Preface
This may have been covered before, but upon a search I couldn't readily find anything about it. I concede that I may not have searched back far enough.
Additionally, I'm not a chemist nor a trained biologist. I can search for and comprehend studies well, but not with the educational context of many here. So, forgive my layman's understanding.
Last, I have a ton of school work to do right now, and so I haven't searched extensively on this. My insight on this has come from both short term use as well as...drumroll....wikipedia as a starting source.
Admit it, your excited to comment on this already
My Supplementation Habits
I'm an extremely cautious experimenter as a matter of instinct. Although, I suppose that such an approach is out of a sense of self preservation, it seems to hinder me more than help. I'm trying to break myself of adhering too strongly to imagined models of stacking supplements that could really use a lot of adjustment.
Case in point: I had several months of racetam use, previously, but stuck to DMAE as a choline source. I think that may have severely limited my experience, but I thought that "choline was choline".
Additionally, although I had ALACAR on hand, I hardly tried it out of some fancied belief that pricaetam on its own was the way to nootropic bliss. When you start with all of this, its very difficult to quickly gain a comprehensive model of how these supplements behave and interact. Furthermore, which ones have extreme value and which have less so.
My point is, that although I have been supplementing for a while, on and off, the following might seem like a "basic" revelation in terms of the supplements combined.
Topic
Today I took a dose of ALCAR that amounted to 1/10th or less of a "00" Capsule. I waited twenty minutes and felt something, but very subtle
At the twenty minute mark, I ingested a very small amount of choline(5 drops mixed with an acid) that was actually just a stabilizing agent used in "Biosil" (I have choline bitartrate on order). I had before noticed that this choline had helped me recover from a post huperzine migraine after the first day that I had taken the huperzine, and so today I purposely took the Biosil solely for the choline content - to determine how it would interact with the ALCAR. Initially, I noticed a decrease in cognitive awareness, starting with an immediate increase in my hearing issues. However, about seven minutes later that subsided and I felt fantastic. I mean, really good. I noticed significant neuroprotective effect against my light sensitivity issues and an overall felling of well being that seemed to mimic a 200 mg does of huperzine, but more intense and with a better overall feeling of health about it. It lasted about four hours. Remember, this was with miniscule amounts of both substances.
So, in-between my studies today, I was reading about acetylcholine on wikipedia. Just to make sure I had the model of action fairly correct in my head. The brief upregulation of my hearing issue worried me, and so I wanted to make sure that I wasn't further doing anything that would be ototoxic.
About halfway down the page, under, "Drugs acting on the acetylcholine system", there is a list with this text above it:
"These are drugs that mimic acetylcholine on the receptor. In low doses, they stimulate the receptors, in high they numb them due to depolarization block."
Then, the first 'drug' listed is ALCAR.
Question
I know that many people here take daily doses of ALCAR that range from 250 mg up to a few grams per day, sometimes several times per day. However, if assertion of the wikipedia entry is correct, and this depolarization block occurs to a degree in the brain, thus preventing ACh release, then high does ALCAR would have the opposite effect of what is desired.
In the context of the depolarization block assertion, and in theory, a very low dose of ALCAR(perhaps the lower the better) in addition to choline 20-30 minutes later, and perhaps a B complex vitamin, would lead to a significant enhancement effect professed to be desired with ALCAR or choline alone.
It feels like , if one so desired to experiment, one could then take to another level with huperzine - assuming that you would desire that and one did not consume too much choline. Although, that may be setting the stage for too much ACh, regardless. Or, maybe its great.
It has already been determined that the way to prevent ALCAR induced mitochondrial ROS is with a lose dose. Perhaps, that mechanism also speaks to a low dose having a superior effect, in general.
Conclusion
This model might explain why some people get bad reactions from ALCAR. I would be willing to bet that anyone that doesn't understand the hype, or has had issues, has always taken a high dose, or if the have taken it at a very low dose then they haven't followed it up with choline.
Experimenting with both low and high doses of choline, post low dose ALCAR, seems to be warranted.
I'm ready to get criticized on my understanding of this. However, maybe even if I am off, then this will open up a discussion of the possible benefits of extremely low dose ALCAR.
