The one indisputable finding from the literature so far is that many people are seeking cognitive enhancement. Beyond that, the literature yields only partial and tentative answers to the questions just raised. Given the potential impact of cognitive enhancement on society, more research is needed. For research on the epidemiology of cognitive enhancement, studies focused on the cognitive-enhancement practices and experiences of students and nonstudent workers are needed. For research on the cognitive effects of prescription stimulants, larger samples are needed. Only with substantially larger samples will it be possible to assess small but potentially important benefits, as well as risks, and to distinguish individual differences in drug response. Large samples would also be required to compare these effects to the cognitive effects of improved sleep, exercise, nutrition, and stress management. To include more ecologically valid measures of cognition in academic and work environments would in addition require the equivalent of a large clinical trial.

The evidence? Ritalin is FDA-approved to treat ADHD. It has also been shown to help patients with traumatic brain injury concentrate for longer periods, but does not improve memory in those patients, according to a 2016 meta-analysis of several trials. A study published in 2012 found that low doses of methylphenidate improved cognitive performance, including working memory, in healthy adult volunteers, but high doses impaired cognitive performance and a person’s ability to focus. (Since the brains of teens have been found to be more sensitive to the drug’s effect, it’s possible that methylphenidate in lower doses could have adverse effects on working memory and cognitive functions.)
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.
“The author’s story alone is a remarkable account of not just survival, but transcendence of a near-death experience. Cavin went on to become an advocate for survival and survivors of traumatic brain injuries, discovering along the way the key role played by nutrition. But this book is not just for injury survivors. It is for anyone who wants to live (and eat) well.”
I took the first pill at 12:48 pm. 1:18, still nothing really - head is a little foggy if anything. later noticed a steady sort of mental energy lasting for hours (got a good deal of reading and programming done) until my midnight walk, when I still felt alert, and had trouble sleeping. (Zeo reported a ZQ of 100, but a full 18 minutes awake, 2 or 3 times the usual amount.)
Analyzing the results is a little tricky because I was simultaneously running the first magnesium citrate self-experiment, which turned out to cause a quite complex result which looks like a gradually-accumulating overdose negating an initial benefit for net harm, and also toying with LLLT, which turned out to have a strong correlation with benefits. So for the potential small Noopept effect to not be swamped, I need to include those in the analysis. I designed the experiment to try to find the best dose level, so I want to look at an average Noopept effect but also the estimated effect at each dose size in case some are negative (especially in the case of 5-pills/60mg); I included the pilot experiment data as 10mg doses since they were also blind & randomized. Finally, missingness affects analysis: because not every variable is recorded for each date (what was the value of the variable for the blind randomized magnesium citrate before and after I finished that experiment? what value do you assign the Magtein variable before I bought it and after I used it all up?), just running a linear regression may not work exactly as one expects as various days get omitted because part of the data was missing.
It’s basic economics: the price of a good must be greater than cost of producing said good, but only under perfect competition will price = cost. Otherwise, the price is simply whatever maximizes profit for the seller. (Bottled water doesn’t really cost $2 to produce.) This can lead to apparently counter-intuitive consequences involving price discrimination & market segmentation - such as damaged goods which are the premium product which has been deliberately degraded and sold for less (some Intel CPUs, some headphones etc.). The most famous examples were railroads; one notable passage by French engineer-economist Jules Dupuit describes the motivation for the conditions in 1849:
Many studies suggest that Creatine helps in treating cognitive decline in individuals when combined with other therapies. It also helps people suffering from Parkinson’s and Huntington’s disease. Though there are minimal side effects associated with creatine, pretty much like any nootropic, it is not entirely free of side-effects. An overdose of creatine can lead to gastrointestinal issues, weight gain, stress, and anxiety.
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.
I have no particularly compelling story for why this might be a correlation and not causation. It could be placebo, but I wasn’t expecting that. It could be selection effect (days on which I bothered to use the annoying LED set are better days) but then I’d expect the off-days to be below-average and compared to the 2 years of trendline before, there doesn’t seem like much of a fall.
During the 1920s, Amphetamine was being researched as an asthma medication when its cognitive benefits were accidentally discovered. In many years that followed, this enhancer was exploited in a number of medical and nonmedical applications, for instance, to enhance alertness in military personnel, treat depression, improve athletic performance, etc.
The one indisputable finding from the literature so far is that many people are seeking cognitive enhancement. Beyond that, the literature yields only partial and tentative answers to the questions just raised. Given the potential impact of cognitive enhancement on society, more research is needed. For research on the epidemiology of cognitive enhancement, studies focused on the cognitive-enhancement practices and experiences of students and nonstudent workers are needed. For research on the cognitive effects of prescription stimulants, larger samples are needed. Only with substantially larger samples will it be possible to assess small but potentially important benefits, as well as risks, and to distinguish individual differences in drug response. Large samples would also be required to compare these effects to the cognitive effects of improved sleep, exercise, nutrition, and stress management. To include more ecologically valid measures of cognition in academic and work environments would in addition require the equivalent of a large clinical trial.
Only two of the eight experiments reviewed in this section found that stimulants enhanced performance, on a nonverbal fluency task in one case and in Raven’s Progressive Matrices in the other. The small number of studies of any given type makes it difficult to draw general conclusions about the underlying executive function systems that might be influenced.

