Nicotine
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2008-07-15T15:07:19Z
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{{otheruses4|the chemical compound|other uses|Nicotine (disambiguation)}}
{{Drugbox|
|IUPAC_name = ''(S)-3-(1-Methyl-2-pyrroli-
dinyl)pyridine''
| image=Nicotine-2D-skeletal.png
| image2=Nicotine-3D-vdW.png
| CAS_number=54-11-5
| ATC_prefix=N07
| ATC_suffix=BA01
| ATC_supplemental=
| PubChem=942
| smiles = C1=CC=NC=C1[C@@H]2CCCN2C
| DrugBank=
| C=10 | H=14 | N=2 |
| molecular_weight = 162.26 g/mole
| density= 1.01
| boiling_point= 247
| melting_point= -79
| bioavailability=
| metabolism =
| elimination_half-life= 2 hours
| excretion =
| pregnancy_US = D
| legal_AU = Unscheduled
| legal_CA =
| legal_UK = Unscheduled
| legal_US =
| legal_status =
| routes_of_administration= [[Tobacco smoking|Smoked (as tobacco)]], [[Insufflate]]d (as snuff), [[Nicotine gum|Chewed]]
| dependency_liability = Medium to high
}}
'''Nicotine''' is an [[alkaloid]] found in the [[nightshade]] family of plants (''Solanaceae''), predominantly in [[tobacco]], and in lower quantities in [[tomato]], [[potato]], [[eggplant]] (aubergine), and [[Bell pepper|green pepper]]. Nicotine can also be found, along with [[cocaine]], in the leaves of the [[coca]] plant. Nicotine has been found to constitute approximately 0.6 - 3.0% of dry weight of tobacco,<ref>{{cite web |url=http://dccps.nci.nih.gov/tcrb/monographs/9/m9_3.PDF |title=Smoking and Tobacco Control Monograph No. 9}}</ref> with [[biosynthesis]] taking place in the [[root]]s, and accumulating in the [[leaves]]. It functions as an [[Plant defense against herbivory|antiherbivore chemical]], being a potent [[neurotoxin]] with particular specificity to [[insect]]s; therefore nicotine was widely used as an [[insecticide]] in the past, and currently nicotine derivatives such as [[imidacloprid]] continue to be widely used.
In low concentrations (an average [[cigarette]] yields about 1 mg of absorbed nicotine), the substance acts as a [[stimulant]] in [[mammal]]s and is one of the main factors responsible for the dependence-forming properties of [[tobacco smoking]]. According to the [[American Heart Association]], "Nicotine [[addiction]] has historically been one of the hardest addictions to break." The pharmacological and behavioral characteristics that determine tobacco addiction are similar to those that determine addiction to drugs such as [[heroin]] and [[cocaine]].<ref>[http://www.americanheart.org/presenter.jhtml?identifier=4753 American Heart Association] and Nicotine addiction.</ref>
== History and name ==
Nicotine is named after the tobacco plant ''[[Nicotiana tabacum]]'', which in turn is named after [[Jean Nicot]], [[France|French]] ambassador in [[Portugal]], who sent tobacco and seeds from [[Brazil]] to [[Paris]] in 1560 and promoted their medicinal use. Nicotine was first isolated from the tobacco plant in [[1828]] by [[Germany|German]] chemists Posselt & Reimann.<!--might be in: Magazin der Pharmacie 24. 138. 1828-->{{Fact|date=April 2008}} Its chemical [[empirical formula]] was described by Melsens in [[1843]],<ref>{{cite journal
| title = Ueber das Nicotin
| author = Melsens
| journal = [[Journal für Praktische Chemie]]
| volume = 32
| issue = 1
| pages = 372–377
| year = 1844
| url =
| doi = 10.1002/prac.18440320155 }}</ref> and it was first synthesized by A. Pictet and Crepieux in [[1893]].{{Fact|date=April 2008}}
For thousands of years, people have smoked or chewed the leaves of the tobacco plant, Nicotiana tabacum. Tobacco was first found and cultivated in the Americas, perhaps as early as 6000 B.C. Following the discovery and colonization of North and South America by Europeans, the tobacco plant was exported widely, to continental Europe and the rest of the civilized world. Even in its early days, tobacco use was controversial. Some hailed its medicinal properties. For example, tobacco was supposed to be protective against the ravages of the Plague. As early as the 1600s, people speculated that there might be a link between diseases, like cancer, and tobacco use.{{Fact|date=April 2008}} Since then, modern research methods have provided evidence of this link, and public service announcements that warn of tobacco's health risks and addictive nature are seen regularly on several media.
