Nicotine and Multiple Sclerosis: The Research
Smoking raises the risk of multiple sclerosis while Scandinavian snus users show lower risk, which points away from nicotine and toward smoke, and animal studies of nicotine in experimental autoimmune encephalomyelitis report less brain inflammation. This page collects the published research on nicotine and multiple sclerosis, each paper summarised in plain language with its PubMed record.
This collection is research only: papers found on PubMed, each described as its own abstract reports it. Cell and animal results are labelled as such, and harms are listed beside benefits. It is not medical advice.
Table of Contents
Research at a Glance
What kind of study each paper on this page is, and when the papers were published. Hover over a bar for its count.
The Papers (29)
Newest first. Study types on this page — Human trial: 1 · Human observational study: 9 · Review: 7 · Animal study: 11 · Other: 1. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.
Personality traits in patients with multiple sclerosis: their association with nicotine dependence and polypharmacy
Human observational study, 2024. Researchers studied 375 people with multiple sclerosis at two German clinics, using personality questionnaires (NEO-FFI and TCI-R) and the Fagerstrom test for smoking dependence. Among current smokers with MS, those with severe nicotine dependence had higher neuroticism scores and higher harm-avoidance scores, plus lower scores for reward dependence, self-directedness, and cooperativeness, compared to those with mild or moderate dependence. People with MS who also had polypharmacy (taking multiple medications) showed a similar pattern of higher neuroticism and lower extraversion, persistence, self-directedness, and cooperativeness.
Meißner J, Frahm N, Hecker M et al. (2024). Personality traits in patients with multiple sclerosis: their association with nicotine dependence and polypharmacy. Ther Adv Neurol Disord. — PubMed PMID: 39411724 · doi:10.1177/17562864241279118
Phytochemicals derived from Nicotiana tabacum L. plant contribute to pharmaceutical development
Review, 2024. This review looks at compounds found in the tobacco plant — including nicotine, solanesol, cembranoid diterpenes, and tobacco oils — separate from smoke's toxic components. Drawing on about 20 years of published research, it describes laboratory and mechanistic findings suggesting these compounds have antioxidant, anti-inflammatory, and metabolism-related effects, and discusses their potential as supplements for conditions including neurodegenerative diseases, inflammatory diseases such as multiple sclerosis, and metabolic conditions like obesity. The paper is a literature summary of molecular mechanisms rather than a new experiment.
Zhang W, Pan X, Fu J et al. (2024). Phytochemicals derived from Nicotiana tabacum L. plant contribute to pharmaceutical development. Front Pharmacol. — PubMed PMID: 38681197 · doi:10.3389/fphar.2024.1372456
Influence of oral tobacco versus smoking on multiple sclerosis disease activity and progression
Human observational study, 2023. Researchers tracked over 9,000 people with multiple sclerosis in Sweden for up to 15 years, comparing those who smoked, were exposed to secondhand smoke, or used oral snuff (smokeless tobacco) against non-users. People who kept smoking after their MS diagnosis had faster disability progression and worse scores on quality-of-life and thinking-speed tests than non-smokers, and secondhand smoke exposure showed a similar pattern. Those who quit smoking after diagnosis did better than those who kept smoking. Snuff users, by contrast, had slower disability progression than people who never used snuff, leading the authors to suggest nicotine replacement therapy might help smokers quit.
Wu J, Olsson T, Hillert J et al. (2023). Influence of oral tobacco versus smoking on multiple sclerosis disease activity and progression. J Neurol Neurosurg Psychiatry. — PubMed PMID: 37001984 · doi:10.1136/jnnp-2022-330848
Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects
Review, 2022. This review looks at how nicotine affects inflammation across a range of diseases, including inflammatory bowel disease, arthritis, multiple sclerosis, sepsis, and oral inflammation. Drawing on studies from the past 20 years, the authors report that nicotine is mostly anti-inflammatory, especially in ulcerative colitis, arthritis, sepsis, and endotoxemia, but it can worsen oral conditions like periodontitis and gingivitis. The paper also summarizes dosage ranges and possible mechanisms, such as effects on immune cells and the vagus nerve/acetylcholine pathway.
