This is an archive of past discussions with User:Seppi333. Do not edit the contents of this page. If you wish to start a new discussion or revive an old one, please do so on the current talk page.
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I'm going to go ahead and just find the study and use that as a source. However, it's actually Wikipedia policy that it's better to use a secondary news source reporting on a study than it is to use the study itself. I'm not sure why this is the case, but I remember someone linking it to me after I made the same point you just did on my user page. Also, it's almost always better to try to fix something yourself or to leave the almost-sufficient version in place (after commenting about it in the talk page) than it is to delete it. Thanks. Exercisephys (talk) 22:06, 21 June 2013 (UTC)
False accusation of vandalism
Please retract this inappropriate accusation of vandalism. I see you are a new editor, which may well explain your misunderstanding of the meaning of "vanadalism". Please note that accusing a good-faith contributor of vandalism is a personal affront to an editor's integrity. Please read WP:NOT VANDALISM. Thank you. :) 81.157.7.7 (talk) 10:39, 25 June 2013 (UTC)
I appreciate your interest in improving the article and that section; however, piecewise deletion of non-supporting material of a specific viewpoint along with re-casting and mis-citing the results of academic research only hurts wikipedia. You did bring to my attention the specific policy on primary sources though, so I've tried to address your issues w.r.t. wp:npov by disassociating it from the context of test-taking. Seppi333 (talk) 10:56, 25 June 2013 (UTC)
I didn't directly address your claims of nonvandalism because it's highly subjective; even the policy you linked to stated this in the first two sentences. That said, I still consider skewing the content of an article so much that its citations don't agree at all with the text on the page to be vandalism. Seppi333 (talk) 13:46, 25 June 2013 (UTC)
Thank you for at least replying. This is a content dispute, NOT vandalism. Vandalism is something else and not an accusation to be made lightly. I reiterate my requests to desist in making such accusations and, where possible, redact those you have already made.81.157.7.7 (talk) 14:07, 25 June 2013 (UTC)
Seppi333, the IP came to my talk page because I put a welcome template on his talk page. I looked over all the edits and it doesn't appear to be vandalism to me. It appears he's just acting like a WP:NEWBIE. It might be helpful to stop calling him a vandal. He doesn't appear to have that behaviour and you can be blocked for saying it. Instead, I suggest whenever he does something that isn't a good idea like reverting, etc., instead of arguing with him, point him to the policy. This is clearly a content dispute, not vandalism. I don't know the article or it's subject, but as you know questions about sources can be handled at the RS board. I've explained some of the rules to him and pointed him to some of the policies. He is using the talk page. He's trying to do things the right way or he wouldn't have asked for help. Please try to help him where needed. Thanks. Malke 2010 (talk) 15:29, 25 June 2013 (UTC)
I did exactly what you said, stating the precise policies I performed the revert under before performing the revert. I don't know why you wrote that I didn't direct him to the policy when I very clearly did so on the talk page of that article. It was after he reverted a second time (IE after I stated the policies I reverted under and had amended the page once) without any discussion that I issued a vandalism warning. So, just for your reference so that you actually do read all the edits: Talk:Amphetamine_mixed_salts_(medication). If after reading that you still find my actions do not suffice, I'd like to know what I should have done instead, since I already did everything you said. Seppi333 (talk) 16:11, 25 June 2013 (UTC)
In fact, between our last correspondence and after I explicitly asked everyone not to make any further edits pending discussion on the talk page and in the edit history, he restored the misattributed edits I deleted under an entirely different section. I'd ask you what I should do now, since he has literally just circumvented my attempt to pause edits and discuss the issue by moving the edits that are in contention to a different section. See Amphetamine mixed salts (medication) revision history. Seppi333 (talk) 16:35, 25 June 2013 (UTC)
That said, maybe I can ask you the same question I asked Malke about those edits. What would you do if our roles were reversed? Seppi333 (talk) 17:29, 25 June 2013 (UTC)
Thanks for the pointer; I'll do that in the future. Given the status, I can appreciate why you use an IP as a proxy account for editing. Still, I'd appreciate it if you'd wait for the talk page discussion to come to a consensus. Seppi333 (talk) 17:44, 25 June 2013 (UTC)
Please do not remove the conclusions from a Cochrane review and you must paraphrase sources rather than copy and paste from them. Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:55, 5 August 2013 (UTC)
Note to other users reading these old comments: these issues were discussed in a section in the Wikipedia_talk:WikiProject_Medicine archive, titled "COPY AND PASTE" as well as in several sections in Jmh649's talkpage archive.
It's nice to see someone else with a degree in Psychopharmacodynamics (you said psychopharmacology on your user page, but since you're contributions are mainly about effects that drug have on the body, I'm assuming your degree is in pharm-d rather than pharm-k. Also, I should add that I haven't graduated yet. However, I will complete my 6th year of medical this year!) contributing to Wikipedia! You add great information to the articles and I'm glad someone, who's educated on the subject, contributes so much to the Amphetamine, Methamphetamine, and Methylphenidate articles. Especially since there is so many misconceptions out there about these drugs.
It's very frustrating when people who have no knowledge on a subject edit the articles just because they believe everything the media tells them. Again, I applaud you for, essentially, moderating the articles and keeping the information factual, rather than speculative.
Thanks for the kind words. I agree - there's way too much misinformation out there - hopefully improving wikipedia articles will change that to some extent. Regards, Seppi333 (talk) 03:21, 15 October 2013 (UTC)
Hi there, I'm pleased to inform you that I've begun reviewing the article Amphetamine you nominated for GA-status according to the criteria. This process may take up to 7 days. Feel free to contact me with any questions or comments you might have during this period. Message delivered by Legobot, on behalf of Sasata -- Sasata(talk)01:10, 17 October 2013 (UTC)
Hi Seppi. Just saw your "censored comment" about Sleep aid. And noticed that the three articles wikilinked above redirect to three different articles. Perhaps we should decide which article is the best to redirect to? --Hordaland (talk) 11:50, 19 October 2013 (UTC)
Hey Hordaland - good catch. My initial thought was to redirect the page to that section since it's the only article (section) I found that actually covers the three classic non-prescription sleep aids - H1 antihistamines, melatonin, and valerian; it has pretty broad coverage of more general depressants and sedatives as well, so I figured it was the best place for a redirect on that topic. I'm not familiar with all the sleep articles though, so there may be a better place for those redirects. Seppi333 (talk) 13:02, 19 October 2013 (UTC)
Hi again, Seppi333. Thanks again for your edits to amphetamine, an important page which is very much in need of development. I'd like to point out that you should always make sure you aren't removing correct and notable information when copy-editing and revising. People devote a lot of time to finding information and accompanying sources that belong in these pages, and it shouldn't be deleted haphazardly. I remember previously mentioning this when you deleted a section involving working memory from the page as well.
Hey Exercise, thanks for the feedback. If you're referring to the recent edits in pharmacokinetics and cytochrome p450 enzymes - I couldn't find any sources regarding humans to that material after an hour of searching google and pubmed. The best I could find was animal studies which mentioned those enzymes; without a source, I deleted it per medrs because it's currently GA nominated (I'd rather not put CN tags if I can't find the information myself). Regards, Seppi333 (talk) 01:37, 1 October 2013 (UTC)
I'll admit I don't have a high attention to detail, so if I unwittingly deleted a medrs-quality source that contained that information, please let me know which it was and I'll restore the content after I check it. Seppi333 (talk) 02:02, 1 October 2013 (UTC)
I've been very busy and haven't been able to get involved with this debate. However, I'll be around for the next few days. My concern was more general. I saw many of the improvements I made to stimulant-related pages reverted or removed, and I found many of the same errors and biases that I had corrected once again present (for example, improper treatment of enantiomerism in the amphetamine mixed salts page). Additionally, there were some opinions injected into the amphetamine- and methylphenidate-related pages that went against medical consensus and hued instead to the rather paranoid and faddish movement of vilifying or devaluing these chemicals. I want to make sure that these pages remain informational and unbiased, and I admittedly feel a little demoralized seeing my hard work disregarded and thrown away. Exercisephys (talk) 02:25, 13 October 2013 (UTC)
Hey again Exercisephys. If I've removed any of your edits which were MEDRS-cited and aren't already reflected in a change I've made, I would strongly appreciate it if you added it back into the article. If I removed it because it was included in a section I moved onto the page, I frankly wouldn't even mind/care if you edited it back to the presentation/wording of your liking. I don't have any desire to force presentation of article content in any particular manner. I just don't really have the time/interest to go through sections to add only new material piece-by-piece because a large update would like I just did would take forever.
Like I mentioned on the adderall talk page a moment ago though, I very well may have oversited something and deleted something that I shouldn't have, so I'd actually encourage you to go through all the edits I just made on that page if you're interested in doing so and make any changes you see fit. Regards, Seppi333 (talk) 02:43, 13 October 2013 (UTC)
Not a huge deal, but here's another example of what I'm talking about, from Talk:Amphetamine: "anatomically narrow angles" not sure what this means Fixed by deleting it (I'm not sure either) Googling (well, StartPaging) the term gave me a definition, and StartPaging the term followed by "amphetamine" gave me sources. Exercisephys (talk) 22:21, 25 October 2013 (UTC)
I didn't see the point in spending extra time to elaborate on an optical contraindication when I didn't do so for a far direr one, like people with heart disease, who are at risk of experience sudden cardiac death when using it. Even potential blindness is a triviality in comparison to that. If you want to add the source and a clarified version of the text back in, feel free to do so. Seppi333 (talk) 22:51, 25 October 2013 (UTC)
I don't understand your point; there are more serious side-effects of amphetamine, so it's okay to ignore this one? I suppose my main point is that in trying to make amphetamine a GA or FA you're being too aggressive in your deletion of anything that could be seen as incohesive or undercited instead of taking the time to properly incorporate it. Patience is key; a lot of people put a lot of work into making that article thorough. I appreciate your concern and your work, you've largely been doing a good job. However, that last comment seemed a little oppositional. It isn't on me to cite valid yet uncited sentences/paragraphs that I didn't add. If you need help doing so, appeal to the community, but don't just silently yank them. (Refer to my user page) Exercisephys (talk) 03:54, 26 October 2013 (UTC)
(outdent) The point I was trying to make is the same one as in WP:UNDUE - or "balance w.r.t. prominence." In the future, to address your concerns, I'll make a new thread in the talk page, move deleted material there, and notify you with Exercisephys (talk·contribs) to inform you of material I've cut and that I don't think is worth investing my time finding citations for (as long as I don't doubt it's validity). Is this a satisfactory solution for you?
Just as an aside, one sentence that I've done this for already is in the collapse tab in Talk:Amphetamine#Article improvement. I have no interest in looking to recite that material even though it's true. Seppi333 (talk) 06:36, 26 October 2013 (UTC)
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P-hydroxynorephedrine, which you submitted to Articles for creation, has been created. The article has been assessed as Stub-Class, which is recorded on the article's talk page. You may like to take a look at the grading scheme to see how you can improve the article.
You are more than welcome to continue making quality contributions to Wikipedia. Note that because you are a logged-in user, you can create articles yourself, and don't have to post a request. However, you may continue submitting work to Articles for Creation if you prefer.
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Is there anything I can do to improve the section I wrote about stimulant drugs in the treatment of ADHD? I'd be happy to add, edit or remove information to better comply with Wikipedia standards. Just let me know, and I'd be happy to put in my extra time to helping out! :)
My main concern is really just the length of the section in relation to other uses, but fortunately a lot of what's mentioned is already mentioned elsewhere (especially in the next section on performance-enhancing). So, in an effort to reduce redundancy in the article, I more or less condensed the paragraphs into the main points and merged them into the existing text. It's effects on motivation and cognitive control aren't unique to ADHD, which is why that's mentioned in the performance-enhancing section instead of medical uses section. Nonetheless, I kept the parts on its effects in children where the sources elaborate a bit more. I also cut few sentences from the original page on primates due to one source demonstrating long term safety/efficacy in humans in the revised portion.
Edit: I'm probably not going to be done with this until tomorrow, since I've got a lot of formatting work to do for text flow/readability in order to merge the two parts after I finish adding the remainder. Seppi333 (talk) 03:31, 14 November 2013 (UTC)
Keep the layout clear: Keep the talk page attractively and clearly laid out, using standard indentation and formatting conventions. Avoid repetition, muddled writing, and unnecessary digressions. Talk pages with a good signal-to-noise ratio are more likely to attract continued participation. See Talk page layout.
Repeating something in another section is not repetitive. If you want to reformat it to remove the talkquote, I don't really care about that. If tabbing a statement I make to clarify the language used, I will remove the tab unless it's actually justified (which in this case, it wouldn't be). Seppi333 (talk) 21:17, 15 November 2013 (UTC)
Excessive use of bold, outlining your text in boxes, inserting them in the middle of other discussion, and making the background of the text blue is disruptive. Please cease this. --Kim D. Petersen21:19, 15 November 2013 (UTC)
The Mediation Committee has received a request for formal mediation of the dispute relating to "Amphetamine". As an editor concerned in this dispute, you are invited to participate in the mediation. Mediation is a voluntary process which resolves a dispute over article content by facilitation, consensus-building, and compromise among the involved editors. After reviewing the request page, the formal mediation policy, and the guide to formal mediation, please indicate in the "party agreement" section whether you agree to participate. Because requests must be responded to by the Mediation Committee within seven days, please respond to the request by 14 December 2013.
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Hello, Seppi333. Please check your email; you've got mail! It may take a few minutes from the time the email is sent for it to show up in your inbox. You can remove this notice at any time by removing the {{You've got mail}} or {{ygm}} template.
Hi, Seppi333. I responded to your comment on my talk page. I appreciate your subtle olive-branch in attempting to gain more understanding of one another's points of view.
I didn't want to fully address this in that response, but there's one other thing that causes me to be sometimes oppositional to you. I feel that you sometimes stymie changes or corrections because the originals' citations are sufficient/MEDRS. Wikipedia isn't about compiling MEDRS sources, it's about compiling accurate, complete information. Sources, even ones meeting MEDRS standards, can be wrong, opinionated, outdated or incomplete. This is especially true when we find a new MEDRS that contradicts an already-cited one. There isn't a grandfather clause for sources or facts.
Editors should work together to try to find facts and truth where they can, not vigorously defend existing passages just because they have sufficient citations.
Dexamphetamine is the D-amphetamine of the amphetamine type" Amphet is L and D" althogh Dexamphetamine is only the D-amphetamine" chemically a type") :) Adderal is Amphetamine as it contains 50/50 of D and L. Dexamphetamine contains 100% of pure D therefore speaking chemically being a type of amphetamine" But still amphetamine but only 1 type of the amphetamine" Cheers mate" if you want to chat more email PM me — Preceding unsigned comment added by 101.171.85.55 (talk) 16:45, 13 December 2013 (UTC)
Re your message
Hi Seppi. No worries. My colleague is pushing for publication soon for some reason. ENT is only working on paper 2 so we no longer wait for that stage. You have already reviewed the "interventions" section and commented. Were you happy with the conclusions I wrote? Many thanks, Lesion (talk) 15:34, 30 December 2013 (UTC)
@Lesion: Ah, alright, I was going to look into the statistical methodologies of the various refs for comparisons, but that might take too long. Even so, I can still comb through all the stats in the paper today just to make sure everything is sound. As for the interventions conclusions, the conclusions that were based upon statistics were all sound since the hypothesis test results supported them. I didn't see anything even slightly unusual/off when I checked the section, so it was good. Beyond the statistical component (and checking for typos ), I can't really do much else since I'm not really familiar with the subject/field. Seppi333 (Insert 2¢) 16:05, 30 December 2013 (UTC)
As you probably have guessed, it was not a systematic review or anything... didn't use any particularly structured method of searching literature. So, considering we spend only one short paragraph on each study, there is perhaps no need to spend time analyzing the methodology of each... Main things are: (i) that nothing strange has been said when discussing the studies, and (ii) that the wording of the results was ok. If you have finished your final check just drop me a note. Please feel free to raise any other concerns in the manuscript. Just a notification before publication that you were happy with everything. Thank you for your input. Lesion (talk) 23:10, 30 December 2013 (UTC)
@Lesion: I don't have access to Al-Abassi 2009, but I probably don't need to go through it since any two studies with distinct datasets will have some degree of heterogeneity. So in a nutshell, your heterogeneity statement in that paragraph is almost certainly going to be valid. As for everything else, the stats and the inference from the hypothesis tests all seem ok. I made a comment in the draft about a possible typo with "Al-Abassi et al 2008" under comparison of interventions - not sure if that was intended or not. The only comment I have besides that is that appending "et al" to papers with only one author (like the Al-Abassi citation) isn't necessary, although I don't think it's incorrect to add it anyway. In any event, the stats look fine! Regards, Seppi333 (Insert 2¢) 23:33, 30 December 2013 (UTC)
That paper had almost identical study design to Finkelstien et al. 2004. In fact those 2 studies were the only ones which were closely similar. I can send you the paper if you wish. Thanks for spotting dates and et al error. I don't think supposed to use et al. if there are 2 authors either, since it means "and others" plural. OK great, thank you for final check. I will email you again when submit to journal, hopefully in a day or so. Kind regards, Lesion (talk) 23:53, 30 December 2013 (UTC)
Few comments on style
If there is not controversy between high quality sources one can just state the facts. One does not need to preface it with "A Cochrane Review" Of "A study in the BMJ".
Would typically try to summarize the sources rather than quote them
Generics do not need capitals.
The article could use some simplification. Wording is currently a little complicated.
Do all 7 of the refs support the last sentence of the lead? More than 2 or 3 refs is often a red flag. I would simply you the two best sources. Doc James (talk · contribs · email) (if I write on your page reply on mine) 13:36, 6 January 2014 (UTC)
Eh, after the first commenter in the amphetamine FA review complained about how refs in the lead made it hard to read (first bullet), I moved them to the end of the paragraph instead of by sentence. I cited only the 1st sentence of the lead besides that, just because I think stating something is a neurotoxin upfront is a bit contentious. I can put them into notes or distribute them if you think it looks better.Seppi333 (Insert 2¢) 13:40, 6 January 2014 (UTC)
So technically per WP:LEAD you do not need refs in the lead as long as it is supported by the body of the text. What I do however (as people will tag the article with cs tags if you don't) is add hidden refs like this <!-- Ref here -->
Per the references guidelines the refs should be behind the sentence they support not at the end of the paragraph.Doc James (talk · contribs · email) (if I write on your page reply on mine) 13:52, 6 January 2014 (UTC)
Anyway I disagree with that advice you have received at the FA for amphetamine and would recommend you switch it back and do the above :-) Doc James (talk · contribs · email) (if I write on your page reply on mine) 13:56, 6 January 2014 (UTC)
@Jmh649: that's a good idea. I'll do that with meth's lead citations before I GA-nominate it then. I'm going to wait and see what the commenter in the FA review thinks - assuming he ever replies. Otherwise I'll just do it on amph anyway.Seppi333 (Insert 2¢) 14:03, 6 January 2014 (UTC)
Also per image sizes, usually they are left at default or given a fraction of default per [2] This allows registered users to set how large they want to see them rather than forcing a specific size upon people. Some many details... Doc James (talk · contribs · email) (if I write on your page reply on mine) 14:05, 6 January 2014 (UTC)
@Jmh649: normally I'd just use thumbs and do that, but since all but 2 images (the free base and the structure of lysdexamfetamine) in the body are diagrams, their usefulness is a bit limited unless they're displayed at a size that they can be viewed normally and read. At 300px, some of those would be pretty difficult to read - especially the one in pharmacodynamics. Seppi333 (Insert 2¢) 14:11, 6 January 2014 (UTC)
Yes some may be of sufficient important to require stretching across the entire screen. This may however give some undue weight IMO. Just something to keep in mind. Doc James (talk · contribs · email) (if I write on your page reply on mine) 14:15, 6 January 2014 (UTC)
You are seriously impugning the man's character. Do you have any good evidence to back up your assertion that he is likely to or is the kind of person who would doctor the data in a publication? --Anthonyhcole (talk · contribs · email) 19:03, 11 January 2014 (UTC)
@Anthonyhcole: oh. Meh, I don't really care about removing it tbh - I was being the peanut gallery. Even so, you'd be surprised how often researchers screw up their stats. Though something blatantly spurious like that does make me raise an eyebrow. I also don't have qualms with making a charge like that. Seppi333 (Insert 2¢) 19:32, 11 January 2014 (UTC)
Arrgh. I've seen some atrocious statistical work in social neuroscience. There was a scandal a few years back around this article. The authors excoriated a couple of research teams over their assignment of correlation without adequate statistical power. The paper was originally named "Voodoo Correlations in Social Neuroscience". It tragically, in my opinion, sank the entirety of one paper, despite the statistical error affecting only part of it. The sound part of the study supported the overlap of physical and social pain (rejection) in the brain.
Hi there, I'm pleased to inform you that I've begun reviewing the article Methamphetamine you nominated for GA-status according to the criteria. This process may take up to 7 days. Feel free to contact me with any questions or comments you might have during this period. Message delivered by Legobot, on behalf of DendroNaja -- DendroNaja(talk)23:50, 24 January 2014 (UTC)
logic
I cannot resist. I am on your side, but this is too much fun. He is ACTUALLY wrong, not logically wrong, basically because most circumcisions are USA plus Islam, and Islam is not the vast majority of the sum. That aside, I will take his side deductively on two points. First it was MY reference, and pinning it on him when he only used it to refute me is at best a rhetorical point, which seems common on WP. As for the remainder of your point:
the vast majority of circumcisions practiced in the world are due to religious and cultural reasons
The existence of a cultural region where your statement is not true (i.e., the % of population citing medical reasons is greater than cultural reasons) constitutes a logical contradiction with your statement (i.e., the statement needs to be qualified to particular regions in order to be true, since its validity is conditional upon geography).
He said (most X are Y) is true for the set of all X
You said (most X are Y) is not true for all subsets of all X.
