With subtle effects, we need a lot of data, so we want at least half a year (6 blocks) or better yet, a year (12 blocks); this requires 180 actives and 180 placebos. This is easily covered by $11 for Doctor’s Best Best Lithium Orotate (5mg), 200-Count (more precisely, Lithium 5mg (from 125mg of lithium orotate)) and $14 for 1000x1g empty capsules (purchased February 2012). For convenience I settled on 168 lithium & 168 placebos (7 pill-machine batches, 14 batches total); I can use them in 24 paired blocks of 7-days/1-week each (48 total blocks/48 weeks). The lithium expiration date is October 2014, so that is not a problem
I can test fish oil for mood, since the other claimed benefits like anti-schizophrenia are too hard to test. The medical student trial (Kiecolt-Glaser et al 2011) did not see changes until visit 3, after 3 weeks of supplementation. (Visit 1, 3 weeks, visit 2, supplementation started for 3 weeks, visit 3, supplementation continued 3 weeks, visit 4 etc.) There were no tests in between the test starting week 1 and starting week 3, so I can’t pin it down any further. This suggests randomizing in 2 or 3 week blocks. (For an explanation of blocking, see the footnote in the Zeo page.)
From the standpoint of absorption, the drinking of tobacco juice and the interaction of the infusion or concoction with the small intestine is a highly effective method of gastrointestinal nicotine administration. The epithelial area of the intestines is incomparably larger than the mucosa of the upper tract including the stomach, and the small intestine represents the area with the greatest capacity for absorption (Levine 1983:81-83). As practiced by most of the sixty-four tribes documented here, intoxicated states are achieved by drinking tobacco juice through the mouth and/or nose…The large intestine, although functionally little equipped for absorption, nevertheless absorbs nicotine that may have passed through the small intestine.
Farah was one of several scholars who contributed to a recent article in Nature, "Towards Responsible Use of Cognitive Enhancing Drugs by the Healthy". The optimistic tone of the article suggested that some bioethicists are leaning towards endorsing neuroenhancement. "Like all new technologies, cognitive enhancement can be used well or poorly," the article declared. "We should welcome new methods of improving our brain function. In a world in which human workspans and lifespans are increasing, cognitive-enhancement tools - including the pharmacological - will be increasingly useful for improved quality of life and extended work productivity, as well as to stave off normal and pathological age-related cognitive declines. Safe and effective cognitive enhancers will benefit both the individual and society." The BMA report offered a similarly upbeat observation: "Universal access to enhancing interventions would bring up the baseline level of cognitive ability, which is generally seen to be a good thing."
The NIDA research study focused on 10 healthy male participants. The men were subjected to two rounds of PET brain scans after consuming either Provigil (200 mg or 400 mg) or a placebo. The scans demonstrated that the Provigil users had an increase in the amount of dopamine in the brain. Dopamine is a key neurological messenger in the brain’s reward system. Cocaine and methamphetamine have a similar effect on the brain, but they are more potent and faster-acting than Provigil. As cocaine and amphetamines are addiction-forming, the reasoning here is that Provigil may also be addictive.
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.
Vinpocetine: This chemical is a semi-synthetic derivative of an extract from periwinkle. It acts as a potent anti-inflammatory agent, and has also received some testing as a supplement for memory enhancement. While research results are inconclusive right now, this chemical has been shown to increase blood circulation and metabolism in the brain and may slow down neuron loss. Some tests have also shown that it can improve concentration and attention.
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:
The low-carb & high-fat diet (includes keto-diet) are not good for you because the brain needs glucose for fuel. It can burn fat. But, the brain’s preferred energy source is glucose. The key is to provide the brain with glucose without raising glucose/serum blood level. You do that by avoiding sugar and eating complex carbohydrates (fresh produce) that convert into glucose.
Past noon, I began to feel better, but since I would be driving to errands around 4 PM, I decided to not risk it and take an hour-long nap, which went well, as did the driving. The evening was normal enough that I forgot I had stayed up the previous night, and indeed, I didn’t much feel like going to bed until past midnight. I then slept well, the Zeo giving me a 108 ZQ (not an all-time record, but still unusual).
Is 200 enough? There are no canned power functions for the ordinal logistic regression I would be using, so the standard advice is to estimate power by simulation: generating thousands of new datasets where we know by construction that the binary magnesium variable increases MP by 0.27 (such as by bootstrapping the original Noopept experiment’s data), and seeing how often in this collection the cutoff of statistical-significance is passed when the usual analysis is done (background: CrossValidated or Power Analysis and Sample Size Estimation using Bootstrap). In this case, we leave alpha at 0.05, reuse the Noopept experiment’s data with its Magtein correlation, and ask for the power when n=200
It wasn't always helpful, but it does work sometimes. The first two days gave me stomach and head pain, so I began to test with taking before or after food, and with or without food. The bottle says to take before food, but I preferred taking this with food, more food is better. This doesn't go well in the stomach with something like chocolate, so take this with something like bread or a meal. More importantly, stay very hydrated unless you want a headache, these pills are very hydro-demanding. The pills also work better if you get your blood moving, just a short walk is fine. Energy drinks and coffee go very well with these, as I had a very clear minded experience when taking these with a Monster Java, it was like a cool breeze blowing away the mental fog.