Zhang W, Lin H, Zou M et al. (2022). Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects. Front Immunol. — PubMed PMID: 35251010 · doi:10.3389/fimmu.2022.826889
Cotinine as a measure of smoking in observational studies of multiple sclerosis
Human observational study, 2021. This Swedish case-control study looked at how smoking is measured when studying multiple sclerosis (MS) risk and progression. It found that defining smokers by self-reported smoking history versus by cotinine (a nicotine breakdown product) levels gave very different results: the increased risk of converting to secondary progressive MS among smokers showed up with self-reported history but not with cotinine-based measurement. The authors conclude that using cotinine levels without accounting for different nicotine sources can produce biased estimates of the smoking-MS relationship.
Hedström AK, Olsson T, Alfredsson L (2021). Cotinine as a measure of smoking in observational studies of multiple sclerosis. Mult Scler. — PubMed PMID: 33170069 · doi:10.1177/1352458520968803
A silent agonist of α7 nicotinic acetylcholine receptors modulates inflammation ex vivo and attenuates EAE
Animal study, 2020. Researchers tested whether a lab-made molecule that selectively calms a specific nicotine-receptor type (the alpha7 nicotinic receptor) without fully activating it could reduce inflammation in mouse immune cells and in mice with an induced multiple-sclerosis-like disease. In mouse white blood cells grown in a dish, this molecule and a separate receptor-blocking drug both reduced the number of inflammatory immune cells and lowered their production of inflammatory signaling proteins. In live mice with the MS-like disease, the molecule significantly improved disease symptoms, and it also reduced chronic inflammatory pain in mice.
Godin JR, Roy P, Quadri M et al. (2020). A silent agonist of α7 nicotinic acetylcholine receptors modulates inflammation ex vivo and attenuates EAE. Brain Behav Immun. — PubMed PMID: 31874200 · doi:10.1016/j.bbi.2019.12.014
Attenuation in Nicotinic Acetylcholine Receptor α9 and α10 Subunit Double Knock-Out Mice of Experimental Autoimmune Encephalomyelitis
Animal study, 2019. Mice with a model of multiple sclerosis (experimental autoimmune encephalomyelitis, or EAE) were studied, comparing normal mice to mice genetically engineered to lack nicotinic receptor subunits called alpha9 and alpha10. Mice missing both subunits had less severe disease, later onset, less immune cell invasion of the brain and spinal cord, fewer reactive oxygen species, and less nerve-fiber damage (demyelination) than normal mice. These effects looked the same as those seen in nicotine-treated normal mice or in mice missing only the alpha9 subunit, suggesting the alpha9 nicotinic receptor subunit plays a role in driving inflammation and autoimmune damage in this mouse model.
Liu Q, Li M, Whiteaker P et al. (2019). Attenuation in Nicotinic Acetylcholine Receptor α9 and α10 Subunit Double Knock-Out Mice of Experimental Autoimmune Encephalomyelitis. Biomolecules. — PubMed PMID: 31817275 · doi:10.3390/biom9120827
Transcriptomic Characterization of the Human Habenula Highlights Drug Metabolism and the Neuroimmune System
Other, 2018. Researchers studied gene activity in the habenula (a small brain region) using tissue from three adult and four fetal human brains. They found that the habenula strongly expresses nicotinic receptors, the genes nicotine acts on, along with GPR151 and cilia-related genes. Genes already linked to smoking and nicotine response from genetic studies were also especially active in this brain region, alongside immune-related genes tied to several other diseases.
Le Foll B, French L (2018). Transcriptomic Characterization of the Human Habenula Highlights Drug Metabolism and the Neuroimmune System. Front Neurosci. — PubMed PMID: 30429765 · doi:10.3389/fnins.2018.00742
Nicotine and autoimmunity: The lotus' flower in tobacco
Review, 2018. This review gathers earlier research on how nicotine affects the immune system in autoimmune diseases, including multiple sclerosis, type 1 diabetes, rheumatoid arthritis, sarcoidosis, Behçet's disease and inflammatory bowel diseases. The authors say the findings conflict. Some studies suggest nicotine increases inflammatory signals and makes a type of white blood cell (neutrophils) die and release their contents, which the immune system can then attack as if they were foreign. Other studies suggest nicotine calms inflammation, mainly by binding to the alpha-7 nicotinic receptor, which can increase regulatory T cells and lower inflammatory signals; the authors name addiction and the side effects of each nicotine product sold as the main problems with nicotine.
