Продукты питания при ревматизме — практические советы по пит

Kapitel in Buch

Ernährungspyramide S. 1106 entspricht nicht konsequent den gewonnenen Erkenntnissen, sondern bringt v.a. eine Abschwächung der schädlichen Faktoren.

Omega-3 fatty acids are immunoregulatory. Vitamin D has multiple immunosuppressive effects. Antioxidants can be acquired through the diet. Adipose tissue is metabolically active and has effects on the inflammatory response.

Importance of the Balance of n-3 and n-6 Fatty Acids in the Inflammatory Process The balance of AA and EPA can be altered through dietary fatty acid intake.

Production of reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, are part of the normal immune response. Acting through transcription factors such as NF-κB, ROS increase production of proinflammatory eicosanoids and cytokines, including PGE2, TNF, and IL-1β. Thus unchecked production of ROS may cause inflammation and tissue damage. Antioxidant enzymes such as superoxide dismutase and glutathione peroxidase remove superoxide, thereby providing protection from oxidative damage. Vitamin C (ascorbic acid), vitamin E (α-tocopherol), and β-carotene are acquired through the diet and can act as ROS scavengers.

Obesity might affect disease activity and outcomes in RA. Increased BMI predisposes to gout. Obesity is associated with knee osteoarthritis (OA). Direct biomechanical effects of obesity contribute to OA. Increased leptin provides another link between obesity and OA.

Trotzdem ist das Fazit verhalten: Omega-3 fatty acids modestly reduce disease activity and NSAID requirements. There is no evidence for the benefit of antioxidants in the management of RA. Fasting, vegetarian/vegan, and elimination diets are difficult to sustain, and it is difficult to predict which patients may respond

DOI: 10.1016/B978-0-323-31696-5.00068-1

Book: moderate evidence

Narratives Review

Effects of Dietary Cholesterol and Egg Intake on Lipoprotein Metabolism and Immune Inflammation

Diets rich in cholesterol appear to have the capacity to regulate immune function through modulation of cellular cholesterol levels and lipoprotein metabolism . The effects of dietary cholesterol and cholesterol-rich foods, specifically eggs, on plasma lipids have been reviewed by Blesso and Fernandez ; thus, the following sections focus on the effects of dietary cholesterol on immunomodulatory lipid pathways. In interpreting these findings, it is important to note that human studies evaluating the effects of dietary cholesterol often use whole eggs as the intervention treatment. Eggs are considered to be a rich source of dietary cholesterol, providing approximately 186 mg of cholesterol per large egg.

Rheumatoid Arthritis

RA is a chronic autoimmune disorder characterized by severe joint inflammation and damage. Activated T lymphocytes are found within synovial joint fluid from RA patients, yet they exhibit impaired TCR responsiveness and proliferative capacity [87,88]. Proinflammatory HDL and reduced HDL-mediated cholesterol efflux has additionally been observed in RA patients [94,181,182,183], whereas RA treatment improves markers of HDL function [184] and increases PBMC mRNA ABCA1 expression [185]. Increases in HDL-cholesterol have additionally been associated with improvements in radiographic hand osteoarthritis [186]. However, it is unclear whether cholesterol metabolism or lipid raft formation is modified within activated T cell populations, or whether cholesterol-rich diets can directly modulate HDL dysfunction and T lymphocyte activity in joint tissues of RA patients [24,101]. Interestingly, dietary regimens that are low in cholesterol or cholesterol-free—including medically supervised fasting (7–10 days), vegan diets, and lactovegetarian diets—have been shown to reduce inflammation and improve clinical measures of RA [187]. Hafström et al. [171] demonstrated that a greater percentage of RA patients following a gluten-free vegan diet for at least nine months exhibited clinical improvement according to the American College of Rheumatology 20 (ACR20) criteria, as compared to patients consuming a non-vegan diet. Patients following a 4-week, very low-fat diet (10%) vegan diet additionally experienced improved RA symptoms, including a reduction in pain, joint swelling, and joint mobility [172]. Vegan and vegetarian diets have further been shown to reduce total cholesterol and LDL-cholesterol levels in RA patients [188,189], as well as reduce leukocyte counts and pro-inflammatory CRP [173,174]. Conversely, high cholesterol diets have been shown to exasperate joint inflammation and osteoarthritis development in APOE*3Leiden.CETP mice, potentially due to cholesterol-induced inflammation and joint cartilage degradation [28,190,191]. These findings suggest that dietary cholesterol restriction improves RA outcomes, yet further research is warranted to elucidate the mechanisms by which this occurs.

DOI: 10.3390/nu10060764

Study: weak evidence

Narratives Review

Effects of Dietary Cholesterol from Egg Intake on LDL-C, HDL-C, and the LDL-C/HDL-C Ratio

Berger et al. [29] examined the serum lipid responses to dietary cholesterol across 19 intervention trials. Dietary cholesterol intake, which came mostly from eggs, was shown to significantly increase both serum LDL-C (6.7 mg/dL net change) and HDL-C (3.2 mg/dL net change), resulting in only a marginal increase in the LDL-C/HDL-C ratio (0.17 net change) [29]. Using the LDL-C/HDL-C ratio may provide an estimate of how much cholesterol is delivered to plaques via LDL, as well as potentially how much is being removed by HDL [47]. An LDL-C/HDL-C ratio <2.5 is considered optimal based on individual lipoprotein recommendations, while evidence suggests there is an increase in the risk for cardiovascular events above this level in some populations . Table 1 summarizes results from clinical studies examining the effects of added dietary cholesterol via egg intake on serum lipids during weight maintenance in healthy and hyperlipidemic populations. In children and adults with normal cholesterol levels, consumption of 2–4 eggs per day vs. yolk-free egg substitute significantly increased both LDL-C and HDL-C in most studies, with no change in the LDL-C/HDL-C ratio . Healthy men who were classified as hyper-responders (15 out of 40 participants) did show a significant increase in the LDL-C/HDL-C ratio with the consumption of three eggs per day for 30 days, however, the mean ratio (2.33 ± 0.80) was still within the optimal range of <2.5 [45]. Similar responses were observed in hyperlipidemic adults; consuming two eggs per day resulted in elevated HDL-C without a change in LDL-C in hypercholesterolemic adults, while there was an increase in both LDL-C and HDL-C in combined hyperlipidemics (elevated serum cholesterol and triglycerides) [49]. In older adults taking statins, consuming either two or four eggs per day did not significantly increase LDL-C, whereas HDL-C was increased with both doses of eggs.

DOI: 10.3390/nu10040426

Study: weak evidence

prospektive Kohortenstudie

Importance  Cholesterol is a common nutrient in the human diet and eggs are a major source of dietary cholesterol. Whether dietary cholesterol or egg consumption is associated with cardiovascular disease (CVD) and mortality remains controversial.

Objective  To determine the associations of dietary cholesterol or egg consumption with incident CVD and all-cause mortality.

Design, Setting, and Participants  Individual participant data were pooled from 6 prospective US cohorts using data collected between March 25, 1985, and August 31, 2016. Self-reported diet data were harmonized using a standardized protocol.

Exposures  Dietary cholesterol (mg/day) or egg consumption (number/day).

Main Outcomes and Measures  Hazard ratio (HR) and absolute risk difference (ARD) over the entire follow-up for incident CVD (composite of fatal and nonfatal coronary heart disease, stroke, heart failure, and other CVD deaths) and all-cause mortality, adjusting for demographic, socioeconomic, and behavioral factors.

Results  This analysis included 29 615 participants (mean [SD] age, 51.6 [13.5] years at baseline) of whom 13 299 (44.9%) were men and 9204 (31.1%) were black. During a median follow-up of 17.5 years (interquartile range, 13.0-21.7; maximum, 31.3), there were 5400 incident CVD events and 6132 all-cause deaths. The associations of dietary cholesterol or egg consumption with incident CVD and all-cause mortality were monotonic (all P values for nonlinear terms, .19-.83). Each additional 300 mg of dietary cholesterol consumed per day was significantly associated with higher risk of incident CVD (adjusted HR, 1.17 [95% CI, 1.09-1.26]; adjusted ARD, 3.24% [95% CI, 1.39%-5.08%]) and all-cause mortality (adjusted HR, 1.18 [95% CI, 1.10-1.26]; adjusted ARD, 4.43% [95% CI, 2.51%-6.36%]). Each additional half an egg consumed per day was significantly associated with higher risk of incident CVD (adjusted HR, 1.06 [95% CI, 1.03-1.10]; adjusted ARD, 1.11% [95% CI, 0.32%-1.89%]) and all-cause mortality (adjusted HR, 1.08 [95% CI, 1.04-1.11]; adjusted ARD, 1.93% [95% CI, 1.10%-2.76%]). The associations between egg consumption and incident CVD (adjusted HR, 0.99 [95% CI, 0.93-1.05]; adjusted ARD, −0.47% [95% CI, −1.83% to 0.88%]) and all-cause mortality (adjusted HR, 1.03 [95% CI, 0.97-1.09]; adjusted ARD, 0.71% [95% CI, −0.85% to 2.28%]) were no longer significant after adjusting for dietary cholesterol consumption.

Conclusions and Relevance  Among US adults, higher consumption of dietary cholesterol or eggs was significantly associated with higher risk of incident CVD and all-cause mortality in a dose-response manner. These results should be considered in the development of dietary guidelines and updates.

DOI: 10.1001/jama.2019.1572

Study: moderate evidence

Narratives Review

Traditionally considered an episodic crystal-induced arthritis, gout is now increasingly recognized as a disease with underlying dysregulation of innate immune memory mechanisms. Growing evidence supports the central hypothesis of this review: that trained immunity, defined as persistent epigenetic and metabolic reprogramming of innate immune cells, plays a critical role in gout pathogenesis and progression, contributing to heightened inflammatory responsiveness even in the presence of urate-lowering therapy (ULT). Understanding these mechanisms opens new therapeutic opportunities by directly targeting the maladaptive immune memory that sustains chronic inflammation [10].

Up to this date, observational studies have demonstrated that innate immune cells can undergo epigenetic, transcriptional, and metabolic reprogramming resulting in a heightened and sustained response to future triggers/stimuli [14–16]. Metabolism and epigenetics serve as fundamental pillars of trained immunity, engaging in a dynamic and reciprocal interplay [17]. Altered metabolic pathways not only provide the energy and biosynthetic precursors for immune activation but also generate key metabolites, such as acetyl-CoA and fumarate, which directly modify the epigenetic landscape by influencing histone acetylation and methylation, thereby regulating pro-inflammatory gene expression [18]. Consequently, recent research increasingly implicates these interconnected pathways in gout and related rheumatic diseases [10].

Despite the growing interest in trained immunity and immune modulation, it is important to emphasize that hyperuricemia remains the essential upstream driver of gout. The innate immune cascade cannot be activated in the absence of elevated uric acid levels, as no MSU crystals form in normouricemic conditions. Therefore, ULT remains the cornerstone of gout management. In parallel with therapies targeting immune pathways, ongoing research into novel agents that modulate uric acid synthesis, renal excretion, and metabolism, including xanthine oxidase inhibitors, uricosurics, recombinant uricase, and newer dual-mechanism agents, offers additional opportunities for comprehensive disease control.

DOI: 10.37349/emd.2025.1007103

Study: weak evidence

Narratives Review

The gut microbiota plays a crucial role in chronic inflammation associated with HUA. Dysbiosis increases intestinal permeability, which promotes the translocation of bacteria or their products, such as lipopolysaccharide (LPS), into the bloodstream[8]. High serum levels of LPS induce chronic inflammation, thus increasing the risk of HUA[19]. This information on the underlying mechanisms can provide insights into the complexity of HUA and the potential for targeted interventions[20].