Next, if these theorized safe and effective pills don't just get you through a test or the day's daily brain task but also make you smarter, whatever smarter means, then what? Where's the boundary between genius and madness? If Einstein had taken such drugs, would he have created a better theory of gravity? Or would he have become delusional, chasing quantum ghosts with no practical application, or worse yet, string theory. (Please use "string theory" in your subject line for easy sorting of hate mail.)


However, when I didn’t stack it with Choline, I would get what users call “racetam headaches.” Choline, as Patel explains, is not a true nootropic, but it’s still a pro-cognitive compound that many take with other nootropics in a stack. It’s an essential nutrient that humans need for functions like memory and muscle control, but we can’t produce it, and many Americans don’t get enough of it. The headaches I got weren’t terribly painful, but they were uncomfortable enough that I stopped taking Piracetam on its own. Even without the headache, though, I didn’t really like the level of focus Piracetam gave me. I didn’t feel present when I used it, even when I tried to mix in caffeine and L-theanine. And while it seemed like I could focus and do my work faster, I was making more small mistakes in my writing, like skipping words. Essentially, it felt like my brain was moving faster than I could.

Took pill #6 at 12:35 PM. Hard to be sure. I ultimately decided that it was Adderall because I didn’t have as much trouble as I normally would in focusing on reading and then finishing my novel (Surface Detail) despite my family watching a movie, though I didn’t notice any lack of appetite. Call this one 60-70% Adderall. I check the next evening and it was Adderall.

Some people aren’t satisfied with a single supplement—the most devoted self-improvers buy a variety of different compounds online and create their own custom regimens, which they call “stacks.” According to Kaleigh Rogers, writing in Vice last year, companies will now take their customers’ genetic data from 23andMe or another source and use it to recommend the right combinations of smart drugs to optimize each individual’s abilities. The problem with this practice is that there’s no evidence the practice works. (And remember, the FDA doesn’t regulate supplements.) Find out the 9 best foods to boost your brain health.