Gomes JP, Watad A, Shoenfeld Y (2018). Nicotine and autoimmunity: The lotus' flower in tobacco. Pharmacol Res. — PubMed PMID: 29051105 · doi:10.1016/j.phrs.2017.10.005
Interactions between genetic, lifestyle and environmental risk factors for multiple sclerosis
Review, 2017. This review looks at how genetic and environmental or lifestyle factors combine to raise or lower the risk of multiple sclerosis. It lists established risk factors like high latitude, smoking, low vitamin D and Epstein-Barr virus infection, and notes that use of nicotine, along with alcohol, cytomegalovirus infection and high coffee intake, is associated with a reduced risk of developing MS.
Olsson T, Barcellos LF, Alfredsson L (2017). Interactions between genetic, lifestyle and environmental risk factors for multiple sclerosis. Nat Rev Neurol. — PubMed PMID: 27934854 · doi:10.1038/nrneurol.2016.187
Serum Cotinine Does Not Predict Neutralizing Antibodies Against Interferon Beta in an Austrian MS Cohort
Human observational study, 2016. Researchers measured cotinine, a breakdown product of nicotine used to objectively confirm smoking status, in blood from 160 people with multiple sclerosis who were being tested for neutralizing antibodies against their interferon beta medication. About 34% of antibody-negative patients and 39% of antibody-positive patients were classified as smokers by cotinine levels, a difference that was not statistically significant. The study also found that patients' self-reported smoking status did not always match their cotinine-based status (a mismatch in 7 of 37 patients with known smoking history).
Auer M, Hegen H, Luft T et al. (2016). Serum Cotinine Does Not Predict Neutralizing Antibodies Against Interferon Beta in an Austrian MS Cohort. J Interferon Cytokine Res. — PubMed PMID: 27918711 · doi:10.1089/jir.2016.0054
Environmental factors and their interactions with risk genotypes in MS susceptibility
Review, 2016. This review discusses environmental and lifestyle factors linked to multiple sclerosis risk, including Epstein-Barr virus, sun exposure/vitamin D, smoking, obesity, organic solvents, shift work, alcohol, and coffee. It notes that nicotine, along with alcohol and high coffee consumption, is associated with a decreased risk of MS, and discusses how such factors can interact with genetic susceptibility to affect disease risk.
Hedström AK, Alfredsson L, Olsson T (2016). Environmental factors and their interactions with risk genotypes in MS susceptibility. Curr Opin Neurol. — PubMed PMID: 27035899 · doi:10.1097/WCO.0000000000000329
Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis
Animal study, 2016. In mice with an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis), researchers tested whether nicotine could change the numbers of inflammatory immune cells (proinflammatory monocytes and neutrophils) entering the brain and spinal cord. Nicotine significantly reduced the infiltration of these cells into the central nervous system at the time points when they normally drive disease damage, acting through two nicotinic receptor subtypes (alpha7 and alpha9). Nicotine-treated mice also had lower levels of two chemical signals (CCL2 and CXCL2) in the brain that normally attract these inflammatory cells, and this drop occurred before the cell infiltration became severe.
Jiang W, St-Pierre S, Roy P et al. (2016). Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. — PubMed PMID: 26810225 · doi:10.4049/jimmunol.1501613
Nicotinic receptor activation negatively modulates pro-inflammatory cytokine production in multiple sclerosis patients
Human observational study, 2015. Researchers studied immune blood cells from people with relapsing-remitting multiple sclerosis and healthy donors, looking at nicotinic receptors. Patients had higher levels of two inflammatory signals (IL-1β and IL-17) than healthy donors. When the blood cells were treated with nicotine, these inflammatory signals decreased, and nicotine increased the amount of a specific nicotinic receptor subtype (α7) only in the MS patients' cells. The authors suggest this receptor may help control inflammation in MS.
Reale M, Di Bari M, Di Nicola M et al. (2015). Nicotinic receptor activation negatively modulates pro-inflammatory cytokine production in multiple sclerosis patients. Int Immunopharmacol. — PubMed PMID: 26209886 · doi:10.1016/j.intimp.2015.06.034
Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis
Animal study, 2015. Researchers studied animals with experimental autoimmune encephalomyelitis, a lab model of multiple sclerosis-like disease, to see whether nicotine changes the nerve stem cells in the spinal cord that help with repair. In untreated animals with the disease, the spinal cord's own repair response was limited and delayed, and the cells lining the spinal cord's central canal multiplied less than in healthy animals. Nicotine lowered inflammation in that area, partly restored the multiplication of those lining cells, and increased the number of oligodendrocytes, the cells that make the protective coating around nerves. These results come only from animals, and the authors present them as a new insight into how nicotine eases this disease model.