He did not make a deductive fallacy. You just wore him down.
@Bob the goodwin: Yeah...I realized that while writing a formal proof of the argument, though you probably noticed I tweaked my argument slightly to account for how his statement could cover subsets of the population in 2 distinct cases when I wrote that proof. =P By that time, I also knew he wouldn't really catch/follow it, so... hehe. Seppi333 (Insert 2¢) 08:35, 25 January 2014 (UTC)
ADOS
...and in all honestly I have to say I jacked it from someone else in turn. The kitten however, remains nonreturnable ;p Lesion (talk) 09:33, 25 January 2014 (UTC)
Wow, what a lot of comments have been added since I looked last! Please keep up your effort; I'll try to do my bit when I've got some more leisure. Cheers --ἀνυπόδητος (talk) 14:15, 19 January 2014 (UTC)
Sorry to see the nomination has been closed. Do you intend to fix the remaining issues? Actually, what are they? I'm a bit overwhelmed by the amount of discussion added meanwhile. If you point me to the problematic points of the article, I might be of assistance. Cheers, ἀνυπόδητος (talk) 13:45, 25 January 2014 (UTC)
@Anypodetos: There wasn't any issue that wasn't addressed at the time it was closed... =/ I think they just don't like having old FAC's lingering on the page so they closed it. I'm frankly kind of annoyed by it. I intend to open another FAC for it once the mandatory 2 week renomination block has passed.Seppi333 (Insert 2¢) 13:54, 25 January 2014 (UTC)
Quite unexpected. I was for promotion, and my questions/comments were not conditions, but rather suggestions on where the article can be improved. Should I have mentioned that within the discussion? The Sceptical Chymist (talk) 23:57, 2 February 2014 (UTC)
@The Sceptical Chymist: I think the main issue is that it just didn't have enough supports at the time it closed. Your feedback was definitely both rigorous and comprehensive (and rather helpful IMO), so I think your review was fine. I'm going to reopen a new amphetamine FAC in two days (Feb 5th) and ask several individuals who're familiar with parts of the subject to do a review; consequently, I'll probably be able to gather enough reviews when the nomination closes this time around.
I think the FAC coordinators take into account supports/reviews from recent prior FAC nominations, but if you want to reaffirm your support or offer additional comments in the second FAC, it certainly wouldn't hurt (it could help, depending on what the closing FAC coordinator thinks). Also, thanks again for all the feedback you provided in your first review. I know comprehensive reviews take a bit of time, so I appreciate the effort you put into it. Seppi333 (Insert 2¢ | Maintained) 05:55, 3 February 2014 (UTC)
Thanks! Wasn't too difficult since I had amphetamine to serve as an outline - and several sections I just copied from amphetamine (although I rewrote them to make the pages look different) and cited the Desoxyn Rx info instead of the Adderall one, hehe. Boghog did the synthesis section because I'm an idiot when it comes to chemistry (I didn't take a college level chem course, just lots of physics). I am learning as I go along though. ;P Seppi333 (Insert 2¢ | Maintained) 17:32, 3 February 2014 (UTC)
Why was the page that was previously "Amphetamine mixed salts" changed back to Adderall? We had a long discussion about that had and it changed the other way in the past year. Exercisephys (talk) 01:09, 29 January 2014 (UTC)
Honestly, I don't see the justification for the move, and I really which you would let me know before reverting major changes that I spent a lot of time on. I don't think we should use a brand name for a medication that is primarily prescribed as a generic. Exercisephys (talk) 04:04, 30 January 2014 (UTC)
I think that it should be listed under a generic name like every other non-historic generic drug on Wikipedia. Do you have a preferred place to publicly discuss this? I'm not trying to be a jerk, but I really don't see the reason in listing it under "Adderall".
I should add, as someone who has worked in an American pharmacy, that it's filled by default as a generic under the name "amphetamine salts". Additionally, I think the best precedent for this is Ritalin. The brand "Ritalin" is probably more ubiquitous than "Adderall" and (unlike amphetamine) no one knows what the hell methylphenidate is. Regardless, the title of the article is methylphenidate. Exercisephys (talk) 15:46, 30 January 2014 (UTC)
Hey! This is just a little note to say, "Thanks for all your hard work." And while I'm at it, here's another one for your work on the Amphetamine article:
It's always nice to see Wikipedians improving high-traffic articles that people clearly read and care about. Hopefully, these awards act as small tokens of my and others' appreciation.
Hi... I notice that you uploaded the File:Catecholamine and trace amine biosynthesis.png – nice job! I was wondering if you might make a couple of tweaks? The vertical bonds to the carboxylate groups in the structures on the left should point to the C-atom not to the O-atom. Similarly in the structures on the right, the bonds to the NHCH3 should point to the N-atom and not the C-atom. I suspect that both the NHCH3 and CO2H groups are aligned centre when they should be left-aligned. Thanks. EdChem (talk) 05:11, 30 January 2014 (UTC)
Addendum... also the hydroxyl groups on the ethyl chain, the bonds point between the OH instead of at the O-atom. Thanks for the quick response. EdChem (talk) 05:15, 30 January 2014 (UTC)
Hi Seppi. As promised, I have been working to expand the synthesis section of the amphetamine article (see amphetamine sandbox). I know you were planning to redo the graphics but I needed to create new graphics to match the text I was writing. I hope you don't mind. I was also planning to redo the methods 1, 2, and 3 in the "Amphetamine synthesis routes" graphics to match the style of the other graphics in this section. How does it look so far? One worry I have is that the section is becoming too long and some reviewers seem to be allergic to organic chemistry ;-) I was not planning to expand it any further and the present version may need to be trimmed somewhat. Thoughts? Boghog (talk) 06:52, 24 February 2014 (UTC)
@Boghog:No problem on the graphics! I was just going to do that part to take some of the workload off of you, but if you have time to do that, you'd do a better job than me. :P
Looks good so far; depending on the number of graphics in the final version, I might organize it with {{multiple images}}, but I'll wait until you've finished to worry about the layout. Just for consistency with the rest of the amphetamine page, the synthesis would need citations to each sentence, though I could probably do that part easily enough after you've finished. I really appreciate all your help with the chemistry-related content btw. Seppi333 (Insert 2¢ | Maintained) 07:02, 24 February 2014 (UTC)
I have redone the all the graphics so that they are use a consistent style and merged all the graphics into one template. While the cited review articles in turn cited all the synthetic routes contained in the section, I have also added citations to the primary literature for each of the reactions. Unfortunately the graphics now spill over into the next section (I have included the history section in the sandbox just to see how this would look). This is a general problem most synthetic review articles have. I could work on expanding the text to reduce the spill over, but the text is already probably detailed enough for a general article about amphetamine. Thoughts? Boghog (talk) 19:06, 24 February 2014 (UTC)
Thanks for adjusting the images. I have made a number of additional edits and I think it is ready to be inserted in the article. Thoughts? Boghog (talk) 21:33, 25 February 2014 (UTC)
What do you think about a supplementary section "harmful/toxic impurities/byproducts of clandestine preparation"? --Hm20 (talk) 16:14, 26 February 2014 (UTC)
I can help with that. I use Photoshop CC (CS6). If you'd like to collaborate, I'll make up a diagram similar to the one in the link then we can figure out how to include the information from your's in a manner that is intuitive to a layperson. Does that work for you? Ian Furst (talk) 22:48, 26 February 2014 (UTC)
I gotta confess, I am new to this and don't have time/patience to figure out this cryptic interface to get a message posted.. hope this is okay.
I have issue with first part of the Methamphetamine article. It fails to cite source for the "opposite of amphetamine" statement on neurotoxicity: "Entirely opposite to the long-term use of amphetamine, there is evidence that methamphetamine causes brain damage from long-term use in humans". This statement is without citation and suggests a hint of bias, as it needlessly compares this one drug to another. My personal experience is that both of these drugs are equally dangerous. To say that one is more harmful by a particular measure is fine, but I do not believe that any of these classes of drugs should be presented as being more or less dangerous than the others. If the statement is true, let's cite the source. Otherwise, I submit that it should be deleted.
I am no fan of meth, but I am also very sensitive to seeing misinformation about it. It is very important that information be correct and verifiable, else doubt may be cast on the rest.
Another time, please don't use a dummy edit to make a comment. Such comments are appropriate for the talk page. Further, it is not unlikely that the editor is not done editing. The part of my edit summary that said "revert and restore valid diffs" implies that I will be making at least one more edit. Your making such a dummy edit forced me to resolve an edit conflict. Even though your edit was just adding a space, it caused additional work on my part for a not very good reason. I would not have had as much of a problem with your doing so, if the only thing that I had reverted was your use of User:Ohconfucius/script/MOSNUM dates. Looking up the article history to determine which date format should be used did not take that long. I had already done so prior to reverting your edit. However, there were changes by Citation bot which I also reverted, and I was attempting to decide the best way to resolve getting the good parts of that edit back in the article without the munged authors which it has been putting in every edit I have seen it do in the past couple of days (only looked at those that hit my watchlist).
I appreciate that you desired to have the dates in Nootropic be consistent. In doing so, it is appropriate to go through the history of the page to determine what format was used first (see WP:DATERET). The history page has a link to show the oldest edits. In most cases is it easy to just pick the first and the last, maybe the middle (or a binary search) on that page of the history. Doing so usually shows enough information to determine which format was used first. In some cases, a more detailed effort is required. — Makyen (talk) 05:57, 24 March 2014 (UTC)
@Makyen: Whenever that occurs, click the text box, hit ctrl-a, ctrl-c, highlight the entire existing article, and paste the contents of your clipboard over it. That will circumvent the need to fix a dummy edit. Even so, that edit summary didn't seem to suggest to me that you were making another edit. Seppi333 (Insert 2¢ | Maintained) 06:03, 24 March 2014 (UTC)
Resolving the edit conflict, once I determined that it was a dummy edit, was relatively easy. It was, of course, just copy and pasting. However, I have to take the time to determine what edits were made because I can not assume that the edit is just a dummy edit.
Yes, you changed 4 dates from mdy to dmy and I changed 5 from dmy to mdy. The significant majority of dates were YYYY-MM-DD or malformed. If something is that close, then it is a good idea to go back to determine the format of dates first placed in the article. Unfortunately, date formats are something that people people will change back and forth. If it is at all unclear it is best to go back to the most basic test which is the first date entered in the article. If the article has organically grown to be 50-1 uses in the other direction, that is a different story. Finding the first use and explaining it in the edit summary can prevent edit skirmishes in the future.
I see that you have changed date formats on several articles. In your edit summaries, you claim that your edits are "per WP:MOSNUM". However that guideline does not support your edits. MOS:DATEFORMAT indicates that the style "2001-08-22" is suitable for references.
If you wish to undertake stylistic formatting changes throughout a whole article, you should discuss this on the article's talk page first, especially when the article is a featured one. Axl¤[Talk]15:57, 24 March 2014 (UTC)
@Axl: If you look through my edits, I actually changed a minority of dates by selecting the majority style, unless it was a malformed one. The edit summary "date formats per WP:MOSNUM by script" was from a script. Anything that followed that was my edit summary. Almost none of our FA's had consistent dates. That means they'd all fail at that FA criteria. I made them consistent, and chose the dominant format (DMY or MDY) of the two current variants that have "use XYZ dates" templates. YMD apparently isn't MOSNUM, but unfortunately, a lot of older refs use YMD. Seppi333 (Insert 2¢ | Maintained)
Before your edit to "Lung cancer", there were eight access dates in the format "yyyy-mm-dd", two with the format "Month dd, yyyy", and only one in the format "dd Month yyyy". Journal dates are typically in the format "Month yyyy". Axl¤[Talk]13:07, 27 March 2014 (UTC)
(Sorry about the late reply.) You seem to be taking this personally. This is just a simple disagreement between two editors—this isn't about you. We both know that you're a great editor. Moreover, if you don't "give the slightest iota of a fuck" about the format, why should you give a fuck about the opinion of some random faceless guy on the internet? That's the approach that I take when editing disagreements start to stress me.
@Axl: You're right - I owe you an apology for coming off aggressively like that; sorry. I became frustrated from the repeated allusions on WT:MED to the incident where a dispute arose over the specific format used. My concern is/was really only consistency, regardless of format, in our FAs due to the FA criteria regarding consistent ref formatting. My reasoning for doing it was my judgment that it's better to fix the FA criteria errors in our FAs and bypass a consensus than to get tied up in talkpage discussions about who prefers what date format for each article where there was no dominant format.
As for the particular article you mentioned, I'd have converted the dates to the YMD format in that article if the script provided an option for that; unfortunately, it's the only date format that it doesn't include. It would've taken me too much time to manually convert the dates in the 5-10% of articles which had inconsistent citations and YMD as the most prevalent format. I don't plan on changing the dates in other articles in case you're concerned about that. Seppi333 (Insert 2¢ | Maintained) 06:48, 9 April 2014 (UTC)
I agree with you that a consistent formatting style is preferable. I am not convinced that one specific style is better than another. I was not aware that your script makes it easier to use one particular style.
My suggestion would be to post a note on the article's talk page prior to making the edits. Propose to change the dates to the new consistent format, perhaps something like: "The access dates in the references have different format styles. I propose to change all of these to the format: dd month yyyy." Then give it a few days to see if anyone objects. The featured articles tend to be watched quite well. If there are no objections, make the change.
With specific regard to "Lung cancer", if you had made this proposal on the talk page, I would have asked "Why not make them consistent with the current prevalent style: yyyy-mm-dd?" You would have informed me that your tool only supports certain formats. With that knowledge, I would not have objected to your proposal. Axl¤[Talk]11:22, 9 April 2014 (UTC)
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It's my understanding that edit disagreements are best discussed on the talk page of the site where the edits are occurring. Are you OK with that approach? If so I'll leave you a note on the Ghrelin talk page for your response. Thanks.
Thanks for the quick response. Two questions for my education: 1) do I keep this response at the margin, or indent (::) under your response? 2) have you ever taken part in arbitration re an inability to resolve a difference over an edit? If so, could you give me a word or two about the process?
I've just found the WP:BRT page which answered all my questions about the process, so I'll retract my question asking you to explain it. Unless you have any useful anecdotes from you personal experience from being involved in it.
BRT says I should revert your edit back to mine, then have the discussion on the talk page, but I'm going to leave yours there for now. Plenty of time to talk!
I'm back to talk more about your recent edits to Ghrelin. I would still prefer to chat with you a bit more here, and if we don't come to an agreement at some point, we can take the discussion to the Ghrelin talk page and get an Administrator involved to choose.
The first issue is to describe Ghrelin as a neuropeptide. My reading tells me that that designation is reserved for peptides made by neurons. Since the ghrelin cell is not a neuron, ghrelin is not a neuropeptide. Ghrelin is certainly a peptide, and the receptor is certainly on a neuron, but that does not make it a neuropeptide. If you think I am wrong, would you provide me a reference addressing this?
The second issue is that ghrelin cells are found in the CNS. Certainly ghrelin receptors are found in the CNS, but I find no references that the cell is the CNS. The citation you linked to this doesn't mention CNS ghrelin cells in the abstract (I don't have access to full text).
So similar request: if you think I am wrong, would you provide me a reference addressing this?
Thanks for "retracting" the produced in the CNS part. Before I saw the changes you made, I was coming here to tell you that I think I am wrong and you are right re whether it is a neuropeptide! Purely by accident, I was reading about gastrin: secreted by the gastric G cell, a peptide that has a receptor in the CNS - identical situation to ghrelin, and that author referred to gastrin as a "neuropeptide"! Now I see that of the 3 papers you cited to me, two said it is a neuropeptide, a third said it acts like a neuropeptide. The third one is probably anal like me and is being a literalist. I'm thinking "acts like a neuropeptide" is a great compromise, but I'd like to change the wording a bit and see what you think. If you don't like it, we'll keep talking.
IiKkEe (talk) 22:19, 8 May 2014 (UTC)
Two more issues. One, are you really OK with my parenthetical description of what is the function of the VTA? I think the chemical addiction part is OK but I really don't know about the sexual desire part. Delete that part, modify it, or leave it as is? I hope you 'll make the last call on that or I'll need to do some reading.
Two, Boghog left a note on the talk page about 2 sentences he wanted in the lead that I had placed in the Structure section which I completely rewrote. I deleted them 2 May, he reverted 2 May 06:36. I deleted, not realizing he put them back. He reverted 4 May 07:25, I deleted 07:29, he reverted 09:58. I was in the middle of a complete rewrite of the lead, and didn't realize he was reverting. I just thought the system was not accepting my deletions. Then I saw the message on the Talk page. I rewrote his first sentence for word economy and clarity, and he didn't revert those changes, so I assume he's OK with it as is. Now that the that I have expanded and rewritten the rest of the lead to the point I think it is "perfect", it's time to discuss these two sentences.
You added a concurrence with his wishes on the talk page at the time. Now that the lead has been updated and expanded and the Structure section has been expanded to include the info in these 2 sentences, do you still think these should be included? I think they are minor facts not of sufficient importance to make the lead - especially the second sentence which is not really about ghrelin, rather the parent molecule. Just interested to know your position before I negotiate with him, so I know if I am discussing this with one or two who see it differently. If he still thinks they belong, we can move on to arbitration by an Administrator. Since its just personal preference, it shouldn't be too painful if I lose!
I noticed on your user page a rating system for such articles. If this is part of your WP interest, would you as time permits read Platelets, Leptin, Ghrelin, and Essential thrombocythaemia and see if their is sufficient improvement with recent edits to warrant a review for potential rating upgrade?
If that's not one of your interests, or you review them and think the current rating is appropriate, please let me know and I'll accept your judgment and move on!
Hi Seppi333 -
Because of your addition to the Ghrelin lead re its effect on the VTA, I am suspecting that you have some knowledge and interest in the VTA. I am pasting a comment here that I left on the VTA Talk page a few moments age, and would like your response if I guessed right about your involvement with the topic: respond there or on my User talk page if you are so inclined. Am I anywhere close to right?
"As I understand it, the VTA is the brain center that allows human beings to become addicted to all the drugs listed; to food; and to become addicted to sexual intercourse, masturbation, viewing pornography, sexual stalking, sexual possessiveness, sexual rage, sexual violence, rape, and murder.
I understand that the mechanism for this is that with increasing intensity and frequency of sensory input to the VTA from the above stimuli, repetitive dopamine assaults on the dopamine receptors in the VTA cause a compensatory reduction in their number in order to modulate the response; so that the next comparable "dose" of input results in a lesser "reward" ; or restated, a greater input is required to create can comparable intensity of satisfaction. More and more input creates ever lesser gratification, and withdrawal creates intense cravings. If the "inputs" are readily available, the result is addiction.
The evolutionary advantage of the VTA to early humans was that because food and sex were extremely difficult to obtain, there was survival value for a neural mechanism promoting these intense behavior seeking desires. But now that in modern society food, sexual stimuli, and addicting drugs are readily available to us all, the presence of the VTA, which used to promote survival, now creates antisocial and self destructive survival-averse behavior. In other words, it explains most of the woes of the modern world.
I have no references to any of the above at my fingertips. I will leave this here for a few days to see if there are any comments, reactions, or corrections. If not, I will add the above three paragraphs to the lead."
The VTA is really more of a communication node in DA pathways than the structure responsible for those things. The nucleus accumbens is the primary brain structure involved in addiction and sexual arousal. The VTA is interacts with the nucleus accumbens as part of the mesolimbic pathway. I'll copyedit that text on the Ghrelin page when I have some spare time and relevant sources for it. Seppi333 (Insert 2¢ | Maintained) 00:50, 13 May 2014 (UTC)
Nootropics
Hello! I saw the template. Are you still working on the article? A few days ago, at the Romanian Wikipedia, we started our own work on the article. Perhaps we could help each other. Regards, Wintereu (user talk) 23:43, 9 May 2014 (UTC)
I notice you re-added the AfD notice to this page; I removed it as it was improperly added without a discussion page and it was unclear whether an AfD or Prod was meant. After I explained this here it was accepted by the editor posting the notice. I don't want to edit war over this so won't revert you but it can't be left in this state.--JohnBlackburnewordsdeeds16:29, 24 May 2014 (UTC)
Dear Sep333, I noticed you made some changes in Statistics recently. I haven't incorporated your changes in my new version, please be aware that this is unintentionally, since I was working from an earlier version of the article. I'll try if I can easily insert your recent changes either today or later this week. Marcocapelle (talk) 20:04, 26 May 2014 (UTC)
Diffs are listed from oldest to newest, dates are in UTC
15:36, 24 May 2014 (edit summary: "Reverted 1 edit by JohnBlackburne: WP:AFD and WP:PM are distinct/disjoint processes. Also note the "Please do not remove or change this AfD message until the issue is settled" text. (TW)")
22:18, 28 May 2014 (edit summary: "Expanded the existing intro without removing anything on the page to once again...cut the POV fork. Leaving the coatrack for npov noticeboard")
This looks to be seven six reverts since 24 May. Please agree to wait for a talk page consensus before reverting the article again. This will help to avoid any admin action. Thank you, EdJohnston (talk) 02:46, 29 May 2014 (UTC)
Amended my report to show six reverts. The article once again contains some <onlyinclude> code that John Blackburne had removed, so if you want credit for a self-revert you should do it fully. I doubt that you have any consensus for this change. EdJohnston (talk) 03:09, 29 May 2014 (UTC)
@EdJohnston: The net change of what was displayed on that page was only an addition of content. Are you suggesting I need consensus to add material to Wikipedia? In any event, see talk:statistics if you care to know about the current state of that page. Seppi333 (Insert 2¢ | Maintained) 03:14, 29 May 2014 (UTC)
I don't know his reasoning for wanting to retain the page, but my concern is primarily about keeping the page summarized on or fully contained in statistics (or not exist) instead of exist as a POV fork suggesting they're distinct fields. Seppi333 (Insert 2¢ | Maintained) 04:59, 29 May 2014 (UTC)
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Hi, Seppi333. I shall have some spare time this week. Is there an article that you would like me to look at? Axl¤[Talk]11:45, 2 June 2014 (UTC)
@Axl: Sorry for the late reply! My laptop broke a week and a half ago, so I haven't been on wikipedia lately. There was/is no article that I need assistance with, but thank you for offering to help – I appreciate it! Seppi333 (Insert 2¢ | Maintained) 18:55, 13 June 2014 (UTC)
Hi from Wil
Howdy, I was wondering if you have ADHD yourself. Although I've had many good experiences on Wikipediocracy, I just had a very tough one when I mentioned ADHD. If you can believe it, everyone was uncomfortable talking about it, accused me of somehow hiding (what, they didn't specify) behind it, or refused to believe there was anything good about it. I've run in to the first two many times, but the third was new to me. In any case, every bad experience is an opportunity to build better ones, so I decided to go on-wiki to meet other ADHDers. I know that WP is a reference work and is not intended to convince anyone of anything or debate conflicting viewpoints, but I figured I'd go through some of the more common disorders and make sure that they contain solidly referenced descriptions of the some of the more prevalent gifts that are highly correlated with many disorders, starting with ADHD. Would love to see you drop by on my talk page, too. I hear some of the most influential Wikipedians hang out there, tho some for all the wrong reasons. I'd like to think that they're increasingly showing up for better ones. Hope to run in to you again soon. ,Wil (talk) 23:34, 15 June 2014 (UTC)
@Wllm: Hi Wil. I do, but I don't believe it's a necessarily a handicap. The ADHD article is actually quite well referenced and has a large number of medical editors watching over it to maintain article quality (i.e., edits that fail to satisfy the WP:Good article criteria, WP:MEDRS/WP:MEDMOS, or WP:POV are almost always reverted immediately). Content changes are often discussed on the talk page first as well - Talk:ADHD. Seppi333 (Insert 2¢ | Maintained) 00:40, 16 June 2014 (UTC)
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I wanted to be sure you were aware that you have been mentioned in several posts made by the IP-hopping Telus customer from Edmonton, Canada (75.15x.xxx.xxx) who sometimes signs their posts "Bohgosity BumaskiL," and who intentionally uses peculiar spelling ("iz", "haz"). I am sure you know who I am talking about. In particular this editor has mentioned you:
In this section on the User Talk page of administrator Jehochman
In this section on the User Talk page of administrator Steve_Smith
In this section on the User Talk page of administrator Qwyrxian
This editor has neglected to provide you the courtesy of a {{ping}} when making these posts; that is why I am bringing it to your attention here. The editor may have mentioned you to other administrators but used different IP addressed that I haven't tracked down here.
