Smoking is one of the best-established modifiable risk factors in multiple sclerosis (MS). It is associated not only with a higher likelihood of developing MS, but also with faster disability accumulation after diagnosis. In AQP4-positive NMOSD and MOGAD, the picture is different: a convincing increase in disease incidence has not been demonstrated, but newer data from 2025–2026 link smoking to poorer recovery after attacks and a greater likelihood of residual neurological disability.
Several important publications appeared in 2026 and allow this topic to be discussed more precisely. A large umbrella review of MS combined 11 systematic reviews and 97 unique studies; the prospective NationMS cohort provided new data on disability progression; and a separate meta-analysis in NMOSD and MOGAD quantified the effect of smoking on recovery after relapses.
The association between smoking and MS risk is one of the most consistent epidemiological findings in neuroimmunology. Meta-analyses indicate that smokers have, on average, approximately a 1.5-fold higher risk of developing MS than never-smokers. Many studies also demonstrate a dose–response relationship: the greater the cumulative smoking exposure, the higher the risk.
In the study Smoking Attributable Risk in Multiple Sclerosis, which included 9,419 people with MS and an equal number of population controls, the estimated proportion of MS cases attributable to smoking was 13.1%. This is a population-level estimate, not an individual prediction. It does not mean that a particular person has a 13% risk of MS; rather, it illustrates how substantial the contribution of smoking may be at the population level.
The 2026 umbrella review confirmed the overall pattern: active cigarette smoking, as well as waterpipe smoking, was consistently associated with increased MS risk. The authors also emphasized that most available evidence is observational, that there is heterogeneity between studies, and that causality cannot be measured with the same certainty as in a randomized trial.
The most likely explanation is a combination of mechanisms rather than a single pathway. Tobacco smoke causes chronic airway inflammation, alters innate and adaptive immune responses, increases oxidative stress and may interact with genetic susceptibility to MS. Interactions between smoking and HLA risk alleles have been reported, supporting a “genetics + environment” model rather than a single-cause explanation.
One particularly interesting concept is the lung irritation hypothesis: combustion products and inflammation in the respiratory tract may be more important to MS risk than nicotine itself. This has practical implications when choosing smoking-cessation strategies.
After MS has been diagnosed, smoking remains an unfavorable factor. Across multiple cohorts it has been associated with faster accumulation of physical disability, worsening walking function and earlier transition to secondary progressive disease.
A particularly important 2026 publication is the prospective NationMS cohort. Investigators analyzed 1,374 people with MS and assessed EDSS, walking speed, cognitive measures and MRI. Smoking was associated with a higher likelihood of reaching unfavorable EDSS and Timed 25-Foot Walk thresholds and with worse longitudinal trajectories in these outcomes.
Interestingly, the same study found no significant association between smoking and the number of T2 lesions or gadolinium-enhancing lesions. This is an important nuance: the adverse effect of smoking in MS cannot be reduced simply to “more lesions on MRI.” It may operate through chronic inflammation, neurodegeneration, vascular mechanisms, comorbidity and reduced neurological reserve.
Thus, a person may have a relatively stable routine MRI while still experiencing a long-term adverse effect from continued smoking.
Systematic reviews support an association between smoking, disability accumulation and a higher risk of transition to secondary progressive MS. The effect generally becomes stronger with greater cumulative exposure, meaning that pack-years matter in addition to smoking status itself.
This distinction is clinically important because some patients are afraid of nicotine replacement therapy — patches, gum or sprays — and therefore continue smoking.
A large Swedish cohort published in 2023 included 9,089 people with MS and compared active smoking, second-hand smoke exposure and the use of smokeless oral tobacco. Active and passive exposure to smoke was associated with faster EDSS progression. Use of snuff did not show the same adverse association with disease progression.
This does not mean that nicotine is harmless, and it is certainly not a recommendation to use snuff. Smokeless tobacco carries its own risks. The practical implication is different: nicotine replacement therapy should not be equated with the risk of continuing to smoke. For a person who cannot stop cigarettes without pharmacological support, a nicotine patch or another approved nicotine-replacement strategy is generally preferable to continued inhalation of tobacco smoke.
Evidence on second-hand smoke and the risk of developing MS is less consistent than the evidence on active smoking. In the 2026 umbrella review, results for passive smoke exposure were mixed. However, in the Swedish cohort of people already diagnosed with MS, current passive exposure was associated with faster EDSS progression.
In practical terms, a person with MS should try to minimize not only their own smoking but also regular exposure to indoor tobacco smoke.
Waterpipe smoking is not a “milder” form of smoking. A systematic review and meta-analysis published in 2025 also identified waterpipe tobacco smoking as an unfavorable exposure in the context of MS. In the 2026 umbrella review, active waterpipe smoking was among the smoking exposures consistently associated with MS onset risk.
Risk and prognosis depend on cumulative exposure. Therefore, “I only smoke a few cigarettes” is not equivalent to no risk. From a medical perspective, the goal remains complete cessation of inhaled tobacco smoke rather than merely reducing the number of cigarettes.
It would be incorrect to claim that smoking reduces the effectiveness of all disease-modifying therapies in the same way. However, observational signals exist for some treatments.
For example, in a 2023 study of people with relapsing MS treated with dimethyl fumarate or fingolimod, current smoking was associated with a higher risk of relapse and overall disease activity. After multivariable adjustment, the risk of relapse remained higher among current smokers. Former smokers were closer to never-smokers in measures of disease activity.
This study was relatively small and does not prove a universal pharmacological interaction between smoking and all MS therapies. Nevertheless, it supports an important practical principle: effective MS treatment does not remove the need to stop smoking.
