Whole pill at 3 AM. I spend the entire morning and afternoon typing up a transcript of Earth in My Window. I tried taking a nap around 10 AM, but during the hour I was down, I had <5m of light sleep, the Zeo said. After I finished the transcript (~16,600 words with formatting), I was completely pooped and watched a bunch of Mobile Suit Gundam episodes, then I did Mnemosyne. The rest of the night was nothing to write home about either - some reading, movie watching, etc. Next time I will go back to split-doses and avoid typing up 110kB of text. On the positive side, this is the first trial I had available the average daily grade Mnemosyne 2.0 plugin. The daily averages all are 3-point-something (peaking at 3.89 and flooring at 3.59), so just graphing the past 2 weeks, the modafinil day, and recovery days: ▅█▅▆▄▆▄▃▅▄▁▄▄ ▁ ▂▄▄█. Not an impressive performance but there was a previous non-modafinil day just as bad, and I’m not too sure how important a metric this is; I must see whether future trials show similar underperformance. Nights: 11:29; 9:22; 8:25; 8:41.
In a broad sense, this is enhancement; in a stricter one, it’s optimisation. “I think people think about smart drugs the way they think about steroids in athletics,” Arnsten says, “but it’s not a proper analogy, because with steroids you’re creating more muscle. With smart drugs, all you’re doing is taking the brain that you have and putting it in its optimal chemical state. You’re not taking Homer Simpson and making him into Einstein.”
Of all the smart drugs in the world, Modafinil is most often touted as the best. It’s a powerful cognitive enhancer, great for boosting alertness, and has very few, mild side effects that most healthy users will never experience. And no, you can’t have any. Sorry. Modafinil is a prescription medication used to treat disorders like narcolepsy, shift work sleep disorder, and for those who suffer from obstructive sleep apnea.
A big part is that we are finally starting to apply complex systems science to psycho-neuro-pharmacology and a nootropic approach. The neural system is awesomely complex and old-fashioned reductionist science has a really hard time with complexity. Big companies spends hundreds of millions of dollars trying to separate the effects of just a single molecule from placebo – and nootropics invariably show up as “stacks” of many different ingredients (ours, Qualia , currently has 42 separate synergistic nootropics ingredients from alpha GPC to bacopa monnieri and L-theanine). That kind of complex, multi pathway input requires a different methodology to understand well that goes beyond simply what’s put in capsules.
Overall, the studies listed in Table 1 vary in ways that make it difficult to draw precise quantitative conclusions from them, including their definitions of nonmedical use, methods of sampling, and demographic characteristics of the samples. For example, some studies defined nonmedical use in a way that excluded anyone for whom a drug was prescribed, regardless of how and why they used it (Carroll et al., 2006; DeSantis et al., 2008, 2009; Kaloyanides et al., 2007; Low & Gendaszek, 2002; McCabe & Boyd, 2005; McCabe et al., 2004; Rabiner et al., 2009; Shillington et al., 2006; Teter et al., 2003, 2006; Weyandt et al., 2009), whereas others focused on the intent of the user and counted any use for nonmedical purposes as nonmedical use, even if the user had a prescription (Arria et al., 2008; Babcock & Byrne, 2000; Boyd et al., 2006; Hall et al., 2005; Herman-Stahl et al., 2007; Poulin, 2001, 2007; White et al., 2006), and one did not specify its definition (Barrett, Darredeau, Bordy, & Pihl, 2005). Some studies sampled multiple institutions (DuPont et al., 2008; McCabe & Boyd, 2005; Poulin, 2001, 2007), some sampled only one (Babcock & Byrne, 2000; Barrett et al., 2005; Boyd et al., 2006; Carroll et al., 2006; Hall et al., 2005; Kaloyanides et al., 2007; McCabe & Boyd, 2005; McCabe et al., 2004; Shillington et al., 2006; Teter et al., 2003, 2006; White et al., 2006), and some drew their subjects primarily from classes in a single department at a single institution (DeSantis et al., 2008, 2009; Low & Gendaszek, 2002). With few exceptions, the samples were all drawn from restricted geographical areas. Some had relatively high rates of response (e.g., 93.8%; Low & Gendaszek 2002) and some had low rates (e.g., 10%; Judson & Langdon, 2009), the latter raising questions about sample representativeness for even the specific population of students from a given region or institution.
The leadership position in the market is held by the Americas. The region has favorable reimbursement policies and a high rate of incidence for chronic and lifestyle diseases which has impacted the market significantly. Moreover, the region's developed economies have a strong affinity toward the adoption of highly advanced technology. This falls in line with these countries well-develop healthcare sectors.

