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all 33 comments

[–]Poop_Slow_Think_Long 4 points5 points  (4 children)

That stuff made my vision sharper than it's ever been before - for a few hours, among other things. sorry to hear it didn't work for you.

[–][deleted] 1 point2 points  (2 children)

That was a one-time experience for me on my 2nd dose. Totally unexpected, and I didn't realize it had something to do with the noopept until later. It sounds stupid but I happened to be watching Silent Hill and was completely mesmerized by it, thinking it was the most visually stunning HD of all HD films I'd ever seen (maybe it was just Radha Mitchell in various states of dishevelment... i swear i could count the beads of sweat on her sternum).

Then I watched it again the next day without having taken noopept, and thought "Eh, it's OK, but it looks different" (like watching a non-HD version relative to previous viewing) and realized the connection. Never had experienced that since, after many uses of noopept. I still use it once in a while because it causes a funny feeling in my head, no idea of any cognitive benefits however.

[–]yeah-ok 5 points6 points  (1 child)

I still use it once in a while because it causes a funny feeling in my head, no idea of any cognitive benefits however.

Spoken like a true nootropist.

[–][deleted] 0 points1 point  (0 children)

thankfully we have ppl like gwern who are peculiarly particularly well-equipped for reports based on careful analysis. for the rest of us folks i think "funny feelings" are arguably more accurate than reporting based on half-way pretensions of objectivity.

[–][deleted] 0 points1 point  (0 children)

He chose a book for reading

[–]FrigoCoder 0 points1 point  (0 children)

A linear regression, which included other concurrent experiments as covariates & used multiple imputation for missing data, indicates a small benefit to the lower dose levels and harm from the highest 60mg dose level, but no dose nor Noopept as a whole was statistically-significant. It seems Noopept’s effects are too subtle to easily notice if they exist, but if one uses it, one should probably avoid 60mg+.

I remember a ratty experiment where the optimal dosage was the human equivalent of 2x8 or 2x9 mg IIRC, and there was a sharp decline in benefits at larger doses.

Would be nice to see a prolonged study with strict 2x10 mg dosages. Possibly cosupplemented with Magnesium and Phosphatidylcholine precursors.

[–][deleted]  (2 children)

[deleted]

    [–]MisterYouAreSoDumbNatrium Health & Nootropics Depot 4 points5 points  (0 children)

    Hey hey, P21 is not Russian!

    [–]gwerngwern.net[S] 0 points1 point  (0 children)

    Aside from Noopept, no. (Pretty much everything I've ever experimented with chemical-wise is listed on my nootropics page, so if you're ever curious if I've experimented with something, you can search it.)

    [–]JohnMcPineapple -1 points0 points  (2 children)

    It certainly helped me by increasing my brain receptivity. I never perceive any immediate effects from it, but I was surprised that when I tried to study a complex topic recently, which I didn't really understand half a year ago, I had no problems grasping it.

    But mind you that I kind of suffer from constant tireness, which probably increases its effect on me. It's denoted as to have no effect on a well functioning brain after all.

    [–][deleted]  (1 child)

    [deleted]

      [–]gwerngwern.net[S] 1 point2 points  (0 children)

      I'd like to note that repeatedly approaching some topics can do wonders.

      Yep. Through spaced repetition and memory consolidation, if nothing else.

      [–]economyx -1 points0 points  (18 children)

      N=1, multiple concurrent confounders.

      Just because you can use experimental methods and run analyses in R doesn't make this scientific.

      [–]gwerngwern.net[S] 6 points7 points  (17 children)

      I formulated a hypothesis, designed it with power in mind, removed the largest confounder of all by blinding, controlled for others, used randomization to enable causal inference, and then tested the hypothesis. The internal validity is out the wazoo. Not scientific?

      Haters going to hate.

      [–]Synzael 4 points5 points  (12 children)

      I would not use an oral roa

      [–]MisterYouAreSoDumbNatrium Health & Nootropics Depot 4 points5 points  (11 children)

      I have typed out my sublingual case many times now. At 9.8% oral bioavailability, Gwern's highest dose is only roughly 5mg. That's half the dosage I use sublingually. His 12mg oral dose is almost nothing. Can't neglect the fact that it is a peptide, and should be taken in a ROA that bypasses the GI tract.

      Not that I am saying changing the ROA will for sure give him results. But it needs to be accounted for before I take the results seriously.

