Smoking is one of the best-established modifiable risk factors in multiple sclerosis (MS). It is associated not only with a higher probability of developing MS, but also with faster accumulation of disability after diagnosis. The picture is different for AQP4-positive NMOSD and MOGAD: convincing evidence of an increased risk of developing these diseases has not been shown, but new data from 2025–2026 link smoking with 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 in MS combined 11 systematic reviews and 97 unique studies; the prospective NationMS cohort provided new data on 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 people who smoke have, on average, approximately a 1.5-fold higher probability of developing MS than never-smokers. Many studies also show a dose-response relationship: the greater the cumulative smoking exposure, the higher the risk.
In the Smoking Attributable Risk in Multiple Sclerosis study, which included 9,419 people with MS and the same number of population controls, the estimated proportion of MS cases attributable to smoking was 13.1%. This is a population measure, not an individual prediction: it does not mean that any particular person's risk of MS is 13%. It reflects how substantial the contribution of smoking may be at the population level.
The 2026 umbrella review confirmed the overall picture: active cigarette smoking and waterpipe smoking were consistently associated with a higher risk of MS. The authors also emphasized that most available evidence remains observational, studies are heterogeneous, and a causal effect cannot be measured with the same precision as in a randomized clinical trial.
The most likely explanation is a combination of mechanisms rather than a single pathway. Tobacco smoke causes chronic inflammation of the airways, changes the function of innate and adaptive immune cells, increases oxidative stress and may interact with genetic susceptibility to MS. Studies have described interactions between smoking and HLA risk alleles, supporting a “genetics + environment” model rather than a single-cause explanation.
One hypothesis of particular interest is lung irritation: combustion products and airway inflammation may be more important for MS risk than nicotine itself. This distinction has practical implications when choosing smoking-cessation methods.
After diagnosis, smoking remains an unfavorable factor. Across different cohorts it has been associated with faster accumulation of physical disability, worsening walking ability and earlier development of secondary progressive MS.
The prospective NationMS cohort published in 2026 is particularly important. Researchers analyzed 1,374 people with MS and assessed EDSS, walking speed, cognition and MRI. Smoking was associated with a greater likelihood of reaching unfavorable EDSS and Timed 25-Foot Walk thresholds and with worse trajectories of these measures during follow-up.
Interestingly, the same study did not find a significant association between smoking and the number of T2 lesions or gadolinium-enhancing lesions. This is an important clarification: the harmful effect of smoking in MS cannot be reduced to “more MRI lesions”. It may act through chronic inflammation, neurodegeneration, vascular mechanisms, comorbidity and loss of functional reserve.
A patient may therefore have relatively stable routine MRI findings and still experience a long-term adverse effect from continued smoking.
Systematic reviews show an association between smoking, a higher risk of disability accumulation and transition to secondary progressive MS. The effect is generally stronger with greater cumulative smoking exposure, meaning that pack-years matter in addition to current smoking status.
This question is important because some patients are afraid of nicotine-replacement therapy — patches, gum or sprays — and continue smoking as a result.
A large Swedish cohort published in 2023 and including 9,089 people with MS compared active smoking, passive smoking and smokeless oral tobacco. Active and passive smoke exposure were associated with faster EDSS progression. Use of snuff did not show the same adverse association with progression.
This does not mean that nicotine is harmless, and it is certainly not a recommendation to use snuff. Smokeless tobacco has its own risks. The data do, however, support a practical conclusion: nicotine-replacement therapy should not be equated with continued smoking. For a patient who cannot stop cigarettes without pharmacological support, a nicotine patch or another approved nicotine-replacement method is usually far preferable to inhaling tobacco smoke.
Evidence on passive smoking and the risk of developing MS is less consistent than evidence on active smoking. In the 2026 umbrella review, findings on passive smoke exposure were mixed. However, in the Swedish cohort of people with established MS, current passive smoking was associated with faster EDSS progression.
In practice, it is reasonable for a person with MS to minimize not only their own smoking but also regular exposure to tobacco smoke indoors.
Waterpipe smoking is not a “milder” form of smoking. A systematic review and meta-analysis published in 2025 also identified waterpipe smoking as an unfavorable exposure in the context of MS. In the 2026 umbrella review, active waterpipe smoking was among forms of smoking consistently associated with the risk of MS onset.
Risk and prognosis depend on cumulative exposure. “I only smoke a few cigarettes” does not mean absence of risk. From a medical perspective, the ultimate goal remains complete avoidance of inhaled tobacco smoke rather than merely reducing the number of cigarettes.
