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Nicotine addiction[edit]

Sorry if this is a stupid question, but should a reader typing in "Nicotine addiction" be redirected to Nicotine#Reinforcement_disorders(now Nicotine#Reinforcement disorders and cognitive effects), or Nicotine dependence? I realize that there exist differing definitions of substance dependence and addiction, but a reader may not (and perhaps the adverse consequences of smoking, and the fact that most smokers want to quit,[1][2] make it a bit moot). Is content quality in Nicotine dependence a factor? HLHJ (talk) 06:05, 21 October 2018 (UTC)

I know ICD treats addiction and dependence as synonyms (see .2 at F10-F19). Other narcotic addictions redirect to either a "use disorder" or "dependency" article, rather than the article on the substance – or a subsection thereof; examples opioid addiction, cocaine addiction and cannabis addiction. Little pob (talk) 12:16, 21 October 2018 (UTC)
Addiction and dependence are not synonymous, but the distinction is probably lost on the average reader. Seppi333 (Insert ) 23:59, 21 October 2018 (UTC)
The Nicotine dependence article discusses both use as synonyms and distinctions, without refs, so I've taken the liberty of adding your ref, Little pob. The article also discusses things that are addiction by any definition. Perhaps a rename of the article would be the best way to deal with this?
Separately, the Nicotine article is in terrible shape. I had a go at it to try and make it vaguely conform to MOS:MED, but it still contains a lot of contradictions and some dubious sources. Doc James, I've seen you fix up such things before, and know that you are much better at it than I. Could you possibly have a look at it? If I've made it worse I apologize. HLHJ (talk) 05:27, 27 October 2018 (UTC)
Nicotine is not strictly a drug. It should be structured like Alcohol, not like Aspirin. WhatamIdoing (talk) 15:21, 27 October 2018 (UTC)
Thank you, WhatamIdoing. Alcohol and Ethanol seem to be structured quite differently; what guidelines would apply here? HLHJ (talk) 16:34, 27 October 2018 (UTC)
How does one reach the conclusion that alcohol and nicotine are not strictly drugs?--Literaturegeek | T@1k? 17:34, 27 October 2018 (UTC)
Nicotine is not just a medication but also a drug of abuse I think is what WAID means. Doc James (talk · contribs · email) 17:55, 27 October 2018 (UTC)
Also that nicotine has uses that have nothing to do with human consumption, most famously as an insecticide, and that it is a naturally occurring substance whose existence is independent of any uses that we might put it to.
There are various definitions of drug. The FDA's definition is that a drug is whatever they've approved. A more generic is anything that you give with the intent to treat a condition. In that model, a glass of water is a drug if you give it to someone with a dehydration headache, and a cup of orange juice is a drug if you give it to someone whose blood sugar is low. I see the utility of this definition, but I don't subscribe to it. My personal definition of drug never includes water, and it is not even broad enough to encompass lime juice, even though that lime juice has been given with the intention of treating a deadly disease. Lime juice IMO is a food, and only tangentially a treatment for nutritional deficiency. Nicotine's claim to being "a drug" is debatable – it falls somewhere on the drug–non-drug spectrum between lime juice and cyclophosphamide – but I personally place it closer to lime juice than to cyclophosphamide. WhatamIdoing (talk) 01:00, 29 October 2018 (UTC)
I think WaID is being just a bit reductive here for argument's sake. The FDA's definition of "drug" is found in 21 USC 321 as seen here. Good luck deciphering what all the "and"s mean. Tobacco products fall under their own definition. LeadSongDog come howl! 19:08, 29 October 2018 (UTC)
(edit conflict) Seppi333, you reverted all of my edits (except one fairly minor edit), stating that "Content on performance enhancement goes under uses; several new statements (e.g., cognitive decline and carcinogenicity) cite sources that state this about smoking and tobacco, but not nicotine (WP:V); lastly, non-clinical neuropsychopharnacology claims requires only SCIRS, not MEDRS" and "I reverted a few constructive edits, but the majority of the changes made were not an improvement". I'd like to put the constructive edits back, so I'd like to clear up what the problems were. I've re-tagged some of my concerns.
I'm not sure why a "Psychoactive effects" section came right at the head of the article. Initially, I just tried to balance it by adding info about the negative mental effects of nicotine (with MEDRS). This was the first edit you reverted; I assume that you objected to the use of a review on the effects of nicotine in cigarettes. However, the review discusses measurements of blood nicotine and statements about nicotine.
I think you are acting on the assumption that e-cigarettes deliver just nicotine, so studies using e-cigarettes can be used to make statements about the effects of nicotine, while studies using cigarettes cannot. I don't think either of these views are supported by MEDRS. E-cigs essentially emit a wet low-temperature smoke, as they char a tobacco extract and simultaneously vapourize the water it was suspended in. Then they cool the vapour into a cloud of wet steam, which visually hides the smoke generated by pyrolysing the tobacco extract (though it still smells like pipe smoke). MEDRS seem to draw conclusions about the effects of nicotine from NRT studies and from findings of similar effects from a variety of nicotine-delivery devices; snus, cigarettes, and e-cigs are all relevant (the carcinogenicity statement was made about snus and drawn from a review on the global disease burden from smokeless tobaccos). Conclusions are also drawn from animal studies. I think that if MEDRS makes statements about nicotine, Wikipedia can.
The section on the use of nicotine as a performance-enhancing drug contains no sources that actually say that it is used in this manner. The section on fetal harms seems structured to bury information on the fetal harms of nicotine. You removed two good MEDRS sources I added there, and a fix of another ref that had failed to include two institutional authors; were those the constructive edits you reverted? The statement "Nicotine also extends the duration of positive effects of dopamine and increases the sensitivity of the brain's reward system to rewarding stimuli" seems to me to be about biochemistry and need MEDRS; can you explain why not?
Overall, I was worried that the article starts off by giving the impression that the mental effects of nicotine are all positive, and it isn't harmful. This does not seem to me to reflect MEDRS. These statements are mixed with bits of neuroscience which have far to little context to actually support the general statements, but lend a certain scienciness to them. HLHJ (talk) 19:03, 27 October 2018 (UTC)

───────────────────────── I’ll restore the constructive edits by tomorrow evening. I’m very busy off-wiki. The real issue with the edits is that the nicotine article is about pure nicotine and most of the sources you cited made statements about tobacco and smoking. The only form of pure nicotine commercially available is NRT, so reviews of clinical studies involving that are appropriate for the article. Drug monographs could also be used.

The statement requires SCIRS because it’s not clinical. I would, however, remove “positive” - that part is nonsensical.

Seppi333 (Insert ) 20:28, 27 October 2018 (UTC)

Thank you. I'll try and make sure future statements about nicotine are directly supported by source statements about nicotine. I withdraw my suggestion that you view e-cigarette use to be nicotine consumption, as I think it was unfair. Sorry. HLHJ (talk) 22:30, 27 October 2018 (UTC)

Content still not OK[edit]

Hi, Seppi333. I'm sorry, but I'm not really happy with the current state of the article. Obviously I don't want an edit war with you and QuackGuru. I would like to discuss the issues below. I'd also welcome more third-party views.
I didn't get pinged from this, so my apologies for my late response. Seppi333 (Insert ) 07:58, 14 November 2018 (UTC)

Brain damage[edit]

