Diet and Rheumatoid Arthritis

Almost everyone with rheumatoid arthritis is eventually told that diet matters. The trouble is that the advice arrives with the volume turned all the way up in both directions — one source says food is irrelevant and you should just take your methotrexate, another says the right elimination diet will put you in remission and let you throw the drugs away. Neither of those is what the research actually shows.

What the research shows is narrower and more useful: food is a real but modest lever on RA disease activity, and a large lever on the things RA drags along with it — heart disease, weight, fatigue, and how well your medication works. Some dietary findings in RA are genuinely striking. Others are famous mostly because they were interesting, not because they held up. This page separates those two piles honestly, and then puts the surviving material into a week of ordinary food you could actually cook.

This page assumes you are already on, or discussing, disease-modifying treatment. Nothing here replaces it. If a diet page ever tells you to stop a DMARD, close the page.

Table of Contents

  1. What Diet Can and Cannot Do in RA
  2. The Mediterranean Pattern: Best-Tested, Modest Effect
  3. Fasting Followed by a Vegetarian Diet
  4. The Gut, the Mouth, and the Mucosal-Origins Hypothesis
  5. Elimination Diets and Personal Trigger Foods
  6. Body Weight and Fat Tissue as a Driver of Disease
  7. Alcohol: A Confusing Signal, Handled Carefully
  8. Salt: A Mechanism Worth Knowing, Evidence Still Thin
  9. Vitamin D Status
  10. A Practical Week of Eating
  11. How to Test a Diet Change on Yourself
  12. Key Research Papers
  13. Connections
  14. Featured Videos

1. What Diet Can and Cannot Do in RA

Think of RA disease activity as a dial with several hands on it. Your DMARD or biologic has the strongest grip — it can move the dial from severe to near-normal. Smoking has a strong grip in the wrong direction. Diet has a real grip, but a lighter one: in the trials that measured it properly, dietary change moved standard disease-activity scores by an amount that is detectable and worth having, but smaller than what a well-matched medication does.

That framing matters because it sets expectations correctly in both directions:

One more honesty note. RA naturally flares and settles on its own. That property makes it exceptionally easy to believe a diet worked when you simply caught the downswing of a natural cycle. It is why uncontrolled testimonials about RA diets are so abundant and so unreliable, and why the sections below lean hard on randomized trials even when those trials are small and old.

2. The Mediterranean Pattern: Best-Tested, Modest Effect

If you only change one thing, change to a Mediterranean-style pattern. It has the most supportive trial evidence in RA, the least risk, and by far the strongest general-health case.

The pattern in plain terms: olive oil as the main fat; oily fish several times a week; vegetables and fruit at most meals; beans, lentils, and chickpeas; nuts; whole grains including brown rice; garlic, onions, and herbs used generously; meat present but not central; very little in the way of packaged, refined, industrially-produced food.

What the trials found

A Swedish randomized trial by Sköldstam and colleagues put people with active RA on a Mediterranean-style diet for three months against an ordinary Swedish control diet, in a setting where both groups were fed the same way to remove the "someone is cooking for me" effect. The Mediterranean group ended with lower disease-activity scores and better physical function. It took several weeks to show up — not days.

A Scottish pilot by McKellar and colleagues did something more practical: it taught 130 women with RA in deprived areas of Glasgow how to cook Mediterranean food, in six weekly two-hour hands-on classes, and then followed them for six months. Pain scores, morning stiffness, and patients' own global assessment improved compared with a control group who were handed written advice only. That study is worth knowing about because it tested the realistic version of the intervention — teaching, not supplying — and it still worked.

More recently the Swedish ADIRA crossover trial fed participants a portfolio-style anti-inflammatory diet (oily fish, whole grains, probiotic dairy, fruits and vegetables, olive-family fats) versus a control diet for ten weeks each, with food delivered to their homes. The intervention period produced a difference in disease activity favouring the anti-inflammatory diet — but a small one, small enough that on its own it would not change a treatment decision. The trial was later the subject of a published correction in the same journal, which is a reason to treat its numbers gently rather than quote them precisely.

