Diet as a DMARD? The Evidence Is Still Hard to Swallow Save

Dietary interventions are rarely taken as seriously as pharmacological therapies in rheumatology. Yet patients ask about them constantly, and an increasing number of studies suggest that nutrition may influence disease outcomes. Two randomized controlled trials presented at EULAR 2026 add to this growing literature in PsA and RA. However, before we start prescribing Mediterranean diets, the data deserve a closer look.

In abstract OP070, Eder and colleagues presented the DIPSA randomized controlled trial which compared a Mediterranean diet, a calorie-restricted DASH diet and standard dietary advice in 92 overweight and obese patients with active PsA. After 24 weeks, all groups experienced improvements in disease activity, pain, fatigue and patient-reported outcomes. This being said, there was no significant differences between either dietary intervention and the control arm. The most compelling finding was that greater weight loss correlated with greater clinical improvement, regardless of which diet patients followed. In other words, the study provides stronger evidence that losing weight improves PsA outcomes than it does for any particular dietary pattern. This particularly matters in the context of obesity being increasingly recognised as a driver of systemic inflammation in PsA, and recent data with GLP-1 receptor agonists have reinforced the concept that weight reduction itself can improve disease activity (OP069, OP0112). 

Abstract OP0207 approached the question from a different angle. In this placebo-controlled trial, Daien and colleagues evaluated inulin supplementation in patients with active RA. Patients receiving fibre daily were more likely to achieve a EULAR response at 4 weeks (OR 4.65) and showed improvements in the Th17/Treg balance. In MTX users, mean ΔDAS28 was –1.00 with fibre vs –0.34 with placebo, while no effect was seen in non-MTX patients (n=6).

The findings are certainly intriguing and fit with increasing interest in the gut microbiome as a therapeutic target in RA. However, the study included fewer than 50 patients and lasted only 30 days. While the immunological and microbiome analyses provide biological plausibility, they remain exploratory. At this stage, it is difficult to know whether fibre supplementation itself is enhancing treatment response or whether we are observing downstream metabolic effects that accompany dietary modification.

Taken together, these studies suggest that nutritional interventions may have a role in inflammatory arthritis, but neither trial definitively demonstrates that diet itself is acting as a disease-modifying therapy. The PsA study largely points towards weight loss as the key driver of benefit, while the RA study provides an interesting signal that requires confirmation in larger and longer studies.

For now, the evidence supporting weight reduction as a strategy to improve inflammatory arthritis outcomes appears stronger than the evidence supporting any specific diet. Whether particular dietary patterns exert independent anti-inflammatory effects remains an open question—and one that future studies will need to answer before diet or microbiome restauration can truly be considered a DMARD.