Hi all,
it's been quite awhile since I've posted here, but this pharmacological quandary has been on my mind for quite some time now, and I've decided to come here and share my experiences and theories with those of you here that I have come to know have great knowledge and understanding of the minutiae and various intricacies of the dopamine system that I do not possess (I have a pretty good idea conceptually, but due to incomplete research, I have yet to learn about this system in depth).
First off, before trying Ethylphenidate, I read horror stories online of people binging and having full-blown stimulant psychosis, a product of WAY too much dopamine (Schizophrenics have a surplus of dopamine, which contributes to the hallucinations). I read about people seeing the dreaded "shadow people" and paranoia, setting traps in their houses to prevent the imaginary "intruders" from surprising them. So you can imagine I was a bit worried. I considered the sources, however, and since they were both from drug forums, and these accounts came from people that were known to have binging and addiction problems (the amounts they did I later found to be exorbitant, as well). My research on Eth showed that it was a DNRI, or Dopamine/Norepinephrine Re-uptake Inhibitor, and that it primarily worked on dopamine, not so much Norepinephrine (this fit exactly with my experience; more on this later). It actually had a very low affinity for the dopamine receptor, so agonism seemed to not be it's primary role, just re-uptake inhibition. I uncovered the curious fact that Ethylphenidate is actually created in the body when Methylphenidate (Ritalin) and Alcohol are consumed together, much like how Cocaine and Ethanol (Alcohol) combine to form Cocaethylene, a completely new compound as well. Methylphenidate seems to inhibit Norepinephrine re-uptake more than Dopamine, and Ethyl seems to be it's inverse. This seemed great to me, as I wanted more Dopamine and didn't quite like the tweaky feel that Norepinephrine provides (this is the speedy part, that causes bruxism (jaw clenching), appetite suppression, and general the more "tweaky" effects of stimulants. I decided to try it, but cautiously.
I started low, and since 100mg was listed as a strong dose, I decided to use my 10mg scoop to bump my first 10mg dose via insufflation. I had heard this route was painful and caused nose bleeds, but after about a week and a half of daily use (albeit light), my nose is better than ever. The small amounts at a time help (10mg), and I don't exceed 100mg in any day. My impression? I LOVE IT. It has all the benefits of a stimulant, but doesn't seem to have the negative side effects associated with them (and I am usually very sensitive to stimulant side effects). It wakes you up for sure, but does not "tweak" you out. It gives me the OPTION and ABILITY to be awake and alert if I want to be, but doesn't INSIST I be that way like amphetamines or methylphenidate. I can do a bump and then eat a full meal and then take a nap- this is just unheard of for me, as following stimulants I usually cannot eat for at least 24hrs and cannot sleep without pharmacological intervention. I attribute these positive effects bereft of the negative to Eth having little Norepinephrine re-uptake activity.
So my dilemma? I love Eth and have been productive and feeling great, but my mind knows that this is not sustainable and probably not good for the dopamine system. It can't be HORRIBLE; people take larger doses of Methylphenidate daily for years. I don't want to be those people, however. I've been devising ways to reduce it's impact on my dopamine system, and am open to new ideas. Here are a few things I have been trying:
-Sulbutiamine! Why? Sulbutiamine is reported to up-regulate dopamine receptors. Hopefully this combats tolerance and dopamine down-regulation a bit.
-SAM-e and L-Tyrosine! Why? SAM-e is a methyl donater, and it has been proposed that taking SAM-e in tandem with neurotransmitter precursors can methylate them and allow them to cross the BBB. Using a lot of dopamine? Yes. I figured having plenty of precursors may help not burning out the receptor.
I plan to cycle off of it soon, but I was wondering if any of you had any other thoughts in terms of mitigating wear and tear on the dopamine system. I forgot to mention that I am taking Alpha Lipoic Acid and N-Acetyl-Cysteine for antioxidant protection as well as Oxiracetam and Phenylpiracetam. I ceased my Suni+Uni combination to mitigate excitotoxicity. So- any ideas, bright people?