      [–]gwerngwern.net[S] 4 points5 points  (8 children)

      I would be more impressed by that observation if the highest dose hadn't had the worst results. (There also seems to be no particular consensus in the anecdotes on /r/nootropics about sublingual being all-important.)

      I have typed out my sublingual case many times now.

      Could you link to it? Searching through your profile as far as Reddit will go, I don't see one. There's a link to WP, but the two articles there (Boiko et al 2000 & Boiko et al 2004) don't compare sublingual at all; and Examine discusses almost entirely oral administration in rats & humans, with the suggested oral doses being well below my max and likewise with the cited human study Neznamov & Teleshova 2009 which had positive results (using 20mg, no mention of sublingual).

      [–]MisterYouAreSoDumbNatrium Health & Nootropics Depot 1 point2 points  (7 children)

      You're completely ignoring the complex pharmacodynamics of noopept. Of course high oral doses are going to lead to more side effects, with less of the wanted effects. That is because the metabolites are still active, but in different ways. You want to get the full structure across the BBB BEFORE is gets broken apart, or the PGP structure is not going to exert its nootropic effect. That is the key to making nooept work.

      There also seems to be no particular consensus in the anecdotes on /r/nootropics[1] about sublingual being all-important.

      Why are you suddenly placing weight on anecdotes, when there is evidence for the pharmacodynamic issues?


      Oral administration of noopept reaches much lower plasma concentrations than IV and sublingual. A lot of people quote a Russian study as saying that it's oral bioavailability is 97%, but that is incorrect.

      The study showing that is in Russian and was done on rats and chinchilla rabbits. Their finding was actually 98.67% bioaccessibility of oral tablets in comparison to the oral parent compound via a feeding tube. The actual finding of peroral in comparison to IV was 9.33%. That means that only roughly 10% of the oral dose makes it to your bloodstream. Those quoting the 97% number have not read the actual study. I'll link the full text for you below.

      Full Text

      The absolute bioaccessibility was on the average AUC p.o./ AUC i.v. = 9.33 +-1.30%, which is evidence of a pronounced effect of the “first passage” via the gastrointestinal tract and the liver. In comparison with rats, rabbits are characterized by slower absorption of the parent substance, which is manifested by an almost twofold increase in MRT and by decrease in the C max AUC 0 ratio in the latter case.

      Peptides are easily ripped apart by digestive enzymes, and noopept is not immune to these effects. It's only saving grace is that it is a very small dipeptide. This means that it has a higher likelihood of being absorbed before being ripped apart than larger peptides that are almost 0% bioavailable. The longer it takes to get to your bloodstream, the more it will be broken apart. It will be ripped into it's 3 parts, the glycine, proline, and phenylacetyl esters. If this happens peripherally, the molecules are useless to the brain. They must pass the BBB before being metabolized. This is much less likely if you allow it to undergo first pass metabolism. The only thing noopept has going for it is size, which as you can see from the study doesn't help much.

      Noopept is active orally, but much less than sublingual. Even the Russian pharmaceutical instructions state that it should be taken sublingually. The study I linked used 10mg/kg IV, and 50mg/kg peroral, and still the oral was unable to get close to the Cmax of IV.

      Thus, the results of our investigation showed that the absolute (peroral) bioaccessibility of noopept is 7.09% in rats and 9.33% +-1.30% in rabbits.

      Here is another Russian study on the matter:

      Similar plasma level of GVS- 111 was observed after 5 mg/kg parenteral and 50 mg/kg oral administration.

      So it took 50mg/kg peroral to reach the plasma concentration of 5mg/kg paenteral. A very substantial difference.

      Considerable differences related to the administration route were revealed in GVS-111 metabolism. After parenteral administration, apart from the unchanged GVS-111 molecule, the plasma contained 2 phenylacetyl metabolites phenylacetylproline and phenylacetic acid, which were not detected after oral administration. At the same time, plasma chromatograms after oral administration showed a peak which was eluted before GVS-111 and differed from the known phenylacetyl-derivatives by the elution time. It could be either hydroxylated or methylated GVS-111 metabolite. This difference in GVS-111 metabolism in different administration routes seems to be due to the fact that parenterally administered peptide is hydrolyzed preferentially by plasma peptidases, while metabolic transformations after oral administration occur during its first passage through the liver.