What effect size is realistic

Put together, these trials point to the same honest conclusion. A Mediterranean pattern in RA produces a small-to-moderate reduction in disease activity and a clearer improvement in pain and function, appearing over weeks to months rather than immediately. It does not produce remission. Someone whose swollen joint count is in the double digits will not eat their way to zero.

The 2009 Cochrane review of dietary interventions in RA, led by Hagen and colleagues, reached a comparable verdict from a stricter angle: the trials are small, hard to blind, and prone to dropouts, so the evidence for any single diet remains weak — while noting that dietary changes were nonetheless associated with improvement in several studies. Both statements are true at once. The trials are real; they are also small.

The case for doing it anyway is that the downside is very small. Unlike a drug, an eating pattern built on olive oil, fish, vegetables, beans, and brown rice carries no toxicity, no monitoring bloodwork, and a large independent benefit for your heart — which, in RA, is not a side issue.

Not quite zero, though, and the same Cochrane review is the reason to say so. Across the trials it pooled, people assigned to dietary manipulation dropped out about 10% more often than controls and lost significantly more weight — on average around 3 kg. Its authors concluded that potential adverse effects should not be ignored. For most people that weight change is neutral or welcome. If you are already thin, or already losing weight without meaning to, it is not; see the weight section, where unintentional loss is treated as a warning sign rather than a win.

3. Fasting Followed by a Vegetarian Diet

This is the most dramatic result in the RA diet literature, and it is also the one most often quoted without its caveats.

The Norwegian trial

In 1991, Kjeldsen-Kragh and colleagues published a controlled trial in The Lancet that has shaped the conversation ever since. People with RA underwent a supervised fast of roughly a week to ten days, then moved to a gluten-free vegan diet for several months, then to a lacto-vegetarian diet for the remainder of a year. A control group ate an ordinary diet. Foods were reintroduced one at a time, and anything that reproduced symptoms was dropped again.

The results were substantial and, unusually for a diet trial, showed up in objective measures: fewer tender and swollen joints, less pain, better grip strength, and lower ESR and C-reactive protein. Improvement appeared within about four weeks and — the part that made the study famous — the diet group still held an advantage over controls at one year.

A related Finnish trial by Nenonen and colleagues tested an uncooked, lactobacilli-rich vegan diet and also reported improvement in subjective and some objective measures, with symptoms returning after participants went back to their usual food.

Why the results are hard to bank on

Four problems sit on top of these findings, and none of them is fatal, but together they explain why fasting-plus-vegetarian never became standard advice.

The modern repeat

That last objection was tested directly. The German NutriFast exploratory randomized trial, published by Hartmann and colleagues in 2022, compared a seven-day fast followed by eleven weeks of a plant-based diet against twelve weeks of standard national dietary recommendations, in patients on contemporary treatment. The primary endpoint was not statistically significant. Both groups improved on disease-activity and function measures over twelve weeks; the fasting group's improvement in function arrived faster, within the first week, while the comparison group caught up later.

That is an honest and instructive result. It suggests the fasting effect is real but front-loaded, that a good ordinary diet gets to a similar place more slowly, and that against modern treatment the extra advantage of the dramatic version shrinks considerably.

Is any of it worth trying?

A supervised medical fast is not a casual experiment, and it is a genuinely bad idea without medical oversight if you take prednisone, methotrexate, diabetes medication, or blood-pressure medication, or if you have kidney disease, are underweight, or have any history of an eating disorder. This is the one place on this page where the "talk to your rheumatologist first" instruction is not filler.

The transferable lesson, though, is free: the diet that people landed on after the fast — largely plant-based, vegetable-heavy, built on whole unrefined food — overlaps heavily with the Mediterranean pattern. You can adopt the destination without the fast.

4. The Gut, the Mouth, and the Mucosal-Origins Hypothesis

Here is the most interesting idea in RA research right now, and it needs to be labelled clearly: this is a hypothesis with supportive evidence, not established fact. It is presented as such below because that is what the evidence supports, and because it is exactly the area where diet marketing runs furthest ahead of the science.

