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^ Sattler, Sebastian; Mehlkop, Guido; Graeff, Peter; Sauer, Carsten (February 1, 2014). "Evaluating the drivers of and obstacles to the willingness to use cognitive enhancement drugs: the influence of drug characteristics, social environment, and personal characteristics". Substance Abuse Treatment, Prevention, and Policy. 9 (1): 8. doi:10.1186/1747-597X-9-8. ISSN 1747-597X. PMC 3928621. PMID 24484640.
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If you’re concerned with using either supplement, speak to your doctor. Others will replace these supplements with something like Phenylpiracetam or Pramiracetam. Both of these racetams provide increased energy levels, yielding less side-effects. If you do plan on taking Modafinil or Adrafinil, it’s best to use them on occasion or cycle your doses.
At dose #9, I’ve decided to give up on kratom. It is possible that it is helping me in some way that careful testing (eg. dual n-back over weeks) would reveal, but I don’t have a strong belief that kratom would help me (I seem to benefit more from stimulants, and I’m not clear on how an opiate-bearer like kratom could stimulate me). So I have no reason to do careful testing. Oh well.
Gamma-aminobutyric acid, also known as GABA, naturally produced in the brain from glutamate, is a neurotransmitter that helps in the communication between the nervous system and brain. The primary function of this GABA Nootropic is to reduce the additional activity of the nerve cells and helps calm the mind. Thus, it helps to improve various conditions, like stress, anxiety, and depression by decreasing the beta brain waves and increasing the alpha brain waves. It is one of the best nootropic for anxiety that you can find in the market today. As a result, cognitive abilities like memory power, attention, and alertness also improve. GABA helps drug addicts recover from addiction by normalizing the brain’s GABA receptors which reduce anxiety and craving levels in the absence of addictive substances.
An additional complexity, related to individual differences, concerns dosage. This factor, which varies across studies and may be fixed or determined by participant body weight within a study, undoubtedly influences the cognitive effects of stimulant drugs. Furthermore, single-unit recordings with animals and, more recently, imaging of humans indicate that the effects of stimulant dose are nonmonotonic; increases enhance prefrontal function only up to a point, with further increases impairing function (e.g., Arnsten, 1998; Mattay et al., 2003; Robbins & Arnsten, 2009). Yet additional complexity comes from the fact that the optimal dosage depends on the same kinds of individual characteristics just discussed and on the task (Mattay et al., 2003).
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.↩
Among the questions to be addressed in the present article are, How widespread is the use of prescription stimulants for cognitive enhancement? Who uses them, for what specific purposes? Given that nonmedical use of these substances is illegal, how are they obtained? Furthermore, do these substances actually enhance cognition? If so, what aspects of cognition do they enhance? Is everyone able to be enhanced, or are some groups of healthy individuals helped by these drugs and others not? The goal of this article is to address these questions by reviewing and synthesizing findings from the existing scientific literature. We begin with a brief overview of the psychopharmacology of the two most commonly used prescription stimulants.
Smart drug, also called nootropic or cognitive enhancer, any of a group of pharmaceutical agents used to improve the intellectual capacity of persons suffering from neurological diseases and psychological disorders. The use of such drugs by healthy individuals in order to improve concentration, to study longer, and to better manage stress is a subject of controversy.
Specifically, the film is completely unintelligible if you had not read the book. The best I can say for it is that it delivers the action and events one expects in the right order and with basic competence, but its artistic merits are few. It seems generally devoid of the imagination and visual flights of fancy that animated movies 1 and 3 especially (although Mike Darwin disagrees), copping out on standard imagery like a Star Wars-style force field over Hogwarts Castle, or luminescent white fog when Harry was dead and in his head; I was deeply disappointed to not see any sights that struck me as novel and new. (For example, the aforementioned dead scene could have been done in so many interesting ways, like why not show Harry & Dumbledore in a bustling King’s Cross shot in bright sharp detail, but with not a single person in sight and all the luggage and equipment animatedly moving purposefully on their own?) The ending in particular boggles me. I actually turned to the person next to me and asked them whether that really was the climax and Voldemort was dead, his death was so little dwelt upon or laden with significance (despite a musical score that beat you over the head about everything else). In the book, I remember it feeling like a climactic scene, with everyone watching and little speeches explaining why Voldemort was about to be defeated, and a suitable victory celebration; I read in the paper the next day a quote from the director or screenwriter who said one scene was cut because Voldemort would not talk but simply try to efficiently kill Harry. (This is presumably the explanation for the incredible anti-climax. Hopefully.) I was dumbfounded by the depths of dishonesty or delusion or disregard: Voldemort not only does that in Deathly Hallows multiple times, he does it every time he deals with Harry, exactly as the classic villains (he is numbered among) always do! How was it possible for this man to read the books many times, as he must have, and still say such a thing?↩
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 placebo24.) 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.