Nicotine is known to cause permanent cognitive and behavioural deficits; it's a developmental neurotoxin not only in fetuses, but in children, teens, and young adults.[3] The lede currently summarizes this as "The general medical position is that nicotine itself poses few health risks, except among certain vulnerable groups".
Since essentially all people who get hooked on nicotine do so before the age of 25, this is a rather serious omission of highly relevant information. My attempt to insert this information is the lede by adding ", such as young adults" to the end of the sentence was changed, to a statement about adolescents added deeper in the article. Most people getting addicted are also desperately trying to be very grown-up, and identify as young adults. Stating, incorrectly, that nicotine is just bad for adolescents is a well-known way to get more adolescents addicted. So this is not just wrong, but wrong in a way that seriously misleads (and harms) readers. HLHJ (talk) 03:00, 8 November 2018 (UTC)
I'm not sure that "young adult" would be a fair summary of the sentence later in the article that you describe as being about "adolescents". WhatamIdoing (talk) 16:18, 8 November 2018 (UTC)
Hello, WhatamIdoing. The sentence added was "Adolescents seems to be vulnerable to the negative effects of nicotine on the central nervous system". The Surgeon General's report discusses human (correlations, dose-response relationship) and animal (causality) data for adolescents and young adults, and underlying mechanisms, then says "The effects of nicotine exposure on cognitive function after adolescence and young adulthood are unknown" (the US SG also put out a video pointing out that no-one would volunteer their child for a test of how nicotine damaged their cognitive development). I'm not sure how best to summarize this; suggestions? HLHJ (talk) 01:26, 9 November 2018 (UTC)
It appears that the evidence is strongest for an effect in utero, and the picture gets murkier as the user gets older. So why did you choose to emphasize "certain vulnerable groups, such as young adults"? Why did you not choose something uncontroversial, such as "certain vulnerable groups, such as children" or even "certain vulnerable groups, such as children and teenagers"? WhatamIdoing (talk) 16:36, 9 November 2018 (UTC)
Basically, because the lede already covered harms to fetuses (it doesn't cover breastfeeding, but I missed that). I don't think that the non-whole-tobacco nicotine use evidence for post-weaning children is particularly different from that for any older group, with the exception of that single long-term NRT study on adults. The source does not use the well-defined word "teenagers" in relation to cognitive effects; it uses "adolescents" and "young adults". "Adolescents" is extensively used to refer to rats, in the source and its sources, many of which are also MEDRS. The source does not specify these groups by chronological age; it fairly vaguely classifies them by developmental stage, talking about developing brains (fairly necessary if you are going to draw analogies to rats, which don't generally celebrate their fourth birthdays even with the best of care). It mentions that the (human) brain development continues longer than previously thought, into young adulthood.
I've come across this area of research separately in research on learning and memory; as I recall, age and development seem not to be that tightly correlated, especially at older ages, and activities and experiences seem to have a strong effect. Humans generally change cognitive environment with age, and these life-stage-related changes have changed over time (e.g. a couple of generations ago, many English speakers expected to leave school at 16, take a job, and work at the same company until they were 65). So it's difficult to study such age-related changes in a way that makes it clear that we are not just measuring cultural customs. There is obviously a cultural link between "ages where you are doing lots of new stuff" and "ages of 11-25" or some such. The source (and many of its sources) are vague about chronological age, and that probably actually reflects reality.
So I wanted to be non-specific in a way that reflected the sources. I'd read a fair bit of research saying that no-one identifies as an adolescent, and that telling teens that a product was bad for adolescents tended to cause them to think it was safe for them (because they themselves are unusually mature and basically adults). The term "adult" has commonly been used as including teens by people around me, which I realize is a cultural bias I wasn't paying attention to (most age categories are culture-specific; no one says "There's a lot of ephebi on Wikipedia"). "Young adults" seemed sourced and likely to give an accurate impression, communicating information missing from the existing information. It was also short. I thought it likely that I was going to face opposition, and did not want to write a long text before the basic issue of including the information or not was settled.
Rough summary of the info I've seen follows. Evidence is strongest for in-utero and for breastfeeding babies, because their mothers often take NRT. There is a bit of a gap for young children. While some small children do use nicotine, and photos and even old ads show them doing so, I do not know of any research on the effects on them. There is evidence for the harms of second-hand smoke, and children in this age group often die of acute nicotine poisoning, being more susceptible to it, even allowing for body weight, and very prone to stick things (including the tobacco suspensions used to fill e-cigs) in their mouths. At an age around seven or so, children become more independent, and a fair proportion start using nicotine before the age of ten.[1] We have little experimental data on the effects of long-term non-whole-tobacco nicotine use on post-weaning children, teens, and twens. There's hardly much more on long-term use in adults.
Nicotine taken in adulthood (including by eating peppers and tomatoes) may have a protective effect on age-related cognitive decline, especially Parkinson's, and this effect is seen in independent studies too, so I think including it in the article is a good idea. There are prospective observational studies showing that smoking is associated with faster cognitive decline, but of course there are a lot of confounding factors there; for instance, low socieo-economic status seems to make people smoke more and get ill more even when they don't smoke. ("Smoking is a prospective risk factor for impaired cognitive function in later life"[2], based on [3][4]) Some of these prospective studies followed people from birth; some made extensive efforts to eliminate confounding factors. Apart from evidence of developmental neurotoxicity, they found some negative mental effects. Some cognitive abilities oscillate around normal, following blood nicotine levels, averaging out about the same. However, mood goes down with withdrawal and a hit just brings it back to where it would otherwise be, meaning smoking worsens average mood ("Nicotine/smoking thus comprised an additional source of psychobiological distress, irrespective of experiential background... No prospective study has found that the uptake of smoking leads to psychobiological gains. Instead they show the opposite, with smoking leading to increased levels of stress and depression"[4]).
The chance of an ethics committee passing a study that randomizes nonusers to a long-term dose of nicotine is pretty low. Experimentally giving ten-year-olds something that the medical research community thinks likely to lead to emotional distress, addiction, and long-term cognitive impairment seems even less likely to meet with ethical approval. Such an experiment would be likely to cause suicides. I think our choice is between describing the best guesses of reliable sources as such and not mentioning the issue at all. HLHJ (talk) 08:50, 14 November 2018 (UTC)

───────────────────────── I don't see where in this source - [3] - it says that nicotine causes either brain damage or cognitive deficits. The only thing I found in this source that refers to cognitive deficits pertains to smoking: Smoking during adolescence has been associated with lasting cognitive and behavioral impairments, including effects on working memory and attention, although causal relationships are difficult to establish in the presence of potential confounding factors (Goriunova and Mansvelder 2012). That's not sufficient to claim that nicotine causes cognitive deficits or even might cause cognitive deficits, because tobacco contains a very large number of bioactive compounds. If I missed something, please quote the statement from the source so that I know what you're referring to. Seppi333 (Insert ) 08:03, 14 November 2018 (UTC)

Sure, Seppi333; from the intro of that 2014 SGUS report: "The evidence is sufficient to infer that nicotine exposure during fetal development, a critical window for brain development, has lasting adverse consequences for brain development... The evidence is suggestive that nicotine exposure during adolescence, a critical window for brain development, may have lasting adverse consequences for brain development". In chapter five, "Nicotine exposure during adolescence also appears to cause long-term structural and functional changes in the brain... Thus, adolescents appear to be particularly vulnerable to the adverse effects of nicotine on the CNS[central nervous system]. Based on existing knowledge of adolescent brain development, results of animal studies, and limited data from studies of adolescent and young adult smokers, it is likely that nicotine exposure during adolescence adversely affects cognitive function and development. Therefore, the potential long-term cognitive effects of exposure to nicotine in this age group are of great concern". By 2016 the doubt seems much reduced; again just from the intros: "Nicotine exposure can also harm brain development in ways that may affect the health and mental health of our kids [obviously a press summary]... Compared with older adults, the brain of youth and young adults is more vulnerable to the negative consequences of nicotine exposure. The effects include addiction, priming for use of other addictive substances, reduced impulse control, deficits in attention and cognition, and mood disorders. Furthermore, fetal exposure to nicotine during pregnancy...Nicotine exposure during adolescence can cause addiction and can harm the developing adolescent brain... Nicotine can cross the placenta and has known effects on fetal and postnatal development. Therefore, nicotine delivered by e-cigarettes during pregnancy can result in multiple adverse consequences, including sudden infant death syndrome, and could result in altered corpus callosum, deficits in auditory processing, and obesity."[5]
I used the term "brain damage" in the heading after I found myself trying to write something like "neurodevelopmental toxicity causing alteration to structural and functional aspects of the central nervous system and associated long-term cognitive and behavioural deficits" and decided to go for succinct. It is not, to my knowledge, found in the reports by the surgeon general's office, nor the article, and if there are reasons not to summarize it that way, please let me know and I'll avoid it too. HLHJ (talk) 06:05, 15 November 2018 (UTC)
I've edited this again in response to QuackGuru. Also added content on the differing addictive potential of different delivery forms. HLHJ (talk) 06:07, 15 November 2018 (UTC)
Brain damage typically refers to lesions in the brain; this sounds more like maladaptive neuroplasticity. Seppi333 (Insert ) 01:55, 16 November 2018 (UTC)
WhatamIdoing, I've added a specific statement with specific chronological ages to the lede, with solid sourcing to a 2016 US surgeon general's report; I've tried to make it unambiguous, any criticism welcome. HLHJ (talk) 07:16, 16 November 2018 (UTC)


I inserted two good MEDRS sources on the effects of nicotine (specifically nicotine), in pregnancy; you reverted this to the current content, which has a long paragraph on how other components of smoke are bad, and ends with what sounds like its lede. Could you please explain why? The removed content:

During pregnancy and breastfeeding, mothers are advised not to use any products containing nicotine,[6] as nicotine harms the fetus.[7] One 2010 review concluded "Overall, the evidence provided in this review overwhelmingly indicates that nicotine should no longer be considered the ‘‘safe’’ component of cigarette smoke. In fact, many of the adverse postnatal health outcomes associated with maternal smoking during pregnancy may be attributable, at least in part, to nicotine alone".[6]

Thanks. HLHJ (talk) 03:00, 8 November 2018 (UTC)
Given the quoted statement - "The use of any products containing nicotine likely will have adverse effects of fetal neurological development." - I'm fine with re-adding the assertion:

During pregnancy and breastfeeding, mothers are advised not to use any products containing nicotine since nicotine could harm the fetus.[6][8]

Seppi333 (Insert ) 08:05, 14 November 2018 (UTC)
I've added this to the section you linked above. Seppi333 (Insert ) 08:08, 14 November 2018 (UTC)
Thanks. I've reordered the section so that it doesn't start with specific statements about smoking. We probably need some more up-to-date refs (here's [ a 2016 one). HLHJ (talk) 09:13, 14 November 2018 (UTC)
Looks good. Seppi333 (Insert ) 09:27, 14 November 2018 (UTC)
Also edited again in response to QG, who had a point that the quotes and the statements did not line up any more. HLHJ (talk) 06:32, 15 November 2018 (UTC)

