Herbs and Supplements for Rheumatoid Arthritis

If you have rheumatoid arthritis, you have almost certainly been handed a bottle by someone who loves you. A neighbour swears by turmeric. A cousin sends a link about thunder god vine. The shop assistant recommends collagen. And you are left holding a capsule with no idea whether it is medicine, food, or wishful thinking — and no idea whether it will quietly interfere with the methotrexate that is actually holding your joints together.

This page is an honest audit of the non-omega-3 natural adjuncts people take for RA. (Fish oil gets its own page, because its evidence base is larger than everything here combined.) Every item below gets an explicit evidence tier, and where a supplement has documented harm, that harm sits in the same paragraph as the claim — not buried in a footnote where nobody reads it.

Two things worth saying once, clearly, so the rest of the page does not have to keep repeating them. First: nothing here is a substitute for a DMARD. RA is a disease that eats cartilage and bone, and the erosion happens whether or not you feel better. Feeling better on a herb while joint damage continues is the worst possible outcome. Second: tell your rheumatologist what you are taking, by name and dose. Not out of vague caution — several items on this page have documented interactions, or overlapping organ toxicity, with methotrexate, leflunomide, warfarin and the direct oral anticoagulants, and your prescriber cannot manage a risk they do not know about.

Table of Contents

  1. How to Read an Evidence Tier
  2. Curcumin and Turmeric
  3. Boswellia serrata (Indian Frankincense)
  4. Thunder God Vine (Tripterygium wilfordii)
  5. White Peony and Total Glucosides of Paeony
  6. Cat's Claw (Uncaria tomentosa)
  7. Ginger
  8. GLA: Borage, Evening Primrose, Blackcurrant Seed
  9. Vitamin D
  10. Probiotics
  11. Collagen
  12. Interactions That Actually Matter
  13. A Sane Order of Operations
  14. Key Research Papers
  15. Connections
  16. Featured Videos

How to Read an Evidence Tier

Supplement marketing collapses everything into one phrase: "clinically proven." That phrase does an enormous amount of dishonest work. A study in twelve mice and a thousand-patient randomised trial can both be described as clinical research by someone with a product to sell. So this page uses four tiers, and states which one applies before making any claim.

Two more points matter before the list starts. Osteoarthritis is not rheumatoid arthritis. OA is mechanical wear with secondary inflammation; RA is an autoimmune attack on the joint lining. A supplement that dulls OA knee pain may do nothing at all to an autoimmune synovium — and a very large share of the "arthritis supplement" literature is OA research wearing an RA label on the bottle. Wherever that borrowing is happening below, it is flagged.

And a small unblinded trial in a single centre is a hypothesis, not a finding. That is not snobbery. Joint pain is one of the most placebo-responsive symptoms in medicine; RA itself flares and remits on its own; and people who volunteer for a supplement trial are, by selection, people who expect supplements to work. Any of those three can manufacture an improvement with no drug effect whatsoever.

Curcumin and Turmeric

Tier: Preliminary. Genuinely promising mechanism, genuinely small trials, and one real safety signal that has grown in recent years.

Curcumin is the yellow pigment in turmeric root. In the laboratory it blocks NF-κB, the master switch that turns on the inflammatory genes driving RA synovitis — broadly the same territory several prescription drugs attack from other angles. That mechanism is not marketing; it is well characterised. The problem has always been getting the molecule into your blood.

The human trials

The most-quoted RA study is a small three-arm pilot in which patients received curcumin, diclofenac (a standard anti-inflammatory), or both. Patients on curcumin alone improved on disease-activity scoring at least as much as those on diclofenac, and tolerated it better. That result circulates online as though it settled the question. It did not: it was a pilot, it was small, and critically it had no placebo arm — so there is no way to separate a drug effect from the effect of being enrolled in a study and watched closely for weeks.

A later randomised, double-blind, placebo-controlled trial using a high-bioavailability curcumin formulation did find improvement in RA symptoms and inflammatory markers against placebo, at two different doses. Better design, real result. It is still one trial, in a small group, funded the way formulation studies usually are. One good trial plus one flawed trial equals "preliminary," not "proven."