Singh AK, Durairajan SSK, Iyaswamy A, Williams LL. Elucidating the role of gut microbiota dysbiosis in hyperuricemia and gout: Insights and therapeutic strategies. World J Gastroenterol 2024; 30(40): 4404-4410 [PMID: 39494101 DOI: 10.3748/wjg.v30.i40.4404]

Gout treatment is complex, with the main challenges related to low rates of urate-lowering therapy initiation and continuation, along with the side effects of traditional drugs. These side effects include gastrointestinal toxicity, tolerance, allopurinol hypersensitivity syndrome, nephrotoxicity, and contraindications in patients with other prevalent comorbid conditions[34-36]. About 40% of gout patients are affected by chronic kidney disease and a decrease in glomerular filtration rate[37]. Even the use of NSAIDs, colchicine, and uricosuric medications has limitations[38]. Therefore, safer treatment methods that can effectively intervene in gout development are urgently needed.

Singh AK, Durairajan SSK, Iyaswamy A, Williams LL. Elucidating the role of gut microbiota dysbiosis in hyperuricemia and gout: Insights and therapeutic strategies. World J Gastroenterol 2024; 30(40): 4404-4410 [PMID: 39494101 DOI: 10.3748/wjg.v30.i40.4404]

Several important directions for future research and development have emerged. A well-designed human clinical trial is needed to evaluate the efficacy of microbiome-targeted interventions for treating gout with respect to their effect on clinically relevant endpoints, UA, and inflammation. Personalized treatment strategies for gout based on the makeup of the microbiome of each person should be developed using the capabilities of high-throughput sequencing and machine-learning tools for deducing microbial signatures associated with susceptibility to gout or response to treatment. Future research should focus on elucidating the complex relationships between the gut microbiome and gout pathogenesis, particularly examining specific metabolites and signaling pathways involved in microbiota-host interactions related to UA metabolism and inflammation. Microbiome studies offer promising avenues for developing novel therapeutic agents, including designer probiotics, UA degradation methods, and targeted prebiotics that selectively promote beneficial bacteria growth. In the future, microbiome data analysis and other omics technologies need to be combined to gain deeper insights into the systemic effects of gut microbiota dysbiosis in gout patients.

Singh AK, Durairajan SSK, Iyaswamy A, Williams LL. Elucidating the role of gut microbiota dysbiosis in hyperuricemia and gout: Insights and therapeutic strategies. World J Gastroenterol 2024; 30(40): 4404-4410 [PMID: 39494101 DOI: 10.3748/wjg.v30.i40.4404]

DOI: 10.3748/wjg.v30.i40.4404

Study: weak evidence

Klinische Beobachtungsstudie mit cross-sectional design (Querschnittsstudie)

Camilla et al. highlighted that WHO projections suggest that gout mortality may increase by 55% by 2060.

Hyperuricemia represents the primary risk factor for gout. However, epidemiological studies indicate that the majority of individuals with hyperuricemia remain asymptomatic throughout their lifetime; only approximately 10% progress to clinically evident gout (14). One-third of patients have normal SUA levels during acute flares of gouty arthritis. Interestingly, the proportion of MSU deposits in patients with early clinical gout (one or two joint flares) seems similar to that in asymptomatic hyperuricemic patients according to ultrasound scans (15). Thus, it is difficult to predict gout attack by monitoring the uric acid level or deposits of MSU crystals, and more factors that have not yet been studied should be considered.

An increasing number of studies have shown that the gut microbiota may modulate local immune responses in mice and that the human gut microbiota is linked to inflammatory cytokine production (20, 21). However, few studies have examined the association between the gut microbiota and hyperuricemia in humans.

DOI: 10.3389/fendo.2025.1643566

Study: moderate evidence

Narratives Review

Today, gout and hyperuricemia are recognized as systemic metabolic disorders associated with a range of comorbidities, including cardiovascular diseases, chronic kidney disease, metabolic syndrome, and hepatic steatosis. These associated conditions, if left unaddressed, can significantly impact the patient quality of life and long-term health outcomes. Thus, the effective management of gout necessitates a comprehensive approach that considers the underlying metabolic disturbances and comorbid conditions, rather than focusing solely on joint pain management.

...and discuss the clinical implications for optimizing patient care. In doing so, we highlighted the need for a holistic approach that addresses both gout itself and its broader health impacts.

Hyperuricemia does not necessarily lead to gout. It has been reported that only up to 36% of hyperuricemic individuals develop gout attacks [22].

Many pharmacologic agents influence SUA levels. The drugs that increase SUA levels include diuretics (particularly thiazide diuretics), low-dose aspirin, nicotinic acid, testosterone, xylitol, the anti-tubercular drugs pyrazinamide and ethambutol, and some immunosuppressants, such as ciclosporin, tacrolimus, and mizoribine [80]. Cytotoxic chemotherapy may induce tumor lysis syndrome, which leads to an increase in SUA levels due to the massive breakdown of tumor cells [81]. Tumor lysis syndrome has also been reported following treatment with dexamethasone, zoledronic acid, thalidomide, bortezomib, rituximab, and ibrutinib [82].

Several drugs prescribed for indications other than treating hyperuricemia decrease the SUA levels. These include losartan, calcium channel blockers, high-dose aspirin, leflunomide, statins, fenofibrates, sodium glucose co-transport 2 (SGLT2) inhibitors, and estrogen [83].

Dietary modifications should also be considered. Patients with gout and hyperuricemia should be advised to limit purine-rich foods, such as red meats, seafood, and legumes, and to avoid sugar-sweetened drinks and foods rich in fructose. Alcohol avoidance should be encouraged as well.

DOI: 10.3390/jcm13247616

Study: weak evidence

Querschnittsstudie (cross-sectional study) in einer Kohortenstudie

Results: This cohort included 211 RA patients: D2TRA-PIRRA (n=32), DT2RA-NIRRA (n=34), non-D2TRA (n=145). At least one EULAR comorbidity was present in 46% of patients (range 0 to 4). The most represented EULAR comorbidities were cardiovascular diseases (29.5%), osteoporosis (19.5%) and gastrointestinal diseases (8.0%). The number of EULAR comorbidities was similar across groups (p=0.581 by Kruskal-Wallis test), and it was moderately correlated with age at RA onset (r=0.439, p<0.0001). When separately analyzing each comorbidity, there were no significant differences yet a numerical increase in the prevalence of gastrointestinal diseases (15.6% vs 7.3% vs 0.0%, p=0.162) and serious infections (12.5% vs 6.0% vs 5.9%, p=0.328) in D2TRA-PIRRA compared to D2TRA-NIRRA and non-D2TRA patients (Figure 1A). With regard to comorbidities not encompassed in the EULAR domains, fibromyalgia was highly prevalent among D2TRA-NIRRA (23.5%) compared to DT2-RAPIRRA (3.1%) and non-D2TRA (2.7%) patients (p<0.0001; Figure 1A). Extra-articular manifestations were recorded in 27.2% of non-DT2RA, 25.0% of DT2RA-PIRRA and 17.62% of DT2RA-NIRRA (p=0.787), without significant differences in single manifestations. DT2RA-PIRRA patients had numerically more serositis, inflammatory eye disease, and interstitial lung disease than non-D2TRA, while D2TRA-NIRRA patients only showed features of serositis and Sjogren's syndrome (Figure 1B).

DOI: 10.1136/annrheumdis-2023-eular.1864

Study: moderate evidence

Book: strong evidence

Book: strong evidence

Narratives Review

Siehe Tabelle S. 4: Although findings are inconsistent, some studies suggest that fish or fish oil intake decreases the risk of RA, mostly due to long-chain n-3 polyunsaturated fatty acids (PUFAs) content [102–104]. Especially long-term intake of more than 0.21 g/day long-chain n-3 PUFAs was associated with a decreased risk of developing RA [105]. As the estimated dietary intake of n-3 PUFAs may not correlate with their plasma levels, the percentage of long-chain n-3 PUFAs in erythrocyte membranes may serve as a surrogate measure [106]. Higher erythrocyte membrane content of n-3 PUFAs was associated with a lower prevalence of anti-CCP antibodies and RF in subjects at risk for RA and a lower risk of transition from anti-CCP positivity to inflammatory arthritis [107–109]. However, in a large prospective cohort study, no association between n-3 PUFAs, but a significant inverse association with n-6 PUFA linoleic acid levels and risk of RA was described [110]. Other foods are considered in association with the risk of RA, although findings are inconsistent as well. Moderate alcohol intake [111,112], fruit and vitamin C [113], olive oil, cooked vegetables [114], mushrooms, beans, poultry, and dairy products [115] are considered protective in RA. The protective effect of alcohol intake was included in the risk calculation formula of RA development [116]. Interestingly, an inverse relationship between the presence of RA and the consumption of alcohol at or before disease onset was predominantly confined to ACPApositive RA, while a non-significant association was observed for ACPAnegative RA [117]. The possible mechanisms for the protective effect of alcohol are via attenuation of the innate inflammatory response shown in vitro and in vivo or via intrinsic corticosteroid production [112,118–120].

DOI: 10.1016/j.autrev.2021.102797

Study: weak evidence

Bidirektionale Mendelian Randomisation (MR)-Analyse basierend auf grossen GWAS-Datensätzen

A recent observational study suggested that excessive SFA intake might trigger inflammation and muscle degradation in patients with RA, possibly leading to sarcopenia and inflammatory processes. The American College of Rheumatology dietary guidelines for RA recommend a Mediterranean diet with limited SFA intake. Nevertheless, given the extant controversies and inherent biases in observational research methodologies, it is imperative to rigorously assess the causative implications of SFAs for RA.

DOI: 10.3389/fnut.2024.1337256

Study: weak evidence

Querschnittsstudie (cross-sectional study) innerhalb einer grossen Kohorte

Results: A total of 1,388 participants (mean age 61.3 years, 57.4% women) were included in the study, of whom 72 had symptomatic hand OA (prevalence of symptomatic hand OA 5.2%). Beta-diversity of the gut microbiome, but not α-diversity, was significantly associated with the presence of symptomatic hand OA (P = 0.003). Higher relative abundance of the genera Bilophila and Desulfovibrio as well as lower relative abundance of the genus Roseburia was associated with symptomatic hand OA. Most functional pathways (i.e., those annotated in the KEGG Ortholog hierarchy) that were observed to be altered in participants with symptomatic hand OA belonged to the amino acid, carbohydrate, and lipid metabolic pathways.

Conclusion: This large, population-based study provides the first evidence that alterations in the composition of the gut microbiome were observed among study participants who had symptomatic hand OA, and a low relative abundance of Roseburia but high relative abundance of Bilophila and Desulfovibrio at the genus level were associated with prevalent symptomatic hand OA. These findings may help investigators understand the role of the microbiome in the development of symptomatic hand OA and could contribute to potential translational opportunities.

