Talk:Nootropic/Archive 3

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Archive 1 Archive 2 Archive 3

Lede

This statement is factual and general for the lede: "While many substances are purported to improve cognition, research is at a preliminary stage as of 2018, and the effects of these agents are not fully determined." This statement is vague, factually incorrect, and provides little general knowledge for the common user: "While many substances are purported to improve cognition, the number of substances with cognition-enhancing properties that have been established by meta-analysis of clinical research is very small." Properties are not "established by meta-analysis" of primary research, such as this PMID 24423151. That's a single-dose analysis, too vague and preliminary for an encyclopedia. There is no MEDRS-quality review proving the specific type of nicotinic receptor involved in attention, PMID 28607947 - a non-MEDRS opinion article. Reverting and warning about WP:3RR. --Zefr (talk) 22:19, 10 July 2018 (UTC)

Re: the lead - my only problem with the statement is that it's a blanket statement that applies even to drugs with well-established effects like caffeine, nicotine, and amphetamine (hence, factually incorrect) . I agree that the average reader wouldn't understand my version given that most won't know what a meta-analysis is; however, it was not factually incorrect; most substances do not have established cognitive enhancing properties on the basis of meta-analysis of RCTs. Nonetheless, I've refined your version to address the problem with it. Seppi333 (Insert 2¢) 22:45, 10 July 2018 (UTC)
Re: the methylphenidate study - that removal actually seems fine to me based upon your rationale. Seppi333 (Insert 2¢) 22:45, 10 July 2018 (UTC)
Re: the nicotine receptor statements - that has absolutely nothing to do with claiming that nicotine affects attention. If those studies were cited in a manner to suggest that nicotine improves attention without having first established that, it would constitute WP:OR/WP:SYNTH. The reason for inclusion was to explain the neuropsychopharmacology of nicotine's effect on attention by stating (1) a biomolecular target that mediates effects on attention and (2) nicotine's binding affinity at that target, after having first established (3) nicotine affects attention (citing WP:MEDRS compliant sources). Note that neither (1) or (2) require a WP:MEDRS because they're not medical claims; they're required to satisfy WP:SCIRS. Seppi333 (Insert 2¢) 22:48, 10 July 2018 (UTC)
@Zefr: I've revised the statement regarding nicotinic receptors since it wasn't accurate as written in the reverted version. In any event, I would appreciate it if you didn't allege that I'm POV pushing; you and I are both required to comply with WP:AGF.
Also, we'd waste less time reverting one another if you explained specifically what's wrong with the original version on the talk page. I realize that it takes longer to do this in the short run, but it'll end up saving you (and me) time since you'll end up doing it again and again as you and I revert one another before we end up discussing this on the talk page. As is clearly evident from [1], I'm perfectly fine with others making large revisions (e.g., completely rephrasing a statement or deleting text) to articles that I've written – or essentially deleted and rewrote – provided that there's a reason for those changes. Policy-compliant article expansions are always fine with me. Seppi333 (Insert 2¢) 23:10, 10 July 2018 (UTC)
I didn't notice this earlier, but I'm not sure why you changed every sentence to past tense. Seppi333 (Insert 2¢) 04:48, 11 July 2018 (UTC)
Use of the present tense gives to the non-specialist reader the impression these are established, universally-accepted properties; this is a form of POV-pushing. They are not established properties. We present systematic reviews and meta-analyses of preliminary research as evidence of ongoing assessment of the possible properties of these drugs on healthy people. The most neutral position is to use the past tense of findings from the research, as summarized in the reviews. These are not confirmed pharmacological properties. --Zefr (talk) 14:56, 12 July 2018 (UTC)
They are established. Get broader consensus. Seppi333 (Insert 2¢) 17:30, 12 July 2018 (UTC)
You can’t simply violate 3RR to revert me on the grounds that I’m citing fringe theories. For one thing, if this was fringe, why are you the first person to notice? Why do so many sources corroborate it? Why are you not providing a source that backs up the non-fridge POV? And lastly, why are you skewing the text so that it is no longer verifiable? Seppi333 (Insert 2¢) 18:44, 12 July 2018 (UTC)

Coverage of CNS stimulants

Notified WT:MED, WT:PHARM, and WT:NEURO.

I'm requesting feedback on two revisions of the section on CNS stimulants on the basis of the neutrality and verifiability of the statements in each revision.

Please take note of (1) past vs present verb tense to reflect editorial opinion of the sources (i.e., the intended purpose of this revision, as stated in the #Lede discussion above), (2) the accuracy of the statements relative to the cited + quoted sources, and (3) content on "Amphetamine", "Methylphenidate", and "Nicotine" from version 1 which was removed in version 2.

Which version of this content is more appropriate for the article on the basis of content policy (specifically, WP:V, WP:NPOV, and WP:FRINGE)? Seppi333 (Insert 2¢) 07:52, 13 July 2018 (UTC)