The idea

RA is diagnosed in the joints, but there is good reason to think it does not start there. The antibodies that define seropositive RA — anti-CCP antibodies, which target proteins modified by a process called citrullination — can be detectable in blood years before a single joint hurts. Something is triggering an immune response somewhere else, and the joints are where the resulting immune activity eventually lands.

The mucosal-origins hypothesis, laid out by Holers and colleagues in Nature Reviews Rheumatology, proposes that this "somewhere else" is a mucosal surface — the lung, the gums, or the gut lining. Each of those is a place where your immune system meets the outside world and has to decide what is friend and what is foe. The hypothesis is that at one of these surfaces, tolerance breaks down, citrullinated proteins are generated and presented in an inflammatory context, and an antibody response begins that later finds matching targets in joint tissue.

This fits several things that were otherwise loose ends. Smoking, the strongest environmental risk factor for RA, is a lung insult. Gum disease is repeatedly associated with RA. And the gut is the largest immune interface in the body.

What was actually found about Prevotella copri

Scher and colleagues reported in eLife in 2013 that the gut bacterium Prevotella copri was substantially over-represented in the stool of people with new-onset, untreated RA compared with healthy controls and with people with chronic treated RA. The mouse work in that paper is widely reported as showing that P. copri causes arthritis. It does not. What the authors showed in mice was that P. copri could take over the intestinal microbiota and that colonised animals became more sensitive to chemically induced colitis — a gut result, not a joint one. The arthritis link in that paper is the human correlation in its title, not an animal experiment.

Two later findings are important for calibrating what this means. Zhang and colleagues, in Nature Medicine, found that both the gut and oral microbiomes were altered in RA and that the alterations partly normalized after DMARD treatment — which raises the awkward question of how much of the difference is cause and how much is consequence of the disease or its treatment. And Alpizar-Rodriguez and colleagues looked at people who were antibody-positive and at risk but did not yet have RA, and found Prevotella-related signals in that pre-clinical group too — which pushes the finding earlier in the timeline, closer to cause.

What this does and does not license

The honest summary: the mucosal-origins picture is the most promising explanatory framework RA has had in a generation, and it currently justifies eating more plants and flossing — not buying anything.

5. Elimination Diets and Personal Trigger Foods

Ask ten people with RA about food triggers and you will get ten different lists. Dairy, wheat, tomatoes, peppers, aubergine, citrus, red meat, coffee, corn — every one of these has a devoted constituency. The research on this is genuinely strange, and the strangeness is the finding.

What the trials show

Darlington and colleagues published a placebo-controlled, blinded study of dietary manipulation in RA in The Lancet in 1986 — a serious attempt to test the trigger-food idea rather than assume it. Systematic elimination-and-reintroduction protocols of this kind have repeatedly found that some patients do react reproducibly to some foods.

But here is the part that matters: the specific foods do not reproduce across people, and often do not reproduce across trials. There is no RA trigger food. There is no nightshade effect, no dairy effect, no gluten effect that shows up reliably at group level in people without coeliac disease. What exists is a minority of individuals with idiosyncratic, personally-consistent reactions to foods that vary from person to person.

Why this happens

Several explanations are on the table and they are not mutually exclusive. Genuine individual food sensitivities exist and are heterogeneous. RA's spontaneous flare-and-settle cycle generates false associations at a high rate. And expectation is powerful: in unblinded testing, people find what they are looking for. The value of blinded challenge protocols is precisely that they strip out the last two.

How to run an elimination sensibly, if you want to

Elimination diets are not harmless. They shrink the diet, they cost social life and pleasure, and long restriction risks real nutritional gaps — calcium and vitamin D in particular, which matter enormously in a disease treated with steroids and associated with bone loss. If you are going to do it, do it as a short experiment with a defined end, not a lifestyle.

  1. Pick one suspect at a time. Removing eight foods at once tells you nothing about which one mattered.
  2. Give it three to four weeks. Shorter than that and you are reading noise.
  3. Track something numeric. Morning stiffness in minutes, a 0–10 pain score, and a tender-joint count — written down daily, before you decide anything.
  4. Reintroduce deliberately. Add the food back and watch. A trigger that only works one direction is not a trigger.
  5. Repeat once. If removal helps and reintroduction hurts twice, you have found something real for you. If not, put the food back and move on.
  6. Stop after two or three failed suspects. The yield falls fast, and the cost of a shrinking diet keeps rising.
  7. Never eliminate a whole food group indefinitely without replacing what it supplied. Dropping dairy without a calcium plan is a bad trade in a disease that already threatens bone.