For NMOSD and MOGAD, the question differs fundamentally from MS. At present, there is no comparably convincing association between smoking and the probability of developing these diseases. Instead, increasing evidence suggests that smoking may worsen recovery after an attack that has already occurred.
| Disease | What is known about disease risk | What is known about outcomes in smokers |
|---|---|---|
| MS | Risk is increased; supported by meta-analyses and an umbrella review | Faster disability accumulation and higher risk of progression |
| AQP4-NMOSD | No convincing increase in incidence has been demonstrated | Poorer recovery after attacks and more residual disability |
| MOGAD | Evidence for increased disease-onset risk is insufficient | Association with incomplete recovery after attacks and greater disability |
The 2026 meta-analysis included 10 studies published between 2014 and 2026. In AQP4-NMOSD, smoking was not significantly associated with disease incidence. However, among people with NMOSD or MOGAD, smokers had a higher risk of incomplete recovery after relapse, with a pooled RR of 1.73.
When analyzed separately, the association was stronger in MOGAD: RR 2.41. In AQP4-NMOSD it was RR 1.62. The authors also identified a signal toward poorer MRI lesion resolution in smokers, while the effect of smoking on relapse frequency remained inconsistent.
In a multicenter study of 442 patients, current smokers with MOGAD had a higher likelihood of residual disability after the initial attack and after the first episode of optic neuritis. In AQP4-NMOSD, current smoking was also associated with a higher risk of residual neurological deficit after the first attack.
A 2026 multicenter MOGAD cohort from 21 centers in China found that a history of smoking was associated with an increased risk of disability. The association with relapses became weaker and lost statistical significance after adjustment. This again suggests that the principal adverse effect of smoking in MOGAD may relate less to the number of attacks and more to the quality of recovery and accumulation of residual deficit.
In these diseases, a single severe attack — such as optic neuritis or myelitis — can itself leave substantial irreversible disability. Therefore, even a factor that does not increase relapse frequency but worsens recovery may have major clinical importance.
At present, there are no high-quality clinical data showing that vaping or heated tobacco products are safe for people with MS, NMOSD or MOGAD.
Importantly, the 2026 umbrella review specifically assessed this question and reached a clear conclusion: among the included reviews, no studies directly evaluated the effect of e-cigarettes or vaping on MS onset or progression. Therefore, the statement “vaping is safe for MS” is not evidence-based.
Experimental studies suggest that e-cigarette aerosols can cause endothelial dysfunction, inflammation and disruption of the blood–brain barrier. These are mainly preclinical data, however, and they cannot be translated directly into precise numerical risks for humans.
Practical conclusion: switching from cigarettes to vaping should not be regarded as a proven neurologically safe long-term strategy. If an e-cigarette is used as a temporary step toward complete smoking cessation, the plan should ideally be time-limited and have a predefined endpoint: no smoking.
The data here are particularly important: the adverse effect of smoking does not mean that “once you have smoked, it is too late to change anything.” On the contrary, studies show clinical benefit from smoking cessation after MS diagnosis.
In the study by Tanasescu and colleagues, each additional year without smoking was associated with a gradual reduction in the risk of reaching EDSS 4 and EDSS 6. In a large UK cohort of nearly 8,000 patients, smoking cessation was associated with slower worsening of motor outcomes; after quitting, the rate of motor decline became similar to that seen in never-smokers.
In the Swedish cohort of 9,089 patients, those who continued smoking after diagnosis had worse long-term outcomes than those who stopped.
For NMOSD and MOGAD, there are fewer long-term studies specifically examining the effect of cessation. However, given the increasingly consistent association between current smoking and poorer recovery after attacks, stopping smoking is a clinically reasonable component of preventing accumulated disability.
The overall approach is similar to smoking cessation in the general population: the best results usually come from combining pharmacological and behavioral support.
In MS, fatigue, cognitive symptoms and reduced physical activity may make standard cessation programs more difficult. The plan therefore needs to be realistic and should not rely on “willpower” alone.
From a medical perspective, it is strongly discouraged. Smoking is associated with a higher risk of developing MS and with faster disability accumulation after diagnosis. Smoking cessation should be considered part of long-term MS management alongside effective disease-modifying therapy, physical activity and control of other risk factors.
Yes. Cohort studies show that after smoking cessation, the rate of deterioration decreases. The earlier smoking stops, the less additional cumulative exposure occurs.
The results are not uniform. Some earlier studies reported greater MRI inflammatory activity, but the 2026 prospective NationMS cohort found no significant association with the number of T2 or gadolinium-enhancing lesions. This does not mean smoking is harmless: clinical progression in smokers was worse in the same cohort.
MS itself is not a contraindication to nicotine replacement therapy. Observational evidence supports the view that a substantial part of the adverse effect of smoking is related to smoke exposure and airway irritation rather than nicotine alone. The specific cessation method should still be selected with a clinician, taking cardiovascular status and other medications into account.
There are insufficient data to consider vaping safe in MS. The 2026 umbrella review found no studies directly evaluating the effect of e-cigarettes on MS outcomes. Vaping should therefore not be regarded as a proven safe substitute for conventional cigarettes.
No. Waterpipe smoking also causes exposure to combustion products and is not a safe alternative. Contemporary reviews include waterpipe smoking among tobacco exposures associated with unfavorable MS risk.
For AQP4-NMOSD, the 2026 meta-analysis did not show a significant increase in disease incidence among smokers. For MOGAD, evidence that smoking increases the risk of disease onset is also insufficient. However, smoking is associated with poorer recovery after attacks in both conditions.
Because disability in these disorders can arise directly from a single severe attack. If recovery after optic neuritis or myelitis is worse, the same number of attacks can still result in greater residual disability.