The bioavailability caveat, which is really the whole story

Turmeric powder is only a few percent curcuminoids by weight, and what little you swallow is poorly absorbed, rapidly conjugated by the gut wall and liver, and excreted. Eating curry is a delightful habit and an unreliable drug-delivery system. Every serious curcumin product therefore does something to fix absorption:

Documented harm

For most people curcumin causes nothing worse than loose stools, reflux and a stained countertop. But the US Drug-Induced Liver Injury Network published a case series of ten turmeric-associated liver injuries, and those numbers are worth reading rather than filing under "rare": the injury was hepatocellular in nine of the ten, five patients were hospitalised, and one died of acute liver failure. Onset was typically one to four months after starting. Seven of the ten carried the HLA-B*35:01 allele, several times its background frequency — which suggests a genetically susceptible minority rather than a dose-dependent poison, and is no help to you at all, because nobody types for it before selling you a capsule. Three of the seven products chemically analysed also contained piperine, which by design pushes more of everything into the bloodstream.

This matters more in RA than in the general population, for one specific reason: methotrexate and leflunomide are already the liver's problem. Stacking a supplement with a documented hepatotoxicity signal on top of a drug that requires periodic liver monitoring is not a theoretical concern. If you take curcumin alongside a DMARD, your prescriber should know, and your liver function tests are what catch trouble early.

Curcumin also shows mild antiplatelet activity in laboratory work. On its own, unimportant. On top of warfarin, a DOAC, aspirin or a daily NSAID, it belongs on the list you hand your doctor.

Boswellia serrata (Indian Frankincense)

Tier: Preliminary — and largely borrowed from osteoarthritis.

Boswellia is the resin of a tree used in Ayurvedic medicine for joint complaints for a very long time. Its boswellic acids — particularly AKBA, acetyl-11-keto-β-boswellic acid — inhibit 5-lipoxygenase, the enzyme that manufactures leukotrienes. That is a genuinely different target from the COX pathway NSAIDs block, which is the interesting part: an anti-inflammatory route ibuprofen does not touch.

The clinical evidence is real but almost all of it is in knee osteoarthritis. A small double-blind crossover trial of Boswellia serrata extract in knee OA reported less pain, better knee flexion and longer walking distance than placebo. A later placebo-controlled trial of an AKBA-enriched extract in knee OA found improvement in pain and function, together with a fall in a cartilage-degrading enzyme measured in joint fluid.

Notice what is missing: rheumatoid arthritis. Boswellia has been tested in RA far less often, in smaller numbers, and with distinctly less encouraging results than the OA work. Anyone telling you Boswellia is "proven for rheumatoid arthritis" is quoting osteoarthritis trials at you. It may still help — leukotrienes are involved in RA synovitis and the mechanism is plausible — but "may still help" is exactly what Preliminary means.

Documented harm: Boswellia is one of the better-tolerated items on this page. Reported effects are mostly gastrointestinal — nausea, reflux, diarrhoea — with occasional rash. It has been shown to affect drug-metabolising enzymes in laboratory systems, so if you take a narrow-margin drug it belongs on your list, though there is no well-documented clinical interaction disaster to point at. Practical note: products vary enormously in boswellic acid content, and standardisation to AKBA specifically (rather than to total boswellic acids) is what the better trials used.

Thunder God Vine (Tripterygium wilfordii)

Tier: Reasonable evidence for efficacy — alongside genuine, documented, sometimes irreversible toxicity. Both halves of that sentence are true at the same time, and you should not read one without the other.

This is the most important entry on the page, because it is the one where the usual reassurance — "it probably won't work, but it probably won't hurt" — is exactly backwards. Thunder god vine probably does work. It can also seriously hurt you.

The efficacy evidence is not weak

A Chinese randomised trial compared a Tripterygium wilfordii extract on its own, methotrexate on its own, and the two combined, in patients with active RA over roughly six months. Extract monotherapy was not inferior to methotrexate, and the combination outperformed methotrexate alone. Earlier, a US randomised trial compared a Tripterygium extract with sulfasalazine and found significantly more patients reaching the standard ACR20 improvement benchmark on the extract — although dropout was high in both arms, which weakens the result.

