Snus and Multiple Sclerosis: Dr. Ardis on the Swedish Snuff Research
Multiple sclerosis (MS) is a disease in which the body’s own immune system attacks myelin, the fatty insulation that wraps nerve fibres in the brain, spinal cord and optic nerves. Sweden has an unusual natural experiment for anyone curious about nicotine and MS: millions of Swedes take snus, a moist oral snuff tucked under the upper lip, which delivers high doses of nicotine with no smoke at all. Dr. Bryan Ardis names MS as the third disease, after Parkinson’s and Alzheimer’s dementia, where he says nicotine stands out, and he points to a Swedish study of snuff users as his evidence.
This page sets out his position as he gives it, then walks through the research Swedish epidemiologists have published on snuff, smoking and MS since 2009, and the animal studies on nicotine in experimental autoimmune encephalomyelitis (EAE), the laboratory model of MS.
Table of Contents
- What Dr. Ardis Says
- Snus, Smoke and MS: The Terms
- The 2009 Swedish Study in Neurology
- “Nicotine Might Have a Protective Effect” (2013)
- The Swedish Construction Workers Cohort
- EIMS and GEMS: The Later Swedish Papers
- Smoke Versus Nicotine: The Authors’ Own Point
- Nicotine in the MS Animal Model (EAE)
- Which Study Dr. Ardis Describes
- Safety Notes
- Dr. Ardis’s Own Work
- Key Research Papers
- Connections
- Featured Videos
1. What Dr. Ardis Says
Dr. Ardis set this out in a 2025 podcast appearance (Culture Apothecary) and in his book Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity, where, he says, the nicotine chapter carries “the research link to a study out of Sweden.”
He introduces MS straight after describing nicotine as a nootropic — “a brain stimulator” that “turns the brain on,” in his words “like caffeine, except better” — and calls multiple sclerosis “the third” disease on his list. His account of the Swedish study runs in these steps:
- The study came out of Sweden and, he says, ended during the pandemic.
- It was a 20-year study comparing the general population with people who use snuff — who put tobacco in their lips, “multiple times a day,” every day.
- The question, as he frames it, was the risk of developing and being diagnosed with MS over the next 20 years in the general population versus in those using the tobacco products.
- The researchers, he says, expected MS to be “skyrocketedly higher” in the tobacco-using group.
- After 20 years, he states, the snuff users “not only had the lowest risk of developing MS over the entire general population” — and those who did more than they were asked, who started smoking cigarettes as well as dipping snuff, “had the lowest of all risk factors for multiple sclerosis.”
For Dr. Ardis the result fits his wider position that nicotine itself protects the nervous system and calms inflammation, a position set out on the Nicotine Hypothesis page. The sections below describe the published Swedish research on snuff and MS, paper by paper, in the words and figures the authors report.
2. Snus, Smoke and MS: The Terms
A few terms make the research easier to read.
- Swedish snuff (snus, moist snuff). Ground tobacco kept moist and placed between the upper lip and gum, loose or in small pouches. Nicotine is absorbed through the lining of the mouth. Nothing is burned, so the user inhales no smoke. The Swedish papers use “snuff,” “moist snuff” and “oral tobacco” for the same product.
- Case-control study. Researchers recruit people newly diagnosed with a disease (cases) and people from the same population without it (controls), then compare their past habits. The result is an odds ratio (OR): an OR of 1.0 means no difference, above 1.0 means the habit was more common among people with MS, below 1.0 means less common. An OR of 0.3 is roughly a 70% lower odds.
- Cohort study. Researchers record habits in a large group first, then follow them for years to see who develops the disease. The result is usually a relative risk (RR), read the same way as an odds ratio.
- Pack-years. A measure of cumulative smoking: one pack a day for one year is one pack-year.
- EAE. Experimental autoimmune encephalomyelitis, an MS-like disease induced in mice or rats by immunising them against myelin proteins. It is the standard laboratory model for testing ideas about MS.
3. The 2009 Swedish Study in Neurology
The first paper to separate snuff from smoking in MS came from the Karolinska Institutet in Stockholm. Anna K. Hedström, Maria Bäärnhielm, Tomas Olsson and Lars Alfredsson published “Tobacco smoking, but not Swedish snuff use, increases the risk of multiple sclerosis” in Neurology in September 2009.
