At small effects like d=0.07, a nontrivial chance of negative effects, and an unknown level of placebo effects (this was non-blinded, which could account for any residual effects), this strongly implies that LLLT is not doing anything for me worth bothering with. I was pretty skeptical of LLLT in the first place, and if 167 days can’t turn up anything noticeable, I don’t think I’ll be continuing with LLLT usage and will be giving away my LED set. (Should any experimental studies of LLLT for cognitive enhancement in healthy people surface with large quantitative effects - as opposed to a handful of qualitative case studies about brain-damaged people - and I decide to give LLLT another try, I can always just buy another set of LEDs: it’s only ~$15, after all.)
When you hear about nootropics, often called “smart drugs,” you probably picture something like the scene above from Limitless, where Bradley Cooper’s character becomes brilliant after downing a strange pill. The drugs and supplements currently available don’t pack that strong of a punch, but the concept is basically the same. Many nootropics have promising benefits, like boosting memory, focus, or motivation, and there’s research to support specific uses. But the most effective nootropics, like Modafinil, aren’t intended for use without a prescription to treat a specific condition. In fact, recreational use of nootropics is hotly-debated among doctors and medical researchers. Many have concerns about the possible adverse effects of long-term use, as well as the ethics of using cognitive enhancers to gain an advantage in school, sports, or even everyday work.
“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.
“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!”

As Sulbutiamine crosses the blood-brain barrier very easily, it has a positive effect on the cholinergic and the glutamatergic receptors that are responsible for essential activities impacting memory, concentration, and mood. The compound is also fat-soluble, which means it circulates rapidly and widely throughout the body and the brain, ensuring positive results. Thus, patients with schizophrenia and Parkinson’s disease will find the drug to be very effective.

