Can nutrition prevent the onset of Rheumatoid Arthritis? A mini review of dietary risk and progression from pre-clinical autoimmunity
1. GKT School of Medical Education, King’s College London, London, United Kingdom
2. Department of Life Sciences, School of Life and Health Sciences, University of Nicosia, Nicosia, Cyprus
3. Department of Nutritional Sciences, King’s College London, London, United Kingdom
4. Centre for Rheumatic Diseases, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King’s College London, London, United Kingdom
5. Centre for Education, Faculty of Life Sciences and Medicine, King’s College London, London, United Kingdom
6. Department of Rheumatology, King’s College Hospital, London, United Kingdom
Article metrics
View details
Abstract
Rheumatic and musculoskeletal diseases are major causes of disability worldwide, and many have inflammation at their core. Rheumatoid Arthritis (RA), in particular, is preceded by a prolonged “pre-clinical” phase in which genetic susceptibility and modifiable exposures, including diet, interact. Nutrition is thought to play an important role as an ‘external’ but modifiable factor in inflammatory diseases. The existing literature suggests that it may act as a lever for prevention and risk modification through direct or indirect effects on adiposity, systemic inflammation, mucosal immunity, the gut microbiome, and cardiometabolic comorbidity. In this mini review, we synthesize and critically appraise the evidence linking dietary patterns and targeted nutritional interventions with RA risk.
1 Introduction
Rheumatoid Arthritis (RA) is a systemic autoimmune disease characterized by joint inflammation (1) and is estimated to have a global prevalence of 460 per 100,000 population (2). These inflammatory processes lead to joint and bone damage, pain, and stiffness (3). RA symptoms are progressive and vary among individuals; pain, stiffness, fatigue, and deformity can disrupt physical, psychological, and sexual functioning (4). Furthermore, the inflammatory effects of RA spread beyond the joints, increasing morbidity and mortality through complications in the heart, lungs, nervous system, and vascular system (5).
RA incidence and prevalence vary globally; a 2025 systematic review identified wide variation between regions and countries (6) with a prevalence of 541–779 per 100,000 in the UK (7), 680 per 100,000 in Canada (8) and 1,500 per 100,000 in Korea (9). These geographic variations may reflect ambiguous diagnostic criteria (10), and uncertainty due to insidious onset and gradual symptom progression (11). Many genetic, socioeconomic, and environmental factors have been identified as potential influences on RA prevalence (12). The complex interaction between genetic, hormonal, immune systems, and environmental factors on the expression of autoimmune disease has been referred to as the ‘mosaic of autoimmunity’ (13), whereby the above factors converge to produce unique rheumatological presentations.
Regarding environmental exposures, several studies have highlighted the beneficial effect of an anti-inflammatory diet in established disease on both RA-disease activity (14), and patient-reported pain (15). Chronic inflammatory states are thought to stem from hyperresponsivity to normally benign stimuli, loss of protective cellular barrier function, inflammatory cell infiltration, and overproduction of inflammatory mediators such as chemokines, cytokines, and oxidants (16). In this context, anti-inflammatory diets may decrease inflammatory cell production, promoting greater intestinal cell barrier function, and increasing anti-inflammatory responses (16). Characteristics of anti-inflammatory diets include being high in monounsaturated fats (for example, extra virgin olive oil; EVOO) and n-3 long-chain polyunsaturated fatty acids (PUFAs), while also being low in glycemic index, saturated fat, and added sugar and rich in fiber and phytonutrients, through a variety of fruits, nuts and seeds, vegetables, and legumes (17). An anti-inflammatory diet aligns closely with the Mediterranean diet (MD), and thus some researchers recommend that the MD be used alongside standard medical treatments in RA management (17–19).
Dietary intake influences an individual’s body mass index (BMI) and adiposity (20, 21). In turn, excess adipose tissue has been shown to harbor greater inflammatory cells (such as neutrophils, lymphocytes and macrophages), thus contributing to systemic inflammation (22). Macrophages, which are particularly abundant in adipose tissue, are responsible for the secretion of pro-inflammatory cytokines (22), of which tumor necrosis factor (TNF) and interleukin (IL) 1 and 6, are heavily implicated in RA (23). Strong associations have been drawn between adiposity and increased risk of developing RA (21), highlighting that nutrition may be implicated in disease development via increasing BMI.
Furthermore, bacterial colonization in the gut, particularly Prevotella copri (Pc) and Collinsella aerofaciens, may result in pro-inflammatory intestinal environments, a potential mechanism driving progression to RA (24). This suggests a direct link between diet, the microbiome, and RA risk. Additionally, nutrition may be associated with the development of metabolic comorbidities common in RA, such as several cardiovascular comorbidities, including myocardial infarction, congestive heart failure, and atrial fibrillation (25). Prioritizing diet in RA patients may therefore not only reduce inflammation and improve disease status, but also slow the progression of cardiometabolic comorbidities (26).