Who was studied. A population-based case-control study in Sweden: 902 people with newly diagnosed MS and 1,855 randomly selected controls from the same population. This was the Swedish EIMS study (Epidemiological Investigation of Multiple Sclerosis).
What they reported.
- Smokers of both sexes had an increased risk of MS: OR 1.4 for women and OR 1.8 for men.
- The increase appeared even among people who had smoked moderately (5 pack-years or fewer), rose with the cumulative amount smoked, and remained for up to 5 years after stopping.
- In contrast, taking Swedish snuff for more than 15 years was associated with a lower risk of developing MS: OR 0.3 (95% confidence interval 0.1–0.8).
The authors’ conclusion. Snuff use “is not associated with elevated risk for MS, which may indicate that nicotine is not the substance responsible for the increased risk of developing MS among smokers.”
4. “Nicotine Might Have a Protective Effect” (2013)
Four years later the same group returned to the question with far larger numbers. Hedström, Jan Hillert, Olsson and Alfredsson published “Nicotine might have a protective effect in the etiology of multiple sclerosis” in Multiple Sclerosis Journal in 2013.
Who was studied. Two Swedish population-based case-control studies pooled together: 7,883 people with MS and 9,437 controls. The two studies are EIMS and GEMS (Genes and Environment in Multiple Sclerosis).
Why they looked. The authors note that moist snuff “leads to exposure to high doses of nicotine” and that recent studies indicated nicotine could modulate immune responses.
What they reported.
- People who took snuff had a lower risk of developing MS than people who had never used moist snuff: OR 0.83 (95% CI 0.75–0.92).
- The more snuff a person had used over their lifetime, the lower the risk — what the authors call “clear evidence of an inverse dose-response correlation.”
- People who both smoked and took snuff had a significantly lower MS risk than smokers who had never used moist snuff, even after adjusting for how much they smoked.
The authors’ conclusion. “Our results add evidence to the hypothesis that nicotine exerts anti-inflammatory and immune-modulating effects in a way that might decrease the risk of developing MS.”
This is the paper whose finding on combined use comes closest to the second half of Dr. Ardis’s account: the snuff-plus-smoking group is compared with smokers who did not use snuff, and the snuff users fare better.
5. The Swedish Construction Workers Cohort
The one long-term Swedish cohort that has reported on snuff and MS is a study of construction workers. Cecilia Carlens and colleagues at the Karolinska Institutet published “Smoking, use of moist snuff, and risk of chronic inflammatory diseases” in the American Journal of Respiratory and Critical Care Medicine in 2010.
Who was studied. 277,777 men in a cohort of Swedish construction workers who reported their tobacco use at health check-ups between 1978 and 1993. The researchers linked them to the national hospital discharge register and followed them through 2004 — a follow-up of up to about 26 years — for five diseases: rheumatoid arthritis, ulcerative colitis, Crohn’s disease, sarcoidosis and MS.
What they reported for MS.
- Ever-smoking was associated with a higher risk of MS: RR 1.9 (95% CI 1.4–2.6).
- Ever-use of moist snuff, adjusted for smoking, was not associated with MS in either direction: RR 1.0 (95% CI 0.8–1.4). The same neutral result held for the other four diseases.
The authors’ conclusion. Smokeless tobacco does not increase the risk of these chronic inflammatory diseases, “suggesting that inhaled nonnicotinic components of cigarette smoke are more important than nicotine itself in the etiology of these diseases.”
6. EIMS and GEMS: The Later Swedish Papers
The two Swedish case-control studies, EIMS and GEMS, have since become one of the largest collections of lifestyle data on MS anywhere, and snuff appears in several of the later papers.
Relapsing and progressive MS (2021)
Published in May 2021, during the pandemic, in the Journal of Neurology, Neurosurgery and Psychiatry, “Factors affecting the risk of relapsing-onset and progressive-onset multiple sclerosis” (Hedström, Hillert, Olsson, Alfredsson) analysed 7,520 relapsing-onset cases, 540 progressive-onset cases and 11,386 controls. Smoking, obesity and high antibody levels against the Epstein–Barr virus were associated with higher risk of both forms of MS; snuff use, alcohol consumption and sun exposure were associated with reduced risk of both.