These are not herbal-supplement studies in the usual sense. They are head-to-head comparisons against real DMARDs, with real endpoints, and the herb held its own. That is rare enough on this page to deserve emphasis: thunder god vine has the strongest efficacy signal of anything listed here.

Read that sentence carefully, though, because it is the one most likely to be misused. "Not inferior to methotrexate, in a controlled trial, using a pharmaceutical-grade Chinese extract, in patients whose blood counts and liver were being checked" is a completely different claim from "you can stop your DMARD and buy this instead." Nobody in those trials swapped a prescription for a supplement; they took a quality-controlled drug inside a study that was watching for the harms described next. Neither trial showed the herb protecting joints from erosion, either — both measured symptom response, not X-rays.

And the toxicity is why it is not standard care

A systematic review of randomised trials of Tripterygium in RA concluded that although efficacy signals were present, the trials were methodologically weak and adverse events were frequent enough to be a serious limitation. The documented adverse effects include:

What that means in practice

In China, Tripterygium preparations are pharmaceutical products with defined extraction, quality control and prescriber oversight. Outside China they are sold as dietary supplements, which means nobody has verified what is in the bottle, which plant part it came from, or how it was extracted — and that verification is precisely the step separating a DMARD-grade extract from a poison. A supplement-grade thunder god vine product is a bet on a supply chain you cannot inspect.

The honest summary: real drug-level activity, real drug-level toxicity, and no drug-level quality control in Western markets. If you are seriously considering it, that is a conversation with a rheumatologist, with baseline and repeated blood counts and liver and kidney testing — not a purchase.

White Peony and Total Glucosides of Paeony

Tier: Reasonable evidence within the Chinese clinical literature; weakly replicated outside it.

Total Glucosides of Paeony (TGP) is an extract of the root of Paeonia lactiflora — white peony, bai shao in traditional Chinese medicine — standardised mainly to paeoniflorin. Unlike almost everything else on this page, TGP is not a supplement in its home market: it is a licensed anti-rheumatic medicine in China, prescribed as an add-on to conventional DMARDs rather than instead of them.

Its proposed mechanism is unusual and worth understanding. TGP behaves as an immune modulator rather than a blanket immune suppressant — in experimental work it dampens overactive T-cell and macrophage responses while leaving baseline immune function comparatively intact. Whether that elegance translates into a clinically meaningful advantage is a separate question from whether the theory is attractive.

What emerges from systematic review is interesting in an unexpected way. TGP used as adjuvant therapy in RA is associated not only with symptom benefit but with a lower rate of adverse events than conventional therapy alone — in particular, fewer liver-enzyme elevations in patients taking methotrexate or leflunomide. In other words, its most reproducible effect in the literature may be as a liver-protective companion to DMARD therapy rather than as an anti-inflammatory in its own right. If that holds up, it is a genuinely useful role, just not the one the marketing emphasises.

The honest caveat: nearly all of this evidence comes from Chinese trials, many of them small, with blinding and allocation concealment frequently unclear. That is a description of the evidence base, not an accusation. Trials run where a therapy is already standard practice tend to be positive, and independent replication elsewhere is thin. The tier reflects exactly that: strong within one literature, unconfirmed outside it.

Documented harm: the main one is dose-related diarrhoea and abdominal discomfort, common enough to be the usual reason people stop. Rash and dizziness are reported. It is not recommended in pregnancy. And because it is taken alongside DMARDs, and plausibly alters how the liver handles them, it belongs on the list you give your rheumatologist — even though the direction of that particular interaction currently looks favourable.

Cat's Claw (Uncaria tomentosa)

Tier: Preliminary, resting on essentially one small trial — with a documented kidney safety signal in autoimmune disease.