This mini review aims to synthesize and critically appraise the current evidence linking dietary patterns and targeted nutritional interventions with RA risk. To inform the review, a search was carried out in PubMed and Google Scholar using the following search terms: Rheumatoid Arthritis, Arthralgia, Diet, Nutrition, Mediterranean Diet, Western Diet, Anti-Inflammatory Diet and Pre-Clinical Rheumatoid Arthritis. Systematic reviews, observational studies and interventional studies were included based on their relevance to the development of RA.
2 Rheumatoid Arthritis risk and Mediterranean diet, Western diet, and overall dietary quality
A commonly studied dietary pattern in relation to RA risk is the MD, characterized by abundant plant foods such as unrefined cereals, fruit, vegetables, legumes, EVOO, moderate consumption of poultry, dairy products, and eggs, and limited consumption of sweets and red meat (17). In the French E3N-EPIC prospective cohort study in women (1990–2017), adherence to a MD in those with established smoking history was associated with a lower risk of RA (HR 0.91 [95% CI 0.84–0.99]) (27). No association, however, was seen in non-smoking women. This highlights the effect of environmental influences on RA risk, such as smoking, as demonstrated by a dose–response meta-analysis of 10 studies, showing that the risk of RA in those with a 21–30 pack-year smoking history, compared to never-smokers, was increased by 94% (RR 1.94 [95% CI 1.65–2.27]) (28). The association between greater adherence to the MD and reduced RA risk, in both men and women, has also been supported by evidence from a cohort study and systematic review including 117,341 participants, where those in the highest quartile of MD adherence had a lower risk of RA development than those in the lowest quartile (HR 0.71 [95% CI 0.58–0.88]) (29). This association appeared to differ according to seropositive status. Johansson et al. (30) reported that greater adherence to the MD was associated with a reduced risk of RF-positive RA (OR 0.69, 95% CI 0.54–0.88), whereas no significant association was observed for RF-negative RA.
In contrast the ‘Western Diet’ (WD) – characterized by high intakes of red and processed meat, refined carbohydrates, added sugars, high salt, and ultra-processed foods (UPFs) – has been proposed as a potential driver of autoimmune disease (19). Red meat may contribute to a pro-inflammatory dietary pattern, partly through arachidonic acid (31). UPFs are industrial formulations with five or more ingredients (32), and additives such as preservatives, emulsifiers, sweeteners, and artificial colors/flavors (33). Examples include breakfast cereals, processed meats, soft drinks, and pre-packaged frozen meals (34). Although most foods undergo some processing, additives dictate the degree of processing: standard steel-cut oats are minimally processed, become processed when they contain sugar, and ultra-processed through the addition of flavors/colorings (35). The low fiber content of the WD is associated with fewer fiber-degrading bacteria and increased expression of virulence factors (36), reducing microbial diversity and depriving beneficial gut bacteria of fermentable substrates. This reduces production of protective short-chain fatty acids such as butyrate which regulate immune cells (37). Reduced butyrate may increase intestinal permeability, facilitating microbial product translocation into the circulation and promoting inflammation (38).
High consumption of UPFs is also associated with a higher obesity prevalence (36) and increased RA risk. In 207,012 participants of the UK Biobank study who were free from RA at baseline, high consumption of UPFs was associated with a 6% increase in RA risk per standard deviation increase in UPF intake (HR 1.06 [95% CI 1.01–1.11]) (39). UPFs are thought to contribute to systemic inflammation, leading to a rise in inflammatory markers such as C-reactive protein (CRP) and leucocytes (39).
Conversely, better diet quality is associated with lower RA risk. In a prospective study of 170,000 women from the Nurses’ Health Study who were free from RA at baseline, greater long-term adherence to the 2010 Alternative Healthy Eating Index (AHEI-2010) was associated with a lower risk of seropositive RA among women aged ≤55 years (HR 0.67 [95% CI 0.51–0.88]) (40). Similarly Di Giuseppe et al. (41) prospectively followed 32,232 women for 7.5 years, as part of the Swedish Mammography Cohort. Findings included a non-statistically significant 29% (RR 0.71 [95% CI 0.48–1.04]) reduced RA risk in women who consistently ate ≥1 serving of fish per week and a 52% (RR 0.48 [95% CI 0.29–0.67]) lower risk in those who consumed >0.21 g/day of n-3 PUFAs. Omega-3 fatty acids [synonymous with n-3 PUFAs (42)], found in fatty fish, seafood, walnuts, and linseeds (43), are an essential fatty acid component of the human diet. They exert anti-inflammatory effects partly by competing with arachidonic acid for cyclooxygenase enzymes, thereby reducing the production of pro-inflammatory arachidonic acid-derived prostaglandin E2 and favoring formation of the less inflammatory prostaglandin E3 (44).