      So taking noopept orally is going to lead to high levels of the metabolites glycine, proline, and phenylacetyl esters. What it will not do is get the coveted proline-glycine-proline structure to the brain in meaningful amounts. That PGP structure is what we want, and is what leads to both Selank's and Semax's nootropic effects. So taking larger doses of noopept orally would be similar to taking huge doses of Selank and Semax orally. It does not make any sense.

      Again, I am not trying to impress anyone with observations. I am simply stating that any peptide is going to be EXTREMELY dependent on route of administration. Your test results sublingually could show the exact same results. I am not saying that is not a possibility. But that should be accounted for in your study design.

      [–]gwerngwern.net[S] 2 points3 points  (6 children)

      You're completely ignoring the complex pharmacodynamics of noopept.

      I'm not, but I don't see any reason to believe that sublingual is massively more effective than oral, or that it has >6x more bioavailability (and so your 10mg sublingual dose is a larger effective dose than my 60mg doses were)

      You want to get the full structure across the BBB BEFORE is gets broken apart, or the PGP structure is not going to exert its nootropic effect.

      The studies you cited on Wikipedia seem to indicate that Noopept gets across the BBB fine.

      Why are you suddenly placing weight on anecdotes, when there is evidence for the pharmacodynamic issues?

      Because the anecdotes seem to generally be oral doses smaller than mine, so now we have a problem: either I've effectively disproven all the anecdotes and the anecdotes are being driven by (surprise surprise) placebo, self-justification, non-random consumption patterns, biased data collection etc, or you have disproven them with your sublingual argument; either way, why should I believe you - you don't seem able to produce a study showing that sublingual pwns oral, so you must be going off your personal experience... the same personal experience which has just been disproven by either you or me.

      The study showing that is in Russian and was done on rats and chinchilla rabbits. Their finding was actually 98.67% bioaccessibility of oral tablets in comparison to the oral parent compound via a feeding tube.

      Sure. As I said, it didn't compare with sublingual, although it's nice to know that swallowed tablets or powders basically don't differ from a slurry directly to the stomach.

      That means that only roughly 10% of the oral dose makes it to your bloodstream.

      Yeah but we're not comparing tablets/slurries to IVs/injections.

      Even the Russian pharmaceutical instructions state that it should be taken sublingually.

      Where do they say that? When I was looking through human trials on Pubmed, none of them seem to specify sublingual in the abstracts that I could tell.

      Thus, the results of our investigation showed that the absolute (peroral) bioaccessibility of noopept is 7.09% in rats and 9.33% +-1.30% in rabbits.

      OK, but what's the sublingual bioaccessibility? Your counterargument is meaningless if the sublingual accessibility is, say, 8.09% in rats and 10.33%. Then sublingual is better as one would expect, but not importantly so.

      Here is another Russian study on the matter: https://hotfile.com/dl/239810985/dc74e87/Bioavailability_of_noopept.pdf.html

      Similar plasma level of GVS- 111 was observed after 5 mg/kg parenteral and 50 mg/kg oral administration.

      So it took 50mg/kg peroral to reach the plasma concentration of 5mg/kg paenteral. A very substantial difference.1

      Hold on, your quote doesn't say 'peroral', it says 'parenteral'. Parenteral is also IV. (Boikos 2000, the paper you seem to be citing here, is itself alluding to an earlier 1997 paper which I can't find but given the term the translator chose, it seems likely to be IV or another form of injection.) Again, this is not what is in question: I agree that of course injection has higher bioavailability. What I want to know is how oral compares with sublingual in bioavailability. IV is not relevant. I am not taking Noopept via IV; you are not taking Noopept via IV; no one on /r/nootropics or Longecity is taking Noopept via IV that I know of; the people in any human studies are not taking Noopept via IV; and so on.

      (All your hotfile.com links are broken since the site is dead. You should include at least titles with your links when you use filesharing sites you know will likely be gone in a year or two.)

      So taking noopept orally is going to lead to high levels of the metabolites glycine, proline, and phenylacetyl esters. What it will not do is get the coveted proline-glycine-proline structure to the brain in meaningful amounts.

      ...And the same paper also observes that there is plenty of GVS-111 in the brain too.


      So let me ask again clearly: you say sublingual may have much higher bioavailability and so I underdosed hugely by going oral. Do you have any studies or citations showing that sublingual administration has substantially higher bioavailability, such as 6x, than that of oral administration?

      If you do not and your case is entirely that last quote about IV/injections having different metabolites, why do you think that the metabolites for sublingual would look like IV/injections rather than oral's metabolites?