Snuff, smoking and how MS progresses (2023)
Jing Wu, Olsson, Hillert, Alfredsson and Hedström followed 9,089 patients from the two studies for up to 15 years after diagnosis through the Swedish MS registry, published in the same journal in 2023. Current smokers had faster disability progression than non-smokers, and passive smoking was linked to faster progression too. People who stopped smoking after diagnosis did better than those who continued. Snuff users had a more favourable course on the disability scale (EDSS) than people who had never used snuff. The authors wrote that this suggested “nicotine replacement therapy could be an attractive way to increase the chance of quitting smoking among patients with MS.”
Passive smoking (2011)
Restricting the EIMS data to people who had never smoked (695 cases, 1,635 controls), Hedström and colleagues reported in 2011 that exposure to other people’s smoke was associated with a higher MS risk (OR 1.3), rising with years of exposure. Because snuff use did not carry the same risk, the authors proposed that the critical effect of smoke “may be the result of irritations in the lungs.”
Stopping smoking after diagnosis (2015)
Using 728 GEMS patients who smoked at diagnosis, Ramanujam and colleagues reported in JAMA Neurology that each additional year of smoking after diagnosis brought forward the move to secondary progressive MS by 4.7%; those who quit reached that stage later (at ages 56 versus 48 in the Kaplan–Meier curves). Snuff use was one of the factors adjusted for in the model.
7. Smoke Versus Nicotine: The Authors’ Own Point
Across these papers the Swedish researchers draw the same distinction themselves. Smoking delivers nicotine together with thousands of combustion products into the lungs; snus delivers nicotine through the mouth with no smoke. In their data the two habits pull in different directions:
- Smoking, and even other people’s smoke, is associated with a higher risk of developing MS and with faster progression afterwards (sections 3, 5 and 6).
- Snuff is associated with no change in risk in the construction-worker cohort, and with lower risk and slower progression in the EIMS/GEMS case-control data (sections 3–6).
The 2009 paper concludes that nicotine “is not the substance responsible” for the smokers’ extra risk; the 2010 paper points to “inhaled nonnicotinic components of cigarette smoke”; the 2011 paper to irritation of the lungs; and the 2013 paper adds that nicotine may itself have anti-inflammatory, immune-modulating effects that lower risk. The laboratory work in the next section tests that last idea directly.
8. Nicotine in the MS Animal Model (EAE)
Immune cells carry nicotinic acetylcholine receptors, the same family of receptors nicotine acts on in the brain (see Nicotinic Acetylcholine Receptors). One subtype, the α7 receptor, is central to what researchers call the cholinergic anti-inflammatory pathway: signals through it damp down the release of inflammatory messengers. Several groups have tested nicotine in mice with EAE.
Shi and colleagues, Phoenix (2009)
Fu-Dong Shi, Lukas and colleagues reported in the Journal of Immunology that nicotine exposure “significantly delays and attenuates” the inflammatory and autoimmune response to myelin in mouse EAE. Outside the brain, nicotine slowed the multiplication of myelin-reactive T cells and changed their cytokine profile; inside the brain and spinal cord it reduced the numbers of infiltrating dendritic cells, monocytes and resident microglia, and lowered the molecules those cells use to present antigens to T cells.
Nizri, Brenner and colleagues, Jerusalem (2009)
Nizri, Brenner and colleagues in Jerusalem reported, also in the Journal of Immunology, that the α7 receptor sits on the surface of CD4+ T cells and increases when they are activated. Nicotine reduced T-cell multiplication against a myelin antigen and cut the inflammatory Th1 messengers (TNF-α, interferon-γ) and Th17 messengers (IL-17 and related cytokines), while raising IL-4 — a shift toward the calmer Th2 type. In live mice, nicotine at 2 mg/kg under the skin reduced the severity of EAE, with less immune-cell infiltration, less demyelination and less axon loss. T cells from mice lacking the α7 receptor did not respond to nicotine.
Hao and colleagues (2011)
Hao, Simard and colleagues reported in Experimental Neurology that nicotine’s dampening of brain and spinal-cord inflammation in EAE involved both α7 and non-α7 nicotinic receptors.
Gao and colleagues, Stony Brook (2014)
Gao, Tsirka and colleagues at Stony Brook University separated nicotine from the rest of cigarette smoke in a PLoS One study. Nicotine reduced the severity of EAE — less demyelination, better body weight, less microglial activation — and nicotine given after symptoms had begun prevented further worsening. The remaining smoke components, given as cigarette smoke condensate, did the opposite: they brought symptoms on earlier and made them worse in the early stages, and the authors identified acrolein, a smoke compound, as one possible culprit.