The ‘Brain-Gut Axis’ is a term used to describe the two-way communication system between our digestive tract and the brain. A growing body of research into this axis demonstrates how much influence the gut can have over the brain and vice versa (1). When we speak about reactions to foods, we most commonly understand them as immediate and often dangerous allergic responses, such as the constriction of the throat and trouble breathing, or dizziness and fainting. It is usually easy to pinpoint the food that causes these reactions because of the immediate immune system response, caused by a type of immune cell known as IgE antibodies. In contrast to this, food intolerances are mediated by IgG antibodies and these reactions can take up to 48 hours to have an effect. Symptoms related to IgG reactions can often be manifested as chronic issues like joint ache, IBS and depression or anxiety, which are often overlooked and not associated with what we eat.
2ml is supposed to translate to 24mg, which is a big dose. I do not believe any of the commercial patches go much past that. I asked Wedrifid, whose notes inspired my initial interest, and he was taking perhaps 2-4mg, and expressed astonishment that I might be taking 24mg. (2mg is in line with what I am told by another person - that 2mg was so much that they actually felt a little sick. On the other hand, in one study, the subjects could not reliably distinguish between 1mg and placebo25.) 24mg is particularly troubling in that I weigh ~68kg, and nicotine poisoning and the nicotine LD50 start, for me, at around 68mg of nicotine. (I reflected that the entire jar could be a useful murder weapon, although nicotine presumably would be caught in an autopsy’s toxicology screen; I later learned nicotine was an infamous weapon in the 1800s before any test was developed. It doesn’t seem used anymore, but there are still fatal accidents due to dissolved nicotine.) The upper end of the range, 10mg/kg or 680mg for me, is calculated based on experienced smokers. Something is wrong here - I can’t see why I would have nicotine tolerance comparable to a hardened smoker, inasmuch as my maximum prior exposure was second-hand smoke once in a blue moon. More likely is that either the syringe is misleading me or the seller NicVape sold me something more dilute than 12mg/ml. (I am sure that it’s not simply plain water; when I mix the drops with regular water, I can feel the propylene glycol burning as it goes down.) I would rather not accuse an established and apparently well-liked supplier of fraud, nor would I like to simply shrug and say I have a mysterious tolerance and must experiment with doses closer to the LD50, so the most likely problem is a problem with the syringe. The next day I altered the procedure to sucking up 8ml, squirting out enough fluid to move the meniscus down to 7ml, and then ejecting the rest back into the container. The result was another mild clean stimulation comparable to the previous 1ml days. The next step is to try a completely different measuring device, which doesn’t change either.
Its high levels of collagen help reduce intestinal inflammation, and healing amino acids like proline and glycine keep your immune system functioning properly and help improve memory. Bone broth is what I prescribe most frequently to my patients because it truly helps heal your body from the inside out. You’ll also be surprised at how simple and economical it is to make at home with my Beef Bone Broth Recipe.
On the other hand, sometimes you’ll feel a great cognitive boost as soon as you take a pill. That can be a good thing or a bad thing. I find, for example, that modafinil makes you more of what you already are. That means if you are already kind of a dick and you take modafinil, you might act like a really big dick and regret it. It certainly happened to me! I like to think that I’ve done enough hacking of my brain that I’ve gotten over that programming… and that when I use nootropics they help me help people.
Harriet Hall, MD also known as The SkepDoc, is a retired family physician who writes about pseudoscience and questionable medical practices. She received her BA and MD from the University of Washington, did her internship in the Air Force (the second female ever to do so), and was the first female graduate of the Air Force family practice residency at Eglin Air Force Base. During a long career as an Air Force physician, she held various positions from flight surgeon to DBMS (Director of Base Medical Services) and did everything from delivering babies to taking the controls of a B-52. She retired with the rank of Colonel. In 2008 she published her memoirs, Women Aren't Supposed to Fly.
The BoredAt websites - which allow college students to chat idly while they're ostensibly studying - are filled with messages about Adderall. Posts like these, from the BoredAtPenn site, are typical: "I have some Adderall - I'm sitting by room 101.10 in a grey shirt and headphones"; "I have Adderall for sale 20mg for $15"; "I took Adderall at 8pm, it's 6:30am and I've barely blinked." On the Columbia site one poster complains that her friends take Adderall "like candy", adding: "I don't want to be at a disadvantage to everyone else. Is it really that dangerous? My grades weren't that great this year and I could do with a bump." A Columbia student responds: "It's probably not a good idea if you're not prescribed", but offers practical advice anyway: "Keep the dose normal and don't grind them up or snort them." Occasional dissenters ("I think there should be random drug testing at every exam") are drowned out by testimonials like this one, from the BoredAtHarvard site: "I don't want to be a pusher or start people on something bad, but Adderall is amazing."
