Wikipedia:Featured article candidates/Amphetamine/archive5: Difference between revisions
→Comments from AmericanLemming: putting all my comments from peer review/4th FAC into a collapsed table for convenience |
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:I quickly went through the ''Interactions'' subsection to give you some new comments to work with, but I need a few days to reread the first half of the article, both to refamiliarize myself with the material and tweak the prose further if need be. I also need to look at the "Overdose" section again and take a look at the changes you've made in response to my comments. Reviewing this is priority number one for my Christmas break, so I should be able to finish it before classes start up again. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 08:11, 15 December 2014 (UTC) |
:I quickly went through the ''Interactions'' subsection to give you some new comments to work with, but I need a few days to reread the first half of the article, both to refamiliarize myself with the material and tweak the prose further if need be. I also need to look at the "Overdose" section again and take a look at the changes you've made in response to my comments. Reviewing this is priority number one for my Christmas break, so I should be able to finish it before classes start up again. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 08:11, 15 December 2014 (UTC) |
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{{collapse top|1=American Lemming's comments from peer review/4th FAC}} |
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'''Lead''' |
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Just finished reading through this part. It looks well-written, well-organized, and well-sourced. The first paragraph is a bit on the long side, as is the lead as a whole, but I'm not really sure you can cut anything out without losing something important. My four comments/questions are as follows: |
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* “At therapeutic doses, this causes emotional and cognitive effects such as euphoria, change in libido, increased arousal, and improved cognitive control. It induces physical effects such as decreased reaction time, fatigue resistance, and increased muscle strength.” This wording implies to me that there aren’t any side effects at therapeutic doses, which probably isn’t the case. |
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:* After rereading it, I think I agree about the sentence on physical effects. The statement on psychological effects seems more or less neutral, since increased arousal can lead to insomnia or increased wakefulness. Similarly, changes in libido can be desirable or undesirable depending on the individual. I'll tweak the the physical effects clause over the next day or so to address this. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::*Now that I look at it again, just leave the sentence alone. Sometimes less is more, and I think making it any wordier would decrease the intelligibility to the general reader. Besides, it is correct as it stands. |
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::::Good point; I'm okay with that. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 08:59, 10 August 2014 (UTC) |
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* “Very high doses can result in a psychosis (e.g., delusions and paranoia) which rarely occurs at therapeutic doses even during long-term use.” First, “a psychosis” sounds awkward to me. If it’s consistent with medical terminology, then by all means keep it, but otherwise I would drop the “a”. Second, so it’s pretty difficult to die of an overdose of amphetamine? That’s the impression I’m getting here. |
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:* There's different types of psychoses, though I agree it sounds weird so I'd be ok with removing it. As for overdoses, it's pretty rare to die from an overdose when medical treatment is sought. The doses that recreational users take are roughly 10-100 times higher than the maximum dose when its used medically. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::*I've gone and removed the "a". |
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* “Unlike methamphetamine, amphetamine's salts lack sufficient volatility to be smoked.” So if you can inhale amphetamine (see infobox), why can’t you smoke it? Or am I confusing smoking cigarettes and smoking other drugs? |
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:*The salts can't be smoked, but they can be snorted (insufflated) as a powder. That's really only a recreational route though. The medical route involves inhaling small amounts of the freebase via an inhaler (e.g., [[:File:Benzedrine_inhaler_for_wiki_article.jpg]]). Unlike the salts, the freebase is a liquid at room temperature and CAN be smoked. Illicit amphetamine is almost never trafficked/sold as the freebase, which I'm assuming is due to its volatility. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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* “Amphetamine is also chemically related to the naturally occurring trace amine neurotransmitters, specifically phenethylamine and N-methylphenethylamine” Two questions here: 1. Does phenethylamine = trace amine neurotransmitters? 2. Is it that amphetamine is chemically related to trace amine neurotransmitters but is most closely related to phenethylamine and N-methylphenethylamine? That’s what it sounds like to me. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 06:26, 4 August 2014 (UTC) |
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:*Both phenethylamine and N-methylphenethylamine are trace amines; N-methylphenethylamine is the most closely chemically-related trace amine to amphetamine since it's an amphetamine isomer. If you can think of a better way to word it, feel free to change it! [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 19:06, 5 August 2014 (UTC) |
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::*I've taken a shot at that; please do double-check to make sure it's accurate. |
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::::Looks good. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 08:59, 10 August 2014 (UTC) |
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I've made two edits to the lead, and I think that will do. The lead is meant to be the most accessible part of the article, and it really isn't the place to be explaining nuances and technicalities. |
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'''Medical''' |
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* Question about this section in general: when we’re talking about medical uses of amphetamine, we’re almost always talking about Adderall, right? |
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:* Adderall (no generic name - i.e., a [[United States Adopted Name|USAN]]/[[International Nonproprietary Name|INN]] - even though it's almost always sold as a generic), dextroamphetamine (tons of brand names/generic forms), and lisdexamfetamine (brand:Vyvanse, still patented) are the currently available amphetamine-based pharmaceuticals; it covers this group of drugs. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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* “Magnetic resonance imaging studies suggest that long-term treatment with amphetamine decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function of the right caudate nucleus.” So it decreases abnormalities in brain structure and function in general and improves function of the right caudate nucleus in particular? If that’s so, I would suggest changing the second half to “ADHD; in particular, it improves the function of the right caudate nucleus.” |
