5-MeO-DALT causing neurotoxicity: hospitalization, catatonia, & seizures

[endotropic]

I'm not "worried about loosing my buzz", I'm a pharmacologist who works with etizolam and 5-MeO-DALT as part of my job. I'm sorry that you had a bad reaction but your conduct is extremely reckless. So now eventually it will be 10 times as hard to purchase etizolam and 5-MeO-DALT for studies. And probably 90% of the potential research projects with etizolam or 5-MeO-DALT will never happen if they are scheduled, so some interesting questions will never be answered.

As a scientist apparently working within the drug abuse field I'm surprised how readily you condemn an individual clearly suffering from a drug dependence. You realize the event that will restrict your access to these chemicals requires two players right? First the user that overdoses and dies, then the regulators who start the emergency scheduling protocol. If you get mad at the overdosing drug user in that scenario then I actually feel bad for you.

No one can control what a drug user does or doesn't put into their body, decades of failed prohibitionist policies have proven that beyond a shadow of a doubt. That means we need to concentrate on changing the other side of that equation.

 

[serotonin2A]

This report was primarily about 5-MeO-DALT, and that substance isn't addictive. So it's not like he lost control over his ability to ingest 5-MeO-DALT. Sometimes when people loose control of their drug intake bad things happen, and unfortunately the outcome is still their responsibility. I'm not saying he set out to cause the events that this will help to set in motion, but he still bears some blame. It's not any different then getting in an accident while drinking and driving.

If you think I'm getting mad at an "overdosing drug addict" then you are not hearing what I am saying. I'm not saying he was reckless to use etizolam or to use 5-MeO-DALT. But I am saying that he was reckless to combine such an extremely high dose benzodiazepine addiction with a drug like 5-MeO-DALT. It is just inherently dangerous to do that.

 

[endotropic]

This report was primarily about 5-MeO-DALT, and that substance isn't addictive. So it's not like he lost control over his ability to ingest 5-MeO-DALT. Sometimes when people loose control of their drug intake bad things happen, and unfortunately the outcome is still their responsibility. I'm not saying he set out to cause the events that this will help to set in motion, but he still bears some blame. It's not any different then getting in an accident while drinking and driving.

I agree that he's responsible for his own medical situation, what happened after that was really out of his control. This smells like an ambitious doctor trying to get his name out in a neurology journal with some sexy unknown drug. Let's see how much emphasis the final report puts on the etizolam before we jump to any conclusions though.

As long as odure provided his physicians with all of the relevant information I find it hard to fault him for how they interpreted the situation. It's really the doctor's responsibility to determine what led up to those events at that point.

 

[serotonin2A]

I really have to disagree. It wasn't like he woke up and took his daily dose of etizolam, took too much, and woke up in the hospital. This isn't a case where he thought he was buying etizolam and someone sold him 5-MeO-DALT. His use of 5-MeO-DALT didn't happen by mistake. If he had just overdosed, or simply had a bad reaction to one of the drugs then that would have simply been an accident. But at some point, all of his actions, taken together, start to look reckless to me.

 

[St3ve]

I think many people here would anticipate that combining 40 mg/day etizolam with 5-MeO-DALT could easily produce a bad outcome.

By what mechanism would huge amounts of etizolam and 5 meo dalt cause the series of events reported by the OP? As far as I know there's absolutely no published data on 5-meo-dalt's pharmacodynamics. You could reasonably assume it might cause problems when taken during benzo withdrawal, anything other than another tranquilizer could cause all sorts of hyperactivity in the brain leading to convulsions, etc. But I don't really see how it would cause problems if taken on the usual amount of etizolam.

 

[serotonin2A]

By what mechanism would huge amounts of etizolam and 5 meo dalt cause the series of events reported by the OP? As far as I know there's absolutely no published data on 5-meo-dalt's pharmacodynamics. You could reasonably assume it might cause problems when taken during benzo withdrawal, anything other than another tranquilizer could cause all sorts of hyperactivity in the brain leading to convulsions, etc. But I don't really see how it would cause problems if taken on the usual amount of etizolam.

40 mg/day is an extremely high dose of etizolam, probably equivalent to 400 mg/day of diazepam. Anyone on such a high dose needs to be extremely cautious about taking any other substances, especially something like 5-MeO-DALT where the pharmacology is almost completely unknown. 5-MeO-DALT could be a weak GABA-A antagonist, either directly or indirectly. Etizolam may also have some off-target serotonergic effects that may not be manifest unless it is taken at an extremely high dose, and that could cause an interaction with 5-MeO-DALT. The fact is that anyone taking a high dose of a benzodiazepine needs to be extremely carefull when they take other drugs, because they are much more likely to experience an adverse drug interaction.