DOI: 10.1002/art.41729

Study: moderate evidence

Querschnittsstudie (cross-sectional observational study)

Results. CC were most common in FM, followed by SLE. FM comorbidity was dominated by depression, mental illness, and symptom-type comorbidity (e.g., gastrointestinal and genitourinary disorders). In SLE, there were substantial increases in hypertension, depression, cataract, fractures, and cardiovascular and cerebrovascular, neurologic, lung, gall bladder and endocrine disorders compared with RA. Any current CC reduced the EQ-5D utility by 0.08 to 0.16 units. The lowest EQ-5D score was noted for current psychiatric illness (0.55) and current depression (0.60). Conclusion. Four patterns of comorbidity emerged: that associated with aging; that associated with aging but enhanced by the index condition, as in SLE and cardiovascular disease; comorbidity that is part of the symptoms complex of the index condition; and CC that represent lifetime traits or manifestations of the underlying illness. Depression was the most strongly associated correlate of EQ-5D quality of life, and current depression was present in about 15% of patients with RA or NIRD and 34% to 39% of those with SLE and FM. (First Release January 15 2010; J Rheumatol 2010; 37:305–15; doi:10.3899/jrheum.090781).

DOI: 10.3899/jrheum.090781

Study: moderate evidence

Prospektive Kohortenstudie

her population samples. In this prospective observational study, we have found no strong evidence to suggest that increased dietary intake of antioxidant nutrients protects against the incidence of knee OA. Knee OA progression, however, and the development of knee pain, appears to be reduced in people with high intakes of vitamin C and possibly other antioxidants. The possibility that dietary modification might contribute to the secondary prevention of this public health problem requires further investigation.

DOI: 10.1002/art.1780390417

Study: moderate evidence

Narratives Review

The most important bioactive chemical constituents of turmeric are curcuminoids, including curcumin, demethoxycurcumin and bis-demethoxycurcumin, which are extracted from the rhizome of the herb Curcuma longa which belongs to the Zingiberaceae family. The best known, curcumin, is a hydrophobic polyphenol which, thanks to its antioxidant and anti-inflammatory properties, seems to be effective in the prevention of various pathologies, including autoimmune and inflammatory ones, going to interact with numerous molecular targets.

Curcumin, in particular, has shown an interesting preventive effect, proving effective in the prevention of RA. In vitro, curcumin showed antiproliferative and anti-inflammatory action in fibroblast-like synoviocytes in rheumatoid arthritis (RA-FLS) inducing apoptosis and causing inhibition of COX-2 pathways leading to the production of prostaglandin E2 (PGE2). Furthermore, the exposure of RA-FLS to curcumin led to the decrease of cytokines and growth factors, such as Interleukin-6 (IL-6) and the growth factor of the vascular endothelium and the deactivation of the nuclear factor kB (NF-kB). The influence of curcumin on specific signal transduction pathways is therefore an interesting point, because the activation of these pathways can alter the threshold for immune activation in rheumatoid arthritis. In animal model studies, curcumin has been shown to increase anti-inflammatory cytokines, reduce pro-inflammatory cytokines and activate the antioxidant defense system.

DOI: 10.1016/j.clnu.2020.08.020

Study: weak evidence

Narratives Review

High fat consumption can cause excessive accumulation of triglycerides, inducing increased fat mass and obesity. It has been reported that overweight/obesity was connected with 60% of hyperuricemia cases in a clinical trial of 14,624 adults [70], possibly due to lipid metabolic disorder promoting purine metabolism by elevating XO activity [71].

Sugar-sweetened beverages containing high-fructose corn syrup and sucrose or almost equal amounts of fructose and glucose, which account for approximately one-third of added sugar consumption in the diets of American adults [80], have been thought to be closely connected with a high prevalence of hyperuricemia in Western countries [81]. Long-term high sugar consumption has been found to accelerate the accumulation of uric acid and promote MSU deposition in fly renal tubules, suggesting that a similar problem may occur in human excretory systems under dietary challenges [82]. In a follow-up study of 650 participants, the results confirmed that a high-sugar diet participates in kidney dysfunction and uric acid metabolism disorders [82].

For example, the plasma concentrations of vitamin C saturation ranges daily from 200 to 400 mg, implying that exceeding the recommended supplemental dose has little effect on the consequences [120]. More importantly, taking high-dose and long-term supplements of vitamin C may be associated with adverse effects, and the resulting excessive uric acid excretion could elevate the risk of kidney stones in gouty patients [121,122].

The typical dietary patterns include a DASH and Mediterranean diet, both of which are comprised of fruits, vegetables, and low-fat dairy products with reductions in total and saturated fats. Increasing evidence supports that consuming a DASH diet can continuously attenuate SUA in hyperuricemia patients and reduce the incidence of gout in participants [34,45]. Similar SUA-lowering effects have been observed in a research investigations of the Mediterranean diet [58]. Moreover, intervention with the DASH diet combined with adequate sodium and plant-derived protein shows more beneficial functions in reducing SUA levels [33,37].

Therefore, our recommendation is for individuals to follow a healthy diet for prevention purposes, and for patients with mild gout, we recommend the DASH and Mediterranean diet, which focus on plant-based components. Additionally, we recommend a reduction in the consumption of high-fat foods (fast food and cream products), especially foods with trans fatty acids (such as margarine and butter), and for individuals to pay attention to the amount of nutrient supplements consumed. For patients with severe gout, dietary modification and medication should be combined, and health care providers should remind patients of food–drug interactions to achieve synergistic effects.

DOI: 10.3390/nu14173525

Study: weak evidence

Narratives Review

Excessive consumption of products with high fructose content can cause hyperuricemia and gout. In addition, the increase in uric acid resulting from excessive consumption of fructose, and overall and sustained high serum uric acid levels have been shown to cause various disorders that will give rise to metabolic syndrome. In this review, the interwoven relationships between hyperuricemia—an increase in serum uric acid levels—and the resulting gout, as well as metabolic syndrome, and the role excessive fructose consumption plays in these, have been investigated.

Alcohol, fructose-sweetened foods and beverages, and purine-rich foods are dietary factors that cause an increase in uric acid levels.

Metabolic syndrome is a condition related to type 2 diabetes, hypertension, dyslipidemia, and abdominal obesity. Cardiovascular diseases and NAFLD are also associated with metabolic syndrome. It is stated that the prevalence of gout and metabolic syndrome increases in parallel with each other.40

DOI: 10.5152/cjm.2024.24001

Study: weak evidence

Narratives Review

Consumption, and Metabolic Syndrome Metabolic syndrome is a condition related to type 2 diabetes, hypertension, dyslipidemia, and abdominal obesity. Cardiovascular diseases and NAFLD are also associated with metabolic syndrome. It is stated that the prevalence of gout and metabolic syndrome increases in parallel with each other.40

DOI: 10.1016/j.autrev.2018.05.009

Study: weak evidence

Mendelian Randomization (MR)-Studie mit genetischen Daten

Although many studies have found an association between other factors such as vitamin supplementation, appropriate coffee citation, and improvement in IA disease activity, the fact that our study did not find a causal association cannot be excluded from being related to the insufficient sample size for the inclusion of several exposure factors of interest in the study, suggesting that the sample size should be continued to be expanded in the future to obtain more stable results.

It also identifies causal relationships between several dietary modalities and different types of IA. These findings have significant implications for the prevention and management of IA through dietary modification.

Unhealthy diets, such as those high in sugar, salt, trans fats, and ultra-processed foods, can lead to imbalances in the gut microbiota, increased oxidative stress, and activation of inflammatory genes. In addition, vitamin and mineral deficiencies and insufficient intake of omega-3 fatty acids have also been linked to inflammation. Healthy eating habits, such as increased intake of fruits, vegetables, and fiber-rich foods, may help to reduce inflammation (41) and may also assist in regulating gut microbiota diversity and stability to prevent disease (42).

IA, a major disease characterized by a long-term chronic inflammatory state, has become increasingly prevalent in recent years, and the identification of modifiable risk factors (e.g., dietary factors) is an achievable way to halt the onset and progression of this type of disease. To overcome the problem of the low inclusion of dietary factors and the homogeneity of the diseases studied in previous studies, we conducted this comprehensive study to assess the causal relationship between several dietary factors (cereals, bread, vegetables and fruits, meat and fish, beverages, dairy products, salt, vitamins, minerals) and IA.

DOI: 10.3389/fnut.2024.1426125

Study: weak evidence

Narratives Review

Developed societies, although having successfully reduced the burden of infectious disease, constitute an environment where metabolic, cardiovascular, and autoimmune diseases thrive. Living in westernized countries has not fundamentally changed the genetic basis on which these diseases emerge, but has strong impact on lifestyle and pathogen exposure. In particular, nutritional patterns collectively termed the “Western diet”, including high-fat and cholesterol, high-protein, high-sugar, and excess salt intake, as well as frequent consumption of processed and ‘fast foods’, promote obesity, metabolic syndrome, and cardiovascular disease. These factors have also gained high interest as possible promoters of autoimmune diseases. Underlying metabolic and immunologic mechanisms are currently being intensively explored. This review discusses the current knowledge relative to the association of “Western diet” with autoimmunity, and highlights the role of T cells as central players linking dietary influences to autoimmune pathology.

DOI: 10.1007/s11882-013-0404-6

Study: weak evidence

Narratives Review

As current treatment options in OA are very limited, OA patients would benefit greatly from some ability to self-manage their condition. Since diet may potentially affect OA, we reviewed the literature on the relationship between nutrition and OA risk or progression, aiming to provide guidance for clinicians. For overweight/obese patients, weight reduction, ideally incorporating exercise, is paramount. The association between metabolic syndrome, type-2 diabetes and OA risk or progression may partly explain the apparent benefit of dietary-lipid modification resulting from increased consumption of long-chain omega-3 fatty-acids from oily fish/fish oil supplements. A strong association between OA and raised serum cholesterol together with clinical effects in statin users suggests a potential benefit of reduction of cholesterol by dietary means. Patients should ensure that they meet the recommended intakes for micronutrients such as vitamin K, which has a role in bone/cartilage mineralization. Evidence for a role of vitamin D supplementation in OA is unconvincing.

DOI: 10.1093/rheumatology/key011

Study: weak evidence

Narratives Review

Despite gout being one of only a few ‘curable’ rheumatic diseases (through the use of pharmacological urate-lowering therapies (ULTs)), management of the disease is inadequate in many parts of the world, owing to low uptake of ULT and patient adherence to these medications.

It is difficult to estimate the global occurrence of gout accurately owing to a lack of data for many countries and the highly variable prevalence estimates across different geographical regions and populations that are obtained using different disease definitions (Fig. 1; Table 1). A gout diagnosis should ideally be based on classification criteria or the demonstration of monosodium urate crystals in aspirated joint fluid or tophi, but most studies rely on self-reported diagnosis or identification of diagnostic codes or prescription of gout-specific medication in medical registries, which are prone to recall or misclassification bias. Underascertainment is possible due to long intercritical periods between flares, individuals not consulting for flares that they self-manage, or when prevalence and/or incidence are measured in Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors Mats Dehlin1, Lennart Jacobsson 1 and Edward Roddy 2,3 ✉ Abstract | Gout is the most common inflammatory arthritis and occurs when hyperuricaemia, sustained elevation of serum urate levels resulting in supersaturation of body tissues with urate, leads to the formation and deposition of monosodium urate crystals in and around the joints. Recent reports of the prevalence and incidence of gout vary widely according to the population studied and methods employed but range from a prevalence of <1% to 6.8% and an incidence of 0.58–2.89 per 1,000 person-years. Gout is more prevalent in men than in women, with increasing age, and in some ethnic groups. Despite rising prevalence and incidence, suboptimal management of gout continues in many countries. Typically, only a third to half of patients with gout receive urate-lowering therapy, which is a definitive, curative treatment, and fewer than a half of patients adhere to treatment. Many gout risk factors exist, including obesity, dietary factors and comorbid conditions. As well as a firmly established increased risk of cardiovascular disease and chronic kidney disease in those with gout, novel associations of gout with other comorbidities have been reported, including erectile dysfunction, atrial fibrillation, obstructive sleep apnoea, osteoporosis and venous thromboembolism. Discrete patterns of comorbidity clustering in individuals with gout have been described. Increasing prevalence and incidence of obesity and comorbidities are likely to contribute substantially to the rising burden of gout. 1Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. 2Primary Care Centre Versus Arthritis, School of Primary, Community and Social Care, Keele University, Keele, UK. 3Haywood Academic Rheumatology Centre, Haywood Hospital, Midlands Partnership NHS Foundation Trust, Stoke-on-Trent, UK. ✉e-mail: e.roddy@keele.ac.uk https://doi.org/10.1038/ s41584-020-0441-1 REVIEWS Nature Reviews | Rheumatology secondary or tertiary care registries rather than primary care where most patients with gout are managed. A 2015 meta-analysis of 71 studies of gout prevalence published between 1962 and 2012 found a pooled global prevalence of 0.6% (95% CI 0.4–0.7%), although there was marked statistical heterogeneity among the included estimates2 .

