|>> || |
Nootropics are tricky, as each nootropic is liable to have differing pharmacokinetics and/or pharmacodynamics, meaning each substance has to be taken with respect to its own optimum dose range and dosing regimens, taking into account the interactions between each respective nootropic in a stack in addition to how you yourself respond to the substance.
You take 300mg of Phenylpiracetam with 300mg to boost 4-5hrs later (with a choline source, I prefer pre-loaded but I've never found this to be necessary) and you will very likely experience some notable nootropic effect in time for that daunting test with the essay question you know is just waiting to inscribe the meaning of pain into your dominant palm.
In contrast, if you took 300mg Piracetam and boosted after 6 hours with another 300, it's doubtful you'll experience much nootropic effect in time for the exam. Not only does Piracetam tend to require doses of 1-2g+ (in total throughout the day, split into 2-3 doses) before starting to shine, it also doesn't really start to shine until you've been keeping up your regimen consistently for weeks (IME, and in the experience of many others).
My experience is mostly with racetams, I wouldn't consider the likes of L-Tyrosine or other amino acid/neurotransmitter precursors to be any more nootropic than a large serving of meat & alternatives. They're nutrients. They only become nootropic once you're on actual nootropics that partially diminish or exhaust stores of neurotransmitters.
IME racetams shine in stacks, and I've found no partner more comp[limentary to nootropic effect than the original "smart drug," amphetamine. IIRC, they compliment one another quite amicably both pharmacologically, on paper, and cognitively, in practice. The only concern I could muster (aside from not yet-well-studied-but-nonetheless-seemingly-negligible-if-present-whatsoever long-term side effects (in excess of 30 years, 1 week for some of these new racetams) was a potential for glutamate excitotoxicity and resultant apoptosis, dopamine excitotoxicity " ", and a very weak link to what I imagine might cause a lowering of the seizure threshold as a result of AMPA/kainate receptor modulation, but I didn't get far into that reading before my ADHD took me on a detour.
Speaking of which: for fuck's sake, I got distracted for three seconds just now and stumbled upon this:
Don't let the "nature" tag fool you, this is a real medical journal. Apparently, amphetamine coaxing more dopamine out of those neurons might mitigate some of the glutamatergic impacts on its own.
Regardless of the neurotransmitter causing excitotoxicity, the actual process of cell death is closely linked to the production of reactive oxygen and nitrogen species in the uh... Cytoplasm? Insubstantial. What matters is that these chemicals are powerful oxidizers that contribute to the complex chain of events leading to the destruction of nerve terminals. This process can be interrupted, slowed, and it's damage reduced (if not prevented entirely) by generous loads of antioxidants. Here's the catch: generous loads. Ketamine or dextromethorphan can protect against glutamatergic excitotoxicity IIRC, but my readings suggest that my favourite drug here-to-shake-up-the-pharmaceutical-industry, cannabis (namely THC, CBD, and no doubt the hundreds of other cannabinoids found within its buds) contains antioxidant properties that are substantial, if my interpretation of the literature is accurate. In a nutshell, constantly keeping cannabinoid levels up in your bloodstream can contribute to a multi-faceted antioxidant and anti-inflammatory defense that I'd bet my neurons on.
Then again, there is documentation of cannabis and some psychedelics inducing neurogenesis in regions of the brain, most notably the hippocampus (perhaps my assertions that cannabis and psychedelics applied correctly are nootropics shall be realized as commonplace in time!).
I have a feeling that even if I accidentally the whole hippocampus, recovery from neuronal cell loss as a result of this stack (or others, or diseases such as Huntington's or Parkinson's, take your pick) could be possible.
Anyhow, I tire. Basically, you gotta know your nootropic(s).