Googling, you sometimes see correlational studies like Intake of Flavonoid-Rich Wine, Tea, and Chocolate by Elderly Men and Women Is Associated with Better Cognitive Test Performance; in this one, the correlated performance increase from eating chocolate was generally fairly modest (say, <10%), and the maximum effects were at 10g/day of what was probably milk chocolate, which generally has 10-40% chocolate liquor in it, suggesting any experiment use 1-4g. More interesting is the blind RCT experiment Consumption of cocoa flavanols results in acute improvements in mood and cognitive performance during sustained mental effort11, which found improvements at ~1g; the most dramatic improvement of the 4 tasks (on the Threes correct) saw a difference of 2 to 6 at the end of the hour of testing, while several of the other tests converged by the end or saw the controls winning (Sevens correct). Crews et al 2008 found no cognitive benefit, and an fMRI experiment found the change in brain oxygen levels it wanted but no improvement to reaction times.
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.)
-Phosphatidylserine, which occurs naturally in high concentrations in the brain and has been shown to lower stress, cortisol and physical fatigue, improve attention-deficit and forgetfulness and increase mental processing and memory. Research indicates an effective dose of 100 mg three times daily, but anything over that may lead to adverse side effects like insomnia.
After many years recruiting teens from across the city to join us for a year of culinary adventures, we’re relying on the city’s network of talented youth service providers to fill the gap and cultivate the next generation of smart, resilient youth leaders. While this isn’t where we wanted to be, we’re reaching for gratitude and sharing KUDOS one last time.
But according to Professor David Weinshenker of Emory University, most people who take Provigil do not report euphoria or even a level of stimulation close to the effects of caffeine. For Weinshenker, the addiction potential of Provigil is limited, and it’s used in various treatment contexts. Provigil may be an effective medication therapy for depression, ADHD, autism and other disorders.
That really says it all: there’s an initial spike in MP, which reads like the promised stimulative effects possibly due to fixing a deficiency (a spike which doesn’t seem to have any counterparts in the previous history of MP), followed by a drastic plunge in the magnesium days but not so much the control days (indicating an acute effect when overloaded with magnesium), a partial recovery during the non-experimental Christmas break, another plunge, and finally recovery after the experiment has ended.
But it's not the mind-expanding 1960s any more. Every era, it seems, has its own defining drug. Neuroenhancers are perfectly suited to the anxiety of white-collar competition in a floundering economy. And they have a synergistic relationship with our multiplying digital technologies: the more gadgets we own, the more distracted we become and the more we need help in order to focus. The experience that neuroenhancement offers is not, for the most part, about opening the doors of perception, or about breaking the bonds of the self, or about experiencing a surge of genius. It's about squeezing out an extra few hours to finish those sales figures when you'd really rather collapse into bed; getting a B instead of a B-minus on the final exam in a lecture class where you spent half your time texting; cramming for the GREs (postgraduate entrance exams) at night, because the information-industry job you got after college turned out to be deadening. Neuroenhancers don't offer freedom. Rather, they facilitate a pinched, unromantic, grindingly efficient form of productivity.
It would be like saying: 'No, you can't use a cell phone. It might increase productivity!'" If we eventually decide that neuroenhancers work, and are basically safe, will we one day enforce their use? Lawmakers might compel certain workers - A&E doctors, air-traffic controllers - to take them. (Indeed, the US Air Force already makes modafinil available to pilots embarking on long missions.) For the rest of us, the pressure will be subtler - that queasy feeling I get when I remember that my younger colleague is taking Provigil to meet deadlines. All this may be leading to a kind of society I'm not sure I want to live in: a society where we're even more overworked and driven by technology than we already are, and where we have to take drugs to keep up; a society where we give children academic steroids along with their daily vitamins.
A picture is worth a thousand words, particularly in this case where there seems to be temporal effects, different trends for the conditions, and general confusion. So, I drag up 2.5 years of MP data (for context), plot all the data, color by magnesium/non-magnesium, and fit different LOESS lines to each as a sort of smoothed average (since categorical data is hard to interpret as a bunch of dots), which yields:
Blueberries. "Brainberries" is what Steven Pratt, MD, author of Superfoods Rx: Fourteen Foods Proven to Change Your Life, calls these tasty fruits. Pratt, who is also on staff at Scripps Memorial Hospital in La Jolla, Calif., says that in animal studies researchers have found that blueberries help protect the brain from oxidative stress and may reduce the effects of age-related conditions such as Alzheimer's disease or dementia. Studies have also shown that diets rich in blueberries significantly improved both the learning capacity and motor skills of aging rats, making them mentally equivalent to much younger rats. Ann Kulze, MD, author of Dr. Ann's 10-Step Diet: A Simple Plan for Permanent Weight Loss & Lifelong Vitality, recommends adding at least 1 cup of blueberries a day in any form -- fresh, frozen, or freeze-dried.