The importance of hyperuricaemia as a risk factor for the development of gout has been confirmed in recent studies.

As a result, hyperuricaemia alone is insufficient to enable a diagnosis of gout without the presence of typical clinical features or evidence from joint aspiration. Obesity and dietary factors Obesity is an important risk factor for gout and is thought to be a major contributor to the rising prevalence and incidence of gout. 

Although the role of dietary factors in the pathogenesis of gout has been suspected for centuries, supporting epidemiological evidence has only emerged over the past 15 years. Consumption of red meat, seafood and shellfish, fructose, sugar-sweetened soft drinks and alcoholic drinks (particularly beer) increase the risk of incident gout...

Most studies have investigated epidemiological associations between gout and single comorbidities, whereas multiple comorbidities commonly coexist. However, little is known about the associations between these multiple comorbidities. Metabolic syndrome is a constellation of interrelated conditions, including obesity, dyslipidaemia, hypertension and insulin resistance, and is associated with increased risk of atherosclerosis. The prevalence of metabolic syndrome in individuals with gout in a Korean university hospital86 and the US NHANES-III (ref.87) was 51% and 63%, respectively, and the NHANES-III patients with gout had three times the odds of having metabolic syndrome than age-matched and sex-matched controls without gout.

DOI: 10.1038/s41584-020-0441-1

Study: weak evidence

Narratives Review

Rheumatoid arthritis (RA) is a chronic immune-driven inflammatory disease characterised by joint swelling, joint tenderness, destruction of synovial joints and systemic inflammation, ultimately causing severe disability and premature mortality. Early mortality has been largely attributed to an increased rate of cardiovascular (CV) events that is independent of traditional CV risk factors and associated with increased systemic inflammation.

SCFAs are an energy source for gut epithelial cells, having an indirect anti-inflammatory effect by improving the assembly of tight junctions and enhancing intestinal barrier function.

DOI: 10.3390/nu12113504

Study: weak evidence

Narratives Review

In summarizing the mechanisms by which polyphenols targeting the UPS to ameliorate metabolic disorders, the four possible pathways are proposed: lipid metabolism, inflammation, insulin resistance, and oxidative stress. Hence, the relationship between UPS and these four metabolic pathways is comprehensively summarized.

Polyphenols interact the UPS activity. Polyphenolic compounds such as EGCG, curcumin, quercetin, and resveratrol modulate UPS function by either promoting the degradation of proteins indirectly through UPS interactions or directly regulating intracellular proteasome levels.

EGCG modulates the UPS process to regulate lipid metabolism

EGCG modulates the UPS process to exert antioxidative and anti-inflammatory effect

Curcumin modulates the UPS process to improve lipid metabolism and insulin resistance

Curcumin regulates the UPS process to exert anti-inflammatory effects

Quercetin modulates the UPS process to improve lipid metabolism

Quercetin regulates the UPS process to exert anti-inflammatory effects

Resveratrol modulates the UPS process to improve lipid metabolism

Resveratrol regulates the UPS process to show anti-inflammatory and antioxidative effects

Other polyphenols modulates UPS process to protect metabolic disorders

DOI: 10.3389/fnut.2024.1445080

Study: weak evidence

Narratives Review

Rheumatoid arthritis (RA) is a progressive autoimmune disease that leads to severe functional impairment and a significantly reduced quality of life. Recent estimations suggest that the global prevalence of RA is approximately 0.5%. This condition typically manifests as painful and swelling small joints of the hands and feet. The pathogenesis of RA is complex and involves interactions between articular and immune cells. Fibroblast-like synoviocytes (FLSs) are considered to be the major drivers of the development of RA. T cells, which are categorised into several subtypes, among which Th17 cells are highly implicated in the progression of the disease.

According to contemporary studies, eating > 100 g/day of red meat is associated with a 2-year earlier onset of RA [134]. In a study from Kuwait, patients with active RA had markedly higher consumption of red meat, along with butter, soft drinks, and pastries [135]. Even the large USA National Health and Nutrition Examination Survey (NHANES) has seemingly confirmed the detrimental effect of red meat intake on RA: the authors reported a relationship between beef intake and RA prevalence.

DOI: 10.3390/nu16183215

Study: weak evidence

The dietary changes do not reverse joint deformities, but the pain diminishes because the improved diet helps reduce the inflammation in the joints.

At the TrueNorth Health Center, we see many people experience a decrease in their osteoarthritis after changing their diets.

The incidence of arthritis is lower, and the ability to manage it is higher, in places where people consume smaller quantities of animal fat and animal protein than we do in the US. For instance, vegetarian and vegan diets have been shown to decrease arthritis pain and inflammation; even the more moderate Mediterranean diet, characterized by lower consumption of animal products, is associated with a lower risk of rheumatoid arthritis.^[7][8]

A study published in the Lancet supports the contention that diet plays a role in controlling numerous arthritis symptoms.^[9] Compared to a control group, individuals randomized to fast before transitioning to vegan and vegetarian diets for a year showed significant improvement in several measures, including pain score, duration of morning stiffness, health assessment questionnaire, and strength.

If a person suffering from rheumatoid arthritis wants to identify their food sensitivities, the best method is to undertake a period of fasting (ingesting only pure water), followed by a period of rotational feeding. Many arthritis patients have fasted at the TrueNorth Health Center. During the fasting period, it is common for joint pain and swelling to totally disappear.

This pain-free period provides welcome relief, but proper refeeding after the fast is crucial. In fact, there is no point in undertaking a fast if your intention is to revert to your previous way of eating because this behavior is part of the problem (possibly the major part).

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The microbiome isn’t just about digesting food—it’s a master conductor in the orchestra of human health. Trillions of microbes communicate with our immune system, shape our metabolism, and even influence how we think and feel. Far from being passive passengers, these microscopic partners generate metabolites that regulate inflammation, signal through the vagus nerve to the brain, and produce neurotransmitters like serotonin, which governs mood, appetite, and sleep. Increasingly, scientists describe the microbiome as an endocrine organ in its own right through which imbalances can ripple across the body, affecting everything from chronic disease risk to mental well-being.

Immune Modulation
Microbes educate both our innate and adaptive immune systems, helping distinguish harmful pathogens from benign or beneficial ones. This training is foundational to maintaining immune balance and preventing overreactions.

 Studies show that dietary diversity is a strong predictor of microbial diversity, a quality linked to lower rates of inflammation, obesity, and metabolic disease. A diet rich in vegetables, fruits, legumes, whole grains, nuts, and seeds supplies hundreds of distinct phytochemicals and fibers that together shape a more balanced, adaptive microbial community.

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Es ist wahrscheinlich, dass die Quellen nachträglich hinzugefügt wurden, da der Text keine hochgestellten Quellennummern enthält. Somit ist der Bezug zwischen Text und Literaturverzeichnis lose.

Systematische Kommentare über die Rolle der Ernährung und konkret umsetzbare Tipps haben wir im Quellenverzeichnis keine gefunden. Die anwendbarsten Tipps beschränken sich auf eine Auflistung von schädlichen und förderlichen Inhaltsstoffen - oder aber auf die mediterrane Diät, was wir so nicht vollkommen unterstützen können, siehe Text.

Quellen 18 und 22 beleuchten wichtige Zusammenhänge im Detail, geht aber auch nicht in die Praxis der Ernährung. (Quelle 21 ist ein Doppel zu 18)

Quelle 1 informiert über Einzelfakten, Ernährungsfaktoren und Einflüsse auf die Krankheit, ist aber risikenfokussiert und nicht besonders lösungsorientiert.

Quelle 3 zeigt zwar das Problem des leaky guts, diskutiert aber keine konkreten Ernährungsmassnahmen dagegen (streift aber Fecal microbiota transplantation und live biotherapeutics)

Quellen 9 und 17 erwähnen Ernährungsstrategien am Rand, zweitere etwas genauer.

Quelle 14 ist sehr allgemein gehalten und informiert über Ernährung und Entzündungen. Auch Quelle 16 ist sehr allgemein.

Quelle 15 ist leider theoretisch und nicht menschbezogen: In addition, several dietary manipulations can alter the course of SLE, which may be partly mediated by effects on the gut microbiota as hypothesized above. Studies have shown that caloric restriction prevents the progression of lupuslike disease in NZB and (NZB NZW)F1 mice41,42 as well as the SLE-associated antiphospholipid syndrome (APS) in (NZW BXSB)F1 mice.43 Other dietary interventions or factors, such as polyunsaturated fatty acids, vitamins A, D, and E, and phytoestrogens also lead to improved outcome in animal models of SLE, mostly via reduction in proteinuria and glomerulonephritis.44 Furthermore, using two isocaloric diets that differed in their fat composition, Reifen et al. showed that enrichment with n-3 polyunsaturated fatty acids prevents fetal loss and other clinical manifestations of lupus-associated APS.45

Quelle 23 schlussfolgert immerhin: In particular, widespread evidence highlighted the importance of a diet rich in vitamins (mainly A, B₆, C, D and E) and MUFA/PUFA (particularly n-3 PUFA and MUFA) with an adequate fibre intake, protein and Na restriction and moderate energy consumption in reducing co-morbidities and preventing SLE flares, thus minimising unnecessary burden in patients with SLE. It is also remarkable the promising role of dietary polyphenols included in the diet through vegetables, fruits, cereals, legumes and drinks such as tea and wine in the management of SLE. Likewise, it is important to encourage patients to stop smoking, avoid being overweight and optimise their blood pressure, lipid profile, and control of disease activity to decrease cardiovascular morbidity. Den Hinweis auf Wein unterstützen wir nicht.

Quelle 26 zeigt klar positive Effekte von roh-veganer Ernährung, aber an 2 (!) PatientInnen.

Quelle 31 ist seriös recherchiert, deckt sich aber mit unserer Quelle 1 neueren Datums.

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When you are trying to heal your body, all foods that increase inflammation must be avoided. The following three steps focus on three such food groups.

Step 1: Eliminate Animal Products - Details dort

Step 2: Eliminate Added Oils - Details dort

Step 3: Eliminate Processed Foods - Details dort

When I teach this information to my clients, their first question is “how do I get calcium?” They fear that they will weaken their bones without dairy products. Research has shown that dairy products actually cause bone loss; countries that have the highest rates of dairy consumption, like the USA, Canada, Norway, Sweden, Australia, and New Zealand, also have the highest rates of osteoporosis.^[10][11] The lowest rates are among people who eat the fewest animal-derived foods, like natives of rural Asia and rural Africa.^[10][11] These people also have lower overall calcium intake than dairy-consuming cultures do. Calcium is abundant and easy to absorb from green leafy vegetables like kale and broccoli, which come without the risks accompanying dairy products.

