I have finals right now and have been taking DMAE with Smart Focus Formula (huperzine A, a bit of vinpocetine and rhodiola) regularly for about 2 weeks. I recently procured a cap of concerta. Would it be safe to take these all together? What about if I have been preloading the others for 2 weeks, but didn't take them on the day I took the methylphenidate? I just want to know if anyone thinks there's a risk.
Thanks for your help!
EDIT: forgive the typo in the title, meant to write DMAE.
It would be interesting to get the exact dosages contained within the Smart Focus Formula.
Methylphenidate actually works as a dopamine and norepinephrine reuptake inhibitor, increasing the presence of these neurotransmitters. I'm not really sure if an abundance of Dopamine causes health concerns, but based on some of the findings Vinpocetine increases dopamine[1] and Rhodiola is supposedly responsible for creating a balance within serotonin and dopamine levels, hence the term adaptogen. You probably already know that though.
DMAE mainly affects acetylcholine levels within the brain, though I personally believe it seems to have more of an anticholinergic effect mentally, giving thoughts a viscosity that can be detrimental for creative thought (I had a weird experience with it). I kind of feel though that the combination of the two precursors of stimulatory neurotransmitters will backfire a bit. Especially considering you're using both huperzine, which decreases the chemical responsible for the breakdown of acetylcholine and DMAE, which supposedly is a much stronger precursor of ACh. Though i stipulate that the levels found within the Smart Focus Formula are quite low, maybe to the point of not being cost effective?
Those are mainly assumptions though, but I'm wondering, if you've taken the combination before, did you feel overly active? Sounds like an interesting combination nonetheless, but experimentation during finals doesn't sound like a great idea

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[1]
Increases in neuronal levels of DOPAC, a metabolic breakdown product of dopamine, have been shown to occur in striatal isolated nerve endings as a result of exposure to vinpocetine.[12] Such an effect is consistent with the biogenic pharmacology of reserpine, a structural relative of vinpocetine, which depletes catecholamine levels and may cause depression as a side-effect of the cardiovascular and anti-psychotic effects.[13]
http://en.wikipedia....iki/Vinpocetine