Discussion

  • I haven't gone through every detail, but what immediately stood out to me is that Version 1 says "unambiguously enhance cognition in the healthy individuals", which is an awfully strong statement to make about a very fuzzy area of neuropharmacology, and tends to have the effect of telling readers what to do. On that basis alone, I think that Version 2 better satisfies WP:NPOV. --Tryptofish (talk) 15:40, 13 July 2018 (UTC)
    • I've struck that adjective from version 1 since I agree with you. In any event, if others think that distinct parts of both versions have greater merit (or if alternative wording for this section is proposed), I think creating a "version 3" based upon consensus would actually be a better approach than picking one or the other. Seppi333 (Insert 2¢) 16:39, 13 July 2018 (UTC)
      • Removing that word is a step in the right direction, but I would just change it to "when taken at low doses, enhanced cognition in healthy people" as per Version 2, which is much better wording all around. --Tryptofish (talk) 17:05, 13 July 2018 (UTC)
        • Substituting that phrase in version 1 would be fine with me if it's written in present tense; the differences in wording between the two are really a non-issue to me. What I find concerning with version 2 is the use of past tense when stating a fact, the deletion of 4 sentences (1 from the entry on amphetamine, 1 from methylphenidate, and 2 from the entry on nicotine) for no apparent reason, and how it conveys a subjective opinion about the underlying evidence or distorts what the references assert. By this last issue, I'm referring to the changes like 41 double-blind, placebo-controlled studies → 41 preliminary human studies (see the cited meta-analysis) and Methylphenidate – a benzylpiperidine that improves a range of cognitive functions to Methylphenidate – a benzylpiperidine that had cognitive effects (see quotes from the cited refs below). Seppi333 (Insert 2¢) 18:00, 13 July 2018 (UTC)
          • No, I think the verb needs to be in past tense. That is because the sentence is about what the various studies have found (not what they are continuing to find). The other issues that you mention are things I don't have time to look into now, but my first concern is what I have already been saying. --Tryptofish (talk) 18:48, 13 July 2018 (UTC)
            @Tryptofish: This is version 2: Systematic reviews and meta-analyses of clinical research in humans established that certain central nervous system stimulants, when taken at low doses, enhanced cognition in healthy people. Read this sentence over in your head. If it helps, cut out the verbiage between the two underlined verbs:
            Systematic reviews and meta-analyses of clinical research in humans established that... stimulants... enhanced cognition in healthy people.
            Now, compare that to the same sentence using the present tense for the 2nd verb:
            Systematic reviews and meta-analyses of clinical research in humans established that... stimulants... enhance cognition in healthy people.
            The first verb conveys that studies have found something. The 2nd conveys the studies' findings. The sentence seems extremely awkwardly written to me when that second verb uses the past tense; if I were to adopt this practice and use the past tense to describe any finding from clinical research, I'd end up writing literally every sentence on safety/efficacy in a drug article in the past tense (e.g., X was effective for treating Y; side effects included A, B, and C; "Relatively high doses of stimulants caused cognitive deficits"). Anyway, it occurred to me that dating this statement would better articulate the fact that these findings come from previously published studies and not all studies on an ongoing basis: A systematic review and a meta analysis that were published in 2015 and assessed clinical research in humans found that certain certain central nervous system stimulants, when taken at low doses, enhance cognition in healthy people. Does that wording address the issue you were getting at? Seppi333 (Insert 2¢) 02:18, 14 July 2018 (UTC)
            Yes, I see that I missed the construction with two different verbs. But continuing with that, and looking to make the writing more direct and less complicated, as well as to not over-sell provisional research findings, I think it would be even better to make the sentence: Systematic reviews and meta-analyses of clinical human research found enhanced cognition in healthy people associated with low doses of certain central nervous system stimulants;. --Tryptofish (talk) 17:16, 14 July 2018 (UTC)
            Your proposed wording is fine with me. Seems like an improvement since it’s succinct/concise. See #Version 3 from discussion. Seppi333 (Insert 2¢) 22:24, 14 July 2018 (UTC)

Version 1

See also: Yerkes–Dodson law
Hebbian version of the Yerkes–Dodson law

Systematic reviews and meta-analyses of clinical research in humans established that certain central nervous system stimulants, when used at low (therapeutic) concentrations, unambiguously enhance cognition in the healthy individuals;[1][2][3][4] in particular, the classes of stimulants that demonstrate cognition-enhancing effects in humans act as direct agonists or indirect agonists of dopamine receptor D1, adrenoceptor A2, or both receptors in the prefrontal cortex.[1][2][4][5] Relatively high doses of stimulants cause cognitive deficits.[4][5]

Section reflist

References

  1. ^ a b c d Spencer RC, Devilbiss DM, Berridge CW (June 2015). "The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex". Biol. Psychiatry. 77 (11): 940–950. doi:10.1016/j.biopsych.2014.09.013. PMC 4377121. PMID 25499957. The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. ... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation. ... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.
  2. ^ a b c d e Ilieva IP, Hook CJ, Farah MJ (January 2015). "Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis". J. Cogn. Neurosci. 27: 1–21. doi:10.1162/jocn_a_00776. PMID 25591060. The present meta-analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short-term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty-eight studies (total of 1,409 participants) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short-term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long-term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be valuable, although it is also possible that healthy users resort to stimulants to enhance their energy and motivation more than their cognition. ... Earlier research has failed to distinguish whether stimulants' effects are small or whether they are nonexistent (Ilieva et al., 2013; Smith & Farah, 2011). The present findings supported generally small effects of amphetamine and methylphenidate on executive function and memory. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ...