3 Progression from pre-clinical autoimmunity to clinically apparent disease
3.1 Pre-clinical Rheumatoid Arthritis and risk
Pre-clinical RA is the period preceding the clinical phase of RA by several years (45) during which initial inflammatory processes and sub-clinical synovial inflammation may develop before symptom manifestation. Patients may exhibit anti-citrullinated protein antibodies (ACPAs) or RF positivity during this phase (3). Notably, some patients only develop ACPAs after the onset of clinically-apparent RA, therefore, ACPAs cannot reliably be used as a biomarker of pre-clinical RA (46). The pre-clinical phase is thought to be influenced by genetic and environmental factors: non-modifiable genetic factors contributing approximately 30–60% of susceptibility to RA development (46), with the remainder attributed to environmental factors (47). High decaffeinated coffee consumption, smoking history, and exposure to air pollution have been associated with increased susceptibility to RA, potentially through gene–environment interactions that promote the development of autoimmunity (46). Lifestyle modification (including diet alteration to favor anti-inflammatory diets such as the MD) has been associated with a lower risk of RA development (45), potentially modulating the gene–environment interaction (48).
3.2 Dietary links and immune activation
Anti-inflammatory diets such as the MD may reduce inflammation through cytokine regulation by lowering the production of pro-inflammatory molecules, such as IL-6 and oxidative stress markers (49). Furthermore, n-3 PUFAs, key components of the MD, may counteract the secretion of pro-inflammatory IL-6 in vascular tissues, exerting anti-inflammatory effects (50). Some evidence for this stems from a nested case–control study in a population without RA but at high genetic risk, where anti-CCP2 positivity was inversely associated with n-3 PUFA concentrations in erythrocytes (OR 0.47 [95% CI 0.24–0.92] per standard deviation increase) (51). It is of note, however, that subsequent progression to clinical RA was not studied.
Beyond these systemic anti-inflammatory effects, diet may influence immune processes at mucosal surfaces. The mucosal origins hypothesis provides a conceptual rationale for the potential role of these effects in RA initiation. The hypothesis argues that immune dysregulation at mucosal sites may contribute to systemic autoimmunity that precedes clinically apparent synovitis (52). Mucosal immunity is promoted through ingestion of soluble fibers from fruit, vegetables, and legumes, which nurture the growth of beneficial gut bacteria, protecting the intestinal barrier and reducing systemic inflammation (49). In contrast, WDs are thought to disrupt microbial diversity and increase expression of microbial virulence factors (36). They may also promote inflammation through diet-induced obesity, whereby the accumulation of white adipose tissue contributes to a pro-inflammatory state through its endocrine activity, including the production of TNF-α and IL-6, and modulation of T-cell responses (53).
Furthermore, WD constituents may directly trigger localized intestinal inflammation (through factors such as oxidized LDL cholesterol and saturated fatty acids), alongside indirectly triggering inflammation through microbial alteration (54). WDs can contribute to dysbiosis as they typically contain a higher concentration of UPFs and inflammatory foods (55). In particular, WDs are rich in additives (such as salt and artificial sweeteners), which have been associated with reduced numbers of beneficial gut bacteria Lactobacillus and Bifidobacteria (55). As such, gut dysbiosis may be promoted through the loss of beneficial organisms, growth of harmful bacteria and overall reduction in microbial diversity (56). Such dysbiosis may shift immune responses toward inflammatory pathways, including Th17 responses (52), and may facilitate abnormal modification of proteins such as citrullination (57). Given the physiological homeostasis between the gut microbiome and the immune system (56), pro-inflammatory diets which adversely alter microbial composition may also contribute to immune dysregulation. For example, Pc has been proposed as a potential contributor to the progression of pre-clinical to established RA, evidenced by significant abundance of Prevotella species (p = 0.04) in individuals with pre-clinical RA compared to first-degree relative controls (58), and anti-CCP-positive individuals at risk of RA showing a trend toward higher IgG anti-Pc-p27 levels (59).
Metabolic syndrome and obesity also contribute to chronic inflammatory states through increased oxidative stress, circadian rhythm disruption (60) and inappropriate activation of immune cells (61) such as T cells (53). Pathways described in Figure 11 – The Role of Diet in the Onset of Rheumatoid Arthritis, suggest that diet could influence RA development and is a plausible component of a wider gene–environment interaction in pre-clinical RA. It is of note, however, that evidence remains limited.
4 Discussion
Cumulative evidence suggests that diet is important in the development of RA through a variety of anti-inflammatory and pro-inflammatory mechanisms. The available observational evidence generally suggests an association between greater adherence to the MD and lower RA risk (27, 29, 30, 41) exerted through anti-inflammatory components such as n-3 PUFAs (41, 50, 62) and plant-based foods and fiber promoting the growth of beneficial microbial bacteria (49). On the contrary, the WD is typically associated with pro-inflammatory changes (19, 36, 39, 53, 54, 56). In genetically susceptible people, particularly in the presence of other exposures such as smoking or obesity (63), these inflammatory changes may promote autoantibody formation, years before apparent joint swelling.