Cat's claw is a woody Amazonian vine whose bark and root have long been used for inflammatory and infectious complaints. The RA evidence is a single small randomised, double-blind trial in which a freeze-dried extract was added to existing DMARD therapy and produced a reduction in the number of painful joints compared with placebo. Around forty patients, one centre, never convincingly repeated. That is a hypothesis, not a finding.

There is also a chemistry problem most product labels ignore. Uncaria tomentosa occurs as two chemotypes: one dominated by pentacyclic oxindole alkaloids (POAs), the other by tetracyclic oxindole alkaloids (TOAs). Laboratory work suggests the TOAs antagonise the POAs' immune effects, and the trial above deliberately used a POA-only preparation. Most retail products state neither chemotype — so a given bottle of cat's claw may contain the chemistry that was tested, the chemistry that opposes it, or an unknown mixture of both.

Documented harm: mostly mild — nausea, diarrhoea, headache, dizziness. But there is a published case report of acute kidney injury attributed to a cat's claw remedy in a patient with systemic lupus erythematosus, and that case carries weight here precisely because the patient had an autoimmune disease. Cat's claw is also widely marketed as an "immune booster," which is a strange thing to want in a disease where the immune system is the aggressor. There is no trial evidence that it worsens RA — but the marketing logic and the disease logic point in opposite directions, and that is worth noticing before you spend money on it.

Ginger

Tier: Preliminary for RA; better, though still modest, evidence in osteoarthritis.

Ginger's pungent compounds — gingerols and shogaols — inhibit both the COX and the lipoxygenase arms of inflammation, which is a broader block than an NSAID achieves. The mechanism is sound and the food is safe, which together make ginger one of the easier things on this page to justify trying.

In knee osteoarthritis, a reasonably sized randomised trial of a standardised ginger extract found a modest but statistically real reduction in knee pain on standing compared with placebo. Modest is the operative word — and, again, that is OA.

In actual rheumatoid arthritis, the best study is a randomised trial in which ginger supplementation over three months shifted the expression of immune-regulatory genes in patients' blood cells — increasing the regulatory T-cell transcription factor and decreasing pro-inflammatory ones — alongside improvement in disease activity. That is a mechanistically satisfying and genuinely interesting result. It is also a gene-expression study in a small group, and gene expression is not a swollen joint.

Documented harm: heartburn, reflux and a burning aftertaste, mostly at higher doses. The one usually flagged is ginger's antiplatelet activity, and it deserves an honest description rather than the standard blanket warning. Ginger inhibits platelet aggregation in laboratory work, and scattered case reports describe raised INRs — but a controlled crossover study in healthy volunteers found that ginger at recommended doses did not measurably change clotting status, or the pharmacokinetics or effect of warfarin. So the accurate position is unresolved: not an established interaction, and not a cleared one either, particularly at the gram-per-day doses supplements deliver on top of warfarin, a DOAC, aspirin, or the daily NSAID many RA patients are quietly still taking. That is a reason to write it on the list you give your prescriber, and to stop it a week or two before a planned dental extraction, joint injection or operation. It is not a reason to worry about the ginger in your cooking, which is nowhere near these doses.

GLA: Borage, Evening Primrose and Blackcurrant Seed Oil

Tier: Reasonable evidence — the best-supported non-omega-3 supplement on this page, from trials that are old, small, and used doses far above what most people actually swallow.

Gamma-linolenic acid is an omega-6 fatty acid, which sounds wrong until you follow the chemistry. Most dietary omega-6 travels down a pathway ending in arachidonic acid and inflammatory prostaglandins. GLA is a fork in that road: the body converts it largely to dihomo-gamma-linolenic acid, which feeds the series-1 prostaglandins — the anti-inflammatory ones — and competes with arachidonic acid along the way. It is one of the few genuinely counterintuitive results in nutritional immunology, and unusually, it held up when it was tested.

Two placebo-controlled randomised trials in rheumatoid arthritis reported reductions in joint tenderness and swelling. The earlier one gave 1.4 grams of GLA a day from borage seed oil over six months; the later one gave 2.8 grams a day of purified GLA as the free fatty acid against a sunflower-seed-oil placebo, and saw meaningful improvement in 14 of 22 patients versus 4 of 19 on placebo. Note the units: grams per day, not the milligrams in a typical capsule. A Cochrane review of oral herbal therapies for RA concluded that GLA — from evening primrose, borage or blackcurrant seed oil — showed potential benefit, while noting that the trials were small and often incompletely reported. In the crowded field of RA supplements, "the Cochrane review says it might work" is a comparatively strong position to occupy.