After a month of testing nootropics, I’m not ready to commit to them permanently. They’re simply too untested, and while “move fast and break things” might be a good approach to building software, it’s not what I want for my brain. Still, I think we’ll likely hear more about nootropics, especially as recreational users of more powerful prescription drugs like Adderall and modafinil look for less harsh alternatives. Sometimes, when you’re working, you don’t want to put your brain on jet fuel—a little unleaded gas will do. And for those moments, nootropics could be a fertile testing ground for the intrepid body-hacker.
Factor analysis. The strategy: read in the data, drop unnecessary data, impute missing variables (data is too heterogeneous and collected starting at varying intervals to be clean), estimate how many factors would fit best, factor analyze, pick the ones which look like they match best my ideas of what productive is, extract per-day estimates, and finally regress LLLT usage on the selected factors to look for increases.
Mosconi holds a dual PhD in neuroscience and nuclear medicine. She is the associate director of the Alzheimer’s Prevention Clinic at Weill Cornell Medical College/New York-Presbyterian Hospital, and the founder of the Nutrition and Brain Fitness Lab at New York University School of Medicine. With her training and experience, she ought to understand and practice rigorous science. She makes all the right noises about scientific literacy and recognizing pseudoscience, but she seems unable to look in the mirror and see her own errors.
Although piracetam has a history of “relatively few side effects,” it has fallen far short of its initial promise for treating any of the illnesses associated with cognitive decline, according to Lon Schneider, a professor of psychiatry and behavioral sciences at the Keck School of Medicine at the University of Southern California. “We don’t use it at all and never have.”
Nootroo and Nootrobox are two San Francisco nootropics startups that launched last year. Their founders come from the tech scene and their products are squarely aimed at the tech crowd seeking the convenience of not having to build their own combinations. Each claims big-name Silicon Valley entrepreneurs and investors among their users, though neither will name them.
It is incredibly easy to abuse and become addicted to methylphenidate, and misuse is shockingly prevalent, even among so-called “non-affected” users: with students, biohackers, soccer moms and busy executives popping it – and many of the other smart drugs below – like candy. It’s also not all it’s cracked up to be. Side effects include insomnia, stomach ache, headache and anorexia. Overdoses (which may occur easily as it can be difficult to estimate and regulate dosage) can lead to agitation, hallucinations, psychosis, lethargy, seizures, tachycardia (rapid heart rate), dysrhythmia (irregular heart rhythms), hypertension and hyperthermia. Methylphenidate is particularly hazardous to developing brains, especially those of younger students who are frequently prescribed the drug or who – often in high school and college – use it without a prescription. The prefrontal cortex, located behind the forehead, is responsible for cognition, personality-expression and decision-making, and develops well into the mid-20s, at which point it takes over as the “rational” part of the brain. In the central nervous system, and particularly in the prefrontal cortex, dopamine levels must have a natural rise and fall in order for healthy rational processes (executive control) to develop. By influencing dopamine levels, methylphenidate can negatively impact this healthy cognitive development, especially when it is abused or used too frequently.
Takao Hensch, a Harvard professor of cellular biology and part of a Boston Children’s Hospital team, found that the drug encouraged the brain to learn new skills as quickly as the sponge-like brain of an infant in her patient Shannon, an otherwise normal 14-year-old girl who suffers from extremely poor eyesight brought on by amblyopia, commonly known as lazy eye. In a matter of months, the drug helped Shannon’s brain relearn how to use her eye which resulted in markedly improved vision.
Although research linking diet and dementia is still in its infancy, there are a few important relationships between nutrients and brain health that are worth exploring. Having a nourishing, well rounded diet gives our brain the best chance of avoiding disease. If your diet is unbalanced for whatever reason, you may want to consider a multivitamin and mineral complex and an omega-3 fatty acid supplement to help make up a few of the essentials. If you are considering taking a supplement it is best to discuss this with your GP or qualified healthcare professional.
First half at 6 AM; second half at noon. Wrote a short essay I’d been putting off and napped for 1:40 from 9 AM to 10:40. This approach seems to work a little better as far as the aboulia goes. (I also bother to smell my urine this time around - there’s a definite off smell to it.) Nights: 10:02; 8:50; 10:40; 7:38 (2 bad nights of nasal infections); 8:28; 8:20; 8:43 (▆▃█▁▂▂▃).
And when it comes to your brain, it’s full of benefits, too. Coconut oil works as a natural anti-inflammatory, suppressing cells responsible for inflammation. It can help with memory loss as you age and destroy bad bacteria that hangs out in your gut. (5) Get your dose of coconut oil in this Baked Grouper with Coconut Cilantro Sauce or Coconut Crust Pizza.