    The results of this meta-analysis cannot address the important issues of individual differences in stimulant effects or the role of motivational enhancement in helping perform academic or occupational tasks. However, they do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.
  3. ^ a b c d e Bagot KS, Kaminer Y (April 2014). "Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review". Addiction. 109 (4): 547–557. doi:10.1111/add.12460. PMC 4471173. PMID 24749160. Modafinil appears to improve reaction time (P ≤ 0.04), logical reasoning (P ≤ 0.05) and problem-solving. Methylphenidate appears to improve performance in novel tasks and attention-based tasks (P ≤ 0.05), and reduces planning latency in more complex tasks (P ≤ 0.05). Amphetamine has been shown to improve consolidation of information (0.02 ≥ P ≤ 0.05), leading to improved recall. Across all three types of prescription stimulants, research shows improved attention with lack of consensus on whether these improvements are limited to simple versus complex tasks in varying youth populations.
  4. ^ a b c d e Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014). "Psychostimulants and cognition: a continuum of behavioral and cognitive activation". Pharmacol. Rev. 66 (1): 193–221. doi:10.1124/pr.112.007054. PMC 3880463. PMID 24344115.
  5. ^ a b c d e Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 14: Higher Cognitive Function and Behavioral Control". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 9780071827706. Mild dopaminergic stimulation of the prefrontal cortex enhances working memory. ...
    Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in individuals with ADHD and, at higher doses, in normal subjects. Positron emission tomography (PET) demonstrates that methylphenidate decreases regional cerebral blood flow in the doroslateral prefrontal cortex and posterior parietal cortex while improving performance of a spatial working memory task. This suggests that cortical networks that normally process spatial working memory become more efficient in response to the drug. ... [It] is now believed that dopamine and norepinephrine, but not serotonin, produce the beneficial effects of stimulants on working memory. At abused (relatively high) doses, stimulants can interfere with working memory and cognitive control ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors.
    Stimulant prescriptions have engendered controversy because these drugs are potentially abusable (when drugs are used at higher than therapeutic doses), because they are used even in young children (as early as age 3), and because they may be used with benefit by individuals with only mild or even absent symptoms, in which case they are being used for cognitive enhancement rather than treatment. ... Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention. Drugs used for this purpose include, as stated above, methylphenidate, amphetamines, atomoxetine, and desipramine     Cite error: The named reference "NHMH_3e-Higher Cognitive Function" was defined multiple times with different content (see the help page).
  6. ^ Urban, KR; Gao, WJ (2014). "Performance enhancement at the cost of potential brain plasticity: neural ramifications of nootropic drugs in the healthy developing brain". Frontiers in Systems Neuroscience. 8: 38. doi:10.3389/fnsys.2014.00038. PMC 4026746. PMID 24860437.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ Mereu M, Bonci A, Newman AH, Tanda G (October 2013). "The neurobiology of modafinil as an enhancer of cognitive performance and a potential treatment for substance use disorders". Psychopharmacology. 229 (3): 415–34. doi:10.1007/s00213-013-3232-4. PMC 3800148. PMID 23934211.
  8. ^ Meulen, Ruud ter; Hall, Wayne; Mohammed, Ahmed (2017). Rethinking Cognitive Enhancement. Oxford University Press. p. 116. ISBN 9780198727392.
  9. ^ Rogers, P. (2007). "Caffeine, mood and mental performance in everyday life". Psychology Today. 32 (1): 84–89. doi:10.1111/j.1467-3010.2007.00607.x.
  10. ^ Kiefer, I. (2007). "Brain Food". Scientific American Mind. 18 (5): 58–63. doi:10.1038/scientificamericanmind1007-58. Retrieved November 1, 2009.
  11. ^ Heishman SJ, Kleykamp BA, Singleton EG (June 2010). "Meta-analysis of the acute effects of nicotine and smoking on human performance". Psychopharmacology. 210 (4): 453–69. doi:10.1007/s00213-010-1848-1. PMC 3151730. PMID 20414766.
  12. ^ Sarter M (August 2015). "Behavioral-cognitive targets for cholinergic enhancement". Current Opinion in Behavioral Sciences. 4: 22–26. doi:10.1016/j.cobeha.2015.01.004.
  13. ^ "Nicotine: Biological activity". IUPHAR/BPS Guide to Pharmacology. International Union of Basic and Clinical Pharmacology. Retrieved February 7, 2016. Kis as follows; α2β4=9900nM [5], α3β2=14nM [1], α3β4=187nM [1], α4β2=1nM [4,6]. Due to the heterogeneity of nACh channels we have not tagged a primary drug target for nicotine, although the α4β2 is reported to be the predominant high affinity subtype in the brain which mediates nicotine addiction [2–3].

Version 2

See also: Yerkes–Dodson law
Hebbian version of the Yerkes–Dodson law

Systematic reviews and meta-analyses of clinical research in humans established that certain central nervous system stimulants, when taken at low doses, enhanced cognition in healthy people;[1][2][3] in particular, the classes of stimulants that demonstrated cognition-enhancing effects in humans act as direct agonists or indirect agonists of dopamine receptor D1, adrenoceptor A2, or both types of receptor in the prefrontal cortex.[1][2][4][5] Relatively high doses of stimulants caused cognitive deficits.[4][5]

A 2014 systematic review noted that low doses of amphetamine also improved memory consolidation, in turn leading to improved recall of information in non-ADHD youth.[3] It also improved task saliency (motivation to perform a task) and performance on tedious tasks that required a high degree of effort.[2][4][5]

  • Methylphenidate – a benzylpiperidine that had cognitive effects (e.g., working memory, episodic memory, and inhibitory control, aspects of attention, and planning latency) in healthy people.[1][2][3] It also may improve task saliency and performance on tedious tasks.[5] At above optimal doses, methylphenidate had off–target effects that decreased learning.[6]
  • Eugeroics (armodafinil and modafinil) – are classified as "wakefulness promoting" agents; modafinil increased alertness, particularly in sleep deprived individuals, and was noted to facilitate reasoning and problem solving in non-ADHD youth.[3][7] Modafinil did not produce improvements in mood, memory, and motivation in sleep deprived or non-sleep deprived individuals.[8]
  • Xanthines (most notably, caffeine) – were shown in a 2007 study to increase alertness, performance, and, in some studies, memory.[4][9] Children and adults who consumed low doses of caffeine showed increased alertness, yet a higher dose was needed to improve performance.[10]
  • Nicotine – A meta-analysis of 41  preliminary human studies concluded that nicotine or smoking caused small improvements in fine motor abilities, alerting and orienting attention, and episodic and working memory.[11]
Section reflist

References

  1. ^ a b c Spencer RC, Devilbiss DM, Berridge CW (June 2015). "The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex". Biol. Psychiatry. 77 (11): 940–950. doi:10.1016/j.biopsych.2014.09.013. PMC 4377121. PMID 25499957. The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. ... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation. ... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.
  2. ^ a b c d Ilieva IP, Hook CJ, Farah MJ (January 2015). "Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis". J. Cogn. Neurosci. 27: 1–21. doi:10.1162/jocn_a_00776. PMID 25591060. The present meta-analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short-term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty-eight studies (total of 1,409 participants) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short-term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long-term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be valuable, although it is also possible that healthy users resort to stimulants to enhance their energy and motivation more than their cognition. ... Earlier research has failed to distinguish whether stimulants' effects are small or whether they are nonexistent (Ilieva et al., 2013; Smith & Farah, 2011). The present findings supported generally small effects of amphetamine and methylphenidate on executive function and memory. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ...