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:* The caudate nucleus was one example that was highlighted in one of the reviews; there's improvement in function in more than one brain structure along the dopamine pathways that it acts upon. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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* “but high doses of dextroamphetamine in such people should be avoided.” Because of the side effects? Long-term damage to some part of the body? |
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:* It exacerbates motor tics in people with Tourette's, which is a harmless but undesirable/annoying side-effect. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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* “task saliency” this may warrant a quick note to define saliency; the Wikipedia article on the subject isn’t terribly helpful. |
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:* Good point; I'll go through later today and add this based upon the definition used in the textbook that cited that passage. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::{{added}} - [https://en.wikipedia.org/w/index.php?title=Amphetamine&diff=620611114&oldid=620324694 Diff] [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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* “but this is prohibited at events regulated by the World Anti-Doping Agency.” From what I can gather, the World Anti-Doping Agency regulates just about every international and professional sporting event. I think this warrants another note/quick explanation in text, perhaps. |
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:* <s>That's fine with me if you'd like to add this.</s> Found a suitable ref, how's this look? [https://en.wikipedia.org/w/index.php?title=Amphetamine&diff=620712448&oldid=620660052 Diff] {{P|1}} [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::* Better and worse. On one hand, I think adding the "regulated by collegiate, national, and international anti-doping agencies" does a much better job of explaining that amphetamine is widely prohibited in sporting events; on the other hand, expanding the tidbit about the World Anti-Doping Agency (WADA) turned the sentence into a run-on. I've trimmed the part on WADA to fix the sentence, and I think you could cut it out entirely if you wanted to. Your fix (adding "regulated by collegiate, national, and international anti-doping agencies") was a lot better than the one I suggested, and we don't need both. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 06:30, 11 August 2014 (UTC) |
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::::{{Removed}} the WADA mention - {{noping|Shudde}} insisted I add it during the FAC review that he didn't finish. I didn't really want it to include it anyway - seemed like trivia. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 16:00, 11 August 2014 (UTC) |
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* “In healthy people at oral therapeutic doses, amphetamine has been shown to increase physical strength, etc.” It may be worthwhile mentioning that there are some minor side-effects, even in healthy people at oral therapeutic doses. Otherwise, why aren’t we all on amphetamine? :) |
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:* There's actually a lot of discussion among the academic community about the use of performance enhancing agents in the general population (e.g., [http://www.ncbi.nlm.nih.gov/pubmed/23767434 this paper elicited quite a lot of responses]). It was only recently determined that low doses of ADHD psychostimulants improve cognitive control in everyone via their effect on [[dopamine D1 receptor]]s in the [[prefrontal cortex]]. |
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:: Back to the issue: I tried to keep this section disjoint from the side effects section to avoid redundancy and maintain neutrality when covering it. I think it'd be alright to mention that there are additional physical side effects in that paragraph; however, I'm not sure it's a good idea to re-list the physical side effects alongside these, since it's both redundant with the side effects section and isn't relevant to the performance enhancing effect. This list of physical enhancement effects isn't included in the side effects section for the same reason. That said, I'll go ahead and add a clause mentioning the presence of additional side effects if that's what you had in mind. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::: I would suggest adding something along the lines of "At these doses, the side effects are minimal." That's enough to help the reader keep the existence of side effects in mind without the unnecessary repetition of listing them all in two places. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 06:47, 11 August 2014 (UTC) |
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::::{{added}} – [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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* Also, with that same sentence, it does seem that this is one place where [[WP:OVERKILL]] might apply. I understand that the article’s on a fairly technical subject, but do you really need four inline citations of the exact same two sources for four words in a row? I suggest you put all three sources at the end of the sentence, like you do elsewhere. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 09:03, 6 August 2014 (UTC) |
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:* I'd be okay with grouping them at the end of the sentence, though the main reason I did this is because the performance enhancing use of these drugs has generated much controversy, and until recently there hasn't been much high quality research/review supporting these effects in humans. I imagine that some people reading this article might come into it with a bias, which is why I cited them by effect. I'll go ahead and group the citations if you think it improves readability - let me know. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::* I recommend doing that. Besides, you quote directly from the source in the inline citation, so if someone doubts whether the sentence is true they can just mouse over the citation and read it for themselves. And as it currently stands it's just hard to read. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 06:53, 11 August 2014 (UTC) |
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::::{{done}} – [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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Sorry for the late follow-up; I've been pretty busy this past week. <s>I'll address these points momentarily!</s> Regards, [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 16:16, 9 August 2014 (UTC) |
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'''Contraindications''' |
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* I don’t think there’s anything in the manual of style against a one-paragraph section, but it does look somewhat odd. What do you think about combining the “Contraindications” section with the “Interactions” section? The “Interactions” section does a nice job of explaining why people with certain conditions or on certain drugs (MAOIs, for instance) shouldn’t take amphetamine. |
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:: I actually agree that it would make sense to combine these, since serious drug interactions give rise to contraindications; however, the current layout of level-2 headers is indicated in [[MOS:MED]], so I can't really deviate from the present state. Barring unusual or unique circumstances, there isn't much wiggle room in the section ordering. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 14:19, 11 August 2014 (UTC) |