Notably most evidence reviewed is derived from studies on established RA, rather than pre-clinical and at-risk individuals, and direct evidence that dietary modification can alter the progression to clinical RA remains limited. With this caveat in mind, several confounding factors, including smoking, may alter the effect of diet on the pre-clinical RA course (27). It is thus crucial to acknowledge the concept of the mosaic of autoimmunity when considering modifiable risk factors for RA, as some factors may prove challenging to separate. Another important consideration is adherence to the MD (29, 30), which can be challenging to assess across different populations and study designs, thereby limiting comparability between studies. Moreover, although evidence on diet in pre-clinical RA is largely observational, evidence on the impact of diet on established RA may still provide useful mechanistic and clinical insights. For example, a systematic review of clinical trials evaluating dietary interventions in RA found that their effects were more notable for subjective rather than objective measures of RA disease activity (64). This provides foundational evidence that dietary interventions can play a role in RA; however, there remains scope to focus more specifically on how diet can influence the pre-clinical RA course, rather than established disease. Identifying pre-clinical RA can be challenging due to the variety of causes of arthralgia and the lack of universal, highly sensitive serological markers. Although RF and ACPA positivity may provide insight into a patient’s pre-clinical RA phase, not all patients who develop RA will exhibit these autoantibodies during this period (46). This is important given that higher MD adherence in pre-clinical RA patients with RF positivity was associated with 31% lower odds of RA development (OR 0.69 [95% CI 0.54–0.88]) (30).
An additional point to consider is the effect of other well-known diets on RA risk, although available evidence is primarily based on established rather than pre-clinical RA. The ketogenic diet has been reported to have anti-inflammatory effects in established RA through suppression of IL-1 and TNF-α (65) and vegan diets have also been associated with symptom reduction in established RA, likely due to the antioxidant effects and favoring the growth of Lactobacillus (66). These foundations provide evidence for the involvement of diet in RA disease activity, although further research is needed to assess the impact of a variety of diets on the pre-clinical RA disease course.
Despite cumulative evidence suggesting that anti-inflammatory diets may modulate RA outcomes, understanding patient and clinician perspectives is important for implementing dietary advice into current medical practice. Through surveying 100 individuals at risk of RA (who reported arthralgia and were seropositive for RF/ACPAs), Boheemen et al. (67) found that all patients were willing to change at least 1 lifestyle component: mainly opting to increase fruit and vegetable intake. Rheumatologists (n = 49) however, were not issuing lifestyle counseling to all at-risk RA patients, due to a perceived shallow supporting evidence base. Notably, the small sample sizes limit generalizability of findings.
4.1 Limitations and clinical implications
Evidence on RA risk relies heavily on observational studies, which cannot establish causality between diet and symptom burden. Furthermore, assessing dietary quality can be challenging, as the use of different dietary indices, such as MD adherence or the AHEI-2010, may reduce comparability between studies. Additionally, as pre-clinical RA cannot be reliably diagnosed, existing studies have not specifically recruited patients with pre-clinical RA but rather at-risk or general populations who were followed up to incident RA diagnosis. This limits the conclusions that can be drawn regarding the pre-clinical-to-clinical RA transition.
Nevertheless, growing evidence suggests that adoption of an anti-inflammatory MD may improve RA disease activity and reduce inflammation (17). Thus, the potential implications of diet on pre-clinical RA are considerable. Such a dietary pattern emphasizes plant-based foods including legumes, a variety of vegetables, whole grains, unsalted nuts and seeds, seasonal fruit (especially those rich in phytochemicals, such as berries), n-3 PUFAs (such as fatty fish), lean protein sources, moderate consumption of eggs and dairy products, fermented foods, and limited, if at all, consumption of red meat and UPFs. By targeting modifiable dietary risk factors in the pre-clinical RA phase, through, if necessary, individualized dietary advice provided by registered dietitians, it may be possible to alter the course of progression to clinical RA (48). However, further research is necessary to better understand which dietary interventions are most beneficial, the time-period of implementation and the population group to be targeted. A close collaboration between rheumatologists and registered dietitians is also important.
5 Conclusion
In conclusion, evidence suggests that dietary modification toward a Mediterranean dietary pattern may exert anti-inflammatory effects and beneficially influence the gut microbiome. In contrast, the WD is perceived to pose an environmental risk factor, either directly through inflammation or indirectly through its association with a higher risk of obesity, potentially increasing the risk of RA and co-morbidities. However, definitive evidence that adopting a MD alters progression from pre-clinical autoimmunity to clinical disease, is still lacking. Existing evidence is primarily observational and derived from general-population cohorts or individuals with established RA, rather than confirmed at-risk individuals. Future research should continue to evaluate the effects of specific anti-inflammatory dietary interventions during the pre-clinical phase of RA using robust, rigorously designed methodologies.