    The results of this meta-analysis cannot address the important issues of individual differences in stimulant effects or the role of motivational enhancement in helping perform academic or occupational tasks. However, they do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.
  3. ^ a b c d Bagot KS, Kaminer Y (April 2014). "Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review". Addiction. 109 (4): 547–557. doi:10.1111/add.12460. PMC 4471173. PMID 24749160. Modafinil appears to improve reaction time (P ≤ 0.04), logical reasoning (P ≤ 0.05) and problem-solving. Methylphenidate appears to improve performance in novel tasks and attention-based tasks (P ≤ 0.05), and reduces planning latency in more complex tasks (P ≤ 0.05). Amphetamine has been shown to improve consolidation of information (0.02 ≥ P ≤ 0.05), leading to improved recall. Across all three types of prescription stimulants, research shows improved attention with lack of consensus on whether these improvements are limited to simple versus complex tasks in varying youth populations.
  4. ^ a b c d Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014). "Psychostimulants and cognition: a continuum of behavioral and cognitive activation". Pharmacol. Rev. 66 (1): 193–221. doi:10.1124/pr.112.007054. PMC 3880463. PMID 24344115.
  5. ^ a b c d Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 14: Higher Cognitive Function and Behavioral Control". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 9780071827706. Mild dopaminergic stimulation of the prefrontal cortex enhances working memory. ...
    Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in individuals with ADHD and, at higher doses, in normal subjects. Positron emission tomography (PET) demonstrates that methylphenidate decreases regional cerebral blood flow in the doroslateral prefrontal cortex and posterior parietal cortex while improving performance of a spatial working memory task. This suggests that cortical networks that normally process spatial working memory become more efficient in response to the drug. ... [It] is now believed that dopamine and norepinephrine, but not serotonin, produce the beneficial effects of stimulants on working memory. At abused (relatively high) doses, stimulants can interfere with working memory and cognitive control ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors.
    Stimulant prescriptions have engendered controversy because these drugs are potentially abusable (when drugs are used at higher than therapeutic doses), because they are used even in young children (as early as age 3), and because they may be used with benefit by individuals with only mild or even absent symptoms, in which case they are being used for cognitive enhancement rather than treatment. ... Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention. Drugs used for this purpose include, as stated above, methylphenidate, amphetamines, atomoxetine, and desipramine
  6. ^ Urban, KR; Gao, WJ (2014). "Performance enhancement at the cost of potential brain plasticity: neural ramifications of nootropic drugs in the healthy developing brain". Frontiers in Systems Neuroscience. 8: 38. doi:10.3389/fnsys.2014.00038. PMC 4026746. PMID 24860437.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ Mereu M, Bonci A, Newman AH, Tanda G (October 2013). "The neurobiology of modafinil as an enhancer of cognitive performance and a potential treatment for substance use disorders". Psychopharmacology. 229 (3): 415–34. doi:10.1007/s00213-013-3232-4. PMC 3800148. PMID 23934211.
  8. ^ Meulen, Ruud ter; Hall, Wayne; Mohammed, Ahmed (2017). Rethinking Cognitive Enhancement. Oxford University Press. p. 116. ISBN 9780198727392.
  9. ^ Rogers, P. (2007). "Caffeine, mood and mental performance in everyday life". Psychology Today. 32 (1): 84–89. doi:10.1111/j.1467-3010.2007.00607.x.
  10. ^ Kiefer, I. (2007). "Brain Food". Scientific American Mind. 18 (5): 58–63. doi:10.1038/scientificamericanmind1007-58. Retrieved November 1, 2009.
  11. ^ Heishman SJ, Kleykamp BA, Singleton EG (June 2010). "Meta-analysis of the acute effects of nicotine and smoking on human performance". Psychopharmacology. 210 (4): 453–69. doi:10.1007/s00213-010-1848-1. PMC 3151730. PMID 20414766.

Version 3 from discussion

Systematic reviews and meta-analyses of clinical human research found enhanced cognition in healthy people associated with low doses of certain central nervous system stimulants;[1][2][3][4] in particular, ...

Section reflist

References

  1. ^ Cite error: The named reference Unambiguous PFC D1 A2 was invoked but never defined (see the help page).
  2. ^ Ilieva IP, Hook CJ, Farah MJ (January 2015). "Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis". J. Cogn. Neurosci. 27: 1–21. doi:10.1162/jocn_a_00776. PMID 25591060. The present meta-analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short-term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty-eight studies (total of 1,409 participants) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short-term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long-term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be valuable, although it is also possible that healthy users resort to stimulants to enhance their energy and motivation more than their cognition. ... Earlier research has failed to distinguish whether stimulants' effects are small or whether they are nonexistent (Ilieva et al., 2013; Smith & Farah, 2011). The present findings supported generally small effects of amphetamine and methylphenidate on executive function and memory. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ...