Gao Z, Nissen JC, Legakis L et al. (2015). Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis. Neuroscience. — PubMed PMID: 25813705 · doi:10.1016/j.neuroscience.2015.03.031
The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components
Animal study, 2014. Mice with an induced MS-like disease (experimental autoimmune encephalomyelitis) were treated with nicotine or with cigarette smoke condensate containing the non-nicotine components of smoke. Nicotine made the disease milder, with less nerve-fiber damage, better weight maintenance, and calmer immune-cell activity in the brain, and starting nicotine after symptoms appeared kept the disease from getting worse. In contrast, the non-nicotine smoke components, especially a compound called acrolein, made early disease symptoms worse. The study ties these opposite effects to how nicotine versus the other smoke components affect brain immune cells called microglia.
Gao Z, Nissen JC, Ji K et al. (2014). The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. — PubMed PMID: 25250777 · doi:10.1371/journal.pone.0107979
Novel therapeutic approach by nicotine in experimental model of multiple sclerosis
Animal study, 2013. Researchers tested nicotine in mice with an induced autoimmune brain disease used as a lab model of multiple sclerosis, giving nicotine either before or after the disease was triggered. They also tested nicotine's effect on cell proliferation and inflammatory markers in a cell line in the lab. Nicotine reduced how severe and how early the disease appeared in the mice, and brain tissue examined under the microscope showed less of the typical nerve-damaging plaque in the nicotine-treated groups compared to untreated mice.
Naddafi F, Reza Haidari M, Azizi G et al. (2013). Novel therapeutic approach by nicotine in experimental model of multiple sclerosis. Innov Clin Neurosci. — PubMed PMID: 23696955
Differential modulation of EAE by α9*- and β2*-nicotinic acetylcholine receptors
Animal study, 2013. Mice with experimental autoimmune encephalomyelitis (EAE, the lab model of multiple sclerosis) were treated with nicotine or had the genes for two types of nicotinic receptors (alpha9 or beta2) deleted. Nicotine delayed disease onset and reduced severity in normal mice, and mice missing the alpha9 receptor did just as well without needing nicotine, while mice missing the beta2 receptor never recovered from their worst symptoms even though nicotine still reduced severity for them. The two receptor types were also linked to different levels of immune cell activity and inflammation markers in the brain and spinal cord before disease onset.
Simard AR, Gan Y, St-Pierre S et al. (2013). Differential modulation of EAE by α9*- and β2*-nicotinic acetylcholine receptors. Immunol Cell Biol. — PubMed PMID: 23399696 · doi:10.1038/icb.2013.1
Nicotine might have a protective effect in the etiology of multiple sclerosis
Human observational study, 2013. This study used two Swedish population-based case-control studies (7,883 people with multiple sclerosis and 9,437 people without it) to see whether using moist snuff, a smokeless tobacco that delivers high doses of nicotine, was linked to the risk of developing multiple sclerosis. People who used snuff had a lower risk of multiple sclerosis than people who had never used it (odds ratio 0.83), and the more snuff someone had used over time, the lower the risk. Smokers who also used snuff had a lower risk than smokers who had never used snuff, even after the amount of smoking was taken into account. The authors say this supports the idea that nicotine may calm inflammation and change immune responses in a way that might lower the risk of multiple sclerosis, but this kind of study shows a link and cannot prove that nicotine is the cause.
Hedström AK, Hillert J, Olsson T et al. (2013). Nicotine might have a protective effect in the etiology of multiple sclerosis. Mult Scler. — PubMed PMID: 23319071 · doi:10.1177/1352458512471879
Smoking as a risk factor for multiple sclerosis
Human observational study, 2013. Researchers measured cotinine, a breakdown product of nicotine, in blood samples collected years before disease onset from 192 people who later developed multiple sclerosis and 384 matched people who did not. People with elevated cotinine levels (10 ng/ml or higher) had about a 1.5 times higher risk of developing multiple sclerosis, and this link was stronger in younger people (under about 26 years old), where the risk was about 2.2 times higher.