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There’s no single known cause for the immune dysregulation associated with more than 80 different autoimmune diseases, but possible triggers include:^[6]

• Poor gut health or leaky gut.
• Excess of stressors from diet, environment, and/or physical and emotional burdens.

For example, elevated levels of immune cells specific to a particular protein in cow’s milk have been discovered in people with type 1 diabetes.^[9] The molecular mimicry theory suggests these proteins are similar to proteins in the pancreas, which causes an immune reaction that targets not only the milk proteins but also pancreatic “self” cells.

Other dietary triggers may be related to foods’ effects on gut health. According to one study, additives in highly processed foods may increase intestinal permeability. This can allow antigens and pathogens to pass out of the gut and into the bloodstream, where immune cells subsequently target and attack them.^[10] Many of these same foods also affect short-chain fatty acid production in the gut, further contributing to permeability and potentially preventing T-reg cells from maturing properly.^[11]

High-sodium diets may also play a role. Salt appears to increase levels of immune cells involved in inflammation and autoimmunity, which makes another case for avoiding highly processed foods.^[12] Eating other proinflammatory foods^[13] like meat, dairy, and processed vegetable oils puts additional stress on the immune system and may make autoimmune diseases worse.

Website

A whole food, plant-based (WFPB) diet in particular may be beneficial in several key areas associated with autoimmunity.

Eliminating the Biggest Offenders

Lowering Inflammation

Healing the Gut

Supporting Immune Health

Specific plant foods contain nutrients and antioxidants to modulate the immune system^[10][11] and support healthy immune responses:

• Carotenoids and flavonoids: brightly-colored vegetables and fruits, especially berries^[12]
• B Vitamins: grains, nuts, seeds, leafy greens, root vegetables, and nutritional yeast
• Vitamin C: bell peppers, oranges, papayas, broccoli, tomatoes^[13]
• General immune support: leafy greens, mushrooms, ginger, garlic, and onions^[14]

Supplementing with high-quality plant-based vitamin D may provide additional support if vitamin D levels are low.

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Randomisierte kontrollierte Studie (RCT)

Dietary manipulation is commonly used among rheumatoid arthritis (RA) patients despite the relative lack of data from controlled studies of these regimens.

This is the first controlled study to demonstrate a long-term (1 yr) effect of a vegan diet free of gluten on signs and symptoms of RA. In addition, a decrease in serum levels of IgG antibodies to gliadin and b-lactoglobulin was selectively recorded in the group of patients who responded positively to the vegan diet.

DOI: 10.1093/rheumatology/40.10.1175

Study: strong evidence

Narratives Review

Flaxseed, hempseed and canola oil are the main sources of ALA.  Nuts and seeds are important sources of ALA and other micronutrients. As for the ALA content of nuts and seeds, 28 g of hempseed or walnuts exceeds the adequate intake for ALA, which is ideally set at 1.1 g/day for women and 1.6 g/day for men. 

Humans evolved on a diet with an omega-6/omega-3 ratio of about 1, while Westerners (e.g., those on Western diets) have a ratio of 15/1–16/1. These diets are deficient in omega-3 fatty acids and contain excessive amounts of omega-6 fatty acids. Excessive amounts of omega-6, including LA, or a very high unbalanced omega-6/omega-3 ratio, promote the pathogenesis of many diseases, including cardiovascular, cancer and inflammatory/autoimmune diseases.

DOI: 10.3390/ijms241814319

Study: weak evidence

Interventionsstudie mit klinischer Beobachtung: 53 Patienten mit Rheumatoider Arthritis (RA).

The beneficial effect of a 1-yr vegetarian diet in RA has recently been demonstrated in a clinical trial. We have analysed stool samples of the 53 RA patients by using direct stool sample gas-liquid chromatography of bacterial cellular fatty acids. Based on repeated clinical assessments disease improvement indices were constructed for the patients At each time point during the intervention period the patients in the diet group were then assigned either to a group with a high improvement index (HI) or a group with a low improvement index (LI). Significant alteration in the intestinal flora was observed when the patients changed from omnivorous to vegan diet. There was also a significant difference between the periods with vegan and lactovegetarian diets. The faecal flora from patients with HI and LI differed significantly from each other at 1 and 13 months during the diet. This finding of an association between intestinal flora and disease activity may have implications for our understanding of how diet can affect RA

Briefly, the study was a 13-month prospective, single-blind, randomized trial. Fifty-three patients (45 women and eight men) with active RA were enrolled in the study. Twenty-seven patients were randomized to a diet group and 26 to a control group. The patients in the diet group spent the first month at a health farm, while the patients in the control group were sent to a convalescent home. For the test group the dietary intervention began with a fast of 7-10 days. The vegan diet period lasted 3.5 months and the lactovegetarian period 9 months. The vegan diet contained no meat, fish, eggs, dairy products, refined sugar, added salt, preservatives, tea, coffee, alcoholic beverages or strong spices. In addition, gluten and citrus fruits were excluded. After the fast a 'new' food item was added to the diet every second day, and if any increase in RA symptoms was observed within 48 h it was omitted for 7 days. If the reintroduction of the food item after 7 days re-exacerbated the symptoms, it was excluded from the diet for the remaining study period (individual adjustment of diet).

Alterations in the intestinal flora will change the antigenic challenge and in turn, this may be of importance for the disease activity in RA. A clinically important change in the faecal flora is not necessarily due to changes of a single or a few bacterial species. It may be due to a combination of changes in a large number of different species, as a response to an environmental factor such as diet. The GLC method readily detects changes, differences or similarities between the fatty acid profiles of the stool samples.

The finding that significant differences in the faecal flora were observed between the HI group and the LI group suggests strongly an association between intestinal bacteria and clinical improvement of RA. Based on this, it is tempting to speculate whether antimicrobials, which usually change faecal flora, might be of use in controlling the disease activity in RA. Further studies within this field are warranted, since, at least, clotrimazole [27, 28], metronidazole [29] and minocyclin [30-32] have been claimed to have some effect in RA.

The early appearance (at 1 month) of the difference in faecal flora between HI and LI groups suggests that the primary change would be in the faecal flora rather than in disease improvement This gives support to the idea that changes in faecal flora may be one of the mechanisms through which certain diets and other factors affect disease activity in RA patients.

DOI: 10.1093/rheumatology/33.7.638

Study: moderate evidence

Narratives Review

Fasting/vegetarian/vegan diet

Exclusion diet

DOI: 10.2147/NDS.S6922

Study: weak evidence

Experimentelle In-vitro-Studie mit humanen Zellen

We found that IL-17 stimulated FLS to produce RANKL and tocotrienol decreased this IL-17-induced RANKL production. Tocotrienol decreased the IL-17-induced activation of mammalian target of rapamycin, extracellular signal-regulated kinase, and inhibitor of kappa B-alpha. When monocytes were incubated with IL-17, RANKL, IL-17-treated FLS or Th17 cells, osteoclasts were differentiated and tocotrienol decreased this osteoclast differentiation. Tocotrienol reduced Th17 cell differentiation and the production of IL-17 and sRANKL; however, tocotrienol did not affect Treg cell differentiation.

Tocotrienol inhibited IL-17- activated RANKL production in RA FLS and IL-17-activated osteoclast formation. In addition, tocotrienol reduced Th17 differentiation. Therefore, tocotrienol could be a new therapeutic choice to treat bone destructive processes in RA.

6 A subsequent study (n = 42) that tested the effects of an uncooked vegan diet rich in lactobacilli in RA patients reported that the uncooked vegan diet decreased subjective symptoms of RA compared to the control group. Moreover, it was reported that large doses of live lactobacilli consumed daily may also have positive effects on objective measures of RA.17 Nevertheless, additional randomized long-term studies are needed to confirm efficacy by improved methodologically convincing data.12

DOI: 10.3904/kjim.2019.372

Study: weak evidence

Narratives Review

Tocotrienols are found in certain cereals and vegetables such as palm oil, rice bran oil, coconut oil, barley germ, wheat germ and annatto [34, 35]. Palm oil and rice bran oil contain particularly higher amounts of tocotrienols (940 and 465 mg/kg, respectively) [36]. Other sources of tocotrienols include grape fruit seed oil, oats, hazelnuts, maize, olive oil, Buckthorn berry, rye, flax seed oil, poppy seed oil and sunflower oil (Fig. 2) [37].

Tocotrienols occur in photosynthetic plants in varying amounts, and the vegetable oils such as sunflower, corn, safflower and cottonseed provide a useful source for these vitamin E forms. 

DOI: 10.1007/s12154-014-0127-8

Study: weak evidence

Narratives Review

In the past, lowered serum concentration of trace micronutrients has been demonstrated as a frequent event in autoimmune diseases. Epidemiological reports proved that a low Se status can be a risk factor for RA, indicating the significance of antioxidants in controlling the maintenance and progression of the disease.

In this study, they reported a meta-analysis from 14 case control studies that included 716 participants and showed significant association between RA and low serum Se concentration.

It has been reported that Se supplementation improves the condition of patients as well as reduces inflammation levels in experimental models, such as the granuloma pouch exudate, and in lupus mice or in the adjuvant arthritis in rats. Evidence has suggested that Se can decrease inflammation in autoimmune disorders. One report revealed that Se supplementation has an antioxidant effect as it upregulates selenoproteins and downregulates inflammation in autoimmune disorders.

DOI: 10.3390/nano11082005

Study: weak evidence

Narratives Review

Food sources of ARA: ARA is found only in animal-derived foods because plants cannot synthesize C-20 LCPUFAs. The main food sources of ARA are meat, poultry, eggs, fish and dairy foods.

This review of dietary surveys of ARA intake indicates that ARA is obtained from a wide variety of animal foods, such as meat, poultry, egg, fish and dairy foods, and that the amount of ARA intake is 100–250 mg/day in advanced counties. Meanwhile, ARA intake may be in the tens of mg/day in developing countries. The review also demonstrates that ARA supplementation (82 or 120 mg/day for 3–4 weeks) at a dose equal to or less than the dietary ARA intake increases plasma ARA composition; that plasma ARA composition is ARA dose-dependently increased in the range of 82–3600 mg/day; and that ARA supplementation decreases plasma LA composition, but not DHA/EPA composition. ARA intake from foods or supplementation is thought to have a great impact on LCPUFA metabolism. The continued accumulation of evidence from large and well-designed dietary surveys and clinical trials is expected to confirm this.

DOI: 10.1186/s12944-019-1039-y

Study: weak evidence

Narratives Review

Humans are host to trillions of microbes that form an ecosystem which is required for the homeostasis of the immune system. Disruption to that ecosystem can cause dysbiosis with abnormal immune system function. Since the gut contains the maximum number of microorganisms, alteration in microbial composition due to environmental factors can disrupt the homeostatic milieu in the gut. It can also provide an opportunity for the expansion of a pathogenic microbe. Subsequently, this could lead to becoming involved in continuous low-grade inflammation, which can easily break tolerance in the event of insult to the immune system. Indeed, preclinical autoreactivity can be present in patients with RA for up to 10 years prior to transitioning from asymptomatic to clinical onset of disease. Smoking has been suggested as one of the factors that can cause preclinical autoreactivity; one can speculate that endogenous factors such as the gut microbiota might play a role in preclinical autoreactivity.