@Zad68: Thanks for the notice Zad; I appreciate it. I'm not really concerned about what he's doing though. He's within his right to troll talkpages with illiterate writing if he wishes, and I'm within my right to be a WP:DICK and express my disapproval (e.g., my sarcastic Facepalm ) of his asinine behavior. Until he stops his mockery/trolling with the intentional use of broken English, I'm probably not going to level with him. Fortunately, TPG gives me autonomy to delete his irrelevant warning notices if he intends to continue spamming my talkpage with them. Seppi333 (Insert 2¢ | Maintained) 02:57, 14 July 2014 (UTC)
Dextroamphetamine article
Hi, I noticed you removed all the references from the lead section of the dextroamphetamine article and I'd like to know why. I understand you pruning the information about side effects as I will grant you it was a bit too long so I understand that sort of pruning, I also understand that I did in fact get the pharmacology wrong as I was misreading the journals and their results, but I do not understand why you cut all the references out that I had placed in the lead, after all they were secondary sources which permitted and even favoured by WP:MEDRS. After all Wikipedia is never going to be respected as a high-quality source on its own, hence the fundamental need for verifiability, hence I think at least some of the major points in the lead, like its use by the military, its medical uses and its pharmacologic action needs referencing. I understand cutting the reference number for each point (like its military use, medical use and pharmacology) down to say one review article, but I do not understand why they should be cut entirely. I read the lead guideline and it didn't make any argument against referencing so long as they do not clutter the lead. I do understand also that you moved those references to the pharmacology section, but I fail to see the harm of citing these references in the lead as well. Brenton (contribs · email · talk · uploads) 20:37, 18 July 2014 (UTC)
@Fuse809: We can include them if you want - I'm just trying to keep the lead citation standard consistent. All the other articles currently use either no citations (e.g., methamphetamine) or a paragraph endnote style like amphetamine. The lead doesn't require citations because it's essentially just supposed to summarize the article content which should be cited. But again, I'm not opposed to it - it's just simpler in the short term because citing the lead requires going through the whole article to pick out relevant refs that were already used. For consistency, it just needs to have the references contained in a [sources #] tag using the {{#tag:ref| place-references-here |group="sources"}} wikicode placed at the end of each paragraph. Seppi333 (Insert 2¢ | Maintained) 20:54, 18 July 2014 (UTC)
Sexual Addiction edit
Hi Seppi333, I'm curious about your edit to the Sexual Addiction article. Your comment is that the Neurochemical Theory is outdated and conflicts with subsequent info in the article in level two. First, where is the conflicting info -- I don't understand what you're referring to by level two. Since the section you've edited is a list of prevalent theories, how could there be conflicting info -- is it that this isn't an existing theory? Also how is the neurochemical theory outdated? As I understand it, this is a major prevailing theory for explaining sex addiction. I think probably this information should remain, but I wanted to reach out to you for an explanation of your reasoning first. TBliss (talk) 19:56, 11 August 2014 (UTC)
Hi TBliss, there's a large amount of neuroscience/neuroimaging research supporting the role of ΔFosB in sex addictions, but I'll do my best to summarize the key points. The role that ΔFosB induction in the nucleus accumbens (NAcc) plays in addiction isn't theoretical; it's been experimentally demonstrated (via viral vector-mediated gene transfer experiments) as being a crucial element in the pathological signaling cascades involved in virtually any form addiction. This is mentioned in nearly every citation on the FosB page. ΔFosB is essentially a bottleneck in these cascades (as illustrated in the diagram below), so the overexpression of that factor alone is sufficient to induce addictive disorders. This human-relevant literature review, PMID 21459101, which is entirely on non-drug addictions, points out that natural reinforcers induce ΔFosB in the NAcc; so in a nutshell, with chronic acquisition, they all have the capacity to produce pathological signaling cascades which result in a behavioral addiction. This is also stated in numerous references on the FosB page.
In regards to the section I deleted, merely stating that the neurochemical component is a theory contradicts the whole section on ΔFosB, which covers experimental evidence. The text in the section I deleted was cited by a reference that was 30 years old and mentioned a defunct concept (an "adrenaline rush") which couldn't possibly mediate reinforcement effects. People don't abuse epinephrine pens or NRIs because excessive α/β-adrenergic activity in the central nervous system feels just plain awful. The role of dopamine in reinforcement neurotransmission has been in medical literature for at least a couple decades (e.g., there were about 100 papers published between 1970 and 1990 which are relevant to humans and that include the terms "dopamine" and "reinforcement"), so it was very outdated information.
What I meant by level 2 header was the section heading that uses the "==Section title==" in the source code. The number of equal signs included determines the HTML heading level for that section. As an example, this talkpage section has a level 2 heading, while "User talk:Seppi333" at the very top of this page appears with a level 1 heading.
With all that said, I mentioned previously on the talkpage that amphetamine and sexual reward produce nearly identical signaling cascades to induce NAcc ΔFosB, but I didn't provide any explanation or reference of this. This recent paper - http://www.jneurosci.org/content/33/8/3434.full.pdf - investigated the interactions/relationship between amphetamine reward and sex reward (or just amphetamine and orgasms) and literally states outright in the abstract that the two posses very similar cascades (act on similar mechanisms). This is perfectly consistent with what is observed in human neuroimaging studies with amphetamine and orgasms. The addiction-related pathway that amphetamine acts upon is the mesocorticolimbic pathway, which includes ventral tegmental area, prefrontal cortex, and nucleus accumbens. Not surprisingly, reviews of neuroimaging during human orgasms (see review 1 & review 2) show that all three of these structures have increased activity during sex, and in the NAcc during orgasm, due to increased neurotransmission of dopamine along the associated pathway. So, in a nutshell, that basically means that the post-synaptic signaling cascade in the NAcc resulting from excessively frequent orgasms or amphetamine abuse looks like this.
Large diagram illustrating the psychostimulant (and orgasm) post-synaptic addiction cascades
This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamateco-release by such psychostimulants,[4][5]postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[4][6][7] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors;[4][8][9]c-Fosrepression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.[10] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process.[8][9] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[8][9]
^Lindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends in Pharmacological Sciences. 26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID15860375.
^Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". European Journal of Pharmacology. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID24374199.
^ abcRenthal W, Nestler EJ (September 2009). "Chromatin regulation in drug addiction and depression". Dialogues in Clinical Neuroscience. 11 (3): 257–268. doi:10.31887/DCNS.2009.11.3/wrenthal. PMC2834246. PMID19877494. [Psychostimulants] increase cAMP levels in striatum, which activates protein kinase A (PKA) and leads to phosphorylation of its targets. This includes the cAMP response element binding protein (CREB), the phosphorylation of which induces its association with the histone acetyltransferase, CREB binding protein (CBP) to acetylate histones and facilitate gene activation. This is known to occur on many genes including fosB and c-fos in response to psychostimulant exposure. ΔFosB is also upregulated by chronic psychostimulant treatments, and is known to activate certain genes (eg, cdk5) and repress others (eg, c-fos) where it recruits HDAC1 as a corepressor. ... Chronic exposure to psychostimulants increases glutamatergic [signaling] from the prefrontal cortex to the NAc. Glutamatergic signaling elevates Ca2+ levels in NAc postsynaptic elements where it activates CaMK (calcium/calmodulin protein kinases) signaling, which, in addition to phosphorylating CREB, also phosphorylates HDAC5. Figure 2: Psychostimulant-induced signaling events
^Broussard JI (January 2012). "Co-transmission of dopamine and glutamate". The Journal of General Physiology. 139 (1): 93–96. doi:10.1085/jgp.201110659. PMC3250102. PMID22200950. Coincident and convergent input often induces plasticity on a postsynaptic neuron. The NAc integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex (PFC), as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses (Goto and Grace, 2005). The converse was also shown to be true; stimulation at PFC potentiates PFC–NAc synapses but depresses hippocampal–NAc synapses. In light of the new functional evidence of midbrain dopamine/glutamate co-transmission (references above), new experiments of NAc function will have to test whether midbrain glutamatergic inputs bias or filter either limbic or cortical inputs to guide goal-directed behavior.
^Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. ... Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain.
^ abcRobison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nature Reviews Neuroscience. 12 (11): 623–637. doi:10.1038/nrn3111. PMC3272277. PMID21989194. ΔFosB serves as one of the master control proteins governing this structural plasticity. ... ΔFosB also represses G9a expression, leading to reduced repressive histone methylation at the cdk5 gene. The net result is gene activation and increased CDK5 expression. ... In contrast, ΔFosB binds to the c-fos gene and recruits several co-repressors, including HDAC1 (histone deacetylase 1) and SIRT 1 (sirtuin 1). ... The net result is c-fos gene repression. Figure 4: Epigenetic basis of drug regulation of gene expression
^ abcNestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clinical Psychopharmacology and Neuroscience. 10 (3): 136–143. doi:10.9758/cpn.2012.10.3.136. PMC3569166. PMID23430970. The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives. ... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure. ... ΔFosB overexpression in nucleus accumbens induces NFκB ... In contrast, the ability of ΔFosB to repress the c-Fos gene occurs in concert with the recruitment of a histone deacetylase and presumably several other repressive proteins such as a repressive histone methyltransferase
^Nestler EJ (October 2008). "Transcriptional mechanisms of addiction: Role of ΔFosB". Philosophical Transactions of the Royal Society B: Biological Sciences. 363 (1507): 3245–3255. doi:10.1098/rstb.2008.0067. PMC2607320. PMID18640924. Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch—from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure
I see you've done something similar in the substance dependence article. While the FOSB stuff looks plausible, I think it's radically oversimplifying things to state that it is the mechanism of addiction, as if the matter was settled beyond doubt, and these massive text dumps go way beyond what's needed.
What would make more sense, and would meet the WP:NPOV requirement, would be a statement on the lines of "Several researches, most notably Dr. X and Professor Y, have put forward the hypothesis that ...", and then point the reader at the FOSB article for more detail. -- The Anome (talk) 23:33, 9 September 2014 (UTC)
I can't put it any more clearly: the reviews you are quoting make clear statements that delta FOSB is implicated in the process of sexual addiction, but other practitioners, equally legitimately, claim that sexual addiction is not actually a real thing. Logically, they can't both be right, and there is thus a legitimate difference of opinion between experts. In this case, WP:NPOV is the only way this can be resolved. -- The Anome (talk) 21:02, 13 September 2014 (UTC)
@The Anome: The distinction has to do with how addiction is being modeled. In the DSM diagnostic framework and the addiction pharmacology paradigm, sexual addiction literally cannot be diagnosed by anything other than an observation of true compulsive behavior. The metrics the DSM uses are designed/intended for drugs, and it ends up being relatively useless for behavioral addictions. If you look up table 1 in the review that cites the giant table I transclude, you'll notice that sex addiction is the exception to withdrawal symptoms of any sort. I excluded that row from the wikipedia table because withdrawal can occur for non-addictive drugs (i.e., it's not entirely useful for determining if a drug is addictive; it's probably useless for determining "addictive behaviors". There's no dependence associated with sex because withdrawal doesn't occur. Tolerance also makes no sense in this context, so it's effectively useless for diagnosis. So, it SHOULD be difficult to diagnose in that framework.
The "reward-reinforcement" framework I mentioned isn't too much more complicated than what is taught in college intro psych classes. An addictive drug is literally defined as one which is both (positively-)reinforcing and rewarding (involves reward center activation). Several behaviors implicated in behavioral addictions, including sex, fit all the characteristics of a being "rewarding" as well as "reinforcing" (the use of these terms comes up frequently in the sex addiction papers). It's a neuropsychological model, and it's much more useful for identifying and determining relationships between addictive drugs (or addictive behaviors, or between the two types) for some obvious and some esoteric reasons. It's also the current basis of clinically identifying what behaviors are addicting, from which a more useful diagnostic framework can be developed. All of this research is simply the foundation for identifying metrics to clinically identify behavioral addictions without them having to become ruinously compulsive before identifying. Established diagnostic criteria (what clinicians use) does not precede the research used in establishing those criteria or identifying the addiction (which is model specific) in the first place.
With that said, the ONLY way an argument in current "debate" could be relevant to this, is if a "clinician" or researcher argues that sex can not result in a compulsive disorder of any kind (as in the lead sentence of addiction, which is accurately defined). It's worth noting that if the term "dependence" is used in an argument to refer to an addiction, the argument model-specific to a distinct paradigm, and therefore not relevant to ΔFosB (the two frameworks have nothing notable in common). If there's current peer reviewed literature (preferably a medical review, but I'd be ok with a primary source that's published by a credible group) arguing that truly compulsive sexual behavior (analogous to the definition in addiction) is not possible, or it argues against the rewarding/reinforcing properties of sex, I'll accept your reworded version involving controversy. Seppi333 (Insert 2¢ | Maintained) 22:17, 13 September 2014 (UTC)
Two things I probably should note as well:
Clinicians don't ever use the research framework of addiction, so I'd be surprised if they make any arguments relevant to it.
If this material actually did conflict with another authoritative body of research, I find it highly highly doubtful that any respectable journal would ever go through with publishing a medical review that makes significant claims without any qualification or coverage of differing viewpoints somewhere in the review. It's called a literature review for a reason. Seppi333 (Insert 2¢ | Maintained) 22:27, 13 September 2014 (UTC)
Highly respectable journals publish all sorts of things, and science and medicine contain many disparate communities of researchers. I think you can say with great certainty that one particular community of serious scientists working in the context of one particular conceptual model of addiction now all agree that what they call "sexual addiction" is certainly correlated with, and quite possibly entirely explained by, FOSB activity. But they are not the only group of people studying sexual addiction. Various groups of equally serious clinicians and psychologists have also studied it from their own perspective, and come up with entirely different conclusions.
You say above "clinicians don't ever use [the] research framework of addiction, so I'd be surprised if they make any arguments relevant to it." That's exactly my point. They are talking in entirely different terms of reference. You might as well say that the reward-reinforcement people aren't talking in terms of models used by clinicians, and that they don't make any arguments relevant to it.
It's not clear who's right, and it's not our position as Wikipedians to say that one group of researchers are right, and another wrong. In fifty years' time, this will probably be settled science. But at the moment, we just have no way of knowing which group is right. We just can't say that molecular biology and neuroscience trump psychology or clinical medicine because one is "real" science and the other isn't. Hence WP:NPOV.
Myself, I'm quite prepared to believe in the FOSB hypothesis, but I think we should wait for the experts in those respective fields to resolve their differences before Wikipedia reports it as uncontroversial fact, and NPOV is no longer needed. -- The Anome (talk) 23:01, 13 September 2014 (UTC)
On review: Actually, I think this is a key insight. The article is called "sexual addiction", but different groups of people use that name to mean entirely different things, and that's why it's hard to achieve a consensus on this. The reward-reinforcement people mean one thing (that thing you make rats do that is found to correlate to FOSB activity when you autopsy them), psychologists another (the thing where people say they're unhappy they're having so much sex, and can't seem to stop), psychiatrists another (the thing that does not appear to have any objective attributes to define it as a real thing, and therefore doesn't "exist" in any meaningful sense), and the moralists another (the thing where someone you disapprove of is having more sex than you are). And the public and popular press are even more confused: it vacillates between "that sexy thing it's tittilating to read about, and here's a picture of an alleged sufferer in her underwear", and "that awful menace that threatens our children". As a result, it's very hard to write a single article on the topic.
Do you agree that this might be the problem here? If so, perhaps one way to proceed would be to put more emphasis on the differences between the different conceptions of the term. -- The Anome (talk) 23:33, 13 September 2014 (UTC)
@The Anome: That's exactly the point I've been trying to make! There's actually little coverage of these topics on wikipedia, which is unfortunate; but, I've been rewriting the addiction section of a textbook that Nestler coauthored, so hopefully I'll be able to put this material somewhere.
This is their definition of addiction.[1] This is a snippet on the pharmacology addiction model.[2] This is a snippet on the reward-reinforcement model.[3] That chapter of the textbook does a very good job at explaining addiction and both models if you're interested in reading about them. Seppi333 (Insert 2¢ | Maintained) 23:47, 13 September 2014 (UTC)
References
^Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–365, 375. ISBN9780071481274. The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
compulsive eating, shopping, gambling, and sex–so-called "natural addictions"– ... these pleasurable behaviors may excessively activate reward-reinforcement mechanisms in susceptible individuals. ...{{cite book}}: line feed character in |quote= at position 120 (help)CS1 maint: multiple names: authors list (link)
^Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. ISBN9780071481274. Familiar pharmacologic terms such as tolerance, dependence, and sensitization are useful in describing some of the time-dependent processes that underlie addiction. Tolerance refers to... Pharmacokinetic tolerance is caused by..., whereas pharmacodynamic tolerance is a result... Sensitization, also referred to as reverse tolerance, occur when... Dependence is defined as an adaptive state that develops in response to repeated drug administration, and is unmasked during withdrawal, which occurs when drug taking stops. Dependence from long-term drug use may have both a somatic component, manifested by physical symptoms, and an emotional–motivation component, manifested by dysphoria. While physical dependence and withdrawal occur with some drugs of abuse (opiates, ethanol), these phenomena are not useful in the diagnosis of addiction because they do not occur with other drugs of abuse (cocaine, amphetamine) and can occur with many drugs that are not abused (propranolol, clonidine).
The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2000), which makes distinctions between drug use, abuse, and substance dependence, is flawed. First, diagnosis of drug use versus abuse can be arbitrary and reflect cultural norms, not medical phenomena. Second, the term substance dependence implies that dependence is the primary pharmacologic phenomenon underlying addiction, which is likely not true, as tolerance, sensitization, and learning and memory also play central roles. It is ironic and unfortunate that the Manual avoids use of the term addiction, which provides the best description of the clinical syndrome.{{cite book}}: line feed character in |quote= at position 171 (help)CS1 maint: multiple names: authors list (link)
^Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 365–366. ISBN9780071481274. The reinforcing effects of drugs can be demonstrated in animals, where rodents and nonhuman primates readily self-administer certain drugs … The strength with which certain drugs reinforce behavior in animals correlates well with their tendency to reinforce drug-seeking behavior in humans.
The neural substrates that underlie the perception of reward and the phenomenon of positive reinforcement are a set of interconnected forebrain structures called brain reward pathways; these include the nucleus accumbens (NAc; the major component of the ventral striatum), the basal forebrain (components of which have been termed the extended amygdala, as discussed later in this chapter), hippocampus, hypothalamus, and frontal regions of the cerebral cortex. Addictive drugs are rewarding and reinforcing because they act in brain reward pathways to enhance dopamine release or the effects of dopamine in the NAc or related structures, or because they produce effects similar to dopamine.{{cite book}}: line feed character in |quote= at position 297 (help)CS1 maint: multiple names: authors list (link)
Excellent! I think we are in agreement about the problem. In regard to the reward-reinforcement model, I think you're spot on -- there really is no serious disagreement that the FOSB hypothesis is the current settled scientific consensus in that specific context. But not everyone is talking about the same thing when they use the term "sexual addiction". I'll put my list below, to invite your comments...