== Chemistry ==
Nicotine is a [[hygroscopy|hygroscopic]], oily liquid that is [[miscible]] with [[water (molecule)|water]] in its [[base (chemistry)|base]] form. As a [[nitrogenous base]], nicotine forms [[salt]]s with [[acid]]s that are usually solid and water soluble. Nicotine easily penetrates the [[skin]]. As shown by the physical data, [[Freebase (chemistry)|free base]] nicotine will burn at a temperature below its boiling point, and its vapors will combust at 308K (35°C or 95°F) in air despite a low [[vapor pressure]]. Because of this, most of the nicotine is burned when a cigarette is smoked; however, enough is inhaled to provide the desired effects.
==Pharmacology==
===Pharmacokinetics===
As nicotine enters the body, it is distributed quickly through the [[blood]]stream and can cross the [[blood-brain barrier]]. On average it takes about seven seconds for the substance to reach the [[brain]] when inhaled. The half life of nicotine in the body is around two hours<ref>{{cite web |url=http://jpet.aspetjournals.org/cgi/content/citation/221/2/368 |title=Interindividual variability in the metabolism and cardiovascular effects of nicotine in man}}</ref>. The amount of nicotine inhaled with tobacco smoke is a fraction of the amount contained in the tobacco leaves. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. For [[chewing tobacco]], [[dipping tobacco]] and [[Snuff (tobacco)|snuff]], which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco. Nicotine is [[metabolized]] in the [[liver]] by [[cytochrome P450]] enzymes (mostly [[CYP2A6]], and also by [[CYP2B6]]). A major metabolite is [[cotinine]].
===Pharmacodynamics===
Nicotine acts on the [[nicotinic acetylcholine receptor]]s, specifically the [[ganglion type nicotinic receptor]] and one [[CNS type nicotinic receptor]]. The former is present e.g. in the [[adrenal medulla]] and the latter in the CNS. In small concentrations it increases the activity of these receptors.
====In adrenal medulla====
By binding to [[ganglion type nicotinic receptor]]s in the adrenal medulla nicotine increases flow of [[adrenaline]] (epinephrine), a stimulating [[hormone]]. By binding to the receptors, it causes cell depolarization and an influx of [[calcium]] through voltage-gated calcium channels. Calcium triggers the [[exocytosis]] of [[Chromaffin cell|chromaffin granules]] and thus the release of [[epinephrine]] (and norepinephrine) into the [[bloodstream]].
The release of adrenaline causes an increase in [[heart rate]], [[blood pressure]] and [[respiration]], as well as higher [[blood glucose]] levels <ref> Human Anatomy and Physiology. Elaine N Marieb & Katja Hoehn. 2007, Pearson Education. </ref>
[[Cotinine]] is a byproduct of the metabolism of nicotine which remains in the blood for up to 48 hours and can be used as an indicator of a person's exposure to smoke.
====In CNS====
By binding to [[CNS type nicotinic receptor]]s, nicotine increases [[dopamine]] levels in the [[reward circuit]]s of the [[brain]]. In this way, it activates the reward system and generates feelings of [[pleasure]].
Furthermore, nicotine activates the [[sympathetic nervous system]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/8140174?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVBrief Paper published on PubMed]</ref>, acting via [[splanchnic nerves]] to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the [[bloodstream]].