      [–]MisterYouAreSoDumbNatrium Health & Nootropics Depot 3 points4 points  (5 children)

      There are no studies investigating sublingual administration of noopept, and the relative bioavailabilities compared to oral/injection. Yes we are making a jump, albeit an educated jump. We know that sublingual bypasses first pass metabolism, and that noopept is extensively metabolized via the liver. That is not the same thing as anecdotal evidence. It may not be the type of evidence you are looking for. However, it would have been easy for you to include that in your study. Again, the results would be limited to you personally. However, the results would be interesting.

      The studies you cited on Wikipedia seem to indicate that Noopept gets across the BBB fine.

      It does. That is why injections work. We are worried about the enzymes in the GI tract and liver, though. That is the issue with oral. If you bypass those, then it has a much greater chance to pass the BBB. If the GI tract and liver breaks it down, it never gets a chance to pass the BBB.

      Because the anecdotes seem to generally be oral doses smaller than mine, so now we have a problem: either I've effectively disproven all the anecdotes and the anecdotes are being driven by (surprise surprise) placebo, self-justification, non-random consumption patterns, biased data collection etc, or you have disproven them with your sublingual argument; either way, why should I believe you - you don't seem able to produce a study showing that sublingual pwns oral, so you must be going off your personal experience... the same personal experience which has just been disproven by either you or me.

      I am discussing mechanisms, not anecdotes. You cannot equate the educated assumption that sublingual has increased bioavailability, when we know it is extensively metabolized in the GI tract and liver, to people self reporting results. There is no study doing a direct comparison of sublingual to oral, so we have to go on assumptions based on mechanisms. If I had said believe me, I feel it more vial sublingual, then we would be talking anecdotes.

      Where do they say that? When I was looking through human trials on Pubmed, none of them seem to specify sublingual in the abstracts that I could tell.

      This was in Russian, and was translated by another Redditor. Unfortunately I do not have the link handy, and have not verified with anyone else whether or not his translation was correct.

      Hold on, your quote doesn't say 'peroral', it says 'parenteral'. Parenteral[2] is also IV.

      Yes, that was the point. Peroral took 10 times the dosage to reach the same concentration as injection. The later study showed that oral administration did not lead to any of the good metabolites, but that IV did. Again, I cannot show you a study that proves sublingual does the same. But the enzymes in your plasma are different than the enzymes in your GI tract and liver. The enzymes that sublingual would hit are the same as IV, with the exception of a few in your mouth. So bypassing those enzymes in the GI tract and stomach are going to drastically eliminate the initial metabolism, and make the sublingual metabolites much closer to the IV metabolites. Again, I cannot prove that to you, since nobody has thought to do a sublingual study.

      So you are right, I cannot provide you with a study proving what I am saying. All I can give you is evidence for the mechanisms behind the theory. Until someone does a sublingual study, or we fund one ourselves, that is all we can go on. For you to include a sublingual aspect to your personal study would not be difficult, and could give us more relevant data. Saying that you do not think it should be done, because nobody else has done a sublingual study, seems silly to me. It's not done until someone does it. Again, that is why I made it clear that I am not saying it would for sure alter the results of your testing. But this is a very valid variable to be tested.

      [–]gwerngwern.net[S] 1 point2 points  (4 children)

      There are no studies investigating sublingual administration of noopept, and the relative bioavailabilities compared to oral/injection.

      Alright fine, so when you wrote "At 9.8% oral bioavailability, Gwern's highest dose is only roughly 5mg. That's half the dosage I use sublingually. His 12mg oral dose is almost nothing.", you were speculating out your ass about what my highest dose translated to and how it's 'almost nothing'. Please mention that in the future when you are exasperatedly telling people how you've written up a billion times how sublingual is infinitely superior.

      However, it would have been easy for you to include that in your study...For you to include a sublingual aspect to your personal study would not be difficult, and could give us more relevant data. Saying that you do not think it should be done, because nobody else has done a sublingual study, seems silly to me.

      No, it would not have. Sublingual breaks blinding because I have no idea where to find a placebo which tastes exactly like Noopept's particular foulness. And without blinding, all it would have shown (besides, of course, being unpleasant to consume and a huge amount of work to double the already-huge-sample-size to allow any remotely accurate comparison of the effect sizes from oral and sublingual) is 'placebo effects are big'. This is why I was hoping your confident pronouncements were based on hard biochemical data showing that sublingual was several times more bioavailable - because estimating the difference is impossible from behavioral mechanisms in the absence of a workable placebo.

