprotective means that something will prevent injury if applied before or about the time of injury. Once we become dependent on benzos, the injury is complete. There's nothing to protect anymore.

 

Jordan Peterson's case at this point is unresolved. He mentioned once he was treated in Serbia (we don't know what with), and he was feeling better. This was the latest we heard about him. But the fact that he felt well at that point doesn't mean he is feeling well now. How many people go to rehab who are given some drug to mask their benzo symptoms (barbiturates, anti-psychotics, and the list goes on) and once the effect of those drugs subsides, they are thrown back to the throws of benzo withdrawal.

 

I think I'm curious enough. That's why I became a scientist. Positive too. I believe in scientific progress. But that can only happen when the scientific method is used. The scientific method is not based on logic (deduction or board forums) only. It also requires induction, experiments. I never disrespected anybody here. I might have argued with their opinions but that's not disrespect.

 

I'm tapering my benzo very slowly and gradually and feeling perfectly fine other than having tinnitus. I don't complain.

[[Ma...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

[[wo...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

 

What is the definition of failure? I really don't know how you can say they fail when there are many many studies showing success working for people with benzo dependence. I did a search through these forums very few people talk about them or following lets say some of the protocols that are mentioned in the research studies where anticonvulsants did help.

 

If your setting the gold standard that success is a perfect reversal of all symptoms in 100% of patients, you will be hard pressed to find any medicines today that fit that description in any field. If anyone was brave enough, they could take low dose gabazine for a few weeks and pray they don't have seizure (hopefully with an anticonvulsant) and maybe that would reverse benzo withdrawal in the "perfect" inverse way. The goal is to make the process as comfortable as possible and prevent as many adverse reactions, at minimum anticonvulsants could prevent seizures in people who do rapid tapers or cold turkey (in this category they can be close to 100% effective). At most they can help speed the healing process and return life to normal for as many people as possible. As you said, it took months/years to change our bodies with benzos, it would take weeks/months to change it back...

 

[[Ma...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

 

What is the definition of failure? I really don't know how you can say they fail when there are many many studies showing success working for people with benzo dependence. I did a search through these forums very few people talk about them or following lets say some of the protocols that are mentioned in the research studies where anticonvulsants did help.

 

If your setting the gold standard that success is a perfect reversal of all symptoms in 100% of patients, you will be hard pressed to find any medicines today that fit that description in any field. If anyone was brave enough, they could take low dose gabazine for a few weeks and pray they don't have seizure (hopefully with an anticonvulsant) and maybe that would reverse benzo withdrawal in the "perfect" inverse way. The goal is to make the process as comfortable as possible and prevent as many adverse reactions, at minimum anticonvulsants could prevent seizures in people who do rapid tapers or cold turkey (in this category they can be close to 100% effective). At most they can help speed the healing process and return life to normal for as many people as possible. As you said, it took months/years to change our bodies with benzos, it would take weeks/months to change it back...

 

https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832

[[Ha...]]

That's all well and good, but what about the ones of us that couldn't tolerate the benzos to complete a taper?

[[wo...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

 

What is the definition of failure? I really don't know how you can say they fail when there are many many studies showing success working for people with benzo dependence. I did a search through these forums very few people talk about them or following lets say some of the protocols that are mentioned in the research studies where anticonvulsants did help.

 

If your setting the gold standard that success is a perfect reversal of all symptoms in 100% of patients, you will be hard pressed to find any medicines today that fit that description in any field. If anyone was brave enough, they could take low dose gabazine for a few weeks and pray they don't have seizure (hopefully with an anticonvulsant) and maybe that would reverse benzo withdrawal in the "perfect" inverse way. The goal is to make the process as comfortable as possible and prevent as many adverse reactions, at minimum anticonvulsants could prevent seizures in people who do rapid tapers or cold turkey (in this category they can be close to 100% effective). At most they can help speed the healing process and return life to normal for as many people as possible. As you said, it took months/years to change our bodies with benzos, it would take weeks/months to change it back...

 

https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832

 

 

I opened that link on https://sci-hub.se/https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832, the only thing relevant to our discussion here is table 5 on page 9, where your own guy lists carbamapazepine as an approach with a "moderate" level of evidence. You say its a failure. Can you please tell me where in the article it states that anticonvulsants are a failure. I only see limited evidence, maybe when he wrote it, he didn't do a thorough search on how effective anticonvulsants can be.