The dose problem nobody puts on the label

The RA trials used gram-level daily doses of GLA. The oils differ enormously in how much GLA they actually contain:

Do that arithmetic and the implication is stark: a typical evening primrose capsule regimen delivers a small fraction of the GLA used in the positive trials. A great many people have concluded "GLA didn't work for me" after taking a dose that was never tested in the first place. If you try GLA, the number to look for on the label is milligrams of GLA — not milligrams of oil.

Documented harm: the important one is specific to borage. Borage plants contain pyrrolizidine alkaloids, liver toxins capable of causing veno-occlusive disease with sustained exposure. Reputable borage oil is processed and certified PA-free, but that certification is exactly what a cheap product omits — and in someone already taking methotrexate, an uncertified borage oil is a poor gamble. Look for explicit "PA-free" or "certified free of pyrrolizidine alkaloids" labelling, and do not buy without it.

Beyond that: GI upset and soft stools are common at gram doses; the GLA oils have mild antiplatelet activity; and benefit in the trials took months to appear. If you are going to test GLA, test it for a season, not a fortnight.

Vitamin D

Tier: Reasonable evidence for preventing autoimmune disease and for correcting a deficiency. Weak evidence that it reduces disease activity once RA is established. Those are different claims, and they are constantly conflated.

Vitamin D is a hormone that regulates T-cell behaviour, and low vitamin D is very common in people with RA. Those two facts get welded together into a third claim — that taking vitamin D will calm your RA — which the evidence does not really support.

What the evidence does support:

Trials of vitamin D supplementation aimed specifically at lowering disease activity in established RA have been mixed and mostly unimpressive. The reasonable position: get your level measured, correct a deficiency because deficiency is worth correcting on its own terms, and do not expect a DMARD effect from it.

Documented harm: vitamin D is fat-soluble and does accumulate. Sustained very high intakes cause hypercalcaemia — nausea, confusion, kidney stones, kidney injury. The risk concentrates in people taking large doses long-term without ever testing, and in those also taking calcium supplements or thiazide diuretics. That is an argument for measuring rather than guessing, not an argument for avoidance.

Probiotics

Tier: Preliminary — and the joint-outcome evidence has been getting weaker rather than stronger.

The theory is genuinely compelling. RA is increasingly understood as a disease that may begin at mucosal surfaces — gum, gut, lung — before it ever reaches a joint, and the gut microbiome shapes the regulatory T cells that are supposed to prevent autoimmunity in the first place. Reset the microbiome, the argument goes, and you might reset the disease.

What the trials show is more sober, and the two meta-analyses that exist do not agree with each other — which is itself the finding. The first pooled nine trials in 361 patients and reported that the inflammatory cytokine IL-6 was significantly lower on probiotics but that disease activity score did not differ from placebo at all. The second, published a year later, found close to the mirror image: the inflammatory markers, IL-6 among them, did not move, C-reactive protein shifted only borderline, and yet disease activity score did improve. When two pooled analyses of largely overlapping small trials point opposite ways on both the biomarker and the clinical outcome, the honest reading is neither "probiotics work" nor "probiotics fail" — it is that the underlying trials are too small, and too varied in strain, dose and duration, to settle the question either way.

It is also worth knowing that one of the most-cited individual RA probiotic trials, frequently quoted in supplement marketing, now carries an Expression of Concern from its journal. That is not a retraction and not proof of wrongdoing, but it means the record is under question, and any summary leaning on that trial is leaning on something unstable. This page names it rather than quietly citing it.