Used because addictive, not because medicinal[edit]

The current article says that nicotine is used for its stimulant effects, replacing content that said that it is used because it is addictive (source says : "Most smokers use tobacco regularly because they are addicted to nicotine"; QuackGuru, why is this FV, given that I specified that it was mostly smoked for its addictive effects?).
Content citing surveys to state that most smokers use unwillingly were removed on grounds that they were not MEDRS. I'm not sure that stats on smokers' own opinions on why they smoke are biomedical claims (removed article text: "Adult smokers mostly want to quit and can't; they commonly feel addicted, and feel misery and disgust at their inability to quit, according to surveys done in the US.") I realize that some nicotine users are not smokers, but a very large proportion of nicotine use is by smokers. Cigarettes are the best-studied nicotine product, so I think studies on cigarettes making statements relevant to nicotine are on-topic. Content about smokers is highly relevant to the point here, namely: according to admittedly imperfect evidence, nicotine is mostly used by addicts because they can't stop. Not just by people who like the mental effects, which are, on average, negative.
Users crave nicotine for its acute effects on mood, which are positive; however, negative mood effects set in shortly after use (20–60 minutes after a cigarette, in smokers)[9]. This rapid mood oscillation is associated with addictiveness. Smokers need the nicotine hits to feel normal.[4][10] Regular use causes chronic depressed moods (including higher reported stress and less energy) which are reversible on quitting[9] (unlike some of the cognitive harms, which are probably permanent effects of the brain).[3]
All this is inadequately covered in the current Nicotine#Reinforcement disorders section, which is confused and self-contradictory.
Finally, the article has a large section under "Uses" on an unsourced use of nicotine as a performance-enhancing drug. I do not think this is a significant use; I think this is unfounded marketing puffery (like a lot of dodgy health claims which circulate on the internet and are naively added to Wikipedia). I therefore think this section should be removed. If you disagree, please let me know why. HLHJ (talk) 03:00, 8 November 2018 (UTC)
I did not tag it as FV. I tagged another sentence as FV content. The content was removed because it was off-topic. QuackGuru (talk) 20:46, 8 November 2018 (UTC)
If content saying that nicotine is used because it is addictive is off-topic, why is content saying that nicotine is used because it is a stimulant on-topic, QuackGuru? HLHJ (talk) 01:17, 9 November 2018 (UTC)
The content added did not state that nicotine is used because it is addictive. You stated in part no source with statement on reasons for nicotine use as a whole found, so using statements about smoking clearly identified as such. Smoking and nicotine are different topics. It is better to use sources that are directly related to recreational drug use. The section name is "Recreational". Content about recreational drug use pertaining to nicotine is on-topic. Current wording is "Nicotine is used as a recreational drug.[42] Recreational drug users commonly use stimulants such nicotine for its mood-altering effects.[43]" Both sources I cited are related to recreational nicotine use. QuackGuru (talk) 03:21, 9 November 2018 (UTC)
Quack, do you think that the statement is actually untrue? Do you believe, or disbelieve, the claim that some nicotine users use nicotine because they're addicted?
(Just so we're all on the same page, "recreational drug use" means "drug use for any purpose other than to treat a disease." Taking nicotine to raise your blood pressure, if you have hypotension, is not recreational. Taking it because you like it is recreational.) WhatamIdoing (talk) 16:42, 9 November 2018 (UTC)
It is irrelevant if it is true or not true. The definition of "recreational drug use" is also irrelevant. The content is relevant when the source indicates it is discussing recreational nicotine use.
The section name is "Recreational". Sources that are not specifically about recreational nicotine use are generally off-topic to the section. QuackGuru (talk) 17:40, 9 November 2018 (UTC)
Nearly all nicotine use by humans recreational, according to that definition. Therefore, nearly all sources about nicotine in general are on topic. Indeed, the recreational use so overwhelms other uses that I would accept all sources that don't say that they're specifically talking about some rare medicinal or functional use as being on topic for that section. WhatamIdoing (talk) 22:38, 11 November 2018 (UTC)
would generally agree w/ WAID--Ozzie10aaaa (talk) 10:58, 20 November 2018 (UTC)

People don't use a drug that's addictive (i.e., rewarding and reinforcing) merely because it's addictive unless they're addicted to it. I can't imagine most people would casually use nicotine due to its rewarding effects because it's not a particularly euphorogenic substance (i.e., nicotine consumption doesn't induce a pleasurable affective state like certain other psychostimulants do). Case in point: I use nicotine lozenges periodically solely to improve my focus at times when I find it difficult to concentrate; nicotine has a very well-established attentional performance-enhancing effect in humans based upon meta-analyses of clinical trials. I don't take it merely because it's reinforcing and I certainly don't use it for modifying my affect (NB: I've never noticed it having any effect on my affect), which is what I assume you mean by "people take it because it's addictive" (to be clear, many addictive drugs induce a positively-valenced or "pleasurable" affective state when consumed, but this is not typical for nicotine). In any event, I doubt we have a source which asserts that people use nicotine recreationally simply because it's "addictive". Seppi333 (Insert ) 08:20, 14 November 2018 (UTC)

I am not sure why you put "addictive" in scare quotes with respect to nicotine. I'd put "recreational", as something that makes you depressed is not my idea of recreation. If we are to go by anecdote, all of the nicotine users I know or have ever known are addicted to it, including the ones who insisted they weren't. The mood swings were pretty obvious; they got antsy and short-tempered before they used it. When given excellent medical reasons to give it up, namely cancer, they could not. I am not arguing that all nicotine use is because it is addictive; that would be absurd, as obviously someone using it for the first time is not using it because they are addicted. I am arguing that most use is because it is addictive. The same source cited for the statement "Recreational drug users commonly use stimulants such as nicotine for its mood-altering effects" actually clarifies it in a way that agrees with your statement about euphorogenicity; it also says "Stimulant drug users suffer a range of negative states when off-drug and feel better in numerous ways when on-drug, hence the strong addictiveness of every CNS stimulant." If you are an addict, you have chronic mild low mood, briefly relieved by a nicotine hit, which brings mood up to normal for a few tens of minutes. I've found a source for the statement that most use is due to nicotine's addictiveness, and I've modified the mood-alteration statement to accord with the source (and what you say):

It is widely used because it is highly addictive.[11] People addicted to nicotine suffer depressed mood, and commonly take nicotine for its mood-normalizing effects.[4][9]

I hope this is OK. HLHJ (talk) 09:49, 14 November 2018 (UTC)
Just to be clear, the term “addictive” describes a drug property. An addiction is a brain disorder which is induced by drugs with that property. People only use addictive drugs compulsively if they have an addiction to one of those drugs.
With that in mind, I think what you mean to say is, “It is widely used because many people are addicted to it.” The clause “because it is highly addictive” comes off sounding like it’s a motivation for using it (i.e., it suggests that people use it because they want to develop an addiction); consequently, that wording is really awkward. I’m sure you’re aware that many people begin using tobacco products for social reasons (e.g., fitting in with a group, a belief that it’s perceived as cool, etc.), not because their goal is to become an addict. Face-tongue.svg
What you’ve described in the second sentence pertains to psychological dependence and the associated emotional-motivational withdrawal symptoms, not an addiction. So, just change “People addicted to nicotine” to “People dependent upon nicotine” and that sentence will be fine. Seppi333 (Insert ) 02:13, 15 November 2018 (UTC)
On the second, I'd changed it to "dependent" before seeing this. I've changed the first to "Nicotine has become widely used because it is highly addictive, which makes it hard to quit using it" now, as I agree that the idea of aspirational addiction is odd. HLHJ (talk) 06:17, 15 November 2018 (UTC)
Performance-enhancing drug[edit]

I still think this Nicotine#Enhancing performance section should go; we have no independent source that this use is significant, and the only sourced sentence with the context to make it comprehensible is isolated from important context found in the Nicotine#Reinforcement disorders section (that the effects are acute and counterbalanced by negative effects of dependence, such that dependent nicotine users are not cognitively better off on average). I have tagged the section accordingly. HLHJ (talk) 06:29, 15 November 2018 (UTC)

You’re conflating cognitive deficits that arise from an addiction with a short-term drug effect, so I don’t see a reason to cut that section. A number of articles on other addictive performance-enhancing drugs use that same section to cover the effects on performance. Seppi333 (Insert ) 07:30, 15 November 2018 (UTC)
The "Use/Enhancing performance" section reads:

Nicotine-containing products are sometimes used for the performance-enhancing effects of nicotine on cognition.[citation needed] A meta-analysis of 41 double-blind, placebo-controlled studies concluded that nicotine or smoking had significant positive effects on aspects of fine motor abilities, alerting and orienting attention, and episodic and working memory.[12] A 2015 review noted that stimulation of the α4β2 nicotinic receptor is responsible for certain improvements in attentional performance;[13] among the nicotinic receptor subtypes, nicotine has the highest binding affinity at the α4β2 receptor (ki[equals sign that won't render in talkquote template]1 nM) which is also the biological target that mediates nicotine's addictive properties.[14] Nicotine has potential beneficial effects, but it also has paradoxical effects, which may be due to the inverted U-shape of the dose-response curve or pharmacokinetic features.[15]

