Editorial NexoScience
A weekly serving of salmon will not cure multiple sclerosis. But according to a large Swedish study that followed patients for up to fifteen years, it might slow down how fast the disease takes away their mobility.
Researchers tracked 2,719 people newly diagnosed with multiple sclerosis (MS) through the Swedish MS registry, using data from the nationwide Epidemiological Investigation of Multiple Sclerosis. Everyone reported how often they ate lean fish (cod, haddock, pollock) and oily fish (salmon, mackerel, herring, tuna) around the time of their diagnosis, and the team then watched what happened to their disability over the following years.
People who ate the most fish saw their risk of worsening cut by roughly a third. Patients in the highest fish consumption group had a 34% lower risk of confirmed disability worsening compared with those who rarely or never ate fish (hazard ratio 0.66). The protective association held up across three separate disability milestones, including reaching EDSS 3 and EDSS 4, two standard checkpoints doctors use to track how much a patient’s mobility and function have declined.
The benefit showed up whether the fish was lean or oily. People who ate both lean and oily fish weekly had the lowest risk of all, but even eating just one type regularly was linked to some protection. That pattern matters because it suggests the effect is not purely about omega-3 fatty acids, which are concentrated mostly in oily fish. The researchers point to taurine, an amino acid abundant in fish and seafood in general, as a possible additional player, alongside the way diet can reshape gut bacteria linked to inflammation.
Changing habits after diagnosis still mattered. In 2021, the team sent a follow-up questionnaire to check whether people had changed their fish intake since being diagnosed. About a quarter had. Those who went from rarely eating fish to eating it several times a week saw their risk of disability worsening drop by 20%, and the small group who made the most dramatic jump, from almost never eating fish to eating it daily, cut their risk by more than half. Patients who kept a consistently high fish intake throughout the follow-up period showed the strongest protection of all.
Vitamin D does not appear to explain the pattern. Because oily fish is also a dietary source of vitamin D, the researchers checked whether that nutrient was driving the results. It was not: vitamin D levels barely changed the relationship between fish consumption and disability progression, and on their own, baseline vitamin D levels showed no clear trend with how the disease progressed.
As with any study built on questionnaires and observation rather than a controlled trial, this one cannot prove that fish itself is what slows the disease. People who eat more fish may also differ in other habits, resources, or overall health that were not fully captured, and the researchers themselves call for replication before the findings move into clinical advice. Still, the size of the cohort, the 15-year follow-up, and the fact that people who changed their diet after diagnosis also changed their trajectory make this more than a passing correlation.
The study, “Impact of fish consumption on disability progression in multiple sclerosis,” was published in the Journal of Neurology, Neurosurgery & Psychiatry (DOI: 10.1136/jnnp-2024-335200).