Documented harm: for most people, gas and bloating in the first week and nothing more. The exception matters in RA specifically: in people who are substantially immunosuppressed — high-dose steroids, rituximab, combination biologic therapy, neutropenia — there are case reports of bacteraemia and fungaemia caused by the organisms in probiotic products. Rare, but real, and RA is a population where heavy immunosuppression is common. If you are on a biologic, ask before starting one.

Where the microbiome argument stands on firmer ground is food rather than capsules: fibre, fermented foods, and an eating pattern that feeds a diverse microbiome. That is covered on the diet page.

Collagen

Tier: Preliminary for undenatured type II collagen in RA — a fascinating early result that did not replicate. Essentially no RA evidence for the hydrolysed collagen powder sold in shops.

Collagen is scientifically the most interesting story on this page and the most badly misrepresented in retail, because two entirely different products share one word.

Undenatured type II collagen: the oral-tolerance idea

The idea is not "eat cartilage, build cartilage." It is immunological. Feeding an antigen in small amounts can teach the gut-associated immune system to tolerate it — the same principle underlying oral immunotherapy for food allergy. Since RA involves an immune attack on joint cartilage, feeding tiny doses of intact type II collagen might, in theory, retrain that response rather than suppress it.

An early trial published in Science tested exactly that and reported decreases in swollen and tender joint counts with oral chicken type II collagen, including a handful of complete remissions in the collagen group and none on placebo. It was a striking result and it launched a decade of follow-up work. The follow-up was much less exciting: a larger multicentre randomised placebo-controlled trial found only marginal effects overall, with a hint of benefit at the lowest dose — a dose-response pattern that is biologically plausible for oral tolerance and statistically fragile in practice.

So: a real mechanism, one dramatic early trial, weak replication. Preliminary. Not disproven, and not established either.

Hydrolysed collagen peptides: a different product entirely

The collagen powder sold for skin, hair and joints is hydrolysed — deliberately broken into short peptides and amino acids. That processing destroys the intact protein structure the oral-tolerance mechanism depends on. Whatever hydrolysed collagen does, it is not performing the Science trial's trick. There is some osteoarthritis evidence for undenatured type II collagen supplements affecting joint symptoms, and some general nutritional case that collagen peptides supply glycine and proline usefully — but for rheumatoid arthritis specifically the evidence for hydrolysed collagen is close to absent. It does not even qualify as Traditional use only, because a modern processed powder has no tradition standing behind it either. It is simply untested in this disease.

Documented harm: minimal. Mild GI upset, occasional unpleasant taste, and the usual allergy caveat for people sensitive to the source species (chicken, bovine, fish, eggshell membrane). Collagen is one of the few things on this page whose main cost is your money rather than your liver.

Interactions That Actually Matter

Most "herb-drug interaction" warnings are theoretical, derived from cell culture, and clinically irrelevant. A few are not. These are the ones worth acting on if you have RA.

If you take methotrexate or leflunomide

The organ to protect is the liver, and the mistake to avoid is stacking.

If you take warfarin, a DOAC, or daily aspirin

Bleeding risk is additive and largely invisible until suddenly it is not. A published review of clinically evidenced herb-warfarin interactions is the sober version of this list: many popular claims turn out to be poorly supported, and a handful are well documented.

If you take a biologic or a JAK inhibitor

Here the honest answer is that the evidence is thin and most of the caution is theoretical. Herbs marketed as "immune boosters" — echinacea, cat's claw, astragalus — rest on a premise that sits awkwardly beside a drug prescribed to suppress immunity, but there is no trial evidence that they neutralise a biologic. The documented risk is narrower and more concrete: live probiotic organisms in the significantly immunosuppressed, as described above. And grapefruit juice inhibits CYP3A4, which is relevant to several oral RA drugs — worth a specific question about your specific drug rather than a blanket rule.

A Sane Order of Operations

If you have read this far looking for a protocol, here is the honest one — ordered by benefit per unit of risk and expense.