It cannot be stated that smoking reduces the effectiveness of every disease-modifying therapy to the same extent. 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, relapse risk remained higher in current smokers. Former smokers had activity measures closer to those of never-smokers.
The study was relatively small and does not prove a universal pharmacological interaction between cigarettes and all MS therapies. It does, however, support 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 similarly convincing evidence that smoking increases the probability of developing these diseases. Increasing evidence does suggest, however, that smoking may worsen recovery after an attack has already occurred.
| Disease | What is known about disease risk | What is known about prognosis 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 disease incidence has been shown | Poorer recovery after attacks and greater residual disability |
| MOGAD | Evidence for an increased risk of onset 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, no significant association was found between smoking and disease incidence. Among smokers with NMOSD or MOGAD, however, the risk of incomplete recovery after relapse was higher: pooled RR 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 noted 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 probability 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 Chinese centers found that a history of smoking was associated with a higher risk of disability. The association with relapses weakened and was no longer significant after statistical adjustment. This again suggests that the main adverse effect of smoking in MOGAD may be expressed less through a greater number of attacks and more through 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 major irreversible disability. Therefore, even a factor that does not increase relapse frequency but worsens recovery can have substantial clinical importance.
At present there are no high-quality clinical data allowing e-cigarettes or heated-tobacco systems to be considered safe for people with MS, NMOSD or MOGAD.
The 2026 umbrella review specifically assessed this question and reached an important conclusion: among the included reviews, there were no studies directly evaluating the effect of e-cigarettes or vaping on MS risk or progression. The statement “vaping is safer for MS” therefore does not have an adequate evidence base.
Experimental studies show that e-cigarette aerosols can produce endothelial dysfunction, inflammation and disruption of the blood-brain barrier. These are mainly preclinical data and cannot be directly converted into numerical risks for humans.
Practical conclusion: switching from cigarettes to vaping should not be considered a proven neurologically safe long-term strategy. If an e-cigarette is used as a temporary step toward complete smoking cessation, it is preferable to time-limit that plan and define the final goal in advance — no smoking.
The data here are especially important: the adverse effect of smoking does not mean that “if someone has already smoked, it is too late to change anything”. On the contrary, studies show clinical benefit from smoking cessation after the diagnosis of MS.
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 almost 8,000 people with MS, smoking cessation was accompanied by slower deterioration in motor outcomes; after quitting, the rate of motor decline became comparable with that of 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.
There are fewer long-term studies specifically evaluating smoking cessation in NMOSD and MOGAD. However, given the convincing association between current smoking and poorer recovery after attacks, smoking cessation is a logical and clinically justified component of reducing the risk of accumulated disability.
The overall approach is the same as in people without a demyelinating disease: the best outcomes usually come from combining pharmacological and behavioral support.
In MS, fatigue, cognitive symptoms and reduced physical activity should also be taken into account because they can make standard cessation programs more difficult. The plan should be realistic and should not rely only on “willpower”.
From a medical perspective, it is not advisable. Smoking is associated with a higher risk of developing MS and with faster accumulation of disability after diagnosis. Smoking cessation should be considered part of long-term MS management alongside modern disease-modifying therapy, physical activity and control of accompanying risk factors.
Yes. Cohort studies show that deterioration slows after smoking cessation. The earlier someone stops, the lower their future cumulative exposure.
Results are inconsistent. Some earlier studies reported greater MRI activity, but the prospective NationMS cohort in 2026 did not find a significant association with the number of T2 or gadolinium-enhancing lesions. This does not mean smoking is harmless: clinical progression in smokers was still worse in the same cohort.
MS itself is not a contraindication to nicotine-replacement therapy. Observational evidence supports the idea that an important part of the harm from smoking may be related to smoke and airway irritation rather than nicotine alone. The specific cessation method should be chosen 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 assessing 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 involves inhalation of combustion products and is not a safe alternative. Current reviews include waterpipe smoking among smoking exposures associated with unfavorable MS risk.
For AQP4-NMOSD, a 2026 meta-analysis did not show a significant increase in disease incidence among smokers. For MOGAD, convincing evidence of a higher risk of onset is also lacking. Smoking is nevertheless associated with poorer recovery after attacks in both disorders.
Because in these diseases disability may result directly from a single severe attack. If recovery after optic neuritis or myelitis is poorer, the same relapse frequency may still lead to greater residual disability.