Nootropic (new-tro-pik) is the term for supplements, also known as smart drugs, that improve brain function. They can be food substances like phenethylamine and L-Theanine, found in chocolate and green tea, respectively. Nootropics also include extracted and purified components of medicinal plants, as well as substances synthesized from chemical precursors, such as piracetam, the world's first official nootropic (piracetam was created in 1964 in Belgium by a team of scientists whose leader, Dr. Corneliu E. Giurgea, coined the term). Since then piracetam has been widely used as a cognitive enhancer and to treat neurological diseases like Alzheimer's.
The real culprit at the heart of the problem may be impossible to regulate – the human desire to have a supercharged brain. For now, this wish is still largely relegated to the domain of fiction. Researchers point out that increasing the power of certain parts of the brain, such as areas responsible for learning and focus, would likely deprive other parts of the brain that are needed to live. Despite the appeal of a super-brain, a better goal is still to maintain a balanced brain and lifestyle.
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I’ve spent over a million dollars hacking my own biology. The lion’s share has gone to making my brain produce as much energy as it can. I even wrote a book, Head Strong, about neurofeedback, oxygen deprivation, supplements, deeper sleep, meditation, cold exposure, and about a dozen other brain hacks, and how you can use them to make your brain stronger than you thought possible.
I almost resigned myself to buying patches to cut (and let the nicotine evaporate) and hope they would still stick on well enough afterwards to be indistinguishable from a fresh patch, when late one sleepless night I realized that a piece of nicotine gum hanging around on my desktop for a week proved useless when I tried it, and that was the answer: if nicotine evaporates from patches, then it must evaporate from gum as well, and if gum does evaporate, then to make a perfect placebo all I had to do was cut some gum into proper sizes and let the pieces sit out for a while. (A while later, I lost a piece of gum overnight and consumed the full 4mg to no subjective effect.) Google searches led to nothing indicating I might be fooling myself, and suggested that evaporation started within minutes in patches and a patch was useless within a day. Just a day is pushing it (who knows how much is left in a useless patch?), so I decided to build in a very large safety factor and let the gum sit for around a month rather than a single day.
I noticed what may have been an effect on my dual n-back scores; the difference is not large (▃▆▃▃▂▂▂▂▄▅▂▄▂▃▅▃▄ vs ▃▄▂▂▃▅▂▂▄▁▄▃▅▂▃▂▄▂▁▇▃▂▂▄▄▃▃▂▃▂▂▂▃▄▄▃▆▄▄▂▃▄▃▁▂▂▂▃▂▄▂▁▁▂▄▁▃▂▄) and appears mostly in the averages - Toomim’s quick two-sample t-test gave p=0.23, although a another analysis gives p=0.138112. One issue with this before-after quasi-experiment is that one would expect my scores to slowly rise over time and hence a fish oil after would yield a score increase - the 3.2 point difference could be attributable to that, placebo effect, or random variation etc. But an accidentally noticed effect (d=0.28) is a promising start. An experiment may be worth doing given that fish oil does cost a fair bit each year: randomized blocks permitting an fish-oil-then-placebo comparison would take care of the first issue, and then blinding (olive oil capsules versus fish oil capsules?) would take care of the placebo worry.

If all of this sounds great to you, get ready to level up your brain to game like a god with GodMode. Unless, you know, you're under 18, pregnant, potentially have any pre-existing medical conditions, are taking any prescription medications, are otherwise ingesting caffeine or taking other stimulants, or you don't want to drop $60 on gamer pills. Then, you know, don't.


50 pairs of active/placebos or 100 days. With 120 tablets and 4 tablets used up, that leaves me 58 doses. That might seem adequate except the paired t-test approximation is overly-optimistic, and I also expect the non-randomized non-blinded correlation is too high which means that is overly-optimistic as well. The power would be lower than I’d prefer. I decided to simply order another bottle of Solgar’s & double the sample size to be safe.
The basic idea is to remedy a deficiency (not look for acute stimulant effects) and magnesium has a slow excretion rate18, so week-long blocks seem appropriate. I can reuse the same methodology as the lithium self-experiment. The response variables will be the usual mood/productivity self-rating and, since I was originally interested in magnesium for possible sleep quality improvements, a standardized score of sleep latency + # of awakenings + time spent awake (the same variable as my potassium sleep experiment).
Caffeine dose dependently decreased the 1,25(OH)(2)D(3) induced VDR expression and at concentrations of 1 and 10mM, VDR expression was decreased by about 50-70%, respectively. In addition, the 1,25(OH)(2)D(3) induced alkaline phosphatase activity was also reduced at similar doses thus affecting the osteoblastic function. The basal ALP activity was not affected with increasing doses of caffeine. Overall, our results suggest that caffeine affects 1,25(OH)(2)D(3) stimulated VDR protein expression and 1,25(OH)(2)D(3) mediated actions in human osteoblast cells.
It looks like the overall picture is that nicotine is absorbed well in the intestines and the colon, but not so well in the stomach; this might be the explanation for the lack of effect, except on the other hand, the specific estimates I see are that 10-20% of the nicotine will be bioavailable in the stomach (as compared to 50%+ for mouth or lungs)… so any of my doses of >5ml should have overcome the poorer bioavailability! But on the gripping hand, these papers are mentioning something about the liver metabolizing nicotine when absorbed through the stomach, so…
Systematic reviews and meta-analyses of clinical human research using low doses of certain central nervous system stimulants found enhanced cognition in healthy people.[21][22][23] In particular, the classes of stimulants that demonstrate cognition-enhancing effects in humans act as direct agonists or indirect agonists of dopamine receptor D1, adrenoceptor A2, or both types of receptor in the prefrontal cortex.[21][22][24][25] Relatively high doses of stimulants cause cognitive deficits.[24][25]
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