“Small disconnected facts, if you take note of them, have a way of becoming connected.”
— Walker Percy
Multiple sclerosis is a “chronic autoimmune disease of the central nervous system, in which the immune system mistakenly attacks the myelin sheath (the protective covering) of nerve fibres (axons) in the brain, spinal cord and optic nerves. This causes inflammation, demyelination, formation of scar tissue (sclerosis), and resultant interruption of nerve impulse transmission, leading to a wide range of neurological symptoms.[1]”
At first glance, such a complex autoimmune disease would seem to have little to do with something as prosaic as diet, let alone ultraprocessed foods (UPFs). And yet, as discussed in a recent presentation at the 2025 Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), there seems to be a connection.
- This observational study followed patients over 5 years.
- It was a secondary analysis of 451 participants from the Betaferon/Betaseron in Newly Emerging MS for Initial Treatment trial cohort.
- The original trial examined whether early interferon beta-1b treatment after a clinically isolated syndrome (CIS) could slow progression to MS, reduce relapses, and improve MRI outcomes; after 15 years of follow-up, results confirmed an advantage for an early start with interferon beta-1b.
- The current study used the NOVA food classification (which classifies ultra-processed foods as NOVA Group 4) and metabolomic proxies to identify UPF consumption.
- Study outcomes included time to clinically definite MS (CDMS) or MRI-based MS, relapse rates, and MRI lesion metrics.
- UPF consumption did not significantly predict whether someone converted from CIS to clinically definite MS.[2]
- At baseline (CIS onset), higher UPF consumption correlated with a larger T1-hypointense lesion volume and lower neurological function scores.
- Those consuming the greatest amount of UPFs at 2 years had more new active lesions and greater increases in T2 lesion volume.
- At the end of the five-year follow-up, those patients in the highest quartile of UPF consumption had a statistically significant, 30% greater risk for relapse than those in the lowest quartile.
The Caveat:
Although not immediately apparent upon the surface, with deeper exploration, it should not be surprising. UPFs have been linked to too many chronic inflammatory conditions, such as obesity, type II diabetes, cardiovascular disease, and certain types of cancer. High consumption of ultraprocessed foods has also been correlated with an increased risk of early mortality, where for every 10% increase in UPFs in the diet, the risk for early mortality is statistically significantly increased by 10%.[3]
In the current analysis, 208 patients with CIS converted to MS over the five-year observation period, while 243 did not. UPF scores did not differ between those who converted and those who did not, suggesting that UPF dietary exposure may not trigger MS onset, according to lead researcher and neurologist Gloria Dalla Costa, MD, of the Harvard T.H. Chan School of Public Health.
However, among patients who developed full-blown MS, those who consumed more ultra-processed foods had significantly greater T1 hypointense lesion volume and a lower Multiple Sclerosis Functional Composite Scores than those who ate less ultraprocessed foods.
The highest quartile of ultraprocessed food consumers —those who ate the most ultraprocessed foods —suffered more relapses and had more new active lesions. One of the takeaways, according to Dr. Dalla Costa, is to incorporate avoidance of ultraprocessed foods into an early MS management support strategy. She suggested that, beyond the known pro-inflammatory effects of ultraprocessed foods (UPFs), UPFs could directly or indirectly contribute to greater MS activity by impairing central nervous system defenses or by causing metabolic stress that hinders repair.
The findings suggest that ultraprocessed foods may act as a chronic inflammatory accelerant, rather than a causal trigger for the development of multiple sclerosis. However, Dr. Della Costa also acknowledged that these are correlational findings from an observational study and that further investigation is required. To that end, she noted that a prospective randomized trial is planned to confirm the findings of this study.
[1] (Tafti, 2025)
[2] Clinically Isolated Syndrome (CIS) refers to a first episode of neurological symptoms caused by inflammation or demyelination of the central nervous system (CNS) that lasts for at least 24 hours, and which is not yet sufficient to fulfil the diagnostic criteria for MS.
[3] (Liang, 2025)
Additional references:
Tafti, Dawood; Ehsan, Moavia; Xixis, Kathryn L. Multiple Sclerosis. Stat Pearls Publishing. 2025.