If someone dependent on a high dose of etizolam or another benzodiazepine ends up loosing consciousness for some reason and is hospitalized, they could easily end up having seizures, because the doctors wouldn't know that the patient would eventually lapse into withdrawal without intervention. And comatose patients are sometimes treated with naloxone or flumazenil, which could contribute to seizures. These are things that someone taking hight doses of benzodiazepines needs to understand and mitigate.

I'm not trying to be insensitve, because the OP had a horrible experience, and paid a terrible price. But I think he was irresponsible and I'm going to call him out for that.

 

[AlphaOdure]

By what mechanism would huge amounts of etizolam and 5 meo dalt cause the series of events reported by the OP? As far as I know there's absolutely no published data on 5-meo-dalt's pharmacodynamics. You could reasonably assume it might cause problems when taken during benzo withdrawal, anything other than another tranquilizer could cause all sorts of hyperactivity in the brain leading to convulsions, etc. But I don't really see how it would cause problems if taken on the usual amount of etizolam.

This is exactly my conundrum... and why I am perplexed.

I had tripped numerous amounts of times, in higher doses, when dependent upon etizolam; carisoprodol; & barbiturates (from 2008/2009 till Oct 31 2014; well started my taper Sept 31, completely off all GABAergics--well except for low doses of phenibut--as of my lorazepam taper concluded Oct 31 2014). I even used it out of the same batch while on these high doses of etizolam. And i was stabilized at this level for some time, 40mg/day etizolam (again, stressing I am no longer dependent, thank god).

 

[AlphaOdure]

40 mg/day is an extremely high dose of etizolam, probably equivalent to 400 mg/day of diazepam. Anyone on such a high dose needs to be extremely cautious about taking any other substances, especially something like 5-MeO-DALT where the pharmacology is almost completely unknown. 5-MeO-DALT could be a weak GABA-A antagonist, either directly or indirectly. Etizolam may also have some off-target serotonergic effects that may not be manifest unless it is taken at an extremely high dose, and that could cause an interaction with 5-MeO-DALT. The fact is that anyone taking a high dose of a benzodiazepine needs to be extremely carefull when they take other drugs, because they are much more likely to experience an adverse drug interaction.

If someone dependent on a high dose of etizolam or another benzodiazepine ends up loosing consciousness for some reason and is hospitalized, they could easily end up having seizures, because the doctors wouldn't know that the patient would eventually lapse into withdrawal without intervention. And comatose patients are sometimes treated with naloxone or flumazenil, which could contribute to seizures. These are things that someone taking hight doses of benzodiazepines needs to understand and mitigate.

I'm not trying to be insensitve, because the OP had a horrible experience, and paid a terrible price. But I think he was irresponsible and I'm going to call him out for that.

Well if you're supposedly a pharmacologist as you claim.. that must resort to shady means to obtain "research chemicals", maybe you should change your trade. I'd be interested in some insight nonetheless rather than the drugs are bad argument, b/c bluelight is here for harm reduction, we're all aware 40-80x the introductory dose of something isn't good. But BL & harm reduction should be about warning of specific instances such as these, case study or not. I don't see how possibly dissuading people from posting similar experiences does any good.

And, as stated, I had used 5-MeO-DALT, miprocin, iprocin, psilocybe mushrooms, DALT, 2c-c, and many other psychedelics during this time--and at higher doses--w/o any adverse effect.

 

[chaos_destroy]

And, as stated, I had used 5-MeO-DALT, miprocin, iprocin, psilocybe mushrooms, DALT, 2c-c, and many other psychedelics during this time--and at higher doses--w/o any adverse effect.

Then how can you (or the doctors) be so sure the 5-MeO-DALT caused this then? Not saying its not at least part to blame but it seems like a common theme in a lot of drug horror stories you read involve some daily massive dose of some other drug that apparently played no part in it.

You said you took 60mg but also say you have no recollection of taking it so how do you know how much you took? Was it taken orally? Had you taken it orally or snorted before from the same batch? nBMeO's would likely be active in their parental 2c compound dose range orally but snorted would be much more potent. Could you have been sold a nBMeO by mistake? Maybe this time you snorted some?