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:: After further thought, I think it may be better to keep these sections separate; most of the drug databases we link to in the drugbox don't provide this information together. The FDA uses distinct sections for the information as well. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 18:17, 12 August 2014 (UTC) |
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::: I agree with you; you really can't go against the MOS, especially when you want to get the article to FA status. As the next best alternative, I've added explanatory hatnotes to each section that tell the reader what the section is about and that direct them to the other section if that's not what they were looking for. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 06:39, 13 August 2014 (UTC) |
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::::I think it might be best to use {{tl|see also}} templates here, since some of the contraindications aren't substance-related. It seemed a bit difficult for me to summarize the relationship in a hatnote without it being really long. The first sentence of each section (I think) more or less implies how they're related though. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 09:31, 13 August 2014 (UTC) |
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* “Due to the potential for stunted growth, the USFDA advises monitoring the height and weight of children and adolescents prescribed amphetamines.” This contradicts the statement in the first paragraph of the “Medical uses” section that “humans experience normal development and nerve growth”. Do humans experience normal development when using amphetamine or not? [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 07:20, 11 August 2014 (UTC) |
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:: It's technically a transient effect due to a rebound growth spurt associated with a temporary cessation of treatment. IIRC, all dopaminergic stimulants suppress growth hormone release in adolescents (see [https://docs.google.com/viewer?a=v&pid=sites&srcid=ZGVmYXVsdGRvbWFpbnxzZXBwaWx1cnZlc3BhbmNha2VzfGd4OjcwNTJhNGQ5N2FkYTJiNQ page 4, paragraph 2 in this ref]), so it's not unique to amphetamine. See section 5.3 of [http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf this ref] for more detail. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 14:19, 11 August 2014 (UTC) |
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:::Follow-up: After rereading the sentence I wrote in medical uses, I noticed there isn't actually a contradiction here. The full statement in medical uses is:<blockquote>Long-term amphetamine exposure in some species is known to produce <u>abnormal dopamine system development</u> or nerve damage,[35][36] but humans experience <u>normal development</u> and nerve growth.</blockquote> The "normal development" is in reference to the development of neural systems (not just dopaminergic systems) and the brain, as opposed to the body and physical development. All the citations included in that sentence are confined to this context as well. <br />I've clarified the point in the contraindications section. [https://en.wikipedia.org/w/index.php?title=Amphetamine&diff=620947321&oldid=620789989 diff] These are the references cited: [https://docs.google.com/viewer?a=v&pid=sites&srcid=ZGVmYXVsdGRvbWFpbnxzZXBwaWx1cnZlc3BhbmNha2VzfGd4OjU0ZGJjN2RhYTkwNTlhNmI see P125-127], [https://docs.google.com/viewer?a=v&pid=sites&srcid=ZGVmYXVsdGRvbWFpbnxzZXBwaWx1cnZlc3BhbmNha2VzfGd4OjcwNTJhNGQ5N2FkYTJiNQ see page 2-4], [https://docs.google.com/viewer?a=v&pid=sites&srcid=ZGVmYXVsdGRvbWFpbnxzZXBwaWx1cnZlc3BhbmNha2VzfGd4OjNhMzBjOGJiN2E4YjQ2OTg see P546]. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 18:17, 12 August 2014 (UTC) |
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:::I've changed "normal development" to "normal brain development" and similarly tweaked the note added in the "Contraindications" section. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 06:54, 13 August 2014 (UTC) |
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'''Side effects''' |
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* “Amphetamine may reduce gastrointestinal motility (i.e., intestinal peristalsis) if intestinal activity is high, or increase motility if the smooth muscle of the tract is relaxed.” I have no idea what this sentence means. You do a really nice job explaining what “contraction of the urinary bladder sphincter” means in plain English earlier in this paragraph; I would use that as a model here. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 07:20, 11 August 2014 (UTC) |
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::{{added}} clarification earlier - I forgot to reply here after I did this. Please let me know if the current section is understandable! The current version:<blockquote>If intestinal activity is high, amphetamine may reduce [[gastrointestinal motility]], i.e., the rate at which content moves through the digestive system; however, amphetamine may increase motility when the [[smooth muscle tissue|smooth muscle]] of the tract is relaxed.</blockquote>[[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 18:19, 12 August 2014 (UTC) |
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:::Much better. I've put the definition in parentheses. Personally, I'm curious to know ''what'' causes the smooth muscle of the gastrointestinal tract to relax, but I'm not sure if the average reader shares my interest. :) [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 07:02, 13 August 2014 (UTC) |
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::::I'm not entirely sure to be honest. The [[enteric nervous system]] isn't well understood at the moment. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 20:47, 15 August 2014 (UTC) |
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'''Overdose''' |
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'''Update''': I've finished going through the prose of the Overdose section, though I do plan to go through it again, as it's hard to catch everything the first time around. One general note: I have some issues with the organization of the section, particularly with the beginning and ending and with the subheadings. See the suggestions below. I would like to log in every day and keep an eye on developments here, but in reality we're probably looking at middle to end of next week or possible next weekend; I'm kind of busy through Wednesday. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 09:09, 14 September 2014 (UTC) |
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:1. This section is technical enough that I think a introduction paragraph is warranted. Give the general reader the bottom line about the most effective treatments, give a simplified description of the bimolecular mechanism of addiction, ditto with psychosis, toxicity, and withdrawal. Don't make them go digging for what they're looking for, especially when some of the content is highly technical. |
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:2. Also, I don't think the "Psychosis" and "Toxicity" sections are long enough to warrant their own level 3 headings when "Dependence and addiction" is a level 3 heading with five paragraphs and those two are half-paragraphs. I suggest either significant expansion, consolidation of the two into one level 3 heading subsection, or addition to the top of the section with the rest of the overdose symptoms. |
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:3. Put the Overdose symptoms into a chart as we talked about above and then move the giant annotated image further down so we're not sandwiching text between images. |
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:4. I have some more ideas for rearranging and adding/moving subsection headers, but I'll wait on those until we've decided what to do with the above three proposals. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 09:09, 14 September 2014 (UTC) |