Statements
Funding
The author(s) declared that financial support was not received for this work and/or its publication
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest
Generative AI statement
The author(s) declared that Generative AI was used in the creation of this manuscript. We acknowledge the use of Generative AI in facilitating the production of this manuscript. ChatGPT was used to suggest ideas and a potential research plan, to assist in the generation of Figure 1, and to assist in rewording and shortening text
Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher
Supplementary material
The Supplementary material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fnut.2026.1864271/full#supplementary-material
Footnotes
1.^Although several associations have been described as illustrated by Figure 1, many require further confirmation
References
van der WoudeDvan der Helm-van MilAHM. Update on the epidemiology, risk factors, and disease outcomes of rheumatoid arthritis. Best Pract Res Clin Rheumatol. (2018) 32:174–87. doi: 10.1016/j.berh.2018.10.005
2.
AlmutairiKNossentJPreenDKeenHInderjeethC. The global prevalence of rheumatoid arthritis: a meta-analysis based on a systematic review. Rheumatol Int. (2021) 41:863–77. doi: 10.1007/s00296-020-04731-0
3.
Di MatteoAEmeryP. Rheumatoid arthritis: a review of the key clinical features and ongoing challenges of the disease. Panminerva Med. (2024) 66:427–42. doi: 10.23736/S0031-0808.24.05272-8
4.
ParentiGTomainoSCMCipollettaS. The experience of living with rheumatoid arthritis: a qualitative metasynthesis. J Clin Nurs. (2020) 29:3922–36. doi: 10.1111/jocn.15428
5.
FigusFAPigaMAzzolinIMcConnellRIagnoccoA. Rheumatoid arthritis: extra-articular manifestations and comorbidities. Autoimmun Rev. (2021) 20:102776. doi: 10.1016/j.autrev.2021.102776
6.
UkePMaharajAAdebajoA. A review on the epidemiology of rheumatoid arthritis: an update and trends from current literature. Best Pract Res Clin Rheumatol. (2025) 39:102036. doi: 10.1016/j.berh.2025.102036
7.
ScottICWhittleRBaileyJTwohigHHiderSLMallenCDet al. Rheumatoid arthritis, psoriatic arthritis, and axial spondyloarthritis epidemiology in England from 2004 to 2020: an observational study using primary care electronic health record data. Lancet Reg Health Eur. (2022) 23:100519. doi: 10.1016/j.lanepe.2022.100519
8.
NairBTaylor-GjevreRWuLJinSQuailJM. Incidence and prevalence of rheumatoid arthritis in Saskatchewan, Canada: 2001-2014. BMC Rheumatol. (2019) 3:28. doi: 10.1186/s41927-019-0077-4
9.
JeongHBaekSYKimSWEunYHKimIYKimHet al. Comorbidities of rheumatoid arthritis: results from the Korean National Health and nutrition examination survey. PLoS One. (2017) 12:e0176260. doi: 10.1371/journal.pone.0176260
10.
Di MatteoABathonJMEmeryP. Rheumatoid arthritis. Lancet. (2023) 402:2019–33. doi: 10.1016/S0140-6736(23)01525-8
11.
RaduAFBungauSG. Management of rheumatoid arthritis: an overview. Cells. (2021) 10:2857. doi: 10.3390/cells10112857
12.
FinckhAGilbertBHodkinsonBBaeSCThomasRDeaneKDet al. Global epidemiology of rheumatoid arthritis. Nat Rev Rheumatol. (2022) 18:591–602. doi: 10.1038/s41584-022-00827-y
13.
de CarvalhoJFPereiraRMRShoenfeldY. The mosaic of autoimmunity: the role of environmental factors. Front Biosci. (2009) 1:501–9. doi: 10.2741/e46
14.
VadellAKBärebringLHulanderEGjertssonILindqvistHMWinkvistA. Anti-inflammatory diet in rheumatoid arthritis (ADIRA)—a randomized, controlled crossover trial indicating effects on disease activity. Am J Clin Nutr. (2020) 111:1203–13. doi: 10.1093/ajcn/nqaa019
15.
SchönenbergerKASchüpferACGloyVLHaslerPStangaZKaegi-BraunNet al. Effect of anti-inflammatory diets on pain in rheumatoid arthritis: a systematic review and meta-analysis. Nutrients. (2021) 13:4221. doi: 10.3390/nu13124221
16.
CalderPCAlbersRAntoineJMBlumSBourdet-SicardRFernsGAet al. Inflammatory disease processes and interactions with nutrition. Br J Nutr. (2009) 101:1–45. doi: 10.1017/S0007114509377867
17.