One of the most widely known classes of smart drugs on the market, Racetams, have a long history of use and a lot of evidence of their effectiveness. They hasten the chemical exchange between brain cells, directly benefiting our mental clarity and learning process. They are generally not controlled substances and can be purchased without a prescription in a lot of locations globally.
Use of prescription stimulants by normal healthy individuals to enhance cognition is said to be on the rise. Who is using these medications for cognitive enhancement, and how prevalent is this practice? Do prescription stimulants in fact enhance cognition for normal healthy people? We review the epidemiological and cognitive neuroscience literatures in search of answers to these questions. Epidemiological issues addressed include the prevalence of nonmedical stimulant use, user demographics, methods by which users obtain prescription stimulants, and motivations for use. Cognitive neuroscience issues addressed include the effects of prescription stimulants on learning and executive function, as well as the task and individual variables associated with these effects. Little is known about the prevalence of prescription stimulant use for cognitive enhancement outside of student populations. Among college students, estimates of use vary widely but, taken together, suggest that the practice is commonplace. The cognitive effects of stimulants on normal healthy people cannot yet be characterized definitively, despite the volume of research that has been carried out on these issues. Published evidence suggests that declarative memory can be improved by stimulants, with some evidence consistent with enhanced consolidation of memories. Effects on the executive functions of working memory and cognitive control are less reliable but have been found for at least some individuals on some tasks. In closing, we enumerate the many outstanding questions that remain to be addressed by future research and also identify obstacles facing this research.

But there would also be significant downsides. Amphetamines are structurally similar to crystal meth – a potent, highly addictive recreational drug which has ruined countless lives and can be fatal. Both Adderall and Ritalin are known to be addictive, and there are already numerous reports of workers who struggled to give them up. There are also side effects, such as nervousness, anxiety, insomnia, stomach pains, and even hair loss, among others.
This would be a very time-consuming experiment. Any attempt to combine this with other experiments by ANOVA would probably push the end-date out by months, and one would start to be seriously concerned that changes caused by aging or environmental factors would contaminate the results. A 5-year experiment with 7-month intervals will probably eat up 5+ hours to prepare <12,000 pills (active & placebo); each switch and test of mental functioning will probably eat up another hour for 32 hours. (And what test maintains validity with no practice effects over 5 years? Dual n-back would be unusable because of improvements to WM over that period.) Add in an hour for analysis & writeup, that suggests >38 hours of work, and 38 \times 7.25 = 275.5. 12,000 pills is roughly $12.80 per thousand or $154; 120 potassium iodide pills is ~$9, so \frac{365.25}{120} \times 9 \times 5 = 137.
Dosage is apparently 5-10mg a day. (Prices can be better elsewhere; selegiline is popular for treating dogs with senile dementia, where those 60x5mg will cost $2 rather than $3531. One needs a veterinarian’s prescription to purchase from pet-oriented online pharmacies, though.) I ordered it & modafinil from Nubrain.com at $35 for 60x5mg; Nubrain delayed and eventually canceled my order - and my enthusiasm. Between that and realizing how much of a premium I was paying for Nubrain’s deprenyl, I’m tabling deprenyl along with nicotine & modafinil for now. Which is too bad, because I had even ordered 20g of PEA from Smart Powders to try out with the deprenyl. (My later attempt to order some off the Silk Road also failed when the seller canceled the order.)
DNB-wise, eyeballing my stats file seems to indicate a small increase: when I compare peak scores D4B scores, I see mostly 50s and a few 60s before piracetam, and after starting piracetam, a few 70s mixed into the 50s and 60s. Natural increase from training? Dunno - I’ve been stuck on D4B since June, so 5 or 10% in a week or 3 seems a little suspicious. A graph of the score series26:
At this point, I began thinking about what I was doing. Black-market Adderall is fairly expensive; $4-10 a pill vs prescription prices which run more like $60 for 120 20mg pills. It would be a bad idea to become a fan without being quite sure that it is delivering bang for the buck. Now, why the piracetam mix as the placebo as opposed to my other available powder, creatine powder, which has much smaller mental effects? Because the question for me is not whether the Adderall works (I am quite sure that the amphetamines have effects!) but whether it works better for me than my cheap legal standbys (piracetam & caffeine)? (Does Adderall have marginal advantage for me?) Hence, I want to know whether Adderall is better than my piracetam mix. People frequently underestimate the power of placebo effects, so it’s worth testing. (Unfortunately, it seems that there is experimental evidence that people on Adderall know they are on Adderall and also believe they have improved performance, when they do not5. So the blind testing does not buy me as much as it could.)