If you are a slow caffeine metabolizer and consume too much caffeine, you run the risk of mild to severe complications, such as cardiovascular disease. There’s also the sleep disruption problem of having too much caffeine left in your bloodstream late in the day as a result of a longer caffeine half-life, a problem not faced by fast caffeine metabolizers (it’s so unfair if you love your cup of joe, right?). In addition, fast caffeine metabolizers actually run a reduced risk of cardiovascular complications if they consume at least one cup of coffee per day. While anyone can be a slow caffeine metabolizer, there are certain ethnic backgrounds that are indeed associated with slower and faster caffeine metabolisms. For example, it’s known that people with Asian and African ethnic backgrounds generally have slower rates of caffeine metabolism. To find out if you’re a fast or slow caffeine metabolizer, you can have a relatively inexpensive salivary genetic test performed by a company like 23andme and then use the online dashboard to jump straight to your CYP1A2 gene. When you’re there, you type into the search bar “rs762551”. If your rs762551 SNP variant is AA, then you’re a fast caffeine metabolizer, but if your variant is AC or CC, you’re a slow caffeine metabolizer. Fortunately, many genetic testing companies will now simply report directly on your results whether you’re a slow or fast metabolizer, without you needing to go through the SNP searching trouble.
Choline is a nootropic: it enhances your ability to pay attention and learn efficiently, probably because you use a lot of acetylcholine during mentally-demanding tasks, and choline helps you synthesize enough to work harder and go longer. Choline also links to decreased brain inflammation in a dose-dependent manner — the more choline you eat, the less inflamed your brain tends to be.
1. Stough, C., Lloyd, J., Clarke, J., Downey, L. A., Hutchison, C. W., Rodgers, T., & Nathan, P. J. (2001). The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology (Berl), 156(4), 481-484. 2. Ishaque, S., Shamseer, L., Bukutu, C., & Vohra, S. (2012). Rhodiola rosea for physical and mental fatigue: a systematic review. BMC Complementary and Alternative Medicine, 12(1), 70. doi:10.1186/1472-6882-12-703. Pase, M. P., Kean, J., Sarris, J., Neale, C., Scholey, A. B., & Stough, C. (2012). The cognitive-enhancing effects of Bacopa monnieri: a systematic review of randomized, controlled human clinical trials. J Altern Complement Med, 18(7), 647-652. doi:10.1089/acm.2011.03674. Raghav, S., Singh, H., Dalal, P. K., Srivastava, J. S., & Asthana, O. P. (2006). Randomized controlled trial of standardized Bacopa monniera extract in age-associated memory impairment. Indian J Psychiatry, 48(4), 238-242. doi:10.4103/0019-5545.315555. Neale, C., Camfield, D., Reay, J., Stough, C., & Scholey, A. (2013). Cognitive effects of two nutraceuticals Ginseng and Bacopa [...]: a review and comparison of effect sizes. British Journal of Clinical Pharmacology, 75(3), 728-737. doi:10.1111/bcp.120026. Prynne, C. J., Thane, C. W., Prentice, A., & Wadsworth, M. E. (2005). Intake and sources of phylloquinone (vitamin K(1)) in 4-year-old British children: comparison between 1950 and the 1990s. Public Health Nutr, 8(2), 171-180.7. Ferland, G. (2012). Vitamin K and the nervous system: an overview of its actions. Adv Nutr, 3(2), 204-212. doi:10.3945/an.111.0017848. Zeidan, Y. H., & Hannun, Y. A. (2007). Translational aspects of sphingolipid metabolism. Trends in molecular medicine, 13(8), 327-336.9. Beulens, J. W., Bots, M. L., Atsma, F., Bartelink, M. L., Prokop, M., Geleijnse, J. M., . . . van der Schouw, Y. T. (2009). High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis, 203(2), 489-493. doi:10.1016/j.atherosclerosis.2008.07.01010. Geleijnse, J. M., Vermeer, C., Grobbee, D. E., Schurgers, L. J., Knapen, M. H., van der Meer, I. M., . . . Witteman, J. C. (2004). Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. J Nutr, 134(11), 3100-3105.11. Theuwissen, E., Magdeleyns, E. J., Braam, L. A., Teunissen, K. J., Knapen, M. H., Binnekamp, I. A., . . . Vermeer, C. (2014). Vitamin K status in healthy volunteers. Food Funct, 5(2), 229-234. doi:10.1039/c3fo60464k12. Barros, M. P., Poppe, S. C., & Bondan, E. F. (2014). Neuroprotective properties of the marine carotenoid astaxanthin and omega-3 fatty acids, and perspectives for the natural combination of both in krill oil. Nutrients, 6(3), 1293-1317.13. Pashkow, F. J., Watumull, D. G., & Campbell, C. L. (2008). Astaxanthin: a novel potential treatment for oxidative stress and inflammation in cardiovascular disease. Am J Cardiol, 101(10a), 58d-68d. doi:10.1016/j.amjcard.2008.02.01014. Annweiler, C., Schott, A. M., Berrut, G., Chauvire, V., Le Gall, D., Inzitari, M., & Beauchet, O. (2010). Vitamin D and ageing: neurological issues. Neuropsychobiology, 62(3), 139-150. doi:10.1159/00031857015. Brown, J., Bianco, J. I., McGrath, J. J., & Eyles, D. W. (2003). 1,25-dihydroxyvitamin D3 induces nerve growth factor, promotes neurite outgrowth and inhibits mitosis in embryonic rat hippocampal neurons. Neurosci Lett, 343(2), 139-143.16. Naveilhan, P., Neveu, I., Wion, D., & Brachet, P. (1996). 1,25-Dihydroxyvitamin D3, an inducer of glial cell line-derived neurotrophic factor. Neuroreport, 7(13), 2171-2175.17. Tangpricha, V., Pearce, E. N., Chen, T. C., & Holick, M. F. (2002). Vitamin D insufficiency among free-living healthy young adults. Am J Med, 112(8), 659-662.18. Annweiler, C., Allali, G., Allain, P., Bridenbaugh, S., Schott, A. M., Kressig, R. W., & Beauchet, O. (2009). Vitamin D and cognitive performance in adults: a systematic review. European Journal of Neurology, 16(10), 1083-1089. doi:10.1111/j.1468-1331.2009.02755.x19. Annweiler, C., Montero-Odasso, M., Llewellyn, D. J., Richard-Devantoy, S., Duque, G., & Beauchet, O. (2013). Meta-analysis of memory and executive dysfunctions in relation to vitamin D. J Alzheimers Dis, 37(1), 147-171. doi:10.3233/jad-13045220. Balion, C., Griffith, L. E., Strifler, L., Henderson, M., Patterson, C., Heckman, G., . . . Raina, P. (2012). Vitamin D, cognition, and dementia A systematic review and meta-analysis. Neurology, 79(13), 1397-1405.21. Dean, A. J., Bellgrove, M. A., Hall, T., Phan, W. M. J., Eyles, D. W., Kvaskoff, D., & McGrath, J. J. (2011). Effects of Vitamin D Supplementation on Cognitive and Emotional Functioning in Young Adults – A Randomised Controlled Trial. PLoS One, 6(11), e25966. doi:10.1371/journal.pone.002596622. Etgen, T., Sander, D., Bickel, H., Sander, K., & Forstl, H. (2012). Vitamin D deficiency, cognitive impairment and dementia: a systematic review and meta-analysis. Dement Geriatr Cogn Disord, 33(5), 297-305. doi:10.1159/00033970223. Fontani, G., Corradeschi, F., Felici, A., Alfatti, F., Migliorini, S., & Lodi, L. (2005). Cognitive and physiological effects of Omega-3 polyunsaturated fatty acid supplementation in healthy subjects. Eur J Clin Invest, 35(11), 691-699. doi:10.1111/j.1365-2362.2005.01570.x24. Huhn, S., Masouleh, S. K., Stumvoll, M., Villringer, A., & Witte, A. V. (2015). Components of a Mediterranean diet and their impact on cognitive functions in aging. Frontiers in aging neuroscience, 7.25. Bradbury, J. (2011). Docosahexaenoic Acid (DHA): An Ancient Nutrient for the Modern Human Brain. Nutrients, 3(5), 529-554. doi:10.3390/nu305052926. Einother, S. J., & Giesbrecht, T. (2013). Caffeine as an attention enhancer: reviewing existing assumptions. Psychopharmacology (Berl), 225(2), 251-274. doi:10.1007/s00213-012-2917-427. Johnson, L. C., Spinweber, C. L., & Gomez, S. A. (1990). Benzodiazepines and caffeine: effect on daytime sleepiness, performance, and mood. Psychopharmacology (Berl), 101(2), 160-167. 28. Smith, A., Kendrick, A., Maben, A., & Salmon, J. (1994). Effects of breakfast and caffeine on cognitive performance, mood and cardiovascular functioning. Appetite, 22(1), 39-55. doi:10.1006/appe.1994.100429. Smith, A. P., Kendrick, A. M., & Maben, A. L. (1992). Effects of breakfast and caffeine on performance and mood in the late morning and after lunch. Neuropsychobiology, 26(4), 198-204. doi:11892030. Smith, B. D., Davidson, R. A., & Green, R. L. (1993). Effects of caffeine and gender on physiology and performance: further tests of a biobehavioral model. Physiol Behav, 54(3), 415-422. 31. Warburton, D. M. (1995). Effects of caffeine on cognition and mood without caffeine abstinence. Psychopharmacology (Berl), 119(1), 66-70. 