Originally Posted by
Alyzarin
I think this belongs here.... I don't normally post in ED, so excuse me if it doesn't. This is just a theory right now, not based on a bunch of studies or anything (at least not that I know of), this is just the kind of stuff I think about in my free time and I thought this might add up.
To my knowledge, it's been up to this point assumed that the ego death comes along with the other core effects of psychedelic hallucinations, generally thought to be caused by activation of serotonin receptors, particularly 5-HT2A. I'm no longer certain I believe this. My current theory is the effects related to ego death are actually caused by adrenergic receptors. Lately I've been reading up on the effects of adrenaline (epinephrine) and norepinephrine on the body and mind, and I've been surprised at what I found.
Powerful adrenaline rushes (like really powerful) have been known to exhibit a wide range of effects, including strong time dilation, feelings of being in a dream or separate from normal reality, tunnel vision (i.e., loss of peripheral vision), loss of rational thought, loss of ability to comprehend colors, etc..... Basically, the more adrenergic activity you have, the more your brain starts shutting off different functions to put as much energy as it possibly can into increasing your focus on the moment. Now, how far this effect can go from adrenaline rushes alone is limited, because your body will either shut itself off when it realizes what's going on or you're going to have a heart attack, or a stroke, or something else terrible. All of that adrenaline isn't only causing central nervous system effects, but peripheral ones as well. BUT, some drugs can activate adrenergic receptors, or cause adrenergic activity to increase, with varying levels of activity relevant to the CNS and PNS. So with certain chemicals it's entirely possible to experience CNS adrenergic effects more intense than any normal adrenaline rush would get you without presenting the same physical danger.
Now, what's interesting about this is that I had before had reason to think that increased adrenergic activity (especially norepinephrine) lowered NMDA receptor activity, which is the mechanism used by dissociative hallucinogens. If you know anything about dissociatives (which you probably do if you know anything about psychedelics), you'll know that the list of CNS effects I've given also matches up pretty well. I'd say one of the biggest differences is that the adrenergic effects cause you to focus intently, and pure dissociative effects cause you to unfocus. This would most likely be, in my opinion, because the adrenergic effects are shutting down everything BUT the part of your mind made to focus, and the pure dissociatives aren't keeping even that up. Another thing would be that when the effects are brought around by the adrenaline and norepinephrine, there's a much higher chance that you're going to be afraid than when going straight through the dissociative mechanism.
Now, what does this have to do with anything? Well, if you know very much about the psychedelic ego death, you've probably already picked up on that. Fear, focus on the moment, time dilation, separation from reality, loss of ability to think rationally or comprehend the world.... These effects are crucial to the ego death experience! And most psychedelics (at least, most of the well-known ones) are extremely safe as far as effects on the PNS go, you can take absurd doses of them without becoming physically in danger. Nearly all psychedelics (and certainly all of them associated with ego death) have some adrenergic activity as well. So could it be that the ego death is actually a result of pushing these adrenaline-related effects beyond the limit of what is normally possible, all the way up to a total shutdown of all normal brain processing other than focus?
So let's get to some drug examples. First, with psychedelics. I always found it bizarre that psychedelics could induce ego death at such varying levels of serotonergic hallucinations if these effects are supposedly activated through the same mechanism. Let's for instance take LSD and DMT. Anyone with experience with both of these chemicals will tell you that you can achieve ego death from LSD at a level of hallucination that looks like a joke compared to DMT. However, DMT "breakthroughs", a full out-of-body sensory overload experience brought on by serotonergic hallucinations, can be totally without ego death, something which is almost unimaginable with LSD, where a dose required to make you trip that hard would blow a hole through the fabric of reality. DMT is extremely similar to the tryptamines in your body (and is in fact one of them) like serotonin, and as a result very likely has far more serotonergic than adrenergic activity. LSD on the other hand is known to have a pretty good amount of adrenergic and even dopaminergic activity. So doesn't that seem to correlate? This can also be said of mescaline.
And on that note, a perhaps even more sturdy example would be the difference between 5-MeO-DMT and bufotenine, two other endogenous psychedelic tryptamines. 5-methoxy tryptamines are often found to share similarities with psychedelic phenethylamines like mescaline and the 2Cs, and like them 5-MeO-DMT has been found to have some activity in inhibiting the reuptake of monoamines, including norepinephrine. 5-MeO-DMT is also known to cause an unbelievably strong level of ego death when smoked, despite having very little (if any?) 5-HT2A activity. Bufotenine on the other hand, which is the most similar psychedelic in structure to serotonin (with bufotenine being 5-hydroxy-N,N-dimethyltryptamine and serotonin being 5-hydroxytryptamine), likely has a higher serotonergic to adrenergic activity ratio than any other psychedelic, and it's known to create POWERFUL serotonergic hallucinations, with reports stating them to be much stronger than those created by DMT, and yet with little to no removal from reality or ego death-like effects whatsoever.
On the subject of reuptake inhibitors, let's look at two important factors: serotonin reuptake inhibitors (SRIs) and norepinephrine reuptake inhibitors (NRIs), preferably selective. If the ego death is a result of high serotonergic activity, why don't any SRIs exhibit effects related to ego death? Overdose of them usually involves some mild sensory hallucinations, at best. Even kanna, which contains mesembrine (a supposed natural SRI that seems to be much safer physically than medical SRIs), when taken in large doses creates the normal psychedelic sensory hallucinations, but not ego death-like effects. However, atomoxetine, a NRI currently being used to treat ADHD, among other things, CAN create powerful dissociative experiences in overdose. I think that alone goes a long way in saying something here. Lastly, I'd like to mention dextromethorphan (DXM). There's a lot of debate in the drug community over whether dissociatives can cause ego deaths like psychedelics can (and of course with my theory here they absolutely can), but even among dissociatives DXM is often touted to be especially psychedelic-like. To my knowledge, DXM is also the only widely-used dissociative hallucinogen to have not insignificant effects on norepinephrine reuptake. Hmmm....
However, where I think this is most interesting, personally, is its relation to naturally accessing the body's dissociative mechanisms. By which I refer to things like sleep paralysis and OBEs. I remember reading before of some monks (maybe monks? it's been a while since I looked it up) who practiced meditation and things like yoga nidra and other yogas to move beyond the dream state into a state of clear white light. Just like that experienced at the peak of ego death. Is it possible that, with this theory in mind, ego death is simply a step further than OBE in this mechanism and the point of that meditation is to reach it by being able to focus yourself so much that you can continue to push past the OBE and dream states? Of course, that part's mainly me thinking out loud for now....
So that's where I'm at right now. Any thoughts? I know I didn't list any sources or anything, a lot of this is just using knowledge I've built up over a long, long period of research, so feel free to ask me about anything if you want to.