After I ran out of creatine, I noticed the increased difficulty, and resolved to buy it again at some point; many months later, there was a Smart Powders sale so bought it in my batch order, $12 for 1000g. As before, it made Taekwondo classes a bit easier. I paid closer attention this second time around and noticed that as one would expect, it only helped with muscular fatigue and did nothing for my aerobic issues. (I hate aerobic exercise, so it’s always been a weak point.) I eventually capped it as part of a sulbutiamine-DMAE-creatine-theanine mix. This ran out 1 May 2013. In March 2014, I spent $19 for 1kg of micronized creatine monohydrate to resume creatine use and also to use it as a placebo in a honey-sleep experiment testing Seth Roberts’s claim that a few grams of honey before bedtime would improve sleep quality: my usual flour placebo being unusable because the mechanism might be through simple sugars, which flour would digest into. (I did not do the experiment: it was going to be a fair amount of messy work capping the honey and creatine, and I didn’t believe Roberts’s claims for a second - my only reason to do it would be to prove the claim wrong but he’d just ignore me and no one else cares.) I didn’t try measuring out exact doses but just put a spoonful in my tea each morning (creatine is tasteless). The 1kg lasted from 25 March to 18 September or 178 days, so ~5.6g & $0.11 per day.
“Love this book! Still reading and can’t wait to see what else I learn…and I am not brain injured! Cavin has already helped me to take steps to address my food sensitivity…seems to be helping and I am only on day 5! He has also helped me to help a family member who has suffered a stroke. Thank you Cavin, for sharing all your knowledge and hard work with us! This book is for anyone that wants to understand and implement good nutrition with all the latest research to back it up. Highly recommend!”
The question of whether stimulants are smart pills in a pragmatic sense cannot be answered solely by consideration of the statistical significance of the difference between stimulant and placebo. A drug with tiny effects, even if statistically significant, would not be a useful cognitive enhancer for most purposes. We therefore report Cohen’s d effect size measure for published studies that provide either means and standard deviations or relevant F or t statistics (Thalheimer & Cook, 2002). More generally, with most sample sizes in the range of a dozen to a few dozen, small effects would not reliably be found.
The evidence? A 2012 study in Greece found it can boost cognitive function in adults with mild cognitive impairment (MCI), a type of disorder marked by forgetfulness and problems with language, judgement, or planning that are more severe than average “senior moments,” but are not serious enough to be diagnosed as dementia. In some people, MCI will progress into dementia.
AMP and MPH increase catecholamine activity in different ways. MPH primarily inhibits the reuptake of dopamine by pre-synaptic neurons, thus leaving more dopamine in the synapse and available for interacting with the receptors of the postsynaptic neuron. AMP also affects reuptake, as well as increasing the rate at which neurotransmitter is released from presynaptic neurons (Wilens, 2006). These effects are manifest in the attention systems of the brain, as already mentioned, and in a variety of other systems that depend on catecholaminergic transmission as well, giving rise to other physical and psychological effects. Physical effects include activation of the sympathetic nervous system (i.e., a fight-or-flight response), producing increased heart rate and blood pressure. Psychological effects are mediated by activation of the nucleus accumbens, ventral striatum, and other parts of the brain’s reward system, producing feelings of pleasure and the potential for dependence.

“Such an informative and inspiring read! Insight into how optimal nutrients improved Cavin’s own brain recovery make this knowledge-filled read compelling and relatable. The recommendations are easy to understand as well as scientifically-founded – it’s not another fad diet manual. The additional tools and resources provided throughout make it possible for anyone to integrate these enhancements into their nutritional repertoire. Looking forward to more from Cavin and Feed a Brain!!!!!!”

Vitamin B12 is also known as Cobalamin and is a water-soluble essential vitamin.  A (large) deficiency of Vitamin B12 will ultimately lead to cognitive impairment [52]. Older people and people who don’t eat meat are at a higher risk than young people who eat more meat. And people with depression have less Vitamin B12 than the average population [53].
I’ve been actively benefitting from nootropics since 1997, when I was struggling with cognitive performance and ordered almost $1000 worth of smart drugs from Europe (the only place where you could get them at the time). I remember opening the unmarked brown package and wondering whether the pharmaceuticals and natural substances would really enhance my brain.
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