32. Wilhelmus, M. M., Hay, J. L., Zuiker, R. G., Okkerse, P., Perdrieu, C., Sauser, J., . . . Silber, B. Y. (2017). Effects of a single, oral 60 mg caffeine dose on attention in healthy adult subjects. J Psychopharmacol, 31(2), 222-232. doi:10.1177/026988111666859333. Fredholm, B. B., Battig, K., Holmen, J., Nehlig, A., & Zvartau, E. E. (1999). Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev, 51(1), 83-133. 34. Borzelleca, J. F., Peters, D., & Hall, W. (2006). A 13-week dietary toxicity and toxicokinetic study with l-theanine in rats. Food Chem Toxicol, 44(7), 1158-1166. doi:10.1016/j.fct.2006.03.01435. Kimura, K., Ozeki, M., Juneja, L. R., & Ohira, H. (2007). L-Theanine reduces psychological and physiological stress responses. Biol Psychol, 74(1), 39-45. doi:10.1016/j.biopsycho.2006.06.00636. Tian, X., Sun, L., Gou, L., Ling, X., Feng, Y., Wang, L., . . . Liu, Y. (2013). Protective effect of l-theanine on chronic restraint stress-induced cognitive impairments in mice. Brain Res, 1503, 24-32. doi:10.1016/j.brainres.2013.01.04837. Unno, K., Fujitani, K., Takamori, N., Takabayashi, F., Maeda, K., Miyazaki, H., . . . Hoshino, M. (2011). Theanine intake improves the shortened lifespan, cognitive dysfunction and behavioural depression that are induced by chronic psychosocial stress in mice. Free Radic Res, 45(8), 966-974. doi:10.3109/10715762.2011.56686938. Unno, K., Tanida, N., Ishii, N., Yamamoto, H., Iguchi, K., Hoshino, M., . . . Yamada, H. (2013). Anti-stress effect of theanine on students during pharmacy practice: positive correlation among salivary alpha-amylase activity, trait anxiety and subjective stress. Pharmacol Biochem Behav, 111, 128-135. doi:10.1016/j.pbb.2013.09.00439. Dodd, F. L., Kennedy, D. O., Riby, L. M., & Haskell-Ramsay, C. F. (2015a). A double-blind, placebo-controlled study evaluating the effects of caffeine and L-theanine both alone and in combination on cerebral blood flow, cognition and mood. Psychopharmacology (Berl), 232(14), 2563-2576. doi:10.1007/s00213-015-3895-040. Rogers, P. J., Smith, J. E., Heatherley, S. V., & Pleydell-Pearce, C. W. (2008). Time for tea: mood, blood pressure and cognitive performance effects of caffeine and theanine administered alone and together. Psychopharmacology (Berl), 195(4), 569-577. doi:10.1007/s00213-007-0938-141. Foxe, J. J., Morie, K. P., Laud, P. J., Rowson, M. J., de Bruin, E. A., & Kelly, S. P. (2012). Assessing the effects of caffeine and theanine on the maintenance of vigilance during a sustained attention task. Neuropharmacology, 62(7), 2320-2327. doi:10.1016/j.neuropharm.2012.01.02042. Giesbrecht, T., Rycroft, J. A., Rowson, M. J., & De Bruin, E. A. (2010). The combination of L-theanine and caffeine improves cognitive performance and increases subjective alertness. Nutr Neurosci, 13(6), 283-290. doi:10.1179/147683010x1261146076484043. Haskell, C. F., Kennedy, D. O., Milne, A. L., Wesnes, K. A., & Scholey, A. B. (2008). The effects of L-theanine, caffeine and their combination on cognition and mood. Biol Psychol, 77(2), 113-122. doi:10.1016/j.biopsycho.2007.09.00844. Kahathuduwa, C. N., Dassanayake, T. L., Amarakoon, A. M., & Weerasinghe, V. S. (2016). Acute effects of theanine, caffeine and theanine-caffeine combination on attention. Nutr Neurosci. doi:10.1080/1028415x.2016.114484545. Owen, G. N., Parnell, H., De Bruin, E. A., & Rycroft, J. A. (2008). The combined effects of L-theanine and caffeine on cognitive performance and mood. Nutr Neurosci, 11(4), 193-198. doi:10.1179/147683008x30151346. Einother, S. J., Martens, V. E., Rycroft, J. A., & De Bruin, E. A. (2010). L-theanine and caffeine improve task switching but not intersensory attention or subjective alertness. Appetite, 54(2), 406-409. doi:10.1016/j.appet.2010.01.00347. Deijen, J. B., van der Beek, E. J., Orlebeke, J. F., & van den Berg, H. (1992). Vitamin B-6 supplementation in elderly men: effects on mood, memory, performance and mental effort. Psychopharmacology (Berl), 109(4), 489-496.48. Lewerin, C., Matousek, M., Steen, G., Johansson, B., Steen, B., & Nilsson-Ehle, H. (2005). Significant correlations of plasma homocysteine and serum methylmalonic acid with movement and cognitive performance in elderly subjects but no improvement from short-term vitamin therapy: a placebo-controlled randomized study. Am J Clin Nutr, 81(5), 1155-1162. 49. Bryan, J., Calvaresi, E., & Hughes, D. (2002). Short-term folate, vitamin B-12 or vitamin B-6 supplementation slightly affects memory performance but not mood in women of various ages. J Nutr, 132(6), 1345-1356. 