Salzer J, Hallmans G, Nyström M et al. (2013). Smoking as a risk factor for multiple sclerosis. Mult Scler. — PubMed PMID: 23257617 · doi:10.1177/1352458512470862
Smoking cessation for the neurologic patient
Review, 2012. This is a review article aimed at health care providers about helping patients quit smoking, including patients with neurologic conditions like stroke, dementia, and multiple sclerosis. It discusses counseling, nicotine replacement therapies, and other medications as the main treatments, and notes that even brief advice from a provider can improve a patient's chances of quitting.
Tavee J (2012). Smoking cessation for the neurologic patient. Neurol Clin Pract. — PubMed PMID: 29443310 · doi:10.1212/CPJ.0b013e31825a7812
Attenuation of CNS inflammatory responses by nicotine involves α7 and non-α7 nicotinic receptors
Animal study, 2011. This study in mice tested whether nicotine affects experimental autoimmune encephalomyelitis, a mouse model of the immune attack on the brain and spinal cord seen in multiple sclerosis. Nicotine made the disease less severe, and that protection largely disappeared in mice bred without the alpha-7 nicotinic receptor. Even without that receptor, nicotine still partly cut the number of immune cells entering the brain and spinal cord, slowed the growth of self-attacking T cells, and increased calming regulatory T cells. The authors conclude that the alpha-7 receptor plays an important role but other nicotinic receptor types also contribute to nicotine's anti-inflammatory effects; these results come from mice only.
Hao J, Simard AR, Turner GH et al. (2011). Attenuation of CNS inflammatory responses by nicotine involves α7 and non-α7 nicotinic receptors. Exp Neurol. — PubMed PMID: 20932827 · doi:10.1016/j.expneurol.2010.09.020
Smoking, use of moist snuff, and risk of chronic inflammatory diseases
Human observational study, 2010. This study followed 277,777 Swedish male construction workers for years to compare cigarette smoking with moist snuff (a smokeless, nicotine-containing tobacco product) and their risk of several inflammatory diseases. Smoking raised the risk of rheumatoid arthritis, Crohn's disease, multiple sclerosis, and ulcerative colitis (in ex-smokers), and lowered the risk of sarcoidosis. Moist snuff use, which delivers nicotine without smoke, showed no increased or decreased risk for any of these five diseases. The researchers concluded that the inhaled non-nicotine parts of cigarette smoke, rather than nicotine itself, appear to be the more important factor behind these disease risks.
Carlens C, Hergens MP, Grunewald J et al. (2010). Smoking, use of moist snuff, and risk of chronic inflammatory diseases. Am J Respir Crit Care Med. — PubMed PMID: 20203245 · doi:10.1164/rccm.200909-1338OC
Activation of the cholinergic anti-inflammatory system by nicotine attenuates neuroinflammation via suppression of Th1 and Th17 responses
Animal study, 2009. This study looked at what happens when nicotine switches on a receptor called the alpha7 nicotinic receptor, which sits on immune cells called T cells. In lab experiments with T cells, nicotine lowered T cell multiplication and cut the release of several inflammatory signalling chemicals. It also shifted the cells toward a less inflammatory type, with one controlling protein falling by 50% and another rising by 350%. T cells from mice bred without this receptor did not respond to nicotine. In mice with an MS-like disease of the brain and spinal cord, nicotine injections (2 mg/kg) made the disease less severe and reduced immune cell entry into the nervous system, nerve coating damage and nerve fibre loss. These results come only from cells and mice.
Nizri E, Irony-Tur-Sinai M, Lory O et al. (2009). Activation of the cholinergic anti-inflammatory system by nicotine attenuates neuroinflammation via suppression of Th1 and Th17 responses. J Immunol. — PubMed PMID: 19846875 · doi:10.4049/jimmunol.0902212
The cholinergic anti-inflammatory system limits T cell infiltration into the neurodegenerative CNS, but cannot counteract complex CNS inflammation
Animal study, 2009. Researchers studied mice that either had or lacked a nicotinic receptor (nAChRalpha7), the receptor activated by nicotine or the body's own acetylcholine, which is part of a pathway that normally helps calm inflammation. In a nerve-injury model, mice without this receptor showed more immune T cells entering the damaged brain-stem region, showing the receptor normally limits that T-cell entry. However, in a more complex brain inflammation model similar to multiple sclerosis (experimental autoimmune encephalomyelitis), having or lacking this receptor made no difference, meaning this pathway could not control the broader inflammation in that model.
