Higher intake of ultra-processed foods (UPFs) may exacerbate disease activity in early multiple sclerosis (MS), according to new research presented at the 41st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS 2025).
Researchers found that increased UPF consumption was linked to more frequent relapses and greater MRI-detected lesion activity, highlighting the potential role of diet as a complementary strategy in disease management.
The study, led by Dr. Gloria Dalla Costa, analyzed data from 451 patients with clinically isolated syndrome – the first clinical presentation of MS – who were enrolled in the BENEFIT trial and followed for up to five years. A previously validated metabolomic signature of UPF intake, comprising 39 plasma metabolites developed by Harvard colleagues, was applied to baseline plasma samples to calculate individual UPF scores.
While UPF scores were not associated with conversion to clinically definite MS, higher scores at baseline were linked to greater T1 hypointense lesion volume, indicative of more severe tissue damage, and lower neurological function scores. Over the five-year follow-up, participants in the highest UPF quartile experienced approximately 30% more relapses than those in the lowest quartile.
By two years, they also had a higher rate of new active lesions, representing ongoing inflammation, and a larger increase in T2 lesion volume, a marker of accumulating tissue changes. These associations remained significant after adjustment for age, sex, treatment allocation, baseline disease burden, BMI, vitamin D, and smoking.
This pattern suggests ultra-processed foods act as a chronic inflammatory accelerant rather than a disease trigger, amplifying existing inflammatory processes in MS rather than determining whether someone develops the disease in the first place.”
Dr. Gloria Dalla Costa
“The biological mechanisms behind this effect may involve disruption of the gut barrier by additives such as emulsifiers and preservatives, which can allow bacterial endotoxins to enter the bloodstream and trigger immune activation that reaches the brain,” she explained. “Elevated ceramides and modified lipids suggest UPF consumption may also alter membrane composition, making myelin – the insulating layer that forms around nerves – and the cells that produce it more vulnerable to autoimmune attack.”
“In addition, metabolic stress signatures such as elevated C4-OH carnitine point to impaired cellular energy production, limiting the brain’s ability to withstand and repair damage during inflammatory episodes. Overall, our findings suggest UPF consumption creates a cascade of biological disruptions that amplify MS inflammatory activity.”
Discussing the clinical implications of the findings, Dr Dalla Costa said, “I would recommend UPF reduction as a valuable supporting strategy for early MS management. Similar to vitamin D supplementation or smoking cessation advice, this is not about replacing established therapies, but about complementing them. It’s a low-risk, potentially high-benefit intervention.”
Looking ahead, the team plans to replicate these results in other MS cohorts, integrate microbiome analysis, and design intervention studies. “We are finalizing a comprehensive manuscript which will provide the evidence base needed to inform clinical practice guidelines and establish the foundation for future dietary intervention studies,” Dr. Dalla Costa concluded.
Source:
41st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS 2025)