      It does. That is why injections work.

      ...and 10% of it also gets past the BBB when administered orally, as Boiko et al 2000 shows.

      You cannot equate the educated assumption that sublingual has increased bioavailability, when we know it is extensively metabolized in the GI tract and liver, to people self reporting results.

      If Noopept only works injected and oral is extensively metabolized, why do the oral studies show positive results?

      The later study showed that oral administration did not lead to any of the good metabolites, but that IV did.

      How do we know these metabolites are necessary and sufficient? The Noopept is getting to the brain either administration route, so what justifies this claim? You seem to be making leap after leap here: sublingual metabolizes like injection, the metabolites are meaningfully different (as best as we can tell from some shitty animal experiments, which I have criticized constantly in the past), the metabolites are the entire reason for the effect... None of these seem particularly plausible, and all together, it's just privileging the hypothesis.

      [–]MisterYouAreSoDumbNatrium Health & Nootropics Depot 1 point2 points  (3 children)

      We can certainly make you a solution that masks the taste. That is not hard at all. And I was not speculating out my ass. Your lowest dose of 12mg is almost nothing, when you take into account the oral bioavailability. You have the studies, and conceded that it is around 10%. I was merely mentioning that your highest oral dose, when taking bioavailability into account, was half the sublingual dose I take. There was no mention of anything being superior. I even mentioned many times that your results might not differ at all with sublingual. You are the one putting words in my mouth now. I brought up an extremely valid variable, that we can even help you control for with blinding, and you are getting upset at me for mentioning it.

      You know what, don't worry about it. I'll figure out a way to run a trial for it.

      [–][deleted]  (1 child)

      [deleted]

        [–]MisterYouAreSoDumbNatrium Health & Nootropics Depot 0 points1 point  (0 children)

        Route of administration.

        [–]economyx 0 points1 point  (3 children)

        "used randomization to enable causal inference"..?

        Explain to me how you eliminated all the confounders (other experimental compounds you were taking), and I'll explain to you the difference between correlation and an actual treatment effect.

        [–]gwerngwern.net[S] 1 point2 points  (2 children)

        I'll explain to you the difference between correlation and an actual treatment effect

        Please explain to me how randomized a treatment does not enable one to calculate the mean effect of the treatment. I'm sure Fisher, Student, Rubin, Pearl etc will all be fascinated to hear why RCTs don't actually turn out to work.

        [–]economyx 0 points1 point  (1 child)

        First, none of those authors are reading your study, so let's not speak for whether or not they would agree with your randomization method.

        Then, let's look at your confounders. While you've randomized some of the new compounds in with the noopept (assuming all have lost effect by the time you've switched), you either choose not to, or fail to control for others (modafinil, which you say you minimized taking, but still took some of the time, and magnesium citrate, which you handle by correlating it's effect rather than isolating it). That's sloppy at best, misleading at worst.

        The idea behind randomization is to make the statement that all other factors are ignorable, so that you can show that the ONLY variation must be due to a treatment effect. While you're flirting with that concept, you haven't controlled for a while host of other potential confounders (your relative health for each time period, for instance).

        Finally, this brings us to the real point of randomization in a controlled study. Individual characteristics are likely too difficult to accurately measure and control for, which is why the medical industry affects randomization via large numbers of clinical trial patients, who receive either placebo or treatment. The idea is, on average, underlying characteristics that cannot be controlled for will vary randomly if the patient is selected randomly. Your N=1 study doesn't sufficiently prove you've attempted to handle that kind of (very real!) variation.

        Maybe a deeper read of Rubin and Pearl, and a look at some relevant medical literature, can provide a better explanation, but you're in the pseudoscience realm with this "study". I don't think you're wearing a foil hat, but these are the same mistakes made by people trying to prove chemtrails and colonic benefits.

        [–]gwerngwern.net[S] 1 point2 points  (0 children)

        While you've randomized some of the new compounds in with the noopept (assuming all have lost effect by the time you've switched), you either choose not to, or fail to control for others (modafinil, which you say you minimized taking, but still took some of the time,

        No, I said I didn't take it. Therefore it cannot be an issue since it was the same in all time periods, and even if I had been taking it, how would it undermine the results given the randomization of the intervention in question?

        and magnesium citrate, which you handle by correlating it's effect rather than isolating it).

        The magnesium citrate was randomized and blinded as well, aside from the incorporation as a covariate to explain variance; and dropping it from the analysis entirely doesn't change the conclusion.