Studies have shown that other ingredients in inhaled tobacco smoke (as opposed to pure nicotine) inhibit the production of [[monoamine oxidase]] (MAO)<ref>{{cite journal |author=Fowler JS, Volkow ND, Wang GJ, Pappas N, Logan J, MacGregor R, Alexoff D, Wolf AP, Warner D, Cilento R, Zezulkova I |title=Neuropharmacological actions of cigarette smoke: brain monoamine oxidase B (MAO B) inhibition. |journal=Journal of addictive diseases |year=1998 |pmid=9549600}}</ref>, an [[enzyme]] responsible for breaking down [[monoamine|monoaminergic neurotransmitters]], such as dopamine, in the brain. The compounds responsible for this effect are beta-carboline alkaloids such as [[harmane]] and [[norharmane]].
==Psychoactive effects==
Nicotine's [[Mood (psychology)|mood]]-altering effects are different by report. First causing a release of [[glucose]] from the liver and [[epinephrine]] (adrenaline) from the [[adrenal medulla]], it causes [[stimulation]]. Users report feelings of [[relaxation]], [[calmness]], and [[alertness]]. <ref>Gilbert Lagrue, François Lebargy, Anne Cormier, "From nicotinic receptors to smoking dependence: therapeutic prospects" ''Alcoologie et Addictologie'' Vol. : 23, N° : 2S, juin 2001, pages 39S - 42</ref> It is even reported to produce a mildly [[Euphoria (emotion)|euphoric]] state. By reducing the [[appetite]] and raising the [[metabolism]], some [[smoker]]s may [[weight loss|lose weight]] as a consequence.<ref>Jean-Claude Orsini, "Dependence on tobacco smoking and brain systems controlling glycemia and appetite" ''Alcoologie et Addictologie'' Vol. : 23, N° : 2S, juin 2001, pages 28S - 36S</ref><ref>http://uninews.unimelb.edu.au/articleid_1898.html</ref> It also allows the mouth to be stimulated without food, and the taste of tobacco smoke may curb the [[appetite]].{{Fact|date=January 2008}}
When a [[cigarette]] is smoked, nicotine-rich blood passes from the [[lung]]s to the [[brain]] within seven seconds and immediately stimulates the release of many chemical messengers including [[acetylcholine]], [[norepinephrine]], [[epinephrine]], [[vasopressin]], [[arginine]], [[dopamine]], and [[beta-endorphin]]. This results in enhanced pleasure, decreased [[anxiety]], and a state of alert [[relaxation]]. Nicotine enhances [[attention|concentration]] and [[learning]] due to the increase of [[acetylcholine]]. It also enhances [[alertness]] due to the increases of [[acetylcholine]] and [[norepinephrine]]. [[Arousal]] is increased by the increase of [[norepinephrine]]. [[Pain]] is reduced by the increases of [[acetylcholine]] and [[beta-endorphin]]. [[Anxiety]] is reduced by the increase of [[beta-endorphin]]. Nicotine also sensitises brain reward systems.<ref>Kenny PJ, Markou A. "Nicotine self-administration acutely activates brain reward systems and induces a long-lasting increase in reward sensitivity"
''Neuropsychopharmacology'' (2006) 31, 1203–1211.</ref> The effects of nicotine last from five minutes to two hours. Most cigarettes (in the smoke inhaled) contain 0.1 to 2.8 milligrams of nicotine.<ref>http://www.erowid.org/chemicals/nicotine/nicotine_dose.shtml</ref>
Research<ref>{{cite book
| last = Einstein
| first = Stanley
| authorlink = Stanley Einstein
| title = Drug and Alcohol Use: Issues and Factors
| publisher = [[Springer]]
| date = 1989
| pages = 101-118
| isbn = 0306413787
}}</ref> suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine. This stimulates [[action potential|nerve transmission]]. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of [[nerve impulses]], producing a mild sedative effect. At low doses, nicotine potently enhances the actions of [[norepinephrine]] and [[dopamine]] in the brain, causing a drug effect typical of those of [[psychostimulants]]. At higher doses, nicotine enhances the effect of [[serotonin]] and [[opiate]] activity, producing a calming, [[analgesic|pain-killing]] effect. Nicotine is unique in comparison to most [[drug]]s, as its profile changes from [[stimulant]] to [[sedative]]/[[pain killer]] in increasing [[dosage]]s and use.