 

Now the counterevidence:

 

Here is also another metastudy (a study of studies with review of all options and explations):

http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

He specifically reviews 27 studies which review efficacy of anticonvulsants as adjuncts in benzodiazepine withdrawal. I read this article in pretty good detail, the evidence looks pretty compelling to me, i challenge people here to read the case studies. We have Sci-hub, we can download each of the articles we find relevant and see which one helps where and have efficacious each treatment was relative to placebo, the point is nowhere is it clear that they are failures. they can help help, they are not cures. For people suffering from benzo withdrawal where someone is on the razors edge they might be the difference between relapse and success or suicide. Same with xenon and other treatments.

 

[[Ma...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

 

What is the definition of failure? I really don't know how you can say they fail when there are many many studies showing success working for people with benzo dependence. I did a search through these forums very few people talk about them or following lets say some of the protocols that are mentioned in the research studies where anticonvulsants did help.

 

If your setting the gold standard that success is a perfect reversal of all symptoms in 100% of patients, you will be hard pressed to find any medicines today that fit that description in any field. If anyone was brave enough, they could take low dose gabazine for a few weeks and pray they don't have seizure (hopefully with an anticonvulsant) and maybe that would reverse benzo withdrawal in the "perfect" inverse way. The goal is to make the process as comfortable as possible and prevent as many adverse reactions, at minimum anticonvulsants could prevent seizures in people who do rapid tapers or cold turkey (in this category they can be close to 100% effective). At most they can help speed the healing process and return life to normal for as many people as possible. As you said, it took months/years to change our bodies with benzos, it would take weeks/months to change it back...

 

https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832

 

 

I opened that link on https://sci-hub.se/https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832, the only thing relevant to our discussion here is table 5 on page 9, where your own guy lists carbamapazepine as an approach with a "moderate" level of evidence. You say its a failure. Can you please tell me where in the article it states that anticonvulsants are a failure. I only see limited evidence, maybe when he wrote it, he didn't do a thorough search on how effective anticonvulsants can be.

 

Now the counterevidence:

 

Here is also another metastudy (a study of studies with review of all options and explations):

http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

He specifically reviews 27 studies which review efficacy of anticonvulsants as adjuncts in benzodiazepine withdrawal. I read this article in pretty good detail, the evidence looks pretty compelling to me, i challenge people here to read the case studies. We have Sci-hub, we can download each of the articles we find relevant and see which one helps where and have efficacious each treatment was relative to placebo, the point is nowhere is it clear that they are failures. they can help help, they are not cures. For people suffering from benzo withdrawal where someone is on the razors edge they might be the difference between relapse and success or suicide. Same with xenon and other treatments.

 

The article you cited does not talk about glutamate receptor antagonists. Carbamazepine, which the article you cited discusses, is a sodium channel blocker and not a glutamate receptor antagonist, like xenon. You're comparing apples with oranges.

 

Nevertheless, all of us would welcome any type of agent that helps. Carbamazepine, the evidence for which in my opinion is hardly compelling, is a very dangerous drug and one its most severe side effects is bone marrow failure.

[[ra...]]

All,

 

I meant ketamine is an NMDA "ANTagonist."  I have got to stop posting my cogfog is just too sick with this cold.  Between that and "GABA receptors releasing GABA," I am just mucking things ups. Sorry.  I am trying to say xenon is different and good.  That is all I have in brain power right now.  This is so frustrating.

 

Hopefully this thread and my mind will improve in a few weeks.  Good luck.

 

Ramcon1

[[wo...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

 

What is the definition of failure? I really don't know how you can say they fail when there are many many studies showing success working for people with benzo dependence. I did a search through these forums very few people talk about them or following lets say some of the protocols that are mentioned in the research studies where anticonvulsants did help.

 

If your setting the gold standard that success is a perfect reversal of all symptoms in 100% of patients, you will be hard pressed to find any medicines today that fit that description in any field. If anyone was brave enough, they could take low dose gabazine for a few weeks and pray they don't have seizure (hopefully with an anticonvulsant) and maybe that would reverse benzo withdrawal in the "perfect" inverse way. The goal is to make the process as comfortable as possible and prevent as many adverse reactions, at minimum anticonvulsants could prevent seizures in people who do rapid tapers or cold turkey (in this category they can be close to 100% effective). At most they can help speed the healing process and return life to normal for as many people as possible. As you said, it took months/years to change our bodies with benzos, it would take weeks/months to change it back...