    The results of this meta-analysis cannot address the important issues of individual differences in stimulant effects or the role of motivational enhancement in helping perform academic or occupational tasks. However, they do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.
  3. ^ Bagot KS, Kaminer Y (April 2014). "Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review". Addiction. 109 (4): 547–557. doi:10.1111/add.12460. PMC 4471173. PMID 24749160. Modafinil appears to improve reaction time (P ≤ 0.04), logical reasoning (P ≤ 0.05) and problem-solving. Methylphenidate appears to improve performance in novel tasks and attention-based tasks (P ≤ 0.05), and reduces planning latency in more complex tasks (P ≤ 0.05). Amphetamine has been shown to improve consolidation of information (0.02 ≥ P ≤ 0.05), leading to improved recall. Across all three types of prescription stimulants, research shows improved attention with lack of consensus on whether these improvements are limited to simple versus complex tasks in varying youth populations.
  4. ^ Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014). "Psychostimulants and cognition: a continuum of behavioral and cognitive activation". Pharmacol. Rev. 66 (1): 193–221. doi:10.1124/pr.112.007054. PMC 3880463. PMID 24344115.

Continued discussion

Thanks, Seppi, for the Version 3 revision. Assuming that we have consensus to use that language along with language from either Version 1 and/or Version 2, I'd like to understand better what the remaining differences are. I can see some differences in what drug groups are listed, but I do not understand what the disagreements are about such differences. --Tryptofish (talk) 17:30, 15 July 2018 (UTC)

In a nutshell, Zefr deleted 4 sentences without explanation, changed every verb that was written in the present tense to past tense, and made odd changes to the wording like “methylphenidate ... had cognitive effects (e.g., working memory, ... )”. He didn’t explain anything except for the change in tense, for which his explanation was Use of the present tense gives to the non-specialist reader the impression these are established, universally-accepted properties; this is a form of POV-pushing. They are not established properties. We present systematic reviews and meta-analyses of preliminary research as evidence of ongoing assessment of the possible properties of these drugs on healthy people. The most neutral position is to use the past tense of findings from the research, as summarized in the reviews. These are not confirmed pharmacological properties.. He’s doing exactly what WP:MEDASSESS says not to do by assessing the evidence as opposed to the source. It’s ironic because he’s POV-pushing while saying not doing it is POV-pushing. I don’t agree with the changes he made. Seppi333 (Insert 2¢) 18:47, 15 July 2018 (UTC)
@Zefr: what do you think? --Tryptofish (talk) 21:03, 15 July 2018 (UTC)
Wait for further editor input. Grammatical revision to "Systematic reviews and meta-analyses of clinical human research using low doses of certain central nervous system stimulants found enhanced cognition in healthy people. In particular..." Keep the past tense, assure the excessive quoting is eliminated, and retain the rest of version 2. --Zefr (talk) 21:41, 15 July 2018 (UTC)
I don't see that the class "xanthines" is supported by the refs provided; caffeine is. Not sure what the 2007 study mentioned there is. The Scientific American and Psych today refs are not good. I'm OK with the lead sentence as stated. Jytdog (talk) 07:36, 16 July 2018 (UTC)
I've cut the xanthines part and replaced it with just "Caffeine". Feel free to edit that part. I haven't looked at those refs. If you think the whole thing is poorly referenced, I can look for newer refs; I'm sure there's suitable meta-analyses out there. Seppi333 (Insert 2¢) 18:27, 29 July 2018 (UTC)

@Zefr: Why did you cut "Amphetamine – systematic reviews and meta-analyses report that amphetamine benefits a range of cognitive functions (e.g., inhibitory control, episodic memory, working memory, and aspects of attention) in the general population, and these effects are especially notable in individuals with ADHD.[1][2][3][5]"? Seppi333 (Insert 2¢) 18:28, 29 July 2018 (UTC)

That's really the main omission between your version and the original version that concerns me. Seppi333 (Insert 2¢) 18:29, 29 July 2018 (UTC)
Think about what your sentence says when contracted: "Amphetamine benefits the general population and in individuals with ADHD." The research on amphetamines in healthy people is still preliminary (the reviews offered summarize preliminary research), provides no high-quality evidence of "benefit", and remains controversial clinically for ADHD, such as this Cochrane review and the withdrawal of this Cochrane review. --Zefr (talk) 16:36, 30 July 2018 (UTC)
@Zefr: Re: The research on amphetamines in healthy people is still preliminary (the reviews offered summarize preliminary research), provides no high-quality evidence of "benefit", and remains I don't see where in those reviews that they assert their own evidence is not high quality; have I misread them, or is this your own interpretation? The only thing I came across when looking through them again was this statement:

Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities.
–PMID 25591060

Re: and remains controversial clinically for ADHD, such as this Cochrane review and the withdrawal of this Cochrane review. I don't see what the controversy about the addiction liability for stimulants and their use in ADHD has to do with this article. Can you explain why you mentioned this? Seppi333 (Insert 2¢) 06:16, 2 August 2018 (UTC)

Looking over the sources for caffeine, I agree those were bad. We already had a meta-analysis in the article, but its coverage of caffeine in the article seems to have been removed at one point. Anyway, I re-added that, deleted the low-quality refs, and re-added the statement discussed above. Seppi333 (Insert 2¢) 05:11, 4 August 2018 (UTC)

Just a note that I'm going to take this page off my watchlist because it looks like edits are moving along for the time being. Please do not hesitate to ping me if anyone would like me to check back, particularly if the discussion comes to a specific decision point. --Tryptofish (talk) 17:51, 4 August 2018 (UTC)

Modafinil as cognitive enhancer

Hi guys, I would like to propose that the systematic review of the effects of Modafinil rather be used. Refernce is: Battleday RM, Brem AK. Modafinil for cognitive neuroenhancement in healthy non-sleep-deprived subjects: A systematic review. European Neuropsychopharmacology. 25(11): 1865-1881 (2015). Anyone have a reason not to? Tirab (talk) 21:22, 5 August 2018 (UTC)

