Alcohol Was this Klonopin or Alcohol WD? Would taking Klonopin EARLIER have prevented it? Do I need to quit drinking?

[Mycophile]

It wouldn't matter if we had doctors or not. This is on the edge of emerging neuroscience and combinatorial reactions to multiple receptor systems because you're not supposed to be taking large doses of benzodiazepines, opioids, herbal opioids like kratom in an uncontrolled manner like you are.

I mean you're almost doing investigational experimentation in one of two categories either

PLAY STUPID GAMES, WIN STUPID PRIZES!

or

FUCK AROUND AND FIND OUT!

While it is thin and very very loosely supported, there is evidence that seizures occur when kratom is used by people with gabaergic dysfunction caused by either benzodiazepine abuse or epilepsy.

We're not sure if you have breakthrough seizures that have been hidden by your benzodiazepine used for years.

What we do know is that you used an excessive amount of benzodiazepines, that you have recently lowered your dose extremely. That would instigate gabaergic dysfunction because you're still in a partially with drawn state even with no symptoms.

There is absolute evidence that kratom acts at the benzodiazepine site of the GABA receptor.

So you know you have the evidence, you have the observed effects, but you still want to argue against what you've seen.

No, I'm just not sure that your explanation is correct, and I'm not sure you are either. I do thank you for your theory, and I did ask for theories, but we still don't know.

I don't use an excessive amount of benzos. I take only 1.0mg of Klonopin per day, 0.5 in the morning and 0.5 at night. You could call it excessive use of GABA drugs, especially the first time with Phenibut. I don't know if you really could the 2nd time with a lot of alcohol and a little bit of Klonopin.

I think we do know that its likely I'm not having "breakthrough seizures hidden by my Klonopin for years" because I actually was taken abruptly (and criminally I might add) off Klonopin cold turkey about 9-10 years back, and I didn't even have side effects which was odd. Certain people on here have also told me that what I experienced was NOT a seizure. I'm hoping they are correct. Wouldn't a seizure mean you were totally unconscious?

I'm not really into the comments about me "playing stupid games" lol. We all know most of us on here have done that, and I would guess you've probably done it with certain drugs yourself. I just wanted to understand more about exactly how bad what I did to myself was and also what drugs I would need to exclude in the future for it to not happen again.

If you still wanted to use SOME of the drugs in this equation, but not all of them, and you didn't want this to happen again, what combo would you use?

Because I don't want to have to quit drinking altogether, or weed, and I'd prefer to be able to use kratom from time to time. I am probably not going to use Phenibut again, or at least I know it's a bad idea. Most of all, I have a very hard time imagining life without EVER being able to drink.

 

[snmfmy]

No, I'm just not sure that your explanation is correct, and I'm not sure you are either. I do thank you for your theory, and I did ask for theories, but we still don't know.

I don't use an excessive amount of benzos. I take only 1.0mg of Klonopin per day, 0.5 in the morning and 0.5 at night. You could call it excessive use of GABA drugs, especially the first time with Phenibut. I don't know if you really could the 2nd time with a lot of alcohol and a little bit of Klonopin.

I think we do know that its likely I'm not having "breakthrough seizures hidden by my Klonopin for years" because I actually was taken abruptly (and criminally I might add) off Klonopin cold turkey about 9-10 years back, and I didn't even have side effects which was odd.

I'm not really into the comments about me "playing stupid games" lol. We all know most of us on here have done that, and I would guess you've probably done it with certain drugs yourself. I just wanted to understand more about exactly how bad what I did to myself was and also what drugs I would need to exclude in the future for it to not happen again.

If you still wanted to use SOME of the drugs in this equation, but not all of them, and you didn't want this to happen again, what combo would you use?

Because I don't want to have to quit drinking altogether, or weed, and I'd prefer to be able to use kratom from time to time. Most of all, I have a very hard time imagining life without EVER being able to drink.

But you did. You said you were using 10 mg a day at one point. And 10 mg of Klonopin a day is excessive.

It's quite obvious that regardless of the seizures you're not going to stop taking what you're taking.

So I don't even know why you're bothering to be concerned.

The fact that the Klonopin prevents the seizures significantly points to gaba involvement, specifically at the benzodiazepine binding site.

The Klonopin occupies the receptor and or pushes the kratom molecule off the receptor so it's action on the GABA receptor that was causing the seizures can't happen.