  1. Take the DMARD. Nothing on this page has been shown to change radiographic progression. Methotrexate and the biologics do. Every month of undertreated inflammation is joint you do not get back.
  2. Take the folate you were prescribed, and correct a measured vitamin D deficiency. These are the two supplements with the clearest role in RA, and one of them is prescribed rather than chosen.
  3. Change one thing at a time, and give it three months. RA fluctuates on its own. Starting four supplements in one week guarantees you will never learn which, if any, did anything — and if a liver enzyme rises, nobody will know which bottle to stop.
  4. Keep a written list of everything you take, with doses, and give a copy to your rheumatologist and your pharmacist. This one habit prevents most of the harms described on this page.
  5. Judge by joints, not by feelings. Morning stiffness duration, swollen joint count, and your CRP or ESR are outcomes you can actually check. "I think it's helping" is the least reliable instrument in the room — in both directions.
  6. Set a stop rule before you start. Decide in advance what would count as failure — no change in morning stiffness at twelve weeks, say — and then actually stop. Supplement cupboards grow because nobody ever writes down the exit condition.

And the point that deserves repeating: if you are drawn to thunder god vine precisely because it is the one with real efficacy data, then take its toxicity data every bit as seriously as its efficacy data. They come from the same trials.

Key Research Papers

  1. Chandran B, Goel A. A randomized, pilot study to assess the efficacy and safety of curcumin in patients with active rheumatoid arthritis. Phytotherapy Research, 2012;26(11):1719–1725.
  2. Amalraj A, Varma K, Jacob J, et al. A novel highly bioavailable curcumin formulation improves symptoms and diagnostic indicators in rheumatoid arthritis patients: a randomized, double-blind, placebo-controlled, two-dose, three-arm, and parallel-group study. Journal of Medicinal Food, 2017;20(10):1022–1030.
  3. Shoba G, Joy D, Joseph T, et al. Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers. Planta Medica, 1998;64(4):353–356.
  4. 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.
  5. Kimmatkar N, Thawani V, Hingorani L, Khiyani R. Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee — a randomized double blind placebo controlled trial. Phytomedicine, 2003;10(1):3–7.
  6. Sengupta K, Alluri KV, Satish AR, et al. A double blind, randomized, placebo controlled study of the efficacy and safety of 5-Loxin for treatment of osteoarthritis of the knee. Arthritis Research & Therapy, 2008;10(4):R85.
  7. Lv QW, Zhang W, Shi Q, et al. Comparison of Tripterygium wilfordii Hook F with methotrexate in the treatment of active rheumatoid arthritis (TRIFRA): a randomised, controlled clinical trial. Annals of the Rheumatic Diseases, 2015;74(6):1078–1086.
  8. Goldbach-Mansky R, Wilson M, Fleischmann R, et al. Comparison of Tripterygium wilfordii Hook F versus sulfasalazine in the treatment of rheumatoid arthritis. Annals of Internal Medicine, 2009;151(4):229–240.
  9. Canter PH, Lee HS, Ernst E. A systematic review of randomised clinical trials of Tripterygium wilfordii for rheumatoid arthritis. Phytomedicine, 2006;13(5):371–377.
  10. Liu B, Meng X, Ma Y, et al. Clinical safety of total glucosides of paeony adjuvant therapy for rheumatoid arthritis treatment: a systematic review and meta-analysis. BMC Complementary Medicine and Therapies, 2021;21(1).
  11. Mur E, Hartig F, Eibl G, Schirmer M. Randomized double blind trial of an extract from the pentacyclic alkaloid-chemotype of Uncaria tomentosa for the treatment of rheumatoid arthritis. The Journal of Rheumatology 2002;29(4):678–681. PubMed. — no DOI is registered for this article; the link runs a PubMed search for it.
  12. Hilepo JN, Bellucci AG, Mossey RT. Acute renal failure caused by 'cat's claw' herbal remedy in a patient with systemic lupus erythematosus. Nephron, 1997;77:361.
  13. Altman RD, Marcussen KC. Effects of a ginger extract on knee pain in patients with osteoarthritis. Arthritis & Rheumatism, 2001;44(11):2531–2538.