List of possible meanings of the term "sexual addiction" in descending order of seriousness
A specific model of behaviour used by neuroscientists and molecular biologists to describe animal behavior, and therefore also very likely has correspondences to similar human behavior
a term not used as a diagnosis by the psychiatric community, due to lack of non-subjective criteria to diagnose it, and therefore regarded by some of them as completely meaningless
a term used by psychologists to describe a person's experience when they are having more sex than they would like to have, and it distresses them that they cannot stop doing it
a term used by moralists to disparage those who are having more sex than they admit to having themselves
a term used by the popular press to desribe promiscuity, often in a salacious manner
a term used by the popular press to create moral panic
a concept that has no meaning at all to the general public, who have been exposed to any or all of these, and don't know what to think
Note that the first two groups both have science on their side, and both have, from their respective terms of reference, clear justification for their beliefs. The neuroscientists have clearly identifiable biochemical pathways, and animal experiments which meet the statistical standards of proper science. The psychiatrists point to the fuzziness of the human conception of "sexual addiction", which is so far undefined as a clinical entity, because of the absence of any serious evidence that such a thing exists in humans in a way that might meet the serious standards of evidence-based medicine.
Good! We've got our work cut out, though, to make the article reflect this, as it will need a complete refactoring to do it. Sadly, I've got to stop editing for now, but I'll be very happy to work with you over the forthcoming days to refactor the article into a form that I believe will be satisfactory from both of our viewpoints. -- The Anome (talk) 00:19, 14 September 2014 (UTC)
Amphetamine
Hi! My apologies (again...) for not reacting to your ping. I've been more or less off-wiki lately, and I'm of course completely out of sync with your FA review. Anything I can do? Cheers, ἀνυπόδητος (talk) 08:18, 14 September 2014 (UTC)
@Anypodetos: Hey! Thanks for leaving the note; the FA reviewers suggested I contact everyone from previous nominations for any input on the article for feedback. The article is more or less the same since you reviewed it, with exception to the overdose section which has a lot of new content on the mechanism of amphetamine addiction and behavioral treatments. If you have the time, it'd be great if you could do a short review of that at the current FA nomination page; don't worry about it if you don't have the time though! Also, thanks again for your thorough review in the earlier FA nomination! Seppi333 (Insert 2¢ | Maintained) 07:20, 16 September 2014 (UTC)
October 17, 2014
I'm glad to see that you haven't disappeared off the face of the earth. :) Unfortunately, I am really busy with schoolwork at the moment, so I won't be able to take another look at the article or your changes until next Friday, after my second biochemistry test. AmericanLemming (talk) 15:27, 8 October 2014 (UTC)
I don't know how to say this, Seppi, but I've come to the conclusion that I don't have the time to both do justice to the article and keep up with my studies. I would be be happy to pick up the peer review in mid-December once my semester's finally over, if you'd still be interested in working with me. Again, my apologies, but I thought I'd be upfront about it rather than leaving you in the dark. You've chosen an extraordinarily difficult article to try to take to FA status, and the lack of interest from reviewers at FAC recently hasn't helped matters much.
And until somebody (that is, me, since I don't think anyone else will step up to the plate) goes through it line by line, taking it to FAC again likely won't be successful. (BTW, I should mention that I've really enjoyed working with you and would be happy to do so again once I have the time.) Anyway, just a heads up, and hopefully you can find some other articles to improve in the meantime. :) AmericanLemming (talk) 11:04, 19 October 2014 (UTC)
With regards to your good faith edit here[3]. The things that you considered uncontroversial aren't really :) The aerosol vs. vapor discussion can be found here. The "likely small risk" i've changed into something that actually is verifiable from the reference[4] --Kim D. Petersen17:41, 15 October 2014 (UTC)
Thanks for your note. I appreciated your comments regarding the MEDRS issue over at the cannabis or THC page (I forget which one it was) as well, and your work on MDMA. You are clearly a friend of MEDRS, so I'll consider you a friend of mine as well. Keep up the excellent work. Formerly 98 (talk) 23:27, 19 October 2014 (UTC)
I see that you've been active in editing the Neurotransmitter page on Wikipedia. I just wanted to give you a heads up that my group and I are currently updating this page as well as part of a PSYCH course assignment. Edits will continue throughout the current academic semester, so don't be surprised if you see tweaks/edits in the content and format of the page. Any recommendations/suggestions/comments are most welcome, as we're all beginner-level editors here aiming to improve the quality of the information on this page. Thanks! --IDidThisForSchool (talk) 14:23, 22 October 2014 (UTC)
Regarding this edit[5], your comment is WP:OR. The source Durmowicz(2014) which is used as the reference, only uses "dependence", no mention of addiction is mentioned in the source at all. Since "dependence" and "addiction" are different, you cannot override what the medical reference is actually saying. --Kim D. Petersen16:24, 12 November 2014 (UTC)
@KimDabelsteinPetersen: Your comment above this is WP:OR. The preceding and following sentences are WP:OR as well. Luckily none of our comments are in any wikipedia articles, because that's a lot of WP:OR! Just for the record, considering how much I edit the entire suite of addiction/dependence articles (and definition templates!), I'm pretty sure I know all the nuances in associated terminology and models better than you do. Why do you even care, again? Seppi333 (Insert 2¢ | Maintained) 16:54, 12 November 2014 (UTC)
Since you state that you edit within this topic, then i'm curious as to how you defend strengthening the language of a source as an editor. Once more: Durmowicz does not refer to addiction, even a single time within the whole body of text. On the other hand Durmowicz uses the wording dependence 3 times. Dependence != Addiction. You may yourself think that Durmowicz really means addiction, but as a Wikipedia editor you are not supposed to make your own conclusions. Please adhere to the source, not your personal interpretation. --Kim D. Petersen17:00, 12 November 2014 (UTC)
When I see the term "dependence" used in an article, I typically can't tell what it's referring to in about a third to a half of all cases, because the term "dependence" has 4 meanings: "substance dependence", which is, quite literally, a diagnosticians borked medical term used to replace the word "addiction"; physical dependence, which is a pharmacological phenomenon associated mostly with strong CNS depressants and opiates; psychological dependence, which is another pharmacological phenomenon associated with specific transient psychological symptoms that last ~2 weeks; and then just generic drug dependence which means one or both of the 2 preceeding forms of dependence. There is only 1 definition of addiction and it encompasses all of the above, since it is a disease which may involve one of the 2 forms of pharmacological dependence. Now with all that said, when I read that paragraph and the abstract of the citation, I didn't know precisely which of the 4 terms "dependence" was referring to. My go-to response in cases like that is to replace the abuse of language that is "dependence" with the simpler and more understandable term "addiction". Seppi333 (Insert 2¢ | Maintained) 17:18, 12 November 2014 (UTC)
Durmowicz is referring to physical dependence (as far as i can tell):
"The abuse liability of e-cigarettes in youth is unknown. Non-clinical studies have identified that exposure to nicotine can cause neuroplastic changes in the developing brain that favour continued use and can impact executive cognitive function later in life. 33 The extent to which e-cigarette use in youth will result in nicotine dependence and subsequent use of othertobacco products is unknown."
And such a dependence can lead to addiction, but is not in and of itself an addiction. I'm wholly concious of the ambiguity here, since Danish, my native language, doesn't have this ambiguity, we only have one word ("afhængig") that encompasses both usages :) --Kim D. Petersen17:35, 12 November 2014 (UTC)
That passage is referring to the diagnostic model-based definition since it's discussing "neuroplastic changes"; there is no neurological model of drug dependence because a generic withdrawal syndrome has a somatic component. But... for all addictions, adverse neuroplastic changes arise largely through accumbal ΔFosB overexpression. In any event, since it matters that much to you, I'll just change it to that term and wikilink it for clarity. Seppi333 (Insert 2¢ | Maintained) 17:53, 12 November 2014 (UTC)
Copyright checks when performing AfC reviews
Hello Seppi333. This message is part of a mass mailing to people who appear active in reviewing articles for creation submissions. First of all, thank you for taking part in this important work! I'm sorry this message is a form letter – it really was the only way I could think of to covey the issue economically. Of course, this also means that I have not looked to see whether the matter is applicable to you in particular.
The issue is in rather large numbers of copyright violations ("copyvios") making their way through AfC reviews without being detected (even when easy to check, and even when hallmarks of copyvios in the text that should have invited a check, were glaring). A second issue is the correct method of dealing with them when discovered.
If you don't do so already, I'd like to ask for your to help with this problem by taking on the practice of performing a copyvio check as the first step in any AfC review. The most basic method is to simply copy a unique but small portion of text from the draft body and run it through a search engine in quotation marks. Trying this from two different paragraphs is recommended. (If you have any question about whether the text was copied from the draft, rather than the other way around (a "backwards copyvio"), the Wayback Machine is very useful for sussing that out.)
If you do find a copyright violation, please do not decline the draft on that basis. Copyright violations need to be dealt with immediately as they may harm those whose content is being used and expose Wikipedia to potential legal liability. If the draft is substantially a copyvio, and there's no non-infringing version to revert to, please mark the page for speedy deletion right away using {{db-g12|url=URL of source}}. If there is an assertion of permission, please replace the draft article's content with {{subst:copyvio|url=URL of source}}.
Some of the more obvious indicia of a copyvio are use of the first person ("we/our/us..."), phrases like "this site", or apparent artifacts of content written for somewhere else ("top", "go to top", "next page", "click here", use of smartquotes, etc.); inappropriate tone of voice, such as an overly informal tone or a very slanted marketing voice with weasel words; including intellectual property symbols (™,®); and blocks of text being added all at once in a finished form with no misspellings or other errors.
Hi there, I'm pleased to inform you that I've begun reviewing the article Adderall you nominated for GA-status according to the criteria. This process may take up to 7 days. Feel free to contact me with any questions or comments you might have during this period. Message delivered by Legobot, on behalf of Jaguar -- Jaguar (talk) 16:20, 2 December 2014 (UTC)
addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences
addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
drug withdrawal – symptoms that occur upon cessation of repeated drug use
psychological dependence – dependence socially seen as being extremely mild compared to physical dependence (e.g., with enough willpower it could be overcome)
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
@Doc James: Assuming I don't collapse it, do you have any suggestion on how I can resolve your concerns without simply omitting all that information from articles that use (and misuse) these terms? This template is as much for editors adding something to the page as it is for readers. Seppi333 (Insert 2¢ | Maintained) 03:41, 7 January 2015 (UTC)
I am supportive of having this template on the 10 articles that it mentions. I am not supportive of having it on every article that mentions one of these terms. That is why we have blue links. If people do not understand the terms they click on the blue links for further details. Doc James (talk · contribs · email) 03:50, 7 January 2015 (UTC)
@Doc James: I completely agree with you in general, but published literature on this topic often uses these terms interchangeably and in turn, the articles themselves reflect the confused use of language in cited sources. If we don't follow a single definitional convention, we're going to end up with inaccurate and misleading statements in our articles. I correct these as I see them, but that doesn't change what editors add in the future when I may not be editing wikipedia anymore. This needs to be fixed/addressed somehow. Seppi333 (Insert 2¢ | Maintained) 03:56, 7 January 2015 (UTC)
Having these glossaries on all pages IMO will not fix the issue in question. Plus it is undue weight much of the time. Many terms get misused. Right now we have a user who wants to emphasis that the use of cavities as a plural is wrong as the term is technically singular.
If people want to figure out the correct usage of these terms than they will go to the articles on them where they will see the table you have created. Doc James (talk · contribs · email) 04:01, 7 January 2015 (UTC)
@Doc James: It's a little different when we have well-intentioned editors adding content but unwittingly using the wrong language versus a zealous (possibly moronic) editor intentionally using incorrect language... Seppi333 (Insert 2¢ | Maintained) 04:05, 7 January 2015 (UTC)
We have editors who are unwittingly doing stuff that is not correct all the time. This just takes consistent reminding. Yes I realize that it is an uphill battle :-) Doc James (talk · contribs · email) 04:07, 7 January 2015 (UTC)
It appears that this template is not just on the 10 articles which has the term within it. I am strongly opposed to adding it to dozens or hundreds of articles. There are many things that some people do not understand and having half the lead of all these articles with these 10 terms is undue weight unless the article is specifically about one of these terms. Yes I realize that we may disagree. Before you add it further please get consensus at WT:MED. If you get consensus there then of course you may add them to the articles within the area you get consensus. Doc James (talk · contribs · email) 04:13, 7 January 2015 (UTC)
@Doc James: I don't see myself adding this to more than ~5 articles in total. I only add this to articles where I've elaborated on the neuroscience of addiction, because most people are simply completely unfamiliar with that model and perhaps even operant conditioning in general. In those cases, it's there for accessibility because there's no article or wiktionary entry for some of the terms, just redirects to more general concepts (e.g., rewarding stimuli) or less general concepts (drug withdrawal vs "withdrawal" from behaviors or drugs in general) than are described in the glossary. A second reason related to editors is that I really want to avoid a case where an editor adds content on ΔFosB's role in "dependence", because whatever is written will very likely be completely wrong (there's only emerging evidence in psychological dependence at this point). In any event, if you prefer that I seek consensus for the few more I might consider adding it to, I'll do so as you request when the time comes. Seppi333 (Insert 2¢ | Maintained) 04:28, 7 January 2015 (UTC)
Just add my 2¢ in case it helps. A box like this doesn't belong in articles. For readers if they are unsure of a term they can follow the link, and technical, potentially unclear terms should be linked. Guides to editing of any kind don't belong in article content. It will annoy/distract/confuse more people than it helps, and probably be unnoticed or ignored by many editors who think their own way of using words is correct. Odd mistakes and errors should simply be fixed. If there are serious and persistent errors that keep being made in articles then there are various options.
Add an editnotice, though as a distraction to all editors this should only be used in extreme cases.
add to the talk page where it can be noticed and referred to, perhaps as a FAQ at the top.
if the problem is not with one but all related articles then add it to a guideline, such as a relevant manual of style. If one doesn't exist then create it, as an essay or as a more formal proposal for guideline. More work but has the advantage of greater authority and is more easily maintained.
The latter two are the best general solutions for a single article and a larger group. Each gives something to link to in edit summaries, usable by editors manually and automated processes.--JohnBlackburnewordsdeeds04:26, 7 January 2015 (UTC)
@Doc James and JohnBlackburne: I went and checked the MOS on linking numerous technical terms in a section, necessitating "link chasing" by a reader, since I remember it coming up in an amphetamine FAC (this is why there's a stupid amount of parenthetical explanation in the OD section...). Here's what the MOS says about it:
Do not unnecessarily make a reader chase links: if a highly technical term can be simply explained with very few words, do so. Also use a link, but do not make a reader be forced to use that link to understand the sentence, especially if this requires going into nested links (a link that goes to a page with another technical term needed to be linked, which goes to a page with a link to another technical term, and so on). Don't assume that readers will be able to access a link at all, as, for example, they might have printed an article and be reading the hard copy on paper. — Wikipedia:Manual of Style/Linking#General points on linking style
There is no restriction for glossary transclusion (MOS:GLOSSARY), save for number of definitions (≥5, ≤25) and relevance to the article. Any addictive drug or addictive behavior article that I add ΔFosB content in will always require the first 5 definitions in the glossary, and frequently includes the 6th. So in these cases, which is the vast majority of articles, excluding the ones linked in the glossary, it violates MOS:LINK to not define these terms in the prose or a glossary transclusion. I am always preferential to the lazy solution (transclude 1 page >>> write the same crap on many). Seppi333 (Insert 2¢ | Maintained) 04:07, 8 January 2015 (UTC)
I didn't reply earlier but should have: MOS:GLOSSARY is not a guideline, it's a proposal that's been around for years without being accepted, and there is no standard for their inclusion. Anyway, seeing no other good argument for keeping it and no hope of persuading you I've raised it at TfD, to bring it to wider attention.--JohnBlackburnewordsdeeds06:03, 15 January 2015 (UTC)
The article Adderall you nominated as a good article has been placed on hold . The article is close to meeting the good article criteria, but there are some minor changes or clarifications needing to be addressed. If these are fixed within 7 days, the article will pass; otherwise it may fail. See Talk:Adderall for things which need to be addressed. Message delivered by Legobot, on behalf of Jaguar -- Jaguar (talk) 17:20, 3 December 2014 (UTC)
The current definition in the box, with the addition of "or compulsive drug use" does not improve on the opening sentence of the article: "Addiction is a state defined by compulsive engagement in rewarding stimuli, despite adverse consequences."
And falls short of the dramatic change in a person's priorities (motivations)
which are viewed by others as so socially dysfunctional to the person
that it is described as a disease - "we know better, this is bad for you".
Not all compulsions are so viewed (eg tapping),
and the degrees that these appear as choices to the person vary.
I believe that addictive compulsions appear to be choices, albeit acknowledged as problematic. — Preceding unsigned comment added by MartinGugino (talk • contribs)
@MartinGugino: Addictions are compulsions. Compulsions are not necessarily addictions. The difference is that the latter includes negative reinforcement, so reward is not a necessary attribute of stimuli. Tapping is obviously not rewarding, so it's not addictive. Addictions are disease states associated with pathologically reinforced stimuli, which is indeed compulsion. The degree of "free will" or "choice" an addicted individual has at any given moment is variable over the short term. I don't really follow the rest of what you said. Seppi333 (Insert 2¢ | Maintained) 18:16, 8 December 2014 (UTC)
The addition is sometimes thought of as a disease. Not human. Pretty extreme, and this attitude of judgemental rejection is not conveyed in the definition( Martin | talk • contribs19:19, 9 December 2014 (UTC))
A minor comment
Adderall is already a GA so maybe you change your editing plan for Adderall to FA. Sorry to bother you. Clr324 23:09, 14 December 2014 (UTC) — Preceding unsigned comment added by Clr324 (talk • contribs)
I get the impression that you're pretty frustrated with Wikipedia right now, especially the featured article process. I've now supported promotion on the FAC page; you may want to read my 721-word explanation of why. Anyway, I just wanted to let you know that I've really enjoyed working with you to improve the amphetamine article. If the current FAC doesn't pass (which is unfortunately a somewhat real possibility) and you find the time and desire to improve it further to finally get that FA star, know that I'd be glad to help you with that. Just address the comments I've already made first, please! :)
If you decide that editing Wikipedia is no longer for you, I understand; I've got an article of my own that I've been trying to get to FA status for the past year (Treblinka extermination camp), and that has been a similarly frustrating experience. If that's the case, I wish you all the best in your future endeavors in real life. AmericanLemming (talk) 05:46, 2 January 2015 (UTC)
I'm actually planning on getting back to the FAC sometime tomorrow (technically, today as of posting this). I just wanted a break from editing wikipedia over the holiday - and that means I haven't looked at the FAC page. I'll do a lot of editing/follow-up in the evening. Thanks for reviewing it! Seppi333 (Insert 2¢ | Maintained) 08:45, 2 January 2015 (UTC)
Sorry for disappearing on you this past week. I just needed a short break from the article myself. Anyway, I'm feeling fit as a fiddle now, which means I can look at your responses to my comments and hopefully proofread most of the rest of this article before Monday, when the spring semester starts. AmericanLemming (talk) 22:58, 8 January 2015 (UTC)
On 05:47 3 January 2015 you added an Addiction glossary to the Caffeine page, with the justification "add addiction glossary to the relevant section so that I hopefully don't need to clarify this again in the future". I thought this addition was a useful one; however another editor deleted it on 12:29 4 January with the justification "Effects: on subpage".
I would like to see this table restored. Would you explain here what you meant by the above "hopefully..."? Has this issue been contentious either here or elsewhere in the past? If so, with whom? Would you consider restoring it and discussing it with the deleting editor? I hope so! Is there anything I can do to help? Thanks. Regards, IiKkEe (talk) 17:50, 4 January 2015 (UTC)
addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences
addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
drug withdrawal – symptoms that occur upon cessation of repeated drug use
psychological dependence – dependence socially seen as being extremely mild compared to physical dependence (e.g., with enough willpower it could be overcome)
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
Basically every article on addiction or dependence, except for the 3 that I've copyedited or rewritten, uses the terms "dependence" and "addiction" interchangeably; they're not the same thing - each refers to a distinct neuropsychological concept and arise from different biomolecular mechanisms. Diagnostic classification systems like the DSM arbitrarily use these terms interchangeably, which is the source of a lot of confusion for people (including me at one point) that edit sections or articles on these topics. I imagine doc james finds the table too large for its purpose/relevance to the article. If you'd prefer to include it, I'll add it as a collapsed table (example included here) to address the issue of its size. Seppi333 (Insert 2¢ | Maintained) 18:23, 4 January 2015 (UTC)
References
^ abMalenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN9780071481274.
^ abNestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 15 (4): 431–443. PMC3898681. PMID24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
^ abVolkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMC6135257. PMID26816013. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe. Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
Thank you for your prompt,thorough and thoughtful response. I see the glossary is back on the Caffeine page: thank you for that too. I'm going to trim it a bit and delete the terms which do not apply directly to caffeine. I hope you will take a look at it when I'm done and give me your reaction/suggestions. Regards, IiKkEe (talk) 20:29, 4 January 2015 (UTC)
@IiKkEe: the template actually transcludes to over 20 other articles besides caffeine (the articles listed here); the terms describe all the relevant concepts necessary to define an addiction, a dependence-withdrawal syndrome, and sensitization-tolerance effects for both addictive drugs and addictive behaviors. If you really want just the shortened version, I'll tweak the template code so that it transcludes just that subset to the caffeine article. Seppi333 (Insert 2¢ | Maintained) 21:04, 4 January 2015 (UTC)
Sorry, I already did what I said I was going to do before I saw that there was a message for me from you. See what you think - I deleted the terms I think do not apply to caffeine.IiKkEe (talk) 21:24, 4 January 2015 (UTC)
Major Depression Hypothesis
Why is the MDD page still showing the Monoamine hypothesis as a primary hypothesis for depression, I know that the page presents other hypotheses for the cause, but currently there is no consensus on a hypothesis for the cause of MDD. The Monoamine hypothesis is just the easiest way to explain it, the most studied hypothesis, but it doesn't explain everything about depression, nor how to treat depression fully.
Doctors tell their patients that it's an 'imbalance' of neurotransmitters, however, there is no true consensus on the actual cause of depression. Docs just say this because it's easier to explain, but it's a lie.