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{{anchor|previous}} |
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::Most of that section is arranged according to [[MOS:MED#Drugs, medications and devices]] and a current proposal on MOS:MED's talkpage. Addiction is in that section because the phenomenon only develops with chronic high-dose use; it literally requires a pathological overactivation of the mesolimbic DA pathway (either directly through DA receptors or indirectly through a possibly [http://www.genome.jp/kegg-bin/show_pathway?hsa05034+2354 complex mechanism, e.g., alcohol]). Toxicity is an indicated subsection of overdose, so it kind of needs to be there. I could merge toxicity and psychosis into one section if you'd prefer. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 03:37, 11 October 2014 (UTC) |
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And now for the prose comments for the rest of the section: |
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*“Cognitive behavioral therapy” Could we give a brief definition in-text? |
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::I'm not sure this would be easy for me to define succinctly... e.g., see [[Cognitive behavioral therapy#Description]]. I could probably define it in a note, I'd be more or less be restating parts of that section. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“Cognitive behavioral therapy is currently the most effective clinical treatment for psychostimulant addiction” So even though it’s the most effective clinical treatment, isn’t that based on extremely limited evidence? Or does the Cochrane Collaboration review from the “Pharmacological treatments” subsection only refer to drugs? |
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::Cochrane's review was just pharmacological therapy.[[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*The last sentence in the “Behavioral treatments” paragraph is pretty much unintelligible to the general reader. While I think the whole sentence is in need of some improvement, the very last part is the worst offender: I’ll start from the beginning of the sentence and take it by parts: |
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*:1. “aerobic exercise decreases psychostimulant self-administration” I added a definition of self-administration in the above paragraph, so this is good. |
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*:2. “attenuates sensitization to the rewarding effects of psychostimulants” So basically you don’t feel as good when you take the drug? |
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:::I'm just deleting that clause because its explanation is a lot longer than the clause itself. I'm not sure it affects reward perception necessarily; psychostimulant sensitization involves an increased of dopamine response in the nucleus accumbens from psychostimulant use, which increases the likelihood of developing an addiction. |
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*:3. “reduces the reinstatement of drug-seeking behavior” So you’re less likely to relapse? |
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:::Yep, I've noted this. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*:4. induces opposite effects on striatal dopamine receptor D2 signaling to those induced by pathological stimulant use.” What are the “opposite effects” on striatal dopamine receptor D2 signaling caused be aerobic exercise, and what are the effects caused by pathological stimulant use? |
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::: I think I've addressed this. Let me know. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“Current models of addiction from chronic drug use involve alterations in gene expression in certain parts of the brain.” Based on what I read later, I take it that “certain parts of the brain” really means the nucleus accumbens. How about “in certain parts of the brain, especially the nucleus accumbens”? |
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:::{{Done}} [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“The most important transcription factors” I would suggest adding a note explaining the role of transcription factors in gene expression. |
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::{{in progress}} I need to find a MEDRS-quality source first, but I intend to do this. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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:::{{done}} Added this as a note next to the first use of the "transcription factor" phrase. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“since its overexpression in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction” I assume you’re referencing necessary and sufficient cause here, but the fact that you neither mention the word “cause” nor link to [[Causality#Logic|Necessary and sufficient causes]] is cause for confusion. Also, why is ΔFosB considered a “necessary and sufficient cause” of these neural changes? And what are these neural adaptations, anyway? If the neural adaptations are talked about in the caption to the giant annotated image, you should add “(see caption below image to the right)” so people can read up on that if they want to. |
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:::I meant to link to [[necessary and sufficient]]; I did it in other articles, but oddly enough, I missed it here. Essentially it means that the plasticity of addiction and ΔFosB overexpression always occur together, never alone. It's necessary and sufficient because it's been observed to produce this plasticity with viral overexpression (using [[viral vector]] gene transfer) and their occurrence doesn't occur with a viral block of ΔFosB expression (i.e., viral overexpression of ΔJunD opposes ΔFosB and hence this plasticity with concurrent drug use). This is rather technical - the reference that quotes that sentence explains it more. As for the plasticity, some of it is indicated in the psychostimulant column of the table below, which I've transcluded to several articles from [[FOSB]]. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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{{:FOSB|Table title=Summary of addiction-related plasticity|class=wikitable mw-collapsible mw-collapsed}} |
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*“Since natural rewards induce ΔFosB just like drugs of abuse do” What does it mean that they “induce” ΔFosB? They cause the body to make more of it? |
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:::It means it increases [[gene expression]] of ΔFosB. I've clarified this and linked to [[inducible gene]] with a pipe as "Since natural rewards [[inducible gene|induce expression]] of ΔFosB..." [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“and amphetamine-induced sex addictions.” Do these amphetamine-induced sex addictions occur frequently at therapeutic and/or recreational doses? How does amphetamine cause sex addictions? Does an amphetamine-induced sex addiction mean that you’re addicted to both amphetamine and sex? I’m not harping on this just because it mentions sex; I feel that the sentence as is introduces a condition/disease without really explaining it. |
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:::I clarified the text a little and added the appropriate quote to the reference ("In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex"). It's simply compulsive sexual behavior as a result of amphetamine use. There is a notable interaction between reward perception with sexual behavior and amphetamine use, and an overactivation of DA networks involved in reward perception and reinforcement mediate that phenomenon. I actually rewrote [[sex addiction]] recently to try to explain that concept better (and because I got into an edit war with another editor...). Let me know if you think it needs more work in the article. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“Psychosis” subsection: I feel that the current length of this section doesn’t do the topic justice. We don’t need four full paragraphs about it, but how about 8-10 sentences instead of the current four? |
