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DOI for Arthritis: A Daily Journal

RhythmSpring said:
It could just be that I'm in an unsettling stage in my life right now (i've got arthritis and I'm 21!)
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I got you beat by about 10 years, I was diagnosed with arthritis at age 11 (although the symptoms first appeared when I was 10).

One last thing, it's a pet peeve of mine when people refer to it as Lymes Disease, it's Lyme Disease (no s). It's named after the town, Lyme, CT, where it was first discovered. Incidentally, I grew up two towns east of Lyme.
 
Jamshyd said:
Fascinating.

I'd be interested to know if this is transferable to something else, like DOM for example :).
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It works for any full 5-HT2a agonist; they're all potent TNFa inhibitors. I think DOI is preferred because of the high specificity and low dose required.

I'm thinking of trying low dose DOI for the heck of it. Lately I've been having aches, low energy and I'm interested in seeing if it can be used as cognitive enhancer; replacement for amphetamine. I think the all day duration would be nice for a cognitive enhancer; I find amphetamine to be too euphoric and after the euphoria is gone (4 hours or so) my motivation/energy drops off when I still want to continue working; which leads to redosing, etc.
 
^ Hmm that's interesting if low dose DOI could be better than amphetamine for this, as I get the same way, I enjoy how alert and ready I am, but as soon as it drops off I'm stuck in fatigue and irritability land. I don't do them often, and I tend to not redose as I have high willpower and know it will lead to a binge.

I would just be afraid to get a hotspot and be doomed to a day of tripping balls I was not prepared for.


In the same respect.... Could you use 25i-nbome for this? I've read it's a plesant acid-like trip in recreational doses (well isn't doi also?) And these chemicals are also somewhat close to each other. if the dose is 800mcg-1500mcg try something like 200-250mcg and work your way from there?
The duration of the nbome is also shorter, It's supposedly 10-12 hours, opposed to DOI's rediculous duration which I've read can be quite long.

Would the nbome be better for people who have more trouble sleeping?

or perhaps even 2c-I, in a few miligrams for someone who would have difficulty with the duration as well as difficulty weighing out chemicals that dose in the microgram range.


I do not suffer from rheumatoid arthritis or anything like that.. (that I know of yet.. at least)
But I do suffer from a more mild arthritis at the same age as yourself OP, as well as back pains due to car-crashes, a general lethargy that I can't seem to shake, and bouts of depression. SSRI's are disgusting.. natural MAOI's work fine short term but can be dangerous so I just smoke them with my weed, which so far cannabis helps me, especially in the morning, I usually don't even buy it anymore so you can't say I'm a pot junkie or anything, but It definitely has helped far more than any SSRI
as for some more back story when I was younger I suffered more from depression that I do now, and I believe it started alleviating after I began taking psychedelics, as these breakthroughs I've had over the years point more toward being positive and happy in life.
 
The R-stereoisomer/enantiomer should be present in equimolar amounts to the S enantiomer, so long as a non-stereoselective synthesis was used. I would be extremely surprised if it had been. On very few occasions has enantiomerically pure material been available on the RC market.

The NBOMe derivatives may not have the same TNFa inhibitory function - however, if this activity truly is secondary to 5-HT2A activation in aortic smooth muscle cells (and is not instead mediated through another pathway) then perhaps it will be just as effective for this function afterall.
Again, if it truly is 5-HT2A mediated, then it would be interesting to know through what signalling trafficking pathway it functions through, and whether psychedelic activity (and so, the concomitant signal trafficking profile) is necessary for TNFa inhibition in this cellular target. As you may know, all serotonergic psychedelics are 5-HT2A agonists, but not all 5-HT2A agonists are psychedelics. Lisuride, for example, is a potent 5-HT2A agonist but is not at all psychedelic. This is because it does not cause the same signal transduction behavior.
This raises the possibility that a non-psychedelic TNFa inhibitor is possible. I suspect it is. I would not be surprised to learn that there already is - I haven't checked the literature recently in respect to this topic! :)
 
Wiki page on TNFa inhibitiors said:
Several 5-HT2A agonist hallucinogens including (R)-DOI, TCB-2, LSD and LA-SS-Az have unexpectedly also been found to act as potent inhibitors of TNFα, with DOI being the most active, showing TNFα inhibition in the picomolar range, an order of magnitude more potent than its action as a hallucinogen.
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Devourer said:
I would just be afraid to get a hotspot and be doomed to a day of tripping balls I was not prepared for.
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I would never weigh anything fully active under 10mg on my scale lol. I would make a 1mg/mL solution of DOI and dose with an oral syringe.