 

https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832

 

 

I opened that link on https://sci-hub.se/https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832, the only thing relevant to our discussion here is table 5 on page 9, where your own guy lists carbamapazepine as an approach with a "moderate" level of evidence. You say its a failure. Can you please tell me where in the article it states that anticonvulsants are a failure. I only see limited evidence, maybe when he wrote it, he didn't do a thorough search on how effective anticonvulsants can be.

 

Now the counterevidence:

 

Here is also another metastudy (a study of studies with review of all options and explations):

http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

He specifically reviews 27 studies which review efficacy of anticonvulsants as adjuncts in benzodiazepine withdrawal. I read this article in pretty good detail, the evidence looks pretty compelling to me, i challenge people here to read the case studies. We have Sci-hub, we can download each of the articles we find relevant and see which one helps where and have efficacious each treatment was relative to placebo, the point is nowhere is it clear that they are failures. they can help help, they are not cures. For people suffering from benzo withdrawal where someone is on the razors edge they might be the difference between relapse and success or suicide. Same with xenon and other treatments.

 

The article you cited does not talk about glutamate receptor antagonists. Carbamazepine, which the article you cited discusses, is a sodium channel blocker and not a glutamate receptor antagonist, like xenon. You're comparing apples with oranges.

 

Nevertheless, all of us would welcome any type of agent that helps. Carbamazepine, the evidence for which in my opinion is hardly compelling, is a very dangerous drug and one its most severe side effects is bone marrow failure.

 

Nowhere in my previous  post do i mention glutamate receptor agonist, i was talking about your claim that anticonvulsants "fail". You quote an article where your author himself says the evidence for anticonvulsants is "moderate." Then you say my article talks about one anticonvulsant, when it talks about pretty much every single anticonvulsant (carbamazepine, depakote, lamictal, topirimate, tiagabine, etc....).

 

Then you make an outrageous claim that carbamazepine is dangerous and list its most adverse (.0000001%) of the oldest most dangerous drug of that class. millions of epileptics, bipolar people, and many more take these every day and very very very few people have bone marrow failure (trust me it would be a much larger public health crisis than coronavirus if it was as dangerous as you claim. Some are very safe drugs, they do not cause dependence in anyway like antidepressants or antipsychotics. Lamictal and Depakote are prescribed to tens of millions of people with minimal side effect profile and more focus should be more on those for benzodiazepine dependence.

 

In this forum we have alot of the hard to treat cases, lots of desperate people who message me,  who are I read are willing to spend tens of thousands of dollars to make this problem go away. I did flumazenil and it helped me, but it cost alot. Does it not make sense to try whats easily available, with the help of a knowledgable psychiatrist or neurologist to help and some suggestion, to try some easily available medication in low doses to see if it helps? People are reaching for rescue doses and doing crazy things and having setbacks when topirimate or depakote can easy symptoms substantially it doesn't make sense, and especially when its readilly available and prescribers are around corner, especially if you can print a few articles and show your doctor and make a good point showing that it can help you if they aren't informed.

 

I agree with Maugham1 that a gradual taper is the best option, but its not an exclusive option. Its not like you have to choose between that and adding depakote to the mix. You can do a gradual taper and add depakote or topirimate or whatever your prescriber thinks is best/most comfortable to this mix. Also my personal opinion is life is short, there's no reason to do a 5 year taper. The faster you can get this over with, the better (not too fast ofcourse, 6 months a year, not 5 years), and thats where it can help.

[[Ma...]]

Thanks for that,

the theory for xenon sounds rather similar to the theory behind ketamine for depression... anyway i hope it works, the only way to know is to see... i'm going to see with my pdoc (i want to lose some covid weight and i'm not working so i don't need to be too bright) to switch to topirimate, what i did find is that topirimate modulates gaba (so does magnesium ),

 

don't be dissuaded, just have some sound logic to do so... even if it doesnt work as you expect it can help or there might be some silver lining....

 

Yes, but xenon appears to be substantially different than other anesthetics like ketamine:

http://bjanaesthesia.org/article/S0007-0912(17)35668-4/pdf

http://www.ane.pl/pdf/6931.pdf

 

That's a good point. Nevertheless, I'm skeptical about using any type of glutamate antagonist to try to treat benzo dependence. Many types of glutamate antagonists have been tried in patients suffering from benzo dependence and failed. Another issue is that xenon can only be administered for a short period of time. Unfortunately, benzo dependence in many people is not a short term journey.