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::I'll look through the Cochrane review soon and see if I can add more material. Most of the content in the [[amphetamine psychosis]] section either isn't particularly relevant (e.g., first paragraph) or isn't cited by a MEDRS-quality source. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 03:47, 11 October 2014 (UTC) |
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*“Toxicity” subsection: Same concern as with the Psychosis subsection. Again, I’d feel much more comfortable with the article’s comprehensiveness with 8-10 sentences here instead of three. |
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::There really isn't much to say about amphetamine toxicity in humans. Direct toxicity simply does not occur. I could probably write a whole paper on direct DA toxicity in rats, but including that in the article would be sort of POV because it's misleading. The mechanics of indirect toxicity are mediated entirely through oxidative events related to excessive dopamine release. I could probably add a sentence or two on its mechanics, but these are necessarily going to be fairly technical descriptions compared to the text currently in that section. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 03:47, 11 October 2014 (UTC) |
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*Actually, as I come to think about it, how about we expand the above two subsections slightly, delete the subsection headings, and then move them to the topic of the section where the other overdose side-effects are found? |
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::Due to the the MOS indications that I mentioned in a [[#previous]] bullet, and the points I raised in the above two bullets, it may be best to simply combine the two sections if you'd prefer to have fewer subsections under the Overdose heading. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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*“Manufacturer prescribing information does not indicate the presence” Which manufacturer? Or are we talking about US FDA prescribing regulations? I’m confused. [[User:AmericanLemming|AmericanLemming]] ([[User talk:AmericanLemming|talk]]) 09:09, 14 September 2014 (UTC) |
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:::This actually refers to the prescribing information from all manufacturers of amphetamine pharmaceuticals. The prescribing information is under copyright, and they vary in format, but they're pretty much standardized in the information in they provide (I can link you to a few examples for amphetamine pharmaceuticals on pubchem if you'd like to see what I mean), even though it is copyrighted. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) |
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::::{{ping|AmericanLemming}} I've pasted this from the review so that I can address/reply the points by issue here. I've added the table for the symptoms - let me know what you think. There was a small addition of content in the behavioral treatments section since you last checked it as well. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']] ([[User Talk:Seppi333|Insert '''2¢''']] | [[Special:WhatLinksHere/User:Seppi333/Maintenance|''Maintained'']]) 01:25, 11 October 2014 (UTC) |
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{{collapsebottom}} |
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'''Interactions''' |
'''Interactions''' |
Revision as of 10:06, 18 December 2014
Amphetamine (edit | talk | history | links | watch | logs)
Toolbox |
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- Nominator(s): Seppi333 (Insert 2¢ | Maintained) & Boghog (talk) 00:25, 6 December 2014 (UTC)
I'd be surprised if anyone doesn't know what this article is about, based from the name alone, so I'll forego a description. Seppi333 (Insert 2¢ | Maintained) 00:25, 6 December 2014 (UTC)
Comments from AmericanLemming
@AmericanLemming: I'm renominating this now, though I assume you'll be busy until later in the month, so no worries. I've made this section for you in advance. Seppi333 (Insert 2¢ | Maintained) 00:25, 6 December 2014 (UTC)
- I quickly went through the Interactions subsection to give you some new comments to work with, but I need a few days to reread the first half of the article, both to refamiliarize myself with the material and tweak the prose further if need be. I also need to look at the "Overdose" section again and take a look at the changes you've made in response to my comments. Reviewing this is priority number one for my Christmas break, so I should be able to finish it before classes start up again. AmericanLemming (talk) 08:11, 15 December 2014 (UTC)
American Lemming's comments from peer review/4th FAC
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Lead Just finished reading through this part. It looks well-written, well-organized, and well-sourced. The first paragraph is a bit on the long side, as is the lead as a whole, but I'm not really sure you can cut anything out without losing something important. My four comments/questions are as follows:
I've made two edits to the lead, and I think that will do. The lead is meant to be the most accessible part of the article, and it really isn't the place to be explaining nuances and technicalities. Medical
Sorry for the late follow-up; I've been pretty busy this past week. Contraindications
Side effects
Overdose Update: I've finished going through the prose of the Overdose section, though I do plan to go through it again, as it's hard to catch everything the first time around. One general note: I have some issues with the organization of the section, particularly with the beginning and ending and with the subheadings. See the suggestions below. I would like to log in every day and keep an eye on developments here, but in reality we're probably looking at middle to end of next week or possible next weekend; I'm kind of busy through Wednesday. AmericanLemming (talk) 09:09, 14 September 2014 (UTC)
And now for the prose comments for the rest of the section:
An Error has occurred retrieving Wikidata item for infobox Protein fosB, also known as FosB and G0/G1 switch regulatory protein 3 (G0S3), is a protein that in humans is encoded by the FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene.[1][2][3] The FOS gene family consists of four members: FOS, FOSB, FOSL1, and FOSL2. These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1. As such, the FOS proteins have been implicated as regulators of cell proliferation, differentiation, and transformation.[1] FosB and its truncated splice variants, ΔFosB and further truncated Δ2ΔFosB, are all involved in osteosclerosis, although Δ2ΔFosB lacks a known transactivation domain, in turn preventing it from affecting transcription through the AP-1 complex.[4] The ΔFosB splice variant has been identified as playing a central, crucial[5][6] role in the development and maintenance of addiction.[5][7][8] ΔFosB overexpression (i.e., an abnormally and excessively high level of ΔFosB expression which produces a pronounced gene-related phenotype) triggers the development of addiction-related neuroplasticity throughout the reward system and produces a behavioral phenotype that is characteristic of an addiction.[5][8][9] ΔFosB differs from the full length FosB and further truncated Δ2ΔFosB in its capacity to produce these effects, as only accumbal ΔFosB overexpression is associated with pathological responses to drugs.[10] DeltaFosBDeltaFosB – more commonly written as ΔFosB – is a truncated splice variant of the FOSB gene.