6. Body Weight and Fat Tissue as a Driver of Disease

This is the section with the strongest evidence and the least glamour, and it is probably the most actionable thing on the page.

Fat tissue is not inert

It helps to stop picturing body fat as padding. Adipose tissue is metabolically busy: it secretes signalling molecules — adipokines such as leptin and adiponectin — and, when it expands, it recruits immune cells and releases inflammatory cytokines including TNF-alpha and interleukin-6. Those are the same messengers that RA drugs are designed to block. Someone carrying substantial excess fat tissue is running a low-grade inflammatory signal in the background of a disease defined by inflammatory signalling.

What the clinical data show

Liu and colleagues conducted a systematic review and meta-analysis of obesity's impact on remission and disease activity in RA. The pattern across studies is consistent: higher body mass is associated with a lower probability of achieving remission and with higher measured disease activity. Sandberg and colleagues, working in early RA, similarly found that being overweight reduced the chance of achieving a good treatment response and low disease activity.

Read that carefully, because it is a different claim from "losing weight cures RA." The claim is that excess fat tissue appears to blunt your response to the treatment you are already taking. That makes weight a modifier of drug efficacy, which is a rather more serious thing than a lifestyle footnote.

Two important caveats

First, causality is not fully settled. Pain and stiffness reduce activity, reduced activity adds weight, and steroids add weight too — so some of the association runs backwards. This is a real limitation and it should temper how forcefully the advice is given.

Second, and going the other way — unintentional weight loss in RA is a warning sign, not a win. Active RA can cause loss of muscle mass, sometimes with fat retained, a pattern sometimes called rheumatoid cachexia. Losing weight without trying is something to report, not to celebrate. The goal is fat loss with muscle preserved, which is why the exercise and joint-protection side of this matters as much as the food side. Adequate protein, plus resistance work within your limits, is what protects muscle while fat comes down.

A note on how weight loss works in the diet trials

An easy assumption is that any benefit from a Mediterranean or vegetarian diet in RA is simply weight loss in disguise. Sköldstam and colleagues examined this directly in a 2005 analysis and concluded that weight reduction was not a major reason for the improvement seen with lacto-vegetarian, vegan, or Mediterranean diets in RA. In other words the food composition seems to be doing something on its own account, not merely acting as a calorie-reduction mechanism.

7. Alcohol: A Confusing Signal, Handled Carefully

Alcohol produces one of the most awkward findings in RA epidemiology. Scott and colleagues conducted a systematic review and meta-analysis and reported a protective association between alcohol consumption and the risk of developing RA. That result is real and it has been replicated.

It is also close to useless as advice, for four reasons.

The sensible reading: this literature is no reason to start drinking, and no reason to feel that a modest amount is sabotaging your treatment. If you are on methotrexate or leflunomide, agree an amount with the person monitoring your liver bloods and stick to it. That conversation is worth having explicitly rather than guessing.

Two methotrexate points that belong on a diet page

8. Salt: A Mechanism Worth Knowing, Evidence Still Thin

Salt entered the autoimmunity conversation through immunology rather than epidemiology. Kleinewietfeld and colleagues reported in Nature in 2013 that high sodium chloride conditions drove the development of pathogenic Th17 cells — a T-cell type central to several autoimmune diseases — and worsened experimental autoimmune disease in mice. That is a striking mechanistic result and it launched a great deal of follow-up work.

On the human side, Sundström and colleagues reported in Rheumatology, from a nested case-control study, that sodium intake showed no association with RA risk across the cohort as a whole. The signal appeared only on stratifying by smoking: among smokers, high sodium intake roughly doubled the risk; among non-smokers it did nothing. That is a subgroup interaction in observational data — suggestive, not decisive, and tangled up with smoking rather than standing alone. The authors were explicit that it did not confirm their original hypothesis.