50. Schneider, Z., & Stroinski, A. (1987). Comprehensive B12: chemistry, biochemistry, nutrition, ecology, medicine: Walter de Gruyter.51. Polich, J., & Gloria, R. (2001). Cognitive effects of a Ginkgo biloba/vinpocetine compound in normal adults: systematic assessment of perception, attention and memory. Hum Psychopharmacol, 16(5), 409-416. doi:10.1002/hup.30852. Subhan, Z., & Hindmarch, I. (1985). Psychopharmacological effects of vinpocetine in normal healthy volunteers. Eur J Clin Pharmacol, 28(5), 567-571. 53. Dollins, A. B., Krock, L. P., Storm, W. F., Wurtman, R. J., & Lieberman, H. R. (1995). L-tyrosine ameliorates some effects of lower body negative pressure stress. Physiol Behav, 57(2), 223-230. 54. Shurtleff, D., Thomas, J. R., Schrot, J., Kowalski, K., & Harford, R. (1994). Tyrosine reverses a cold-induced working memory deficit in humans. Pharmacol Biochem Behav, 47(4), 935-941. 55. Brzezinski, A., Vangel, M. G., Wurtman, R. J., Norrie, G., Zhdanova, I., Ben-Shushan, A., & Ford, I. (2005). Effects of exogenous melatonin on sleep: a meta-analysis. Sleep Med Rev, 9(1), 41-50. 56. Ferracioli-Oda, E., Qawasmi, A., & Bloch, M. H. (2013). Meta-Analysis: Melatonin for the Treatment of Primary Sleep Disorders. PLoS One, 8(5), e63773. doi:10.1371/journal.pone.006377357. Inagawa, K., Hiraoka, T., Kohda, T., Yamadera, W., & Takahashi, M. (2006). Subjective effects of glycine ingestion before bedtime on sleep quality. Sleep and Biological Rhythms, 4(1), 75-77. doi:10.1111/j.1479-8425.2006.00193.x58. Bannai, M., Kawai, N., Ono, K., Nakahara, K., & Murakami, N. (2012). The Effects of Glycine on Subjective Daytime Performance in Partially Sleep-Restricted Healthy Volunteers. Front Neurol, 3, 61. doi:10.3389/fneur.2012.0006159. Yamadera, W., Inagawa, K., Chiba, S., Bannai, M., Takahashi, M., & Nakayama, K. (2007). Glycine ingestion improves subjective sleep quality in human volunteers, correlating with polysomnographic changes. Sleep and Biological Rhythms, 5(2), 126-131. doi:10.1111/j.1479-8425.2007.00262.x60. Tuli, H. S., Kashyap, D., Sharma, A. K., & Sandhu, S. S. (2015). Molecular aspects of melatonin (MLT)-mediated therapeutic effects. Life Sci, 135, 147-157. doi:10.1016/j.lfs.2015.06.00461. Herxheimer, A., & Petrie, K. J. (2002). Melatonin for the prevention and treatment of jet lag. Cochrane Database Syst Rev(2), Cd001520. doi:10.1002/14651858.cd00152062. Deng, X., Song, Y., Manson, J. E., Signorello, L. B., Zhang, S. M., Shrubsole, M. J., . . . Dai, Q. (2013). Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. BMC Med, 11(1), 187. doi:10.1186/1741-7015-11-18763. Murck, H., & Steiger, A. (1998). Mg2+ reduces ACTH secretion and enhances spindle power without changing delta power during sleep in men -- possible therapeutic implications. Psychopharmacology (Berl), 137(3), 247-252. 64. Nielsen, F. H., Johnson, L. K., & Zeng, H. (2010). Magnesium supplementation improves indicators of low magnesium status and inflammatory stress in adults older than 51 years with poor quality sleep. Magnes Res, 23(4), 158-168. doi:10.1684/mrh.2010.0220
Whether you want to optimise your nutrition during exam season or simply want to stay sharp in your next work meeting, paying attention to your diet can really pay off. Although there is no single 'brain food' that can protect against age-related disorders such as Alzheimers' or dementia, and there are many other medical conditions that can affect the brain, paying attention to what you eat gives you the best chance of getting all the nutrients you need for cognitive health.
Qualia Mind, meanwhile, combines more than two dozen ingredients that may support brain and nervous system function – and even empathy, the company claims – including vitamins B, C and D, artichoke stem and leaf extract, taurine and a concentrated caffeine powder. A 2014 review of research on vitamin C, for one, suggests it may help protect against cognitive decline, while most of the research on artichoke extract seems to point to its benefits to other organs like the liver and heart. A small company-lead pilot study on the product found users experienced improvements in reasoning, memory, verbal ability and concentration five days after beginning Qualia Mind.