[11] ΔFosB has been implicated as a critical factor in the development of virtually all forms of behavioral and drug addictions.[6][7][12] In the brain's reward system, it is linked to changes in a number of other gene products, such as CREB and sirtuins.[13][14][15] In the body, ΔFosB regulates the commitment of mesenchymal precursor cells to the adipocyte or osteoblast lineage.[16] In the nucleus accumbens, ΔFosB functions as a "sustained molecular switch" and "master control protein" in the development of an addiction.[5][17][18] In other words, once "turned on" (sufficiently overexpressed) ΔFosB triggers a series of transcription events that ultimately produce an addictive state (i.e., compulsive reward-seeking involving a particular stimulus); this state is sustained for months after cessation of drug use due to the abnormal and exceptionally long half-life of ΔFosB isoforms.[5][17][18] ΔFosB expression in D1-type nucleus accumbens medium spiny neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement while decreasing sensitivity to aversion.[5][8] Based upon the accumulated evidence, a medical review from late 2014 argued that accumbal ΔFosB expression can be used as an addiction biomarker and that the degree of accumbal ΔFosB induction by a drug is a metric for how addictive it is relative to others.[5] Chronic administration of anandamide, or N-arachidonylethanolamide (AEA), an endogenous cannabinoid, and additives such as sucralose, a noncaloric sweetener used in many food products of daily intake, are found to induce an overexpression of ΔFosB in the infralimbic cortex (Cx), nucleus accumbens (NAc) core, shell, and central nucleus of amygdala (Amy), that induce long-term changes in the reward system.[19]Role in addiction
Chronic addictive drug use causes alterations in gene expression in the mesocorticolimbic projection, which arise through transcriptional and epigenetic mechanisms.[6][28][29] The most important transcription factors that produce these alterations are ΔFosB, cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), and nuclear factor kappa B (NF-κB).[6] ΔFosB is the most significant biomolecular mechanism in addiction because the overexpression of ΔFosB in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and behavioral effects (e.g., expression-dependent increases in drug self-administration and reward sensitization) seen in drug addiction.[5][6][8] ΔFosB overexpression has been implicated in addictions to alcohol, cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others.[5][6][28][30][31] ΔJunD, a transcription factor, and G9a, a histone methyltransferase, both oppose the function of ΔFosB and inhibit increases in its expression.[6][8][32] Increases in nucleus accumbens ΔJunD expression (via viral vector-mediated gene transfer) or G9a expression (via pharmacological means) reduces, or with a large increase can even block, many of the neural and behavioral alterations seen in chronic drug abuse (i.e., the alterations mediated by ΔFosB).[9][6] Repression of c-Fos by ΔFosB, which consequently further induces expression of ΔFosB, forms a positive feedback loop that serves to indefinitely perpetuate the addictive state. ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise.[6][12] Natural rewards, similar to drugs of abuse, induce gene expression of ΔFosB in the nucleus accumbens, and chronic acquisition of these rewards can result in a similar pathological addictive state through ΔFosB overexpression.[6][7][12] Consequently, ΔFosB is the key mechanism involved in addictions to natural rewards (i.e., behavioral addictions) as well;[6][7][12] in particular, ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward.[12] Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional reward cross-sensitization effects[note 1] that are mediated through ΔFosB.[7][33] This phenomenon is notable since, in humans, a dopamine dysregulation syndrome, characterized by drug-induced compulsive engagement in natural rewards (specifically, sexual activity, shopping, and gambling), has also been observed in some individuals taking dopaminergic medications.[7] ΔFosB inhibitors (drugs or treatments that oppose its action or reduce its expression) may be an effective treatment for addiction and addictive disorders.[34] Current medical reviews of research involving lab animals have identified a drug class – class I histone deacetylase inhibitors[note 2] – that indirectly inhibits the function and further increases in the expression of accumbal ΔFosB by inducing G9a expression in the nucleus accumbens after prolonged use.[9][32][35][36] These reviews and subsequent preliminary evidence which used oral administration or intraperitoneal administration of the sodium salt of butyric acid or other class I HDAC inhibitors for an extended period indicate that these drugs have efficacy in reducing addictive behavior in lab animals[note 3] that have developed addictions to ethanol, psychostimulants (i.e., amphetamine and cocaine), nicotine, and opiates;[32][36][37][38] however, as of August 2015[update], few clinical trials involving humans with addiction and any HDAC class I inhibitors have been conducted to test for treatment efficacy in humans or identify an optimal dosing regimen.[note 4] Plasticity in cocaine addiction
ΔFosB levels have been found to increase upon the use of cocaine.[40] Each subsequent dose of cocaine continues to increase ΔFosB levels with no apparent ceiling of tolerance.[citation needed] Elevated levels of ΔFosB leads to increases in brain-derived neurotrophic factor (BDNF) levels, which in turn increases the number of dendritic branches and spines present on neurons involved with the nucleus accumbens and prefrontal cortex areas of the brain. This change can be identified rather quickly, and may be sustained weeks after the last dose of the drug. Transgenic mice exhibiting inducible expression of ΔFosB primarily in the nucleus accumbens and dorsal striatum exhibit sensitized behavioural responses to cocaine.[41] They self-administer cocaine at lower doses than control,[42] but have a greater likelihood of relapse when the drug is withheld.[18][42] ΔFosB increases the expression of AMPA receptor subunit GluR2[41] and also decreases expression of dynorphin, thereby enhancing sensitivity to reward.[18]
Summary of addiction-related plasticity
Other functions in the brainViral overexpression of ΔFosB in the output neurons of the nigrostriatal dopamine pathway (i.e., the medium spiny neurons in the dorsal striatum) induces levodopa-induced dyskinesias in animal models of Parkinson's disease.[43][44] Dorsal striatal ΔFosB is overexpressed in rodents and primates with dyskinesias;[44] postmortem studies of individuals with Parkinson's disease that were treated with levodopa have also observed similar dorsal striatal ΔFosB overexpression.[44] Levetiracetam, an antiepileptic drug, has been shown to dose-dependently decrease the induction of dorsal striatal ΔFosB expression in rats when co-administered with levodopa;[44] the signal transduction involved in this effect is unknown.[44] ΔFosB expression in the nucleus accumbens shell increases resilience to stress and is induced in this region by acute exposure to social defeat stress.[45][46][47] Antipsychotic drugs have been shown to increase ΔFosB as well, more specifically in the prefrontal cortex. This increase has been found to be part of pathways for the negative side effects that such drugs produce.[48] See alsoNotes
References
Further reading
External links
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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Interactions
- “Inhibitors of the enzymes that metabolize amphetamine…will prolong its elimination half-life” What the clinical significance of having amphetamine in your system longer? Does that make it easier to overdose on it?