So the honest position is: there is a plausible mechanism and a thin human signal, and no trial showing that cutting salt improves established RA. Nobody should be told that a low-sodium diet treats their arthritis.

Even so, moderating salt is easy to justify on other grounds. RA carries elevated cardiovascular risk; blood pressure matters more in RA than in the general population, not less. And in practice, most dietary sodium does not come from the salt shaker — it comes from packaged and processed food. The Mediterranean-pattern advice above already removes most of it as a side effect, without anybody having to weigh anything. Salt your own cooking to taste; the shaker is not the problem.

9. Vitamin D Status

Low vitamin D is common in RA, and it is worth understanding why that observation is less impressive than it sounds.

Lin and colleagues reviewed and meta-analysed the relationship between serum vitamin D level and RA disease activity and found an inverse association — lower vitamin D, higher disease activity. But people with painful, stiff, fatigued joints go outside less, and sunlight is the main source of vitamin D for most people. Low vitamin D in RA is at least partly a consequence of having RA.

The way to cut that knot is a randomized trial of supplementation, and the largest relevant one is VITAL. Hahn and colleagues reported in the BMJ in 2022 that vitamin D at 2000 IU a day, with or without marine omega-3, reduced incident autoimmune disease by roughly a fifth over about five years of follow-up in older adults. That is a genuinely notable result — a randomized trial showing fewer new autoimmune diagnoses.

Note precisely what it does and does not say. It is about preventing new autoimmune disease in a general older population. It is not evidence that vitamin D supplements reduce disease activity in people who already have established RA. Trials aimed at that question have not produced a convincing treatment effect.

The practical position is still straightforward, and it does not depend on the RA question at all:

10. A Practical Week of Eating

Everything above compresses into one pattern. This week is built entirely from whole foods — things that are recognisably what they were when they came out of the ground, the sea, or the animal. It is deliberately repetitive, because a plan you can execute on a bad-hands morning beats an elegant plan you abandon.

The standing rules

Seven days

Day Breakfast Lunch Dinner
Monday Whole oats cooked in whole milk with blueberries and walnuts Sardines on rye with tomato, red onion, olive oil Baked salmon, roasted broccoli and carrots, brown rice
Tuesday Two eggs scrambled in butter, spinach, orange Lentil soup with garlic and olive oil, apple Roast chicken thighs, brown rice, green beans with almonds
Wednesday Plain whole-milk yogurt, raspberries, pumpkin seeds Leftover chicken with chickpeas, cucumber, parsley, lemon, olive oil Mackerel fillets, roasted sweet potato, kale sauteed with garlic
Thursday Whole oats with grated apple, cinnamon, walnuts White bean and tomato salad with olive oil and basil, boiled egg Beef and vegetable stew (onion, carrot, celery, tomato) over brown rice
Friday Two eggs, tomatoes, avocado Sardines with brown rice, cucumber, olive oil, lemon Herring or salmon, roasted cauliflower, barley with parsley
Saturday Plain yogurt with strawberries and almonds Big salad: greens, chickpeas, olives, feta, olive oil, red onion Lamb with roasted aubergine and peppers, brown rice
Sunday Whole oats with blackberries and pumpkin seeds Vegetable and lentil soup, whole-grain bread, cheese Whole roast fish or chicken, roasted root vegetables, brown rice, green salad

Snacks: a handful of walnuts or almonds, an apple or a pear, plain yogurt, a boiled egg, olives, a square of dark chocolate. Drinks: water, tea, coffee if it agrees with you.

Making it survivable on bad days

RA has days when opening a tin is the hardest thing you will do. Build for those days in advance:

11. How to Test a Diet Change on Yourself

Because RA fluctuates on its own, the only way to learn anything from a personal diet experiment is to measure before you form an opinion. Here is a protocol that respects that.