One reason I'm leaning more towards DOI is the fact that it is in fact an amphetamine and would likely give some CNS stimulation. The other being I have enough DOI to last my lifetime or more and no NBOMEs and I don't have much desire to spend money and expand my collection.
 
I guess since these chemicals are truely not well known and properly researched it all leads to speculation on what purposes each one could be used for.

I'd also like to add that the low doses of 2c-P were a nice all-day uplift for me without being energetic.
I was afraid of the chemical at first when I got it due to the dose/response curve and I started by taking 1-2mg every day for the first week. Of course this killed the OEV component for me when I decided to actually go balls deep, but It worked very well at keeping me in a good state of mind.
 
I got a little boshed on GHB last night but with things going on I decided that today would be the best day to try this.

Let me first say I don't have any real inflammatory medical conditions; I just temporarily have some minor joint aches and general tiredness and wanted to experiment.

I took 0.5mg of racemic DOI. Let me just say DOI works fantastic as a strong psychedelic and absolute shit as a cognitive enhancer. At 0.5mg I have been rolling along at + all day. I've been completely unable to concentrate on Calculus as I have been far more interested in choking my chicken.

I also haven't gotten any anti-inflammatory effects; the psychedelic effect which includes vasoconstriction and muscle tension actually makes things worse.

edit: Upon thinking about it; vasoconstriction would help inflammation but think of how your joints/body generally feels in a psychedelic come-up (don't take too much).

0.5mg is definitely enough to have DOI start doing it's main thing. My 5HT2a receptors are certainly agonized. I don't think I would want to do this too often; deregulation of 5HT2a receptors would lead to diminished future trips and the general discombobulation makes this a no-go for being normally functional.

I might try 0.2mg sometime but I was hoping to find some cognitive enhancement in low dose DOI. Maybe I just didn't go low enough. A definite amphetamine pushing psychedelic though.
 
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MattPsy said:
The R-stereoisomer/enantiomer should be present in equimolar amounts to the S enantiomer, so long as a non-stereoselective synthesis was used. I would be extremely surprised if it had been. On very few occasions has enantiomerically pure material been available on the RC market.
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pretty much what i would have said, but with proper wording :)

MattPsy said:
The NBOMe derivatives may not have the same TNFa inhibitory function - however, if this activity truly is secondary to 5-HT2A activation in aortic smooth muscle cells (and is not instead mediated through another pathway) then perhaps it will be just as effective for this function afterall.
Again, if it truly is 5-HT2A mediated, then it would be interesting to know through what signalling trafficking pathway it functions through, and whether psychedelic activity (and so, the concomitant signal trafficking profile) is necessary for TNFa inhibition in this cellular target. As you may know, all serotonergic psychedelics are 5-HT2A agonists, but not all 5-HT2A agonists are psychedelics. Lisuride, for example, is a potent 5-HT2A agonist but is not at all psychedelic. This is because it does not cause the same signal transduction behavior.
This raises the possibility that a non-psychedelic TNFa inhibitor is possible. I suspect it is. I would not be surprised to learn that there already is - I haven't checked the literature recently in respect to this topic! :)
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about the effect being in aortic smooth muscle cells...i wonder what animals' cells the researchers used, and whether they were doing this in vivo or in vitro. i could try to look up the full paper at school
 
If i'm not mistaken DOI has also been studied in regards to its ability to modulate intraocular pressure consequent to disorders such as glaucoma
 
ahh i was just being a douche.i really dont care for it as a psychedelic;but its good to hear that its of theraputic use..its the only do* im aware of thats super readily available atm. i can get doc too; but not in gram amounts..and its much more expensive than it used to be..

then again, i dont risk ordering directly from china- after ordring some DOC actually a yr or two ago and getting some brownish colored gunk..dont know if they messed up the synth or what but needless to say it was toilet flush material..didnt even bother trying it

(sry if this breaks source rules- lmk and ill edit post)
 
any major dude said:
If i'm not mistaken DOI has also been studied in regards to its ability to modulate intraocular pressure consequent to disorders such as glaucoma
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I was not aware of any research involving peripherally-selective PEA-derived compounds, only indoles (actually, indazoles!) - search for : AL-34662

It would not surprise me that you could do the same with PEA compounds however.
 
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