 

[serotonin2A]

Well if you're supposedly a pharmacologist as you claim.. that must resort to shady means to obtain "research chemicals", maybe you should change your trade. I'd be interested in some insight nonetheless rather than the drugs are bad argument, b/c bluelight is here for harm reduction, we're all aware 40-80x the introductory dose of something isn't good. But BL & harm reduction should be about warning of specific instances such as these, case study or not. I don't see how possibly dissuading people from posting similar experiences does any good.

And, as stated, I had used 5-MeO-DALT, miprocin, iprocin, psilocybe mushrooms, DALT, 2c-c, and many other psychedelics during this time--and at higher doses--w/o any adverse effect.

We don't buy pharmacological agents from research sites, but when chemicals are controlled, it makes it much more difficult to actually perform research. We either have to buy them or make them, and control status adds immensely to the paperwork and price. And if the agents become scheduled then there are many scientists who won't be able to work with the substances.

I never said that you shouldn't post about your experience. But that doesn't mean that I can't give my opinion. You almost got yourself killed and your actions have potentially harmed other people.

 

[AlphaOdure]

Then how can you (or the doctors) be so sure the 5-MeO-DALT caused this then? Not saying its not at least part to blame but it seems like a common theme in a lot of drug horror stories you read involve some daily massive dose of some other drug that apparently played no part in it.

You said you took 60mg but also say you have no recollection of taking it so how do you know how much you took? Was it taken orally? Had you taken it orally or snorted before from the same batch? nBMeO's would likely be active in their parental 2c compound dose range orally but snorted would be much more potent. Could you have been sold a nBMeO by mistake? Maybe this time you snorted some?

Because 60mg was all that was left. And i never snorted psychedelics--well at least in the last 10 years of my use. I most likely used it how I used the rest of the batch--intramuscularly, and w/ no such side effects w/ the prior uses (and an empty baggy was found, i'm guessing the plastic bag in which the 5-meo-dalt was in). I agree, its probably some sort of combination. But I seem to suspect 5-meo-DALT b/c GABAergics were the one thing that were commonplace for the last 5-6 years on a daily basis for me and I had no such side effect. I was curious about some sort of pharmacodynamical interaction I'm not yet aware of--and or if anyone had a similar experience as I did, but it seems i'm still at square one..

 

[atara]

Nobody really knows what causes seizures. It is hard to discount the cumulative effect of long-term etizolam abuse in evaluating your susceptibility, but...

I have no idea how I got there, no memory of taking the 5-meo-DALT

We just don't know. Anywho, the fact that you were on high doses of barbiturates prior to etiz serves mostly to reinforce the theory that some cumulative effect of sedative abuse made you more susceptible to seizures. The effect of GABAergic abuse is cumulative rather than acute; the drugs cause long-term changes in brain structure:

http://en.wikipedia.org/wiki/Effects_of_long-term_benzodiazepine_use#Mental_and_physical_health
http://www.benzo.org.uk/ashbzoc.htm

But this is far afield from my realm of experience.

http://en.wikipedia.org/wiki/Epileptic_seizure#Mechanism

Normally brain electrical activity is non synchronous. In epileptic seizures, due to problems within the brain, a group of neurons begin firing in an abnormal, excessive, and synchronized manner. This results in a wave of depolarization known as a paroxysmal depolarizing shift.

Normally after an excitatory neuron fires it becomes more resistant to firing for a period of time. This is due in part from the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine. In epilepsy the resistance of excitatory neurons to fire during this period is decreased.[10] This may occur due to changes in ion channels or inhibitory neurons not functioning properly. This then results in a specific area from which seizures may develop, known as a "seizure focus".[10] Another cause of epilepsy may be the up regulation of excitatory circuits or down regulation of inhibitory circuits follow an injury to the brain. These secondary epilepsies, occur through processes known as epileptogenesis. Failure of the blood–brain barrier may also be a causal mechanism

The primary function of benzodiazepines is to increase the sensitivity of the inhibitory chloride ion channel linked to the GABA receptor type A. When these receptors are overstimulated, the brain tries to decrease both the number of such ion channels and their sensitivity, producing tolerance. It also increases the availability of stimulating glutamate receptors.

The effect of psychedelics is to increase the sensitivity of certain excitatory receptors in the prefrontal cortex. Normally these receptors are triggered in response to novelty, but on a psychedelic they are triggered much more readily. The subject perceives things as being novel, leading to both an appreciation of everyday life (I'm lucky just to live in a world where avocados exist) and disillusion with coping mechanisms, which stop functioning as coping mechanisms and seem like independent phenomena (on LSD you'll drink the whisky slowly and think about how much it's hurting you). This happens because the signalling cascade is activated more easily.