the larger size of the community enables economies of scale and increases the peak sophistication possible. In a small nootropics community, there is likely to be no one knowledgeable about statistics/experimentation/biochemistry/neuroscience/whatever-you-need-for-a-particular-discussion, and the available funds increase: consider /r/Nootropics’s testing program, which is doable only because it’s a large lucrative community to sell to so the sellers are willing to donate funds for independent lab tests/Certificates of Analysis (COAs) to be done. If there were 1000 readers rather than 23,295, how could this ever happen short of one of those 1000 readers being very altruistic?
A similar pill from HQ Inc. (Palmetto, Fla.) called the CorTemp Ingestible Core Body Temperature Sensor transmits real-time body temperature. Firefighters, football players, soldiers and astronauts use it to ensure that they do not overheat in high temperatures. HQ Inc. is working on a consumer version, to be available in 2018, that would wirelessly communicate to a smartphone app.
As opposed to what it might lead you to believe, Ginkgo Smart is not simply a Ginkgo Biloba supplement. In all actuality, it’s much more than that – a nootropic (Well duh, we wouldn’t be reviewing it otherwise). Ginkgo Smart has actually been seeing quite some popularity lately, possibly riding on the popularity of Ginkgo Biloba as a supplement, which has been storming through the US lately, and becoming one of the highest selling supplement in the US. We were pleasantly pleased at the fact that it wasn’t too hard to find Ginkgo Smart’s ingredients… Learn More...
Fortunately for me, the FDA decided Smart Powder’s advertising was too explicit and ordered its piracetam sales stopped; I was equivocal at the previous price point, but then I saw that between the bulk discount and the fire-sale coupon, 3kg was only $99.99 (shipping was amortized over that, the choline, caffeine, and tryptophan). So I ordered in September 2010. As well, I had decided to cap my own pills, eliminating the inconvenience and bad taste. 3kg goes a very long way so I am nowhere close to running out of my pills; there is nothing to report since, as the pills are simply part of my daily routine.
Smart drugs could lead to enhanced cognitive abilities in the military. Also known as nootropics, smart drugs can be viewed similarly to medical enhancements. What’s important to remember though, is that smart drugs do not increase your intelligence; however, they may improve cognitive and executive functions leading to an increase in intelligence.
Does little alone, but absolutely necessary in conjunction with piracetam. (Bought from Smart Powders.) When turning my 3kg of piracetam into pills, I decided to avoid the fishy-smelling choline and go with 500g of DMAE (Examine.com); it seemed to work well when I used it before with oxiracetam & piracetam, since I had no piracetam headaches, and be considerably less bulky.
ADHD medication sales are growing rapidly, with annual revenues of $12.9 billion in 2015. These drugs can be obtained legally by those who have a prescription, which also includes those who have deliberately faked the symptoms in order to acquire the desired medication. (According to an experiment published in 2010, it is difficult for medical practitioners to separate those who feign the symptoms from those who actually have them.) That said, faking might not be necessary if a doctor deems your desired productivity level or your stress around a big project as reason enough to prescribe medication.

l-theanine (Examine.com) is occasionally mentioned on Reddit or Imminst or LessWrong32 but is rarely a top-level post or article; this is probably because theanine was discovered a very long time ago (>61 years ago), and it’s a pretty straightforward substance. It’s a weak relaxant/anxiolytic (Google Scholar) which is possibly responsible for a few of the health benefits of tea, and which works synergistically with caffeine (and is probably why caffeine delivered through coffee feels different from the same amount consumed in tea - in one study, separate caffeine and theanine were a mixed bag, but the combination beat placebo on all measurements). The half-life in humans seems to be pretty short, with van der Pijl 2010 putting it ~60 minutes. This suggests to me that regular tea consumption over a day is best, or at least that one should lower caffeine use - combining caffeine and theanine into a single-dose pill has the problem of caffeine’s half-life being much longer so the caffeine will be acting after the theanine has been largely eliminated. The problem with getting it via tea is that teas can vary widely in their theanine levels and the variations don’t seem to be consistent either, nor is it clear how to estimate them. (If you take a large dose in theanine like 400mg in water, you can taste the sweetness, but it’s subtle enough I doubt anyone can actually distinguish the theanine levels of tea; incidentally, r-theanine - the useless racemic other version - anecdotally tastes weaker and less sweet than l-theanine.)

Adrafinil is a prodrug for Modafinil, which means it can be metabolized into Modafinil to give you a similar effect. And you can buy it legally just about anywhere. But there are a few downsides. Patel explains that you have to take a lot more to achieve a similar effect as Modafinil, wait longer for it to kick in (45-60 minutes), there are more potential side effects, and there aren’t any other benefits to taking it.