I don’t see why not. Seppi333 (Insert 2¢) 03:55, 6 August 2018 (UTC)
It's a review of weak, preliminary, small-subject size research and tenuous conclusions, barely worth mentioning. The content added was overstating the review's conclusions and pro-modafinil POV-pushing. --Zefr (talk) 15:19, 6 August 2018 (UTC)
You stated it's based upon "weak, preliminary" research, but this review doesn't describe the studies using either of these terms. It does indicate some studies were small, but I don't see where you're seeing the rest of your assertion in this review. Please quote it. Seppi333 (Insert 2¢) 18:07, 6 August 2018 (UTC)
I also didn't see any justification in your edit summary for deleting the review you removed. Seppi333 (Insert 2¢) 18:08, 6 August 2018 (UTC)
Single dose studies using 10-64 subjects each are preliminary research; a review of such preliminary research is still a preliminary source. Wikipedia editors have to read the actual sources, rather than relying only on what authors say; WP:MEDASSESS. Using terms like "appeared to have" or "variably benefit" is leading the reader toward your POV and unencyclopedic; WP:NPOV. The review of primary research here was removed because it is not a conclusive report from high-quality clinical studies, gives the appearance of support when the paper is based on preliminary work, and is not needed for the content of the sentence which I am restoring. --Zefr (talk) 20:02, 6 August 2018 (UTC)
@Zefr: Frankly, I didn't even read the source. I just wanted you to admit to reframing the conclusions of the source to reflect your own beliefs and adding your WP:OR with a statement like "Wikipedia editors have to read the actual sources, rather than relying only on what authors say." WP:MEDASSESS states "'Assessing evidence quality' means editors should determine quality of the type of study. Respect the levels of evidence: Do not reject a high-quality type of study (e.g., a meta-analysis) in favor of a source from lower levels of evidence (e.g., any primary source) because of personal objections to the inclusion criteria, references, funding sources, or conclusions in the higher-level source. ... Editors should not perform detailed academic peer review."
Read the bold statements. Your argument is utter bullshit because you're literally rejecting a high-quality source that you disagree with. You just admitted that in no uncertain terms.
Also, since you apparently don't understand this fairly basic statistical concept: meta-analysis pools samples from independent studies. If it assesses 1000 "preliminary studies" with 30 subjects, meta-analysis of those studies yields a sample size of 30000. You don't need to conduct a single study with 30000 people to obtain a high level of statistical power. Ironically though, what you're worried about is a type I error, not a type II, so I don't see why you even care about large sample sizes. Seppi333 (Insert 2¢) 22:10, 6 August 2018 (UTC)

Lion's Mane Mushrooms

I have seen a lot of hype around Lion's Mane mushrooms as a nootropic and as such have been supplementing them myself. I have seen an positive impact, but personal anecdote aside, I am no expert in this field. But I do wonder if they should be considered for inclusion to this article by someone who is more familiar with nootropics? — Preceding unsigned comment added by Jasonv12 (talk • contribs) 16:20, 30 September 2019 (UTC)

This article is not about Nootropics

Given that the subject of this Wikipedia entry is supposed to be nootropics, I'm wondering why they're barely listed.

The Drugs section goes into detail about various stimulants, none of which are nootropics. The section "racetams" mentions piracetam, aniracetam and oxyracetam, and that is all. There are many nootropic substances besides those and this article lists none of them. Then it goes on to list dietary supplements such as ginkgo biloboa and B-12, which have absolutely nothing to do with the nootropic class of substances.

What does a description of these drugs accomplish? They are not nootropics. The entire article barely mentions any nootropics at all, despite supposedly being an article on them. This is not an article about stimulants or dietary supplements in general.

In my opinion this article is mostly not about nootropics at all, and should be mostly rewritten and irrelevant subject material removed.

Levontaun (talk) 10:56, 5 September 2018 (UTC)

Any source for a definitive list/definition of nootropics? Alexbrn (talk) 11:01, 5 September 2018 (UTC)
This article should probably be renamed Cognition-enhancing substance or Cognition-enhancing drug a la the Performance-enhancing substance/Performance-enhancing drug page given that the word "nootropic" is a WP:neologism that some people define differently than simply a substance that enhances a cognitive function. What do others think? Seppi333 (Insert 2¢) 03:34, 6 September 2018 (UTC)
@Jytdog: Curious to know what your thoughts on this are. Seppi333 (Insert 2¢) 03:36, 6 September 2018 (UTC)
The MESH term is "Nootropic Agents"... Jytdog (talk) 00:08, 7 September 2018 (UTC)

There is disagreement about what counts as a nootropic. Some people count drugs, others do not. There is also disagreement about what counts as a drug and what counts as a supplement. This article seems to define a nootropic as any substance that is a cognitive enhancer. This discussion may be worthy of a section. Wikiman2718 (talk) 19:49, 11 May 2019 (UTC)

I support Wikiman2718's suggestion. --Signimu (talk) 23:27, 3 November 2019 (UTC)

Editing the references for the etymology

The etymology section was quite atrocious. Mixed Latin characters into the Greek words, gave the wrong ancient Greek word for "mind", used a non-existent infinitive form of "τρέπω" i.e. "to turn", plus there was one single parenthesis that was italicized for some reason. I've corrected all these mistakes in etymology, orthography, and formatting, but I need someone to edit the references to remove the current ones and add this entry from Oxford dictionary instead: https://www.lexico.com/en/definition/nootropic. Please and thank you. — Preceding unsigned comment added by 62.228.100.227 (talk) 15:57, 5 October 2019 (UTC)

 Done Seppi333 (Insert 2¢) 11:55, 4 November 2019 (UTC)