There is plenty of evidence that kratom lowers the seizure threshold in susceptible people. What this means is that if you have anything physiologically or pharmaceutically that could cause a seizure like activity, kratom lowers the threshold for that to happen. In other words, it makes it easier for the seizure activity to occur.

It's clear that's happening with you.

 

[Mycophile]

But you did. You said you were using 10 mg a day at one point. And 10 mg of Klonopin a day is excessive.

No I never said that. If I did it was a typo, but at no point did I ever take more than 2.0 mgs per day. So does that change your theory?

 

[snmfmy]

No I never said that. If I did it was a typo, but at no point did I ever take more than 2.0 mgs per day. So does that change your theory?

No because kratom lowers the seizure threshold.

That kind of even supports it somewhat.

Phenibut instigates tonic-colonic seizures at high doses and in susceptible people. So your use of phenibut is a variable that increases the likelihood of seizure.

The use of kratom at the same time lowers the threshold for that to occur, meaning it will occur at a lower dose than if you didn't take kratom.

Normally your klonopin would prevent the seizure activity, because Klonopin raises the seizure threshold, but when you don't have it, the seizure activity breaks through.

Stop taking the combination of phenibut and kratom.

But don't cold turkey because phenibut withdrawal causes seizures.

 

[Mycophile]

But you did. You said you were using 10 mg a day at one point. And 10 mg of Klonopin a day is excessive.

It's quite obvious that regardless of the seizures you're not going to stop taking what you're taking.

So I don't even know why you're bothering to be concerned.

The fact that the Klonopin prevents the seizures significantly points to gaba involvement, specifically at the benzodiazepine binding site.

The Klonopin occupies the receptor and or pushes the kratom molecule off the receptor so it's action on the GABA receptor that was causing the seizures can't happen.

There is plenty of evidence that kratom lowers the seizure threshold in susceptible people. What this means is that if you have anything physiologically or pharmaceutically that could cause a seizure like activity, kratom lowers the threshold for that to happen. In other words, it makes it easier for the seizure activity to occur.

It's clear that's happening with you.

I think you are sure that's what it is, but I don't know for sure you are right. I still appreciate your theory.

I never took more than 2.0mgs per day of Klonopin. I guess there could have been times I exceeded it slightly, but my highest prescribed dose was 2.0, and it hasn't been over 1.5 for a long time.

It's not obvious that I'm going to keep taking what I'm taking. I haven't used anything other than weed since this happened and I doubt I'll ever use Phenibut again, and I never used it much more than once a week so there's no concern of withdrawal.

But, for the sake of argument, if you still wanted to be able to drink but not have these EPISODES (I'm not sure they are seizures), do you think cutting out the Kratom would do it? Or could you take Kratom BY ITSELF another day. And/or if i had simply taken my Klonopin dose earlier do you think it wouldn't have happened? Afterall, it stopped the episode, so why wouldn't using it earlier prevent it?

 

[snmfmy]

I think you are sure that's what it is, but I don't know for sure you are right. I still appreciate your theory.

I never ever took more than 2.0mgs per day of Klonopin. I guess there could have been times I exceeded it slightly, but my highest prescribed dose was 2.0, and it hasn't been over 1.5 for a long time.

It's not obvious that I'm going to keep taking what I'm taking. I haven't used anything other than weed since this happened and I doubt I'll ever use Phenibut again.

But, for the sake of argument, if you still wanted to be able to drink but not have these EPISODES (I'm not sure they are seizures), do you think cutting out the Kratom would do it? And/or if i had simply taken my Klonopin dose earlier do you think it wouldn't have happened? Afterall, it stopped the episode, so why wouldn't using it earlier prevent it?

Like I said, I think it's the phenibut kratom combination.

Based on the evidence that's available, that's the most likely explanation. I think it's very unlikely that you have a seizure condition hidden by 2 mg of Klonopin a day.

I also don't think you're getting seizures from lowering your dose of Klonopin from 2 mg to 1 mg a day.

I also don't think that your alcohol consumption would predispose you to that kind of seizure, but I don't know. Have you had multiple alcohol withdrawals before? That's something that we didn't discuss.

 

[Mycophile]

Like I said, I think it's the phenibut kratom combination.

Based on the evidence that's available, that's the most likely explanation. I think it's very unlikely that you have a seizure condition hidden by 2 mg of Klonopin a day.

