Title: Rheumatoid Arthritis and Diet

Key words: autoimmune disease, chronic inflammation, supplementation, PUFAs, antioxidants, minerals, NSAIDs,

Date: May 1999

Category: 13. Specific Conditions

Type: Article

Author: Dr van Rhijn


Rheumatoid Arthritis and Diet




Rheumatoid Arthritis (RA) is regarded as an autoimmune disease and involves chronic inflammation of the synovial membranes of the joints, with a prevalence of 1-3%. Implementation of dietary adjustments to alleviate discomfort for patients suffering from RA has been done for decades, but with little scientific evidence until recently. Evaluation has been notoriously difficult because RA patients, are a heterogeneous group, whose illnesses are triggered by various factors, with remissions and relapses, as well as confounded by a high placebo response. Symptoms may be alleviated by dietary adjustment and the scientific basis for this recommendation will be discussed.

Dietary Manipulation

Dietary therapy for RA can be divided into elimination and supplementation regimes.


Selective dietary elimination therapy is based on an exclusion phase (fasting or limited food access) lasting approximately a week to 10 days, followed a by a reintroduction phase of foods back into the diet with careful monitoring for reactions. The third phase of confirmatory double blind testing of the suspected culprits, responsible for the symptoms is probably the most reliable method for identification1, 2 and elimination for therapeutic purposes, but may take six to eight weeks to complete. There is convincing evidence to confirm that a significant minority of RA patients responds well to fasting3 and elimination diets4, 5, 6.

Although it is advisable to undertake dietary elimination therapy under medical supervision, it is generally safe provided the fasting period is brief with adequate fluid intake, and can be implemented and monitored by the patients themselves.

The improvement obtained by an elimination diet may be secondary to numerous mechanisms, ranging from reduction in food intolerance, variation in gut flora, change in antioxidant status, placebo response, psychological processes and weight reduction. The latter however does not appear to play a casual role in the improvement of rheumatoid patients7, but fasting followed by vegan and lactovegetarian diets appeared to give good results if continued for one year 8.


Polyunsaturated fatty acids (PUFA’s)

Parent essential fatty acids (EFA), n-6 Linoleic Acid (LA) and n-3 Alpha-Linolenic Acid (LNA) are essential unsaturated oils which have to be obtained from the diet, mainly from plant and fish or oil sources respectively. Gamma-Linolenic Acid (GLA), metabolised from LA or obtained from Evening Primrose Oil (EPO), is the parent substance of prostaglandin 1 (PGE1) and Dihomo-Gamma-Linolenic Acid (DGLA), which both provides anti-inflammatory activity in RA9, 10. This effect is also obtained from eicosapentaenoic (EPO) and docosahexaenoic acid, metabolites from further chain elongation of the n-3 series11.

It is well known that the diet of Greenland Eskimos is rich in oily fish (EFA) and associated with a low incidence of inflammatory and autoimmune disorders. Studies confirmed the anti-inflammatory effects and modest improvement in symptoms of RA following supplementation with fish oils12, 13. They are generally safe to take and enable reduction of NSAID’s, but caution is required in patients suffering from diabetes and those with haemorrhagic tendencies. Extra vitamin E is necessary for metabolism and as an antioxidant14. Significant clinical benefit has also been obtained olive oil was used a placebo in RA trials15. An anti-inflammatory effect can also be obtained from extracts of the green lip muscles (Seatone16 and Lyprinol17).


Highly reactive oxygen species (ROS) can be liberated18 during chronic inflammatory conditions such as RA, causing oxidative stress19, 20 and further joint damage21, 22. Raw vegetables and fruit contain natural antioxidants including enzymes (superoxide dismutase, glutathione peroxidase, dimethyl sulphoxide) and non-enzymes (carotenoids, tocopherols, phenols and ascorbate). Antioxidants counteract the potential inflammatory damage in RA and a low antioxidant status was found in RA patients, especially beta-carotene23. They act synergistically as free radical scavengers and their plasma concentrations are determined by dietary intake.


Selenium also acts as an antioxidant, (component of glutathione peroxidase), and although serum levels are relatively low in RA patients, evidence of clinical benefit after supplementation is conflicting24, 25. Research has also shown copper26 as well as zinc27 to be of benefit in alleviating symptoms of RA.

Other Substances

There is some evidence that supplementation with carbohydrates (Kureha), amino acids (Cysteine & Histidine) and proteolytic enzymes (Bromlain, Papain & Chymotrypsin), Polyphenols (Catechin, Cumerin & Quercetin) and even shark cartilage alleviates symptoms in RA. Claims of benefit from herbs such as Alfalfa, Boswella, Feverfew and Karawatake mushrooms lacks scientific evidence and is based on folklore.

Diet or not to Diet

To adhere to a demanding diet requires compliance and commitment. Practical problems include social disruption and taking the diet to extremes, leading to possible nutritional deficiencies especially in children. Patients require thorough investigation, proper diagnosis and prolonged supervision with regular follow up. The prescribed diet should be nutritionally adequate and balanced as well as financially viable. Patients also require emotional and practical support. Patients on non steroidal anti-inflammatory drugs (NSAID's) are prone to increased gut permeability, allowing absorption of antigens and toxins contributing to the symptoms of RA. Dietary manipulation may reduce pathogenic bacterial gut flora and therefor reducing disease symptoms by restoring the gut defences.