We do not have a MEDRS saying that performance enhancement is, in itself and not as a component of dependence, a significant use of nicotine. The second sentence statement was until recently found later in the article, amid more relevant context. The 2015 review in the third sentence mentions nicotine once, to say "Importantly, the non-selective agonist nicotine is less likely to generate such enhancements, in part because nicotine...", so I'm not sure this sentence isn't WP:SYN. The source for the fourth and last sentence says in the abstract "...potentially intervening in age-related changes in diverse molecular pathways leading to pathology. Although nicotine has therapeutic potential, paradoxical effects have been reported, possibly due to its inverted U-shape dose-response effects or pharmacokinetic factors". It is talking about slowing age-related cognitive decline (a use with MEDRS, so we could include that). The point (that high doses of nicotine can have negative effects on cognition, I think) is also made in the first source,[12] in equally obscure language. Anyone else want to weigh in on what this means?
I templated that paragraph as an ad because it looks like a lot of the sciencey industry marketing materials I've read. It make a bold but unsupported claim in plain English, then follows it with a bunch of scientific terminology and claims that sort of look as if they are relevant, but descend into incomprehensibility. This has been shown to be an effective technique for making readers trust claims.[5] The section also leaves out or obfuscates all of the balancing information (for instance, that the benefits in the review are short-term; that a nicotine habit does not give you improved cognitive abilities, and does give you cognitive fluctuations which can cause distress and deeper dependence, and the negative cognitive effects of the maladaptive neuroplasticity described above, which are long-term, with evidence of them in old age).
There are some problems with the cognitive-effects meta-analysis; they included studies of smokers who had not smoked for up to two hours; as the article says, many smokers would be nicotine-deprived by this point. Nearly half the studies did not state funding or were funded by the nicotine industry, and the authors did not examine whether funding source made a difference. They also did not look for publication bias in these mostly very small studies, or separate NRT from smoking (a study on that here, looking at the effect of NRT and cigarettes with almost no nicotine in them). Unfortunately they also do not publish supplementary data, so the reader can't simply run these tests themselves. The Surgeon Genreal's 2014 report also summarizes the review by saying there is no clear evidence for cognitive benefit except for those in withdrawal. There are, however, other sources for the idea that cognitive abilities fluctuate with blood nicotine level in dependent smokers (and more slowly in NRT users), and this fluctuation helps condition dependence. The idea seems likely to be correct and I think it should be included under the mechanisms of dependence. Given more detail and closer sourcing, would you object?
I do not think the short- and long-term, or pre-dependency and withdrawal-based cognitive effects, are the same. I do think they are a factor in addiction (a statement that was sourced in the article). Someone dependent on nicotine feels muzzy and out-of it, so they take nicotine and feel sharper and more focussed. You removed the sentence "Nicotine has clinically significant cognitive-enhancing acute effects at low doses, particularly in fine motor skills, attention, and memory. These beneficial cognitive effects may play a role in the maintenance of tobacco dependence" citing WP:Crystal ball. I think this is more scientific uncertainty than unfounded speculation. I see you also moved the section on dependency and withdrawal from under "adverse effects" to under "Overdose". While the idea that any dose large and swift enough to cause dependence is an overdose is not without merit, and finds some reflection in the proposals to lower the nicotine levels in commercial products to non-addictive levels, I don't think this terminology is widely used in reliable sources, and dependence is certainly a negative effect. We could resolve this by including the section on overdoses as an adverse effect, but I'm not sure if this is acceptable formatting (comments, anyone?).
This is a difficult paragraph; I've tried not to cause offense, and owe you apologies if I fail. I understand from what you posted above that you personally use nicotine lozenges at a level you judge to be non-dependency-inducing; you gave acute cognitive effects as your reason. I'm not attempting to judge whether you are nicotine-dependent; I can't, I shouldn't, and if you wanted to know you'd presumably ask your doctor. But regardless of dependency, you are motivated to believe that the way you use nicotine is harmless. Regardless of the truth of this belief, that motivation will contribute to your POV bias, just as my POV bias is affected by people having first told me they only used nicotine once or twice a month and weren't addicted, and later that they couldn't stop. I am not in any way suggesting that you are being dishonest or otherwise in bad faith in your conceptions around nicotine dependency. I'm just worried; I have learned from experience not to trust any reasoning affecting self-assessments of nicotine dependence.
I also moved the excessively detailed information about plants containing nicotine out of the lede into a separate section. I am a bit worried about the heavy reliance of this section on one source (Siegumund et al. 1999) as I cannot access it and it seems to contradict at least one other source.[6] HLHJ (talk) 06:37, 16 November 2018 (UTC)
@HLHJ: But regardless of dependency, you are motivated to believe that the way you use nicotine is harmless. I never stated this and I don't think this; I'd suggest not making unfounded assumptions about my beliefs and/or knowledge about drugs in general and nicotine in particular. For me, nicotine lozenges have an unpleasant taste, can cause nausea, and promote stress ulcers when used in combination with amphetamine, among other things. I'm also cognizant of the fact that nicotine has been shown to promote cognitive deficits in the offspring of laboratory animals that consume it via transgenerational epigenetic inheritance of methylated histone amino acid residues (i.e., epigenetic marks), which is something that occurs when nicotine is used at sufficiently high doses over a period of time. The possibility that this phenomenon could occur in humans and knowing that sufficiently high doses and/or frequent use of nicotine induces epigenetic changes in the human brain and sperm cells is just one of three reasons why I only take low doses and avoid using it with any regularity.
Large blob of text – collapsed by Seppi333 (Insert )
In any event, it's not particularly difficult to self-diagnose addiction or dependence so long as one is marginally familiar with a handful of concepts in cognitive and behavioral psychology. Personally, I don't like using nicotine (using it is usually mildly unpleasant) and I've never felt a need to use it. The distinction between what motivates a non-addicted/dependent person like me and a person with an addiction to or dependence upon nicotine to use nicotine is that a non-addicted/dependent individual chooses to use the drug for a perceived benefit that is unrelated to any past or present use of it, whereas a dependent person uses it to stave off an undesirable physical/cognitive state and an addict uses it to satisfy a craving/desire for drug reward. It's worth mentioning that I suffered from an addiction to something in the past (that something was not nicotine; this admission is somewhat of a bombshell since it's the first time I've disclosed this on Wikipedia; it's also why I've written so much about the molecular neurobiology, neuroepigenetics, and cognitive neuropsychology of addiction) and I know unequivocally that I'm not addicted to or even just dependent upon nicotine (NB: it's much easier to become dependent upon a drug than it is to become addicted to it; it's also much easier to overcome dependence than addiction). I don't use nicotine lozenges on regular basis and, on days that I choose to use them, I take them maybe once or twice during that day. In contrast, the way an addiction to a drug works is: an addicted individual uses the drug they're addicted to just once, then they develop a craving for it (NB: if relapse [i.e., the development of an irresistible craving] had not occurred prior to the initial re-use of the drug [this would arise from exposure to an arbitrary conditioned reinforcer], then relapse is extremely likely to occur at this point [the initial re-exposure to the drug] due to the drug functioning as a primary positive reinforcer of continued drug use) and use it again, then again, and again, and again, and again until they either run out of it or reach a physiological limit that forces them to focus on other biological needs like eating or sleeping – that's the form of compulsive use that characterizes an addiction.
I'm not telling you this to try to convince you that I'm not addicted to or dependent upon nicotine; rather, I'm stating this because you don't seem to really understand how people behave when they have an addiction as opposed to dependence. It's not withdrawal symptoms that motivate continued use with an addiction; it's the assignment of an excessive amount of incentive salience to the addictive stimulus, which manifests as a craving (i.e., extreme "wanting"/"desire") for doing/using it. I'm not going to try to explain the cognitive psychology of addiction (i.e., how an addict thinks when they're exposed to conditioned environmental cues or an addictive stimulus) because understanding that thought process requires at least some working knowledge of specific cognitive processes (i.e., incentive salience, inhibitory control, Pavlovian-instrumental transfer, and reward sensitization) and forms of associative learning (namely, operant conditioning and classical conditioning), the awareness of and hence the capacity to recognize changes in the aforementioned cognitive processes in oneself, and the awareness of and capacity to recognize a personal failure to exert inhibitory control over one's behavior in particular.
On an unrelated note, the idea that a psychostimulant like nicotine does not confer any marginal cognitive benefit at low (or in some cases even high) doses in nicotine-naive individuals is almost as absurd as thinking that an addiction to nicotine doesn't induce cognitive deficits. The occurrence of a benefit from the use of a cognition-enhancing drug is always dependent upon one's underlying neurobiological state factors (i.e., things like one's current state of wakefulness/cognitive arousal, capacity to focus attention, degree of psychological stress or relaxation, motivational state, etc.) at the time of use and the current task and/or goal one is working to complete. In a nutshell, what I mean by this is that one can, but not necessarily will, obtain a performance benefit from using a cognition-enhancing drug for a given task. A person needs to be in the right "state of mind" to obtain a benefit from using a cognition-enhancing drug to improve task performance (e.g., as a general rule, the use of a psychostimulant drug while in a state of low arousal will improve performance on almost any simple task, but not necessarily on complex tasks; that should be obvious). That meta-analysis isn't the only literature which supports the occurrence of improvements in attentional performance from nicotine use by nicotine-naive individuals. It's just the only meta-analysis that the article cites. There's also evidence that nicotine has ergogenic effects in humans, but those are not as clear-cut as nicotine's cognitive effects; the article currently says nothing about physical performance-enhancing effects. Seppi333 (Insert ) 03:03, 21 November 2018 (UTC)
  • Re: The point (that high doses of nicotine can have negative effects on cognition, I think) is also made in the first source,[1] in equally obscure language. Anyone else want to weigh in on what this means? That inverted U-shape on a dose-response (i.e., task performance) curve for complex/difficult tasks is applicable to all psychostimulants (e.g., caffeine, amphetamine, methylphenidate, etc.). That's also why that whole clause contains a piped wikilink to the Yerkes-Dodson law. More generally, most psychostimulants improve some aspect of cognitive control (i.e., one or more of the cognitive processes which compose it) in low doses and impair cognitive control at high doses. These phenomena are certainly not unique to nicotine.
  • Re: for instance, that the benefits in the review are short-term; that a nicotine habit does not give you improved cognitive abilities, and does give you cognitive fluctuations which can cause distress and deeper dependence, and the negative cognitive effects of the maladaptive neuroplasticity described above, which are long-term, with evidence of them in old age. Read Amphetamine#Enhancing performance and keep in mind that every one of those effects is "short-term" in the sense that they persist for a period which is less than or equal to amphetamine's duration of action. I also want to draw attention to the fact that an amphetamine addiction entails cognitive deficits. Again, nicotine isn't special; virtually all psychostimulants act as cognition-enhancing drugs with respect to cognitive arousal (i.e., they increase "wakefulness") over their duration of action (NB: the Yerkes–Dodson law article covers the empirical relationship between cognitive arousal and task performance). All addictive psychostimulants necessarily induce cognitive deficits when an individual becomes addicted to one of them. Addiction involves impairments in inhibitory control; that specific cognitive impairment is one of two changes to a cognitive processes that results in compulsive drug use (the other one being the sensitization of incentive salience). Seppi333 (Insert ) 03:07, 21 November 2018 (UTC)

