Multiple sclerosis (MS) is a chronic immune-mediated neurological disease characterised by inflammation, demyelination, and neurodegeneration. Growing evidence implicates oxidative stress in the pathogenesis and progression of MS [1], with studies reporting elevated oxidative stress biomarkers alongside reduced endogenous and dietary antioxidants and lower total antioxidant capacity in people with MS. Although experimental studies have suggested that specific antioxidants may influence disease processes [3], findings from human studies remain limited and inconclusive. As individual antioxidants have distinct biological functions and may act synergistically [2], assessing overall dietary antioxidant intake may better capture their potential effects on MS outcomes than examining single antioxidants in isolation. The aim of this study was to test associations between dietary antioxidant intake, assessed using an energy-adjusted Composite Dietary Antioxidant Index (E-CDAI), and relapse risk among adults with MS over 15 years of follow-up. Data were derived from the AusLong Study, a prospective Australian longitudinal cohort that has followed individuals from the time of a first clinical diagnosis of central nervous system demyelination. Participants with clinically isolated syndrome at or shortly before recruitment who progressed to clinically definite MS by the 15-year follow-up were included in this analysis (n = 163). Participants were required to have plausible energy intakes at all assessment points (males: 800–4,000 kcal/day; females: 500–3,500 kcal/day). Dietary intake was assessed using a validated food frequency questionnaire at baseline and at 5-, 10-, and 15-year follow-ups. E-CDAI scores (per 2000 kcal) were calculated and adjusted for total energy intake using the residual method. Relapses were determined by a neurologist and were assessed longitudinally from study entry. Associations between E-CDAI and relapse risk were examined using multilevel mixed-effects parametric survival models. Analyses were adjusted for age, sex, study region, smoking history, disease-modifying therapy use, and overall diet quality as measured by the alternate Mediterranean Diet Score (aMED). Sex interactions and linearity were explored. There was no evidence of an interaction between sex and E-CDAI with relapse, and the association between E-CDAI and relapse was linear. Higher dietary antioxidant intake was associated with lower risk of relapse over the 15-year follow-up period. After adjusting for potential confounders, each one-unit increase in E-CDAI was associated with lower relapse risk by 8% (adjusted hazard ratio [aHR] 0.92; 95% CI 0.88, 0.97, p=0.001). These findings suggest that the combined effects of multiple dietary antioxidants may contribute to reduced disease activity in MS. Given the role of oxidative stress in MS pathophysiology, antioxidant-rich dietary patterns may represent an important and modifiable component of disease management. However, due to the observational nature of this study, causality cannot be established and reverse causation cannot be excluded. Further investigation in other cohorts of people with MS may be warranted to confirm findings.