[[Image:Nicoderm.JPG||thumb|right|A 21 mg patch applied to the left arm]]
[[Nicotine gum]] and [[nicotine patches]] are available, usually in 2-mg or 4-mg doses of [[gum]], that do not have all the other ingredients in smoked tobacco. They appear to be not as addictive or as pleasurable, and, it is claimed, have fewer side effects {{Fact|date=July 2007}}. Whether all the other psychoactive effects also occur has not been well studied.
==Dependence==
{{see also|Smoking cessation}}
Modern [[research]] shows that nicotine acts on the brain to produce a number of effects. Specifically, its addictive nature has been found to show that nicotine activates reward pathways—the circuitry within the brain that regulates feelings of pleasure and euphoria. <ref>[http://www.nida.nih.gov/researchreports/nicotine/nicotine2.html NIDA - Research Report Series - Tobacco Addiction - Extent, Impact, Delivery, and Addictiveness<!-- Bot generated title -->]</ref>
To reduce the health effects of cigarette smoking, the best thing to do is to quit. Public health authorities do not endorse either smoking fewer cigarettes or switching to lower tar and nicotine brands as a satisfactory way of reducing risk. <ref>[http://www.philipmorrisusa.com/en/cms/Products/Cigarettes/Health_Issues/default.aspx]</ref>
[[Dopamine]] is one of the key [[neurotransmitters]] actively involved in the brain. Research shows that by increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has not been shown to be more addictive than [[cocaine]] and [[heroin]], though chronic treatment has an opposite effect on reward thresholds. Like other physically addictive drugs, nicotine causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. In addition, the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. The net effect is an increase in reward pathway sensitivity, opposite of other drugs of abuse (namely cocaine and heroin, which reduce reward pathway sensitivity){{Fact|date=November 2007}}. This neuronal brain alteration persists for months after administration ceases. Due to an increase in reward pathway sensitivity, nicotine withdrawal is relatively mild compared to ethanol or heroin withdrawal.{{Fact|date=November 2007}} Nicotine also has the potential to cause dependence in many animals other than humans. Mice have been administered nicotine and exhibit [[withdrawal]] reactions when its administration is stopped.<ref>[http://www.nida.nih.gov/NIDA_notes/NNvol19N2/Early.html NIDA - Publications - NIDA Notes - Vol. 19, No. 2 - Research Findings<!-- Bot generated title -->]</ref>
A study found that nicotine exposure in adolescent mice retards the growth of the dopamine system, thus increasing the risk of substance abuse during adolescent.<ref> Nolley E.P. & Kelley B.M. "[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17129706&query_hl=31&itool=pubmed_docsum Adolescent reward system perseveration due to nicotine: Studies with methylphenidate.]," ''Neurotoxicol Teratol.'', 2006 Oct 4</ref>
==Toxicology==
The [[LD50|LD<sub>50</sub>]] of nicotine is 50 mg/kg for [[rat]]s and 3 mg/kg for [[mouse|mice]]. 40–60 mg (0.5-1.0 mg/kg) can be a lethal dosage for adult humans.<ref>{{cite journal
| author = Okamoto M., Kita T., Okuda H., Tanaka T., Nakashima T.
| title = Effects of aging on acute toxicity of nicotine in rats
| journal = Pharmacol Toxicol.
