Still, putting unregulated brain drugs into my system feels significantly scarier than downing a latte or a Red Bull—not least because the scientific research on nootropics’ long-term effects is still so thin. One 2014 study found that Ritalin, modafinil, ampakines, and other similar stimulants could eventually reduce the “plasticity” of some of the brain’s neural networks by providing them with too much dopamine, glutamate and norepinephrine, and potentially cause long-term harm in young people whose brains were still developing. (In fact, in young people, the researchers wrote, these stimulants could actually have the opposite effect the makers intended: “Healthy individuals run the risk of pushing themselves beyond optimal levels into hyperdopaminergic and hypernoradrenergic states, thus vitiating the very behaviors they are striving to improve.”) But the researchers found no evidence that normal doses of these drugs were harmful when taken by adults.
Ampakines are structurally derived from a popular nootropic called “aniracetam”. Their basic function is to activate AMPA glutamate receptors (AMPARs). Glutamate (a neurotransmitter) is the primary mediator of excitatory synaptic transmission in mammalian brains, which makes it crucial for synaptic plasticity (the adaptation of synapses, the space between neurons across which information is sent), learning and memory, so when you activate or stimulate glutamate receptors, you can trigger many of these functions. AMPARs are distributed across the central nervous system and are stimulated by incoming glutamate to begin the neuroenhancing benefits they’re often used for. But it is possible to have too much glutamate activity. When excess glutamate is produced, accumulates and binds to AMPARs, the result is excitotoxicity, which is a state of cell death (in the case of the central nervous system and your brain, neuron death) resulting from the toxic levels of excitatory amino acids. Excitotoxicity is believed to play a major role in the development of various degenerative neurological conditions such as schizophrenia, delirium and dementia.

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In 3, you’re considering adding a new supplement, not stopping a supplement you already use. The I don’t try Adderall case has value $0, the Adderall fails case is worth -$40 (assuming you only bought 10 pills, and this number should be increased by your analysis time and a weighted cost for potential permanent side effects), and the Adderall succeeds case is worth $X-40-4099, where $X is the discounted lifetime value of the increased productivity due to Adderall, minus any discounted long-term side effect costs. If you estimate Adderall will work with p=.5, then you should try out Adderall if you estimate that 0.5 \times (X-4179) > 0 ~> $X>4179$. (Adderall working or not isn’t binary, and so you might be more comfortable breaking down the various how effective Adderall is cases when eliciting X, by coming up with different levels it could work at, their values, and then using a weighted sum to get X. This can also give you a better target with your experiment- this needs to show a benefit of at least Y from Adderall for it to be worth the cost, and I’ve designed it so it has a reasonable chance of showing that.)
(People aged <=18 shouldn’t be using any of this except harmless stuff - where one may have nutritional deficits - like fish oil & vitamin D; melatonin may be especially useful, thanks to the effects of screwed-up school schedules & electronics use on teenagers’ sleep. Changes in effects with age are real - amphetamines’ stimulant effects and modafinil’s histamine-like side-effects come to mind as examples.)
At this point I began to get bored with it and the lack of apparent effects, so I began a pilot trial: I’d use the LED set for 10 minutes every few days before 2PM, record, and in a few months look for a correlation with my daily self-ratings of mood/productivity (for 2.5 years I’ve asked myself at the end of each day whether I did more, the usual, or less work done that day than average, so 2=below-average, 3=average, 4=above-average; it’s ad hoc, but in some factor analyses I’ve been playing with, it seems to load on a lot of other variables I’ve measured, so I think it’s meaningful).

In fact, many nerve gas agents act similarly to Huperzia serrata by blocking the enzyme that breaks down acetylcholine. But research has shown that in smaller doses, Huperzine A, the extract of Huperzia serrata used in nootropics, would likely offer some protection against damage from nerve agents. That the same substance can act as a nerve agent, protect against nerve agents, and give you crazy dreams, underscores how important it is to stay within the recommended doses.
In addition to this, privilege also plays an important role in this epidemic. "Not everyone has access to eat healthily", she mentions. In fact, she recalls an anecdote in which a supermarket owner noticed how people living off food stamps rarely use them to buy fruits and vegetables. Curious about this trend, the owner approached someone with food stamps, to which she admitted she didn't buy them because she didn't know the price prior to weighing them and felt ashamed of asking. His solution? Pre-cutting and packaging fruits in order to make them more accessible to those with lower incomes. 
By the way, before we move on, allow me to clarify what I mean by “slow caffeine metabolizer”. Ever wondered why your co-worker can slam four giant mugs of coffee during a brief morning of work, while one shot of espresso leaves you jittery and irritated? Turns out that not everyone metabolizes caffeine the same. Generally speaking, in healthy adults, caffeine has a half-life that ranges from about 3 to 7 hours. For example, if the half-life of caffeine in your blood is 5 hours, that means that it takes 5 hours for caffeine levels to be reduced by 50%. Then it takes another 5 hours for that amount to be reduced by 50%. While caffeine metabolism time also depends upon age and environmental factors, a big influence on varying caffeine half-life times is your genetic makeup.

Eugeroics (armodafinil and modafinil) – are classified as "wakefulness promoting" agents; modafinil increased alertness, particularly in sleep deprived individuals, and was noted to facilitate reasoning and problem solving in non-ADHD youth.[23] In a systematic review of small, preliminary studies where the effects of modafinil were examined, when simple psychometric assessments were considered, modafinil intake appeared to enhance executive function.[27] Modafinil does not produce improvements in mood or motivation in sleep deprived or non-sleep deprived individuals.[28]
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