Section reflist[edit]


  1. ^ Pechacek TF, Nayak P, Slovic P, Weaver SR, Huang J, Eriksen MP (November 2017). "Reassessing the importance of 'lost pleasure' associated with smoking cessation: implications for social welfare and policy". Tobacco Control. 27 (e2): tobaccocontrol–2017–053734. doi:10.1136/tobaccocontrol-2017-053734. PMID 29183920.
  2. ^ Chaiton M, Diemert L, Cohen JE, Bondy SJ, Selby P, Philipneri A, Schwartz R (June 2016). "Estimating the number of quit attempts it takes to quit smoking successfully in a longitudinal cohort of smokers". BMJ Open. 6 (6): e011045. doi:10.1136/bmjopen-2016-011045. PMC 4908897. PMID 27288378.
  3. ^ a b c "The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General, Chapter 5 - Nicotine" (PDF). Surgeon General of the United States. 2014. pp. 107–138. PMID 24455788.
  4. ^ a b c Parrott, Andrew C (April 2003). "Cigarette-Derived Nicotine is not a Medicine" (PDF). The World Journal of Biological Psychiatry. 4 (2): 49–55. doi:10.3109/15622970309167951. ISSN 1562-2975.
  5. ^ "E-Cigarette Use Among Youth and Young Adults: A Report of the Surgeon General" (PDF). 2016. Retrieved 15 November 2018. |first1= missing |last1= in Authors list (help)
  6. ^ a b c Bruin, Jennifer E.; Gerstein, Hertzel C.; Holloway, Alison C. (2010-04-02). "Long-Term Consequences of Fetal and Neonatal Nicotine Exposure: A Critical Review". Toxicological Sciences. 116 (2): 364–374. doi:10.1093/toxsci/kfq103. ISSN 1096-6080. PMC 2905398. PMID 20363831. Overall, the evidence provided in this review overwhelmingly indicates that nicotine should no longer be considered the ‘‘safe’’ component of cigarette smoke. In fact, many of the adverse postnatal health outcomes associated with maternal smoking during pregnancy may be attributable, at least in part, to nicotine alone.
  7. ^ England, Lucinda J.; Kim, Shin Y.; Tomar, Scott L.; Ray, Cecily S.; Gupta, Prakash C.; Eissenberg, Thomas; Cnattingius, Sven; Bernert, John T.; Tita, Alan Thevenet N.; Winn, Deborah M.; Djordjevic, Mirjana V.; Lambe, Mats; Stamilio, David; Chipato, Tsungai; Tolosa, Jorge E. (31 December 2010). "Non-cigarette tobacco use among women and adverse pregnancy outcomes". Acta Obstetricia et Gynecologica Scandinavica. 89 (4): 454–464. doi:10.3109/00016341003605719. ISSN 1600-0412. The use of any products containing nicotine likely will have adverse effects of fetal neurological development.
  8. ^ England, Lucinda J.; Kim, Shin Y.; Tomar, Scott L.; Ray, Cecily S.; Gupta, Prakash C.; Eissenberg, Thomas; Cnattingius, Sven; Bernert, John T.; Tita, Alan Thevenet N.; Winn, Deborah M.; Djordjevic, Mirjana V.; Lambe, Mats; Stamilio, David; Chipato, Tsungai; Tolosa, Jorge E. (31 December 2010). "Non-cigarette tobacco use among women and adverse pregnancy outcomes". Acta Obstetricia et Gynecologica Scandinavica. 89 (4): 454–464. doi:10.3109/00016341003605719. ISSN 1600-0412. The use of any products containing nicotine likely will have adverse effects of fetal neurological development.
  9. ^ a b c Parrott, Andrew C. (2015). "Why all stimulant drugs are damaging to recreational users: an empirical overview and psychobiological explanation". Human Psychopharmacology: Clinical and Experimental. 30 (4): 213–224. doi:10.1002/hup.2468. ISSN 0885-6222. PMID 26216554. Stimulant drugs such as nicotine and Ecstasy/3, 4-methylenedioxymethamphetamine (MDMA) are taken for positive reasons, yet their regular use leads to deficits rather than gains... The most widely used CNS stimulant drug is nicotine, because it is the only legal substance in this broad class... However, it is often believed that their novice or light social usage is comparatively safe. Hence, another aim is to explain how and why psycho-biological problems can occur with all types of user — because they are a direct psychobiological consequence of drug-induced changes to the CNS (Table 1)... Acute mood gains, followed by mood decrements on drug withdrawal. The periodicity of these mood fluctuations is most frequent in drugs with a rapid onset and rapid withdrawal (nicotine and crack cocaine)... Regular use of all CNS stimulants can lead to chronic mood deficits. Mood states typically improve following drug cessation... Neuroimaging and neurocognitive studies reveal a range of deficits. They may reflect neurotoxicity or neuroadaptive processes. Some recovery may occur on drug cession, while some problems may endure — an important question for future research. [also see section on "Chronic mood effects of stimulant drugs"] Cite error: Invalid <ref> tag; name "Parrott2015" defined multiple times with different content (see the help page).
  10. ^ Parrott AC (January 1998). "Nesbitt's Paradox resolved? Stress and arousal modulation during cigarette smoking" (PDF). Addiction. 93 (1): 27–39. CiteSeerX doi:10.1046/j.1360-0443.1998.931274.x. PMID 9624709.
  11. ^ Siqueira LM (January 2017). "Nicotine and Tobacco as Substances of Abuse in Children and Adolescents". Pediatrics. 139 (1): e20163436. doi:10.1542/peds.2016-3436. PMID 27994114. The highly addictive nature of nicotine is responsible for its widespread use and difficulty with quitting.
  12. ^ a b Heishman SJ, Kleykamp BA, Singleton EG (July 2010). "Meta-analysis of the acute effects of nicotine and smoking on human performance". Psychopharmacology. 210 (4): 453–69. doi:10.1007/s00213-010-1848-1. PMC 3151730. PMID 20414766.
  13. ^ Sarter M (August 2015). "Behavioral-Cognitive Targets for Cholinergic Enhancement". Current Opinion in Behavioral Sciences. 4: 22–26. doi:10.1016/j.cobeha.2015.01.004. PMC 5466806. PMID 28607947.
  14. ^ "Nicotine: Biological activity". IUPHAR/BPS Guide to Pharmacology. International Union of Basic and Clinical Pharmacology. Retrieved 7 February 2016. Kis as follows; α2β4=9900nM [5], α3β2=14nM [1], α3β4=187nM [1], α4β2=1nM [4,6]. Due to the heterogeneity of nACh channels we have not tagged a primary drug target for nicotine, although the α4β2 is reported to be the predominant high affinity subtype in the brain which mediates nicotine addiction
  15. ^ Majdi A, Kamari F, Vafaee MS, Sadigh-Eteghad S (October 2017). "Revisiting nicotine's role in the ageing brain and cognitive impairment". Reviews in the Neurosciences. 28 (7): 767–781. doi:10.1515/revneuro-2017-0008. PMID 28586306.