NikiphorouEPhilippouE. Nutrition and its role in prevention and management of rheumatoid arthritis. Autoimmun Rev. (2023) 22:103333. doi: 10.1016/j.autrev.2023.103333
18.
PapandreouPGioxariADaskalouEGrammatikopoulouMGSkouroliakouMBogdanosDP. Mediterranean diet and physical activity nudges versus usual care in women with rheumatoid arthritis: results from the MADEIRA randomized controlled trial. Nutrients. (2023) 15:676. doi: 10.3390/nu15030676
19.
PaolinoSPaciniGPatanèMAlessandriECattelanFGoeganFet al. Interactions between microbiota, diet/nutrients and immune/inflammatory response in rheumatic diseases: focus on rheumatoid arthritis. Reumatologia. (2019) 57:151–7. doi: 10.5114/reum.2019.86425
20.
AtakanMMKoşarŞNGüzelYTinHTYanX. The role of exercise, diet, and cytokines in preventing obesity and improving adipose tissue. Nutrients. (2021) 13:1459. doi: 10.3390/nu13051459
21.
OhnoTAuneDHeathAK. Adiposity and the risk of rheumatoid arthritis: a systematic review and meta-analysis of cohort studies. Sci Rep. (2020) 10:16006. doi: 10.1038/s41598-020-71676-6
22.
GremeseETolussoBGiganteMRFerraccioliG. Obesity as a risk and severity factor in rheumatic diseases (autoimmune chronic inflammatory diseases). Front Immunol. (2014) 5:576. doi: 10.3389/fimmu.2014.00576
23.
SmolenJSRedlichKZwerinaJAletahaDSteinerGSchettG. Pro-inflammatory cytokines in rheumatoid arthritis. Clin Rev Allergy Immunol. (2005) 28:239–48. doi: 10.1385/CRIAI:28:3:239
24.
Alpízar-RodríguezDFinckhAGilbertB. The role of nutritional factors and intestinal microbiota in rheumatoid arthritis development. Nutrients. (2021) 13:96. doi: 10.3390/nu13010096
25.
ChenJNorlingLVCooperD. Cardiac dysfunction in rheumatoid arthritis: the role of inflammation. Cells. (2021) 10:881. doi: 10.3390/cells10040881
26.
CorraoSCalvoLGiardinaACangemiIFalconeFArganoC. Rheumatoid arthritis, cardiometabolic comorbidities, and related conditions: need to take action. Front Med. (2024) 11:1421328. doi: 10.3389/fmed.2024.1421328
27.
NguyenYSalliotCGelotAGambarettiJMarietteXBoutron-RuaultMCet al. Mediterranean diet and risk of rheumatoid arthritis: findings from the French E3N-EPIC cohort study. Arthritis Rheumatol. (2021) 73:69–77. doi: 10.1002/art.41487
28.
Di GiuseppeDDiscacciatiAOrsiniNWolkA. Cigarette smoking and risk of rheumatoid arthritis: a dose-response meta-analysis. Arthritis Res Ther. (2014) 16:R61. doi: 10.1186/ar4498
29.
HuPLeeEKPLiQTamLSWongSYSPoonPKMet al. Mediterranean diet and rheumatoid arthritis: a nine-year cohort study and systematic review with meta-analysis. Eur J Clin Nutr. (2025) 79:888–96. doi: 10.1038/s41430-025-01628-8
30.
JohanssonKAsklingJAlfredssonLDi GiuseppeDEIRA study group. Mediterranean diet and risk of rheumatoid arthritis: a population-based case-control study. Arthritis Res Ther. (2018) 20:175. doi: 10.1186/s13075-018-1680-2
31.
LiDNgAMannNJSinclairAJ. Contribution of meat fat to dietary arachidonic acid. Lipids. (1998) 33:437–40. doi: 10.1007/s11745-998-0225-7
32.
DickenSJBatterhamRL. Ultra-processed food and obesity: what is the evidence?Curr Nutr Rep. (2024) 13:23–38. doi: 10.1007/s13668-024-00517-z
33.
SteeleEMBaraldiLGda CLMLMoubaracJCMozaffarianDMonteiroCA. Ultra-processed foods and added sugars in the US diet: evidence from a nationally representative cross-sectional study. BMJ Open. (2016) 6:e009892. doi: 10.1136/bmjopen-2015-009892
34.
PagliaiGDinuMMadarenaMPBonaccioMIacovielloLSofiF. Consumption of ultra-processed foods and health status: a systematic review and meta-analysis. Br J Nutr. (2021) 125:308–18. doi: 10.1017/S0007114520002688
35.
MonteiroCACannonGLevyRBMoubaracJCLouzadaMLRauberFet al. Ultra-processed foods: what they are and how to identify them. Public Health Nutr. (2019) 22:936–41. doi: 10.1017/S1368980018003762
36.