I also don't think you're getting seizures from lowering your dose of Klonopin from 2 mg to 1 mg a day.

I also don't think that your alcohol consumption would predispose you to that kind of seizure, but I don't know. Have you had multiple alcohol withdrawals before? That's something that we didn't discuss.

No, I've never had alcohol withdrawal before, which is what makes this so scary. I've had GABA rebound anxiety every time I drink, but never anything like these 2 episodes. And also, the 2nd episode the following week I didn't have any Phenibut at all, so it couldn't just be that combo. That is particularly why i was even more freaked out the 2nd weekend, because i wanted to prove to myself it wouldn't happen without the Phenibut, but it did, and the episode lasted longer than the 1st.

Do you think what happened could likely have killed me? I mean, I'm probably going to start freaking if you say it could have, but as long as I have access to Klonopin would I not be relatively safer? Or could I have simply died? And when I ask that, I mean not like "is it possible" but more "is it likely?"

 

[snmfmy]

No, I've never had alcohol withdrawal before, which is what makes this so scary. I've had GABA rebound anxiety every time I drink, but never anything like these 2 episodes. And also, the 2nd episode the following week I didn't have any Phenibut at all, so it couldn't just be that combo. That is particularly why i was even more freaked out the 2nd weekend, because i wanted to prove to myself it wouldn't happen without the Phenibut, but it did, and the episode lasted longer than the 1st.

Do you think what happened could likely have killed me? I mean, I'm probably going to start freaking if you say it could have, but as long as I have access to Klonopin would I not be relatively safer? Or could I have simply died?

Describe GABA rebound anxiety when you drink.

And secondly, we know phenibut can instigate seizures, we don't know how long the changes phenibut causes in the brain can induce that phenomena.

Although the fact that you didn't have phenibut, That doesn't discount involvement of the GHB subunit of gaba receptors as those are positively allosterically modulated by ethanol as well.

 

[Mycophile]

What are you talking about GABA rebound anxiety when you drink?

Yes, whenever I'm hungover I get rebound anxiety because I take Klonopin and we all know it's not the greatest idea to drink on Klonopin but it doesn't normally kill people. So if I get really drunk then I'm really anxious the next day while hungover, but these 2 times it was like that times 10.

I know it's from that because several years back when I was off Klonopin for 9 months I would drink and not get that anxiety when I was hungover, and actually Kratom REALLY helps with that rebound anxiety, which is even more why I find it odd the assertion that it caused the episodes.

 

[snmfmy]

Yes, whenever I'm hungover I get rebound anxiety because I take Klonopin and we all know it's not the greatest idea to drink on Klonopin but it doesn't normally kill people. So if I get really drunk then I'm really anxious the next day while hungover, but these 2 times it was like that times 10.

I know it's from that because several years back when I was off Klonopin for 9 months I would drink and not get that anxiety when I was hungover, and actually Kratom REALLY helps with that rebound anxiety, which is even more why I find it odd the assertion that it caused the episodes.

I don't understand. You say you get anxiety because you take Klonopin when you're hungover. That doesn't make any sense.

In fact, if you're on a steady dose of Klonopin, that anxiety is most likely because you have low blood sugar from drinking too much.

Ethanol doesn't deplete your GABA. It potentiates the currents at the GABA receptor and at the same time reduces currents at the NMDA glutamate receptors.

If you get anxiety after drinking it's because you have low blood sugar and maybe because your NMDA receptors are no longer inhibited.

If alcohol and kratom combined elicited seizure activity, why would you want to continue it?

 

[Mycophile]

Describe GABA rebound anxiety when you drink.

And secondly, we know phenibut can instigate seizures, we don't know how long the changes phenibut causes in the brain can induce that phenomena.

Although the fact that you didn't have phenibut, That doesn't discount involvement of the GHB subunit of gaba receptors as those are positively allosterically modulated by ethanol as well.

The GABA rebound anxiety is basically like the first time I wake up from drinking my heart is pounding really fast and I'd assume my blood pressure is elevated but I haven't checked. If/when I fall back to sleep and wake up again then the feeling will be significantly decreased. But beyond that, if the rebound anxiety continues, it is basically just excessive emotionality and more worrying than usual and also sometimes thinking about unpleasant things. Like I'm really interested in true crime and came across one case that is very upsetting. So recently when hungover I just kept thinking about what I'd read and watched on this true crime documentary, and I'll just be an anxious mess and very emotional and speedy. That's about it.

