NeighborhoodThreat
Bluelight Crew
oh, silly Richmonders.
-
DPMC Moderators: tryptakid
Kids overdosing on new drug (25I-NBOMe)
- Thread starter 23536
- Start date
BananasAndOranges
Bluelighter
- Joined
- Mar 25, 2010
- Messages
- 1,982
I am very shocked! Who the Fuck gives a real friend a damn research chemical for their first time tripping, Knowing he isnt even into drugs, and one hit of dank would get him toasted. I hope everyone reads this fucking thread. WAKE THE FUCK UP!!! All these chemicals are dangerous as fuck. Im so sick of hearing about reliable sources. Heres something a lot of you may want to knpw. Some of these vendors do not care about you. How many bad reports will it take. This is seriously Annoying to read. Your reliable sources are not reliable. Wake Up. Don't Ever give light weights a fucking research chemical. This is pure stupidity and I Really hope this dudes OK. So Fucked.
HofmannBlotter
Bluelighter
Yes it's indeed very sad to read 
I don't think it's the fault of the 25i-NBOMe, but it can be an allergic reaction to the compounds. Don't know ! I also have many experiences with 25i-NBOMe from a reliable source. It was always amazing and felt clean on the body. But who's knows what can happens...
I don't think it's the fault of the 25i-NBOMe, but it can be an allergic reaction to the compounds. Don't know ! I also have many experiences with 25i-NBOMe from a reliable source. It was always amazing and felt clean on the body. But who's knows what can happens...
are the brain bleedings confirmed to be true ? i wonder about the dosages too ?
why does the reporter say it can be snorted&smoked its like telling "go do a fat line of this shit" and why can't she lose the smile of her face?!
the trip report was scary too... wierd
why does the reporter say it can be snorted&smoked its like telling "go do a fat line of this shit" and why can't she lose the smile of her face?!
the trip report was scary too... wierd
rocknroll702
Bluelighter
really sad for that kid - this has sparked several forums to stop allowing 25i to be spread and offered for the reason being that now it will be gaining so much media attention and most likely asoon to follow ban.
VisualMagic
Bluelighter
The brain bleeding really throws me off, Feels really sensationalist to me. The same thing has been said about LSD and mushrooms. not saying it isn't possible though, just dont understand it. I feel that if dosed properly it's a relatively safe drug. I've had two wonderful experiences at 550ug and 1mg sub lingual. I do think that smoking this is potentially awful for you though, all the unknown carcinogens going into your body and the whatnot.
I felt major brain frying near the end of the trip, most 'fried' ive ever been in my life. So hard to concentrate and think but it goes away as you go more and more back to baseline. This must do something not so good to the brain as it definatley didn't feel healthy
ebola?
Bluelight Crew
Nothing in the report indicates that anyone's brain bled. Why are we even talking about this?
...
My best guess would be that this was an allergic reaction, but this compound is not particularly well researched, so who knows?
ebola
...
My best guess would be that this was an allergic reaction, but this compound is not particularly well researched, so who knows?
ebola
VisualMagic
Bluelighter
The brain bleeding is from the article linked after the report
http://www.nbc12.com/story/16964534/...ng-on-new-drug
http://www.nbc12.com/story/16964534/...ng-on-new-drug
twelvesevndi
Bluelighter
- Joined
- Jan 21, 2011
- Messages
- 481
yeah the article says that the ambulance crew "has learned [that] two of the patients actually had bleeding in the brain after overdosing."
alright well how was this diagnosed? were there CT scans? did the kids have a stroke?
also, the bio-chemistry "expert" Lt. Reese claims she has "heard of one documented case of a patient going into heart failure after overdosing on 25i."
ah yes. documented but somehow completely unknown outside of rumor.
to be fair tho she does seem like a psychopharmacology whiz:
"It's an experimental drug that was being used to research the path of brainwaves with stimulation,"
i don't have any evidence to contradict this story. but it seems like complete drivel.
Last edited:
atara
Bluelighter
This is very weird.
"We" -- not me -- have looked over the binding profile of 25x-NBOMe several times. Long story short, it binds 5-ht2a almost exclusively, 5-ht2c 10x less, mu1 100x less, 5-ht6 100x less:
5-ht2a affinity is subnanomolar, somewhere around 0.3 nM.