Normally, the brain is kind of disorganized, not in sync. But when you take a drug, it affects the whole brain, at once, because it bypasses the normal mechanisms that control neurotransmitter levels -- that's why our favorite drugs are the ones that penetrate the blood-brain barrier, which turns out to be there for a reason. This is itself a sort of synchronization. Especially if the drug is snorted, or otherwise administered rapidly (smoking, injection), in which case the brain undergoes the infamous "rush". It's probably not good to get a rush if you've already drained your psychic brake fluid.

My layperson interpretation is that the seizure starts like hydroplaning: as long as some tiny shred of the brain is still touching the proverbial Earth, it functions as an anchor. But once you cross a sort of "threshold", the car lifts further off the road as water is forced under the tire. And if you have no brakes... hardcore benzo addicts probably shouldn't take stimulants. You get unlucky, then you're wrapped around a tree... you were at risk of a seizure for years, but that's just it, at risk. It happens or it doesn't. My understanding is that a whole lot of drugs can be a trigger: LSD, methamphetamine, et cetera.

As for the duration of the seizure, a likely story is the extent of damage you had already done to yourself.

 

[serotonin2A]

There is a process called kindling, where the threshold for seizure induction progressively decreases over time. PTZ is a GABA antagonist that induces seizures, and psychiatrists actually used to give it to mental patients. Think of it like ECT without those high electric bills! There are doses of PTZ that are too low to induce seizures, but over time, treatment with a low dose can also induce seizures. In a way, it is a sensitization of the glutamatergic system. The Glu system is involved in learning and synaptic plasticity, and for kindling I guess you could describe it as the Glu system being trained to generate seizures.

Glutamate is an excitatory transmitter, and most connections between neurons are glutamatergic. There is a lot of potential for excitation getting out of control because many glutamate neurons that are interconnected. So if cortical neuron A starts firing excessively then it's neighbors may also, and those neurons then can provide additional excitatory input to neuron A. Luckily, glutamate doesn't normally cause seizures because it also excites GABAergic neurons, which tends to offsets the excitation. But if there is less activation of GABA neurons and/or GABA-A receptors then you start to loose that inhibition, and that can causes seizures.

Psychedelics increase glutamate neurotransmission, but they also increase GABA, so they produce a balanced excitation. That's why psychedelics don't normally produce seizures even though they activate the glutamate system. But it is becoming more apparent that at least some psychedelics, such as 25I-NBOMe, can produce seizures at high doses. There have been a few cases where LSD use precipitated a seizure, and it may be that a kindling-like process was involved in those rare cases. Likewise, in this situation, the GABA system could have been dysregulated by chronic etizolam/barbiturate use, and that may predispose someone to seizures induced by 5-MeO-DALT.

 

[St3ve]

Generally seizures can broadly be explained as an imbalance between inhibitory and excitatory systems. The CA3 region in the hippocampus seems to be a particularly likely place for people with epilepsy for seizures to start. It's filled with recurrant connections and thought to make random associations between various stimuli in the creation of episodic memory. These recurrant connections means that through a series of synapses individual neurons can stimulate themselves through positive feedback. Normally if a loop gets out of control inhibitory interneurons become increasingly active and stop the loop. Only when the exctitation gets out of control does a seizure start. It can be a focal one (limited to a specific area), or if the focal seizure expands cause a generalized tonic-clonic seizure. During the tonic phase people generally tense up a lot (excitation dominant), in the clonic phase muscle spasming occurs (this is the inhibitory neurons regaining balance).

We can probably assume that 5-MeO-DALT like other psychedelics is gonna bind to serotonin receptor subtypes. We can only speculate on which ones though, and it might be a releasing agent for all we know as well... Most of the 5-HTR subtypes tend to facilitate cell excitation though, only a few cause an inhibitory effect.

So,I could see how taking something like 5-MeO-DALT during benzo withdrawal could lead to hyperexcitability and seizures. When benzos are taken chronically they will cause changes in the brain while it re-establishes homeostasis. I'd expect that as long as the usual dose is taken your excitation-inhibition balance would be close to normal and you wouldn't get seizures from something like 5-MeO-DALT.

I suppose the excessive use of downers by the OP might've caused very drastic changes that would amplify the effect of a neurostimulant and lead to a risk of seizures...

 

[AlphaOdure]

Just to refine some of my original information on dosages. I originally stated I used 40mg of etizolam a day; i recently came across some documents where I kept records of my buying practices & it appears as if i was actually going through about 125mg of etizolam a day. Wow. I'm surprised i'm still breathing.