9. Which Study Dr. Ardis Describes
Dr. Ardis describes a single Swedish study: 20 years long, ending during the pandemic, comparing snuff users with the general population, in which snuff users had the lowest MS risk and those who also smoked had the lowest of all. The specific study is not identified here; the link he gives is in his book, which was not available for this page. The published Swedish work that matches parts of his description is:
- Long follow-up of snuff users against the population: the construction-worker cohort (section 5), which tracked 277,777 men for up to about 26 years.
- Lower MS risk in snuff users: the 2009 Neurology paper (OR 0.3 after more than 15 years of snuff) and the 2013 Multiple Sclerosis Journal paper (OR 0.83, falling with cumulative dose).
- Snuff plus smoking: the 2013 paper, which reports that people who combined smoking and snuff had a significantly lower risk than smokers who never used snuff.
- Published during the pandemic: the 2021 paper on relapsing- and progressive-onset MS, which lists snuff use among the factors associated with reduced risk, and the 2023 paper on progression.
All are listed with their identifiers under Key Research Papers.
Safety Notes
- Children and pets. Nicotine is poisonous to small children and animals in amounts an adult barely notices. Keep snus, pouches, gum, lozenges and patches — new and used — out of reach, and fold a used patch sticky sides together before throwing it away. If a child or pet swallows or chews any nicotine product, call Poison Control (1-800-222-1222 in the US) or a veterinarian at once.
- Who should not use nicotine without their doctor: pregnancy and breastfeeding; unstable heart disease, a recent heart attack or stroke, serious heart-rhythm problems or uncontrolled high blood pressure.
- Smoke is the part the research flags. The Swedish papers above associate smoking and passive smoking with higher MS risk and faster progression.
- The full list of contraindications and cautions is on the Nicotine Patch Protocol page.
Dr. Ardis’s Own Work
- Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity — his book; the nicotine chapter is where he says he gives the link to the Swedish study.
- Dr. Bryan Ardis Hub — the wing’s main page.
- The Dr. Ardis Show — official site
Key Research Papers
- Hedström AK, Bäärnhielm M, Olsson T, Alfredsson L (2009). Tobacco smoking, but not Swedish snuff use, increases the risk of multiple sclerosis. Neurology. — PubMed PMID: 19720976
- Hedström AK, Hillert J, Olsson T, Alfredsson L (2013). Nicotine might have a protective effect in the etiology of multiple sclerosis. Mult Scler. — PubMed PMID: 23319071
- 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
- Hedström AK, Hillert J, Olsson T, Alfredsson L (2021). Factors affecting the risk of relapsing-onset and progressive-onset multiple sclerosis. J Neurol Neurosurg Psychiatry. — PubMed PMID: 33986119
- 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
- Hedström AK, Bäärnhielm M, Olsson T, Alfredsson L (2011). Exposure to environmental tobacco smoke is associated with increased risk for multiple sclerosis. Mult Scler. — PubMed PMID: 21372120
- Ramanujam R, Hedström AK, Manouchehrinia A, et al. (2015). Effect of Smoking Cessation on Multiple Sclerosis Prognosis. JAMA Neurol. — PubMed PMID: 26348720
- Shi FD, Piao WH, Kuo YP, et al. (2009). Nicotinic attenuation of central nervous system inflammation and autoimmunity. J Immunol. — PubMed PMID: 19155522
- 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
- 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
- Gao Z, Nissen JC, Ji K, Tsirka SE (2014). The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. — PubMed PMID: 25250777
PubMed Topic Searches
Connections
- Dr. Bryan Ardis Hub — the wing’s main page: his nicotine hypothesis and snake-venom theory
- The Nicotine Hypothesis — his wider case for nicotine as an anti-inflammatory
- Nicotinic Acetylcholine Receptors — the α7 receptor behind the EAE studies
- Nicotine in Nightshade Vegetables and Parkinson’s Disease — the first disease on his list
- Nicotine Patch Protocol — his protocol and the full safety list
- Tobacco, Indigenous Medicine and Therapeutic Nicotine — the history he sets nicotine in
- Moving Beyond the COVID-19 Lies — the book that carries his Swedish study link
- Multiple Sclerosis — the site’s full page on the disease
- History of Multiple Sclerosis — how the disease came to be understood
- Optic Neuritis — often the first sign of MS
- Loewi and Dale — the discoverers of acetylcholine, the messenger nicotine mimics