  1. Set a baseline for two weeks before changing anything. Record daily: morning stiffness in minutes, pain 0–10, fatigue 0–10, and how many joints are tender. Two weeks of ordinary variation is your comparison.
  2. Change one thing. Adopt the Mediterranean pattern, or remove one suspect food — not both, and not five foods at once.
  3. Hold it for eight to twelve weeks. The Mediterranean trials took months, not days. Judging at two weeks guarantees a wrong answer.
  4. Keep your medication and your dose constant across the experiment. Changing two variables at once teaches you nothing about either.
  5. Use your bloods. CRP and ESR are drawn routinely anyway, and they are the closest thing you have to an opinion-proof measurement. Ask for your numbers and write them down.
  6. Compare the periods, not your memory. Memory of pain is unreliable and reliably biased toward whatever you hoped would happen.
  7. Tell your rheumatology team what you are doing. Not for permission — so that if your disease activity shifts, they can interpret it correctly rather than adjusting your drugs against a change you caused.

A last piece of perspective. Diet is one of the very few parts of RA you control completely, and that makes it emotionally loaded — which is exactly why it attracts both overpromising and unfair dismissal. A Mediterranean pattern built on whole food, a body weight you can maintain, no cigarettes, movement most days, and a medication regimen that actually controls your inflammation: that combination is supported by evidence, achievable in a real kitchen, and does not require you to buy anything unusual.

12. Key Research Papers

Every citation below was verified against the Crossref DOI registry before publication.

  1. Sköldstam L, Hagfors L, Johansson G. An experimental study of a Mediterranean diet intervention for patients with rheumatoid arthritis. Annals of the Rheumatic Diseases. 2003;62(3):208–214.
  2. McKellar G, Morrison E, McEntegart A, et al. A pilot study of a Mediterranean-type diet intervention in female patients with rheumatoid arthritis living in areas of social deprivation in Glasgow. Annals of the Rheumatic Diseases. 2007;66(9):1239–1243.
  3. Vadell AKE, Bärebring L, Hulander E, et al. Anti-inflammatory Diet In Rheumatoid Arthritis (ADIRA) — a randomized, controlled crossover trial indicating effects on disease activity. The American Journal of Clinical Nutrition. 2020.
  4. Erratum to “Anti-inflammatory Diet In Rheumatoid Arthritis (ADIRA) — a randomized, controlled crossover trial indicating effects on disease activity” [Am J Clin Nutr 111(6) (2020) 1203–1213]. The American Journal of Clinical Nutrition. 2023;118(6):1244. (The published correction referred to in section 2.)
  5. Winkvist A, Bärebring L, Gjertsson I, et al. A randomized controlled cross-over trial investigating the effect of anti-inflammatory diet on disease activity and quality of life in rheumatoid arthritis: the Anti-inflammatory Diet In Rheumatoid Arthritis (ADIRA) study protocol. Nutrition Journal. 2018;17:44.
  6. Kjeldsen-Kragh J, Borchgrevink CF, Laerum E, et al. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. The Lancet. 1991;338(8772):899–902.
  7. Nenonen MT, Helve TA, Rauma AL, Hanninen OO. Uncooked, lactobacilli-rich, vegan food and rheumatoid arthritis. British Journal of Rheumatology. 1998;37(3):274–281.
  8. Hartmann AM, Dell'Oro M, Spoo M, et al. To eat or not to eat — an exploratory randomized controlled trial on fasting and plant-based diet in rheumatoid arthritis (NutriFast-Study). Frontiers in Nutrition. 2022;9:1030380.
  9. Sköldstam L, Brudin L, Hagfors L, Johansson G. Weight reduction is not a major reason for improvement in rheumatoid arthritis from lacto-vegetarian, vegan or Mediterranean diets. Nutrition Journal. 2005;4:15.
  10. Darlington LG, Ramsey NW, Mansfield JR. Placebo-controlled, blind study of dietary manipulation therapy in rheumatoid arthritis. The Lancet. 1986;327(8475):236–238.