Hi, I am a historian on the topic of nootropics, but I am fairly new to Wikipedia so please bear with me while I am still learning the etiquette and formatting (and as a note, User:Signimu , your resources are very helpful in this regard). Thank you for creating the new section on History and moving my text there instead of deleting it. I will work to delineate the history of nootropics in that section and will try to stay away from the etymology of the word nootropics, although I believe it merits discussion. The problem I have, in terms of accuracy, is that there is a clear genesis of the term "nootropic" and the person who invented the word, Corneliu Giurgea, says continually throughout his writing, starting from the very first paper introducing the nootropic concept[1] in 1972 (in French), that nootropics comes from the roots "mind" and "towards" to mean "towards the mind." In Figure 21, titled "Etymologie du mot nootrope" on page 149 of "Vers une pharmacologie de l'activité intégrative du cerveau. Tentative du concept nootrope en psychopharmacologie" (1972) it translates the second half of the word from Greek ("TPOΠEIN") to French ("aller vers") to a parenthesis of English ("towards"). I can provide full scans of this paper if necessary.

You can see numerous other examples of this from the first paper in English from 1973[2]: "A new class is therefore to be considered for which we propose the term Nootropic (from Noos-mind, and tropein-towards). A follow on paper in 1977 states:[3] "The term "nootropic" (noos = mind; tropein = towards) was proposed by us (Giurgea, 1972,1973) to designate psychotropic drugs" and so on.

So the question is then, does the etymology truly stem from the creator of the term, who invented it after 9 years of intense research, or from a dictionary written many years after and which while correctly citing "nootrope" and the "noos" aspects as in the original 1972 nootropics paper, then, with no other sourcing, states the second part to be from "tropē" meaning "turning"? It is not clear where this comes from, nor can I find any other citation or reference to "bending" or "a turning" that doesn't ultimately use Wikipedia as a source. So, I don't understand how we can muddle the direct, repeated, etymology of the term "nootropic" when we have the direct source materials, language, and documentation from the originator of the term? If "etymology" is about the "origin" of the word, it would then be incorrect to say it in any way derives from "turning" and is not meant to be "towards." I am not saying that the Greek "τροπή (tropḗ)" might not mean "turning", however, it is clear that that is not the intended meaning from the source material and therefore would not be accurate as the etymological root of the term "nootropic." NootropicsHistorian (talk) 10:30, 7 November 2019 (UTC)

Hello NootropicsHistorian Ah I'm glad you found the resources useful, you're the first one to give me a feedback about them About your question, that's indeed very interesting and I also wondered about this issue, but since I am no historian I did not take any further step. If indeed you can provide quotes (use the {{citation book|quote=Your quote here}} argument to specify a quote, no need for a scan unless someone else asks you), then I think the best would be to rewrite the Etymology section to both include the original etymology by Giurgea and then other etymologies from other sources (such as the one currently presented), this is something that is often done on Wikipedia when multiple etymologies are provided by various sources. And please feel free to expand the History section, it's always very interesting to know more about the history of compounds and concepts Just make sure to provide appropriate references for each sentence (also to be more precise, feel free to use {{rp|pagenumber}} after a </ref> to precise the page without duplicating references, I can help you for your first tries if you aren't sure how to do it ). --Signimu (talk) 12:04, 7 November 2019 (UTC)

References

  1. ^ Giurgea, C (1972). "Vers une pharmacologie de l'activité intégrative du cerveau. Tentative du concept nootrope en psychopharmacologie". Actualites pharmacologiques. 25: 115–56. PMID 4541214.
  2. ^ Giurgea, C (1973). "The "nootropic" approach to the pharmacology of the integrative activity of the brain". Conditional reflex. 8 (2): 108–15. doi:10.1007/bf03000311. PMID 4736348. A new class is therefore to be considered for which we propose the term Nootropic (from Noos-mind, and tropein-towards)
  3. ^ Giurgea, C.; Salama, M. (January 1977). "Nootropic drugs". Progress in Neuro-Psychopharmacology. 1 (3–4): 235–247. doi:10.1016/0364-7722(77)90046-7. The term "nootropic" (noos = mind; tropein = towards) was proposed by us (Giurgea, 1972,1973) to designate psychotropic drugs

US-weighted coverage

From a cursory read through of this article, there’s 1 statement with a worldwide scope, 1 statement pertaining to Germany, and around a dozen statements pertaining to the United States. There’s too much weight given to the US in this article as of right now. Seppi333 (Insert 2¢) 00:56, 16 May 2019 (UTC)

Seppi333 what do you mean by one statement with a worldwide scope ? Can you please give an exemple of those statements ? thanksWalidou47 (talk) 09:54, 2 February 2020 (UTC)

Can someone review this change

I do not have access to the reference cited. This was the editors first edit here. See this diff —¿philoserf? (talk) 18:59, 6 April 2020 (UTC)

Clear bias in article

This article seems to have been hastily put together by someone with an agenda. The clearest example of this is the incredibly sparse "History" section. One would expect a great deal of information regarding the history of individuals taking cognition-enhancing substances of which people have been documented to have done for millenia. Instead, it is a very short paragraph about the history of "nootropics" with regards to the modern substances referred to under that specific term. I understand that it is marked with "needs expansion" but typically information like its history would be at the forefront of an article, and an article wouldn't even be created if it was missing something like that.

I understand nootropic medications are often experimental, but every single paragraph in the entire article is negative, excluding the history paragraph and opening paragraph. In contrast, the page for Adderall[1], a frequently addictive substance with a multitude of negative short-term and long-term effects, has very little in the way of negatives. I also understand that the idea of wikipedia is that anyone may contribute and add to the article, but I came to the article looking to learn, not expecting that I would have enough knowledge to be contributing.