They should tell patients, that they don't know for certain what causes depression, but this drug seems to help, and we're not entirely sure how it actually works, but it helps some people.
thank you for removing my citation needed for monoamine hypothesis comment on the MDD page, and thank you for whomever added the newer information and citations to this section of the MDD page.Franglish9265 (talk) 19:33, 8 January 2015 (UTC) — Preceding unsigned comment added by Franglish9265 (talk • contribs) 19:40, 7 January 2015 (UTC)
@Franglish9265: I haven't edited that page in months... but as far as the monoamine hypothesis is concerned, the notion that it's an imbalance of neurotransmitters is like 4 decades outdated. There's concrete evidence that, like addiction, depression is governed by epigenetic/pharmacogenomic mechanisms in monoamine signaling pathways. That's why drugs for depression tend to take weeks to take effect, assuming they do at all. Seppi333 (Insert 2¢ | Maintained) 19:47, 7 January 2015 (UTC)
@Seppi333: Yep, I agree with that and thank you for your comments. So, the current evidence is that it's governed by epigenetic and pharmacogenomic mechanisms in MASPs? (so the current consensus is that it's an effect of epigenetic changes due to stress, diet, in-utero environment,... etc. perhaps? what would pharmacogenomic mechanisms be?) How about the BDNF and Neurotrophin related hypothesis? Maybe the SSRIs work indirectly by increasing Neurotrophin levels, because they do cause physical dependence? I've read some abstracts on the Neurotrophins hypothesis, but as of yet not much to it's explanation of how things work.Franglish9265 (talk) 19:46, 8 January 2015 (UTC)
They're not mutually exclusive. Cell signalling can interconnect multiple inputs for a disease along a particular neural pathway via more than 1 signaling pathway/cascade which eventually merges (like in psychostimulant addiction, which has 2 - a cAMP and a calcium pathway) and by involving multiple layers of signaling compounds and proteins. These terminate inside the nuclear membrane (following transcription), which is where the magic (genetics) happens.
It's interesting since that gene transcription factor in the nucleus accumbens governs/modulates virtually every aspect of addiction. Also, I meant pharmacogenomics in terms of the treatment, not the cause. E.g., SSRIs work because of their all-the-way-downstream effects on gene expression through the transcription factors they affect.
In any event, gene transcription factors are the direct regulators of brain plasticity. Intermediate neurotrophic messengers like BDNF signal to these downstream targets, which is what causes the trophic response, not its immediate target (TrkB activation doesn't suddenly grow your brain, in the event what I meant wasn't obvious). Because depression involves altered neuroplasticity, there is without a doubt a pathological genetic component, or that wouldn't occur. Seppi333 (Insert 2¢ | Maintained) 21:03, 8 January 2015 (UTC)
@Franglish9265: The following is from my standard neuropharmacology reference text; it's a rehash of everything I said. This is a quote from page 355 which just summarizes general material; I've bolded the relevant material on the monoamine hypothesis and current theories.[1] (Note: "target neurons of monoamines" refers to the postsynaptic neuron in a monoamine pathway; in case you'd like a complete list of them, I added all of these pathways at neurotransmitter#Brain neurotransmitter systems). It covers the role of genetics/transcription in both current theories (these include the concepts you pointed out) in relation to antidepressant drug effects and depression neuroplasticity on the following 4 pages listed in the citation. Diagrams of depression-related signaling cascades and neural pathways are included in the subsequent pages as well. See the text for more information. Seppi333 (Insert 2¢ | Maintained) 03:21, 9 January 2015 (UTC)
wow quite a bit of things to read before I respond. While I agree that there is a genetic component, I think that there also is a much stronger component of depression, that is situational and epigenetic factors that have a stronger influence. Everyone most likely has the ability to become Major Depressive, given the right circumstances. Stress, Negative experiences, life changing events, events beyond our control, etc. Are you familiar with epigenetics? I most likely have some adverse genetic mutations that predispose me to MDD, but unless they get turned on or off in my offspring or me, it's not something I'm going to worry about. I think that the genetic mutations, etc that we inherit are neutral, in effect. They may have negative implications if they get over-expressed, but one could avoid the negative consequences provided a better understanding of how they get turned on or off, or how to function with MDD. They may have positive implications of they are expressed differently, or not at all.
While I haven't been able to discontinue ADs yet, They seem to work even in an active placebo-ish way for me, but I think they work because they do something else than Selective Serotonin Re-uptake inhibition, they give me hope, and active placebo effects which I'll take any day.Franglish9265 (talk) 16:58, 15 January 2015 (UTC)
Massive reflist
References
^Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 14:Neuropharmacology of Neural Systems and Disorders". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 355–360. ISBN9780071481274. Pharmacologic observations such as these led to a
simple hypothesis: depression is the result of inadequate
monoamine neurotransmission, and clinically effective
antidepressants work by increasing the availability
of monoamines. Yet this hypothesis has failed to
explain the observation that weeks of treatment with
antidepressants are required before clinical efficacy
becomes apparent, despite the fact that the inhibitory
actions of these agents—whether in relation to reuptake
or monoamine oxidase—are immediate. This
delay in therapeutic effect eventually led investigators
to theorize that long-term adaptations in brain function,
rather than increases in synaptic norepinephrine
and serotonin per se, most likely underlie the therapeutic
effects of antidepressant drugs. Consequently,
the focus of research on antidepressants has shifted
from the study of their immediate effects to the investigation
of effects that develop more slowly.
The anatomic focus of research on antidepressants
also has shifted. Although monoamine synapses are
believed to be the immediate targets of antidepressant
drugs, more attention is given to the target neurons of
monoamines, where chronic alterations in monoaminergic
inputs caused by antidepressant drugs presumably
lead to long-lasting adaptations that underlie effective
treatment of depression. The identification of molecular
and cellular adaptations that occur in response to
antidepressants, and the location of the cells and circuits
in which they occur, are the chief goals that guide current
research. The work described toward the beginning
of the chapter on mood-regulating circuits that involve
the subgenual cingulate gyrus, for instance, represent a
significant advance over a narrow focus on monoamine
neuron function. ...
Long-term adaptations in antidepressant action
The several weeks latency in onset of the therapeutic
actions of antidepressants contributes to distress and
clinical risk for those with severe depression. In the
search for treatments of more rapid onset, great effort
has gone into trying to understand the delay in efficacy
of current antidepressants. All current ideas posit that
antidepressant-induced increases in synaptic
monoamine concentrations cause slowly accumulating
adaptive changes in target neurons. Two broad
classes of theories have emerged: (1) Changes in protein
phosphorylation, gene expression, and protein
translation occur in target neurons that ultimately
alter synaptic structure or function in a way that
relieves symptoms; and (2) antidepressant-induced
neurogenesis in the hippocampus and the incorporation
of those new neurons into functional circuits is a
required step in the therapeutic response. Before considering
specific hypotheses, however, it is important
to discuss obstacles in relating research in animal
models to human depression. ...{{cite book}}: line feed character in |quote= at position 50 (help)CS1 maint: multiple names: authors list (link)
@Franglish9265: Didn't notice this until now; when I said behavioral epigenetics, I really meant the effects that drugs and behaviors have on gene expression via their influence on transcription factor expression (those are also genes, but they regulate the expression of other genes). Heritable genetics (by that I mean what you get from your parents) very likely play a role in determining innate risk for developing any brain-related disorders, but they don't govern the actual development/induction of addiction or depression. See this FAQ link from a leading research group in both diseases, specifically: "Q 11. What are transcription factors?" and "Q 12. What role do transcription factors play in addiction and depression?" Seppi333 (Insert 2¢ | Maintained) 05:25, 3 February 2015 (UTC)
Congratulations!
Congratulations on finally getting amphetamine promoted to FA status! It only took you a little over 13 months. :) I'm just as surprised as you are; I thought the FAC coordinators were going to make us go through the entire article word-by-word before they would promote it, which would have taken dozens of hours, another couple of months, and quite likely a sixth FAC. Thankfully, the powers that be have concurred with my argument that the "Pharmacology" and "Physical and chemical properties" sections are so technical that making the prose perfect is unnecessary and (arguably) a waste of time.
However, I probably will proofread and copy-edit the rest of the article (Pharmacology; Physical and chemical properties; and History, society, and culture) on my own at some point in the future. I've made it this far, so I feel like I should finish what I started. Besides, it's like reading a novel; I want to see how it ends. :) Also, when I finally learn about molecular neuropharmacology (probably in med school), I may try to untangle the pharmacodynamics section for the 0.1% of readers who don't know a thing about molecular neuropharmacology but want to read the section anyway.
Anyway, I'm glad I got to help you get the article promoted, and I hope I've restore some of your enthusiasm for Wikipedia after your unpleasant experiences with Shudde, the lack of reviewers at FAC#3, and the long road to FA status (13 months and 5 FACs). Thanks for letting me nitpick the article to death, too. I've enjoyed working with you, and if you ever should feel ready to brave the unfriendly place that is FAC all over again, let me know and I'll try to take a look for you. I'd suggest nominating Adderall next; some two-thirds of the article is transcluded from amphetamine, so it should hopefully have a smoother ride to FA status. AmericanLemming (talk) 04:49, 15 January 2015 (UTC)
some time ago I commented on your substance abuse article, I have a GA nomination forDyslexia I was wondering if you would mind taking a look at it, I of course would be in your debt, thank you--Ozzie10aaaa (talk) 01:58, 29 January 2015 (UTC)
@Ozzie10aaaa: Sure thing; I'll run through it now and see if there's any potential improvements. If I end up with enough time to spare next week, I might actually take on the GA review since I have a general interest in articles on neuropsychiatry/neuropsychology topics. Seppi333 (Insert 2¢ | Maintained) 02:14, 29 January 2015 (UTC)
@Ozzie10aaaa: Hey, I've just been tied up with things outside wikipedia, so I haven't had time to follow up on doing a source review of the article yet - that's rather time intensive work. I'm still planning to go through with reviewing it, it's just going to be more delayed than the 1 day I said it would be. :P Sorry for not following up on that. Seppi333 (Insert 2¢ | Maintained) 18:19, 2 February 2015 (UTC)
Seppi333]]  in the last week I added a few refs so did User:Moxy, "if" you have time to see if theres something missing id appreciate it because of your prior GA knowledge,thanks--Ozzie10aaaa (talk) 23:35, 10 February 2015 (UTC)
Cupcakes
We all know red velvet is the supreme cupcake. — Preceding unsigned comment added by 73.213.24.13 (talk)
I've gone through the title article and made some major revisions which I expect to stimulate some discussion. Given your past interest in articles about psychoactive drugs, thought you might be interested. Thanks. Formerly 98 (talk) 15:23, 29 January 2015 (UTC)
Any reason why you believe addiction is a more appropriate redirect? Per WP:PRIMARY drug addiction would more likely constitute substance dependence. Someone searching for drug addiction would be looking for substance dependence not addiction in general. Valoemtalkcontrib01:20, 27 February 2015 (UTC)
Substance dependence is a diagnosis which includes a drug addiction, but which also includes other drug-related disorders, like a dependence-withdrawal syndrome. Addiction is the closest relevant concept on which we have an article. Seppi333 (Insert 2¢ | Maintained) 20:01, 28 February 2015 (UTC)
A revert on Tail of the ventral tegmental area
Hello Seppi, I'm leaving a message here to discuss an edit on Tail of the ventral tegmental area. I noticed that you reverted an edit I made which removed extensive quotations to copyrighted articles, which represents a copyright violation (close paraphrasing at best) not different from pasting the text in other sections of an article. I'd really appreciate an explanation for keeping the quotes. All the best. --Tilifa Ocaufa (talk) 00:36, 1 March 2015 (UTC)
Hi Tilifa Ocaufa, sorry for the late reply. Excerpting in a citation quote in the context of an excerpt with attribution isn't actually a copyvio so long as the length isn't excessive relative to the total size of the quoted source. This issue actually came up with another editor at in a previous article I worked on (MDMA/Talk:MDMA), however the consensus there was just to keep the total length under a certain word-length. In a nutshell, US government-hosted websites like TOXNET ( e.g., TOXNET MDMA) and PubChem (e.g., PubChem MDMA - all entries with an HSDB link are excerpts) use excerpts w/ attribution to convey information, so it's safe to say that these aren't copyvios so long as the length/manner of quotation is kept in-line with the way these sites do this. I try to also constrain the excerpt's word count to less than 250 words due to the appearance/total length of the reference tooltip. In any event, if you feel very strongly about this, I'd be ok with removing them from this article; I should point out though that there are numerous other articles, some high traffic & heavily reviewed or even FA status, that use excerpts in the citation quote parameter in this manner. Seppi333 (Insert 2¢ | Maintained) 22:21, 3 March 2015 (UTC)
That sounds fine, I read the talk page you pointed to and it's more clear now. In-text attribution appears to be ok for quotations if the text quoted is kept at a minimum. I have no strong feelings either way so if they don't infringe copyright I see no point in removing them. Thanks for answering ;). --Tilifa Ocaufa (talk) 09:12, 4 March 2015 (UTC)
Just to let you know - this edit was a request to revert back to an article title which has stood for several years and was moved without and possibly against consensus. I'll ask for a full move request, but the fact I have to do such a thing to revert a contested move back to an established state is a bit much. SFB20:31, 9 March 2015 (UTC)
@Sillyfolkboy: users don't need to discuss moving a page beforehand, so it isn't necessary to do this. The different between a bold move and a move request is that the latter generates consensus that supports a move beforehand (this provides protection from reverts) while the former may be reverted by anyone at any time. A {{db-g6}} speedy deletion template can be removed by anyone that contents it, like me. You could, however, simply move the page back yourself. I'd ask you to reconsider if you wish to do so though because that page is a really bad disambiguation title for the article for reasons I explained at Talk:Athletics (British).
Again, I'm open to moving these pages to new parenthetical disambiguation titles or another disambiguation approach, but the former page titles don't conform to our article naming policies. We shouldn't even consider using them as an alternative. Seppi333 (Insert 2¢ | Maintained) 20:41, 9 March 2015 (UTC)
I cannot simply move it back because a redirect with history is in the way. Your revert specifically prevented me from doing this, so I find your advice quite odd. I am fully aware that the current choice isn't a great one, but past experience tells me it's the least worst we've got so far. I haven't seen one proposal without a severe flaw – the combination of (a) there being two terms with different meaning in English with very little geographical overlap, and (b) the fact that one term is not easily explained to North American audiences in fewer than a dozen words, means that this is an impossible situation. It's much better to raise a discussion on a page move when there is a clear history of such discussions with many participants visible on that talk page. SFB20:55, 9 March 2015 (UTC)
Sorry, I didn't notice the 4 edits on that page when I wrote the reply. It's still possible to WP:MERGE the entire page back and add the {{copied}} template on the 2 talk pages, but that's a rather messy way to move a page. As for disambiguation, it may be helpful to get input from the editors at WT:WPDAB. Seppi333 (Insert 2¢ | Maintained) 21:00, 9 March 2015 (UTC)
Your GA nom
Hi Seppi, I'd be happy to do the review, since this is a topic that interests me greatly, and I'm ready to pick it up any time you are ready to have it reviewed. In fact if it makes sense to you I could formally start the review now but wait until you're ready to actually do anything. Let me know what you'd prefer. Regards, Looie496 (talk) 15:35, 12 March 2015 (UTC)
Hey Looie496, as long as you're ok with the stable criterion not being met for the next week or so, I'd be ok with that. I've finished rewriting the sections which do not have a maintenance template in it or its parent section. Seppi333 (Insert 2¢ | Maintained) 16:26, 12 March 2015 (UTC)
Hi Seppi. Reiterating what Tilifa Ocaufa wrote above, I have noticed that you are starting to include very long quotations in citations. I have three concerns with this. First, even though the attribution is crystal clear, these long quotations may go beyond fair use and hence represent potential copyright violations. Second, these long quotations may not be necessary and may even obscure the connection between the text and the source used to support that text. Brevity is clarity. Third, the extensive quotations are starting to make the reference section very long so that it starts to overwhelm the rest of the article.
@Boghog: I'd actually encourage you to prune the reference quotes down to the minimum necessary length for WP:V; I know I sometimes overquote beyond what's necessary simply because the way I add article content is to skim a citation for notable information to cover in an article, copy/paste the statements into a ref quote parameter + format an excerpt, and then summarize what I've quoted. Since reviews tend to have a lot of notable information on the topic they're written on, I usually end up with large chunks of quoted text which is sometimes redundant or not relevant to the article text that I write. I don't prune the quotes after I summarize the excerpt solely to provide context for other people, so I'm not concerned about removing parts of an excerpt that are redundant or don't support article text. Seppi333 (Insert 2¢ | Maintained) 02:18, 6 March 2015 (UTC)
If you want to write something in that article which makes a claim like that, it needs to be in the context of all drugs indicated on that page. The ref you provided was not relevant to even half of them; ergo, it's not appropriate for that article. Seppi333 (Insert 2¢ | Maintained)
Precious
Amphetamine
Thank you, Seppi, for quality articles on scientific background in neuropsychopharmacology, such as the rewrite of Amphetamine and Euphoria, for redirects, article talk maintenance and images, for "continuously donate my 2¢ to WT:MED since I'm generous like that", - you are an awesome Wikipedian!
Deleted paragraph regarding increased prescribring of Dexamphetamine in the Netherlands
Hi,
You just deleted the paragraph I wrote regarding the sharp increase in prescribing of Dexamphetamine in the Netherlands, saying it should be moved to the "Legal" section. However, I have to disagree that the "Legal" section would be the most appropriate place to put that paragraph. As it currently is, the "Legal" section lists the legality of (d/l-)amphetamine in several countries, but the paragraph I wrote has little to do with the legality of amphetamine, and more with the medical aspect, as I also mentioned several medical indications for which it can be legally prescribed nowadays, and for what it was prescribed in the past (pre 90's). Maybe you have some better suggestions of where to place the paragraph I wrote?
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@DadaNeem: Hi there. I'm actually in the process of revising the whole thing; I intend to re-add it under a dependence (as opposed to addiction) heading when I commit the edit. Check back in about 10 mins. Seppi333 (Insert 2¢) 22:25, 23 April 2015 (UTC)
@JohnBlackburne:, I've followed through with my statement at the MfD and deleted the subpage. Going forward, I think it would be better if you and I discuss any issues that arise between us and come to a mutually-acceptable solution instead of continue on with our confrontational interactions that began with our dispute at talk:statistics. Seppi333 (Insert 2¢) 23:56, 25 April 2015 (UTC)
I
Seppi, even if the sources are completely muddleheaded about addictions and compulsions, I still wish you had thought of a gentler way to communicate your disgust. I want you here for the long run (also, how do you feel about human cloning? Having six or seven of you would be handy ;-), and I want other editors to stay on your side. You've got friends and allies here. I want you to keep them. If you're frustrated, then come tell me about it. I can't always solve the problems, but I will listen to what you have to say. WhatamIdoing (talk) 01:18, 2 May 2015 (UTC)
Sorry about that, and I appreciate the gesture. I've run into opposition from other editors in the past when I've added/edited content on behavioral addiction and/or dependence pages. The issue always ends up involving the DSM's definitions or controversies which only pertain to clinical/diagnostic models. I've gotten tired of repeating myself. :P Seppi333 (Insert 2¢) 09:10, 2 May 2015 (UTC)
And then when you're finally making some headway with people who "just" needed to be told the same thing twenty times in a row, a total WP:RANDY will show up. Someday (probably after some primary care provider has a spectacular meltdown after telling yet another guy that beer is not a healthful, whole-grain food and that potato chips do not count as vegetables), the frustration of repeating basic facts may even be recognized as a serious mental health stressor. You're dealing with an especially difficult area. You've got sources that seem to choose names based on whether they'll make spectacular headlines instead of whether they'll make any sense. You've got POV pushers from an unusually broad range of interests: pro- and anti- both about substances and behaviors themselves, about regulation, about criminalization, about research money, about commercial interests, about pubic health efforts, and more. You've got an enormous amount of just plain misinformation or ignorance. It's difficult, and you're one of our best editors in that area. Hang in there. We need you.
I don't know how much you know about Cantor. He's pretty good in his subfield. He's maybe got more of an "academia view" than an "editor view": a little more interest in what's going on underneath the surface of a concept than what can be sourced, a little clearer understanding of minor points that even the professional press gets wrong on occasion, and that the lay press completely misses. (I know you're familiar with the problem of the lay press. I once considered buying an empty, sterile plastic syringe, labeling it "Syringe", and mailing it to my local newspaper with a request that they stop saying "syringe" when they meant "needle". An empty syringe is no more dangerous than a ballpoint ink pen with the ink cartridge removed, but you'd never guess that from the breathless stories about a syringe being found in a park.) Anyway, I trust Cantor to know what he's talking about, even if what's really needed to solve the problem quickly in the sources isn't easily available (in this instance, probably a media-friendly compare-and-contrast chart between all the different concepts, plus a promise to shame them publicly if they use the wrong words again). WhatamIdoing (talk) 21:20, 2 May 2015 (UTC)
I expect to be around for a while longer, provided I don't meet an untimely end IRL, hehe. I don't have a problem with Cantor tbh. This is actually the first time I've interacted with him IIRC. I generally don't hold anything against other editors based upon a few interactions unless I perceive a serious behavioral/conduct issue which is outside the purview TPG or related conduct policies. Seppi333 (Insert 2¢) 18:16, 7 May 2015 (UTC)
Congrats!
Hey, Seppi333. A few weeks ago, I visited the home page and saw amphetamine as the featured article. I just wanted to say, congrats! A lot of us really appreciate the work you do. It's a huge selfless societal contribution, and you've done a great job.
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A question
What do you think of the neurodiversity movement? The movement says mental conditions like autism spectrum, ADHD, et. al. should be accepted and celebrated. The movement opposes the idea of "curing" these conditions but many advocates acknowledge the benefits of psychiatric drugs (which is not the same as a cure!) on some and support the right to choose.