  11. Hagen KB, Byfuglien MG, Falzon L, et al. Dietary interventions for rheumatoid arthritis. Cochrane Database of Systematic Reviews. 2009.
  12. Scher JU, Sczesnak A, Longman RS, et al. Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis. eLife. 2013;2:e01202.
  13. Alpizar-Rodriguez D, Lesker TR, Gronow A, et al. Prevotella copri in individuals at risk for rheumatoid arthritis. Annals of the Rheumatic Diseases. 2019;78(5):590–593.
  14. Zhang X, Zhang D, Jia H, et al. The oral and gut microbiomes are perturbed in rheumatoid arthritis and partly normalized after treatment. Nature Medicine. 2015;21(8):895–905.
  15. Holers VM, Demoruelle MK, Kuhn KA, et al. Rheumatoid arthritis and the mucosal origins hypothesis: protection turns to destruction. Nature Reviews Rheumatology. 2018;14(9):542–557.
  16. Liu Y, Hazlewood GS, Kaplan GG, et al. Impact of obesity on remission and disease activity in rheumatoid arthritis: a systematic review and meta-analysis. Arthritis Care & Research. 2017;69(2):157–165.
  17. Sandberg MEC, Bengtsson C, Källberg H, et al. Overweight decreases the chance of achieving good response and low disease activity in early rheumatoid arthritis. Annals of the Rheumatic Diseases. 2014;73(11):2029–2033.
  18. Scott IC, Tan R, Stahl D, et al. The protective effect of alcohol on developing rheumatoid arthritis: a systematic review and meta-analysis. Rheumatology. 2013;52(5):856–867.
  19. Sundström B, Johansson I, Rantapää-Dahlqvist S. Interaction between dietary sodium and smoking increases the risk for rheumatoid arthritis: results from a nested case-control study. Rheumatology. 2015;54(3):487–493.
  20. Kleinewietfeld M, Manzel A, Titze J, et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013;496(7446):518–522.
  21. Hahn J, Cook NR, Alexander EK, et al. Vitamin D and marine omega 3 fatty acid supplementation and incident autoimmune disease: VITAL randomized controlled trial. BMJ. 2022;376:e066452.
  22. Lin J, Liu J, Davies ML, Chen W. Serum vitamin D level and rheumatoid arthritis disease activity: review and meta-analysis. PLOS ONE. 2016;11(1):e0146351.
  23. Hu Y, Sparks JA, Malspeis S, et al. Long-term dietary quality and risk of developing rheumatoid arthritis in women. Annals of the Rheumatic Diseases. 2017;76(8):1357–1364.
  24. Aviña-Zubieta JA, Thomas J, Sadatsafavi M, Lehman AJ, Lacaille D. Risk of incident cardiovascular events in patients with rheumatoid arthritis: a meta-analysis of observational studies. Annals of the Rheumatic Diseases. 2012;71(9):1524–1529.
  25. Shea B, Swinden MV, Tanjong Ghogomu E, et al. Folic acid and folinic acid for reducing side effects in patients receiving methotrexate for rheumatoid arthritis. Cochrane Database of Systematic Reviews. 2013.
  26. Halegoua-DeMarzio D, Navarro V, Ahmad J, et al. Liver injury associated with turmeric — a growing problem: ten cases from the Drug-Induced Liver Injury Network (DILIN). The American Journal of Medicine. 2023;136(2):200–206.

Live PubMed Searches

These links run a fresh search on PubMed, so they stay current as new work is published.

  1. PubMed: Mediterranean diet in rheumatoid arthritis, randomized trials
  2. PubMed: fasting and vegetarian diet in rheumatoid arthritis
  3. PubMed: gut microbiome and rheumatoid arthritis
  4. PubMed: Prevotella copri and rheumatoid arthritis
  5. PubMed: mucosal-origins hypothesis of rheumatoid arthritis
  6. PubMed: elimination diets and food intolerance in rheumatoid arthritis
  7. PubMed: obesity, treatment response and remission in rheumatoid arthritis
  8. PubMed: rheumatoid cachexia and muscle loss
  9. PubMed: alcohol, methotrexate and liver risk in rheumatoid arthritis
  10. PubMed: dietary sodium and Th17 autoimmunity
  11. PubMed: vitamin D and rheumatoid arthritis disease activity
  12. PubMed: periodontitis, P. gingivalis and rheumatoid arthritis
  13. PubMed: dietary fibre, short-chain fatty acids and autoimmune arthritis
  14. PubMed: cardiovascular risk and diet in rheumatoid arthritis

13. Connections

Back to Table of Contents