The Stroop task tests the ability to inhibit the overlearned process of reading by presenting color names in colored ink and instructing subjects to either read the word (low need for cognitive control because this is the habitual response to printed words) or name the ink color (high need for cognitive control). Barch and Carter (2005) administered this task to normal control subjects on placebo and d-AMP and found speeding of responses with the drug. However, the speeding was roughly equivalent for the conditions with low and high cognitive control demands, suggesting that the observed facilitation may not have been specific to cognitive control.
What worries me about amphetamine is its addictive potential, and the fact that it can cause stress and anxiety. Research says it’s only slightly likely to cause addiction in people with ADHD, [7] but we don’t know much about its addictive potential in healthy adults. We all know the addictive potential of methamphetamine, and amphetamine is closely related enough to make me nervous about so many people giving it to their children. Amphetamines cause withdrawal symptoms, so the potential for addiction is there.
With something like creatine, you’d know if it helps you pump out another rep at the gym on a sustainable basis. With nootropics, you can easily trick yourself into believing they help your mindset. The ideal is to do a trial on yourself. Take identical looking nootropic pills and placebo pills for a couple weeks each, then see what the difference is. With only a third party knowing the difference, of course.
If you want to make sure that whatever you’re taking is safe, search for nootropics that have been backed by clinical trials and that have been around long enough for any potential warning signs about that specific nootropic to begin surfacing. There are supplements and nootropics that have been tested in a clinical setting, so there are options out there.
Lebowitz says that if you're purchasing supplements to improve your brain power, you're probably wasting your money. "There is nothing you can buy at your local health food store that will improve your thinking skills," Lebowitz says. So that turmeric latte you've been drinking everyday has no additional brain benefits compared to a regular cup of java.
Texas-based entrepreneur and podcaster Mansal Denton takes phenylpiracetam, a close relative of piracetam originally developed by the Soviet Union as a medication for cosmonauts, to help them endure the stresses of life in space. “I have a much easier time articulating certain things when I take it, so I typically do a lot of recording [of podcasts] on those days,” he says.
Unfortunately, cognitive enhancement falls between the stools of research funding, which makes it unlikely that such research programs will be carried out. Disease-oriented funders will, by definition, not support research on normal healthy individuals. The topic intersects with drug abuse research only in the assessment of risk, leaving out the study of potential benefits, as well as the comparative benefits of other enhancement methods. As a fundamentally applied research question, it will not qualify for support by funders of basic science. The pharmaceutical industry would be expected to support such research only if cognitive enhancement were to be considered a legitimate indication by the FDA, which we hope would happen only after considerably more research has illuminated its risks, benefits, and societal impact. Even then, industry would have little incentive to delve into all of the issues raised here, including the comparison of drug effects to nonpharmaceutical means of enhancing cognition.
At small effects like d=0.07, a nontrivial chance of negative effects, and an unknown level of placebo effects (this was non-blinded, which could account for any residual effects), this strongly implies that LLLT is not doing anything for me worth bothering with. I was pretty skeptical of LLLT in the first place, and if 167 days can’t turn up anything noticeable, I don’t think I’ll be continuing with LLLT usage and will be giving away my LED set. (Should any experimental studies of LLLT for cognitive enhancement in healthy people surface with large quantitative effects - as opposed to a handful of qualitative case studies about brain-damaged people - and I decide to give LLLT another try, I can always just buy another set of LEDs: it’s only ~$15, after all.)
To make things more interesting, I think I would like to try randomizing different dosages as well: 12mg, 24mg, and 36mg (1-3 pills); on 5 May 2014, because I wanted to finish up the experiment earlier, I decided to add 2 larger doses of 48 & 60mg (4-5 pills) as options. Then I can include the previous pilot study as 10mg doses, and regress over dose amount.
As shown in Table 6, two of these are fluency tasks, which require the generation of as large a set of unique responses as possible that meet the criteria given in the instructions. Fluency tasks are often considered tests of executive function because they require flexibility and the avoidance of perseveration and because they are often impaired along with other executive functions after prefrontal damage. In verbal fluency, subjects are asked to generate as many words that begin with a specific letter as possible. Neither Fleming et al. (1995), who administered d-AMP, nor Elliott et al. (1997), who administered MPH, found enhancement of verbal fluency. However, Elliott et al. found enhancement on a more complex nonverbal fluency task, the sequence generation task. Subjects were able to touch four squares in more unique orders with MPH than with placebo.
The truth is, taking a smart pill will not allow you to access information that you have not already learned. If you speak English, a smart drug cannot embed the Spanish dictionary into your brain. In other words, they won't make you smarter or more intelligent. We need to throttle back our expectations and explore reality. What advantage can smart drugs provide? Brain enhancing substances have excellent health and cognitive benefits that are worth exploring.