He recommends a 10mg dose, but sublingually. He mentions COLURACETAM’s taste is more akin to that of PRAMIRACETAM than OXIRACETAM, in that it tastes absolutely vile (not a surprise), so it is impossible to double-blind a sublingual administration - even if I knew of an inactive equally-vile-tasting substitute, I’m not sure I would subject myself to it. To compensate for ingesting the coluracetam, it would make sense to double the dose to 20mg (turning the 2g into <100 doses). Whether the effects persist over multiple days is not clear; I’ll assume it does not until someone says it does, since this makes things much easier.
From its online reputation and product presentation to our own product run, Synagen IQ smacks of mediocre performance. A complete list of ingredients could have been convincing and decent, but the lack of information paired with the potential for side effects are enough for beginners to old-timers in nootropic use to shy away and opt for more trusted and reputable brands. There is plenty that needs to be done to uplift the brand and improve its overall ranking in the widely competitive industry. Learn More...
That study is also interesting for finding benefits to chronic piracetam+choline supplementation in the mice, which seems connected to a Russian study which reportedly found that piracetam (among other more obscure nootropics) increased secretion of BDNF in mice. See also Drug heuristics on a study involving choline supplementation in pregnant rats.↩

Another popular option is nicotine. Scientists are increasingly realising that this drug is a powerful nootropic, with the ability to improve a person’s memory and help them to focus on certain tasks – though it also comes with well-documented obvious risks and side effects. “There are some very famous neuroscientists who chew Nicorette in order to enhance their cognitive functioning. But they used to smoke and that’s their substitute,” says Huberman.


Many studies suggest that Creatine helps in treating cognitive decline in individuals when combined with other therapies. It also helps people suffering from Parkinson’s and Huntington’s disease. Though there are minimal side effects associated with creatine, pretty much like any nootropic, it is not entirely free of side-effects. An overdose of creatine can lead to gastrointestinal issues, weight gain, stress, and anxiety.
Productivity is the most cited reason for using nootropics. With all else being equal, smart drugs are expected to give you that mental edge over other and advance your career. Nootropics can also be used for a host of other reasons. From studying to socialising. And from exercise and health to general well-being. Different nootropics cater to different audiences.
The above information relates to studies of specific individual essential oil ingredients, some of which are used in the essential oil blends for various MONQ diffusers. Please note, however, that while individual ingredients may have been shown to exhibit certain independent effects when used alone, the specific blends of ingredients contained in MONQ diffusers have not been tested. No specific claims are being made that use of any MONQ diffusers will lead to any of the effects discussed above.  Additionally, please note that MONQ diffusers have not been reviewed or approved by the U.S. Food and Drug Administration. MONQ diffusers are not intended to be used in the diagnosis, cure, mitigation, prevention, or treatment of any disease or medical condition. If you have a health condition or concern, please consult a physician or your alternative health care provider prior to using MONQ diffusers.
Results: Women with high caffeine intakes had significantly higher rates of bone loss at the spine than did those with low intakes (−1.90 ± 0.97% compared with 1.19 ± 1.08%; P = 0.038). When the data were analyzed according to VDR genotype and caffeine intake, women with the tt genotype had significantly (P = 0.054) higher rates of bone loss at the spine (−8.14 ± 2.62%) than did women with the TT genotype (−0.34 ± 1.42%) when their caffeine intake was >300 mg/d…In 1994, Morrison et al (22) first reported an association between vitamin D receptor gene (VDR) polymorphism and BMD of the spine and hip in adults. After this initial report, the relation between VDR polymorphism and BMD, bone turnover, and bone loss has been extensively evaluated. The results of some studies support an association between VDR polymorphism and BMD (23-,25), whereas other studies showed no evidence for this association (26,27)…At baseline, no significant differences existed in serum parathyroid hormone, serum 25-hydroxyvitamin D, serum osteocalcin, and urinary N-telopeptide between the low- and high-caffeine groups (Table 1⇑). In the longitudinal study, the percentage of change in serum parathyroid hormone concentrations was significantly lower in the high-caffeine group than in the low-caffeine group (Table 2⇑). However, no significant differences existed in the percentage of change in serum 25-hydroxyvitamin D