| year = 1994
| volume = 75
| issue = 1
| pages = 1–6
| doi =
}}</ref> <ref>[http://www.inchem.org/documents/pims/chemical/nicotine.htm#PartTitle:7.%20TOXICOLOGY IPCS INCHEM]</ref> This designates nicotine as an extremely deadly [[poison]]. It is more toxic than many other alkaloids such as [[cocaine]], which has an LD<sub>50</sub> of 95.1 mg/kg when administered to mice. Spilling liquid nicotine on human skin could result in death.<ref>[http://www.abc.net.au/quantum/poison/nicotine/ted.htm] "Interview with Prof Thoedore Slotkin"</ref>
The [[carcinogen]]ic properties of nicotine in standalone form, separate from tobacco smoke, have not been evaluated by the [[International Agency for Research on Cancer|IARC]], and it has not been assigned to an official carcinogen group. The currently available literature indicates that nicotine, on its own, does not promote the development of [[cancer]] in healthy tissue and has no [[mutagen]]ic properties. Its [[Teratogenesis|teratogenic]] properties have not yet been adequately researched, and while the likelihood of birth defects caused by nicotine is believed to be very small or nonexistent, nicotine replacement product manufacturers recommend consultation with a physician before using a [[nicotine patch]] or [[nicotine gum]] while pregnant or nursing. However, nicotine and the increased [[Nicotinic acetylcholine receptor|cholinergic]] activity it causes have been shown to impede [[apoptosis]]{{Fact|date=April 2007}}, which is one of the methods by which the body destroys unwanted cells ([[programmed cell death]]). Since [[apoptosis]] helps to remove mutated or damaged cells that may eventually become cancerous, the inhibitory actions of nicotine may create a more favourable environment for cancer to develop, though this also remains to be proven.
At least one study has concluded that exposure to nicotine alone, not simply as a component of cigarette smoke, could be responsible for some of the neuropathological changes observed in infants dying from [[Sudden Infant Death Syndrome]] (SIDS).<ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15802186&dopt=Abstract Machaalani et al. (2005)] "Effects of postnatal nicotine exposure on apoptotic markers in the developing piglet brain"</ref>
It has been noted that the majority of people diagnosed with [[schizophrenia]] smoke tobacco. Estimates for the number of schizophrenics that smoke range from 75% to 90%. It was recently argued that the increased level of smoking in schizophrenia may be due to a desire to [[self-medication|self-medicate]] with nicotine. <ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12084420 Schizophr. Res. 2002]</ref>
<ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7864277 Am. J. Psychiatry 1995]</ref> More recent research has found the reverse, that it is a risk factor without long-term benefit, used only for its short term effects.<ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15738502 Br. J. Psychiatry 2005] </ref> However, research on nicotine as administered through a patch or gum is ongoing.
== Nicotine and oxidative stress ==
Nicotine is detoxified by the cytochrome p450 in the liver. Recently it has been published that
it produces [[Radical (chemistry)|free radicals]] in this reaction.{{Fact|date=May 2008}}
<!--
The following paragraph appears to be about "Chronic exposure to tobacco dust". What does this have to do with nicotine by itself?
Study on bidi workers carried out in Solapur
district of Maharashtra state of India revealed that nicotine may be the potent free radical
generetor. [[Sanjay Swami]] et. al. also suggested the carcinogenic effect of nicotine may be due to its free radical generating potential.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/17444052]</ref>
-->
==Link to circulatory disease==
Nicotine has very powerful effects on arteries throughout the body. Nicotine is a stimulant, speeding up the heart by about 20 beats per minute with every cigarette; it raises [[blood pressure]], and is a [[vasoconstrictor]], making it harder for the heart to pump through the constricted arteries. It causes the body to release its stores of fat and [[cholesterol]] into the blood.
Nicotine increases the risk of blood clots significantly. {{Fact|date=February 2008}} If blood clots in an artery, blood flow is reduced or halted, and tissue loses its source of oxygen and nutrients and dies in minutes.
