Pulled from
Seemed like some handy info.
"One of my test subjects was a heavy, frequent user of Cannabis for many years. During the more strenuous portions of his undergraduate studies in the sciences, he found nootropics to be helpful. After a great deal of experimentation, he settled on a small regimen of nootropics to aid in his studying- namely in consolidation and recall, as well as overall vocabulary. In particular, for focus and consolidation, he found that oxiracetam was very helpful, if not a bit short-lived. Pramiracetam proved helpful as well, but was generally too expensive to maintain. He found that piracetam was largely ineffectual for him, though knew others who used it to some success. Aniracetam was helpful, as well, but with a significant deal of emotional side-effects- namely, irritability and anxiety (despite it being touted as a potential anxiolytic).
In terms of combating the more culpable culprit of cannabis-induced memory problems, memory recall, he fond that the most effective compound was l-huperzine. 250µg 5x/week was enough to significantly enhance his semantic and image-based recall, largely enhancing his scientific vocabulary in a time of great need, and producing an oddly photographic state of memory on many occasions during forced recall.
Throughout all of this, he experimented with various sources of choline. If affordable, Alpha-GPC was the most favorable in terms of lifting the cannabis-induced mental-fog. However, he found that choline-citrate was a fully acceptable second. Even without other nootropics, either of these choline sources seems to have a positive effect on cognitive clarity and memory."
Further thoughts:
One leading theory is understanding the effects via a signal/noise ratio problem. Increased quantities of cannabinoid-agonists in the synapse results in the activation of presynaptic CB1 receptors, mimicking the effects of depolarization-induced suppression of inhibition/excitation (DSI/E). In this case, our major concern is with DSI, though DSE plays a role as well. Normally, inhibitory synapses in regions associated with memory (i.e. the hippocampus, amygdala, mammilary bodies, papez-circuit..etc.) are useful to reduce the level of overall neuronal activity (noise) in order to allow the excitatory signals (signal) to be more prominent. If we inhibit these inhibitory synapses, a rise in excitatory noise is achieved, resulting in a lower signal/noise ratio. This may account for the easy distractibility and lack of focus which characterize the deleterious effects of cannabis on memory-oriented cognition. Obviously, that is an oversimplification of what is actually occurring and the compensatory mechanisms which exist to control the situation- however, it is a good starting point.
So, how do we increase the signal/noise ratio? Well, there are a few approaches. One might be to increase the signal. This can be achieved via glutamatergic and cholinergic drugs, which would include most psychomotor stimulants (incl. the prescription nootropic, methylphenidate) and some nootropics (-racetams, l-huperzine). The other option is to decrease the noise, which might be achieved by very low-dose GABAergics (though, if not done accurately this could actually exacerbate the problem) with a low side-effect profile such as alprazolam (start with 100µg or less) or diazepam (start with 750-1,000µg or less).
Of course, there are competing theories on the causes of cannabis-induced memory/cognitive issues-- one of the most interesting, in my opinion, being inhibition of mTOR signaling resulting in decreased protein-synthesis capabilities at the synapse. Then there is the BDNF theory, a non-hippocampal theory, and many more.
-------------------- --------------------------------------------------- Sit up and meditate, there's no time to contemplate. ------------------------------------------------- I have an international Hitech Psytrance project with a friend: BioChronic I make various form of Psytrance as a solo Project Dendriform
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I tried piracetam. I was taking low doses though because whatever the reccomended dose (four times what I took) felt too speedy for my liking. I found it a waste of time, but, I dunno. Maybe this smooths out brain fuzzyness that can be caused by all sorts of variables. Who can say?
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