The other examples of the contribution of pathogenic endogenous bacteria include Prevotella copri, which was observed in new-onset RA patients (NORA) [76], and Subdoligranulum didolesgii isolated from at-risk individuals, which was shown to trigger joint swelling, as well as autoantibodies to CII in germ-free mice [77]. The dysbiosis and expansion of pathogenic microbes can increase intestinal permeability, leading to an egress of bacterial products. RA patients harbor antibodies to peptides derived from P. copri [78]. However, the enrichment of genes in P. copri and its function was dependent on the diet, suggesting an impact of diet on microbial composition and functional status [79], which can contribute to the local milieu.

Microbes can have niche-specific effects, and based on the diet, their gene enrichment may define the impact on the immune system, as indicated by the Prevotella genus in RA, where one Prevotella species is associated with RA onset while another is linked to treatment efficacy, as well as suppressing inflammation [17,59,76,81]. Since P. histicola simulates the action of a biologic drug, the use of commensals as probiotics or prebiotics for reducing inflammation is a possibility, as shown by [18,94]. The role of the diet in healthy aging by modulating the diet and the microbiota has been explored in a comprehensive review [2]. An epigenome–microbiome axis will show that genetic factors and microbial diversity interact. An individual with disease-susceptible genes might harbor certain opportunist commensals which in healthy conditions behave normally, but under certain circumstances such as stress or infections, can expand, resulting in microbial/metabolic dysbiosis.

Generally, investigative research is very focused, thus interactions among various genes and their functions in various organs are bound to be missed. Though genome sequencing can provide genetic associations with diseases, the question is about how we find safer treatments with lower side effects for all conditions. One method could be to achieve eubiosis via modulation of the gut microbiota. This can be accomplished by various means, including the use of selective probiotics, prebiotic supplementation, dietary changes and fecal transplants [82]. One such commensal is P. histicola, which reduces inflammation in a way similar to TNFi, without causing any pathology [17,92,94].

DOI: 10.3390/microorganisms13020255

Study: weak evidence

Querschnitts-/Survey-Studie (Beobachtungsstudie)

Together, this data suggests that increasing the quantity of plant-based foods in the diet, while decreasing processed foods and sugar, is especially beneficial for decreasing SLE symptoms long-term, especially in patients with self-perceived active lupus.

Regarding specific symptoms, weight loss, fatigue, joint/muscle pain and mood were the most cited symptoms that improved from dietary changes. Help with these symptoms was more likely associated with certain dietary changes (Figure 4(c)): For weight loss, the highest percentage of patients indicating improvement undertook vegetarian (66%), low-fat (65%), low/no sugar (63%) and low-carb (62%) eating patterns; For fatigue, improvement was highest with vegan (63%) and low/no dairy (54%) eating patterns; For joint/muscle pain, improvement was highest with vegetarian (54%) and low/no gluten (53%) eating patterns; For most eating patterns examined, 40–50% of respondents indicated that their dietary change helped with mood; however, a low-carb diet had a slightly higher percentage (53%). This suggests that dietary changes involving less animal products and carbohydrates are more effective for patients with SLE who wish to lose weight, increase energy, decrease joint/muscle pain or improve mood.

dietary restraint and changes undertaken over the long-term could increase the clinical benefit to SLE patients, and this data sheds light on patients’ ability to adhere to certain eating patterns; 3) our findings highlight the benefits of a whole-foods, plant-based diet (WFPB) – one that incorporates large amounts of vegetables while limiting processed foods, sugar, red meat and dairy products – to improve symptoms in SLE patients.

In our study, respondents who reported adhering to WFPB eating formats were more likely to experience benefits from dietary change, including significant decreases in SLE symptom severity, especially for SLE patients with initially severe symptoms. WFPB diets have been associated with improvements in chronic low-grade inflammation, including lower serum C-reactive protein, fibrinogen and total leucocyte concentrations,^(18, 19) perhaps due to the anti-inflammatory actions of high dietary fibre. In a recent study, greater consumption of MD foods such as vegetables, fruits, fish and olive oil and abstinence animal products, sugar and pastries was associated with lower SLE activity, damage and CVD risk.⁽²⁰⁾

Conversely, large intakes of compounds found in processed foods such as sugar and gluten is associated with gut dysbiosis, systemic inflammation and exacerbation of SLE symptoms.^{(4, 7, 21, 22)} Petric et al. found that SLE patients in clinical remission who often ate meat, fast food or fried foods had lower levels of C3 than patients who had high intake of vegetables, fruit and fish.⁽¹²⁾

A diet free of gluten, dairy and meat may improve auto-immune symptoms via a reduction in immune-reactivity to these food antigens.⁽²⁶⁾

This suggests that encouraging dietary changes of any duration is a promising approach for reducing SLE patients’ symptoms, but that sustainable long-term changes are most likely to be beneficial. With this respect, it is important to note that not only the food type is important but also the pattern of intake of the dietary change, as suggested in other inflammatory diseases during fasting.^(43, 44)

DOI: 10.1177/09612033211063795

Study: moderate evidence

Narratives Review

Rheumatic and musculoskeletal diseases (RMDs) are chronic systemic immune/inflammatory conditions characterized by the interaction between gene predisposition, autoimmunity and environmental factors. A growing scientific interest has focused on the role of nutrition in RMDs, suggesting its significant contribution to the pathogenesis and prognosis of these diseases. The diet can directly modulate the immune response by providing a wide range of nutrients, which interfere with multiple pathways at both the gastro-intestinal and systemic level. Moreover, diet critically shapes the human gut microbiota, which is recognized to have a central role in the modulation of the immune response and in RMD pathogenesis, such as in rheumatoid arthritis (RA). Choosing the ‘right’ diet is therefore crucial and a form of self-management ‘intervention’ that could impact on disease expression, course and outcome.

DOI: 10.3390/nu14040888

Study: weak evidence

Optimize the Gut Microbiome
The most unique, diverse, and robust microbiomes develop from daily intake of fiber-rich, whole foods.
• Eat fiber-rich foods at each meal (leafy greens and vegetables, berries and whole fruit, nuts and seeds, whole grains, beans, and lentils)
• Foods rich in polyphenols – berries, green tea, flax seed, black olives, capers, and red onion. Spices with polyphenols – cloves, rosemary, oregano, turmeric
• Eat 2 to 3 forkfuls of fermented foods daily (if tolerated) such as sauerkraut, kimchi, kefir, and unsweetened yogurt
• Minimize added sugar and artificial sweeteners
• Keep food and symptom journals to identify potential food sensitivities
• Minimizing stress supports the microbiome. Eat in a calm, relaxed place and sit down while you eat. Chew food well and eat slowly. Try not to eat on the run.

Support the Body’s Natural Detoxification Process
• Include foods high in fiber and rich in antioxidants at every meal (vegetables, berries and whole fruits, nuts and seeds, whole grains, beans and lentils, herbs, and spices)
• Eat cruciferous vegetables daily (arugula, bok choy, Brussel sprouts, broccoli, cabbages, cauliflower, collard greens, daikon, radishes, kale, kohlrabi, and turnips)
• Keep yourself hydrated with water and herbal or green tea
• Avoid artificial sweeteners – especially aspartame, acesulfame K, saccharin, and sucralose

Avoid Nutritional Deficiencies
Deficiencies in certain nutrients may increase muscle pain. Ensure you’re eating foods rich in the following nutrients.
• Vitamin D: Best obtained from safe sun exposure or a supplement
• Folate: Dark leafy greens, asparagus, Brussel sprouts, nuts, beans, and peas Nutrition and Food Services (04/2023) www.nutrition.va.gov Page 2
• Selenium: Brazil nuts (limit to 1 to 2 Brazil nuts per day to avoid selenium toxicity), yellowfin tuna, turkey, and chicken
• Magnesium: Dark leafy greens, pumpkin seeds, sesame seeds, halibut, pollock, avocados, bananas, berries, whole grain, seaweed
• Zinc: Oysters, beef, pork chop, chicken especially dark meat, pumpkin seeds, cashews, chickpeas
• Omega-3: Flax seed or flax seed oil, chia seed, salmon, herring, anchovies, mackerel, sardines, oysters, canola oil, and English and black walnuts
• Lean protein: Eggs, poultry, seafood, grass-fed beef, beans, lentils, nuts, and seeds.

Nutritional Considerations for Worsening Symptoms
The below foods may need to be modified or restricted. Talk to your nutrition provider to determine if this is right for you.
• Red meat: Limiting portions, selecting lower fat cuts, and choosing grass-fed beef may reduce the impact of red meat on inflammation and pain
• Dairy products: Trial non-dairy alternatives. If you choose to consume dairy, fermented dairy (yogurt, kefir) may be better tolerated
• Gluten: Found in wheat, rye, and barley and might contribute to higher levels of pain in some individuals. Talk to your nutrition provider about assessing for a gluten sensitivity.
• Excess added sugar and alternative sweeteners
• Food additives: Including monosodium glutamate (MSG), hydrolyzed protein, protein isolates/concentrates, yeast extract, and aspartame.

Other Lifestyle Factors
• Mind-body practices: Yoga, Tai Chi, meditation, and Qi Gong.
• Exercise: Stress relief and muscle strength.

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Highlights

• Optimal level of 25(OH)D in patients with or at risk of osteoporosis: 30 to 60 ng/mL.

• Intermittent but not daily supplementation may increase the risk of falls.

• Daily vitamin D supplementation (with calcium) may decrease the risk of fractures.

• Daily vitamin D supplementation is a valuable option when possible.

DOI: 10.1016/j.jbspin.2025.105858

Study: weak evidence

Querschnittsstudie (population-based observational study)

In conclusion, PRAL, a marker of dietary acid load, was shown to be an independent predictor of SUA concentrations in cross-sectional analyses of the adult population living in Germany, which suggests potentially SUA-lowering effects of low-PRAL diets. Apart from substantiating already known associations between nutrition-influencing factors, such as the intakes of dairy products or alcohol with SUA, our results show acid-base status to be an additional factor of how metabolism and habitual diets may interfere with SUA concentrations. With regard to the nonpharmacologic treatment of persons suffering from elevated SUA concentrations and gout, PRAL could perhaps become a useful tool to assess the potential of different diets to lower SUA.

DOI: 10.1093/jn/nxx003. PMID: 29378039

Study: moderate evidence

Interventionsstudie mit kontrolliertem Ernährungsregime (klinische Studie), Cross‑Over/Within‑Subject Design

In conclusion, this is the first study investigating the effects of cooking salt in adaptive immunity ex vivo in patients with RA and SLE, suggesting that a restricted sodium dietary intake could contribute to dampen the pro-inflammatory response. Our results add information on a potential new modifiable environmental factor in autoimmune diseases; however, due to the limited sample size, further studies are encouraged to define the utility and modality of dietary habits to ameliorate the outcome in these patients.

DOI: 10.1371/journal.pone.0184449

Study: moderate evidence

Narratives Review

The treatment of FS remains a challenging and complex endeavor due to the multifactorial nature of the disease, involving both metabolic and inflammatory components. Current therapeutic approaches range from non-surgical interventions, such as physical therapy, corticosteroid injections, and manual mobilization, to more invasive procedures, like arthroscopic capsular release and hydrodilation [3]. However, these methods primarily focus on symptom relief and improving shoulder mobility, with limited effectiveness in addressing the underlying inflammatory and fibrotic processes [104].