ADMISSIONSUNDERGRADUATE GRADUATE CONTINUING EDUCATION RESEARCHDIVISIONS RESEARCH IMPACT LIBRARIES INNOVATION AND PARTNERSHIP SUPPORT FOR RESEARCHERS RESEARCH IN CONVERSATION PUBLIC ENGAGEMENT WITH RESEARCH NEWS & EVENTSEVENTS SCIENCE BLOG ARTS BLOG OXFORD AND BREXIT NEWS RELEASES FOR JOURNALISTS FILMING IN OXFORD FIND AN EXPERT ABOUTORGANISATION FACTS AND FIGURES OXFORD PEOPLE OXFORD ACCESS INTERNATIONAL OXFORD BUILDING OUR FUTURE JOBS 牛津大学Staff Oxford students Alumni Visitors Local community
Swanson J, Arnold LE, Kraemer H, Hechtman L, Molina B, Hinshaw S, Wigal T. Evidence, interpretation and qualification from multiple reports of long-term outcomes in the Multimodal Treatment Study of Children With ADHD (MTA): Part II. Supporting details. Journal of Attention Disorders. 2008;12:15–43. doi: 10.1177/1087054708319525. [PubMed] [CrossRef]

We included studies of the effects of these drugs on cognitive processes including learning, memory, and a variety of executive functions, including working memory and cognitive control. These studies are listed in Table 2, along with each study’s sample size, gender, age and tasks administered. Given our focus on cognition enhancement, we excluded studies whose measures were confined to perceptual or motor abilities. Studies of attention are included when the term attention refers to an executive function but not when it refers to the kind of perceptual process taxed by, for example, visual search or dichotic listening or when it refers to a simple vigilance task. Vigilance may affect cognitive performance, especially under conditions of fatigue or boredom, but a more vigilant person is not generally thought of as a smarter person, and therefore, vigilance is outside of the focus of the present review. The search and selection process is summarized in Figure 2.
My answer is that this is not a lot of research or very good research (not nearly as good as the research on nicotine, eg.), and assuming it’s true, I don’t value long-term memory that much because LTM is something that is easily assisted or replaced (personal archives, and spaced repetition). For me, my problems tend to be more about akrasia and energy and not getting things done, so even if a stimulant comes with a little cost to long-term memory, it’s still useful for me. I’m going continue to use the caffeine. It’s not so bad in conjunction with tea, is very cheap, and I’m already addicted, so why not? Caffeine is extremely cheap, addictive, has minimal effects on health (and may be beneficial, from the various epidemiological associations with tea/coffee/chocolate & longevity), and costs extra to remove from drinks popular regardless of their caffeine content (coffee and tea again). What would be the point of carefully investigating it? Suppose there was conclusive evidence on the topic, the value of this evidence to me would be roughly $0 or since ignorance is bliss, negative money - because unless the negative effects were drastic (which current studies rule out, although tea has other issues like fluoride or metal contents), I would not change anything about my life. Why? I enjoy my tea too much. My usual tea seller doesn’t even have decaffeinated oolong in general, much less various varieties I might want to drink, apparently because de-caffeinating is so expensive it’s not worthwhile. What am I supposed to do, give up my tea and caffeine just to save on the cost of caffeine? Buy de-caffeinating machines (which I couldn’t even find any prices for, googling)? This also holds true for people who drink coffee or caffeinated soda. (As opposed to a drug like modafinil which is expensive, and so the value of a definitive answer is substantial and would justify some more extensive calculating of cost-benefit.)
Methylphenidate, commonly known as Ritalin, is a stimulant first synthesised in the 1940s. More accurately, it’s a psychostimulant - often prescribed for ADHD - that is intended as a drug to help focus and concentration. It also reduces fatigue and (potentially) enhances cognition. Similar to Modafinil, Ritalin is believed to reduce dissipation of dopamine to help focus. Ritalin is a Class B drug in the UK, and possession without a prescription can result in a 5 year prison sentence. Please note: Side Effects Possible. See this article for more on Ritalin.