The less I drink and the more I sleep the better it is, and, as I mentioned, Kratom almost completely gets rid of the rebound anxiety during the 1st 4 hours. However, after that I'm still kind of on edge because those other stimulant alkaloids are present in my system. That's the point I was at both times these episodes happened: next day, still hungover, haven't yet taken 2nd dose of Klonopin, it's night time and the more pleasant effects of the Kratom have worn off and I was smoking weed and on edibles both times.

 

[snmfmy]

The GABA rebound anxiety is basically like the first time I wake up from drinking my heart is pounding really fast and I'd assume my blood pressure is elevated but I haven't checked. If/when I fall back to sleep and wake up again then the feeling will be significantly decreased. But beyond that, if the rebound anxiety continues, it is basically just excessive emotionality and more worrying than usual and also sometimes thinking about unpleasant things. Like I'm really interested in true crime and came across one case that is very upsetting. So recently when hungover I just kept thinking about what I'd read and watched on this true crime documentary, and I'll just be an anxious mess and very emotional and speedy. That's about it.

The less I drink and the more I sleep the better it is, and, as I mentioned, Kratom almost completely gets rid of the rebound anxiety during the 1st 4 hours. However, after that I'm still kind of on edge because those other stimulant alkaloids are present in my system. That's the point I was at both times these episodes happened: next day, still hungover, haven't yet taken 2nd dose of Klonopin, it's night time and the more pleasant effects of the Kratom have worn off and I was smoking weed and on edibles both times.

Low blood sugar.
Causes anxiety, tachycardia, etc. maybe some involvement from the kratom.

Well, THC will also give you anxiety and tachycardia.

 

[Mycophile]

I don't understand. You say you get anxiety because you take Klonopin when you're hungover. That doesn't make any sense.

In fact, if you're on a steady dose of Klonopin, that anxiety is most likely because you have low blood sugar from drinking too much.

Ethanol doesn't deplete your GABA. It potentiates the currents at the GABA receptor and at the same time reduces currents at the NMDA glutamate receptors.

If you get anxiety after drinking it's because you have low blood sugar and maybe because your NMDA receptors are no longer inhibited.

If alcohol and kratom combined elicited seizure activity, why would you want to continue it?

I don't take Klonopin because I'm hungover. I just take 0.5mgs each morning and each night because that's what I'm prescribed, but I'm drinking. There have been times I have skipped the nighttime dose when I drink, but it still happens, and it didn't happen during the 9 months I was off Klonopin when I'd drink, so I believe that's the cause.

I don't really understand neuroscience or this:

"Ethanol doesn't deplete your GABA. It potentiates the currents at the GABA receptor and at the same time reduces currents at the NMDA glutamate receptors. If you get anxiety after drinking it's because you have low blood sugar and maybe because your NMDA receptors are no longer inhibited."

HOWEVER...what I do know is that glutamate is in excess when you are hungover or coming down off a lot of gaba drugs. I could be wrong, but I have thought that low level glutamate surge is sort of the same thing as GABA rebound anxiety. Perhaps I'm using the term wrong. Negrogesic said that he'd refer to the FIRST episode as "glutamate surge with akisthisia", but he hasn't responded to this thread on the 2nd episode.

And I don't want to continue to use Kratom combined with alcohol if that caused it. It would be harder not to because I always find that Kratom really helps with that next day anxiety and really makes the hangovers tolerable, but if I really end up believing that was the cause then I won't take kratom the next day. I will most likely be avoiding it in the future and take it on separate days, but generally I've felt like kratom has been the best cure for hangovers...

 

[Mycophile]

Low blood sugar.
Causes anxiety, tachycardia, etc. maybe some involvement from the kratom.

Well, THC will also give you anxiety and tachycardia.

Interesting, but then why didn't it happen during the 9 months I was off Klonopin? I noticed that every time I drank during those 9 months my hangovers were less severe and I didn't get that anxiety.

 

[Skorpio]

I can't really answer most of those questions because I don't know what you're underlying health status is.
And I've been through alcohol withdrawal multiple times and I have never felt like I couldn't control my body temperature and with shivering.

As far as weather was a seizure or not, I really don't know if it was a true seizure. What you describe seem to be seizure like activity.