- “increase plasma catecholamines” I know we’re mentioned it in the lead, but adding “(i.e. norepinephrine and dopamine” after catecholamines may be helpful for the general reader. AmericanLemming (talk) 08:11, 15 December 2014 (UTC)
Comments from Jfdwolff
This is a very good article. Balanced in an area where there's information from numerous domains to compare and weigh. Using every way possible to clarify difficult concepts using notes and tooltips etc.
- While almost all sections are supported heavily by secondary sources, I still find a number of primary sources in some sections. I found one of these to be over 20 years old (e.g. Imperato et al 1993). They may not have been reproduced or included in the current paradigm.
- A number of references currently contains a message that the "chapter" parameter is being ignored. Can this be fixed?
I will see if any other concerns arise from reviews by others (as I cannot claim much expertise in the subject matter) but I have a low threshold for support provided the primary sources concern is addressed. JFW | T@lk 22:18, 6 December 2014 (UTC)
- Don't bother with doing so - I replaced it with a new review. I don't mind cutting primary sources because any that are included are unnecessary for WP:V, so if any others are a concern, let me know. The few primary sources covering medical content in humans are all coupled to WP:MEDRS-quality reviews, as far as I'm aware. I'm quite pedantic about citing anything medical regarding humans with medical reviews or high-quality pharmacology references. In any case, I replaced it with a new medical review covering preclinical evidence (I assume this means "lab animals", so I kept that phrase). That sentence was just meant to provide context to indicate that dopamine and acetylcholine interactions from amphetamine are not unique to humans.
- In the few other cases that I included the primary sources with reviews, I did so because: (1) I found it hard to find the information in the review when re-checking (the review on flavin-containing monooxygenase, where it's in a table instead of the article) or (2) I thought the material was important, but not widely covered in reviews in a relevent context or relevant databases (e.g., the dopamine beta-hydroxylase references). Seppi333 (Insert 2¢ | Maintained) 23:53, 6 December 2014 (UTC)
- Edit: Forgot to note, I'm discussing the citation error issue on the CS1 module talkpage. Will probably have them fixed by tomorrow. Seppi333 (Insert 2¢ | Maintained) 00:35, 7 December 2014 (UTC)
- @Jfdwolff: Everything should be fixed now; let me know if anything is still amiss. Citation errors were really just an error in the module script. Seppi333 (Insert 2¢ | Maintained) 03:51, 8 December 2014 (UTC)
Comments from Axl
This is a point that I made at previous FACs: From "Uses", subsection "Medical", paragraph 4: "A Cochrane Collaboration review on the treatment of ADHD in children with tic disorders indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine in such people should be avoided." Should high doses be avoided in children with tic disorders more so than in children without tic disorders? Axl ¤ [Talk] 10:51, 8 December 2014 (UTC)
- Sorry, I hadn't realized my previous comment didn't address your concern - I reworded the sentence to how I interpreted what Cochrane was essentially saying: "A Cochrane Collaboration review on the treatment of ADHD in children with tic disorders indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in such individuals."
If you'd prefer different wording, feel free to edit that line to your liking. I very seldom revert a reviewers changes to an article in the event you're concerned about it. Seppi333 (Insert 2¢ | Maintained)- No, not in "such individuals", in "some" individuals. Stimulants do not exacerbate tics. *SOME* people may have issues, though. Here are the words from the Cochrane review:
- To evaluate evidence for this reported phenomenon we searched for clinical trials of medications for ADHD used specifically in children with tic disorders. The trials indicate that a number of stimulant and non-stimulant medications are safe and effective treatments for ADHD symptoms and do not worsen tics. High dose stimulants may transiently worsen tics in some children, and worsening tics may limit dose increases of stimulants in some children, but in the majority of children both tics and ADHD symptoms improve with use of stimulant medications.