Table 3 lists the results of 24 tasks from 22 articles on the effects of d-AMP or MPH on learning, assessed by a variety of declarative and nondeclarative memory tasks. Results for the 24 tasks are evenly split between enhanced learning and null results, but they yield a clearer pattern when the nature of the learning task and the retention interval are taken into account. In general, with single exposures of verbal material, no benefits are seen immediately following learning, but later recall and recognition are enhanced. Of the six articles reporting on memory performance (Camp-Bruno & Herting, 1994; Fleming, Bigelow, Weinberger, & Goldberg, 1995; Rapoport, Busbaum, & Weingartner, 1980; Soetens, D’Hooge, & Hueting, 1993; Unrug, Coenen, & van Luijtelaar, 1997; Zeeuws & Soetens 2007), encompassing eight separate experiments, only one of the experiments yielded significant memory enhancement at short delays (Rapoport et al., 1980). In contrast, retention was reliably enhanced by d-AMP when subjects were tested after longer delays, with recall improved after 1 hr through 1 week (Soetens, Casaer, D’Hooge, & Hueting, 1995; Soetens et al., 1993; Zeeuws & Soetens, 2007). Recognition improved after 1 week in one study (Soetens et al., 1995), while another found recognition improved after 2 hr (Mintzer & Griffiths, 2007). The one long-term memory study to examine the effects of MPH found a borderline-significant reduction in errors when subjects answered questions about a story (accompanied by slides) presented 1 week before (Brignell, Rosenthal, & Curran, 2007).
A fancier method of imputation would be multiple imputation using, for example, the R library mice (Multivariate Imputation by Chained Equations) (guide), which will try to impute all missing values in a way which mimicks the internal structure of the data and provide several possible datasets to give us an idea of what the underlying data might have looked like, so we can see how our estimates improve with no missingness & how much of the estimate is now due to the imputation:
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.
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.
“I am nearly four years out from my traumatic brain injury and I have been through 100’s of hours of rehabilitation therapy. I have been surprised by how little attention is given to adequate nutrition for recovering from TBI. I’m always looking for further opportunities to recover and so this book fell into the right hands. Cavin outlines the science and reasoning behind the diet he suggests, but the real power in this book comes when he writes, “WE.” WE can give our brains proper nutrition. Now I’m excited to drink smoothies and eat breakfasts that look like dinners! I will recommend this book to my friends.
That doesn’t necessarily mean all smart drugs – now and in the future – will be harmless, however. The brain is complicated. In trying to upgrade it, you risk upsetting its intricate balance. “It’s not just about more, it’s about having to be exquisitely and exactly right. And that’s very hard to do,” says Arnstein. “What’s good for one system may be bad for another system,” adds Trevor Robbins, Professor of Cognitive Neuroscience at the University of Cambridge. “It’s clear from the experimental literature that you can affect memory with pharmacological agents, but the problem is keeping them safe.”
The use of cognitive enhancers by healthy individuals sparked debate about ethics and safety. Cognitive enhancement by pharmaceutical means was considered a form of illicit drug use in some places, even while other cognitive enhancers, such as caffeine and nicotine, were freely available. The conflict therein raised the possibility for further acceptance of smart drugs in the future. However, the long-term effects of smart drugs on otherwise healthy brains were unknown, delaying safety assessments.