Although research has shown that dietary adjustments only benefit 5 – 40 % of patients suffering from RA, it is still worthwhile because the pharmaceutical alternative (NSAID's) may have substantial and deleterious side effects. Current understanding of the underlying mechanisms requires careful evaluation and more research are needed to clarify the issues. Ignorance about the benefit of dietary manipulation is great among the medical profession and patients alike, and education is urgently needed for both groups.



  1. Jewett, D.L. et al. A double-blind study of symptom provocation to determine food sensitivity. N. Engl. J.Med. 1990; 323: 429 – 433.
  2. Hunter, J.O. Food allergy and intolerance. Presc. J. 37, 4: 193 – 198.
  3. Kroker, G. et al. Fasting and Rheumatoid Arthritis. A multi-centre study. Clin. Ecol. 1984; 2: 137 – 144.
  4. Kavanagh, R. et al. The effect of elemental diet and the subsequent food reintroduction on rheumatoid arthritis. Br. J. Rheum. 1995; 34: 270 – 273.
  5. Beri, D. et al. Effects of dietary restrictions on disease activity in rheumatoid arthritis. Ann. Rheum. Dis. 1988; 47: 69 – 72.
  6. Gamlin, L. & Brostroff, H. Food sensitivity and rheumatoid arthritis. Environ. Toxicol. And Pharmac. 1997; 4: 43 - 49.
  7. Darlington, L.G. et al. Placebo controlled blind study of dietary manipulation therapy in rheumatoid arthritis. Lancet. 1986. I: 236 – 238.
  8. Kjeldsen-Kragh et al. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. 1991; 338: 899 - 902.
  9. Belch, J.J.F. et al. Effects of altering dietary essential fatty acids on requirements for non-steroidal anti-inflammatory drugs in patients with rheumatoid arthritis. Ann. Rheum. Dis. 1988; 47 ; 96 - 104.
  10. Horrobin, D.F. Nutritional and medical importance of gamma-linolenic acid. Prog. Lipid. Res. 1992; 31(2): 163 - 194.
  11. Darlington, L.G. Fish oils: what is the current view on their benefits in various diseases? Med. Dialog. 1994; 429:
  12. Kremer, J. et al. Fish oil fatty acid supplementation in active rheumatoid arthritis. Ann. Inter. Med. 1987; 106: 497 - 503.
  13. Sperling, R.A. et al. Effects dietary supplementation with marine fish oil on leucocyte lipid mediator generation and function in rheumatoid arthritis. Arthritis Rheum. 1987; 30: 988 - 997.
  14. Meydani, M. et al. Effects of long-term fish oil supplementation on vitamin E status and lipid peroxidation in women. J. Nutr. 1991; 121: 484 - 491.
  15. Brzeski, M. et al. Evening primrose oil in patients with rheumatoid arthritis and side effects of non-steroidal anti-inflammatory drugs. Br. J. Rheumat. 1991; 30: 370 - 372.
  16. Gibson, R.G. et al. Perna canaliculus in the treatment of arthritis. Practitioner, 1980; 224: 955 - 960.
  17. Whitehouse, M.W. et al. Anti-inflammatory activity of a lipid fraction (Lyprinol) from the NZ green lipid mussel. Inflammopharmacology. 1997; 5: 237 - 246.
  18. Farrell, A.J. et al. Increased concentrations of nitrite in synovial fluid and serum samples suggest increased nitric oxide synthesis in rheumatic disease. Ann. Rheum. Dis. 1992; 51: 1219 – 1222.
  19. Davies, J.M.S. et al. Inhibition of collagenase activity by N-chlorotaurine, a product of activated neutrophils. Arthritis Rheum. 1994; 37: 424 - 427.
  20. Stevens, C.R. et al. Localisation of xanthine oxidase to synovial endothelium. Ann. Rheum. Dis. 1991; 50: 760 – 762.
  21. Grootveld, M. et al. Oxidative damage to hyaluronate and glucose in synovial fluid during exercise of the inflamed rheumatoid joint. Detection of abnormal low molecular mass metabolites by proton-n.m.r. spectroscopy. Biochem. J. ; 273: 459 – 467.
  22. Chapman, M.L. et al. Increased carbonyl content of proteins in synovial patients with rheumatoid arthritis. J. Rheumat. 1989; 16; 15 – 18.
  23. Heliövaara, M. et al. Serum antioxidants and risk of rheumatoid arthritis. Ann. Rheum. Dis. 1994; 53:1, 51 - 53.
  24. Munthe, E. et al. Trace elements and rheumatoid arthritis pathogenic and therapeutic effect. Acta. Pharm. Toxicol. 1986; 59 (Suppl. 1): 365 - 373.
  25. Chaudière, J. et al. Mechanism of selenium-glutathione peroxidase and its inhibition by mercapto carboxylic acids and other mercapatans. J. Biol. Chem. 1984; 259: 1043 - 1050.
  26. Miesel, R. & Zuber, M. Copper-dependent antioxidases in inflammatory and autoimmune rheumatic diseases. Inflammation. 1993; 17:3, 283 - 294.
  27. Naveh, Y. et al. Zinc metabolism in rheumatoid arthritis: plasma and urinary zinc and relationship to disease activity. J. Rheumat. 1997; 34:4, 643 - 646.