And If the mechanism in play is antagonism of GABA ergic signals meaning reducing the effect of GABA receptors on the brain, that would lead to seizure like activity.

I'm going to paste a citation below. In the paper it describes that kratom alkaloids agonize the mu opioid receptor and antagonize the kappa opioid receptor, apparently this antagonizes gabaergic function:


"Kratom was found to have a higher affinity towards the Kappa opioid receptors rather than the Mu and Delta receptors [7]. Chemically it acts as an agonist at the Mu receptors and an antagonist at the Kappa receptors. These effects lead to the inhibition of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter"

Life-Threatening Hyponatremia Secondary to Chronic Kratom Use: A Case Presentation

Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L. Severe hyponatremia is defined as a serum sodium concentration of less than 125 mEq/L and is a life-threatening complication that must be managed promptly to avoid irreversible ...

www.ncbi.nlm.nih.gov

I'm not really convinced by your source. That statement in the discussion has no citation, and the other about the kappa affinity comes from a review that doesn't mention any impingement on GABA receptors (and yeah I know that mu opioid receptors inhibit GABA neuron terminals in the VTA to increase dopamine release, but local effects on GABA don't equate to global effects). I tend to lend less credence to uncited statements in the discussion section of papers. If you can't infer it from the data or a cited paper, it's about as valid as a forum post here.

Although the fact that you didn't have phenibut, That doesn't discount involvement of the GHB subunit of gaba receptors as those are positively allosterically modulated by ethanol as well.

Do you have any sources showing phenibut having affinity for GHB receptors (also they are GPCRs and unrelated to either GABA A or GABA B receptors)?

@Mycophile

Considering that the common elements to your situations were missing a klonopin dose, a hangover, weed, and kratom, I would say that the hangover and missing a benzo are the most directly correlated with anxiety. I would certainly try and not miss a benzo dose if you drink heavily the day before, and avoiding kratom definately wouldn't hurt. Weed could also amplify any existing anxiety, so I would be careful of it when hung over.

When I refer to circuits, I refer to collections of neurons that link one after another in specific systems. I mentioned the VTA before, so I will use that as an example. The VTA has neurons which release dopamine onto the nucleus accumbens where it coordinates learning and assigning valence to rewarding situations. There are neurons that release GABA onto these dopamine releasing neurons to restrain normal dopamine release. These neurons have mu opioid receptors, and when an agonist binds at them, the mu opioid receptors inhibit the release of GABA, which allows for a larger release of dopamine. It is a circuit level change, as you would be hard pressed to say that mu opioid agonists widely suppress GABA signalling, but they do in the context of modulating the reward circuits.

The effects of a drug are restricted to neurons which have receptors for them. Many GPCRs will then only affect populations of neurons, even if the whole brain is flooded in an agonist.

 

[snmfmy]

I don't take Klonopin because I'm hungover. I just take 0.5mgs each morning and each night because that's what I'm prescribed, but I'm drinking. There have been times I have skipped the nighttime dose when I drink, but it still happens, and it didn't happen during the 9 months I was off Klonopin when I'd drink, so I believe that's the cause.

I don't really understand neuroscience or this:

"Ethanol doesn't deplete your GABA. It potentiates the currents at the GABA receptor and at the same time reduces currents at the NMDA glutamate receptors. If you get anxiety after drinking it's because you have low blood sugar and maybe because your NMDA receptors are no longer inhibited."

HOWEVER...what I do know is that glutamate is in excess when you are hungover or coming down off a lot of gaba drugs. I could be wrong, but I have thought that low level glutamate surge is sort of the same thing as GABA rebound anxiety. Perhaps I'm using the term wrong. Negrogesic said that he'd refer to the FIRST episode as "glutamate surge with akisthisia", but he hasn't responded to this thread on the 2nd episode.

And I don't want to continue to use Kratom combined with alcohol if that caused it. It would be harder not to because I always find that Kratom really helps with that next day anxiety and really makes the hangovers tolerable, but if I really end up believing that was the cause then I won't take kratom the next day. I will most likely be avoiding it in the future and take it on separate days, but generally I've felt like kratom has been the best cure for hangovers...

How do you know that glutamate is in excess?

The reason I ask this is because there's a lot of misinformation and disinformation going around.

Ethanol consumption leads to glutamine depletion. It also lowers the production of glutamate which is made from glutamine and possibly the production of GABA which is also made from glutamine.