        The idea behind randomization is to make the statement that all other factors are ignorable, so that you can show that the ONLY variation must be due to a treatment effect. While you're flirting with that concept, you haven't controlled for a while host of other potential confounders (your relative health for each time period, for instance).

        Huh? Randomization balances unobserved covariates - like my relative health or any modafinil use. It produces an unbiased estimate of the mean effect, it doesn't produce an estimate "that the ONLY variation must be due to a treatment effect", whatever that means. There's always a 'while [sic] host of other potential confounders', that's why we don't simply measure every confound and calculate effects directly!

        Finally, this brings us to the real point of randomization in a controlled study. Individual characteristics are likely too difficult to accurately measure and control for, which is why the medical industry affects randomization via large numbers of clinical trial patients, who receive either placebo or treatment. The idea is, on average, underlying characteristics that cannot be controlled for will vary randomly if the patient is selected randomly. Your N=1 study doesn't sufficiently prove you've attempted to handle that kind of (very real!) variation.

        Um, no, randomization is for allowing causal inference at all.

        You're getting at internal vs external validity - whether my causal results would be the same in other people in the population. I agree that there's no clear external validity because the results are only about me, and there cannot be strong inferences about how much my results will generalize

        (My point in discussing my self-experiments is that anyone reading my self-experiments should have some sort of prior or belief about how much Noopept's effects are the same in every person and they should filter my evidence through that. If they believe Noopept has different effects in, say, people with major depression, then my null result should be of little interest. Where my results should be of most interest is when it is claimed that an intervention is broadly useful in healthy normal people but the evidence for this claim is shit; then my well-done self-experiment may weigh heavy with people - for example, like my LSD microdosing self-experiment - because there is no strong prior reason to expect any particular person to be different and the evidence for no effect in the population after weakening for being on only one person is stronger than the original evidence for an effect in the population.)

        Maybe a deeper read of Rubin and Pearl, and a look at some relevant medical literature, can provide a better explanation, but you're in the pseudoscience realm with this "study".

        Funny, that's how it looks to me: like you don't actually understand what randomization is or what confounds are and are just throwing the terms around.

        So again, please tell me, how does the 'relevant medical literature' show that randomization doesn't work? How does randomizing my consumption of Noopept over dozens of pairs of blocks not allow causal inference about the effect of Noopept? How do these 'confounders', exactly, carefully conspire to oppose the randomization?

        [–]NBC_ToCatchARedditor -2 points-1 points  (5 children)

        Fair enough, but it does work. Although for me I find that it makes me alert for a few hours, but definitely doesn't last the whole day.

        [–]hamsummit 1 point2 points  (4 children)

        but the question isn't if it works, the question is if it is better than placebo

        [–][deleted]  (3 children)

        [deleted]

          [–]norepinephrinex 3 points4 points  (2 children)

          [–]autowikibot 2 points3 points  (0 children)

          N of 1 trial:


          An N of 1 trial is a clinical trial in which a single patient is the entire trial, a single case study. A trial in which random allocation can be used to determine the order in which an experimental and a control intervention are given to a patient is an N of 1 randomized controlled trial. The order of experimental and control interventions can also be fixed by the researcher.

          This type of study has enabled practitioners to achieve experimental progress without the overwhelming work of designing a group comparison study. It can be very effective in confirming causality. This can be achieved in many ways. One of the most common procedures is the ABA withdrawal experimental design, where the patient problem is measured before a treatment is introduced (baseline) and then measured again during the treatment and finally when the treatment has terminated. If the problem vanished during the treatment it can be established that the treatment was effective. A variation of experimental design in single case studies is great. But the N=1 study can also be executed in an AB quasi experimental way; this means that causality cannot be definitively demonstrated. Another variation is non-concurrent experimental design where different points in time are compared with one another. This experimental design also has a problem with causality. But the replication of studies has a great value and can be as effective as a group study. The single case experimental design has been very effective in psychology and other field of behavior science.


          Interesting: Single-subject design | Multinomial distribution | Binomial distribution | Beta distribution

          Parent commenter can toggle NSFW or delete. Will also delete on comment score of -1 or less. | FAQs | Mods | Magic Words

          [–]morphemass -3 points-2 points  (0 children)

          I had my best results from a single 100mg dose, seemed to have a lasting effect for several days afterwards. The recommended 20mg dose did little for me I felt...