Peripheral circulation, arteries going to the extremities, are also highly susceptible to the vasoconstrictor effects of nicotine as well as the increased risk of clots and clogging.{{Fact|date=February 2008}}
== Therapeutic uses ==
The primary therapeutic use of nicotine is in treating nicotine dependence in order to eliminate [[smoking]] with its risks to health. Controlled levels of nicotine are given to patients through gums, dermal patches, lozenges, electric/substitute cigarettes or nasal sprays in an effort to wean them off their dependence.
However, in a few situations, smoking has been observed to apparently be of therapeutic value to patients.
These are often referred to as "Smoker’s Paradoxes"<ref name="cohen">
{{cite journal
| last = Cohen
| first = David J.
| authorlink =
| coauthors = Michel Doucet, Donald E. Cutlip, Kalon K.L. Ho, Jeffrey J. Popma, Richard E. Kuntz
| title = Impact of Smoking on Clinical and Angiographic Restenosis After Percutaneous Coronary Intervention
| journal = Circulation
| volume = 104
| issue =
| pages = 773
| date = 2001
| url = http://www.data-yard.net/34/circulation_2001_104_773.htm
| doi =
| id =
| accessdate = 2006-11-06}}
</ref>. Although in most cases the actual mechanism is understood only poorly or not at all, it is generally believed that the principal beneficial action is due to the nicotine administered, and that administration of nicotine without smoking may be as beneficial as smoking, without the higher risk to health due to [[tar (tobacco residue)|tar]] and other ingredients found in [[tobacco]].
For instance, recent studies suggest that smokers require less frequent repeated [[revascularization]] after [[percutaneous coronary intervention]] (PCI).<ref name="cohen"/> Risk of [[ulcerative colitis]] has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking.<ref name="ohcm">Longmore, M., Wilkinson, I., Torok, E. Oxford Handbook of Clinical Medicine (Fifth Edition) p. 232</ref><ref>
{{cite journal
| last = Green
| first = JT
| authorlink =
| coauthors = Richardson C, Marshall RW, Rhodes J, McKirdy HC, Thomas GA, Williams GT
| title = Nitric oxide mediates a therapeutic effect of nicotine in ulcerative colitis
| journal = Aliment Pharmacol Ther
| volume = 14
| issue = 11
| pages = 1429–1434
| date = November, 2000
| url = http://www.data-yard.net/22/ncbi.htm
| doi =
| pmid =: 11069313
| accessdate = 2006-11-06}}</ref>
Smoking also appears to interfere with development of [[Kaposi's sarcoma]],<ref>
{{cite news
| last =
| first =
| coauthors =
| title = Smoking Cuts Risk of Rare Cancer
| work =
| pages =
| language = English
| publisher = UPI
| date = March 29, 2001
| url = http://www.data-yard.net/10b/kaposi.htm
| accessdate = 2006-11-06}}
</ref>
[[breast cancer]] among women carrying the very high risk [[BRCA]] gene,<ref>
{{cite news
| last = Recer
| first = Paul
| coauthors =
| title = Cigarettes May Have an Up Side
| work =
| pages =
| language = English
| publisher = AP
| date = May 19, 1998
| url = http://www.forces.org/evidence/files/brea.htm
| accessdate = 2006-11-06}}
</ref>
[[preeclampsia]],<ref>
{{cite journal
| last = Lain
| first = Kristine Y.