In addition, dietary modifications, such as time-restricted feeding or intermittent fasting, have been found to modulate leptin levels, offering a potential avenue for metabolic correction in FS patients [105]. However, while restoring leptin sensitivity could theoretically ameliorate fibrosis and inflammation, potential risks remain. Excessive leptin modulation could impact systemic metabolism, potentially influencing appetite regulation, insulin sensitivity, and immune function [113]. Further research is required to determine the optimal balance between therapeutic benefits and metabolic stability in FS treatment.

Emerging research highlights the role of gut microbiota in regulating systemic metabolism, particularly energy balance, glucose homeostasis, and low-grade inflammation associated with obesity [74,75,76]. Alterations in the gut microbiota, such as those caused by a high-fat diet, have been linked to a reduction in beneficial bacterial populations, like Bifidobacterium spp., Lactobacillus spp., and Roseburia spp. [77,78,79]. The interaction between gut microbiota and the immune system is mediated by pattern recognition receptors like Toll-like receptors (TLRs), which detect microbial components such as LPS. Fatty acids can stimulate innate immunity by interacting with the TLR4/CD14 complex, further promoting inflammatory responses [80]. Alterations in the gut microbiota have been implicated in the development of obesity and its related metabolic disorders, with evidence suggesting that modulating the gut microbiota can influence leptin sensitivity and metabolic outcomes [81,82,83].

Interestingly, the gut microbiota also appears to regulate leptin action, with studies showing that dietary interventions, like prebiotics, can improve leptin sensitivity in obese and diabetic mice [84]. This suggests that gut microbiota modulation may offer a novel therapeutic strategy for restoring leptin sensitivity and addressing metabolic dysregulation in FS.

Recent studies have highlighted the role of the gut microbiota in regulating systemic inflammation and metabolic health, including leptin sensitivity [116]. Alterations in gut microbiota composition, often observed in obesity and metabolic syndrome, can exacerbate leptin resistance and inflammatory processes via bacterial translocation and LPS-mediated activation of the JAK-STAT pathway [117]. Probiotic and prebiotic interventions may offer a novel therapeutic strategy to improve metabolic and immune regulation in FS patients, potentially reducing the chronic inflammation and fibrosis associated with the condition [8,118]. However, the precise role of microbiota-driven inflammation in FS remains to be fully elucidated, warranting further clinical investigation.

DOI: 10.3390/jcm14051780

Study: weak evidence

Systematisches Review

3.1. Effect of Diet Interventions on Serum Uric Acid Level and Gout Flares

3.1.1. Calorie Restriction and Fasting

Six studies were found investigating the effect of diet interventions with different grades of calorie restriction or fasting. Maclachlan et al. (1967) studied the effects of combinations of a purine-low diet, fasting, and alcohol intake in a 6-week study [14]. Nine gouty subjects (n = 4 alcoholics) were admitted to hospital. SUA at baseline was measured after urate-lowering therapy (ULT) was discontinued and ranged from 7.2 to 13.9 mg/dL. This level decreased after a 2-week purine-low diet (average = −1.4 mg/dL). After one day of fasting, all subjects showed a rise in SUA levels, with a mean difference of 1.1 mg/dL (1-day fasting) and 2.0 mg/dL (2-day fasting), which returned rapidly to near baseline values after 24 h of refeeding. During a second period of fasting, subjects used alcohol (79–112 g, whiskey) on the two consecutive days of fasting. The mean average increase in SUA in the subjects with gout was 2.4 mg/dL compared to 2.0 mg/dL on fasting without alcohol. Increases in SUA were accompanied by decreases in urate excretion. The subjects experienced 24 gout attacks in total, with most of these attacks (n = 19) directly following an increase of SUA of at least 1 mg/dL.

DOI: 10.3390/nu11122955

Study: strong evidence

prospektive Beobachtungsstudie

In our study, we could confirm a strong correlation between ketonuria and uricemia. It is already known from previous research that as ketone levels in the blood increase, the excretion of uric acid in urine decreases. This happens because ketones and uric acid compete for the same transport mechanisms in the kidneys [44]. Clinically, high uric acid levels are often seen as a problem because they can lead to gout attacks. By contrast, we observed only one case of a gout attack in a patient treated for hyperuricemia in a large cohort of 1422 individuals fasting for up to 21 days, despite high elevations of uric acid (from 338 to 495 µmol/L). Importantly, uric acid acts as a potent antioxidant [45]. In line with our previous findings, we observed that fasting for an extended period led to an increase in the body’s total antioxidant capacity and a decrease in lipid peroxidation [6]. Additionally, the ketone β-hydroxybutyrate has been shown to suppress the activation of the NLRP3 inflammasome [16], thereby reducing the inflammatory response to urate crystals. By contrast, rats that received allopurinol to lower uric acid production experienced reduced physical performance and increased oxidative stress [46].

DOI: 10.3390/nu16121849

Study: moderate evidence

Systematisches Review und Meta-Analyse

RA may cause progressive joint damage and disability. Risk factors for RA are genetic and non-genetic, including smoking, changes in the microbiota, female sex, Western diet, and ethnic factors.

Nutritional therapy for RA aims to attenuate inflammation by altering the ratio of ω-6 to ω-3 fatty acids and increasing antioxidants. The reduction of arachidonic acid (AA), an ω-6 fatty acid, is particularly relevant. AA is the precursor of eicosanoids, which are involved in a variety of cellular functions and reactions. Eicosanoids are also mediators of inflammation, and the amount of AA released from the cell membrane determines the intensity of inflammation. When less AA is present in the cell membrane, less AA is released, and fewer eicosanoids are formed.

The impact of dietary fibers on the composition and metabolic activity of the gut microbiome further contributes to the anti-inflammatory effect of vegetarian, vegan or Mediterranean diets. In RA patients, a high-fiber diet increases anti-inflammatory short-chain fatty acids, decreases pro-inflammatory cytokines, and favorably alters the gut microbiome composition.

Vegetarian diets contain less AA than diets with meat, whereas vegan diets contain virtually no AA. There is evidence from population studies that nutrients of animal origin, as consumed in high amounts in the Western diet, correlate with the occurrence of RA. Therefore, vegetarian and vegan diets may favorably influence inflammation.

The ketogenic diet may reduce eicosanoid formation through the lower generation of reactive oxygen species (ROS) of the ketone metabolism compared to the glucose metabolism. ROS activate phospholipase A2 in the cell membrane of immune cells, which exclusively cleaves AA from phospholipids of the cell membrane. ROS also serve as substrates for the oxidation of AA and lead to excessive eicosanoid formation. In addition, the ketogenic diet increases adenosine, which may alleviate pain and have an anti-inflammatory effect.

DOI: 10.3390/nu13124221

Study: strong evidence

Narratives Review

While it primarily affects young and middle-aged women, FM can affect individuals of any gender or age who chronically suffer from widespread pain in the fibromuscular tissue, tendons, ligaments, and other areas.

Challenges associated with identifying whether vitamin D supplementation has a beneficial effect in RCTs to date include inter-study heterogeneity and relatively small sample numbers for a meta-analysis, with only 5 RCTs included, thus emphasising the need for larger RCTs in different subsets of RA patients to fully elucidate the role, if any, for vitamin D supplementation in the management of RA. In addition, there may be differences in vitamin D-binding protein levels, and other genetic variants, which influence the efficacy of vitamin D supplementation [135]. Vitamin D supplementation in low/moderate doses is not thought to be harmful to patients, has wider health benefits, is relatively inexpensive and has fewer side effects/interactions compared with many other commonly used treatments for RA, such as non-steroidal anti-inflammatory drugs (NSAIDs), or conventional synthetic or biological disease-modifying anti-rheumatic drugs (DMARDs). Evidence is also emerging that vitamin D may augment certain therapies in RA. In one in vitro study, vitamin D 1,25-(OH)₂D3 was shown to act synergistically with the biologic drug abatacept to inhibit T cell activation driven by anti-CD3 cross-linking, and promote a pro-regulatory CD28 phenotype [136]. The potential for enhancing the effects of biologics with simple, low-risk addition of 1,25-(OH)₂D3 is interesting, and further work is required to validate this initial in vitro finding.

DOI: 10.3390/nu17030530

Study: weak evidence

experimentelle Tierstudie (präklinisches Modell)

The correlation between food allergy and RA:

Recent studies have recognized that intestinal immune reactions might be associated with the articular inflammation. Taking into consideration the fact that IgG is the most important antibody playing a role in the pathogenesis of RA, in the present study we measured IgG antibody activities against the “big eight” food antigens using ELISA. As shown in Figure 6i, the results indicated that occurrence of RA is more related to egg- or milk-specific IgG. Furthermore, egg- or milk-specific IgE was determined by RAST and significant elevated concentrations of specific IgE (sIgE) were observed in CIA rats.

DOI: 10.4103/1947-2714.175206

Study: weak evidence

Narratives Review

Hormonal factors such as those associated with long-term stress, or dietary factors, either through increased consumption of foods with a high density of food additives or through the high consumption of gliadin-rich cereals pose threats to the integrity of cell-binding complexes (70). Increased permeability of body barriers is associated with a high risk of endotoxemia, chronic inflammation and insulin resistance (71). In a recent systematic review, most of the included studies showed a higher concentration of lipopolysaccharides (LPS) in diabetic patients than in healthy subjects (72).

A meta-analysis has measured the efficacy of using supplements rich in omega-3 fatty acids and their analgesic effect on inflammatory joint pain, highlighting how eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation reduces the intensity of joint pain, morning stiffness and non-steroidal anti-inflammatory drugs (NSAID) consumption (105).

DOI: 10.3389/fmed.2021.663703

Study: weak evidence

Narratives Review

However, in humans, the majority of vitamin D is synthesised in the skin from the precursor molecule 7-dehydrocholesterol, which undergoes a series of UV light-mediated modifications to generate parental vitamin D3.

DOI: 10.1007/s00223-019-00577-2

Study: weak evidence

Viewpoint-/Meinungsartikel mit narrativem Review-Charakter

Among many consequences, obesity begets more type 2 diabetes, raises blood pressure, promotes systemic inflammation, has haemodynamic impacts that can accelerate progression to chronic kidney disease (CKD) or heart failure (HF), has biomechanical impacts, one of which is to make activity harder [4], or more painful (by accelerating osteoarthritis) and impacts mental health in multiple ways. Obesity is also associated with more infections [3], a finding not well appreciated but important given infection risks inherent in several inflammatory RMDs and attendant therapeutics. It would be important to establish whether obesity impacts infection rates for those on disease-modifying anti-rheumatic drug (DMARDs) and, if so, whether intentional weight loss helps reduce infections in patients with RMDs, allowing more patients to stay on their medications without adverse effects.

Weight also impacts liver fat levels.

Summary of the potential impact of weight loss in RMDs

Likely benefits of intentional weight loss in rheumatological diseasesReduced incidence of RMDs (particularly those with a dominant metabolic component)Reduced disease severity and better outcomesImproved response and persistence of response to disease modifying therapies meaning more likely to remain on such therapies, reducing a need to switch and/or escalate treatment thereby reducing the need for clinic appointmentsReduced adverse effects from current RMD treatments, including possible reduced infections based on data from recent trials in other disease areasImprovement in activities of daily living with potentially reduced pain, fatigue and improvements in mental health, allowing more people to stay in work and remain productive. Potential health economic benefits in some with RMDs?Reduced comorbidities (especially CVD, MASLD, hypertension, and type 2 diabetes)

DOI: 10.1016/j.ard.2025.02.013

Study: weak evidence

Narratives Review

Natural products are rich in dietary fibers, polyphenols, vitamins, minerals, and other beneficial components, and possess many bioactivities, such as antioxidant, anti-inflammatory, anticancer, antidiabetic, antiobesity, hepatoprotective, immunoregulatory, antibacterial, and cardiovascular-protective effects [12–20]. Epidemiological studies found that people consuming more fruits, vegetables, teas, cereals, and nuts had a lower risk of CVDs, and the antioxidants in these natural products were considered as the main contributors [21–23].

