Associations of Dietary Inflammatory Potential, Dietary Diversity, and Micronutrient Adequacy with Rheumatoid Arthritis: A Case–Control Study from India

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease influenced by genetic and environmental factors, including diet. We examined the associations of dietary inflammatory potential, dietary diversity, and micronutrient adequacy with RA and RA-related autoantibodies in an urban Indian population. Methods: In this unmatched case–control study, 301 newly diagnosed RA cases and 314 healthy controls from Hyderabad, India, were enrolled. Dietary intake was assessed using a validated 131-item food frequency questionnaire (FFQ). Dietary inflammatory potential was estimated using the Dietary Inflammatory Index (DII), while dietary quality was assessed using the dietary diversity score (DDS) and mean probability of micronutrient adequacy (MPA). Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies were measured by ELISA. Multivariable regression models adjusted for age, sex, and BMI were used to assess associations. Population attributable fractions (PAFs) were estimated under a theoretical causal framework. Results: Compared with controls, RA cases had lower micronutrient adequacy, lower dietary diversity, and higher dietary inflammatory potential. Each one-unit increase in DII was associated with higher odds of RA (AOR 1.17; 95% CI: 1.10, 1.24), whereas each one-unit increase in DDS (AOR 0.73; 95% CI: 0.66, 0.81) and each 10-percentage-point increase in MPA (AOR 0.88; 95% CI: 0.83, 0.94) were associated with lower odds of RA. Associations with autoantibody concentrations were limited. Higher DDS, when analyzed as a continuous variable, was associated with lower anti-CCP concentrations, but not with RF. Continuous DII and MPA were not significantly associated with either anti-CCP or RF, and associations across categorical analyses were inconsistent. Conclusions: Poorer dietary diversity, lower micronutrient adequacy and a greater dietary inflammatory potential were associated with higher odds of RA. Associations with RA-related autoantibody concentrations were limited and inconsistent, and no significant associations with RF were observed. Given the case–control design, these findings should be interpreted as associations and require confirmation in prospective studies.