@Clr324: Not bothersome or offensive at all - I don't mind.
If you're still interested in knowing where I stand on neurodiversity, I think that the general idea that certain neuropsychiatric disorders aren't necessarily a bad thing (i.e., aren't really a "disorder" at all, for some people) has merit, but I think neurodiversity is centered around the wrong idea. The neurodiversity movement, at its core, considers the existence of such disorders as creating individuality or uniqueness and therefore aren't really disorders, but I think that's a fairly asinine assertion since there are many individuals with neuropsychiatric disorders that strongly desire a "cure" for what makes them "unique". It's analogous to saying that having brain cancer promotes individuality - a malignant tumor in the brain produces neuropsychiatric symptoms, but I doubt anyone would assert that having a malignant brain tumor is even remotely a good thing. That said, some neuropsychiatric "disorders", like ADHD for example, can improve an individual's ability to perform certain tasks while impairing performance in others; lifestyle and occupation/vocation are basically the most important factors in determining whether disorders like ADHD do more good or harm to an individual's quality of life. In virtually every case that I can think of, a majority of individuals with a particular neuropsych disorder finds that the condition reduces quality of life, which is why they're considered medical "disorders".
Personally, I think it really just boils down to whether an individual with a particular neuropsychiatric disorder finds that it enhances or reduces their quality of life overall (that's basically just a cost-benefit analysis of having a neuropsych condition) - this is essentially what determines whether a person would consider their condition as being a "disorder" vs a harmless or even desirable "trait"; unfortunately, I think the neurodiversity movement is going off on a tangent by championing the idea that these disorders are essentially character traits that promote individuality instead of how various disorders can improve quality of life instead of just universally impair it in everyone. Seppi333 (Insert 2¢) 16:31, 15 May 2015 (UTC)
I changed 1 guideline. The other necessarily had to change with it. MOS:MED wasn't an additional change, as it was identical to what I did on MOS:PHARM. Now you get to come up with a different solution/change to the language on MOS:PHARM to fix the issue I had originally addressed. Seppi333 (Insert 2¢) 12:27, 4 June 2015 (UTC)
Can you stop being an asshat and actually read the pages to understand why I made the changes I did? PHARMMOS literally says:
Research
Ongoing investigations into a medication that have not reached clinical usage. Uses that are in clinical trials belong in the Medical uses section.
All I did was add a subsection to medical to make a distinction between approved and non-approved uses. WTF is so controversial about that? Seppi333 (Insert 2¢) 12:31, 4 June 2015 (UTC)
@Doc James: Just for the record, you changed MOS:PHARM just now by deleting that statement with no consensus, but I'm not being a giant dick and reverting you over that. All I care about is that the guidelines are consistent. Seppi333 (Insert 2¢) 13:17, 4 June 2015 (UTC)
Hi Seppi, I'm afraid I had to fail the GA nom, simply because it has been sitting at the top of the queue for three months with no real progress. Feel free to renominate it when it is actually ready for review. Best regards, Looie496 (talk) 16:42, 9 June 2015 (UTC)
@Ozzie10aaaa: They're both good reviews. I haven't read the first ref before, but after skimming through it, it appears to have the same general coverage with other reviews of addiction-related neuroscience. Since gambling isn't a behavior that can be modeled in animals, it probably won't have as much coverage in reviews as other addictive stimuli do. Intracellular mechanisms like ΔFosB probably won't be evidenced for gambling until a diagnosed gambling addict undergoes a brain biopsy to test for it, either alive or postmortem.
I see now, First of all labeling work of a bot "not useful" for just one edit (even though other edits are good) is de-motivating. And It's a simple bug that can be fixed very easily, Don't expect a perfect work at first run. I fixed it for next runs:)Ladsgroupoverleg23:58, 6 July 2015 (UTC)
Yes it is not often that a newer Cochrane review is withdrawn but definitely something the bot should take into account. It is a useful bot just not in that case. Doc James (talk · contribs · email) 04:44, 9 July 2015 (UTC)
Adderall
Thanks for your input on Talk: Adderall -- Chemical Study Aid. I would also appreciate any feedback on the comments I just added since I seem to have a different opinion than some editors on the way WP should address such topics in medical articles. Medicine is not my professional field. Thanks. 172.88.146.9 (talk) 12:15, 15 July 2015 (UTC)
MDMA and BBB
Nice find! I can't find any reference of dosage of MDMA suggesting overdose, though. It only says "BBB dysfunction was observed immediately following acute MDMA treatment and up to 10 weeks following an acute injection. Increased BBB permeability after MDMA treatment was associated with increased parenchymal penetration of endogenous albumin (Sharma and Ali, 2008), increased activation of astrocytes, and microglia (Monks et al., 2004), and increased brain water content suggesting edema (Sharma and Ali, 2008)." — Preceding unsigned comment added by Infinitarian (talk • contribs) 09:44, 7 September 2015 (UTC)
@Infinitarian: Based upon the associated mechanisms involved with methamphetamine-induced BBB dysfunction and the refs on MDMA and the BBB, I suspect that the dose associated with BBB dysfunction varies between individuals. E.g., oxidative stress from excessive dopamine autoxidation and production radical oxygen/nitrogen species, as well as the occurrence of hyperthermia (generally occurs at high doses) or more severe hyperpyrexia (a severe or life-threatening overdose) and the cerebral edema (also a severe OD symptom) that you noted, are all mechanisms which contribute to an inflammatory neuroimmune response that causes BBB dysfunction; for amphetamine, methamphetamine, MDMA, and related substituted amphetamines, the doses necessary to cause excessive production of radical species or overdose symptoms differ between individuals and vary inversely with drug tolerance for a given person. In light of that, it may be difficult to find a precise figure for the doses in humans that affect the BBB, but it's likely in the same ballpark dose range at which toxicity/overdose symptoms of similar severity occur from MDMA use. Most of the known methamphetamine-based mechanisms involved in BBB dysfunction (depicted in the diagram here), excluding the activation sigma-1 receptors, don't occur at lower doses, but transition into toxic cellular responses at doses above its therapeutic range. At sufficiently high doses, I know methamphetamine and MDMA trigger the same toxic reactions in microglia and neurons; MDMA also binds to sigma-1 receptors, presumably as an agonist like meth due to their structural similarity. I haven't read much about the toxic effects of MDMA on astroglia, so I have no clue if it involves different mechanisms of toxicity in those cells.
So, in a nutshell, the doses that begin to induce BBB dysfunction-related mechanisms are likely around the same dose range in which hyperthermia and other mild-moderate overdose symptoms start to appear. Seppi333 (Insert 2¢) 14:25, 7 September 2015 (UTC)
The study with rats used four doses over 8 hours in "trying to approximate a human dosaging pattern". [1] The source you cited [2] found BBB damage at 3-9 mg of methamphetamine intraperitoneally in rats. Converted to oral (x2) human dosage, that's about 70 mg for an average adult. [3] This is well below a typical street dose of 250 mg, and since methamphetamine makes up 80 percent of MDMA by mass (molar weight 190g/mol for methylenedioxy-methamphetamine and 150g/mol for methamphetamine), this is also well below what's in a typical street dose of MDMA.
Infinitarian (talk) 11:31, 8 September 2015 (UTC)
I am under the impression that typical street doses of MDMA-hydrochloride are 100 - 150 mg with one or two doses taken in a usage episode. 250 mg is a rather large dose. Doses in animal studies do not frequently scale obviously to humans. You would have to look to human studies to determine if BBB damage happens at recreational levels. Methamphetamine isn't a major metabolite of MDMA and the methylenedioxy functional group makes quite big difference pharmacologically. It's difficult to draw conclusions from the molecular weight of methamphetamine in MDMA. Sizeofint (talk) 03:13, 9 September 2015 (UTC)
@Infinitarian: Sorry for the late reply - been busy. Replying to the original post: text on this topic should normally go under a section titled "Toxicity" given its context; toxicity is intended as subsection under "Overdose" per the MOS:MED drug section + MOS:PHARM guidelines; however, in this particular article, either is fine IMO. Long-term effects actually contains toxicity info at the moment anyway. In any event, my original statement about it referring to high doses is really just referencing to the content+citations in the meth article's neurotoxicty section that covers the mechanism of indirect neurotoxicity as radical species and dopamine quinones (the autoxidation products). The astroglia mechanism of meth occurs through its binding at astroglia-localized TAAR1; these papers don't specify a dose, but indicate the relevant population is meth abusers, per the wording of both abstracts PMID 22591363 PMID 24950453. The glial cell NF-kB mechanism arises in response to these.
Regarding cross-species pharmacodynamic comparisons, data from an animal study, by itself, isn't applicable to humans for a variety of reasons - this topic is probably covered in animal testing, but I haven't looked. For future reference relative to these compounds, the entire TAAR class has diverged across species over time to the point that each species has its own subset of TAARs genes. Moreover, TAAR1's sequence diverged across species as animals. Rat TAAR1 and human TAAR1 have very dissimilar sequences, and so there are a number of ligands which bind to one receptor but not the other, while the ligands that do have common binding activity often have a significantly different affinity and/or potency at the receptor. E.g., see PMID 17218486 and [15] on a few amphetamine derivative affinities at TAAR1 across species. Seppi333 (Insert 2¢) 19:06, 9 September 2015 (UTC)
No worries, I'm patient. The second source you cited isn't freely accessible, but the first one corroborated what other sources I've found said, that BBB damage is caused by inflammation. It didn't mention the role of TAAR1s. Other sources I've read found that the damage is caused by oxidative stress to the astrocytes, and based on the significant reduction in damage found in coadministration with vitamin C (source: The Agony of Ecstasy, I believe) they assumed this was the primary mechanism. This is what makes me think it's no coincidence that meth and MDMA both cause BBB damage, as they probably metabolize into similar radicals, and the dosage for meth with rats is certainly not one generally considered an overdose. An overdose is defined as a dangerously high dosage, but the damage occurred at dosages simulating human use. We have no way to draw definitive conclusions about dosage from meth studies, but that's all the more reason that we shouldn't specifically label it as overdose, which is to presume we know more than we do. My concern is that a potential MDMA user reading that under the "overdose" section will think he is safe if he takes a normal dosage, whereas the reports I've read from users suggested otherwise. They reported sensations of brain swelling ("brain too big", "brain pushing against skull") months after usage, consistent with findings that MDMA-induced BBB damage increases permeability of the BBB to water and minerals. Of course this isn't my rationale for putting it under long term effects: my rationale is that we don't know if it's caused by an overdose but we do know that it's a long term effect, lasting for at least 10 weeks.
"Brain swelling" - cerebral edema - is a life-threatening condition that involves neurological symptoms. Amphetamine, MDMA, methamphetamine, all dopamine reuptake inhibitors, and all other releasing agents cause the formation of the exact same radicals; these the drugs don't create radicals themselves - dopamine does when it is metabolized. Your brain is forming radicals from dopamine metabolism right now; it's not the presence of radicals which is a problem, it's the formation of too many radicals (superoxide, hydrogen peroxide, peroxynitrite, etc). Seppi333 (Insert 2¢) 14:48, 10 September 2015 (UTC)
I was unaware of the role of dopamine metabolites in oxidative stress until you pointed it out, but there appear to be several mechanisms, including toxic metabolites of MDMA [4] and inhibition of mitochondria [5].
Cerebral edema isn't defined as life-threatening and can be asymptomatic. For example, most children with diabetic ketoacidosis are thought to have cerebral edema, but only 1% is symptomatic. [6] I agree that cerebral edema should be in the overdose section, as it's usually used in symptomatic cases and it would be misleading to put it under long-term effects, but I mentioned it because the asymptomatic cerebral edema caused by non-dangerous doses of MDMA is consistent with findings of increased water/mineral permeability of the BBB, which can itself have more dangerous effects. It's unknown how long the BBB remains damaged, and if it's permanent, it can increase the risk of Alzheimer's disease (which involves amyloids crossing the blood-brain barrier). However, even 10 weeks is a relatively long-term effect, so I think this specifically should be put under long-term side effects. A friend of mine would not have used MDMA if she'd been presented with these findings.
07:36, 13 September 2015 (UTC)
These are 4 of the 20 medical reviews found on the 1st page using the search term "Cerebral edema" or an indexed synonym in the title: PMID 24866063 PMID 24876075 PMID 25941935 PMID 20168229. What the first sentence of these medical reviews have in common is that they all mention the very high mortality rate and/or status of this condition as a medical emergency. This condition isn't just a little "extra water" in the brain - it's swelling which as a consequence of tissue expansion, causes increased intracranial pressure/cranial hypertension, and potentially cerebral hemorrhage. Both edema and hemorrhage can precipitate potentially permanent neurological sequelae, e.g., brain damage, as a consequence. Our article on cerebral edema happens to be pretty shitty at the moment.
Seppi333, Should it be easier for people to know how to post messages properly on talk pages? I'm having a hard time knowing where you want my comment located or if other people would have a hard time knowing how to post to you for other reasons as well. Is there room for improvement on Wikipedia in that area? My original question is: Why do you have 2 letter Ps in you name instead of just one? — Preceding unsigned comment added by Nikpapag (talk • contribs)
@Nikpapag: Ah, sorry about that. Creating a new section anywhere on my talk page is fine with me; page layout can be reformatted so it doesn't really matter to me anyway. I've always spelled it with 2 P's. Seppi333 (Insert 2¢) 17:37, 13 October 2015 (UTC)
Seppi333, Are you reformatting manually a lot or is it somewhat automatic or can it be more? — Preceding unsigned comment added by Nikpapag (talk • contribs)
Hi Seppi, I saw a thread on Reddit about this page and its accuracy, or lack thereof, so I wanted to bring our article to the attention of someone who was familiar with MEDRS and ADHD topics. Do you think you could take a look at it? Thanks, Mark Arsten (talk) 19:18, 19 November 2015 (UTC)
Hello! I noticed that in this revision you changed the medication of choice for treating Giardiasis. The reference listed doesn't support either the old claim nor the new one. It just says that three drugs are used for treatment. I assume you have a good reason for the change you made, so do you know where we might find a reference for the different drug preferences in the U.S. and E.U.? Thanks a bunch! Ajpolino (talk) 18:47, 9 January 2016 (UTC)
Not sure about the EU, although I'd imagine it's stated somewhere on a government website.
Hello Seppi, I have redrawn your annotated amphetamine pathway as c:File:Amph_pathway.svg. Since there went more work from your side into it than just drawing a structural formula, I wanted to ask if you have any objections, especialy regarding copyrights and/or mentioning of you as the original author. I have linked to your original as derived from. I have not replaced any use of your file, I am just browsing the maintenance categories from time to time and redraw some formulae and reaction schemes. --Nothingserious (talk) 10:10, 20 January 2016 (UTC)
Hi there. I don't care about the copyrights or anything, so no concerns there. I may move the transclusions over to the SVG version when I have time - I'd need to resize the image annotations first. Thanks for redrawing it in SVG. Seppi333 (Insert 2¢) 13:38, 20 January 2016 (UTC)
Drugbox names &tc
OK, we agree to isolate to postpone the INN issue :-). But what is your opinion on my current proposal? The demos look great: /testcases9, from here! I need judgements. Pls take a look. -DePiep (talk) 22:28, 24 February 2016 (UTC)
OK, I've been looking at this. I think we can solve the heroin INN issue very fast and without interfering with the big Names discussion. (that won't finish soon I guess). To speed the decision I want to pre-discuss it here with you (pre-cook the proposal).
Situation to be solved: the Infobox title is set, but it is not the INN name. Example: Heroin, LSD.
Basics: The title is either set by default (PAGENAME), or by |drug_name=. WP:PHARMOS states that the title must be the INN name. All fine, for example Aspirin and N,N-Dimethyltryptamine. However, with heroin the page title is chosen for different reasons (most common name), and now the INN-name is totally unconnected.
Solution: I have added |INN= to {{Drugbox}}, only to be used when infobox title and INN differ. It adds a second row to the title: "INN: ...". See /testcases8#Heroin and #Lysergide.
Things not solved:
Only implicitly do we state that the infobox title is INN. (paracetamol should be edited really). Note that my sandbox has now a tooltip (mousehover-text) that says: title=INN).
When there is no INN for a drug, we can not note that. Add: "INN: none" to the title?
Users have asked parameter(s) to add BAN, USAN, AAN somehow. With my change, we still don't have that option. Opening this discussion would involve the overall naming discussion, so is undesired.
Should we take care of variants like rINN and pINN?
FYI, Category:Infobox drug articles with non-default infobox title lists all articles with |drug_name= set. They are potential candidates for using |INN= this way, but it appears most of those 50 pages are adding "(INN)" to the title, which is wrong (because all titles are INN).
@DePiep: Adding the INN as a subheading seems fine IMO. The INN link probably needs to be changed to an {{abbr}} template though - Wikipedia:Manual_of_Style/Infoboxes#Consistency between infoboxes (the bullet: The template should have a large, bold title line. ... It should not contain a link.). Adding "INN: none" for drugs w/o an INN seems fine to me as well. There's no need to address INN variants IMO, since most drug articles don't mention them in the text. Seppi333 (Insert 2¢) 19:16, 25 February 2016 (UTC)
Thanks. Will happen. I'm doubting the abbr thing, it's just a sub-title (my escape reason), and INN was obscure even to me until researching this. -DePiep (talk) 20:08, 25 February 2016 (UTC)
Just to say: I like the result of our quick working in this. LSD is my favorite demo now. For example: adding "(LSD)" to the title to serve our King the Reader!, without being wrong. -DePiep (talk) 21:32, 27 February 2016 (UTC)
Thank you for being one of Wikipedia's top medical contributors!
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The Cure Award
In 2015 you were one of the top 300 medical editors across any language of Wikipedia. Thank you from Wiki Project Med Foundation for helping bring free, complete, accurate, up-to-date health information to the public. We really appreciate you and the vital work you do! Wiki Project Med Foundation is a user group whose mission is to improve our health content. Consider joining here, there are no associated costs, and we would love to collaborate further.
I really have no clue why you'd think that. IMO most of the racetam articles should be deleted because they're full of crap. Seppi333 (Insert 2¢) 01:22, 12 March 2016 (UTC)
Oh yay. i think we have clashed in the past over primary sources... that's why. maybe i am mistaking that. sorry to offend. i do plan on cleaning up the racetam/nootropic stuff so good to know that you think they need work too. anyway, i am all happy. Jytdog (talk) 01:27, 12 March 2016 (UTC)
The concept of stacking is large and warrants its on section on reddit with thousands of members and trackmystack.com is the largest open stack site online, and the community for nootropics especially is very large thus the link. Please explain why it is not relevant to the nootropics article. — Preceding unsigned comment added by 99.247.158.49 (talk) 17:52, 12 March 2016 (UTC)
I'm not the editor who reverted you, but I also think that the notion of "stacking" supplements has very little reason to be mentioned in the nootropics article. The idea that there's some synergistic interaction between compounds is only supported by biomedical research for theanine and caffeine. Everything else is just marketing or opinion based upon subjective personal experience, not hard science. Seppi333 (Insert 2¢) 01:22, 13 March 2016 (UTC)
New title reverted
Hi. The Amphetamine article has a section covering overdose, addiction, dependence and withdrawal, and toxicity and psychosis. I checked a couple of other articles like codeine and oxycodone and there doesn't seem to be any consistency across them. So I gave it a title. Overdose is not a title for eg. addiction. The current layout actually makes no logical sense.
So I was wondering what title I can give it instead (not Other Risks??). Or is the article just plain locked? Can I ask someone to change it? Thanks.
Eloerc (talk) 22:31, 20 March 2016 (UTC)
The layout of that article follows the convention which is laid out in MOS:MED and MOS:PHARM for drug articles. Addiction doesn't occur from supratherapeutic doses of some drugs, but it does for others (e.g., amphetamine), which is why the sections are ordered that way. If you'd like to discuss the more general issue about section layout in medical articles, the appropriate place to discuss the issue would be the MOS:MED talk page, Wikipedia talk:Manual of Style/Medicine-related articles. Seppi333 (Insert 2¢) 22:35, 20 March 2016 (UTC)
Ok thanks. Yep I see the title section of the style guide now. It's pedantic to cover the illegal nature of their use outside of medicine. And very arguable that they're not addictive unless you overdo it. I'll think about the discussion thanks. Eloerc (talk) 23:02, 20 March 2016 (UTC)
LevoAmphetamine S vs R
Thanks for copyediting that intro! I was very confused about the L - S and D - R bit. That the Dextroamphetamine is actually the S enantiomer and vice versa! Even though the latin is wrong, the chemistry is right! xD FOr a while there I was certain wiki was wrong. But if WIki is wrong, then Sigma Aldritch and the NIH also would have been wrong! Glad you fixed my mistake before I had to. -Shibbolethink(♔♕)14:43, 30 March 2016 (UTC)
Hei, thank you for editing dopamine page, where you turned the IUPAC name into bold, and you wrote the comment box that underlining of the contracted letters for dopamine may be ok here. It was I who underlined the letters, assuming a non-chemist would just jump over the chemical term
Are there alternative ways to show the letters that the accronym is made up of, especially if the letters are from a long and foreign? From your comment I suspected that you may guide me to a source, or tell me of an alternative way, for how to more correctly indicate the orign of the acronym.
Kiniena~enwiki has given you a cookie! Cookies promote WikiLove and hopefully this one has made your day better. You can spread the WikiLove by giving someone else a cookie, whether it be someone you have had disagreements with in the past or a good friend.
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KinienaTekie 04:09, 8 April 2016 (UTC)
@Kiniena~enwiki: Thanks for the cookie. Wikipedia:Manual of Style/Text formatting covers text emphasis in articles. Normally, boldface type is only used for alternate names in the introduction of an article (see the MOS:BOLD section of that page). Italic type is the preferred form of emphasis (see MOS:ITALICS), but it isn't really noticeable enough to point out the letters in a contraction. As for text underlining, that manual of style page says that text generally shouldn't be underlined due to potential confusion with a hyperlink; however, in the case of a contraction, underlining only certain letters instead of the entire word wouldn't be confused with a hyperlink because the entire hyperlinked term would be underlined. Seppi333 (Insert 2¢) 04:44, 8 April 2016 (UTC)
A barnstar for you!
