So that "fogginess" you described and slight fatigue when trying to do a mentally taxing task go away with a few days/weeks of abstinence?
I guess that paragraph wasn't that clear. I meant that when doing something mentally taxing, I notice I'm not as good at it as I'm used to, having been on piracetam for months. I don't think this is because I'm having a rebound effect, but just that I'm accustomed to a higher baseline. The possible fogginess I mentioned isn't even something I have a clear memory of, but I wanted to allow for the possibility that there's a very slight readjustment. Piracetam has a good 50 years of usage history, and is probably the most commonly used nootropic there is. You're asking good questions, but I really don't think you have anything to worry about.
If you haven't seen it, check out the
Piracetam Rebound thread. Note that some people that posted were taking like 10g+ per days; I'm sure this accentuates problems. Some of this possibility is definitely due to personal neurochemical makeup, so it's not possible to say with 100% certainty what your experience will be. But I've never heard anyone say say that any effects from piracetam lasted more than a week or maybe two after cessation.
I posted 5 months ago that I thought there was a slight dip below baseline in verbal acumen for a few days after...again, it's so hard to say. Now I've had a lot more time with my new stack, and appreciate how much it improves my attentional difficulties. atm I'm more inclined to attribute this to upshifted expectations concerning my abilities, rather than a rebound due to downregulation. Maybe I'll take a break sometime this summer and see what I notice.
There are no magic pills when it comes to motivation but there might be something which can help me somewhat at least.
Guess you've never taken adderall, then?
This is actually my #1 concern at the moment: trying to find something to replace adderall with regard to motivational effects. Adderall has a lot of downsides, and I too would like something more sustainable (in a number of ways). Things that affect dopamine help: tyrosine, NALT, manganese, and transdermal nicotine have all modulated motivation slightly for me, but none so completely or strongly as adderall. Some are quite weak (manganese), and are only useful if you're prepared to utilize the window. Others are only motivating in a certain way. For instance, I have much the same reaction to NALT that babcock does; it doesn't motivate me to do complex/intellectual things, but really helps me do simple things like clean my room or watch TV, which my mind is usually way too ramped up for. I'm playing with tyrosine this week, but so far it seems slightly more functional. Nicotine is a little more complex...somewhere between tyrosine and NALT, but much warmer, such that it motivates me to be more social.
Deprenyl and galantamine were mentioned a couple of times with regard to motivation, mostly in much older threads. I'm hoping to order deprenyl sometime this month, but it's definitely more of a serious pharmaceutical than a nootropic. Then there are pharmaceutical dopamine agonists of varying selectivity, but my impression is that lots of them have mental or emotional side effects which limit their usefulness.
I think it's worth considering lateral attacks for motivation, as well. Dopamine may be most strongly implicated, but psychologically, this doesn't manifest as a continuum of motivated <-> not motivated. Different emotional systems and behavioral patterns come into play, too. For example, I started taking low dose lithium orotate lately (120/5mg), mostly for neuroprotective effects, but also hoping for a slight mood uplift. At least at the moment, the slight alteration in stress response is making a big difference in what I'm able to motivate myself to do. My difficulties are still there, and pretty severe, but it's easier to implement certain adaptations...actually chipping away at something for 5-10 minutes, rather than avoiding it (even subconsciously) based on how difficult it is to make myself do it (a partially self-fulfilling expectation, it seems). This may only apply to me, because of some thought patterns the last 10 years of my life have imprinted in me, but I think it's worth considering that drugs can have effects on systems which aren't directly implied by their mechanisms.
I honestly have no problem admitting that I'm looking for a magic pill or two; it doesn't bother me in the least that so much of my subjective experience can be modulated via neurochemical mechanisms. In fact, I think it's pretty awesome. Our cultural ideology is really biased against this view; I think we want to believe that we're either the way we are (period), or changeable via frameworks of willpower and effort which are within our conscious control. However, if I thought nootropics/pharmaceuticals were somehow a substitute for trying to make myself a better person through all the other means at my disposal, then I would start to worry
Here's a few paper summaries in my notes on motivation. I think this was for a post at M&M focusing on D1/D2. Mostly rats, but some of these are interesting nonetheless.
19331447 (comment in 19331471): D1/D2 antagonism caused rats to choose lesser rewards requiring less effort. Amphetamine administration blunted this effect, and biased them toward greater effort/reward ("bidirectional modulation of choice behavior"). D3 agonists/antagonists had no effect.
17142306: Evidence that D1 receptors in the anterior cingulate cortex (ACC) encode whether or not an action is worth performing due to expected benefit/cost. Intra-ACC D1 antagonism reduced the tendency to expend effort for greater reward, while ACC D2 antagonism had no effect on this.[rat study]
17805307: "Cost/benefit decisions regarding the relative effort or delay costs associated with a particular response are mediated by distributed dopaminergic and glutamatergic neural circuits." Most relevantly, high doses of amphetamine caused rats to discount greater effort when seeking reward, while low doses allowed them to discount delay. NMDA agonism allowed discounting of both, but did not have as direct an impact on choices made.
15864561: D2 antagonism reduced tolerance for greater effort and delay to attain rewards, while inhibition of serotonin biosynthesis reduced acceptance of only delay.
18668030: Activation of D1/D2 biased rats toward risking painful response for greater reward; antagonism blocked this, and producd risk aversion. D3 operated inversely.