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Or in other words, since the standard deviation of my previous self-ratings is 0.75 (see the Weather and my productivity data), a mean rating increase of >0.39 on the self-rating. This is, unfortunately, implying an extreme shift in my self-assessments (for example, 3s are ~50% of the self-ratings and 4s ~25%; to cause an increase of 0.25 while leaving 2s alone in a sample of 23 days, one would have to push 3s down to ~25% and 4s up to ~47%). So in advance, we can see that the weak plausible effects for Noopept are not going to be detected here at our usual statistical levels with just the sample I have (a more plausible experiment might use 178 pairs over a year, detecting down to d>=0.18). But if the sign is right, it might make Noopept worthwhile to investigate further. And the hardest part of this was just making the pills, so it’s not a waste of effort.
Clarke and Sokoloff (1998) remarked that although [a] common view equates concentrated mental effort with mental work…there appears to be no increased energy utilization by the brain during such processes (p. 664), and …the areas that participate in the processes of such reasoning represent too small a fraction of the brain for changes in their functional and metabolic activities to be reflected in the energy metabolism of the brain… (p. 675).
At this point I began to get bored with it and the lack of apparent effects, so I began a pilot trial: I’d use the LED set for 10 minutes every few days before 2PM, record, and in a few months look for a correlation with my daily self-ratings of mood/productivity (for 2.5 years I’ve asked myself at the end of each day whether I did more, the usual, or less work done that day than average, so 2=below-average, 3=average, 4=above-average; it’s ad hoc, but in some factor analyses I’ve been playing with, it seems to load on a lot of other variables I’ve measured, so I think it’s meaningful).
Core body temperature, local pH and internal pressure are important indicators of patient well-being. While a thermometer can give an accurate reading during regular checkups, the monitoring of professionals in high-intensity situations requires a more accurate inner body temperature sensor. An ingestible chemical sensor can record acidity and pH levels along the gastrointestinal tract to screen for ulcers or tumors. Sensors also can be built into medications to track compliance.
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.
2 commenters point out that my possible lack of result is due to my mistaken assumption that if nicotine is absorbable through skin, mouth, and lungs it ought to be perfectly fine to absorb it through my stomach by drinking it (rather than vaporizing it and breathing it with an e-cigarette machine) - it’s apparently known that absorption differs in the stomach.
Finally, all of the questions raised here in relation to MPH and d-AMP can also be asked about newer drugs and even about nonpharmacological methods of cognitive enhancement. An example of a newer drug with cognitive-enhancing potential is modafinil. Originally marketed as a therapy for narcolepsy, it is widely used off label for other purposes (Vastag, 2004), and a limited literature on its cognitive effects suggests some promise as a cognitive enhancer for normal healthy people (see Minzenberg & Carter, 2008, for a review).
A LessWronger found that it worked well for him as far as motivation and getting things done went, as did another LessWronger who sells it online (terming it a reasonable productivity enhancer) as did one of his customers, a pickup artist oddly enough. The former was curious whether it would work for me too and sent me Speciosa Pro’s Starter Pack: Test Drive (a sampler of 14 packets of powder and a cute little wooden spoon). In SE Asia, kratom’s apparently chewed, but the powders are brewed as a tea.
But, if we find in 10 or 20 years that the drugs don't do damage, what are the benefits? These are stimulants that help with concentration. College students take such drugs to pass tests; graduates take them to gain professional licenses. They are akin to using a calculator to solve an equation. Do you really want a doctor who passed his boards as a result of taking speed — and continues to depend on that for his practice?
Tuesday: I went to bed at 1am, and first woke up at 6am, and I wrote down a dream; the lucid dreaming book I was reading advised that waking up in the morning and then going back for a short nap often causes lucid dreams, so I tried that - and wound up waking up at 10am with no dreams at all. Oops. I take a pill, but the whole day I don’t feel so hot, although my conversation and arguments seem as cogent as ever. I’m also having a terrible time focusing on any actual work. At 8 I take another; I’m behind on too many things, and it looks like I need an all-nighter to catch up. The dose is no good; at 11, I still feel like at 8, possibly worse, and I take another along with the choline+piracetam (which makes a total of 600mg for the day). Come 12:30, and I disconsolately note that I don’t seem any better, although I still seem to understand the IQ essays I am reading. I wonder if this is tolerance to modafinil, or perhaps sleep catching up to me? Possibly it’s just that I don’t remember what the quasi-light-headedness of modafinil felt like. I feel this sort of zombie-like state without change to 4am, so it must be doing something, when I give up and go to bed, getting up at 7:30 without too much trouble. Some N-backing at 9am gives me some low scores but also some pretty high scores (38/43/66/40/24/67/60/71/54 or ▂▂▆▂▁▆▅▇▄), which suggests I can perform normally if I concentrate. I take another pill and am fine the rest of the day, going to bed at 1am as usual.