There is a glutamine rebound several hours after drinking, this does not mean there is a 'glutamate rebound'.

And I'm I'm virtually certain that you did not have a glutamate surge with akathisia. That's a specific sequelae associated with antipsychotic medications that both increase the excess of glutamine in the brain as well as through dopaminergic action potentiates akathisia. It's not going to happen from having several drinks while taking a half a milligram of Klonopin morning and night.

There are plenty of other neurotransmitter systems that alcohol effects that lead to hangover anxiety, number one is actually serotonin, that combined with low blood sugar, and an electrolyte imbalance leads to the tachycardia, the anxiety, the shakiness, etc.

 

[snmfmy]

I'm not really convinced by your source. That statement in the discussion has no citation, and the other about the kappa affinity comes from a review that doesn't mention any impingement on GABA receptors (and yeah I know that mu opioid receptors inhibit GABA neuron terminals in the VTA to increase dopamine release, but local effects on GABA don't equate to global effects). I tend to lend less credence to uncited statements in the discussion section of papers. If you can't infer it from the data or a cited paper, it's about as valid as a forum post here.


Do you have any sources showing phenibut having affinity for GHB receptors (also they are GPCRs and unrelated to either GABA A or GABA B receptors)?

(Some)GHB receptors are simply a specialized subset of GABA A receptors:

α4βδ GABAA receptors are high-affinity targets for γ-hydroxybutyric acid (GHB)​

https://www.pnas.org/doi/full/10.1073/pnas.1204376109

Phenibut is a non-selective agonist of gaba, A receptors. Therefore it effects the same GABA receptors that GHB does.

Now if you're talking about the GHB receptor that is referred to as GPR172A, I don't have any data regarding that.

The paper describing GHB's affinity for alpha 4 subunit extra synaptic gaba receptors is often overlooked.

Of note is that gabapentin agonizes and also increases surface receptor expression in extra synaptic gaba receptors, but not presynaptic receptors.

 

[Mycophile]

I'm not really convinced by your source. That statement in the discussion has no citation, and the other about the kappa affinity comes from a review that doesn't mention any impingement on GABA receptors (and yeah I know that mu opioid receptors inhibit GABA neuron terminals in the VTA to increase dopamine release, but local effects on GABA don't equate to global effects). I tend to lend less credence to uncited statements in the discussion section of papers. If you can't infer it from the data or a cited paper, it's about as valid as a forum post here.


Do you have any sources showing phenibut having affinity for GHB receptors (also they are GPCRs and unrelated to either GABA A or GABA B receptors)?

@Mycophile

Considering that the common elements to your situations were missing a klonopin dose, a hangover, weed, and kratom, I would say that the hangover and missing a benzo are the most directly correlated with anxiety. I would certainly try and not miss a benzo dose if you drink heavily the day before, and avoiding kratom definately wouldn't hurt. Weed could also amplify any existing anxiety, so I would be careful of it when hung over.

When I refer to circuits, I refer to collections of neurons that link one after another in specific systems. I mentioned the VTA before, so I will use that as an example. The VTA has neurons which release dopamine onto the nucleus accumbens where it coordinates learning and assigning valence to rewarding situations. There are neurons that release GABA onto these dopamine releasing neurons to restrain normal dopamine release. These neurons have mu opioid receptors, and when an agonist binds at them, the mu opioid receptors inhibit the release of GABA, which allows for a larger release of dopamine. It is a circuit level change, as you would be hard pressed to say that mu opioid agonists widely suppress GABA signalling, but they do in the context of modulating the reward circuits.

The effects of a drug are restricted to neurons which have receptors for them. Many GPCRs will then only affect populations of neurons, even if the whole brain is flooded in an agonist.

Thanks for responding. I can't say I really understand exactly what your saying with the neuroscience here. Maybe I'd have to read it over a few times and look this stuff up to get it.

But I had already planned on avoiding Phenibut MAYBE forever, at the very least for a long time, but I think it's better off if I don't use it, and I totally agree on not missing my 2nd klonopin dose and avoiding weed the next day. I have generally found that weed makes me very anxious when hungover. I do love how Kratom USUALLY makes me feel better when hungover, but at the very least I will avoid that next time.

Is there anything about these 2 scenarios that leads you to believe I would have to quit drinking altogether? Because that is what would overall be the hardest to do, and I really don't want to have to give up alcohol forever. I just know these episodes freaked me out and I don't want them to happen again.