None of that has kept entrepreneurs and their customers from experimenting and buying into the business of magic pills, however. In 2015 alone, the nootropics business raked in over $1 billion dollars, and web sites like the nootropics subreddit, the Bluelight forums, and Bulletproof Exec are popular and packed with people looking for easy ways to boost their mental performance. Still, this bizarre, Philip K. Dick-esque world of smart drugs is a tough pill to swallow. To dive into the topic and explain, I spoke to Kamal Patel, Director of evidence-based medical database Examine.com, and even tried a few commercially-available nootropics myself.

Another classic approach to the assessment of working memory is the span task, in which a series of items is presented to the subject for repetition, transcription, or recognition. The longest series that can be reproduced accurately is called the forward span and is a measure of working memory capacity. The ability to reproduce the series in reverse order is tested in backward span tasks and is a more stringent test of working memory capacity and perhaps other working memory functions as well. The digit span task from the Wechsler (1981) IQ test was used in four studies of stimulant effects on working memory. One study showed that d-AMP increased digit span (de Wit et al., 2002), and three found no effects of d-AMP or MPH (Oken, Kishiyama, & Salinsky, 1995; Schmedtje, Oman, Letz, & Baker, 1988; Silber, Croft, Papafotiou, & Stough, 2006). A spatial span task, in which subjects must retain and reproduce the order in which boxes in a scattered spatial arrangement change color, was used by Elliott et al. (1997) to assess the effects of MPH on working memory. For subjects in the group receiving placebo first, MPH increased spatial span. However, for the subjects who received MPH first, there was a nonsignificant opposite trend. The group difference in drug effect is not easily explained. The authors noted that the subjects in the first group performed at an overall lower level, and so, this may be another manifestation of the trend for a larger enhancement effect for less able subjects.
The peculiar tired-sharp feeling was there as usual, and the DNB scores continue to suggest this is not an illusion, as they remain in the same 30-50% band as my normal performance. I did not notice the previous aboulia feeling; instead, around noon, I was filled with a nervous energy and a disturbingly rapid pulse which meditation & deep breathing did little to help with, and which didn’t go away for an hour or so. Fortunately, this was primarily at church, so while I felt irritable, I didn’t actually interact with anyone or snap at them, and was able to keep a lid on it. I have no idea what that was about. I wondered if it might’ve been a serotonin storm since amphetamines are some of the drugs that can trigger storms but the Adderall had been at 10:50 AM the previous day, or >25 hours (the half-lives of the ingredients being around 13 hours). An hour or two previously I had taken my usual caffeine-piracetam pill with my morning tea - could that have interacted with the armodafinil and the residual Adderall? Or was it caffeine+modafinil? Speculation, perhaps. A house-mate was ill for a few hours the previous day, so maybe the truth is as prosaic as me catching whatever he had.
The soft gels are very small; one needs to be a bit careful - Vitamin D is fat-soluble and overdose starts in the range of 70,000 IU35, so it would take at least 14 pills, and it’s unclear where problems start with chronic use. Vitamin D, like many supplements, follows a U-shaped response curve (see also Melamed et al 2008 and Durup et al 2012) - too much can be quite as bad as too little. Too little, though, is likely very bad. The previously cited studies with high acute doses worked out to <1,000 IU a day, so they may reassure us about the risks of a large acute dose but not tell us much about smaller chronic doses; the mortality increases due to too-high blood levels begin at ~140nmol/l and reading anecdotes online suggest that 5k IU daily doses tend to put people well below that (around 70-100nmol/l). I probably should get a blood test to be sure, but I have something of a needle phobia.
“Cavin Balaster knows brain injury as well as any specialist. He survived a horrific accident and came out on the other side stronger than ever. His book, “How To Feed A Brain” details how changing his diet helped him to recover further from the devastating symptoms of brain injury such as fatigue and brain fog. Cavin is able to thoroughly explain complex issues in a simplified manner so the reader does not need a medical degree to understand. The book also includes comprehensive charts to simplify what the body needs and how to provide the necessary foods. “How To Feed A Brain” is a great resource for anyone looking to improve their health through diet, brain injury not required.”
Turning to analyses related specifically to the drugs that are the subject of this article, reanalysis of the 2002 NSDUH data by Kroutil and colleagues (2006) found past-year nonmedical use of stimulants other than methamphetamine by 2% of individuals between the ages of 18 and 25 and by 0.3% of individuals 26 years of age and older. For ADHD medications in particular, these rates were 1.3% and 0.1%, respectively. Finally, Novak, Kroutil, Williams, and Van Brunt (2007) surveyed a sample of over four thousand individuals from the Harris Poll Online Panel and found that 4.3% of those surveyed between the ages of 18 and 25 had used prescription stimulants nonmedically in the past year, compared with only 1.3% between the ages of 26 and 49.
Historically used to help people with epilepsy, piracetam is used in some cases of myoclonus, or muscle twitching. Its actual mechanism of action is unclear: It doesn’t act exactly as a sedative or stimulant, but still influences cognitive function, and is believed to act on receptors for acetylcholine in the brain. Piracetam is used off-label as a 'smart drug' to help focus and concentration or sometimes as a way to allegedly boost your mood. Again, piracetam is a prescription-only drug - any supply to people without a prescription is illegal, and supplying it may result in a fine or prison sentence.
Smart drugs could lead to enhanced cognitive abilities in the military. Also known as nootropics, smart drugs can be viewed similarly to medical enhancements. What’s important to remember though, is that smart drugs do not increase your intelligence; however, they may improve cognitive and executive functions leading to an increase in intelligence.