Finally, two tasks measuring subjects’ ability to control their responses to monetary rewards were used by de Wit et al. (2002) to assess the effects of d-AMP. When subjects were offered the choice between waiting 10 s between button presses for high-probability rewards, which would ultimately result in more money, and pressing a button immediately for lower probability rewards, d-AMP did not affect performance. However, when subjects were offered choices between smaller rewards delivered immediately and larger rewards to be delivered at later times, the normal preference for immediate rewards was weakened by d-AMP. That is, subjects were more able to resist the impulse to choose the immediate reward in favor of the larger reward.
Took pill 12:11 PM. I am not certain. While I do get some things accomplished (a fair amount of work on the Silk Road article and its submission to places), I also have some difficulty reading through a fiction book (Sum) and I seem kind of twitchy and constantly shifting windows. I am weakly inclined to think this is Adderall (say, 60%). It’s not my normal feeling. Next morning - it was Adderall.
There are a number of treatments for the last. I already use melatonin. I sort of have light therapy from a full-spectrum fluorescent desk lamp. But I get very little sunlight; the surprising thing would be if I didn’t have a vitamin D deficiency. And vitamin D deficiencies have been linked with all sorts of interesting things like near-sightedness, with time outdoors inversely correlating with myopia and not reading or near-work time. (It has been claimed that caffeine interferes with vitamin D absorption and so people like me especially need to take vitamin D, on top of the deficits caused by our vampiric habits, but I don’t think this is true34.) Unfortunately, there’s not very good evidence that vitamin D supplementation helps with mood/SAD/depression: there’s ~6 small RCTs with some findings of benefits, with their respective meta-analysis turning in a positive but currently non-statistically-significant result. Better confirmed is reducing all-cause mortality in elderly people (see, in order of increasing comprehensiveness: Evidence Syntheses 2013, Chung et al 2009, Autier & Gandini 2007, Bolland et al 2014).
Some cognitive enhancers, such as donepezil and galantamine, are prescribed for elderly patients with impaired reasoning and memory deficits caused by various forms of dementia, including Alzheimer disease, Parkinson disease with dementia, dementia with Lewy bodies, and vascular dementia. Children and young adults with attention-deficit/hyperactivity disorder (ADHD) are often treated with the cognitive enhancers Ritalin (methylphenidate) or Adderall (mixed amphetamine salts). Persons diagnosed with narcolepsy find relief from sudden attacks of sleep through wake-promoting agents such as Provigil (modafinil). Generally speaking, cognitive enhancers improve working and episodic (event-specific) memory, attention, vigilance, and overall wakefulness but act through different brain systems and neurotransmitters to exert their enhancing effects.
Autism Brain brain fuel brain health Brain Injury broth Cholesterol choline DAI DHA Diabetes digestion Exercise Fat Functional Medicine gastric Gluten gut-brain Gut Brain Axis gut health Health intestinal permeability keto Ketogenic leaky Gut Learning Medicine Metabolism Music Therapy neurology Neuroplasticity neurorehabilitation Nutrition omega Paleo Physical Therapy Recovery Science second brain superfood synaptogenesis TBI Therapy tube feed uridine
A number of so-called ‘smart drugs’ or cognitive enhancers have captured attention recently, from stimulants such as modafinil, to amphetamines (often prescribed under the name Adderall) and methylphenidate (also known by its brand name Ritalin). According to widespread news reports, students have begun using these drugs to enhance their performance in school and college, and are continuing to do so in their professional lives.
“Such an informative and inspiring read! Insight into how optimal nutrients improved Cavin’s own brain recovery make this knowledge-filled read compelling and relatable. The recommendations are easy to understand as well as scientifically-founded – it’s not another fad diet manual. The additional tools and resources provided throughout make it possible for anyone to integrate these enhancements into their nutritional repertoire. Looking forward to more from Cavin and Feed a Brain!!!!!!”
Creatine is a substance that’s produced in the human body. It is initially produced in the kidneys, and the process is completed in the liver. It is then stored in the brain tissues and muscles, to support the energy demands of a human body. Athletes and bodybuilders use creatine supplements to relieve fatigue and increase the recovery of the muscle tissues affected by vigorous physical activities. Apart from helping the tissues to recover faster, creatine also helps in enhancing the mental functions in sleep-deprived adults, and it also improves the performance of difficult cognitive tasks.
“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.”
A big part is that we are finally starting to apply complex systems science to psycho-neuro-pharmacology and a nootropic approach. The neural system is awesomely complex and old-fashioned reductionist science has a really hard time with complexity. Big companies spends hundreds of millions of dollars trying to separate the effects of just a single molecule from placebo – and nootropics invariably show up as “stacks” of many different ingredients (ours, Qualia , currently has 42 separate synergistic nootropics ingredients from alpha GPC to bacopa monnieri and L-theanine). That kind of complex, multi pathway input requires a different methodology to understand well that goes beyond simply what’s put in capsules.