basement_shaman
Bluelighter
- Joined
- Dec 14, 2010
- Messages
- 168
About two months ago I ordered 100 grams of pure caffeine powder, intending to simply save a lot of money on Mountain Dew and Monsters.
However I have now come to the conclusion that caffeine will be included as a drug in every single upper-experience I will have in the future. And here's why.
I find that it synergizes awfully well, extremely well actually, with any dopaminergic upper. It provides an actual small rush when snorted in 150+ mg doses and heavily increases the boosted focus that stimulants provide. I redose the caffeine at the same time as the main drug.
Drugs so far that have provided additional euphoria when combined with caffeine:
Methiopropamine
Methylphenidate
Mexthoxetamine (slightly out of category but still valid)
MPA/MDAI combo
Methylphenidate/MDAI combo
MDAI alone (Huge boost!)
Now, I have been thinking about the reasons for this.
First off I suppose that the direct effects of adenosine antagonism (i.e. wards off the sense of having been awake for an extended period) leads to to a combination that's automatically pleasant, but I suspect there is more at play. I started digging in caffeine's pharmacology and these are my conclusions:
Adenosine is released along with some other neurotransmitters, thus the levels are building up as you are awake and decrease when you sleep. Adenosine is also the end product of ATP once the phosphate groups are eaten off for cell energy, thus providing another source for the buildup.
When caffeine enters the body and then brain, it antagonizes the A2A adenosine receptor. When adenosine activates this receptor, release of several neurotransmitters is suppressed. These neurotransmitters are "glutamate, epinephrine, norepinephrine, dopamine, acetylcholine, and to a lesser extent, serotonin" according to wikipedia's main article on caffeine.
So it seems that when caffeine prevents adenosine from acting at the A2A receptor, it directly leads to a "suppression of the suppression" of dopamine release, thus explaining the synergy with methylphenidate and methoxetamine as they are DRIs (I know it's not 100% established for MXE but seemingly it holds true). One possibility as to the mechanism of this is that there exist receptor complexes between the adenosine A2A and dopamine D2 receptors.
Now, why the immense synergy with MDAI?
We pretty much know that the huge euphoria from MDMA is due to the simultaneous release of dopamine and serotonin.
It thus seems that when you add caffeine to the MDAI, you not only have the serotonin release of the MDAI but also the decreased suppression of dopamine release from the caffeine, thus slightly emulating the actions of MDMA. I know that many people including myself have utilized this to combine MDAI with a dopaminergic drug for emulating MDMA. I now propose that simply caffeine may be enough to achieve this.
Any thoughts, comments or criticism?
Some relevant papers:
The novel adenosine A2a antagonist ST1535 potentiates the effects of a threshold dose of l-dopa in unilaterally 6-OHDA-lesioned rats
Adenosine A2A and dopamine D2 heteromeric receptor complexes and their function.
However I have now come to the conclusion that caffeine will be included as a drug in every single upper-experience I will have in the future. And here's why.
I find that it synergizes awfully well, extremely well actually, with any dopaminergic upper. It provides an actual small rush when snorted in 150+ mg doses and heavily increases the boosted focus that stimulants provide. I redose the caffeine at the same time as the main drug.
Drugs so far that have provided additional euphoria when combined with caffeine:
Methiopropamine
Methylphenidate
Mexthoxetamine (slightly out of category but still valid)
MPA/MDAI combo
Methylphenidate/MDAI combo
MDAI alone (Huge boost!)
Now, I have been thinking about the reasons for this.
First off I suppose that the direct effects of adenosine antagonism (i.e. wards off the sense of having been awake for an extended period) leads to to a combination that's automatically pleasant, but I suspect there is more at play. I started digging in caffeine's pharmacology and these are my conclusions:
Adenosine is released along with some other neurotransmitters, thus the levels are building up as you are awake and decrease when you sleep. Adenosine is also the end product of ATP once the phosphate groups are eaten off for cell energy, thus providing another source for the buildup.
When caffeine enters the body and then brain, it antagonizes the A2A adenosine receptor. When adenosine activates this receptor, release of several neurotransmitters is suppressed. These neurotransmitters are "glutamate, epinephrine, norepinephrine, dopamine, acetylcholine, and to a lesser extent, serotonin" according to wikipedia's main article on caffeine.
So it seems that when caffeine prevents adenosine from acting at the A2A receptor, it directly leads to a "suppression of the suppression" of dopamine release, thus explaining the synergy with methylphenidate and methoxetamine as they are DRIs (I know it's not 100% established for MXE but seemingly it holds true). One possibility as to the mechanism of this is that there exist receptor complexes between the adenosine A2A and dopamine D2 receptors.
Now, why the immense synergy with MDAI?
We pretty much know that the huge euphoria from MDMA is due to the simultaneous release of dopamine and serotonin.
It thus seems that when you add caffeine to the MDAI, you not only have the serotonin release of the MDAI but also the decreased suppression of dopamine release from the caffeine, thus slightly emulating the actions of MDMA. I know that many people including myself have utilized this to combine MDAI with a dopaminergic drug for emulating MDMA. I now propose that simply caffeine may be enough to achieve this.
Any thoughts, comments or criticism?
Some relevant papers:
The novel adenosine A2a antagonist ST1535 potentiates the effects of a threshold dose of l-dopa in unilaterally 6-OHDA-lesioned rats
Adenosine A2A and dopamine D2 heteromeric receptor complexes and their function.
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