A 2015 review of various nutrients and dietary supplements found no convincing evidence of improvements in cognitive performance. While there are “plausible mechanisms” linking these and other food-sourced nutrients to better brain function, “supplements cannot replicate the complexity of natural food and provide all its potential benefits,” says Dr. David Hogan, author of that review and a professor of medicine at the University of Calgary in Canada.
This is one of the few times we’ve actually seen a nootropic supplement take a complete leverage on the nootropic industry with the name Smart Pill. To be honest, we don’t know why other companies haven’t followed suit yet – it’s an amazing name. Simple, and to the point. Coming from supplement maker, Only Natural, Smart Pill makes some pretty bold claims regarding their pills being completely natural, whilst maintaining good quality. This is their niche – or Only Natural’s niche, for that matter. They create supplements, in this case Smart Pill, with the… Learn More...
Smart Pill is a dietary supplement that blends vitamins, amino acids, and herbal extracts to sustain mental alertness, memory and concentration. One of the ingredients used in this formula is Vitamin B-1, also known as Thiamine, which sustains almost all functions present in the body, but plays a key role in brain health and function. A deficiency of this vitamin can lead to several neurological function problems. The most common use of Thiamine is to improve brain function; it acts as a neurotransmitter helping the brain prevent learning and memory disorders; it also provides help with mood disorders and offers stress relief.
The use of cognitive enhancers by healthy individuals sparked debate about ethics and safety. Cognitive enhancement by pharmaceutical means was considered a form of illicit drug use in some places, even while other cognitive enhancers, such as caffeine and nicotine, were freely available. The conflict therein raised the possibility for further acceptance of smart drugs in the future. However, the long-term effects of smart drugs on otherwise healthy brains were unknown, delaying safety assessments.
So the chi-squared believes there is a statistically-significant difference, the two-sample test disagrees, and the binomial also disagrees. Since I regarded it as a dubious theory, can’t see a difference, and the binomial seems like the most appropriate test, I conclude that several months of 1mg iodine did not change my eye color. (As a final test, when I posted the results on the Longecity forum where people were claiming the eye color change, I swapped the labels on the photos to see if anyone would claim something along the lines when I look at the photos, I can see a difference!. I thought someone might do that, which would be a damning demonstration of their biases & wishful thinking, but no one did.)
We’d want 53 pairs, but Fitzgerald 2012’s experimental design called for 32 weeks of supplementation for a single pair of before-after tests - so that’d be 1664 weeks or ~54 months or ~4.5 years! We can try to adjust it downwards with shorter blocks allowing more frequent testing; but problematically, iodine is stored in the thyroid and can apparently linger elsewhere - many of the cited studies used intramuscular injections of iodized oil (as opposed to iodized salt or kelp supplements) because this ensured an adequate supply for months or years with no further compliance by the subjects. If the effects are that long-lasting, it may be worthless to try shorter blocks than ~32 weeks.

There is no clear answer to this question. Many of the smart drugs have decades of medical research and widespread use behind them, as well as only minor, manageable, or nonexistent side effects, but are still used primarily as a crutch for people already experiencing cognitive decline, rather than as a booster-rocket for people with healthy brains. Unfortunately, there is a bias in Western medicine in favor of prescribing drugs once something bad has already begun, rather than for up-front prevention. There’s also the principle of “leave well enough alone” – in this case, extended to mean, don’t add unnecessary or unnatural drugs to the human body in place of a normal diet. [Smart Drug Smarts would argue that the average human diet has strayed so far from what is physiologically “normal” that leaving well enough alone is already a failed proposition.]
"Piracetam is not a vitamin, mineral, amino acid, herb or other botanical, or dietary substance for use by man to supplement the diet by increasing the total dietary intake. Further, piracetam is not a concentrate, metabolite, constituent, extract or combination of any such dietary ingredient. [...] Accordingly, these products are drugs, under section 201(g)(1)(C) of the Act, 21 U.S.C. § 321(g)(1)(C), because they are not foods and they are intended to affect the structure or any function of the body. Moreover, these products are new drugs as defined by section 201(p) of the Act, 21 U.S.C. § 321(p), because they are not generally recognized as safe and effective for use under the conditions prescribed, recommended, or suggested in their labeling."[33]
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