Ketogenic diet in rheumatoid arthritis, psoriatic arthritis and psoriasis: A scoping review of clinical and mechanistic evidence
Author(s)
Date Issued
October 2026
Type
article
Volume
25
Issue
10
Journal
Abstract
ackground: Rheumatoid arthritis (RA), psoriasis (PsO), and psoriatic arthritis (PsA) cause substantial disability
and cardiometabolic risk. Ketogenic diets (KDs), including very-low-calorie ketogenic diets (VLCKDs), may influence
disease-relevant immunometabolism, but the clinical evidence remains preliminary.
Objective: To map mechanistic and clinical evidence for KD/VLCKD across RA, PsO, and PsA and to distinguish
direct KD/VLCKD evidence from ketosis-adjacent background evidence.
Methods: Using the Population-Concept-Context (PCC) framework and PRISMA-ScR guidance, MEDLINE/
PubMed, Embase, ClinicalTrials.gov, WHO ICTRP, and reference lists were searched from inception to 30 July
2025. Search strategies are provided in Supplementary Table S1. Eligible direct evidence comprised adult human
KD/VLCKD studies in RA, PsO, or PsA with a ketogenic protocol and reported or protocol-defined nutritional
ketosis. Fasting or low-carbohydrate studies without verified KD/VLCKD were summarized separately. Data
charting was duplicated, and no formal risk-of-bias appraisal was performed.
Results: After reassessment, 29 direct KD/VLCKD studies were retained, while 3 ketosis-adjacent records were
treated as contextual evidence. Mechanistic data support plausible effects of β-hydroxybutyrate on NLRP3
inflammasome signaling, cytokine pathways, immune-cell metabolism, oxidative stress, the gut-skin/gut-joint
axes, and adiposity-related inflammation. Human signals are strongest in psoriatic disease, particularly among
participants with obesity or metabolic dysregulation. However, most studies are short, small, heterogeneous, and
strongly confounded by weight loss.
Conclusions: Current evidence suggests that KD/VLCKD may be a supervised adjunctive dietary approach for
selected people with psoriatic disease and obesity, but it is not yet sufficient to support efficacy claims. RA
evidence is mainly mechanistic or ketosis-adjacent. Adequately powered, at least 24-week randomized trials with
verified ketosis, active comparators, and weight-independent endpoints are needed before routine clinical
implementation
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