PubMed Labs[edit]

A beta site with some new tools that might get incorporated into Pubmed depending on the feedback they receive can be found here CV9933 (talk) 16:48, 29 October 2018 (UTC)

thanks for info--Ozzie10aaaa (talk) 10:01, 31 October 2018 (UTC)
Thanks - the 'PubMed Health' website is different from 'PubMed', and the changes mentioned in your link do not affect the latter (NB please sign your posts with 4 tilde [′~'] marks)! Kitb (talk) 23:43, 8 November 2018 (UTC)
'PubMed Health' was closely connected to the work of Hilda Bastian ( aka User:Hildabast, and also a thoughtful and good-humoured EBM blogger [7][8] :). I believe 'PubMed Health' kept the needs of Wikipedia's medical editing here in mind. I'm sorry to see it go. Among other characteristics, I appreciated its use of DARE appraisals. Thank you @Hilda! (talk) 11:28, 10 November 2018 (UTC)
PubMed Health is now gone, which means one of the links in {{Reliable sources for medical articles}} is obsolete (the link named ..."or to systematic reviews"). I mentioned this on the templates talk page but I don't think anyone noticed (link to discussion: Template talk:Reliable sources for medical articles#PubMed Health will be discontinued 31 October 2018). This link needs to be updated/replaced in the template, which is featured on many articles' talk pages. --Treetear (talk) 23:18, 13 November 2018 (UTC)
I've removed the link for now. --RexxS (talk) 23:36, 13 November 2018 (UTC)

Links to DAB pages in medicine-related articles[edit]

Head of femur

Since my last visit here, I've collected some more pages with bad links which need expert attention. Search for 'disam' in main view and for '{{d' in edit mode. As always, if you solve one of these puzzles, remove the {{dn}} tag from the article and add {{done}} here.

As always, thanks in advance. Narky Blert (talk) 10:50, 5 November 2018 (UTC)

Great work! I'll be back in a month or so with some more :-( Narky Blert (talk) 09:36, 8 November 2018 (UTC)
Thanks for hunting them out for us less experienced folk to work on!! Kitb (talk) 11:31, 8 November 2018 (UTC)
A handy tip someone placed here before, was to go to your user preferences and on the gadgets tab, select the box "Display links to disambiguation pages in orange" CV9933 (talk) 12:25, 8 November 2018 (UTC)
Quick link on above tip: Special:Preferences#mw-prefsection-gadgets -> scroll down to "Appearance" -> select box (5th from bottom) "Display links to disambiguation pages in orange" -> click Save. --Treetear (talk) 21:58, 9 November 2018 (UTC)
thanks Treetear--Ozzie10aaaa (talk) 15:33, 10 November 2018 (UTC)
When I joined WP:DPL, there were c. 40,000 known bad links to WP:DAB pages which had never been looked at or which had been flagged {{dn}} as too difficult. (I was late to the party - I've seen old reports suggesting 200,000 and much worse.)
Once we got that number down below 10,000 or so, I began to ask specialist WikiProjects to help solve some of the remaining problems. Some of those WikiProjects have been utterly indifferent, and therefore utterly useless. However, I can cheerfully say that Wikipedia:WikiProject Medicine is one of the three WikiProjects whose members I have found always to be well-informed and eager to solve puzzles relating to their speciality. Props!
A tip. I or other disambiguators will, sooner or later, pick up bad links to WP:DAB pages, because User:DPL bot flags them as needing attention. However, none of us will ever pick up bad links to WP:SIA pages. Narky Blert (talk) 03:19, 11 November 2018 (UTC)
I've always believed that this group was awesome. :-) WhatamIdoing (talk) 22:41, 11 November 2018 (UTC)
@Narky Blert: Why is a link to a WP:SIA a "bad link"? The reason I ask is that I "disambiguated" the glutamate synthase link in GltS RNA motif by changing that page from a DAB to a SIA, as all of those articles refer to enzymes which catalyze glutamate synthesis. Seppi333 (Insert ) 07:52, 14 November 2018 (UTC)
@Seppi333: SIAs aren't always bad ideas, but they very often are. They are only good ideas if it can be guaranteed that every incoming link is designed to point readers to every article on the page. If even one incoming link is meant for only one of those articles, that confuses readers and degrades the encyclopaedia.
The three enzymes on the glutamate synthase page have different coenzymes. I very much doubt whether every future incoming link will intend to refer to all three.
There is a way to link to a DAB page showing that all articles on it are meant. Link through the (disambiguation) qualifier, and mark it as <!--intentional link to DAB page-->. Narky Blert (talk) 10:28, 14 November 2018 (UTC)

Cleanup needed: Spinal Muscular Atrophy[edit]

I noticed that this article contains a lot of primary references. I removed one sentence that was added (no reference and seemed to be self promo). I will flag it here if anyone has time to take a look: Thanks, JenOttawa (talk) 02:53, 9 November 2018 (UTC)

It's a rare disease. Primary sources are sometimes the best possible sources for standard information about rare diseases. Secondary is not the definition of a good source. It's important to balance multiple considerations around the reliability of sources. A recent primary source from an expert in a respected journal in a relevant area is often better than a review article written by a grad student in a third-tier journal. When we're writing about a common or well-researched condition, we can pick the best of the best of the best (and that's what we wrote MEDRS around), but when we're working on articles about rare diseases, we need to think about sources holistically, and not just through a simplistic primary-bad/secondary-good lens. WhatamIdoing (talk) 16:50, 9 November 2018 (UTC)
Thanks for this clarification, WhatamIdoing - really helpful to us less experienced folk! Kitb (talk) 18:04, 9 November 2018 (UTC)
We have decent reviews on the topic
Doc James (talk · contribs · email) 06:37, 11 November 2018 (UTC)
I agree that those are decent secondary sources, and I would encourage anyone interested in the subject to use them. However, they are not technically review articles, because they are not published in peer-reviewed academic journals. WhatamIdoing (talk) 06:20, 12 November 2018 (UTC)
Thanks for all the feedback @WhatamIdoing and Doc James:. There are many sections of Spinal Muscular Atrophy that are summaries of RCTs/case studies and in vitro/in vivo work. For example,
"Butyrates (sodium butyrate and sodium phenylbutyrate) held some promise in in vitro studies[1][2][3] but a clinical trial in symptomatic people did not confirm their efficacy.[4] Another clinical trial in pre-symptomatic types 1–2 infants was completed in 2015 but no results have been published.[5]"
When you mention above that primary sources are often the best that we have, I do not disagree with you for background info in a Wikipedia article. How do you feel about the above paragraph? It is my understanding that this would not be acceptable as per MEDRS. Similar to @Kitb:, I really appreciate this discussion from a learning point of view.JenOttawa (talk) 14:27, 12 November 2018 (UTC)
User:JenOttawa better to replace with secondary sources IMO Doc James (talk · contribs · email) 02:17, 13 November 2018 (UTC)
I think it depends upon what sources exist. In the case of the sentence about the file drawer problem, the source could be updated to PMID 27490705, which is a 2016 review.
If the three animal studies are the ones cited by the primary source that says it didn't work in humans, then it's a bit like "citing" a historically important paper (which we accept as a valid use): you're putting it there for the convenience of the interested reader, not really as proof that the statement is accurate. The 2016 review mentions both of these substances. WhatamIdoing (talk) 19:27, 13 November 2018 (UTC)


  1. ^ Chang, J. -G.; Hsieh-Li, H. -M.; Jong, Y. -J.; Wang, N. M.; Tsai, C. -H.; Li, H. (2001). "Treatment of spinal muscular atrophy by sodium butyrate". Proceedings of the National Academy of Sciences. 98 (17): 9808–13. Bibcode:2001PNAS...98.9808C. doi:10.1073/pnas.171105098. PMC 55534. PMID 11504946.
  2. ^ Andreassi, C.; Angelozzi, C.; Tiziano, F. D.; Vitali, T.; De Vincenzi, E.; Boninsegna, A.; Villanova, M.; Bertini, E.; Pini, A.; Neri, G.; Brahe, C. (2003). "Phenylbutyrate increases SMN expression in vitro: Relevance for treatment of spinal muscular atrophy". European Journal of Human Genetics. 12 (1): 59–65. doi:10.1038/sj.ejhg.5201102. PMID 14560316.
  3. ^ Brahe, C.; Vitali, T.; Tiziano, F. D.; Angelozzi, C.; Pinto, A. M.; Borgo, F.; Moscato, U.; Bertini, E.; Mercuri, E.; Neri, G. (2004). "Phenylbutyrate increases SMN gene expression in spinal muscular atrophy patients". European Journal of Human Genetics. 13 (2): 256–9. doi:10.1038/sj.ejhg.5201320. PMID 15523494.
  4. ^ Mercuri, E.; Bertini, E.; Messina, S.; Solari, A.; d'Amico, A.; Angelozzi, C.; Battini, R.; Berardinelli, A.; Boffi, P.; Bruno, C.; Cini, C.; Colitto, F.; Kinali, M.; Minetti, C.; Mongini, T.; Morandi, L.; Neri, G.; Orcesi, S.; Pane, M.; Pelliccioni, M.; Pini, A.; Tiziano, F. D.; Villanova, M.; Vita, G.; Brahe, C. (2007). "Randomized, double-blind, placebo-controlled trial of phenylbutyrate in spinal muscular atrophy". Neurology. 68 (1): 51–55. doi:10.1212/01.wnl.0000249142.82285.d6. PMID 17082463.
  5. ^ "Study to Evaluate Sodium Phenylbutyrate in Pre-symptomatic Infants With Spinal Muscular Atrophy (STOPSMA)". Retrieved 28 December 2011.