DOI: 10.1155/2021/6627355

Study: weak evidence

Narratives Review

The autoimmune protocol diet (AIP) is a personalized elimination diet that aims to determine and exclude the foods that might trigger immune responses, leading to inflammation and symptomatology associated with autoimmune diseases.

3.1.1. Elimination phase

During the first phase, grains, legumes, nightshades, nuts, seeds, dairy, eggs, coffee, and alcohol are completely removed from the diet (Table 1). In addition, all refined sugars, oils, processed foods, food additives, artificial colors, and flavorings are excluded due to their contribution to gut dysfunction. The use of non-steroidal anti-inflammatory drugs (NSAIDs) is also avoided during this phase. Patients are encouraged to consume nutrient-dense whole foods, such as vegetables, fruits, mono- and poly-unsaturated fatty acids, tubers, wild game, poultry, organ, and non-processed meats (Table 1) [11]. Gluten-rich grains are avoided, as their glycoprotein extract, gliadin, is implicated in autoimmunity [25]. This phase spans from 6 weeks to 6 months [11]. This prolonged duration stems from plasma B-cells living from a few days to a few months, while immunoglobin G (IgG) antibodies (mostly associated with immune tolerance [26]) have a half-life of 21 days [27]. B-cells contribute to food allergen tolerance by producing allergen-specific IgG antibodies [11].

3.1.2. Reintroduction phase

During the second phase, eliminated foods are reintroduced to identify the ones that trigger individual responses. Generally, there is no rule of thumb on how to initiate the reintroduction. The most common manner is to reintroduce the foods that each patient enjoys the most, or the ones that are less likely to induce negative responses, in an effort to increase the food options. With this in mind, foods have been categorized into four groups based on their likelihood of being well-tolerated [11]. Group 1 consists of egg yolks, legumes, seed oils, and nut oils [11]. Group 2 includes nuts and seeds, cocoa, egg whites, and alcohol [11]. Group 3 comprises cashews and pistachios, eggplant, coffee, and fermented dairy, while Group 4 includes all dairy, white rice, nightshades, alcohol, and gluten-free grains [11]. This phase is time-consuming; if performed methodically however, it results in distinct beneficial health outcomes for each individual.

3.1.3. Maintenance phase

The last AIP phase involves maintaining the protocol and has no specific duration. It aims to provide a healthy diet and lifestyle that will reduce autoimmune responses. In this manner, each patient adopts a dietary pattern associated with a lack of intolerances, considering the reintroduction phase responses.

DOI: 10.1016/j.metop.2024.100342

Study: weak evidence

Systematisches Review und Meta-Analyse

Our systematic review and meta-analysis of prospective cohort studies supports the association between fructose intake and increased risk of developing gout. The strength of evidence for the association between fructose consumption and risk of gout was low, as assessed by GRADE. It means that further research is likely to have a significant impact on our confidence in the effect estimate and is likely to change the estimate.

DOI: 10.1136/bmjopen-2016-013191

Study: strong evidence

Klinische Ernährungsinterventionsstudie (Pilotstudie, teilweise randomisiert)

Haugen et al. [5] have collected data from patients suggesting that extreme vegan diets have alleviated their rheumatic symptoms. `Living food' teachers and consumers have also reported bene®cial e ects of the diet [6±8]. `Living food' is an uncooked vegan diet, rich in lactobacilli, which contains no animal products, ra nated substances or added salt. A detailed descrip tion of the diet is presented by Ha Ènninen et al. [7]. The majority of food items are soaked and sprouted (seeds and grains), and many are fermented. Some items are blended and dehydrated (bread). Fermented products contain high amounts of various lactobacilli [9]. Fermentation and mechanical processing distin guish this diet from other vegan diets.

DOI: 10.1093/rheumatology/37.3.274

Study: moderate evidence

Fall-Kontroll-Studie

 Interestingly, we observed that a higher level of intake of total protein (highest versus lowest tertile) increased the risk of inflammatory polyarthritis by almost 3-fold.

However, it has not been clarified how much nutrients could be harmful, preventive, or healthful. The results of a study showed that food with moderate amounts of proteins and energy substances full of vitamins, minerals, and mono/ polyunsaturated fatty acid prevented tissue damage, suppressed inflammatory actions, and helped to treat systematic lupus erythematosus [4]. Nevertheless, higher amounts of red meat, meat and meat products combined, and protein increased the risk of inflammatory polyarthritis [5]. Researchers revealed that the risk of rheumatoid arthritis increased as a result of higher consumption of meat and protein and lower intakes of fruit, vegetable, and vitamin C [6]. Yet, there have been researches that revealed red meat, poultry, and fish were not associated with RA [2]. Hu et al. also indicated no association between Mediterranean diet and incidence of RA in woman [7].

DOI: 10.1007/s10067-018-4151-x

Study: moderate evidence

Fall-Kontroll-Studie

In intestinal fluid of many RA patients, all three immunoglobulin classes showed increased food specific activities. Except for IgM activity against β‐lactoglobulin, all other IgM activities were significantly increased irrespective of the total IgM level. The RA associated serum IgM antibody responses were relatively much less pronounced. Compared with IgM, the intestinal IgA activities were less consistently raised, with no significant increase against gliadin and casein. Considerable cross reactivity of IgM and IgA antibodies was documented by absorption tests. Although intestinal IgG activity to food was quite low, it was nevertheless significantly increased against many antigens in RA patients. Three of the five RA patients treated with sulfasalazine for 16 weeks had initially raised levels of intestinal food antibodies; these became normalised after treatment, but clinical improvement was better reflected in a reduced erythrocyte sedimentation rate.

Conclusions

The production of cross reactive antibodies is strikingly increased in the gut of many RA patients. Their food related problems might reflect an adverse additive effect of multiple modest hypersensitivity reactions mediated, for instance, by immune complexes promoting autoimmune reactions in the joints.

DOI: -

Study: moderate evidence

Narratives Review

We have performed an umbrella review to understand the impact of food on the development of RA. As described in current clinical guidelines [8], it is true that not all RA patients benefit from dietary intervention; however, following consideration of the research data, a sub-set of RA patients appear to respond favourably to dietary changes. The dietary interventions providing the most significant effect are fasting, gluten-free vegan diets, and/or a customised dietary reintroduction protocol. Although the studies are heterogeneous with regards to the fasting protocol, the time of fast and inclusion criteria for medication use, fasting appears to show the most consistent improvements in both subjective [11–13] and objective [13–19] outcomes measures. At the end of a 1 week fast, significant improvements in objective measures, such as ESR, CRP, and IL-6, have been documented [13, 18–20]. This aligns with significant improvements in disease activity scores [13, 18–22], suggesting that dietary factors may be a source of inflammation in RA. In support of this body of research, a recent study has shown that removal of the gut microbiota with bowel cleansing followed by a 7-day fasting protocol in RA patients, led to a significant decline in DAS-28 scores, and markers of inflammation and mucosal barrier disruption [23].

DOI: 10.1007/s00296-024-05541-4

Study: weak evidence

Food sources of ARA: ARA is found only in animal-derived foods because plants cannot synthesize C-20 LCPUFAs. The main food sources of ARA are meat, poultry, eggs, fish and dairy foods, as shown in Table 1 [20, 21]. ARA is contained in most animal foods [22, 23]

Narratives Review

DOI: 10.1186/s12944-019-1039-y

Study: weak evidence

In this meta-analysis, the pooled SMD was −0.55. For comparison, the established analgesic dose of oral diclofenac (150 mg/day) yields a pooled effect size of SMD –0.56, corresponding to an approximate 14-mm reduction in VAS pain scores (70). The efficacy of omega-3 fatty acid supplementation (SMD –0.55) appears broadly comparable in magnitude; however, unlike nonsteroidal anti-inflammatory drugs (NSAIDs), omega-3 s are associated with a substantially lower risk of gastrointestinal and cardiovascular toxicities. Importantly, omega-3 fatty acids should not be regarded as equivalent to NSAIDs, which remain the first-line therapy for acute pain. Rather, omega-3 s may be best positioned as a safer adjunct or as a long-term strategy in the management of chronic pain.

This finding is consistent with previous reviews suggesting that prolonged supplementation is necessary to achieve clinically meaningful analgesic effects (72). A greater effect was observed in the low-dose group (≤1.35 g day⁻¹; SMD = −0.60), presumably due to saturation of the plasma omega-3 fatty acids curve and better adherence relative to higher doses; nevertheless, doses >1.35 g day⁻¹ remained efficacious. These findings are consistent with prior evidence suggesting that higher doses may not confer additional benefits for chronic pain relief and could even be less effective in certain contexts (31). Accordingly, dosing can be individualized on the basis of cost-effectiveness and patient tolerability.

This meta-analysis demonstrates that omega-3 fatty acid supplementation produces a clinically meaningful, ceiling effect for dose escalation and time-dependent reduction in chronic pain intensity. The analgesic efficacy was most evident in inflammatory pain phenotypes such as rheumatoid arthritis and migraine, whereas evidence remains inconclusive for osteoarthritis and mastalgia. These findings support the use of omega-3 fatty acids as a safe, non-pharmacological adjunct in the management of chronic pain.

Systematisches Review und Meta-Analyse

DOI: 10.3389/fmed.2025.1654661

Study: strong evidence

Fasten gilt seit Jahrhunderten als gesundheitsförderlich. Für Erkrankungen des rheumatischen Formenkreises liegen nur wenige Studien vor, die Effekte des Fastens auf die Aktivität der Entzündung erfasst haben. Eine Untersuchung aus den 1990er Jahren spricht dafür, dass eine Fastenperiode bei rheumatoider Arthritis (RA) Symptome dieser Erkrankung lindern könnte. Positive Effekte werden auch für Betroffene von Bluthochdruck und Diabetes Typ 2 berichtet. Diese Begleiterkrankungen finden sich häufig bei Patient:innen mit rheumatischen Erkrankungen. Die Kommission für Komplementäre Heilverfahren und Ernährung der DGRh hat die vorliegende Evidenz zum Fasten gesichtet: Bei ausgewählten Patient:innen kann diese Methode sinnvoll in ein rheumatologisches Therapiekonzept integriert werden.

Langfristige Ernährungsumstellung kann Ergebnisse des Fastens unterstützen Besonders interessant ist das Fasten in Kombination mit einer nachfolgenden Ernährungsumstellung auf eine mediterrane Kost oder eine andere Kostform mit überwiegend pflanzlicher Nahrung.

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Experimentell finden sich deutliche Hinweise für eine antiinflammatorische Wirkung des Fastens. Mehrere klinische Studien belegen einen symptomatischen Nutzen des längeren modifizierten Fastens (Heilfasten) bei RA. Folgt auf das Fasten eine vegane und vegetarische Ernährung, sind nachhaltige Effekte von bis zu einem Jahr dokumentiert. Für das Intervallfasten sind kardiometabolische, aber keine antirheumatischen Effekte belegt. Ernährung und Fasten sind eine mögliche sinnvolle Ergänzung konventioneller Therapie, werden aber derzeit in der Praxis nur selten berücksichtigt.

Narratives Review

DOI: 10.1007/s00393-024-01557-0

Study: weak evidence