 

What is the definition of failure? I really don't know how you can say they fail when there are many many studies showing success working for people with benzo dependence. I did a search through these forums very few people talk about them or following lets say some of the protocols that are mentioned in the research studies where anticonvulsants did help.

 

If your setting the gold standard that success is a perfect reversal of all symptoms in 100% of patients, you will be hard pressed to find any medicines today that fit that description in any field. If anyone was brave enough, they could take low dose gabazine for a few weeks and pray they don't have seizure (hopefully with an anticonvulsant) and maybe that would reverse benzo withdrawal in the "perfect" inverse way. The goal is to make the process as comfortable as possible and prevent as many adverse reactions, at minimum anticonvulsants could prevent seizures in people who do rapid tapers or cold turkey (in this category they can be close to 100% effective). At most they can help speed the healing process and return life to normal for as many people as possible. As you said, it took months/years to change our bodies with benzos, it would take weeks/months to change it back...

 

https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832

 

 

I opened that link on https://sci-hub.se/https://www.nejm.org/doi/pdf/10.1056/NEJMra1611832, the only thing relevant to our discussion here is table 5 on page 9, where your own guy lists carbamapazepine as an approach with a "moderate" level of evidence. You say its a failure. Can you please tell me where in the article it states that anticonvulsants are a failure. I only see limited evidence, maybe when he wrote it, he didn't do a thorough search on how effective anticonvulsants can be.

 

Now the counterevidence:

 

Here is also another metastudy (a study of studies with review of all options and explations):

http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

He specifically reviews 27 studies which review efficacy of anticonvulsants as adjuncts in benzodiazepine withdrawal. I read this article in pretty good detail, the evidence looks pretty compelling to me, i challenge people here to read the case studies. We have Sci-hub, we can download each of the articles we find relevant and see which one helps where and have efficacious each treatment was relative to placebo, the point is nowhere is it clear that they are failures. they can help help, they are not cures. For people suffering from benzo withdrawal where someone is on the razors edge they might be the difference between relapse and success or suicide. Same with xenon and other treatments.

 

The article you cited does not talk about glutamate receptor antagonists. Carbamazepine, which the article you cited discusses, is a sodium channel blocker and not a glutamate receptor antagonist, like xenon. You're comparing apples with oranges.

 

Nevertheless, all of us would welcome any type of agent that helps. Carbamazepine, the evidence for which in my opinion is hardly compelling, is a very dangerous drug and one its most severe side effects is bone marrow failure.

 

Nowhere in my previous  post do i mention glutamate receptor agonist, i was talking about your claim that anticonvulsants "fail". You quote an article where your author himself says the evidence for anticonvulsants is "moderate." Then you say my article talks about one anticonvulsant, when it talks about pretty much every single anticonvulsant (carbamazepine, depakote, lamictal, topirimate, tiagabine, etc....).

 

Then you make an outrageous claim that carbamazepine is dangerous and list its most adverse (.0000001%) of the oldest most dangerous drug of that class. Tens of millions of epileptics, bipolar people, and many more take these every day and very very very few people have bone marrow failure (trust me it would be a much larger public health crisis than coronavirus if it was as dangerous as you claim, i've been on depakote for 2 years, i've taken topiramate for 3 months, lamictal for 6 months, lithium for 5 years, if the most serious adverse reaction happened to me i would be dead long ago . Anticonvulsants are very safe drugs, they do not cause dependence in anyway like antidepressants or antipsychotics. Lamictal and Depakote are prescribed to tens if not hundreds of millions of people with minimal side effect profile and more focus should be on those.

 

This post was discussing Xenon as a glutamate receptor antagonist. I said that glutamate receptor antagonists failed. Then you said "What is the definition of failure"? I cited an article showing they failed. Then you started talking about anticonvulsants, which are not glutamate receptor antagonists.

 

You then brought carbamazepine up, which is fine by me even though it's not a glutamate receptor antagonist. You say carbamazepine is not dangerous because you are taking depakote, topiramate, lamictal and lithium, which are all NOT carbamazepine. You also say carbamazepine is not dangerous because very few people have bone marrow failure who take it. I disagree. It is dangerous, and that's why people who take carbamazepine have to have their blood counts checked every 3 months: https://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/peripheral_nerve/patient_info/CARBAMAZEPINE_2007.pdf

 

So one lesson from this is that although there are various different drugs that are all called "anticonvulsants", they are chemically different, and have different side effects. Carbamazepine happens to affect the bone marrow.

[[wo...]]

Hi guys,

I've caught up on this thread and wanted to make a few points it spilled over into what i spoke with pacenik with the last few days, i will tell you guys what i told him, since this thread should be renamed glutamate vs gaba. I read the article on Xenon blocking receptors. We have medication that does exactly the same thing (it blocks AMPA, NMDA, and kainate and more!) all of you can get it right now (either over the counter in serbia  or from your doctor with a good explanation in low dose), its called topirimate, here's excerpt from an article and rationale in benzo withdrawal:

 

Topiramate: Topiramate (TPM) is a sulfamate-substituted analog of fructose-1,6-diphosphate, whose efficacy in the treatment of SUD is thought to be through three mechanisms of action. Firstly, TPM facilitates Gamma-Aminobutyric Acid (GABA) transmission by binding to a non-BZD site on GABA-A receptors [75] and inhibits glutamatergic transmission at ionotropic Alpha-amino-3-hydroxi-5-Methilisoxazole-Propionic Acid (AMPA) and kainite glutamate receptors [76], which mediate voltage-dependent sodium [77] and L-type calcium currents [78]. Secondarily to these actions, TPM neuro-stabilizes and downstream reduces DA release in the corticomesolimbic system, which is involved in the mechanism of reward and reinforcement. In addition, TPM's blockade of AMPA-type GLU receptors in the nucleus paragigantocellularis appears to inhibit noradrenergic neuron in the locus coeruleus, the activation of which plays an essential role in producing autonomic symptoms of withdrawal states. Finally, because of its weak inhibition of carbonic anhydrase, it could contribute to an anticonvulsant effect, a potentially important property in the treatment of withdrawal syndromes [79]. It has a specific pharmacokinetic profile, which is characterized by: 1) a biovariability of at least 80%; 2) it reaches its maximum concentration between 1.3-1.7 hours post-ingestion; 3) it has a half-life of 19-23 hours; 4) it reaches steady-state plasma concentration in about 4 days; 5) it has low binding potential to proteins; 6) less than 20% of it undergoes metabolism to inactive metabolites; 7) up to 80% unchanged excretion in the urine; and 9) has little drug-to-drug interactions [32].

 

from: http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

In the article it further describes two cases (a shocking one where some kid was snorting 90mg of midazolam a day over 7 years and was took 500mg of topirimate and tapered off over 3 days (sounds like a miracle to me).

 

I took topirimate 2 years ago, its an interesting medication (for my mood disorder), you can rapidly stop it (although i dont recommend it), anticonvulsants (other than gabapentoids) are nothing like antidepressants/antipsychotics. In higher doses, its called dopamax (because it causes cognitive impairment). Its the best psychiatric med for losing weight for all those interested, they combine it with phen phen for all those who remember than fiasco in the 1990s. I slept better on it for sure

 

Anyway if you want proven glutamate reduction/gaba increase, then why is nobody mentioning lamictal/depakote/topirimate etc? Its very possible (pacenik's idea) that i had a more positive reaction to flumazenil is because i am currently taking 1250mg of depakote every day (which is also an excellent medication!). Anyway something to chew the fat on.

 

Good that you brought this up. Topiramate in clinical studies failed to alleviate symptoms of benzo withdrawal highlighting that this approach is not feasible.

 

I was responding to this above but clicked the last one posted since the word "failed" appeared twice , so apologies from my side. I was never denying the bone marrow issue, every drug has a serious adverse issue. you know tylenol kills people. What percentage of people get the bone marrow issue? how many fatalaties? its still OTC... that doesnt mean its dangerous... 

 

carbamazepine is not firstline treatment for anyone i would try anyway and yes you do have to measure blood levels on it. There are 10 other ones. There is oxcarbamazepine which doesn't require measuring levels and is a much more side effect friendly version of the same. As I said, tens of millions of people take these medications and most of them are considered safe. I hope we can agree on the points above .

 

 

[[Ma...]]

Hi guys,

I've caught up on this thread and wanted to make a few points it spilled over into what i spoke with pacenik with the last few days, i will tell you guys what i told him, since this thread should be renamed glutamate vs gaba. I read the article on Xenon blocking receptors. We have medication that does exactly the same thing (it blocks AMPA, NMDA, and kainate and more!) all of you can get it right now (either over the counter in serbia  or from your doctor with a good explanation in low dose), its called topirimate, here's excerpt from an article and rationale in benzo withdrawal:

 

Topiramate: Topiramate (TPM) is a sulfamate-substituted analog of fructose-1,6-diphosphate, whose efficacy in the treatment of SUD is thought to be through three mechanisms of action. Firstly, TPM facilitates Gamma-Aminobutyric Acid (GABA) transmission by binding to a non-BZD site on GABA-A receptors [75] and inhibits glutamatergic transmission at ionotropic Alpha-amino-3-hydroxi-5-Methilisoxazole-Propionic Acid (AMPA) and kainite glutamate receptors [76], which mediate voltage-dependent sodium [77] and L-type calcium currents [78]. Secondarily to these actions, TPM neuro-stabilizes and downstream reduces DA release in the corticomesolimbic system, which is involved in the mechanism of reward and reinforcement. In addition, TPM's blockade of AMPA-type GLU receptors in the nucleus paragigantocellularis appears to inhibit noradrenergic neuron in the locus coeruleus, the activation of which plays an essential role in producing autonomic symptoms of withdrawal states. Finally, because of its weak inhibition of carbonic anhydrase, it could contribute to an anticonvulsant effect, a potentially important property in the treatment of withdrawal syndromes [79]. It has a specific pharmacokinetic profile, which is characterized by: 1) a biovariability of at least 80%; 2) it reaches its maximum concentration between 1.3-1.7 hours post-ingestion; 3) it has a half-life of 19-23 hours; 4) it reaches steady-state plasma concentration in about 4 days; 5) it has low binding potential to proteins; 6) less than 20% of it undergoes metabolism to inactive metabolites; 7) up to 80% unchanged excretion in the urine; and 9) has little drug-to-drug interactions [32].

 

from: http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

In the article it further describes two cases (a shocking one where some kid was snorting 90mg of midazolam a day over 7 years and was took 500mg of topirimate and tapered off over 3 days (sounds like a miracle to me).

 

I took topirimate 2 years ago, its an interesting medication (for my mood disorder), you can rapidly stop it (although i dont recommend it), anticonvulsants (other than gabapentoids) are nothing like antidepressants/antipsychotics. In higher doses, its called dopamax (because it causes cognitive impairment). Its the best psychiatric med for losing weight for all those interested, they combine it with phen phen for all those who remember than fiasco in the 1990s. I slept better on it for sure

 

Anyway if you want proven glutamate reduction/gaba increase, then why is nobody mentioning lamictal/depakote/topirimate etc? Its very possible (pacenik's idea) that i had a more positive reaction to flumazenil is because i am currently taking 1250mg of depakote every day (which is also an excellent medication!). Anyway something to chew the fat on.

 

Good that you brought this up. Topiramate in clinical studies failed to alleviate symptoms of benzo withdrawal highlighting that this approach is not feasible.

 

I was responding to this above but clicked the last one posted since the word "failed" appeared twice , so apologies from my side. I was never denying the bone marrow issue, every drug has a serious adverse issue. you know tylenol kills people. What percentage of people get the bone marrow issue? how many fatalaties? its still OTC... that doesnt mean its dangerous... 

 

carbamazepine is not firstline treatment for anyone i would try anyway and yes you do have to measure blood levels on it. There are 10 other ones. There is oxcarbamazepine which doesn't require measuring levels and is a much more side effect friendly version of the same. As I said, tens of millions of people take these medications and most of them are considered safe. I hope we can agree on the points above .

 

I accept your apologies

 

To answer your question, about 2% of the people who take carbamazepine have more serious blood issues and mild changes occur in 30% of the people: "Blood dyscrasias (moderate and severe leucopenia and 1 case of thrombocytopenia) occurred with an incidence of 2% with mild changes detected in up to 30% of patients." I got this from here: https://www.medsafe.govt.nz/Profs/PUarticles/carbam.htm

 

Tylenol is a much safer drug.

 

 

[[wo...]]

Hi guys,

I've caught up on this thread and wanted to make a few points it spilled over into what i spoke with pacenik with the last few days, i will tell you guys what i told him, since this thread should be renamed glutamate vs gaba. I read the article on Xenon blocking receptors. We have medication that does exactly the same thing (it blocks AMPA, NMDA, and kainate and more!) all of you can get it right now (either over the counter in serbia  or from your doctor with a good explanation in low dose), its called topirimate, here's excerpt from an article and rationale in benzo withdrawal:

 

Topiramate: Topiramate (TPM) is a sulfamate-substituted analog of fructose-1,6-diphosphate, whose efficacy in the treatment of SUD is thought to be through three mechanisms of action. Firstly, TPM facilitates Gamma-Aminobutyric Acid (GABA) transmission by binding to a non-BZD site on GABA-A receptors [75] and inhibits glutamatergic transmission at ionotropic Alpha-amino-3-hydroxi-5-Methilisoxazole-Propionic Acid (AMPA) and kainite glutamate receptors [76], which mediate voltage-dependent sodium [77] and L-type calcium currents [78]. Secondarily to these actions, TPM neuro-stabilizes and downstream reduces DA release in the corticomesolimbic system, which is involved in the mechanism of reward and reinforcement. In addition, TPM's blockade of AMPA-type GLU receptors in the nucleus paragigantocellularis appears to inhibit noradrenergic neuron in the locus coeruleus, the activation of which plays an essential role in producing autonomic symptoms of withdrawal states. Finally, because of its weak inhibition of carbonic anhydrase, it could contribute to an anticonvulsant effect, a potentially important property in the treatment of withdrawal syndromes [79]. It has a specific pharmacokinetic profile, which is characterized by: 1) a biovariability of at least 80%; 2) it reaches its maximum concentration between 1.3-1.7 hours post-ingestion; 3) it has a half-life of 19-23 hours; 4) it reaches steady-state plasma concentration in about 4 days; 5) it has low binding potential to proteins; 6) less than 20% of it undergoes metabolism to inactive metabolites; 7) up to 80% unchanged excretion in the urine; and 9) has little drug-to-drug interactions [32].

 

from: http://www.heraldopenaccess.us/openaccess/anticonvulsant-agents-for-the-management-of-benzodiazepine-dependence

 

In the article it further describes two cases (a shocking one where some kid was snorting 90mg of midazolam a day over 7 years and was took 500mg of topirimate and tapered off over 3 days (sounds like a miracle to me).

 

I took topirimate 2 years ago, its an interesting medication (for my mood disorder), you can rapidly stop it (although i dont recommend it), anticonvulsants (other than gabapentoids) are nothing like antidepressants/antipsychotics. In higher doses, its called dopamax (because it causes cognitive impairment). Its the best psychiatric med for losing weight for all those interested, they combine it with phen phen for all those who remember than fiasco in the 1990s. I slept better on it for sure

 

Anyway if you want proven glutamate reduction/gaba increase, then why is nobody mentioning lamictal/depakote/topirimate etc? Its very possible (pacenik's idea) that i had a more positive reaction to flumazenil is because i am currently taking 1250mg of depakote every day (which is also an excellent medication!). Anyway something to chew the fat on.

 

Good that you brought this up. Topiramate in clinical studies failed to alleviate symptoms of benzo withdrawal highlighting that this approach is not feasible.

 

I was responding to this above but clicked the last one posted since the word "failed" appeared twice , so apologies from my side. I was never denying the bone marrow issue, every drug has a serious adverse issue. you know tylenol kills people. What percentage of people get the bone marrow issue? how many fatalaties? its still OTC... that doesnt mean its dangerous... 

 

carbamazepine is not firstline treatment for anyone i would try anyway and yes you do have to measure blood levels on it. There are 10 other ones. There is oxcarbamazepine which doesn't require measuring levels and is a much more side effect friendly version of the same. As I said, tens of millions of people take these medications and most of them are considered safe. I hope we can agree on the points above .

 

I accept your apologies

 

To answer your question, about 2% of the people who take carbamazepine have more serious blood issues and mild changes occur in 30% of the people: "Blood dyscrasias (moderate and severe leucopenia and 1 case of thrombocytopenia) occurred with an incidence of 2% with mild changes detected in up to 30% of patients." I got this from here: https://www.medsafe.govt.nz/Profs/PUarticles/carbam.htm

 

Tylenol is a much safer drug.