 

[Mycophile]

How do you know that glutamate is in excess?

The reason I ask this is because there's a lot of misinformation and disinformation going around.

Ethanol consumption leads to glutamine depletion. It also lowers the production of glutamate which is made from glutamine and possibly the production of GABA which is also made from glutamine.

There is a glutamine rebound several hours after drinking, this does not mean there is a 'glutamate rebound'.

And I'm I'm virtually certain that you did not have a glutamate surge with akathisia. That's a specific sequelae associated with antipsychotic medications that both increase the excess of glutamine in the brain as well as through dopaminergic action potentiates akathisia. It's not going to happen from having several drinks while taking a half a milligram of Klonopin morning and night.

There are plenty of other neurotransmitter systems that alcohol effects that lead to hangover anxiety, number one is actually serotonin, that combined with low blood sugar, and an electrolyte imbalance leads to the tachycardia, the anxiety, the shakiness, etc.

Hmmm, well I really don't know.

Negrogesic said that the first episode was very much like one he had where etizolam made it go away, another benzo, just like Klonopin made mine go away.

The first episode, which you might not have read about, simply lasted a few minutes where I was smoking weed, suddenly felt something was wrong as if I wasn't safe inside my own body (akisthesia seems to fit that description when I looked it up) and like i couldn't sit still. Then I got cold and started shivering a little, lay down in bed, my feet started shaking, and then I feel asleep, all within a few minutes. So that's the one that Negrogesic called "glutamate surge with akisthisia."

I don't understand what you mean here at all: "There is a glutamine rebound several hours after drinking, this does not mean there is a 'glutamate rebound'."

What are you saying here?

I read that glutamate is essentially the opposite of GABA, and that overuse of GABA drugs causes you to get those great relaxing feelings we get from alcohol, phenibut, benzos, etc, and then the next day GABA is depleted and its opposite, glutamate, surges, causing anxiety.

Skorpio: Am I correct about that, or am I missing something?

However, Snmfy, you could be right about it being something else that makes me anxious when hungover. I really don't know, and i don't know why it wouldn't have to do with GABA or glutamate, seeing as when I wasn't on Klonopin that stuff didn't happen when i was hungover. I don't know if Klonopin really affects serotonin and the other stuff so much. Maybe it does.

Sucks cause this is the best I can get, different theories from different people who know more than me, but I just can't be sure what's true.

A doctor would just say "don't be stupid, just don't do any of those drugs again, or at least not in combo", but I'd be lying if I said I'm not going to at least drink and smoke weed, and I have always found Kratom to actually be good for hangovers.

If you DO happen to be right it wouldn't be the worst thing in the world cause i think it just essentially means that if I don't do Kratom when hungover or mix kratom and phenibut than this probably won't happen. I do love the kratom/Phenibut combo, but this was bad enough I'll avoid it if necessary, and I can get through hangovers without Kratom.

I think what I'll do is wait a while, then have one night where I do get drunk again, but then the next day take NOTHING recreational, no kratom, no weed, just my prescribed Klonopin and not miss the 2nd dose. My guess is that it won't happen then.

Let me ask you though, does any of this make you think I need to quit drinking permanently?

 

[snmfmy]

Yes and no.

Glutamic acid, also called glutamate which is the ionized version of glutamic acid, is made from the amino acid glutamine. The body can also synthesize glutamic acid directly in small amounts.

Gaba is actually made from glutamate.

So when you supplement with glutamine, glutamate, Even MSG, You're providing the basic building block for both gaba and glutamate.

GABA does not get depleted by positive allosteric modulators like ethanol or benzodiazepines, because they don't cause the release of gaba, they just make the receptors work more efficiently and strongly when gaba does hit them.

However, ethanol is a serotonin and norepinephrine and dopamine releaser. So the hangover anxiety that you're experiencing if it's the result of neurotransmitter depletion would be because of serotonin dopamine and norepinephrine deficit.

Yes, an alcohol hangover is similar to the post adrenaline surge depression that you get after the fight or flight response.

Ethanol also severely impairs insulin metabolism and therefore glucose metabolism. So you have ridiculously unmanaged blood sugar which can make you feel like ass. Which is why forcing yourself to eat a greasy protein and sugar-filled breakfast makes you feel better during a hangover.