The Editor's Barnstar
For your editorial work on dopamine. KinienaTekie 02:18, 9 April 2016 (UTC)
Diphenhydramine is an inverse agonist of the histamine H1 receptor.[38]
That was an edit I made, because I am not good at making more sophisticated changes with the tables and so forth. Another person(s) read my edit and changed the article to reflect the current research. It is worth noting that that drug has been used in the United States and abroad for 70 years before I came along and made that edit. This is extremely distressing. This information has been known for over 5 years, as well.
Of course the scientific article I cite must be studied, but there is no paywall and I will provide the text so it can be quickly examined:
Since all H 1-antihistamines examined to date have shown inverse agonists, it is suggested that the term "H 1-receptor antagonists" be replaced by "H 1-antihistamines." [41],[42]
Constitutional activity is also demonstrated at H 2 receptors. Many H 2 receptor antagonists, such as cimetidine, ranitidine, tiotidine, and famotidine, described previously as pure H 2 antagonists, actually behave as inverse agonists and diminish basal cAMP levels. By using transfected Chinese hamster ovarian (CHO) cells expressing different densities of wild-type H 2 receptors or uncoupled H 2 (Leu124Ala) receptors, considerable agonist-independent H 2 receptor activity was found. [43] Ranitidine and cimetidine acted as inverse agonists (both induced H 2 receptor upregulation), whereas burimamide was shown to be a neutral antagonist.
There are more sophisticated things that the experienced editors can do in order to bring awareness to this problem and restructure it on a level that I cannot attempt, given the fact that we are talking about drug articles here.
That was not the only edit I had made that day:
Cumulative anticholinergic use is associated with an increased risk for dementia.[28][29]
This had been removed before, despite the enormous evidence supporting the notion that this medication is not good to use in the elderly, et al. With the recent research and research on the talk page, it seems to be sticking up there now.
I am willing to take the time to carefully edit each article, studying each drug to make sure my accuracy is as good as can be expected. I have not had anything removed yet, in fact when I have made edits it has tended to encourage others to change the article to reflect the knowledge I bring from the modern papers. On that Benadryl article, I replaced a paper that was published in 1994, kind of distressing since the human genome project was completed in 2003.
The problem is that the organizational structure supporting all these drugs is something that I cannot edit. If you can take care of that, either directly or by putting the gears of Wikipedia into action so that people will begin to recognize the extent of this problem, that will greatly assist not me, but millions of people.
This next bit is a little more theoretical compared to the above but stay with me for a moment:
Studies in rodents have found that the environment exerts an influence on epigenetic changes related to cognition, in terms of learning and memory;[4] environmental enrichment correlated with increased histone acetylation, and verification by administering histone deacetylase inhibitors induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories.[1][28] Research has also linked learning and long-term memory formation to reversible epigenetic changes in the hippocampus and cortex in animals with normal-functioning, non-damaged brains.[1][29] In human studies, post-mortem brains from Alzheimer's patients show increased histone de-acetylase levels.[30][31]
Alzheimer's disease accounts for over 60% of dementia.
This suggest the potential for Anticholinergic drugs, all or almost all of the drugs operating on the H1 receptor, and at least some of the second generation drugs operating on the H2 receptor, to potentially not only share a relationship with Alzheimer's disease, but also potentially induce a negative effect on people by shutting down learning behaviors and so forth, perhaps via epigenetic mechanisms or other unknown mechanisms. The incentive is not there to do anything about it, because no one even knows about this.
Of course that is completely hypothetical (the epigenetic bit), but not totally out to lunch. Allergies, air pollution and lung function all share epigenetic influences [1] and after having been in Southeast Asia and China, I know for a fact that many people are developing allergies. They deal with this by taking medications which after often considered archaic by western standards. If these drugs induce negative epigenetic changes, which is not unfeasible due to their inverse agonist actions (very uncommon to occur naturally in the body, see: [2] for examples, I have studied those in depth already), then we could be talking about an epidemic of Alzheimer's disease in the future.
Wikipedia co-founder Jimmy Wales has said that lack of health information increases preventable deaths in emerging markets and that health information from Wikipedia can improve community health.[29] Wales presented the Wikipedia Zero project as a channel for delivering health information into places where people have difficulty accessing online information.[29]
We can help stop unfathomable amounts of pain (and maybe reinstate learning behaviors? I take Longvida Curcumin, which is one of the most powerful HDAC inhibitors, it truly seems to be very effective, with excellent research demonstrating the preservation of cognitive function) by merely explaining how the drugs actually work. I had gotten started to sit down and edit, but I realized that this problem is bigger than me and I have a duty to try and seek guidance. Regards. Salvia420 (talk) 05:59, 7 May 2016 (UTC)
I would suggest raising these issues on the relevant article talk pages. A lot of medical/pharmaceutical articles need work and are missing notable information. Just keep in mind that medical claims need to be referenced by sources that satisfy WP:MEDRS (e.g., a medical review of literature). Seppi333 (Insert 2¢) 13:13, 10 May 2016 (UTC)
Wondering if I can get insights into your lifestyle recommendations?
I actually have started running for the last 2 weeks now after reading your Wikipedia article and I am constantly telling people about it, such as on my /r/Prebiotics forum on reddit that you already may have heard about, but I have not been able to get your perspective on your actual lifestyle.
Keep in mind it is very hard to do this, it is basically like comparing two libraries to each other, sources for everything are somewhere lurking in Prebiotics.
Essentially I wake up (Talalay pillows, latex and memory foam mattress, I take sleep equipment seriously). Then I take Niacin (to upregulate BDNF and the metabolites stimulate and motivate me), 1200 MG Longvida Curcumin and 400 MG SAM-e. I usually go back to sleep for a bit until the niacin flushing is complete (I always flush with my niacin and I don't think it's effective unless there is a flush).
It takes a while for my brain to turn on and I try very hard to avoid coffee as it is a drug that simulates a 1000 calorie meal and that excessively speeds up metabolism. I have a prebiotic shake with 2 tablespoons of resistant starches and 2 tablespoons of inulin to produce butyric acid. Sometimes I am in ketosis at this point as well, and I think it is ideal to be in that state. I also include creatine and lecithin since much SAM-e is wasted creating these, approximately 70%, and SAM-e makes me incredibly motivated (however that is gene based supplementation).
I then run after I have something to eat (based loosely on nutrigenomics and my genetics testing), I run at least 3 miles and also do some hiking. I focus mainly on my legs.
I also use a standing desk for my computer work to keep my posture straight since a bad posture can lower testoterone and increase cortisol in as little as 2 minutes in humans.(Your Body Language Shapes Who You Are | Amy Cuddy | TED Talks )
I know classical Latin and am studying Hebrew to help increase my executive functions such as inhibitory control. I also am learning python 3 and recently learned how to make a GUI.
There are a lot of other complicated details omitted for brevity but you get the idea.
I have some questions. Is resistance training important? I am aware of skeletal muscles producing large amounts of epigenetic factors. Is this hugely significant?
Are there any resources or sources you can recommend to me that kind of serve as a collection site for people like me that are extremely interested in this stuff? My keyword interests would be "epigenetics, BDNF"
Any other observations, criticisms, etc you could offer me? I think that the sort of stuff you are doing here is absolutely critical to humanities survival. It sounds like a joke but brain health is no joke if we are talking about surviving as a civilization. Regards Salvia420 (talk) 06:24, 5 June 2016 (UTC)
Hmm. I know it sounds extremely basic, but I think basically just a well-rounded lifestyle with a decent diet, regular exercise, and an intellectual hobby is about all I'd be comfortable with recommending to anyone. Resistance exercise and aerobic exercise both exert similar effects on cognitive function, but I assume aerobic exercise generally produces a greater effect overall simply due to the amount of energy expended/physical "work" performed by muscles relative to resistance exercise.
While I regularly use databases for writing wikipedia content, the only place that I'd go to for an information search on epigenetics is pubmed. I'm not aware of any databases dedicated exclusively to neuroepigenetics.
Basic is good. It reminds me of a saying, "the master becomes like a novice". My supplementation can look intimidating, complicated and expensive, and those are all attributes that I despise. In reality I do not want to take expensive supplements, because I want to be able to communicate and induce action in the largest amount of people possible. Curcumin, potato starch, etc, nothing is too sophisticated, because as Ghandi said, be the change you want to see, and my actions express my priorities. Creatine, lecithin is meant to conserve the 70% of SAM-e which would be spent manufacturing it, and SAM-e is very beneficial to me.
I have watched a friend with skitzophrenia degenerate in time, this was aided by his daily consumption of large amounts of coca cola (fructose), which damages 200+ brain genes and of which damage fish oil reverses.
In any case I see you deal with a lot of dopamine related articles. Are you aware that intestinal bacteria can produce significant amounts of dopamine?[1][2] 10.1016/j.tifs.2016.05.001
Part of the reason I connect from time to time is because diet, exercise and prebiotics can actually blur into each other.
Prebiotics can alter brain chemicals and pain response like exercise.[3]
It also increase BDNF, like exercise, and that which niacin upregulates. [4]
In short, the dietary state of ketosis seems interesting to study, if you are studying resistance training then there is a subreddit /r/Ketogains for people on the low carbohydrate diets who lift. However in the latter reference there, there is evidence that fatty acid oxidization increases massively in people adapted to a low carbohydrate diet, allowing similar muscle glucose after extended exercise that is comparable to carbohydrate eaters.
Beta-hydroxybutyrate is produced in ketosis. These guys[7] are very well built, darthluigi has been in ketosis for 13 years and has huge muscles, he is a mod over at ketogains on reddit. I think that it is good to study and know that in depth because it's a pretty practical tool, it's a more recently evolved metabolism (ketosis) and has many benefits (fasting, ghrelin, learning and dopamine). Also see the article on slow wave sleep, low carbohydrate diets and getting hot before sleep (exercise, sauna) increases slow wave sleep.
That's about it, no real reason for this conversation except a knowledge transfer. You clarified things and I am sharing the best I have. Is there any non-invasive mechanism I can utilize? I am not looking for replies or conversation, I am a lone wolf with an axe to grind, tired of seeing companies profit from making my loved ones sick and I want to do something about it, people like you care and I want to arm you with more knowledge.Salvia420 (talk) 09:56, 5 June 2016 (UTC)
I'm not particularly interested in ketogenic diets mainly due to my lifestyle. I'm a distance runner, so depleting my body's glycogen supply with that kind of diet would be fairly retarded (as noted in the ref you linked, ATP production through lipolysis is markedly less than through glycolysis/glycogenolysis). The human body eventually goes into a state where most (excluding the portion derived from gluconeogenesis) of the body's energy production occurs via lipolysis/ketosis after enough energy is expended (i.e., glycogen is depleted) anyway - usually happens after running about 18–22 miles. A second reason would be that I'm prescribed amphetamine, which promotes energy production through ketosis/lipolysis via the peripheral release of norepinephrine.[8][9] Because of that, I don't actually need to eat a ketogenic diet to stimulate a mixed state of glycolysis/ketosis while I'm physically inactive.
It's important to recognize that some compounds that are produced in the periphery (i.e., outside the central nervous system) can't enter the brain due to various brain barriers though (e.g., the 2 most notable being the blood-brain barrier and blood-CSF barrier). This includes dopamine, norepinephrine, and serotonin, and many but not all peptides, so an increase in the concentration of these compounds in peripheral blood plasma doesn't necessarily reflect an increase in cerebral blood plasma.
I'm not aware of anything else besides what you've mentioned that has a significant effect on neurotrophic factor signaling. Seppi333 (Insert 2¢) 05:10, 6 June 2016 (UTC)
Keto has helped me lose 70 pounds, however when I was doing physical work and a car rolled backwards down a hill and crashed into the wall that I was working by, and I talked to the owners of the car and walked past it, and had no idea what happened. It also takes forever to recover from physical labor.
Higher energy production is advantageous at times, there are other times where it is less desirable. Keto has been shown to be neuroprotective in animal studies[10] as well as improving mitochondrial function[11] and there are many other worthwhile studies.
I've explained keto in person to a gold medal winning Olympic athlete but not to convince, I am a fanboy of gray area. I myself use 4F-MPH occasionally, however I am concerned about the effects it might have on neurogenesis in the dentate gyrus[12] which is negatively effected by cortisol and similar chemicals that may be produced from phenethylamines.
I personally take a "yin and the yang" type approach to this sort of stuff, because there are clearly positive and negatives to both metabolic states, or basically everything I speak of here, and therefore a utilitarian type of view, where the states are used as instrumentation to achieve various goals, is ideal, I think. I also think that the body reflects this, since when you are in ketosis for a long time, your muscular insulin resistance builds up and you are actually rewarded for exiting the diet for at least a day.
Also note how I prefer the term metabolic state to "keto diet", because there are many diets out there but only two metabolic states. When we base things off how the body works, then we are guaranteed some level of objectivity. It also helps break the gestalt[13] of this diet being an all day thing or commitment or change; that does not necessarily have to be the case. You can and should be eating carbohydrates every day - not that the macronutrient is necessary at all for human survival, however carbohydrates are necessary for beneficial bacteria that have unique metabolic pathways to ferment carbohydrates.[14]
To close on this point, this is a very gray topic and the language we use to convey these concepts is not ideal. In reality one can and perhaps should reap the benefits of both within a certain day. Carbohydrates before one runs, but as for the type, resistant starches produce the most butyrate, and starch also tends to go to the muscles first. These foods (potatoes for example) are also the most filling. Then later meal choices could focus on decreasing carbohydrates, in order to maximize slow wave sleep[15] which is extremely underrated and by far the most important hours in hour day. A large amount of growth hormone is secreted, and the better your slow wave sleep, the more growth hormone.
I take 4F-MPH occasionally, such as now, because it allows me to become a little more synthetic. Bacteria produce dopamine, very interesting but, "so what". I guess that is all it was, was an interesting point, but it allows me to raise other interesting points. Remember I am the inverse agonist guy, and really that is where the interesting research and gene based medicine is headed[16]. The only endogenous inverse agonists known in the body work quite a lot with dopamine, and also share a powerful relationship with Peptide YY and Neuropeptide Y. These are the Agouti-related peptides and are worth studying.[17]
In particular we want to be looking at the Melanocortin 4 receptor[18]. Just notice how powerful that site is. How many metrics of human health it impacts. Antagonists of this site impact memory, so much so that they are being investigate to treat PTSD. Neuropeptide Y is the same way, a spray could be developed for first responders.[19]
Dopamine and neuropeptide Y interact[20] with each other antagonistically when it comes to food intake. Neuropeptide Y is no joke[21]: increasing food intake and storage of energy as fat, reducing anxiety and stress, reducing pain perception, affecting the circadian rhythm, reducing voluntary alcohol intake, lowering blood pressure, and controlling epileptic seizures.
Study reveals gene expression changes with meditation.[22]
Rapid changes in histone deacetylases and inflammatory gene expression in expert meditators.[23]
That is a very rare paper that explains the mechanisms of meditation. As well as why fasting was recommended to go along with it, perhaps along with dietary recommendations (tumeric and prebiotics in vegetables), it just so happens that a lot of these monks were doing a great deal to inhibit HDAC. I consider that paper the crown jewel of 14 years of research into HDACs.Salvia420 (talk) 22:56, 16 June 2016 (UTC)
Sorry for the late reply, I've been sick the last few days and so have been a bit preoccupied. I'm not sure how meditation induces a cellular stimulus to alter HDAC expression, although I suppose it might be through immediate changes in function of the HPA axis, such as a reduction in plasma cortisol/norepinephrine. If similar changes also occur in certain brain structures in people who meditate, such changes would reflect a phenomenon called activity-dependent neuroplasticity; in a nutshell, the repeated use of certain cognitive functions alters the structure and function, as well as gene expression (a necessary mechanism for these changes), in brain structures that mediate those cognitive functions. This is why I mentioned before that having an intellectual hobby is something that I'd suggest to people. Seppi333 (Insert 2¢) 02:34, 22 June 2016 (UTC)
^Branis NM, Wittlin SD (2015). "Amphetamine-Like Analogues in Diabetes: Speeding towards Ketogenesis". Case Rep Endocrinol. 2015: 917869. doi:10.1155/2015/917869. PMC4417573. PMID25960894. Peripheral norepinephrine concentration rises as well. As demonstrated after Dextroamphetamine administration, plasma norepinephrine can rise up to 400 pg/mL, a level comparable to that achieved during mild physical activity [10, 11]. Cumulative effect on norepinephrine concentration is likely when amphetamine-type medications are given in the setting of acute illness or combined with activities leading to catecholamine release, such as exercise. ... The primary effect of norepinephrine on ketogenesis is mediated through increased substrate availability. As shown by Krentz et al., at high physiological concentrations, norepinephrine induces accelerated lipolysis and increases NEFA formation significantly [14]. Secondly, norepinephrine stimulates ketogenesis directly at the hepatocyte level. As reported by Keller et al. [15], norepinephrine infusion increased ketone bodies concentration to a greater degree when compared to NEFA concentration (155 ± 30 versus 57 ± 16%), suggesting direct hepatic ketogenic effect.{{cite journal}}: CS1 maint: unflagged free DOI (link)
^Keller U, Gerber PP, Stauffacher W (1984). "Stimulatory effect of norepinephrine on ketogenesis in normal and insulin-deficient humans". Am. J. Physiol. 247 (6 Pt 1): E732–9. PMID6150642. Elevation of plasma norepinephrine concentrations to stress levels (1,800 pg/ml) resulted in normal subjects in a significant increase in ketone body production by 155% (determined by use of [14C]acetoacetate infusions), in a decrease of the metabolic clearance rate by 38%, hyperketonemia, and in increased plasma free fatty acid (FFA) levels by 57% after 75 min.
Hello! I requested a reassessment of empty nose syndrome after a full rewrite by Jytdog, contributed to by many people in a discussion that has been long and heated, and included new editors, recruited from an ENS forum who were initially very unhappy with the rewrite. I think we've done a good job under difficult conditions and it would be very good for everyone's morale (as well as the correct decision technically!) if the improved quality were acknowledged. Thank you for considering this. Dubbinu | t | c11:45, 12 June 2016 (UTC)
I suspect that I've thanked you before, but here's a cup of tea. You give so much to Wikipedia and its readers, and we really appreciate it. :-) Exercisephys (talk) 01:46, 20 June 2016 (UTC)
For some reason I always thought methamphetamine was metabolized into dextroamphetamine only, no levoamphetamine. I think this stemmed from a long-past dig through the research literature to find articles comparing dextroamphetamine with methamphetamine because of some ridiculous claims that methamphetamine's action was derived primarily from the dextroamphetamine metabolite and thus it is essentially the same drug (which I was trying to see if I could refute). I just can't get over how stupid it was to miss that, especially after I had just looked up Desoxyn's actual API to confirm that it was racemic... I could have sworn the metabolic pathway in the methamphetamine article said dextroamphetamine, not amphetamine, but apparently not...
I was going to revert your reversion, but if I do so everyones blood pressure gets elevated. So maybe I am missing something, which would not be the first time. Several of these papers look and read like specialized primary references, that is the aspect that concerns me with respect to WP:NOTJOURNAL and WP:SECONDARY, not to mention WP:NOTNEWS[1][2][3].[3][4][5]
@Smokefoot: The first 2 papers you cited are primary sources. The latter 3 are medical reviews. The third reference in that list (PMID 27102537) is a medical review that supports the same statement that the primary sources do (I.e., TMA binds to TAAR5). The primary sources were included just for the hell of it; they're not actually necessary for WP:V. Seppi333 (Insert 2¢) 17:50, 27 June 2016 (UTC)
^Liberles SD, Buck LB (2006). "A second class of chemosensory receptors in the olfactory epithelium". Nature. 442 (7103): 645–50. doi:10.1038/nature05066. PMID16878137.
^Liberles SD (July 2009). "Trace amine-associated receptors are olfactory receptors in vertebrates". Annals of the New York Academy of Sciences. 1170: 168–72. doi:10.1111/j.1749-6632.2009.04014.x. PMID19686131.
You claim I removed high-quality MEDRS sources from articles. Honestly, I can't think of that happening once, and don't recall any angry debates about such sources.
With regard to #s 8-11 in the draft list, all I can say is that there are articles edited by respected editors where such references have been allowed. Let's be constructive and work on making it a better checklist. Thanks, following your response here. --Zefr (talk) 01:04, 5 July 2016 (UTC)
Hydroxyisovalerate: not a MEDRS topic (no collective RCTs or Cochrane summaries) and certainly controversial about its unproved importance, now that I review and recall where we debated before. I'd like you to apologize and remove your comment about my MEDRS editing history on Wikipedia talk:WikiProject Medicine, since there is nothing to support you. I'll give you a couple of hours to take care of this. Thanks. --Zefr (talk) 02:03, 5 July 2016 (UTC)
Always friendly and constructively active at and around WT:PHARM and Template talk:Infobox drug. Seppi was patient and persistent and succeeded in gaining the first pharmacology FA star in over three years.
Your ongoing efforts to improve the encyclopedia have not gone unnoticed: You have been selected as Editor of the Week for work on pharmacology-related articls. Thank you for the great contributions! (courtesy of the Wikipedia Editor Retention Project)
I nominate Seppi333 to be Editor of the Week for bringing Amphetamine to FA status, Adderall and Methamphetamine to GA status, and generally for being friendly and constructive at and around WT:PHARM and Template talk:Infobox drug. The standards for a medical FA are extremely high, but Seppi was incredibly patient and persistent and succeeded in gaining the first pharmacology FA star for over three years.