Hello, it's me again! Is a mucosectomy the same as an endoscopic mucosal resection? de:Mukosektomie through Google Translate says yes, but I have no idea. ♠PMC(talk) 13:03, 10 November 2018 (UTC)

I don't think they're exactly synonyms. I think that mucosectomy is the goal you're trying to achieve, and cutting it out by passing a knife down (or up) the digestive tract is just one of several ways to achieve the goal. Other methods seem to include laparoscopic mucosal resection (stick the knife through a 'keyhole' in your skin) and ablative mucosectomy (destroy the tissue, e.g., by burning or freezing).
It might be reasonable to merge the articles, and describe the different techniques all in the same place, but I don't think that they're exactly the same things. WhatamIdoing (talk) 06:29, 12 November 2018 (UTC)
Hmm ok. I think I'll link mucosectomy from endoscopic mucosal resection and leave a merge for someone else to determine. As always, I appreciate you weighing in. ♠PMC(talk) 07:49, 12 November 2018 (UTC)


There is a move discussion at Talk:Breathing_circuit#Requested_move_4_November_2018. Flooded with them hundreds 08:09, 11 November 2018 (UTC)

commented--Ozzie10aaaa (talk) 11:55, 11 November 2018 (UTC)

Featured quality source review RFC[edit]

Editors in this WikiProject may be interested in the featured quality source review RFC that has been ongoing. It would change the featured article candidate process (FAC) so that source reviews would need to occur prior to any other reviews for FAC. Your comments are appreciated. --Izno (talk) 21:31, 11 November 2018 (UTC)

Help needed improving gene infobox (alternate title: Tom (LT)'s annual gene infobox whinge)[edit]

I need some help from this project to improve an infobox, specifically infobox gene

The article agrees that it's a protein. First line: "Ceruloplasmin (or caeruloplasmin) is a ferroxidase enzyme that in humans is encoded by the CP gene" Yet the infobox... incomprehensible!! Just look at that monster!

I encounter this issue every protein article I visit. They are darned difficult to read!! I can confidently say they are completely incomprehensible to any reader that's not trained to biology at a university level. Is that what we want??

I proposed some changes here, some with consensus, but unfortunately the discussion was archived without any being made.

I would in the wiki way make these changes (including small ones myself), but the infobox is programmed in lua. Whilst I admire the lovingly handcrafted box this means that only a handful of editors can change this 2,000+ line programmed monolith.

I am seeking some help improving the infobox. I'm not too fussed how but some simple suggestions are:

  • primary purpose of the box be summarising key points of information to readers (WP:INFOBOX) - readers who are not biomedically trained
  • Use plain english where possible (WP:TECHNICAL)
  • Decrease the use of images which are unnecessary, such as the mouse karyotype
  • If the gene infobox is used in an article about a protein, include some information about the main functions of that protein (such as what it primarily does, where it is, where it's mostly made in the body) in simple terms. (WP:INFOBOX)

--Tom (LT) (talk) 10:37, 12 November 2018 (UTC)

    • I'd love to see some changes in the gene / protein pages in general. I'm a clinical laboratory geneticist, and my eyes glaze over reading them. There is also significant work on protein / enzyme vs gene, but I don't even know where to begin with that one. The inclusion of all the info for the gene on the page for the protein / enzyme makes things difficult to parse, even if you know what you are looking for. Canada Hky (talk) 20:40, 12 November 2018 (UTC)
      • Infoboxes aren't necessarily for reading are they? I think they are more for referencing information quickly. There could be some information added (although standardizing it would be difficult), but I think the purpose of it is fulfilled. We can use prose in the article itself. Natureium (talk) 21:27, 12 November 2018 (UTC)
        • On a page for the protein, much of the information in the infoboxes is irrelevant and confuses the distinction between gene and protein. That isn't helpful. Canada Hky (talk) 21:37, 12 November 2018 (UTC)
          • I completely agree Canada Hky, the distinction between the gene and protein is lost which adds an additional level of confusion. As a clinical geneticist you don't even find it useful! I wonder if it may be better just to completely recreate a new infobox in wikicode for proteins and then replace the existing set. At least the new ones could be edited and/or sandboxed in a normal manner. --Tom (LT) (talk) 06:47, 14 November 2018 (UTC)

───────────────────────── @Boghog: You might be interested in this thread. Seppi333 (Insert ) 08:31, 14 November 2018 (UTC)

I was hoping for a bit more buy-in from the maintainers of the infobox since Module:Infobox gene is scripted in Lua which I am not very familiar with. Based on the ideas generated in the previous discussion, I will try to hack a prototype when I find time. Boghog (talk) 08:57, 14 November 2018 (UTC)
Template:Infobox protein already exists and has 944 transclusions. I would have thought it would be simplest to make use of that. Further parameters can be added on request.
However, as Template:Infobox gene draws its information from Wikidata, I wondered if you would like me to convert Template:Infobox protein to do the same? I would not code the whole thing in Lua, but simply use Module:WikidataIB to fetch values from Wikidata where no local parameter was supplied. That would allow us to override the Wikidata value whenever we chose, and it would not have any visible effect on existing uses. What do folks think? --RexxS (talk) 15:25, 14 November 2018 (UTC)
We spent several years replacing thousands of {{infobox protein}} transclusions with {{infobox gene}}, so I am not so keen on that solution ;-) Also it really doesn't solve the problem, except perhaps make it easier for non-Lua programmers to implement. The best solution is to get the maintainers of the infobox to implement these changes, but that doesn't seem to be high on their priority list. If we can put together a prototype for community comment, that might catalyze the process.
Please note (this was a source of confusion in previous discussions) that despite the names, both infoboxes are about the gene and the protein. The protein box is still used for special cases (for example families of proteins). Boghog (talk) 17:24, 14 November 2018 (UTC)

Problems today with the PMID tool in visual editor[edit]

Is anyone else having problems? Using Chrome I cannot seem to get the PMID tool to work today (visual editor). I can use the DOI. I got an error message with the PMID: "We couldn't make a citation for you. You can create one manually using the "Manual" tab above." JenOttawa (talk) 16:12, 12 November 2018 (UTC)

sometimes it does happen--Ozzie10aaaa (talk) 20:29, 12 November 2018 (UTC)
Working again now. Just a few hours down! Thanks. JenOttawa (talk) 21:08, 12 November 2018 (UTC)
I asked a dev about this yesterday (we were waiting for a meeting to start), and he said that this kind of behavior is usually due to a server problem somewhere, rather than a software bug. If it happens more frequently, then please let me know. WhatamIdoing (talk) 19:29, 13 November 2018 (UTC)


Could use some additional eyes. --Tryptofish (talk) 21:54, 12 November 2018 (UTC)

Specifically [9] Enigmamsg 00:21, 13 November 2018 (UTC)



Can editors with medical experience please have a look at Phospholipidosis? There's lots of poorly formatted recent editing and an over-reliance on primary sources. Plus there is what appeas to me to be promotion for a company named Nextcea, Inc. Considering one of the major editors of the article is an account named Nextcea (talk · contribs · deleted contribs · logs · edit filter log · block user · block log), I'm sure there is COI/paid editing involved too. Sorry to just drop this here, but this topic is out of my league. Deli nk (talk) 23:38, 12 November 2018 (UTC)

though it has medical aspects, talk page[10] only indicates Wikipedia:WikiProject_Pharmacology--Ozzie10aaaa (talk) 13:36, 13 November 2018 (UTC)
Trimmed the mass of primary sources and tried to better summarize the review. Doc James (talk · contribs · email) 04:11, 14 November 2018 (UTC)
Further comments here Talk:Phospholipidosis would be useful. Doc James (talk · contribs · email) 15:35, 15 November 2018 (UTC)
I left a message and I am happy to help. JenOttawa (talk) 15:52, 15 November 2018 (UTC)
talk[11] indicated COI--Ozzie10aaaa (talk) 17:17, 15 November 2018 (UTC)

Student editors[edit]

We have several articles being edited by students who seem to have not been informed about MEDRS. The following articles would benefit from increased monitoring:

Thanks. Natureium (talk) 00:25, 15 November 2018 (UTC)

thank you for posting--Ozzie10aaaa (talk) 03:00, 16 November 2018 (UTC)
Class seems to be very active right now. JenOttawa (talk) 01:33, 17 November 2018 (UTC)

The MerckManual and MerckHome templates - don't work[edit]

Hi, (well at least one doesn't work, I'm extrapolating...EDIT on the template page of the two examples Folliculitis doesn't work, Lymphadenitis does)

Does anyone know who should be looking after these templates? ( & MerckManual)