Most epidemiological research on nonmedical stimulant use has been focused on issues relevant to traditional problems of drug abuse and addiction, and so, stimulant use for cognitive enhancement is not generally distinguished from use for other purposes, such as staying awake or getting high. As Boyd and McCabe (2008) pointed out, the large national surveys of nonmedical prescription drug use have so far failed to distinguish the ways and reasons that people use the drugs, and this is certainly true where prescription stimulants are concerned. The largest survey to investigate prescription stimulant use in a nationally representative sample of Americans, the National Survey on Drug Use and Health (NSDUH), phrases the question about nonmedical use as follows: “Have you ever, even once, used any of these stimulants when they were not prescribed for you or that you took only for the experience or feeling they caused?” (Snodgrass & LeBaron 2007). This phrasing does not strictly exclude use for cognitive enhancement, but it emphasizes the noncognitive effects of the drugs. In 2008, the NSDUH found a prevalence of 8.5% for lifetime nonmedical stimulant use by Americans over the age of 12 years and a prevalence of 12.3% for Americans between 21 and 25 (Substance Abuse and Mental Health Services Administration, 2009).
Rogers RD, Blackshaw AJ, Middleton HC, Matthews K, Hawtin K, Crowley C, Robbins TW. Tryptophan depletion impairs stimulus-reward learning while methylphenidate disrupts attentional control in healthy young adults: Implications for the monoaminergic basis of impulsive behaviour. Psychopharmacology. 1999;146:482–491. doi: 10.1007/PL00005494. [PubMed] [CrossRef]
“Cavin’s personal experience and humble writing to help educate, not only people who have suffered brain injuries, but anyone interested in the best nutritional advice for optimum brain function is a great introduction to proper nutrition filled with many recommendations of how you can make a changes to your diet immediately. This book provides amazing personal insight related to Cavin’s recovery accompanied with well cited peer reviewed sources throughout the entire book detailing the most recent findings around functional neurology!
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.
I largely ignored this since the discussions were of sub-RDA doses, and my experience has usually been that RDAs are a poor benchmark and frequently far too low (consider the RDA for vitamin D). This time, I checked the actual RDA - and was immediately shocked and sure I was looking at a bad reference: there was no way the RDA for potassium was seriously 3700-4700mg or 4-5 grams daily, was there? Just as an American, that implied that I was getting less than half my RDA. (How would I get 4g of potassium in the first place? Eat a dozen bananas a day⸮) I am not a vegetarian, nor is my diet that fantastic: I figured I was getting some potassium from the ~2 fresh tomatoes I was eating daily, but otherwise my diet was not rich in potassium sources. I have no blood tests demonstrating deficiency, but given the figures, I cannot see how I could not be deficient.

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.
Since dietary supplements do not require double-blind, placebo-controlled, pharmaceutical-style human studies before going to market, there is little incentive for companies to really prove that something does what they say it does. This means that, in practice, nootropics may not live up to all the grandiose, exuberant promises advertised on the bottle in which they come. The flip side, though? There’s no need to procure a prescription in order to try them out. Good news for aspiring biohackers—and for people who have no aspirations to become biohackers, but still want to be Bradley Cooper in Limitless (me).
Brain-imaging studies are consistent with the existence of small effects that are not reliably captured by the behavioral paradigms of the literature reviewed here. Typically with executive function tasks, reduced activation of task-relevant areas is associated with better performance and is interpreted as an indication of higher neural efficiency (e.g., Haier, Siegel, Tang, Abel, & Buchsbaum, 1992). Several imaging studies showed effects of stimulants on task-related activation while failing to find effects on cognitive performance. Although changes in brain activation do not necessarily imply functional cognitive changes, they are certainly suggestive and may well be more sensitive than behavioral measures. Evidence of this comes from a study of COMT variation and executive function. Egan and colleagues (2001) found a genetic effect on executive function in an fMRI study with sample sizes as small as 11 but did not find behavioral effects in these samples. The genetic effect on behavior was demonstrated in a separate study with over a hundred participants. In sum, d-AMP and MPH measurably affect the activation of task-relevant brain regions when participants’ task performance does not differ. This is consistent with the hypothesis (although by no means positive proof) that stimulants exert a true cognitive-enhancing effect that is simply too small to be detected in many studies.
Despite decades of study, a full picture has yet to emerge of the cognitive effects of the classic psychostimulants and modafinil. Part of the problem is that getting rats, or indeed students, to do puzzles in laboratories may not be a reliable guide to the drugs’ effects in the wider world. Drugs have complicated effects on individuals living complicated lives. Determining that methylphenidate enhances cognition in rats by acting on their prefrontal cortex doesn’t tell you the potential impact that its effects on mood or motivation may have on human cognition.
How should the mixed results just summarized be interpreted vis-á-vis the cognitive-enhancing potential of prescription stimulants? One possibility is that d-AMP and MPH enhance cognition, including the retention of just-acquired information and some or all forms of executive function, but that the enhancement effect is small. If this were the case, then many of the published studies were underpowered for detecting enhancement, with most samples sizes under 50. It follows that the observed effects would be inconsistent, a mix of positive and null findings.
Finally, it’s not clear that caffeine results in performance gains after long-term use; homeostasis/tolerance is a concern for all stimulants, but especially for caffeine. It is plausible that all caffeine consumption does for the long-term chronic user is restore performance to baseline. (Imagine someone waking up and drinking coffee, and their performance improves - well, so would the performance of a non-addict who is also slowly waking up!) See for example, James & Rogers 2005, Sigmon et al 2009, and Rogers et al 2010. A cross-section of thousands of participants in the Cambridge brain-training study found caffeine intake showed negligible effect sizes for mean and component scores (participants were not told to use caffeine, but the training was recreational & difficult, so one expects some difference).
The chemical Huperzine-A (Examine.com) is extracted from a moss. It is an acetylcholinesterase inhibitor (instead of forcing out more acetylcholine like the -racetams, it prevents acetylcholine from breaking down). My experience report: One for the null hypothesis files - Huperzine-A did nothing for me. Unlike piracetam or fish oil, after a full bottle (Source Naturals, 120 pills at 200μg each), I noticed no side-effects, no mental improvements of any kind, and no changes in DNB scores from straight Huperzine-A.