| authorlink =
| coauthors = Robert W. Powers, Marijane A. Krohn, Roberta B. Ness, William R. Crombleholme,
James M. Roberts
| title = Urinary cotinine concentration confirms the reduced risk of preeclampsia with tobacco exposure
| journal = American Journal of Obstetrics and Gynecology
| volume = 181
| issue = 5
| pages = 908–14
| date = November 1991
| url = http://www.data-yard.net/2/13/ajog.htm
| doi =
| pmid = : 11422156
| accessdate = 2006-11-06}}
</ref>
and [[atopy|atopic disorder]]s such as [[allergic asthma]].<ref>
{{cite journal
| last = Hjern
| first = A
| authorlink =
| coauthors = Hedberg A, Haglund B, Rosen M
| title = Does tobacco smoke prevent atopic disorders? A study of two generations of Swedish residents
| journal = Clin Exp Allergy
| volume = 31
| issue = 6
| pages = 908–914
| publisher =
| date = June 2001
| url = http://www.data-yard.net/30/asthma.htm
| doi =
| pmid = : 11422156
| accessdate = 2006-11-06}}</ref>
A plausible mechanism of action in these cases may be nicotine acting as an [[Inflammation|anti-inflammatory agent]], and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects.<ref name="sciam">{{cite journal | author=Lisa Melton | title=Body Blazes | journal=Scientific American | date=June 2006 | pages=p.24 | url=http://www.sciam.com/article.cfm?chanID=sa006&colID=5&articleID=00080902-A2CF-146C-9D1E83414B7F0000}}</ref>
With regard to [[neurology|neurological diseases]], a large body of evidence suggests that the risks of [[Parkinson's disease]] or [[Alzheimer's disease]] might be twice as high for non-smokers than for smokers.<ref>
{{cite journal
| last = Fratiglioni
| first = L
| authorlink =
| coauthors = Wang HX
| title = Smoking and Parkinson's and Alzheimer's disease: review of the epidemiological studies
| journal = Behav Brain Res
| volume = 113
| issue = 1-2
| pages = 117–120
|date=August 2000
| url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10942038&dopt=Citation
| doi =
| pmid = : 10942038
| accessdate = 2006-11-06}}
</ref>
Many such papers regarding Alzheimer's disease<ref>
{{cite web
| last = Thompson
| first = Carol
| authorlink =
| coauthors =
| title = Alzheimer's disease is associated with non-smoking
| work =
| date =
| url = http://www.forces.org/evidence/carol/carol16.htm
| format =
| doi =
| accessdate =2006-11-06}}
</ref>
and Parkinson's Disease<ref>
{{cite web
| last = Thompson
| first = Carol
| authorlink =
| coauthors =
| title = Parkinson's disease is associated with non-smoking
| work =
| date =
| url = http://www.forces.org/evidence/carol/carol36.htm
| format =
| doi =
| accessdate =2006-11-06}}
</ref>
have been published. More recent studies find that there's no beneficial link between smoking and Alzheimer's, and in some cases suggest that it actually results in an earlier onset of the disease.<ref>
{{cite web
| last =
| first =
| authorlink =
| coauthors =
| title = Alzheimer's Starts Earlier for Heavy Drinkers, Smokers
| work =
| publisher= Reuters
| date = 2008-17-04
| url = http://www.reuters.com/article/pressRelease/idUS198346+17-Apr-2008+PRN20080417
| format =
| doi =
| accessdate =2008-27-06}}
</ref>
<ref>
{{cite web
| last = Peck
| first = Peggy
| authorlink =
| coauthors =
| title = Smoking Significantly Increases Risk of Alzheimer's Disease Among Those Who Have No Genetic Predisposition
| work =
| date = 2002-25-07
| url = http://www.docguide.com/news/content.nsf/news/8525697700573E1885256C010043BDDC?OpenDocument&c=Smoking%20Related%20Disorders&count=10&id=48dde4a73e09a969852568880078c249
| accessdate = 2008-27-06}}
</ref>
<ref>
{{Citation
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| first =Neelum
| authorlink =
| coauthors = Bienias J.L., Bennett, D.A., et al.