ZinöckerMKLindsethIA. The Western diet-microbiome-host interaction and its role in metabolic disease. Nutrients. (2018) 10:365. doi: 10.3390/nu10030365
37.
MakkiKDeehanECWalterJBäckhedF. The impact of dietary fiber on gut microbiota in host health and disease. Cell Host Microbe. (2018) 23:705–15. doi: 10.1016/j.chom.2018.05.012
38.
De SantisSCavalcantiEMastronardiMJirilloEChieppaM. Nutritional keys for intestinal barrier modulation. Front Immunol. (2015) 6:612. doi: 10.3389/fimmu.2015.00612
39.
ZhaoHBaiYLiuYXingYYanYChenGet al. Association of ultraprocessed food consumption with risk of rheumatoid arthritis: a retrospective cohort study in the UK biobank. Am J Clin Nutr. (2024) 120:927–35. doi: 10.1016/j.ajcnut.2024.08.014
40.
HuYSparksJAMalspeisSCostenbaderKHHuFBKarlsonEWet al. Long-term dietary quality and risk of developing rheumatoid arthritis in women. Ann Rheum Dis. (2017) 76:1357–64. doi: 10.1136/annrheumdis-2016-210431
41.
Di GiuseppeDWallinABottaiMAsklingJWolkA. Long-term intake of dietary long-chain n-3 polyunsaturated fatty acids and risk of rheumatoid arthritis: a prospective cohort study of women. Ann Rheum Dis. (2014) 73:1949–53. doi: 10.1136/annrheumdis-2013-203338
42.
SainiRKPrasadPSreedharRVAkhilender NaiduKShangXKeumYS. Omega-3 polyunsaturated fatty acids (PUFAs): emerging plant and microbial —a review. Antioxidants. (2021) 10:1627. doi: 10.3390/antiox10101627
43.
GargMLWoodLGSinghHMoughanPJ. Means of delivering recommended levels of long chain n-3 polyunsaturated fatty acids in human diets. J Food Sci. (2006) 71:R66–71. doi: 10.1111/j.1750-3841.2006.00033.x
44.
SiriwardhanaNKalupahanaNSMoustaid-MoussaN. Health benefits of n-3 polyunsaturated fatty acids. Adv Food Nutr Res. (2012) 65:211–22. doi: 10.1016/B978-0-12-416003-3.00013-5
45.
WuTLiYLiuYChuCQ. Preclinical RA: how to halt its progression. Best Pract Res Clin Rheumatol. (2025) 39:102030. doi: 10.1016/j.berh.2024.102030
46.
DeaneKDNorrisJMHolersVM. Pre-clinical rheumatoid arthritis: identification, evaluation and future directions for investigation. Rheum Dis Clin N Am. (2010) 36:213–41. doi: 10.1016/j.rdc.2010.02.001
47.
AlarcónGS. Epidemiology of rheumatoid arthritis. Rheum Dis Clin N Am. (1995) 21:589–604. doi: 10.1016/S0889-857X(21)00458-0
48.
MartinsPFonsecaJE. How to investigate: pre-clinical rheumatoid arthritis. Best Pract Res Clin Rheumatol. (2019) 33:101438. doi: 10.1016/j.berh.2019.101438
49.
ItsiopoulosCMayrHLThomasCJ. The anti-inflammatory effects of a Mediterranean diet: a review. Curr Opin Clin Nutr Metab Care. (2022) 25:415–22. doi: 10.1097/MCO.0000000000000872
50.
OppedisanoFMacrìRGliozziMMusolinoVCarresiCMaiuoloJet al. The anti-inflammatory and antioxidant properties of n-3 PUFAs: their role in cardiovascular protection. Biomedicine. (2020) 8:306. doi: 10.3390/biomedicines8090306
51.
GanRWYoungKAZerbeGODemoruelleMKWeismanMHBucknerJHet al. Lower omega-3 fatty acids are associated with the presence of anti-cyclic citrullinated peptide autoantibodies in a population at risk for future rheumatoid arthritis: a nested case-control study. Rheumatology (Oxford). (2016) 55:367–76. doi: 10.1093/rheumatology/kev266
52.
HolersVMDemoruelleMKKuhnKABucknerJHRobinsonWHOkamotoYet al. Rheumatoid arthritis and the mucosal origins hypothesis: external protection becomes internal destruction. Nat Rev Rheumatol. (2018) 14:542–57. doi: 10.1038/s41584-018-0070-0
53.
ManzelAMullerDNHaflerDAErdmanSELinkerRAKleinewietfeldM. Role of “Western diet” in inflammatory autoimmune diseases. Curr Allergy Asthma Rep. (2014) 14:404. doi: 10.1007/s11882-013-0404-6
54.
