I've got a theory that might help explain some peculiarities considering orally taken psychedelics.
-The experiential differences between chaliponga and other DMT-plants.
-The experiential difference between LSD-25, ALD-52, and 1P-LSD.
-The fact that sometimes some effects, like bodyload, stimulation, sedation, or nausea, can be felt even minutes after ingesting a hallucinogen, before the substance could even have reached the brain.
In short: the guts have their own, more or less, autonomous nervous system that is sometimes refered to as "the second brain". Many important receptors that are present within the brain, are also found in this "second brain". This nervous system, though somewhat autonomous, is constantly communicating with the brain. Communication is going in both directions. Some scientists even speculate that bacteria in the intestines may be a major contributor to psychiatric illnesses like depression or OCD.
So one of the main mechanisms of classic psychedelic drugs like DMT, is downregulation of 5-ht2-a. This is an autonomous process that is the result of what the brain perceives as overstimulation of this receptor.
My theory is: even before a classic hallucinogen has crossed the blood-brain barrier, it may have already affected the nervous system of the bowels. The bowels can then send a warning signal to the brain: "incoming serotonin receptor agonist" and thus prime the brain, to be ready to start downregulation. This priming signal could already cause some of the effects associated with psychedelics, like experiencing bodyload, stimulation and mild changes in perception.
Another consequence would be, that although 1P-LSD and ALD-52 are thought to be converted to LSD-25 when passing the blood-brain barrier, they may have their own unique effects on the nervous system outside of the brain. So then within the brain they act in the same way because they are the same substance, but outside of the brain they have different effects, that affect the way the brain responds to LSD-25.
And about chaliponga: ofcourse you could say that perceived differences in effect are the result of the placebo-effect, but that chaliponga also consistently produces diffent effects, physically....projectile vomiting being the most mentionable, is not realy something that can easily be disputed.
Tannins are thought to be the main cause of these physical typicalities.
My thought is that this whole "ejection process", even when it doesn't lead to actual vomiting, could be "jamming" the priming signal to the brain, and thus affecting the way the brain responds to DMT.
-The experiential differences between chaliponga and other DMT-plants.
-The experiential difference between LSD-25, ALD-52, and 1P-LSD.
-The fact that sometimes some effects, like bodyload, stimulation, sedation, or nausea, can be felt even minutes after ingesting a hallucinogen, before the substance could even have reached the brain.
In short: the guts have their own, more or less, autonomous nervous system that is sometimes refered to as "the second brain". Many important receptors that are present within the brain, are also found in this "second brain". This nervous system, though somewhat autonomous, is constantly communicating with the brain. Communication is going in both directions. Some scientists even speculate that bacteria in the intestines may be a major contributor to psychiatric illnesses like depression or OCD.
So one of the main mechanisms of classic psychedelic drugs like DMT, is downregulation of 5-ht2-a. This is an autonomous process that is the result of what the brain perceives as overstimulation of this receptor.
My theory is: even before a classic hallucinogen has crossed the blood-brain barrier, it may have already affected the nervous system of the bowels. The bowels can then send a warning signal to the brain: "incoming serotonin receptor agonist" and thus prime the brain, to be ready to start downregulation. This priming signal could already cause some of the effects associated with psychedelics, like experiencing bodyload, stimulation and mild changes in perception.
Another consequence would be, that although 1P-LSD and ALD-52 are thought to be converted to LSD-25 when passing the blood-brain barrier, they may have their own unique effects on the nervous system outside of the brain. So then within the brain they act in the same way because they are the same substance, but outside of the brain they have different effects, that affect the way the brain responds to LSD-25.
And about chaliponga: ofcourse you could say that perceived differences in effect are the result of the placebo-effect, but that chaliponga also consistently produces diffent effects, physically....projectile vomiting being the most mentionable, is not realy something that can easily be disputed.
Tannins are thought to be the main cause of these physical typicalities.
My thought is that this whole "ejection process", even when it doesn't lead to actual vomiting, could be "jamming" the priming signal to the brain, and thus affecting the way the brain responds to DMT.