- And, surprise, that is correct :) "Some" is the correct word. SandyGeorgia (Talk) 22:09, 10 December 2014 (UTC)
- I don't mind how the statement is worded, though I think this is worth noting: Cochrane's samples were entirely upon individuals with ADHD and some form of tic disorder, so they technically can't generalize the population outside that group without it producing biased statistical inference (i.e., the samples are nonrespresentative of individuals with ADHD in general with or without tic disorders). That's why I assumed their analysis was always in context of the sample and consequently worded that sentence with "such"; in any event, I actually agree completely that dopaminergic-related movement side effects are not specific to individuals with tic disorders. Anyone can develop abnormal involuntary movements and hypersensitive locomotor responses using dopaminergic stimulants because, as in the nucleus accumbens, dopamine (and hence DA stims like amphetamine) induces nigrostriatal ΔFosB in response to chronic sufficiently high dosing.([1] - epigenetics/pharmacogenomics of involuntary motor activity from chronic high-dose L-dopa therapy) Nigrostriatal ΔFosB overexpression, coupled with high-dose amphetamine/methamphetamine, would necessarily produce abnormal motor function and dysregulated motor responses (e.g., substituted amphetamine induced stereotypies). This may or may not contribute to tics though, depending upon which neural pathways give rise to tic disorders. Seppi333 (Insert 2¢ | Maintained) 01:11, 11 December 2014 (UTC)
- Thank you. The current text is fine. Axl ¤ [Talk] 09:48, 12 December 2014 (UTC)
- I don't mind how the statement is worded, though I think this is worth noting: Cochrane's samples were entirely upon individuals with ADHD and some form of tic disorder, so they technically can't generalize the population outside that group without it producing biased statistical inference (i.e., the samples are nonrespresentative of individuals with ADHD in general with or without tic disorders). That's why I assumed their analysis was always in context of the sample and consequently worded that sentence with "such"; in any event, I actually agree completely that dopaminergic-related movement side effects are not specific to individuals with tic disorders. Anyone can develop abnormal involuntary movements and hypersensitive locomotor responses using dopaminergic stimulants because, as in the nucleus accumbens, dopamine (and hence DA stims like amphetamine) induces nigrostriatal ΔFosB in response to chronic sufficiently high dosing.([1] - epigenetics/pharmacogenomics of involuntary motor activity from chronic high-dose L-dopa therapy) Nigrostriatal ΔFosB overexpression, coupled with high-dose amphetamine/methamphetamine, would necessarily produce abnormal motor function and dysregulated motor responses (e.g., substituted amphetamine induced stereotypies). This may or may not contribute to tics though, depending upon which neural pathways give rise to tic disorders. Seppi333 (Insert 2¢ | Maintained) 01:11, 11 December 2014 (UTC)
- No, not in "such individuals", in "some" individuals. Stimulants do not exacerbate tics. *SOME* people may have issues, though. Here are the words from the Cochrane review:
- Sorry, I hadn't realized my previous comment didn't address your concern - I reworded the sentence to how I interpreted what Cochrane was essentially saying: "A Cochrane Collaboration review on the treatment of ADHD in children with tic disorders indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in such individuals."
- From "Contraindications": "It is also contraindicated in people currently experiencing... severe hypertension." The FDA reference states "Moderate to severe hypertension". The Inchem reference just states "hypertension". Axl ¤ [Talk] 11:07, 8 December 2014 (UTC)
- That was probably pruned during previous copyediting - I've cut the word "severe" and left it at hypertension. Seppi333 (Insert 2¢ | Maintained) 13:46, 8 December 2014 (UTC)
- I am wary of adding "elevated blood pressure" in parentheses after "hypertension". Hypertension is more than simply elevated blood pressure. Also, elevated blood pressure is subsequently noted as a cautionary feature that should be monitored. (This statement is in line with the references.)
- That was probably pruned during previous copyediting - I've cut the word "severe" and left it at hypertension. Seppi333 (Insert 2¢ | Maintained) 13:46, 8 December 2014 (UTC)
- I am inclined to delete the "clarification" of the meaning of hypertension from the text. (I note that the subsequent cautionary features such as bipolar disorder, psychosis and Raynaud's phenomenon do not have associated short definitions.) If you insist that a short definition should be included for hypertension, perhaps change it to "persistent blood pressure"? Axl ¤ [Talk] 09:56, 12 December 2014 (UTC)
- Deleted it; I don't care for the parenthetical clarification - I only added them in cases where they were requested. In this case, it was redundant anyway. Seppi333 (Insert 2¢ | Maintained) 09:12, 14 December 2014 (UTC)
- The clarification seems to have been changed to "high blood pressure". Axl ¤ [Talk] 21:40, 16 December 2014 (UTC)
- Deleted it; I don't care for the parenthetical clarification - I only added them in cases where they were requested. In this case, it was redundant anyway. Seppi333 (Insert 2¢ | Maintained) 09:12, 14 December 2014 (UTC)
- I am inclined to delete the "clarification" of the meaning of hypertension from the text. (I note that the subsequent cautionary features such as bipolar disorder, psychosis and Raynaud's phenomenon do not have associated short definitions.) If you insist that a short definition should be included for hypertension, perhaps change it to "persistent blood pressure"? Axl ¤ [Talk] 09:56, 12 December 2014 (UTC)
- From "Side effects", subsection "Physical", paragraph 1: "Cardiovascular side effects can include irregular heartbeat (usually an increased heart rate)." Not all arrhythmias are irregular. Indeed atrial fibrillation is the only common arrhythmia that is irregular. I am aware that the linked article, "Cardiac dysrhythmia", states that "irregular heartbeat" is a synonym. The statement is inaccurate. The reference seems to be inaccessible at the moment. Axl ¤ [Talk] 10:15, 12 December 2014 (UTC)
- I tweaked this as such. Let me know if that works. Wasn't sure how you wanted it. Seppi333 (Insert 2¢ | Maintained) 09:12, 14 December 2014 (UTC)
- No! I recommend "cardiac dysrhythmia (abnormal heart rhythm)." Axl ¤ [Talk] 21:45, 16 December 2014 (UTC)
- I tweaked this as such. Let me know if that works. Wasn't sure how you wanted it. Seppi333 (Insert 2¢ | Maintained) 09:12, 14 December 2014 (UTC)
Comments from Abductive
- I feel that the lead is a bit overlong.
- The lead certainly is too technical, and jumps around between the historical, medical, chemical, abuse, and legal aspects of the topic. I'll break this down by coding each sentence or part of sentence: 1st paragraph; m,hc,c,c,m,ma,la. Second paragraph; h,hm,m,m,m. 3rd; a,am,am,a. 4th; c,ca,m,c. Abductive (reasoning) 04:36, 18 December 2014 (UTC)