As it stands the only thing separating the NBOMe drugs from LSD w.r.t action is: LSD has affinity also at 5-ht1a, 5-ht2c, 5-ht5, 5-ht6, but the absence of this action is likely not too dangerous; however: 25x have potentially much higher intrinsic activity at 5-ht2a than the classical LSD, psilocin, 2C-B, mescaline, comparable instead to DOI, Br-DFLY, etc, and these drugs are indeed more dangerous. LSD is additionally functionally selective at 5-ht2a, preferring arachidonic acid release over phospholipase C activation; I don't know anything about functional selectivity of other ligands, except that DOI is not selective.
There is one other possibility: classical psychedelics have an uncharacteristically high therapeutic index (safety) w.r.t. other similarly powerful recreational drugs, and the "safe" drugs seem to consistently have higher 5-ht1a affinity than others. This includes in particular psilocin, mescaline, LSD, DMT, DPT, MDMA, all 4-HO tryptamines, but does not include any 2C-x, DOx, 25x, etc. 5-ht1a may play a protective role in the effects of the former class of drugs. In particular are 5-ht1a agonists considered serenic, antipsychotic, and empathogenic; this includes cannabidiol, the anxiolytic buspirone, and the antidepressant/hypnotic trazodone. Indeed, DOM, which was the first psychedelic to cause really scary overdoses back in 1969, also lacks any significant 5-ht1a affinity.
In particular, a very intelligent acquaintance had at one point suggested that bronchoconstriction -- which includes shortness of breath and blue lips -- represented a possible risk w.r.t. overdoses on potent 5-ht2a full agonists. I commented at the time that this seemed unlikely, because bronchoconstriction is not seen in serotonin syndrome, which rather includes hyperventilation and hyperthermia (serotonin is a 5-ht2a full agonist obviously), and those in SS do not turn blue.
It appears that I spoke too soon. Turning blue should indicate oxygen depletion (there are other possibilities: methæmoglobinemia). If 5-ht1a is indeed protective, this would explain why users of very high doses of LSD, psilocin, ayahuasca, and mescaline do not have trouble breathing, and why serotonin syndrome does not seem to cause this, but also why Br-DFLY does produce this very undesirable side-effect.
A theory is not complete without errors. The problematic 5-MeO-x tryptamines all have significant affinity at 5-ht1a, which demonstrates that it no guarantor of safety. In one case:
This is consistent with the inflammatory hypothesis suggested by the nameless one. Lots of lung damage, in fact. Except the last symptom, which seems more likely a result of a condition known as "being fucked in the ass". What is really confusing here is that 5-MeO-DiPT is actually a rather weak 5-ht2a agonist, instead having more activity at 5-ht1a.
So there are a couple of acceptable hypotheses:
(1) overdose on NBOMe's causes effects resulting from as-yet-unknown binding to some other, non-psychedelic receptor.
(2) full agonists at 5-ht2a can produce a dangerous inflammatory response, but partial agonists do not; 5-ht1a activity is a red herring
(3) 5-ht1a partially protects from 5-ht2a-mediated inflammatory response and:
(3a) can produce an inflammatory response on its own; there is a necessary, natural "balance" of activity at these receptors
(3b) overdose on 5-MeO-tryptamines results from other, unrelated effects
(4) functional selectivity at 5-ht2a allows LSD, psilocin, et al a wider safety margin: LSD in particular is selective for arachidonic acid release at 5-ht2a over activation of phospholipase C, whereas DOx effects both sorts of activity.
(1) seems unlikely; (2), (3a), (3b), and (4) all seem certainly possible, but I don't really know enough to prefer any of them over the others.
At this point it would be premature and extremely reckless to assume 5-ht1a agonists can protect from the damaging effects of 25x overdoses.
What I don't know is: are psilocin and mescaline also functionally selective in the manner of LSD? That would be enough to confirm or rule out (4). I also don't know about the intrinsic activity of psilocin at 5-ht2a, which would confirm or rule out (2). LSD is almost a full agonist w.r.t. arachidonic acid, but a weak partial agonist w.r.t. phospholipase C. So (2) is already on shaky ground.
In particular (4) implies that TCB-2, which is selective for phospholipase C activation, could be very dangerous.
(3a) and (3b) are wildcards: if 5-ht1a plays a major role, things get confusing and hard to verify, especially because precisely what relative activity is safe at 5-ht2a and 5-ht1a is not clear, and finding compounds which have this mix of activity is much harder than finding agonists of a single receptor.
In the meantime: 500 micrograms is probably too high of a starting dose for 25x. The bioavailability of 25x is very inconsistent: they are up to five times as potent by inhalation, and some people may absorb the drugs easier than others, leading to an unexpectedly powerful dose in the bloodstream. To compensate for this, start small, work your way up, and use a consistent dosing method, i.e. don't switch from sublingual to liquid insufflation once you've found a level you like. Caution is advisable for anyone with a history of asthma.
My guess is that vaporization and maybe liquid insufflation have a consistently higher bioavailability than other non-injection methods. I seemed to need less via liquid insufflation than others did sublingually: my use of 25C never exceeded 550 micrograms, and I hit a +3 at 250 micrograms.
"We" -- not me -- have looked over the binding profile of 25x-NBOMe several times. Long story short, it binds 5-ht2a almost exclusively, 5-ht2c 10x less, mu1 100x less, 5-ht6 100x less:
5-ht2a affinity is subnanomolar, somewhere around 0.3 nM.
As it stands the only thing separating the NBOMe drugs from LSD w.r.t action is: LSD has affinity also at 5-ht1a, 5-ht2c, 5-ht5, 5-ht6, but the absence of this action is likely not too dangerous; however: 25x have potentially much higher intrinsic activity at 5-ht2a than the classical LSD, psilocin, 2C-B, mescaline, comparable instead to DOI, Br-DFLY, etc, and these drugs are indeed more dangerous. LSD is additionally functionally selective at 5-ht2a, preferring arachidonic acid release over phospholipase C activation; I don't know anything about functional selectivity of other ligands, except that DOI is not selective.
There is one other possibility: classical psychedelics have an uncharacteristically high therapeutic index (safety) w.r.t. other similarly powerful recreational drugs, and the "safe" drugs seem to consistently have higher 5-ht1a affinity than others. This includes in particular psilocin, mescaline, LSD, DMT, DPT, MDMA, all 4-HO tryptamines, but does not include any 2C-x, DOx, 25x, etc. 5-ht1a may play a protective role in the effects of the former class of drugs. In particular are 5-ht1a agonists considered serenic, antipsychotic, and empathogenic; this includes cannabidiol, the anxiolytic buspirone, and the antidepressant/hypnotic trazodone. Indeed, DOM, which was the first psychedelic to cause really scary overdoses back in 1969, also lacks any significant 5-ht1a affinity.
In particular, a very intelligent acquaintance had at one point suggested that bronchoconstriction -- which includes shortness of breath and blue lips -- represented a possible risk w.r.t. overdoses on potent 5-ht2a full agonists. I commented at the time that this seemed unlikely, because bronchoconstriction is not seen in serotonin syndrome, which rather includes hyperventilation and hyperthermia (serotonin is a 5-ht2a full agonist obviously), and those in SS do not turn blue.
It appears that I spoke too soon. Turning blue should indicate oxygen depletion (there are other possibilities: methæmoglobinemia). If 5-ht1a is indeed protective, this would explain why users of very high doses of LSD, psilocin, ayahuasca, and mescaline do not have trouble breathing, and why serotonin syndrome does not seem to cause this, but also why Br-DFLY does produce this very undesirable side-effect.
A theory is not complete without errors. The problematic 5-MeO-x tryptamines all have significant affinity at 5-ht1a, which demonstrates that it no guarantor of safety. In one case:
This is consistent with the inflammatory hypothesis suggested by the nameless one. Lots of lung damage, in fact. Except the last symptom, which seems more likely a result of a condition known as "being fucked in the ass". What is really confusing here is that 5-MeO-DiPT is actually a rather weak 5-ht2a agonist, instead having more activity at 5-ht1a.
So there are a couple of acceptable hypotheses:
(1) overdose on NBOMe's causes effects resulting from as-yet-unknown binding to some other, non-psychedelic receptor.
(2) full agonists at 5-ht2a can produce a dangerous inflammatory response, but partial agonists do not; 5-ht1a activity is a red herring
(3) 5-ht1a partially protects from 5-ht2a-mediated inflammatory response and:
(3a) can produce an inflammatory response on its own; there is a necessary, natural "balance" of activity at these receptors
(3b) overdose on 5-MeO-tryptamines results from other, unrelated effects
(4) functional selectivity at 5-ht2a allows LSD, psilocin, et al a wider safety margin: LSD in particular is selective for arachidonic acid release at 5-ht2a over activation of phospholipase C, whereas DOx effects both sorts of activity.
(1) seems unlikely; (2), (3a), (3b), and (4) all seem certainly possible, but I don't really know enough to prefer any of them over the others.
At this point it would be premature and extremely reckless to assume 5-ht1a agonists can protect from the damaging effects of 25x overdoses.
What I don't know is: are psilocin and mescaline also functionally selective in the manner of LSD? That would be enough to confirm or rule out (4). I also don't know about the intrinsic activity of psilocin at 5-ht2a, which would confirm or rule out (2). LSD is almost a full agonist w.r.t. arachidonic acid, but a weak partial agonist w.r.t. phospholipase C. So (2) is already on shaky ground.
In particular (4) implies that TCB-2, which is selective for phospholipase C activation, could be very dangerous.
(3a) and (3b) are wildcards: if 5-ht1a plays a major role, things get confusing and hard to verify, especially because precisely what relative activity is safe at 5-ht2a and 5-ht1a is not clear, and finding compounds which have this mix of activity is much harder than finding agonists of a single receptor.
In the meantime: 500 micrograms is probably too high of a starting dose for 25x. The bioavailability of 25x is very inconsistent: they are up to five times as potent by inhalation, and some people may absorb the drugs easier than others, leading to an unexpectedly powerful dose in the bloodstream. To compensate for this, start small, work your way up, and use a consistent dosing method, i.e. don't switch from sublingual to liquid insufflation once you've found a level you like. Caution is advisable for anyone with a history of asthma.
My guess is that vaporization and maybe liquid insufflation have a consistently higher bioavailability than other non-injection methods. I seemed to need less via liquid insufflation than others did sublingually: my use of 25C never exceeded 550 micrograms, and I hit a +3 at 250 micrograms.
Last edited:
Jesusgreen
Bluelight Crew
Psychedelic Drugs -> Drugs in the Media
(I left a 1 day redirect just so those interested from PD can find it easier)
Very strange, I'm curious.. Where did the actual report come from? Was this passed on to you by someone involved? Because I don't see any mention of it at the media source.
Sounds to me like an allergic reaction - possibly coupled with some inconsistency in the solution used for dosing that led to them receiving more than they thought they were getting.
Still, this is why proper measurement and allergy tests are vital, particularly with compounds so strong. People should be started with < 100ug doses as allergy tests, the smaller the better.
(I left a 1 day redirect just so those interested from PD can find it easier)
Very strange, I'm curious.. Where did the actual report come from? Was this passed on to you by someone involved? Because I don't see any mention of it at the media source.
Sounds to me like an allergic reaction - possibly coupled with some inconsistency in the solution used for dosing that led to them receiving more than they thought they were getting.
Still, this is why proper measurement and allergy tests are vital, particularly with compounds so strong. People should be started with < 100ug doses as allergy tests, the smaller the better.
I do not remember the case of psilocin but afaik it is a general pattern for psychedelics, phenylethylamines most certainly - to not be selective. There is DON that is more selective towards arachidonic acid (AA) release, and 2C-N that activates the AA pathway exclusively. On the other side, there are TCB-2 you mentioned and 2,5-DMA being selective towards phospholipase C pathway.
MikeRWK
Bluelighter
If drugs like lsd and mushrooms were legal this probly wouldnt have happened, i hate RCs because the users are the lab rats.
23536
Bluelight Crew
The report is unique to Bluelight.
https://www.google.com/search?rlz=1...kept+repeating+how+weird+the+living+room+was"
https://www.google.com/search?rlz=1...kept+repeating+how+weird+the+living+room+was"