 

You read what you like to read . Firstly it doesn't say serious blood issues it says the blood issues are mild (thats the heading in big letters), and that they show up with monitoring which is what the point is, it goes away within 2 weeks with switch to another med. The rashes are also mild. Not only that it ends the article with the phrase that carbamazepine is a "relatively safe drug." If it such a relatively safe drug, imagine how safe depakote or lamictal are

 

I opened three prescribing guides on side effects, nobody lists bone marrow suppression as even a "rare side effect." you really had to research hard to find that and i give you kudos for it, your very good at scaring people, and i never even wanted to suggest carbamazepine to anyone and you got me discussing it for the last five posts .  Anyway we need to move on with life, i can't keep trying to refute every misstatement or judgement (or what is in my opinion).

 

I ask kindly if you say something is a failure or doesn't work to say why you think its not a failure and provide some evidence as to why its not (as in the case of topirimate, such as a study where a study or case report where it doesnt work) rather than just say its a failure, and i apologize full for quoting the wrong post when i responded. Goodnight

[[qw...]]

Interested to see where this goes. No intention of going to Europe to get therapy, but more so because this guy is somewhat famous and a reputable psychologist. I’m hoping this story creates some real awareness.

 

These drugs have to go. They are the new opiate crisis and I’m sure that more and more people will start bringing their stories to center stage.

[[Ca...]]

Hmmm... I might be a bit simple, but im still wondering why I got a benzo WD from opiates, so to speak, -and others get the “classic benzo SX” from ADs, and so on..

Personally, for me to consider these things discussed with serious intent, I would have to see these diverse and complex pathways unraveled..

Even with benzo only discontinuations, its often not hard to see when the issues diverge from the trusty “gabba downregulation” or if you will permit, -the typical Ashton experience...

 

I wonder when/if someone stumbles on a “key”, just how gob smacked we all will be..!!??

I do suspect, as perhaps Ramcon is open to, that it might end up an “either or”, a choice of two polarities (or more)..??

 

Till then... Happy hunting... (its all too complex for me..)

 

[[Sh...]]

The worst part about these forums is when fruitful theoretical conversations on science and ideas (literally what ‘chewing the fat’ is for) get hijacked and derailed by a random naysayer reciting the ever-repeated doom and gloom mantra that nothing can help but tapers and time.

 

We all know. We know the mantra. We’ve heard it over and over ad infinitum. With all due respect, if you are uninterested in theoretical science that extends beyond the taper/time mantra, why even post here? There are plenty of other threads about tapering and whatever else you want to talk about. People come here to be hopeful and productive and talk about ideas. We know they’re not proven. We know time is the best answer we’ve got now. But for a lot of us, that’s just not enough. There are not going to be clinical trials. Not any time soon. No way. And if they started tomorrow they’re still a decade away from producing anything of use to mainstream medicine. We would OBVIOUSLY all prefer for tons of brilliant and motivated scientists to come together and dedicate their time to our cause... but that’s not going to happen. All we have is our group, our minds, our energy. If you’re on this page, you should know that mainstream medicine simply doesn’t care. And they never will unless we come together and KEEP talking.

 

Why won’t these issues get solved on benzobuddies?! Why can’t we be the spark? I’ve personally met some brilliant people here and we have something on our side - we CARE about these issues. I’ve met scientists, lawyers, engineers, etc etc all in this circle. I’ve met doctors through people here. I’ve met tons of educated people who are reading and studying and researching and talking to doctors and professionals around the world. Coming up with logical, science-based theories and testing them. Is this the perfect method? No. WE KNOW. But it’s all we’ve got. These threads are for science theories and ideas, we know we’re not talking about facts with 20 years of clinical data and human trials. If we had that we wouldn’t be in this damn position in the first place.... EVERYTHING starts somewhere. No disease has a cure until someone finds it.

 

Ugh. Was hoping the conversation would continue unscathed and I could ignore it, but alas, it continues. I just hate when this happens... Lolol. Forgive me. To return back to the cutting edge discussion and revert away from the pervading mantra that everyone who’s visited this site since its inception knows by heart.......

 

Pacenik!!... have to had your xenon appointment yet? We are nearing the end of the week so just checking in. Did you give it a shot?!

 

Completely agree. Whenever I see Maugham1 posting I immediately feel like leaving the thread. I mean obviously most of this stuff hasnt been studied a lot of it is cutting edge. Personally I dont really care Id rather listen to anecdotal stories of people who told me things worked for them. If I hadnt taken a leap with NAD infusions to cold turkey benzis Id still be polydrugged horribly. I am not healed but im much better and no longer on poison.