  14. Aryaeian N, Shahram F, Mahmoudi M, et al. The effect of ginger supplementation on some immunity and inflammation intermediate genes expression in patients with active rheumatoid arthritis. Gene, 2019;698:179–185.
  15. Zurier RB, Rossetti RG, Jacobson EW, et al. Gamma-linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial. Arthritis & Rheumatism, 1996;39(11):1808–1817.
  16. Leventhal LJ, Boyce EG, Zurier RB. Treatment of rheumatoid arthritis with gammalinolenic acid. Annals of Internal Medicine, 1993;119(9):867–873.
  17. Cameron M, Gagnier JJ, Chrubasik S. Herbal therapy for treating rheumatoid arthritis. Cochrane Database of Systematic Reviews, 2011;(2):CD002948.
  18. 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.
  19. 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.
  20. Mohammed AT, Khattab M, Ahmed AM, et al. The therapeutic effect of probiotics on rheumatoid arthritis: a systematic review and meta-analysis of randomized control trials. Clinical Rheumatology, 2017;36(12):2697–2707. — IL-6 fell; disease activity score did not move.
  21. Aqaeinezhad Rudbane SM, Rahmdel S, Abdollahzadeh SM, et al. The efficacy of probiotic supplementation in rheumatoid arthritis: a meta-analysis of randomized, controlled trials. Inflammopharmacology, 2018;26(1):67–76. — the opposite pattern: inflammatory markers unchanged, disease activity score improved. The two do not agree.
  22. Zamani B, Golkar HR, Farshbaf S, et al. Clinical and metabolic response to probiotic supplementation in patients with rheumatoid arthritis: a randomized, double-blind, placebo-controlled trial. International Journal of Rheumatic Diseases, 2016;19(9):869–879. — this record now carries an Expression of Concern from the journal. It is listed because it is widely cited, not because it should be relied on.
  23. Trentham DE, Dynesius-Trentham RA, Orav EJ, et al. Effects of oral administration of type II collagen on rheumatoid arthritis. Science, 1993;261(5129):1727–1730.
  24. Barnett ML, Kremer JM, St Clair EW, et al. Treatment of rheumatoid arthritis with oral type II collagen: results of a multicenter, double-blind, placebo-controlled trial. Arthritis & Rheumatism, 1998;41(2):290–297.
  25. Lugo JP, Saiyed ZM, Lane NE. Efficacy and tolerability of an undenatured type II collagen supplement in modulating knee osteoarthritis symptoms: a multicenter randomized, double-blind, placebo-controlled study. Nutrition Journal, 2016;15(1).
  26. Jiang X, Williams KM, Liauw WS, et al. Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. British Journal of Clinical Pharmacology, 2005;59(4):425–432. — the controlled study behind the ginger caveat above: no measurable effect on clotting status or on warfarin at recommended doses.
  27. Ge B, Zhang Z, Zuo Z. Updates on the clinical evidenced herb-warfarin interactions. Evidence-Based Complementary and Alternative Medicine, 2014;2014:957362.

Live PubMed Searches

These links run a fresh search every time you click them, so they surface work published after this page was written. They are also the honest way to check anything above that is labelled preliminary — tiers can change, and the evidence base for several of these herbs is still moving.

  1. PubMed: curcumin in rheumatoid arthritis, randomised trials
  2. PubMed: Boswellia serrata and rheumatoid arthritis
  3. PubMed: Tripterygium wilfordii in RA, adverse effects
  4. PubMed: total glucosides of paeony in rheumatoid arthritis
  5. PubMed: Uncaria tomentosa (cat's claw) in rheumatoid arthritis
  6. PubMed: ginger in rheumatoid arthritis, clinical trials
  7. PubMed: gamma-linolenic acid in rheumatoid arthritis
  8. PubMed: borage oil, pyrrolizidine alkaloids and liver toxicity
  9. PubMed: vitamin D supplementation and RA disease activity
  10. PubMed: probiotics in rheumatoid arthritis, randomised trials
  11. PubMed: oral tolerance and type II collagen in RA
  12. PubMed: methotrexate, supplements and liver toxicity
  13. PubMed: herbal supplements, anticoagulants and bleeding risk
  14. PubMed: probiotic bacteraemia in immunocompromised patients

Connections

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