I tried a link, e.g. at the bottom of Miliaria it links to: which is sort of broken, it goes to Lice Infestation. The layout of the site seems to have changed from the section chapter topic format. I assume it ( was trying to translate to the new format, but got the wrong redirection.

e.g. the new place for Miliaria is

I was about to edit the page but found the template, which implies many such links may be broken. ˥ Ǝ Ʉ H Ɔ I Ɯ (talk) 02:41, 15 November 2018 (UTC) Edited ˥ Ǝ Ʉ H Ɔ I Ɯ (talk) 02:55, 15 November 2018 (UTC)

Well, sort of nobody. User:Davidruben created the template, but hasn't edited for over a year, and User:Scottalter, whom I've often asked for help with templates before, has only made a few edits this year.
It doesn't look like there is a clear path from the old path to the new one. We're starting with {{MerckHome|18|206|b||Prickly Heat}} and I don't think that information can be bashed into the new URL. They might require manual updates. The good news is that this will probably require only a few dozen edits, as the templates are not very widely used. WhatamIdoing (talk) 03:40, 15 November 2018 (UTC)

Feedback would be helpful regarding adding two reviews to the PTSD article pertaining to Acupuncture[edit] If you have a chance, gathering a consensus/suggestions would be helpful here. Thanks! JenOttawa (talk) 12:57, 15 November 2018 (UTC)

give opinion(gave mine)--Ozzie10aaaa (talk) 22:22, 16 November 2018 (UTC)

Clinic for Special Children[edit]

Just dropping this here in case anyone is interested to take a look at it. Came across this because of a request at WP:FFU. I basically gutted the article. I did a bit of BEFOREish poking around and I suspect there may be enough to piece together an article with some substance, but it's not my forte. So here is it in case anyone has a particular interest in apparently rare genetic disorders and Amish people. GMGtalk 18:37, 15 November 2018 (UTC)

I will take a look, and can likely source and expand. It is quite an astonishing story and very well regarded genetics clinic and community health initiative. Canada Hky (talk) 18:45, 15 November 2018 (UTC)

School project[edit]

The new article Common Practices in Pain Management with an Emphasis on the Role of Opioids, which appears to be the product of a school assignment, could use medical review. Peacock (talk) 21:01, 15 November 2018 (UTC)

I'm tempted to draftify it, it's clearly an essay rather than an attempt at an encyclopedia article. ♠PMC(talk) 21:03, 15 November 2018 (UTC)
That seems reasonable to me. Peacock (talk) 21:04, 15 November 2018 (UTC)
It was draftified by Praxidicae. Natureium (talk) 21:10, 15 November 2018 (UTC)

IP refspam[edit]

I'm canvassing here for more input on this issue that no one has any proposed solutions for at ANI. Someone has been using a variety of IP addresses (12 that I found) to insert his own primary research papers as references in many biomedical articles. He's done this in batches since 2012. He has been blocked twice but doesn't care. Does anyone have any ideas of how to stop this? Natureium (talk) 21:12, 16 November 2018 (UTC)

If it's the same papers, maybe an edit filter? I don't know how to do them, so I can't help there, but it's a thought. ♠PMC(talk) 21:19, 16 November 2018 (UTC)
Yah not sure of any good solutions. Doc James (talk · contribs · email) 00:45, 17 November 2018 (UTC)
Keeping the content, but replacing the refs with citations to review articles or textbooks might help. He's adding content, not just citations. WhatamIdoing (talk) 16:52, 18 November 2018 (UTC)
But most of the content is supported by his own primary sources, which means there are probably not (yet) any secondary sources to verify it. Natureium (talk) 22:08, 20 November 2018 (UTC)

Sophia Getzowa[edit]

A group of us have been collaborating on this article, though none of us are specialists in medicine. The biographical part is mostly done (except her early life, which is still buried in questions). None of us are comfortable in attempting to discuss her research and expertise. The sources relating to her pathological research are discussed here. If there is anyone from this project that could help explain her research that would be very much appreciated. Thank you. SusunW (talk) 18:41, 17 November 2018 (UTC)

Looks good. Doc James (talk · contribs · email) 19:14, 17 November 2018 (UTC)
Doc James I'd really like help explaining what it was that she discovered. I read the articles, but I do not understand what her research was about. Clearly needs to be written by someone with expertise. Her discovery "solid cell nests" does not have an article, so linking to it isn't even an option. SusunW (talk) 19:25, 17 November 2018 (UTC)

Voting has opened on the community wish list[edit]

  • Have a proposal to improve Wikidata in watchlists HERE

Doc James (talk · contribs · email) 19:43, 17 November 2018 (UTC)

How does that relate to Wikidata/Expand automatic edit summaries? Jo-Jo Eumerus (talk, contributions) 20:04, 17 November 2018 (UTC)
Would be nice to get both done User:Jo-Jo Eumerus. The one I linked is about removing links to edits on Wikidata that do not effect what is displayed on EN WP. Doc James (talk · contribs · email) 01:26, 18 November 2018 (UTC)
Does anyone have any favorite items from the wishlist? I haven't looked at it recently. I remember a proposal about maps, and better map support can be useful to us for some articles (epidemiology, where the outbreak occurred, etc.). What else? WhatamIdoing (talk) 16:56, 18 November 2018 (UTC)

Primary sources[edit]

Hello. I have a quick question in regards to the recent edits by MegGutman (talk · contribs) ([12], [13]). Should we use these sources or is it unnecessary per WP:PSTS? Thanks, Lord Sjones23 (talk - contributions) 04:21, 18 November 2018 (UTC)

Well, I think that the simplest question to resolve is whether "The electrical activity map of the human skin indicates strong differences between normal and diabetic individuals: A gateway to onset prevention" is a good source for such basic information as "Prediabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 DM." This is the sort of thing that we'd normally cite a textbook or even a medical dictionary for, rather than a prototype involving 36 people. WhatamIdoing (talk) 17:01, 18 November 2018 (UTC)
this is a comparative study editor[14] should read MEDRSWikipedia:Identifying_reliable_sources_(medicine)--Ozzie10aaaa (talk) 17:10, 18 November 2018 (UTC)
All of the sources added are primary sources, and each is being used to support some very general biomedical claims. That contravenes MEDRS and is unnecessary. As WAID says, there are bound to be textbooks or good quality reviews that we should be using to support fairly basic claims like the difference in causes and predisposing factors between type 1 and type 2, or a prediabetic condition. --RexxS (talk) 17:23, 18 November 2018 (UTC)
They were unfortunately an account interested in spamming a single author with a number of other accounts also promoting said author. Combine that with the use of primary sources for topics in which much much better sources exist and edit warring... Doc James (talk · contribs · email) 22:31, 19 November 2018 (UTC)

Large genetics class off the rails[edit]

Please see Wikipedia:Education_noticeboard#Large_genetics_class_off_the_rails and the pages linked there, which need checking. Jytdog (talk) 20:10, 18 November 2018 (UTC)

And than we have this one [15] which is also related Doc James (talk · contribs · email) 22:27, 19 November 2018 (UTC)

PCORI hiring a Wikipedian in Residence for a one-year term[edit]

The Patient-Centered Outcomes Research Institute, a Washington D.C.-based nonprofit nongovernmental organization receiving some government funding, is seeking to hire a full-time Wikipedian in Residence for a one year term, perhaps beginning in February 2019. In this role the Wikimedian in Residence will seek to integrate health information from PCORI into Wikipedia.

See the description on the PCORI website. I understand that applications are open. I am passing this message along to WikiProject Medicine. Currently I am Wikimedian in Residence at the Data Science Institute at the University of Virginia, which is not far from DC, and I am keen on collaborating with the person at PCORI by visiting them there and inviting them to my university. Of course I also want someone who engages with WikiProject Medicine and the broader Wikimedia community.

In these roles every organization wants someone who is an expert Wikimedian and an expert in their field. If this is not possible, the next consideration is whether to hire a Wiki-expert with less medical experience, or someone who is proficient with medical information but inexperienced with wiki. Depending on the goals I think either of these could work. If socializing with peers is essential, then I recommend subject-matter experience over wiki experience, and if wiki community outreach is essential, then I recommend wiki experience or at least online community management experience.

Please refer the job posting to anyone whom you think might be interested. Thanks to physician zidovetz of Wiki Project Med Foundation for his visit to this organization in September 2018.

I do not speak for PCORI or have a particular relationship with this organization, but if anyone has questions about Wikimedian in Residence roles in medicine, then I can speak to that as I have been doing this since 2012. Thanks. Blue Rasberry (talk) 17:08, 20 November 2018 (UTC)

National Library of Medicine talking about WikiCite in Webinar[edit]

United States National Library of Medicine is hosting a talk on meta:WikiCite and d:Wikidata:Scholia. This is more of a Wikidata thing but it is medicine. I think that more organizations without a history of regular engagement with Wikimedia projects in medicine are starting to take interest in Wikidata.

Wikidata = 60 million items, 25 million are citations (this slice is mostly WikiCite), 15 million are citations to PubMed.

Dec 7, 2018, 2:00PM - 3:00PM ET

Here is something from this presenter -

Blue Rasberry (talk) 23:18, 20 November 2018 (UTC)