It is not because of the few thousand francs which would have to be spent to put a roof [!] over the third-class carriages or to upholster the third-class seats that some company or other has open carriages with wooden benches. What the company is trying to do is to prevent the passengers who can pay the second class fare from traveling third class; it hits the poor, not because it wants to hurt them, but to frighten the rich. And it is again for the same reason that the companies, having proved almost cruel to the third-class passengers and mean to the second-class ones, become lavish in dealing with first-class passengers. Having refused the poor what is necessary, they give the rich what is superfluous.
It is a known fact that cognitive decline is often linked to aging. It may not be as visible as skin aging, but the brain does in fact age. Often, cognitive decline is not noticeable because it could be as mild as forgetting names of people. However, research has shown that even in healthy adults, cognitive decline can start as early as in the late twenties or early thirties.
One study of helicopter pilots suggested that 600 mg of modafinil given in three doses can be used to keep pilots alert and maintain their accuracy at pre-deprivation levels for 40 hours without sleep.[60] However, significant levels of nausea and vertigo were observed. Another study of fighter pilots showed that modafinil given in three divided 100 mg doses sustained the flight control accuracy of sleep-deprived F-117 pilots to within about 27% of baseline levels for 37 hours, without any considerable side effects.[61] In an 88-hour sleep loss study of simulated military grounds operations, 400 mg/day doses were mildly helpful at maintaining alertness and performance of subjects compared to placebo, but the researchers concluded that this dose was not high enough to compensate for most of the effects of complete sleep loss.

Four of the studies focused on middle and high school students, with varied results. Boyd, McCabe, Cranford, and Young (2006) found a 2.3% lifetime prevalence of nonmedical stimulant use in their sample, and McCabe, Teter, and Boyd (2004) found a 4.1% lifetime prevalence in public school students from a single American public school district. Poulin (2001) found an 8.5% past-year prevalence in public school students from four provinces in the Atlantic region of Canada. A more recent study of the same provinces found a 6.6% and 8.7% past-year prevalence for MPH and AMP use, respectively (Poulin, 2007).
Depending on where you live, some nootropics may not be sold over the counter, but they are usually available online. The law regarding nootropics can vary massively around the world, so be sure to do your homework before you purchase something for the first time. Be particularly cautious when importing smart drugs, because quality control and regulations abroad are not always as stringent as they are in the US. Do not put your health at risk if all you are trying to do is gain an edge in a competitive sport.

When I worked on the Bulletproof Diet book, I wanted to verify that the effects I was getting from Bulletproof Coffee were not coming from modafinil, so I stopped using it and measured my cognitive performance while I was off of it. What I found was that on Bulletproof Coffee and the Bulletproof Diet, my mental performance was almost identical to my performance on modafinil. I still travel with modafinil, and I’ll take it on occasion, but while living a Bulletproof lifestyle I rarely feel the need.
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