WindowEnthuziast557 (talk) 22:51, 3 September 2021 (UTC)

I understand your disappointment. However, a few pointers: a) Sparseness of information is not bias, but reflects that someone must take the effort of collecting information from reputable research. This is in particular important for topics such as medicine/pharmacology. b) Many articles are created despite lacking a history section! Not having a history section is no argument against having an article. c) What exactly do you mean by every single paragraph being "negative"? That studies have not been able to find evidence in support of an increase in cognition? If we are talking about scientific studies, that is not about being "negative", it is just science. And we have high criteria for inclusion (WP:MEDASSESS). Your last sentence basically says "Instead of contributing with the knowledge I have I will just tell people that I know more than them." Which comes of as more annoying than helpful. A more constructive approach would be to go to e.g. Google Scholar, search for new studies of nootropics (I found a few I will add when I have time) to add. Remember, Wikipedia:Be bold! Sda030 (talk) 20:41, 24 February 2022 (UTC)

References

  1. ^ https://en.wikipedia.org/wiki/Adderall

Dubious content

Wargolynch‎ keeps reinserting the following text:

Extended content

It was first introduced by Corneliu Giurgea in 1972 to describe a new classification of molecules that acted selectively towards the central nervous system's higher-level integrative activity. In order for a molecule to qualify as a true nootropic, it must fulfill Giurgea's five criteria for the category.



  1. It should enhance learning and memory.


  1. It should enhance the resistance of learned behaviors/memories to conditions which tend to disrupt them (e.g. electroconvulsive shock, hypoxia...).


  1. It should promote neuroprotection against various physical or chemical injuries (e.g. free radicals, neurotoxins, scopolamine, strong psychostimulants...).


  1. It should increase the efficacy of the cortico-basal ganglia-thalamo-cortical loop mechanisms.


  1. It should not promote strong dopaminergic stimulation (amphetamines, phenidates...), opioidergic stimulation (tianeptine, kratom...) or sedation (benzodiazepines, calcium channel blockers, phenibut...), thus not provoking direct addiction or indirect addictive properties through drug tolerance and homeostasis. At most, it should possess very few temporary side effects and extremely low toxicity.[1]

References

  1. ^ Giurgea, Corneliu E. (1982). "The nootropic concept and its prospective implications". Drug Development Research. 2 (5): 441–446. doi:10.1002/ddr.430020505. S2CID 145059666. The nootropic concept emerged about 10 years ago essentially from the unusual pharmacology of piracetam, which later on was confirmed and extended to human pharmacoclinics and therapeutics. A nootropic drug is characterized by a direct functional activation of the higher integrative brain mechanisms that enhances cortical vigilance, a telencephalic functional selectivity, and a particular efficiency in restoring deficient higher nervous activity.

Two problems:

  • This is a based on a primary source;
  • It does not WP:Verify the text. Thus, removed. Bon courage (talk) 13:27, 5 February 2023 (UTC)
@Wargolynch: can you please address the above concerns? Thanks. M.Bitton (talk) 14:11, 5 February 2023 (UTC)
I'm not the original writer of this section.
You're in fact deleting what was already written before I arrived.
As stated, I've edited the section with more precise and better safety informations.
"Feel free to add new sources" on top of those you can already find in the section plus the ones you can find on the page for Corneliu Giurgea which is linked in the section. Wargolynch (talk) 15:15, 5 February 2023 (UTC)
You are responsible for the text you add; how about addressing the points? Nobody needs your permission to add sources to articles. Bon courage (talk) 15:16, 5 February 2023 (UTC)
There is a citation leading to Giurgea's research. Feel free to read the paper yourself.
https://en.wikipedia.org/wiki/Nootropic#cite_note-4 Wargolynch (talk) 15:23, 5 February 2023 (UTC)
It is a primary source, so not very useful; articles must be based on secondary sources. And what you keep adding is not backed by it. These are the issues. Bon courage (talk) 15:31, 5 February 2023 (UTC)
I've been blocked from this page in despite of the fact I AM NOT THE ORIGINAL WRITER for this section...
Why don't you help finding secondary sources?
This definition is accurate and meaningful.
I've tried to edit the definition by precising how it was the one of Corneliu Giurgea which is basically the inventor of piracetam, it would have helped every reader to better understand it.
You guys are not really helpful. Most people on nootropic communities do agree on the fact strong dopaminergic stimulants, opioidergics and sedatives are not true nootropics but potentially dangerous molecules that can promote neurotoxicity and addiction. It's just common sense from both empirical and experimental points of view.
The page as I edited it was already mentioning these 5 criteria, all I've done was adding more information as why you should be careful with potentially dangerous cognitive enhancers which are not nootropics according to Giurgea's definition.
It's no wonder why some pages are never evolving toward something better. Wargolynch (talk) 16:31, 5 February 2023 (UTC)
@Wargolynch: I am an administrator and am not here to enter into the content dispute, but there is one point you've made more than once that I don't follow. You say that you are not the "original writer of this section". Can you please point to a link or diff in the article that shows what user was the "original writer"? Thanks.--Bbb23 (talk) 16:38, 5 February 2023 (UTC)
I don't want to edit anything on wikipedia anymore.
What I'm doing is just good for both readers and users, it just makes sense. Rather than kicking me out or repeating what I'm sharing is bullshit, maybe these people should just help with achieving something meaningful.
Good bye and good luck, it must be hard to moderate here. Wargolynch (talk) 16:43, 5 February 2023 (UTC)
I was basically editing the section as you kicked me out so people could better understand it was Giurgea's own personal definition, although I think this is the most meaningful definition out there for a plethora of reasons. Wargolynch (talk) 16:46, 5 February 2023 (UTC)
I deleted the article that copied here. I will leave the diff showing the difference between the stable version (before your first edit) and your last edit. Can you please point the part that you're referring to? Thanks. M.Bitton (talk) 16:53, 5 February 2023 (UTC)
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