ChristALauterbachMLatzE. Western diet and the immune system: an inflammatory connection. Immunity. (2019) 51:794–811. doi: 10.1016/j.immuni.2019.09.020
55.
SeverinoATohumcuETamaiLDargenioPPorcariSRondinellaDet al. The microbiome-driven impact of western diet in the development of noncommunicable chronic disorders. Best Pract Res Clin Gastroenterol. (2024) 72:101923. doi: 10.1016/j.bpg.2024.101923
56.
De LucaFShoenfeldY. The microbiome in autoimmune diseases. Clin Exp Immunol. (2018) 195:74–85. doi: 10.1111/cei.13158
57.
BlenkinsoppHCSeidlerKBarrowM. Microbial imbalance and intestinal permeability in the pathogenesis of rheumatoid arthritis: a mechanism review with a focus on bacterial translocation, citrullination, and probiotic intervention. J Am Nutr Assoc. (2024) 43:59–76. doi: 10.1080/27697061.2023.2211129
58.
Alpizar-RodriguezDLeskerTRGronowAGilbertBRaemyELamacchiaCet al. Prevotella copri in individuals at risk for rheumatoid arthritis. Ann Rheum Dis. (2019) 78:590–3. doi: 10.1136/annrheumdis-2018-214514
59.
SeifertJABemisEARamsdenKLowellCPolinskiKFeserMet al. Association of antibodies to Prevotella copri in anti-cyclic citrullinated peptide-positive individuals at risk of developing rheumatoid arthritis and in patients with early or established rheumatoid arthritis. Arthritis Rheumatol. (2023) 75:507–16. doi: 10.1002/art.42370
60.
MonteiroRAzevedoI. Chronic inflammation in obesity and the metabolic syndrome. Mediat Inflamm. (2010) 2010:289645. doi: 10.1155/2010/289645
61.
de HerediaFPGómez-MartínezSMarcosA. Obesity, inflammation and the immune system. Proc Nutr Soc. (2012) 71:332–8. doi: 10.1017/S0029665112000092
62.
HahnJCookNRAlexanderEKFriedmanSWalterJBubesVet al. Vitamin D and marine omega 3 fatty acid supplementation and incident autoimmune disease: VITAL randomized controlled trial. BMJ. (2022) 376:e066452. doi: 10.1136/bmj-2021-066452
63.
DeaneKDDemoruelleMKKelmensonLBKuhnKANorrisJMHolersVM. Genetic and environmental risk factors for rheumatoid arthritis. Best Pract Res Clin Rheumatol. (2017) 31:3–18. doi: 10.1016/j.berh.2017.08.003
64.
PhilippouEPeterssonSDRodomarCNikiphorouE. Rheumatoid arthritis and dietary interventions: systematic review of clinical trials. Nutr Rev. (2021) 79:410–28. doi: 10.1093/nutrit/nuaa033
65.
CiaffiJMitselmanDMancarellaLBrusiVLisiLRuscittiPet al. The effect of ketogenic diet on inflammatory arthritis and cardiovascular health in rheumatic conditions: a mini review. Front Med. (2021) 8:792846. doi: 10.3389/fmed.2021.792846
66.
BadshaH. Role of diet in influencing rheumatoid arthritis disease activity. Open Rheumatol J. (2018) 12:19–28. doi: 10.2174/1874312901812010019
67.
van BoheemenLBoltJWter WeeMMde JongHMvan de SandeMGvan SchaardenburgD. Patients’ and rheumatologists’ perceptions on preventive intervention in rheumatoid arthritis and axial spondyloarthritis. Arthritis Res Ther. (2020) 22:217. doi: 10.1186/s13075-020-02314-9
Summary
Keywords
anti-inflammatory diet, autoimmune disease, gut microbiome, inflammation, Mediterranean diet, pre-clinical RA, Rheumatoid Arthritis
Citation
Karadimova-Watts MVM, Philippou E and Nikiphorou E (2026) Can nutrition prevent the onset of Rheumatoid Arthritis? A mini review of dietary risk and progression from pre-clinical autoimmunity. Front. Nutr. 13:1864271. doi: 10.3389/fnut.2026.1864271
Received
24 April 2026
Revised
22 September 2026
Accepted
05 October 2026
Published
26 October 2026
Volume
13 – 2026
Edited by
Zhenhuan Zhao, Hubei University of Technology, China
Reviewed by
Yuqun Xie, Hubei University of Technology, China
Rhea Hu, University of Otago, New Zealand
Updates
Copyright
© 2026 Karadimova-Watts, Philippou and Nikiphorou
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
†
ORCID: Maria V. M. Karadimova-Watts, orcid.org/0009-0009-7055-1426; Elena Philippou, orcid.org/0000-0003-0300-9572; Elena Nikiphorou, orcid.org/0000-0001-6847-3726
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher
