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Phenethylamines The safety (or lack therof) of DOX chemicals discussion thread

Steamboat: You completely missed the point. But I'm actually not surprised.

As I've already said, I'll do more of an in depth argument and use respectable sources when I have the time to do thorough research, as well as create an outline on how DOXs can be used safely. You only hear what you want to hear and it's annoying having to repeat myself.

Some of the doses are unknown, others or not. The fact that it isn't known, as you claim, means that they are either overdoses or not. It can go either way, so that means it can't be used to "back up" whether they caused deaths at normal doses or not, and I'll retract my claim. In turn, you also wouldn't be able to say they caused deaths at normal dosage levels, just that they caused deaths at all (of which there are thousands of substances that did the same).

Of course you wouldn't be able to find that specific information just using Google. Do you think you're the only one who scoured the regular internet looking for information on DOPr? Google does not have all of the world's information, not even close. They only have what people choose to put up. My point was to share what I learned specifically because it was new. If DOPr was considered dangerous and had negative things to say, I would've posted that too, just like how I didn't leave out any negative experiences with my high dose for safety reasons, even though I blew it out of proportion.

You on the other hand, did not acknowledge how DOx substances can be used safely, even though they can. That speaks volumes about your bias, and especially with how you backed your claims with that faulty Ricuarte study that one time, I simply don't feel the need to heed your warnings. All signs point to you not understanding that it is possible to use DOx substances safely.

And I thought I expressed this to you before, to not post to me and that in turn I would not post towards you. I actually know you in person and refrained from saying many things even though I felt like it at times. Basically, you have no idea how nice I've been towards you considering how backhanded you've been speaking towards me since the beginning. Just realize that your enemy actually has empathy towards you, even if you don't.
 
I would think the DOX chemicals would be safer just due to the chemical being less active at 1mg where as the nbome drugs are extremely active in my opinion, as I have experimented with all of the DOX chemicals and nbome. This would leave more room for error as most people laying these blotters are less experienced most of the time.
 
Since we can't say for sure how safe or unsafe DOx chemicals are, we can only look at all the data and try to infer a relative degree of safety from that. StemboatBill has a very small amount of data that suggests DOx in rare occasions might be potentially unsafe. The vast majority of data suggests that Dox taken at proper doses are relatively safe chemicals.

Given the fact that DOx chemicals have been used for decades, your tiny amount of data, if anything speaks more for the safety of these chemicals than the dangers. The fact is, a lot of people have used these chemicals for a very long time and most of them never experienced a medical emergency. I know you want a scientific study for that but there isn't one and never will be. This is because most people who take DOx aren't reporting about it online, nor are they searching for "2,5-Dimethoxy-4-chloroamphetamine" on Google.

Now if you had dozens and dozens of reports where people were dying from DOx than you would have a lot of data points and something more substantial to look at. But that's just way too small of a sample. What about all the potential variables in those couple of reports that you might not be accounting for? People DO have idiosyncratic reactions to all sorts of things.

Even if we put 100% faith in those studies and reports, all they are really suggesting is that DOx chemicals can, on very rare occasions, be potentially unsafe. But what about alcohol, cars, kitchen knives, Tylenol etc? All of these things can and do kill people. But prohibition doesn't work and people are going to use these things. When you say we should all boycott DOx and choose "safer" chemicals for the sake of harm reduction, isn't that kind of like saying you should be the guy who draws the safety line for all other people? Why should you be that guy? You should draw the safety line for yourself absolutely. Keep in mind, there are plenty of people who would love to boycott your LSD and mushrooms because they are potentially unsafe. And in a sense they're right because LSD and mushrooms ARE potentially unsafe.
 
you backed your claims with that faulty Ricuarte study that one time

You fabricated this. The only controversial Ricaurte research I am familiar with is about the neurotoxicity of MDMA and doesn't mention DOX chemicals. You're fabricating lies and attacking me rather than my arguments. The fact remains you haven't provided any evidence supporting your claims. In fact you haven't provided any evidence. I have repeatedly supported my claims with evidence in this thread.

Although there are few case reports of poisioning, it's hard to tell if they're rare exceptions or something more significant.

You say poisoning, I presume this is emphasizing fatality? Though you didn't provide them in your analysis, I provided multiple reports of fatalities resulting from DOX use.

 
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I don't know if you can count bromo-dragonfly in this discussion... I don't think anyone here would deny it's a sketchy and inappropriately dangerous substance. If you were campaigning against bromo-dragonfly, I would be agreeing with you 100% about how dangerous it is. But it's quite structurally altered from the main DOX family that we've been discussing. That removes 2 of the 5 death cases you posted. 3 deaths out of all this time... it's not many. More than LSD and mushrooms and mescaline, yes. But a lot less than, say, 2C-T-7 or AMT, or MDMA, and a lot less than NBOMes (over a much longer period of time).
 
You fabricated this. The only controversial Ricaurte research I am familiar with is about the neurotoxicity of MDMA and doesn't mention DOX chemicals. You're fabricating lies and attacking me rather than my arguments. The fact remains you haven't provided any evidence supporting your claims. In fact you haven't provided any evidence. I have repeatedly sported my claims with evidence in this thread.

Nah, that's you. I can't count the amount of lies that are coming from you, because there are too many. From your supposed use, which I bet you don't, to all of your other fabricated lies and stories. You should stop projecting yourself onto me, and really that's all I feel like saying on this subject.

Anyone can look up and find their own sources to see if what someone is saying is true. I'm not going to plaster hyperlinks to everything I say, and your supposed "fact" is already untrue so don't make me dig up past posts to prove it. You also haven't shown that your sources prove that DOXs are as dangerous as you say it is at normal doses. Almost everything can be dangerous and life threatening at too high of a dose/overdose. All you do is grab sources on Google and come out with your own conclusions. I've read those studies and a lot more, and of course there are risks but they don't threaten lives enough to warrant such an obsessive view that you take.

I can't even count how many names you use here. You already did with that ridiculous K9 user name. You can deny it all you want, but those that are keen and observant already figured you out. And you say you didn't agree to anything, which you didn't actually say anything, but you sure did a good job of listening to what I said until now. If you truly lived in "Colorado" like you claimed, you wouldn't have listened in the first place.

Anyway, any further posts towards me, unless it's through PM, will be reported from now on. I'm not going to reply to you, and the only reason why I haven't reported your posts yet is because I took your bait and engaged in this ridiculous banter. I won't anymore because you're not much different to me than a virus. Therefore, you will be ignored.
 
Let's chill out a bit, eh? No reason for either side of this debate to get mad at each other. If I had to guess I'd say there is something personal going on here, so it's probably not appropriate for this thread.
 
Let's chill out a bit, eh? No reason for either side of this debate to get mad at each other. If I had to guess I'd say there is something personal going on here, so it's probably not appropriate for this thread.

This isn't personal on my side. My goal has been researching the risks associated with DOX use and somehow these were the responses I received. I am as confused as you. I could use your recommendations on how I should act in this situation. The fact Kl519 has moderator status further complicates things. How should I respond if moderators act this way?


That speaks volumes about your bias, and especially with how you backed your claims with that faulty Ricuarte study that one time

This never happened.


I actually know you in person

I haven't met K1519 in person.


I can't count the amount of lies that are coming from you, because there are too many. From your supposed use, which I bet you don't, to all of your other fabricated lies and stories.

I actually use the drugs my comments report.


I can't even count how many names you use here. You already did with that ridiculous K9 user name.

SteamboatBillJr is my only screen name. Could the screen name K9 actually exist? I thought screen names had minimum lengths.


If you truly lived in "Colorado" like you claimed, you wouldn't have listened in the first place.

I actually live in Colorado. Considering I haven't mentioned my location much and my location isn't mentioned in my profile this is rather creepy. I guess when reading my older comments K1519 was really watching closely.
 
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I am working on my most recent compilation of data does anyone have any additional evidence, new of course.
 
Elaborating on this, binding assays show the pharmacological profile of NBOMe drug is nearly identical. The most significant variation is potency. The DOX drugs we have data on (DOB, DOI, and DOC) also exhibit the same pharmacological profile as 25X-NBOMe drugs. The drugs bind strongly and selectively with 5HT2 receptors. The pathological findings in the overdoses I linked further support this similarity. Fatalities from DOB, DOC, and 25X-NBOMe drugs share the same pathological findings in the medical literature I have read.

The exception is 2C-X drugs. Most of those drugs bind strongly with receptors other than 5HT2 and have increased safety profiles. Alas, further supporting high selectivity at 5HT-2 is associated with toxicity the exception amongst 2C-X drugs is 2C-T-7. 2C-T-7 caused fatalities. 2C-T-7 is different than most other 2C-X drugs and binds abnormally strongly and selectively at 5HT2 receptor types.

Find my full explanation with sources in the appropriate thread.

TLDR: Evidence shows DOB, DOC, 25X-NBOMe, and 2C-T-7 carry this risk of fatality. These risks increase with dose consumed by the user.


In the past I have mentioned drugs with hyper-selectivity at 5HT2A cause fatalities. This includes multiple DOX chemicals and almost every 25X-NBOMe chemical. After discussing this relationship in another topic I am providing my supporting evidence and elaborating on the DOX specific attributes of this.

Recent studies have shown the action of hallucinogenic drugs is the result of the interaction of multiple receptors including 5HT2a. Though other receptors are probably involved, research has demonstrated 5HT1A agonism reduces HTR resulting from 5HT2A agonism. The following data demonstrates the relationship between 5HT1A and 5HT2A. We have verified fatalities from the following chemicals DOB, DOC, 25B-NBOMe, 25C-NBOMe, 25I-NBOMe, and 2C-T-7. I have highlighted those chemicals' 5HT1A/5HT2A ratio in red.


ikoXvpn.jpg


PUapHla.jpg



Notice after selectivity passes ~50X fatalities begin occurring. Also notice the selectivity of safer traditional psychedelics mescaline and LSD is <1 much lower than those associated with significant risks.




Refferences:

Behavioral and neurochemical pharmacology of six psychoactive substituted phenethylamines: Mouse locomotion, rat drug discrimination and in vitro receptor and transporter binding and function
Psychopharmacology (Berl). 2014 Mar
doi: 10.1007/s00213-013-3303-6

Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines.
Rickli A, et al. Neuropharmacology. 2015.
doi: 10.1016/j.neuropharm.2015.08.034

PDSP Ki Database
http://pdsp.med.unc.edu/
 
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Hello all, let me say first of all that I can't give a subjective opinion on this because I have never purposefully taken an identified DOx chemical and I have never taken a NBOMe chemical period, but I do have something to say which I think may be worth contributing to this interesting conversation.

Just from my own personal research, I would have to agree that it does seem likely that the ratio of activity a psychedelic has at 5-HT2A compared to other receptors, especially 5-HT1A, does play some role in how likely it is that said psychedelic will cause seizures. However, I have to point out that it has been said that DOx chemicals are selective 5-HT2A agonists similarly to the NBOMe chemicals, but most of what we used to know about the DOx family was derived either from studies done on rats or from comparing binding data from studies done very differently or at completely different time periods. Instead of relying on those, allow me to offer recent PDSP binding data done on a variety of psychedelics, including DOB, DOI, DOM, and DOET, at human receptor sites, all as part of a single study.

Spreadsheet file.

The study it came from.

Now, it is true that this data paints DOB as a fairly selective 5-HT2 agonist, with 110x selectivity for 5-HT2A over 5-HT1A, but this is pretty different from the >6300x selectivity listed above. By comparison, most NBOMe compounds when tested by the same group with the same procedure do fall into the area of thousands of times selectivity for 5-HT2A as previously stated. Moving on, the same data pegs DOI, the only other tested halogenated amphetamine psychedelic here, with a mere 13x selectivity for 5-HT2A over 5-HT1A. Even worse, DOM only has 7x selectivity, and DOET has nearly 2x selectivity for 5-HT1A.

Again, for comparison, 2C-B in this data has about 9x selectivity for 5-HT2A, and 2C-E has 7x. The PDSP data I referenced earlier gave 1470x selectivity for 25C-NBOMe, whereas the above-referenced data gave 7143x, so going backwards proportionally, you would end up with selectivity for 2C-B and 2C-E in the range of about 35-40x, which matches up fairly closely to the 28x and 34x given. So, if you wanted to adjust the DOx binding numbers the same way, I would say that the upper limits would probably be: 534x for DOB, 63x for DOI, 34x for DOM, and 2x for DOET. Given the proposed theory, I think this could make sense; DOB clearly sores above 50x on this scale and is thought to be the most dangerous, DOI seems like it could get there maybe but I'm aware of people surviving accidental large overdoses without life-threatening problems (but certainly not pleasant trips), DOM of course is known to be quite safe and falls snuggly around 2C-B and 2C-E, and DOET of course is hard to speak for as of yet. However, the lack of side effects that people keep mentioning for DOPR makes me wonder if it continues this trend as well, but of course that's just guessing.

The point of what I'm saying is, I don't think it's really fair to say that the DOx family should definitely be pharmacologically lumped in with the NBOMes yet; based on the most recent data we have on human receptors, it actually seems to me more like DOB is the selective one, and the others are actually really not that far outside of the 2C-x family, but probably just more efficacious. It's true that some of their numbers can get kind of high compared to that 50x mark, but it certainly seems not into the thousands like the NBOMes, and drugs like 2C-T-7 which go over that mark by only about half or less, though known to be dangerous in overdose, are certainly not considered to be extremely risky to use.

Anyway, that's what I've got. Carry on.
 
DOxes are safe, pleasant and healthy. The fact that bad things happen if you decide to take 20x+ a strong dose means nothing. A lot of things can kill you if you are an idiot with them.
 
Hello all, let me say first of all that I can't give a subjective opinion on this because I have never purposefully taken an identified DOx chemical and I have never taken a NBOMe chemical period, but I do have something to say which I think may be worth contributing to this interesting conversation.

Just from my own personal research, I would have to agree that it does seem likely that the ratio of activity a psychedelic has at 5-HT2A compared to other receptors, especially 5-HT1A, does play some role in how likely it is that said psychedelic will cause seizures. However, I have to point out that it has been said that DOx chemicals are selective 5-HT2A agonists similarly to the NBOMe chemicals, but most of what we used to know about the DOx family was derived either from studies done on rats or from comparing binding data from studies done very differently or at completely different time periods. Instead of relying on those, allow me to offer recent PDSP binding data done on a variety of psychedelics, including DOB, DOI, DOM, and DOET, at human receptor sites, all as part of a single study.

Spreadsheet file.

The study it came from.

Now, it is true that this data paints DOB as a fairly selective 5-HT2 agonist, with 110x selectivity for 5-HT2A over 5-HT1A, but this is pretty different from the >6300x selectivity listed above. By comparison, most NBOMe compounds when tested by the same group with the same procedure do fall into the area of thousands of times selectivity for 5-HT2A as previously stated. Moving on, the same data pegs DOI, the only other tested halogenated amphetamine psychedelic here, with a mere 13x selectivity for 5-HT2A over 5-HT1A. Even worse, DOM only has 7x selectivity, and DOET has nearly 2x selectivity for 5-HT1A.

Again, for comparison, 2C-B in this data has about 9x selectivity for 5-HT2A, and 2C-E has 7x. The PDSP data I referenced earlier gave 1470x selectivity for 25C-NBOMe, whereas the above-referenced data gave 7143x, so going backwards proportionally, you would end up with selectivity for 2C-B and 2C-E in the range of about 35-40x, which matches up fairly closely to the 28x and 34x given. So, if you wanted to adjust the DOx binding numbers the same way, I would say that the upper limits would probably be: 534x for DOB, 63x for DOI, 34x for DOM, and 2x for DOET. Given the proposed theory, I think this could make sense; DOB clearly sores above 50x on this scale and is thought to be the most dangerous, DOI seems like it could get there maybe but I'm aware of people surviving accidental large overdoses without life-threatening problems (but certainly not pleasant trips), DOM of course is known to be quite safe and falls snuggly around 2C-B and 2C-E, and DOET of course is hard to speak for as of yet. However, the lack of side effects that people keep mentioning for DOPR makes me wonder if it continues this trend as well, but of course that's just guessing.

The point of what I'm saying is, I don't think it's really fair to say that the DOx family should definitely be pharmacologically lumped in with the NBOMes yet; based on the most recent data we have on human receptors, it actually seems to me more like DOB is the selective one, and the others are actually really not that far outside of the 2C-x family, but probably just more efficacious. It's true that some of their numbers can get kind of high compared to that 50x mark, but it certainly seems not into the thousands like the NBOMes, and drugs like 2C-T-7 which go over that mark by only about half or less, though known to be dangerous in overdose, are certainly not considered to be extremely risky to use.

Anyway, that's what I've got. Carry on.

Thanks for that, interesting post and data.
 
Kaleida,

I am familiar with the study you sourced (Psychedelics and the Human Receptorome) and agree you could derive vague activity relationships from the data, though only vague relationships. I stopped using this data set a while ago and excluded this data from my analysis. This is because the research doesn't list the hot ligand or species used in analysis at each receptor and some of the binding data is in strong disagreement with most research.

Do you realize the study you linked shows DMT (2323 nM) and psilocin (339.6 nM) aren't significantly active at 5HT2a?

These discrepancies and lack of specific explanation of methods in Psychedelics and the Human Receptorome were the reason I excluded this data.
 
Thanks Xorkoth, glad to contribute when I can.

SteamboatBillJr, thank you for the response. I am also familiar with the arguments you presented, I know that this particular study has a bad reputation. Given that this is a matter of opinion, you are welcome to your own and I have no intention of trying to argue you out of it, but I will also present you my own. First, allow me to say that I too had the frustration of thinking that there was really no data given on the binding studies, until I found this hidden in there:

For this study, the NIMH-PDSP (http://pdsp.med.unc.edu/) has assayed sixteen phenylalkylamines, eight tryptamines and one ergoline (twenty-two psychedelics and three controls, Fig. 1) against a panel of fifty-one receptors, transporters, and ion channels. The methodology has been described previously by Glennon et al. [12]. Each compound is initially assayed at 10 µM against each receptor, transporter or ion channel (primary assay). Those that induce >50% inhibition (“hit”) are then assayed at 1, 10, 100, 1,000, and 10,000 nM to determine Ki values (secondary assay). Each Ki value (equilibrium dissociation constant, concentration at which 50% of the hot ligand is displaced by the test ligand) is calculated from at least three replicated assays. Details of how individual assays were conducted can be found at the NIMH-PDSP web site: http://pdsp.med.unc.edu/pdspw/binding.ph​p.

Actually clicking this link at the end takes you to information about the PDSP's standardized procedure for these sorts of tests. There is a page which lists the species of receptors used, and a PDF of their assay protocol book, for which this is a direct link: PDF. In this can be found many details including the hot ligands and several details you did not ask about. For serotonin receptors specifically, this is what we're looking at:

2lca3hk.jpg


As for the discrepancies with other data, again it is your opinion, but I do not personally feel that it is there. One thing I have personally decided after so much research is that comparing affinity numbers from different studies is pointless; for instance, the PDSP Ki Database that you linked before lists the following values for psilocin at 5-HT2A: 12 nM, 25 nM, 107.2 nM, and 370 nM, and for DMT it lists: 42 nM, 462 nM, 558 nM, 1183 nM, 1200 nM, and 230.27 nM. Actually, given these values I don't think that the above 339.6 nM for psilocin and 2323 nM for DMT are really out of the question at all, but my point is that studies always come up with often fairly drastically different numbers for affinity data, and I don't believe we really can say we know enough about why to say which ones of them are the most "accurate". For this reason I am much more interested in finding drugs that are all compared to one another at the same time by the same procedure, because it stands to reason (at least to me) that these values would be the most comparable to each other. In that sense, I would note that that study data shows the following affinity values for 5-HT2A: LSD 11.3 nM, DOB 23.1 nM, 2C-E 43.9 nM, psilocin 339.6 nM, DMT 2323 nM, mescaline >10000 nM. Given the oral potency of each of these compounds in causing psychedelic effects, this progression seems perfectly rational to me. I could say more, but to make a long story short, suffice it to say that I personally have done enough scrutinizing of this data to convince me that it checks out well enough.

As for the relationships that I could derive from this data, I don't see what makes them any more or less than vague than yours.
 
Thanks Kaleida, for providing the source for this recent data. I didn't want to do it myself, and there should be a few more in certain databases, but maybe I'll provide them myself in time. ;)

I didn't really want to waste any more time on this, but if one looks at the whole of this argument (as in look through previous posts), it really can go either way. There still isn't enough data to say whether they are safe or not, because people arbitrarily assign them to what they believe is "safe." So many studies and papers do this, and there doesn't seem to be an agreed upon line between what is safe or not.

What's obvious, which I gathered myself, is that the DOXs are not the same and they shouldn't all be labeled as having the same level of danger. The chart provided here is very similar to what I saw, which is why I pointed out DOB and DOI before, but there is more than this too. Controlling the dose is probably the most important aspect of ensuring that no receptor is agonized to the extent of causing complications.

What's unfair is that one can make a solid case like this for pretty much 95% of RCs out there. Why choose the psychedelic amphetamines specifically, and not heroin IV, datura, etc? It is easy to find what is bad about drugs because of the WOD, and so many studies up until this current century strongly focuses on why drugs shouldn't be consumed. Any argument on this side has a huge advantage because of this discrepancy.

I believe with all of the data in total, it's easy to see that this was blown out of proportion to somehow make this relevant on BL. That's why this topic has been brought up multiple times in different threads, and still finds a way to pop out. I urge people to think about the purpose of this, who's doing it and why DOXs specifically, and not bromo dfly or those other examples from above.

(Above all, this IS a tactic to get everyone's attention by sending a certain message).

Which is why I truly do not want to speak about this again. This topic is beaten to death. I've been sticking to PMs recently and I would be more inclined (ugh) to provide other sources through there if anyone's interested. But I'm not going to waste my time if no one really cares. And I won't be giving any to just anyone, but it has to be someone I trust in my mind.

In any case, everyone should just make up their own minds and decide for themselves what they want to do. It's called freedom of choice, and everyone should, and will, have it.

Anyway, thanks to Kaleida. :) Hopefully I really won't have to speak on this topic again.
 
Ok, I am only going to jump in on a couple points, because I think there are a few issues with some comparisons made.

I don't think 2C T7 has a place on this list. It is commonly known that thio groups at the 4 position give maoi activity and due to that, the dose response curve becomes dangerously steep due to the self inhibition of metabolism. 4mta is an example of this effect without any psychadelic component.

I think it is a mistake to compare DOx compounds with the 25x compounds. 25x compounds are full agonists at 5ht2a, which in my opinion is probably the cause of their toxicity. DOx compounds are partial agonists at 5ht2a, which is probably why the main cause of death in DOx compounds isn't seizures (indicative of gross brain over stimulation, to over simplify). I think that affinity really doesn't paint a very useful picture when talking about overdoses, for example buprenorphine has an extremely high affinity at the mu opiod receptor but is a partial agonist, and will actually send dependant users into precipitated withdrawal, when they are using full agonists with a lower affinity.

25x overdose etiology usually involves intense seizures and then organ damage from rhabdomyalysis. I have not looked, but i have never heard of a case of vasoconstrictive damage occurring from 25x compounds. Please correct me if I am wrong.

While DOx compounds are known to cause seizures their mechanism of toxicity usually stems from long lasting severe vasoconstriction, hence the limb damage that occurs in overdose. In the frame of viewing these compounds based on overdose etiology, DOx shares many more similarities of bromo-dragonfly overdoses. The severe vasoconstriction may be caused by 5ht2a agonism, but it is still usually dissimilar to 25x overdoses in presentation.

I know steamboat will disagree but the margin of safety for dox compounds is an order of magnitude over the margin of safety for nbome compounds in terms of negative effects. Multiple people have been criticized by steamboat for making assumptions in the fatality cases that high doses were involved, while I feel that steamboat is doing the opposite and assuming that low doses were only invoved.

Finally, and probably my weakest point as it is purely anecdotal, but in my town before 2012 DOC was the major fake blotter in town and quite popular, as one enterprising scumbag was selling sheets of it to everybody as acid. There were no hospitalizations from overdoses, and it was not uncommon for the reckless to eat ten strips. After 2012 25i started to take over due to the availability and price, and there were 3 seizure based overdose hospitalizations in that year alone. The only comparitive element to this anecdote is that the supply chain was the same so it was usually the same people dosing, and it changed very rapidly, where DOC was nowhere to be found as soon as 25I hit the markets.

I know that this is in no ways predictive, but for a rather isolated town it does demonstrate a trend that seems to be observed by others here, rather than the use of Web searches as a meter of use. The Google search rate for doc could be explained as both doc and 25i were sold as acid, so while people knew they were getting rcs most did not know the identity, just the blotter prints.
 
DOx are obviously safer than NBOMes. Nobody ever died taking normal dosages of any DOx alone, neither had any problems needing an amputation. Even higher dosages like 6mg of DOC or 20mg of DOM haven't caused any deaths.

We also just can't put all DOx in the same category.
Even DOB and DOI seem to have different affinities, and are visibly more vasoconstrictive.
Also putting Bromo-DragonFLY in the same category is just plain fear-mongering.

About the seizures, it's absurd to say that people only experience mild shaking or dystonia with classical psychedelics. They can definitely cause seizures too.

This has been repeated many many times, but there's no way of convicing the guy.

He's nearly fanatical, trying to come up with all sorts of data. But the only data he can show us is affinity values, which have absolutely no proven correlation with safety.
 
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These are pictures showing the progress of the DOC overdose mentioned earlier in this thread.

Zombie3 said:
Heres some fucked up pics,,,










Like 6 weeks after discharge:






Like 8 weeks after discharge, fell off by itself lol:

quye9.jpg


iq6xm.jpg



Fashiotomy progress, 6 weeks:

This



To this




8 weeks after accident, just had my toes amputated:

Only the two needed to come off, the other 3 will scab off on their own and I won't lose any of those toes! The hole will fill in and create a bit of a new toe pad for me:

 
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