Talk:Nicotine

Connections to other substances MEDRS?

It looks like this new section is supported by mainly primary sources. Should MEDRS apply there? Sizeofint (talk) 21:14, 31 May 2016 (UTC)

Also, should MEDRS apply to Gateway drug theory. That article also includes these primary sources. Sizeofint (talk) 21:16, 31 May 2016 (UTC)

Yes and yes. I have been thinking about what to do with that addition. Jytdog (talk) 21:17, 31 May 2016 (UTC)

Doesn't matter what the article is - matters what the statement is (1st paragraph of MEDRS). I once deleted a poorly sourced medical claim in the Breaking bad article and someone disputed it, but the eventual consensus following discussion was that MEDRS applies because there was a medical claim in that article. Seppi333 (Insert 2¢) 23:11, 31 May 2016 (UTC)

Right, I phrased my question poorly. Sizeofint (talk) 23:21, 31 May 2016 (UTC)

Saidmann, are there any WP:MEDRS compliant sources such as review articles that cover this content? Sizeofint (talk) 23:23, 31 May 2016 (UTC)

I am aware of WP:MEDRS. There you find the rule "Primary sources may be presented together with secondary sources." This has been done in the linked main article Gateway drug theory, which uses these secondary sources:

• D. B. Kandel (Ed.): Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis, Cambridge University Press, 2002, ISBN 978-0-521-78969-1.
• Wayne Hall, Rosalie Liccardo Pacula: Is cannabis a gateway drug? In: Same authors: Cannabis Use and Dependence. Public Health and Public Policy, Cambridge University Press, Cambridge, UK, New York, USA, 2003, ISBN 978-0-521-80024-2, chapt. 10, pp. 104–114.
• Mark A.R. Kleiman, Jonathan P. Caulkins, Angela Hawken: Is marijuana a "gateway drug"? In: Same authors: Drugs and Drug Policy. What Everyone Needs to Know, Oxford University Press, 2011, ISBN 978-0-19-983138-8, chapt. 4, question 8, pp. 81–83.
• Goode, Erich (1974). "Marijuana use and the progression to dangarous drugs". In Miller, Loren (ed.). Marijuana Effects on Human Behavior. Burlington: Elsevier Science. p. 303–338. ISBN 978-1-4832-5811-9.

I have now also added a secondary source in the new section of this article. Please note that in subjects like this one secondary sources usually only present the general frame of subject and research but not the "state of the art", which has to be added by primary sources. This is why we have the rule "Primary sources may be presented together with secondary sources."

References

--Saidmann (talk) 11:11, 1 June 2016 (UTC)

New review

User:Zvi Zig - do not read only the abstract (see WP:NOABSTRACT) - this is basic editing here in WP. The quote from PMID 27079891's conclusion is accurate. Jytdog (talk) 22:46, 26 October 2016 (UTC)

I'm not sure what you're referring to -- the quote I cited is from the body, not the abstract.

The quote from PMID 27079891 is indeed accurate, but it does not represent the review's conclusion accurately. Why is weight given to experimental evidence on biological plausibility, rather than the authors main conclusions on nicotine safety? Zvi Zig (talk • contribs 23:11, 26 October 2016 (UTC)

I see what you are saying -- I added a bit here. That was easily fixable. Jytdog (talk) 23:42, 26 October 2016 (UTC)

Why don't you cite from the next paragraph in that review, which is the ultimate conclusion, rather than WP:JARGON-filled quote confusingly starting off with biological plausibility based on WP:MEDANIMAL evidence Zvi Zig (talk • contribs 00:54, 2 November 2016 (UTC)

If sources disagree in regard to cardiovascular disease risk we do not decide who is "right". Rewording the text can also work rather than deleting all of the conclusion. It also found "Nicotine exerts pharmacologic effects that could contribute to acute cardiovascular events and accelerated atherogenesis experienced by cigarette smokers."[1] QuackGuru (talk) 21:57, 6 November 2016 (UTC)

These sources do not disagree. Rather, they relate to different effects. Some relate to biological plausibility, while others relate to short and long-term human epidemiology. The authors then present the ultimate conclusion, which takes all of these into account, giving each their proper weight.

In regards to the statement quoted above, it is part of the literature review relating to a possible effect, not the conclusion. In fact, authors reject its relevance immediately: "While it is reasonable to conclude that there is a link between nicotine and a more atherogenic lipid profile, multiple cessation studies using nicotine medications (NRT and nicotine nasal spray) report reduced dyslipidemia with significant improvement in HDL/LDL ratios". Zvi Zig (talk • contribs 23:58, 6 November 2016 (UTC)

That is about "Nicotine and dyslipidemia" under a different section. They do not reject the fact that there is a possible link with atherogenesis.

I added the part about dyslipidemia. See "Many quitting smoking studies using nicotine medicines report lowered dyslipidemia with considerable benefit in HDL/LDL ratios.[49]" Sources do disagree about the association with cardiovascular disease. The readers make the ultimate conclusion. QuackGuru (talk) 02:12, 7 November 2016 (UTC)

1. Sorry, I didn't realize you were referring to the statement in the abstract. The abstract's statement on atherogenesis relates to biological plausibility, as you can see in the full-text Conclusion (emph. mine):

   "Studies of the pharmacology and toxicology of nicotine in animals and some epidemiologic studies in people support the biological plausibility that nicotine contributes to acute cardiovascular events in smokers with underlying CVD, and exerts pharmacologic effects that could contribute to accelerated atherogenesis. Short-term nicotine use, such as nicotine medication to aid smoking cessation, appears to pose little cardiovascular risk, even to patients with known CVD. Longer term nicotine use, such as in ST users, appears not accelerate atherogenesis (sic), but may contribute to acute cardiovascular events in the presence of CVD."[2]

2. My statement was about these sources not disagreeing, not the conclusions of other reviews, which are a different discussion. Zvi Zig (talk • contribs 09:05, 7 November 2016 (UTC)

More context was added. See "Brief nicotine use, such as nicotine medicine, seems to incur a slight cardiovascular risk, even to people with established cardiovascular disease.[49] Prolonged nicotine use seems not to increase atherosclerosis.[49]"

There is insufficient data on the long-term effects of nicotine. Since the long-term nicotine use is unknown it is relevant to include it in the WP:LEDE. Even coffee could have negative health effects. QuackGuru (talk) 17:38, 7 November 2016 (UTC)