You can copy the following text to your user page to display a user box proclaiming your selection as Editor of the Week:
{{subst:Wikipedia:WikiProject Editor Retention/Editor of the Week/Recipient user box}}
The minimum requirement for source-quality according to WP:MEDRS is secondary medical sources, such as medical reviews, meta-analyses, and systematic reviews. Randomized controlled trials and everything shown below it don't conform to that sourcing policy. Expert opinion is listed in the orange tab.
Hello Seppi333, why did you remove the content on Pokémon Go surrounding the effects on health? It was properly sourced by references listed on WP:VGRS and it isn't a medical article, so it doesn't entirely need to comply with WP:MEDRS in the same way. Anarchyte(work | talk)08:10, 25 July 2016 (UTC)
The problem with those sources is that the health claims are supported entirely by "expert" opinion. Because Pokemon Go is so new, no medical research at all has been conducted and published on its user base. Since MEDRS requires peer-reviewed secondary medical sources (e.g., professional medical textbooks or literature reviews that are published in medical journals) for sourcing medical statements, there really isn't anything that can be said about Pokemon Go directly in terms of any health effects (see the diagram to the right). It's ok to say something like: "People who play Pokemon go walk significantly more than non-players.[non-medical citation] Walking is associated with such-and-such health benefits.[medical citation]" However, attributing the health effects of walking directly to Pokemon Go would be a WP:SYNTH issue and, like I said at WT:MED, someone going around on a motor scooter is obviously not getting those health benefits. Seppi333 (Insert 2¢) 08:38, 25 July 2016 (UTC)
The first entry reflects the 2nd diff that I mentioned above
I see now that in the 2nd entry that I reverted the addition of the heading "Biomarkers". I just remembered that it was me that created the biomarkers heading in the first place, so this edit doesn't actually constitute anything more than a self-revert as far as I can tell.
The 3rd entry reflects the movement of existing content to an entirely new location where the material has never been previously located - I'm not sure which edit this diff is reverting. If the issue is with section headers, I'd be happy to re-add the research section with a biomarkers subsection and then place a {{empty section}} template there. The movement of existing content to a new position isn't noted as a revert in WP:3RR however. If it were, moving 4 different paragraphs around in 4 different edits in an arbitrary article would violate 3RR.
The 4th entry reflects the 1st diff that I mentioned above.
When the issue is under discussion, if you move a paragraph around 4 times, between which others have also moved that same content, yes it would could.
Fair enough. I don't see which WP policy supports the assertion that boldly moving existing text, which may or may not be under discussion on the talk page, to a new location without undoing a previous edit actually reflect a revert though. Seppi333 (Insert 2¢) 19:00, 14 August 2016 (UTC)
Edit: I struck out the 2nd entry since it was actually me that created that heading when I first added the content on biomarkers. Removing that heading was a self-revert. Seppi333 (Insert 2¢) 19:24, 14 August 2016 (UTC)
I just wanted to clarify something really minor that I had done a bad job articulating in that thread... Even though my library's periodical database does recognize Anti-Cancer Agents in Medicinal Chemistry as a peer-reviewed journal, the review you wanted didn't show in my search results until I unchecked the "peer-reviewed only" filter. Sometimes when that has happened before, I've been able to verify my library was right about certain articles not actually being peer-reviewed despite being published in a journal that is generally peer-reviewed (e.g., Once there was a footnote that said something like "Note: This article has been been reviewed.") Other times I couldn't tell if the library was right or not to filter something out (though there hasn't been a time yet where I knew definitively they were wrong). I can't say for sure how reliable that search feature is, so I was just pointing it out in case there were any indicators that might otherwise be easy to overlook if you were assuming everything printed in the journal had been subject to peer review. Anyway, I haven't even seen the source and I trust your judgment if you choose to use it. I just wanted to clarify what I had been trying to say in the other day. :) —PermStrump(talk)11:03, 27 August 2016 (UTC)
@Permstrump: Ah, that's good to know. In this particular case, it doesn't really make much of a difference anyway since I don't think there's anything worth citing from that review. I was hoping that it would at least mention the clinical trials of the compound for cancer cachexia in humans; however, it's basically just a review of preclinical studies involving the pharmacodynamics of HMB as it relates to the pathophysiology of cancer cachexia, which IMO is way too technical for the HMB article. Seppi333 (Insert 2¢) 11:10, 27 August 2016 (UTC)
Seppi333 I added an image here to attract more editors[27], I went through the article you may want to add [28](i found just 1 mention of bodybuilding)it might be beneficial to the article...IMO(good luck!)--Ozzie10aaaa (talk) 12:58, 9 September 2016 (UTC)
Thanks Ozzie. I've been aware of that systematic review, but it hasn't been published yet. I intend to add it as soon as it comes out. Seppi333 (Insert 2¢) 13:02, 9 September 2016 (UTC)
My responses are indented. --Zefr (talk) 22:25, 12 October 2016 (UTC)
You said:
I can't imagine that you aren't aware of the fact that a medical review is not a primary source for information that it cites, so I think it's fairly safe to assume that there's a non-policy related reason that motivates you to remove content that is cited to some of these sources. If you actually talk to me instead of simply revert my edits or remove other content cited to such sources based upon an irrelevant policy justification, I'd probably be willing to seek a middle ground with you and revise what is written in a manner that's acceptable to both of us. However, since I generally have no clue what the real reason is as to why you're removing material in most cases, I don't know how to begin to go about revising article content so that it's mutually acceptable to us.
I'm open to constructive editing with you. I provide edit summaries which I intend to be informative about my motivation for each edit.
The only thing of which I'm aware that you don't like is the use of medical reviews that cite in vitro evidence or animal studies and make a claim that applies to humans to support a medical claim in an article about humans in vivo. As a general rule, I agree that this is bad unless it is made very clear in the article text that this claim is based upon an extrapolation which may not necessarily be valid/relevant to living humans. However, in some of our past interactions, you've removed medical claims about humans in vivo which is cited to reviews of multiple clinical trials on humans. In the instances that you did this, it really irritated me because I didn't understand why you did this - you simply used a clearly irrelevant policy justification for removing content (e.g., "it [i.e., the source] is primary"). As an example, I know that you're opposed to the current article text in 3-hydroxyisovaleric acid#Medical, but I don't understand why or know which statements in that section that you take issue with.
We cannot assume a typical encyclopedia user reads the whole cited article, especially for in vitro research which we know is years from being applicable to humans. I favor simpler content and sources easy to read per the guidelines at #7 WP:NOTJOURNAL. Except for the HMB article–which, to me, is not WP:N (although well-researched and constructed, to your credit)– I pay close attention to reviews on human studies and do not remove them.
If you're willing to talk to me and explain why you feel that the text in that section and the Niacin#Research section (edit: your most recent revision to that section is fine with me) is problematic, I am willing to revise the content in both of these articles and adjust how I write content in the future in order to reconcile our issues with one another. Seppi333 (Insert 2¢) 21:06, 12 October 2016 (UTC)
This paragraph and no revert or edit war are explanation enough. I'm proceeding as usual. Thanks for being a collaborative editor! --Zefr (talk) 22:25, 12 October 2016 (UTC)
User:Zefr in my view, Seppi made a good faith, extensive effort to figure out a way to work collaboratively with you. In my view, your response is not sufficient and - again in my view - you need to try harder. Please try harder to actually reconcile, per the header of Seppi's note. I for one do not want to see either of you have community-mandated limits put on you, but that is where this is going.
I have said before that both of you are part right and part wrong. In my view Zefr is too aggressive with deletions sometimes in ways that go beyond WP:NOTJOURNAL and you do sometimes remove content supported by reviews that discuss clinical trial data; Seppi as I have said you sometimes do drill in too tightly on detail sometimes. Please do try to find the middle ground (which is where the community consensus really is in my view - it really is between each of your tendencies in editing). Please.
@Zefr: Your statement about HMB's notability is an example of what I was talking about when I mentioned that you sometimes use policy justifications that are clearly irrelevant to the context, based upon the letter of the policy that you cited. As noted in MOS:CHEM#Scope, many compounds are suited to have their own wikipedia article - they need only satisfy WP:N; this policy is often very easy to satisfy for many compounds because they tend to be indexed and described in multiple secondary/tertiary databases (e.g., PubChem Compound, DrugBank, Human Metabolome Database, Hazardous Substances Data Bank, Chemspider, etc.); encyclopedic notability is almost an intrinsic attribute of all human biomolecules because there is usually considerable research interest in ascertaining the function (e.g., biomolecular targets) and the effects of human metabolites on human physiology; hence, these substances usually have a sufficient body of secondary literature published about them. E.g., I've created articles on the fairly recently discovered eoxin compounds – Eoxin A4, Eoxin C4, Eoxin D4, and Eoxin E4 (these are structural analogs of LTA4, LTC4, LTD4, and LTE4) – without citing any sources at all simply because this body of literature exists (for the purpose of satisfying the letter of WP:N, most of the database references and reviews cited in the Eoxin article explicitly mention these four biomolecules - I was just too lazy to export the citations to those articles when I made them). In the case of the HMB article, the WP:N#General notability guideline is satisfied by literally any of the cited medical reviews that are written entirely about HMB (e.g., those that mention the compound in the title) or any of the chemical/biomolecule database entries on HMB, because these are secondary and tertiary reliable (i.e., MEDRS-quality) sources that are written by individuals who have no COI related to the compound (to my knowledge, none of the medical reviews or database references are authored by anyone who works for Metabolic Technologies). Since there isn't just 1, but rather dozens of citations on the page which individually satisfy this notability criterion, I really have no clue why you're saying it's not notable. Based upon the letter of WP:N, its notability seems ineffably obvious to me. Seppi333 (Insert 2¢) 23:37, 13 October 2016 (UTC)
@Doc James: Per your 'copyright expert' here [33], this isn't an issue. Nonetheless, I'm willing to adjust some of the unnecessary quotes in some articles when I find the time and feel like working on that. Seppi333 (Insert 2¢) 23:49, 28 September 2016 (UTC)
She doesn't say it is an issue either, and you specifically asked her to comment about that. Edit: to clarify, my point was that it's not a blatant copyright violation like you make it out to be. Seppi333 (Insert 2¢) 00:00, 29 September 2016 (UTC)
[34] - you don't suggest that this might not be a copyvio; you simply say it is a copyvio. What I don't get is why you're taking issue with it now instead of when it was added over a year ago or subsequently edited months later by another editor to clarify what the abbreviation "VTA" referred to. Seppi333 (Insert 2¢) 00:22, 29 September 2016 (UTC)
I definitely didn't say it isn't an issue. What I said is that there isn't a hard and fast rule, and that extensive quotes are forbidden. In a single instance, footnote 23, we have 224 words, not excluding citations. In one of the more extreme cases I know, Harper & Row v. Nation Enterprises, 300-400 words out of a 500 page book were found to be infringement. That was an extreme cases, but how much is too much depends on multiple factors, as I explained there. I did not have time then and still do not have time to assess each quotation for my own opinion. It can take quite a little while to do properly. Each quotation should be assessed to see if it uses minimal non-free content necessary to educational purposes and if it is transformative in nature. If the question cannot be swiftly determined, User:Doc James, the article can be listed at WP:CP using {{copyvio}}, but it's best not to do that if the quotes can be reasonably assessed and truncated as the backlog there currently stretches some months, I fear. Seppi333, we have identified and addressed potential copyright infringement years after the case. This isn't a situation where it's "immediately or never" but whenever reasonable doubt arises. Our policy is that if in doubt, we default to original language. --Moonriddengirl(talk)15:59, 29 September 2016 (UTC)
(More or less in number of indents) I am traveling and so have really tight time right now, but Stanford may help. Basically, your use of copyrighted content should be building, not just borrowing. Not saying that's what's happening here, because I have no idea - I've only read a bit of the conversation, and haven't heavily reviewed the passages, but we've had issues in the past where people have wanted to copy content from the original sources because they were behind paywalls or because they might go offline. If we are including content only so that our readers don't have to review the original (or even primarily), we could well be pushing the boundaries of transformation as a fair use factor. It would be really nice if there were some simple formula for all of this, but, alas, it just doesn't work that way. :/ --Moonriddengirl(talk)13:43, 1 October 2016 (UTC)
HMB quotes
Quite apart from the copyright concerns, are these long quotations really even necessary? It would be more useful for the reader if these quotations were condensed as much as possible to include only the key points. It is difficult to determine the appropriateness of the long quotes in beta-Hydroxy beta-methylbutyric acid since most of the citations are cited several times. But one quotation sticks out. Do we really need to include detailed statistics? In my opinion, the results should be removed so that the focus is on the conclusions. Boghog (talk) 18:34, 29 September 2016 (UTC)
@Boghog: I included some of the statistics in a few quotes which cover computed effect sizes (e.g., the average difference in lean body mass between the treatment and control groups is quoted in certain citations) simply because I generally didn't mention the effect sizes of HMB treatment over a given period in relation to its specified uses in the article. Only the effect size on muscle damage biomarkers following a single bout of exercise in athletes and the standardized average effect size on lean body mass in sarcopenic adults across a range of study durations are mentioned. The effect size for muscle hypertrophy (i.e., the size of a specific exercised muscle group) in athletes, muscle strength in any population group, and lean body mass in non-sarcopenic population groups (e.g., in people with cancer cachexia) weren't covered in the article, but some of these were mentioned in citation quotes. Nonetheless, I agree that the meta-analysis includes some unnecessary statements in its quote - I'm perfectly fine with deleting the part of the quote on body fat hypothesis test. IMO, the part of the quote that covers the sample size and the computed statistics (mean, confidence interval, P value) involving the lean body mass hypothesis test is useful information. Seppi333 (Insert 2¢) 20:01, 29 September 2016 (UTC)
I suppose a reasonable alternative to putting the lean mass statistics in the quote would be to cover the rest of it in "note 2". I'm okay with covering those statistics either in the quote or in the note, so let me know which you prefer; the note is only missing the p value and sample size from the meta-analysis, so I'll add those there and cut the lean mass statistics in the quote later today if you think that's a better approach. Seppi333 (Insert 2¢) 20:18, 29 September 2016 (UTC)
A slight improvement, but I question why it is necessary to discuss the size of the studies and statistics at all. According to MEDMOSWikipedia should concisely state facts about a subject. It should not discuss the underlying literature at any length. Also splitting the material between citations and notes makes it more difficult for the reader. Eliminating the results to focus on the conclusions would also reduce the copyright concerns. Boghog (talk) 20:58, 1 October 2016 (UTC)
When I add a note after a sentence as was done in this particular case, the note typically covers fairly specific/detailed information about a particular claim that was made in the sentence; I only use a note when I believe that the specificity of the statements that I put in a note is disproportionate to the amount of detail added about other claims in the same paragraph; e.g., it just seems out of place if I talk about the effect of HMB on "A" and "B" in one sentence, then describe how much of an effect that HMB has on "B" (i.e., it's effect size) in a particular context, but mention nothing more about the effect of HMB on "A". FWIW, I normally wouldn't describe the sample size of a meta-analysis, but since this is a dietary supplement, I'd imagine that some readers might be skeptical as to the adequacy of the sample or curious about how large it is. I fall into the latter group. The effect size (the mean and confidence interval) indicates how large an effect is, so I think that's actually rather important to report when available+meaningful. I'm almost always interested in the size of an effect that is reported in a meta-analysis, provided that it has a clear clinical interpretation. Simply saying that "there is an effect" isn't particularly informative since an effect could be statistically significant while being clinically trivial/insignificant (e.g., a tiny effect size like a .01 kg gain in muscle mass in HMB treatment groups relative to controls over a 1 month period). Seppi333 (Insert 2¢) 21:48, 1 October 2016 (UTC)
I saw that :(. I think at this point the article would easily pass WP:GAN. Perhaps take it through the Good Article nomination process while waiting to re-nominate it at FAC. Sizeofint (talk) 16:13, 9 October 2016 (UTC)
I agree that it would probably easily pass a GAN at the moment, but it takes forever to get anyone to take on a GA review. Nominating an article at FAC requires that there not be an active GAN and I plan on renominating the article in 8 days (there's a mandatory 14 day waiting period between the closure of a FAC and its renomination). Seppi333 (Insert 2¢) 14:25, 10 October 2016 (UTC)
Hi Seppi333, thanks for the revert in VMAT2 article, I thought I almost do irreversible damage. I can understand that the scientific basis for the God Gene is not well established. However, if you look at the talk page, I think most of the people there agreed that at least some connection should be given between VMAT2 and God gene. God gene article has different sources of citation and most of them come from popular sources. So I think it is not breaking the walled garden clausal. Do you have other opinion about this? Adeuss (talk) 08:54, 18 November 2016 (UTC)
Great article! I've got another great reference and source whose content I would like to add. After that, please consider nominating this article for "Good" status because it is good. Best Regards,
@Barbara (WVS): While I am familiar with that infection, I started editing that article only recently so there's a lot that I'd need to look over before taking the article through the GA process. Anyway, if you can link me to the reference you mentioned, I'll take a look at it to see what I think is worth adding; feel free to add anything you have in mind though (provided that the ref satisfies WP:MEDRS). I'll review the parts of the cryptosporidiosis article that I haven't edited/reviewed yet and then consider nominating it for GA when I get a chance afterward. I've recently been pretty busy off-wiki though. Seppi333 (Insert 2¢) 01:03, 1 December 2016 (UTC)
This message is meant to be a "just think about it" kind of a message. I am pretty busy right now also. With both of us working on it, it wouldn't be such a chore. Oh, I'm pretty much familiar with MEDRS. Best Regards and Best Wishes,
Hey Seppi, a new FAC has new been opened if you're interested in weighing in with support/opposition/suggestions and your final review of MOS compliance. Thanks! TylerDurden8823 (talk) 15:07, 2 January 2017 (UTC)
The mesolimbic pathways, once thought to be the primary controller of pleasure, is now known to have no role in pleasure.
and
The mesocortical dopaminergic pathways also increase the excitability of the prefrontal cortex, a region particularly important in executive function and goal directed behavior.
are not factually accurate or directly supported by a reference. Both of these examples (there are a handful of others others) are statements that aren't correct, but could be retained in the article after slight modification and the addition of a supporting citation. This is why I added an OR tag until I have to time to fix this later tonight (or possibly tomorrow) instead of deleted them. The first example isn't accurate because the role of dopamine in pleasure cognition hasn't been fully established yet; mesolimbic dopamine release isn't strongly positively correlated with the subjective perception of pleasure, but that does not mean that it does not modulate the perception of pleasure or affect learning/memory related to pleasure cognition. The second isn't accurate because dopamine isn't an excitatory neurotransmitter; it can modulate excitatory/glutamatergic neurotransmission by signaling to glutamate neurons through D1-type receptors, but it is not itself an excitatory neurotransmitter since its two receptor subclasses have opposing effects on the target neurons of dopamine pathways. Seppi333 (Insert 2¢) 00:31, 11 January 2017 (UTC)
The first example was talked about, I think in the berridge source, and the excitation of the PFC in the Maia Frank source. So they are directly supported...Petergstrom (talk) 01:54, 11 January 2017 (UTC)
Like I said, I'll deal with this as soon as I have a chance to update the section with appropriate references (being sidetracked by discussions on two talk pages is not helping me do this). Neither reference that you mentioned actually assert what you've written. They do indeed discuss the topics of dopamine in relation to pleasure and mesocortical neuronal activity in relation to excitatory neurotransmission, but they don't make the assertions that you've written. Seppi333 (Insert 2¢) 02:37, 11 January 2017 (UTC)
Amphetamine
Seppi333, Im curious how does the phosphorylation of DAT explain the "phasic" quick DA release, as an intracellular response would take quite a while wouldn't it? Also, are you positive in increased intracellular Na+ doesn't have any effect on DA release?Petergstrom (talk) 22:51, 14 January 2017 (UTC)
@Petergstrom: DAT is a sodium ion-dependent neurotransmitter symporter, meaning it obtains the energy necessary for transporting dopamine across the plasma membrane by cotransporting sodium ions simultaneously. Changes in the Na+ ion gradient are absolutely necessary for DAT to function, it's just not really that notable in the context of efflux vs uptake because changes in intracellular/extracellular Na+ concentrations by DAT simply reflects active dopamine transport (either as reuptake or efflux) by DAT. It's not actually the mechanism that causes DA efflux as much as it is the mechanism by which DAT operates at all.
IIRC, the phosphorylation of DAT by CAMKII initially triggers a very brief (again, IIRC, on the order of microseconds milliseconds) and massive spike in dopamine release through DAT (~10% of total DA efflux by amphetamine over this time period). I need to look for the source that I'm thinking of which mentions this before linking to it - I'll follow up here once I've found it. Seppi333 (Insert 2¢) 23:16, 14 January 2017 (UTC)
Oh, I got the impression from the outdated source I was using that the Na+ concentration had a larger role in the efflux. Oh well.Petergstrom (talk) 23:20, 14 January 2017 (UTC)
I can't seem to find the source I'm remembering that links CAMKII signaling to the transient burst of dopamine efflux that I've stated here; however, I did find several recent reviews which indicated that this form of amphetamine-induced efflux does occur (i.e., ~10% of total DA release on the order of milliseconds), sans a link to CAMKII. I'll look more later since this is something that I think should be added to the amphetamine article's pharmacodynamics section when I update it with more information on amphetamine-induced kinase-dependent modulation of various transporters. Seppi333 (Insert 2¢) 02:08, 21 January 2017 (UTC)
Yeah... I wouldn't touch that article with a 10 foot pole. Correlations between that ratio and anything are probably just spurious due to issues that often arise when analyzing the relationship between two time series data sets (i.e., a data set of that ratio over time is probably non-stationary). Seppi333 (Insert 2¢) 08:53, 18 January 2017 (UTC)
While I did not add additional comments since January 2017, I had been following the Acne FAC. I think it could be a FA someday, but still needs significant work. As I am somewhat semi-retired from Wikipedia, next time it goes up for a FAC, should you think of me, please email me and I will post a review again. Thank you! (just fyi: I am putting a similar note on a few user pages) --My Core Competency is Competency (talk) 13:50, 8 March 2017 (UTC)
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