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).
Gibson and Green (2002), talking about a possible link between glucose and cognition, wrote that research in the area …is based on the assumption that, since glucose is the major source of fuel for the brain, alterations in plasma levels of glucose will result in alterations in brain levels of glucose, and thus neuronal function. However, the strength of this notion lies in its common-sense plausibility, not in scientific evidence… (p. 185).
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.
I split the 2 pills into 4 doses for each hour from midnight to 4 AM. 3D driver issues in Debian unstable prevented me from using Brain Workshop, so I don’t have any DNB scores to compare with the armodafinil DNB scores. I had the subjective impression that I was worse off with the Modalert, although I still managed to get a fair bit done so the deficits couldn’t’ve been too bad. The apathy during the morning felt worse than armodafinil, but that could have been caused by or exacerbated by an unexpected and very stressful 2 hour drive through rush hour and multiple accidents; the quick hour-long nap at 10 AM was half-waking half-light-sleep according to the Zeo, but seemed to help a bit. As before, I began to feel better in the afternoon and by evening felt normal, doing my usual reading. That night, the Zeo recorded my sleep as lasting ~9:40, when it was usually more like 8:40-9:00 (although I am not sure that this was due to the modafinil inasmuch as once a week or so I tend to sleep in that long, as I did a few days later without any influence from the modafinil); assuming the worse, the nap and extra sleep cost me 2 hours for a net profit of ~7 hours. While it’s not clear how modafinil affects recovery sleep (see the footnote in the essay), it’s still interesting to ponder the benefits of merely being able to delay sleep18.
For instance, they point to the U.S. Army's use of stimulants for soldiers to stave off sleep and to stay sharp. But the Army cares little about the long-term health effects of soldiers, who come home scarred physically or mentally, if they come home at all. It's a risk-benefit decision for the Army, and in a life-or-death situation, stimulants help.
A related task is the B–X version of the CPT, in which subjects must respond when an X appears only if it was preceded by a B. As in the 1-back task, the subject must retain the previous trial’s letter in working memory because it determines the subject’s response to the current letter. In this case, when the current letter is an X, then the subject should respond only if the previous letter was a B. Two studies examined stimulant effects in this task. Rapoport et al. (1980) found that d-AMP reduced errors of omission in the longer of two test sessions, and Klorman et al. (1984) found that MPH reduced errors of omission and response time.
In the largest nationwide study, McCabe et al. (2005) sampled 10,904 students at 119 public and private colleges and universities across the United States, providing the best estimate of prevalence among American college students in 2001, when the data were collected. This survey found 6.9% lifetime, 4.1% past-year, and 2.1% past-month nonmedical use of a prescription stimulant. It also found that prevalence depended strongly on student and school characteristics, consistent with the variability noted among the results of single-school studies. The strongest predictors of past-year nonmedical stimulant use by college students were admissions criteria (competitive and most competitive more likely than less competitive), fraternity/sorority membership (members more likely than nonmembers), and gender (males more likely than females).
Actually, researchers are studying substances that may improve mental abilities. These substances are called "cognitive enhancers" or "smart drugs" or "nootropics." ("Nootropic" comes from Greek - "noos" = mind and "tropos" = changed, toward, turn). The supposed effects of cognitive enhancement can be several things. For example, it could mean improvement of memory, learning, attention, concentration, problem solving, reasoning, social skills, decision making and planning.
"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]