Nicolussi EM, Huck S, Lassmann H et al. (2009). The cholinergic anti-inflammatory system limits T cell infiltration into the neurodegenerative CNS, but cannot counteract complex CNS inflammation. Neurobiol Dis. — PubMed PMID: 19344760 · doi:10.1016/j.nbd.2009.03.010
Nicotinic attenuation of central nervous system inflammation and autoimmunity
Animal study, 2009. Researchers gave nicotine to mice with a lab-induced disease that resembles multiple sclerosis, in which the immune system attacks myelin, the protective coating around nerves in the brain and spinal cord. Nicotine significantly delayed and weakened the inflammatory and autoimmune attack. Outside the brain and spinal cord, it slowed the multiplication of the immune T cells that attack myelin and changed the chemical signals those cells release; inside the brain and spinal cord, it reduced the numbers of several inflammatory immune cell types and lowered the surface markers those cells use to drive an immune response. These results are only in mice, and the authors suggest nicotinic receptors could point to new treatment approaches for inflammatory and autoimmune disorders, including those affecting the nervous system.
Shi FD, Piao WH, Kuo YP et al. (2009). Nicotinic attenuation of central nervous system inflammation and autoimmunity. J Immunol. — PubMed PMID: 19155522 · doi:10.4049/jimmunol.182.3.1730
Smoke exposure increases the risk for multiple sclerosis
Human observational study, 2008. Researchers measured cotinine, a breakdown product of nicotine, in stored blood samples from 109 people with multiple sclerosis and 218 matched people without it. People with higher cotinine levels, even modestly elevated ones, had a higher risk of multiple sclerosis, about three times higher comparing the higher levels to the lowest, and the link was stronger in women than in men. In a smaller group whose samples were taken before their MS began, a similar but smaller, not statistically significant, pattern was seen.
Sundström P, Nyström L, Hallmans G (2008). Smoke exposure increases the risk for multiple sclerosis. Eur J Neurol. — PubMed PMID: 18474075 · doi:10.1111/j.1468-1331.2008.02122.x
Central role of hypothalamic digoxin in conscious perception, neuroimmunoendocrine integration, and coordination of cellular function: relation to hemispheric dominance
Review, 2002. This is a review paper proposing that a hormone-like substance called digoxin, made by the hypothalamus, helps control brain function, hormones, and the immune system, and may be involved in conditions like Parkinson's disease, schizophrenia, brain tumors, and multiple sclerosis. The paper reports that this digoxin can shift the body's chemistry so that certain brain chemicals, including nicotine, serotonin, and others, rise or fall together, and that people who are left-handed with right-brain dominance had higher blood levels of nicotine (along with several other substances) compared to right-handed people. Nicotine here is discussed only as one of several naturally occurring body chemicals whose levels were measured and compared, not as a substance being tested as a treatment.
Kurup RK, Kurup PA (2002). Central role of hypothalamic digoxin in conscious perception, neuroimmunoendocrine integration, and coordination of cellular function: relation to hemispheric dominance. Int J Neurosci. — PubMed PMID: 12325312 · doi:10.1080/00207450290025734
Effects of cigarette smoking on motor functions in patients with multiple sclerosis
Human trial, 1992. Researchers tested how smoking a cigarette affected hand and arm movement right afterward in 21 people with multiple sclerosis and 11 healthy people, using simple motor tests. Sixteen of the 21 MS patients showed a brief worsening of motor performance lasting about 10 minutes after smoking, with scores dropping by 14% on average, while without smoking only 3 of 14 patients got worse and the group actually improved by about 8%. The healthy control group kept improving steadily whether or not they smoked. The researchers concluded that nicotine temporarily worsens motor function in people with MS, possibly through effects on the brain and nervous system or on blood vessel and autonomic responses.
Emre M, de Decker C (1992). Effects of cigarette smoking on motor functions in patients with multiple sclerosis. Arch Neurol. — PubMed PMID: 1449402 · doi:10.1001/archneur.1992.00530360041015
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Connections
- Autoimmunity: When Defence Turns on You — interactive animation
- Nicotine: The Research
- Dr. Bryan Ardis on this subject — his claims, presented on their own pages and kept separate from this research collection
- The Nicotine Patch, animated
- Nicotinic Acetylcholine Receptors
- Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
- Brain and Memory
- Mood and Mental Health
- Inflammation and Immunity
- Cancer Research
- Heart and Blood Vessels
- Metabolism and Weight
- Addiction and Withdrawal
- Patches, Gum and Delivery