| title = The Relation of Cigarette Smoking to Incident Alzheimer's Disease in a Biracial Urban Community Population
| journal = Neuroepidemiology
| volume = 26
| issue = 3
| pages = 140-146
| date =
| url = http://content.karger.com/ProdukteDB/produkte.asp?Doi=91654
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</ref>
<ref>
{{cite web
| last = Lerche Davis,
| first =Jeanie
| authorlink =
| title = Smoking Speeds Dementia, Alzheimer's Disease
| date = 2004-22-03
| url = http://www.webmd.com/smoking-cessation/news/20040322/smoking-speeds-dementia-alzheimers-disease
| accessdate = 2008-27-06}}
</ref>
Recent studies have indicated that nicotine can be used to help adults suffering from [[Autosomal dominant nocturnal frontal lobe epilepsy]]. The same areas that cause seizures in that form of [[epilepsy]] are also responsible for processing nicotine in the brain.<ref>{{cite web |url=http://www.cnsforum.com/commenteditem/3c5dccdc-27fb-4b80-9516-ab81e3e4ea6c/default.aspx |title=Nicotine as an antiepileptic agent in ADNFLE: An n-of-one study}}</ref>
Nicotine and its metabolites are being researched for the treatment of a number of disorders, including [[ADHD]], [[Schizophrenia]] and [[Parkinson's Disease]]. <ref>{{cite web| url=http://www.reutershealth.com/wellconnected/doc30.html |title=Attention-Deficit Hyperactivity Disorder |year=2001 |month=December |work=Reuters Health |publisher=Reuters |archiveurl=http://web.archive.org/web/20060426105219/http://www.reutershealth.com/wellconnected/doc30.html |archivedate=2006-04-26 |quote=Nicotine improves ADHD symptoms. Although such findings should certainly not encourage anyone to smoke, some studies are focusing on benefits of nicotine therapy in adults with ADHD.}}</ref> People with schizophrenia smoke two to three times more than smokers without mental illness; this may be a form of [[self-medication]] to improve attention and short-term memory.<ref>http://www.medicalnewstoday.com/articles/26516.php</ref>
The therapeutic use of nicotine as a means of appetite-control and to promote weight loss is anecdotally supported by many ex-smokers who claim to put on weight after quitting. However studies of nicotine in mice <ref>NIH, online at [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=954834&dopt=Abstract]</ref> suggests it may play a role in weight-loss that is independent of appetite and studies involving the elderly suggest that nicotine affects not only weight loss, but also prevents some weight gain. <ref>Cigarette Smoking and Weight Loss in Nursing Home Residents
[http://www.priory.com/med/cigsmoking.htm]</ref>
== See also ==
*[[Addiction]]
*[[Allen Carr]]
*[[Cigarette]]
*[[Dipping tobacco]]
*[[Drug addiction]]
*[[Myocardial infarction]]
*[[Nicogel]]
*[[Nicotini]]
*[[NicVAX]]
*[[Psychoactive drug]]
*[[Snuff]]
*[[Snus]]
*[[Stroke]]
==External links==
*[http://www.stopsmoking.net/about_add.html Description of nicotine addiction]
*[http://www.howstuffworks.com/nicotine.htm Description of nicotine mechanisms]
==References==
{{reflist|colwidth=35em}}
== Further reading ==
* Nicotine Therapy for ADNFLE: [http://www.cnsforum.com/commenteditem/3c5dccdc-27fb-4b80-9516-ab81e3e4ea6c/default.aspx "Nicotine as an antiepileptic agent in ADNFLE: An n-of-one study"]
* Minna, John D.: [http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=151841 "Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer"]
* [[James Fallon|Fallon, J.H.]], et al. (2005) Gender: A major determinant of brain response to nicotine. International Journal of Neuropharmacology. 8:1-10. [http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=282494]
* West, Kip A., et al.: [http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=151834 "Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells"]
* [http://www.nida.nih.gov/researchreports/nicotine/nicotine.html National Institute on Drug Abuse]
*Erowid information on tobacco[http://www.erowid.org/plants/tobacco/tobacco.shtml]
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{{Drugs used in addictive disorders}}
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[[Category:Health risks]]
[[Category:Neurotoxins]]
[[Category:Nitrogen heterocycles]]
[[Category:Nicotinic agonists]]
[[Category:Plant toxin insecticides]]
[[Category:Pyridines]]
[[Category:Pyrrolidines]]
[[Category:Stimulants]]
[[Category:Tobacco]]
[[Category:Smoking]]
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